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{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nLymphocytes in neuroprotection, cognition and emotion: is intolerance really the answer? Clinical, epidemiological and therapeutic studies indicate that some human depression is associated with proinflammatory cytokines, chronic inflammatory disorders, and inflammation-inducing lifestyle factors. Moreover depression can be induced by administration of proinflammatory cytokines, including IL-2 or IFN-α. However, recent studies in specific pathogen-free (SPF) rodents suggest a different--and potentially contradictory--relationship between immune processes and mental health. These studies suggest that effector T cells specific for central nervous system (CNS) antigens can assist recovery from an array of environmental insults ranging from nerve injury to psychological stress, while in contrast, regulatory T cells (Treg) oppose such recovery. Indeed, some reported effects of this so-called \"protective autoimmunity\" seem of direct relevance to depressive disorders. These findings pose a dilemma for those intending to manipulate inflammatory pathways as a treatment for depression. Should we administer anti-inflammatory treatments, or should we induce self-reactive T cells? We re-examine the rodent findings and outline immunological peculiarities of SPF rodents, the abnormal properties of their regulatory T cells, and the impact of gut microbiota. We find that \"protective autoimmunity\" is likely to be relevant only to very clean SPF animals that lack normal levels of activated T cells, CNS T cell traffic and mature Treg. The data indicate that even in SPF models the effectors of beneficial effects are not the proinflammatory autoimmune cells themselves, but rather unidentified regulatory cells. This reinterpretation of findings relevant to \"protective autoimmunity\" suggests that ongoing, and planned, clinical trials of anti-inflammatory strategies to treat depressive disorders are justified.",
"role": "user"
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"content": "Lymphocytes in neuroprotection, cognition and emotion: is <DDF>intolerance</DDF> really the answer? Clinical, epidemiological and therapeutic studies indicate that some <DDF>human depression</DDF> is associated with <chemical>proinflammatory cytokines</chemical>, <DDF>chronic inflammatory disorders</DDF>, and inflammation-inducing lifestyle factors. Moreover <DDF>depression</DDF> can be induced by administration of <chemical>proinflammatory cytokines</chemical>, including <chemical>IL-2</chemical> or <chemical>IFN-α</chemical>. However, recent studies in <animal>specific pathogen-free (SPF) rodents</animal> suggest a different--and potentially contradictory--relationship between immune processes and mental health. These studies suggest that effector T cells specific for <chemical>central nervous system (CNS) antigens</chemical> can assist recovery from an array of environmental insults ranging from <DDF>nerve injury</DDF> to <DDF>psychological stress</DDF>, while in contrast, regulatory T cells (Treg) oppose such recovery. Indeed, some reported effects of this so-called \"protective autoimmunity\" seem of direct relevance to <DDF>depressive disorders</DDF>. These findings pose a dilemma for those intending to manipulate inflammatory pathways as a treatment for <DDF>depression</DDF>. Should we administer anti-inflammatory treatments, or should we induce self-reactive T cells? We re-examine the rodent findings and outline immunological peculiarities of <animal>SPF rodents</animal>, the abnormal properties of their regulatory T cells, and the impact of <microbiome>gut microbiota</microbiome>. We find that \"protective autoimmunity\" is likely to be relevant only to very clean <animal>SPF animals</animal> that lack normal levels of activated T cells, CNS T cell traffic and mature Treg. The data indicate that even in SPF models the effectors of beneficial effects are not the proinflammatory autoimmune cells themselves, but rather unidentified regulatory cells. This reinterpretation of findings relevant to \"protective autoimmunity\" suggests that ongoing, and planned, clinical trials of anti-inflammatory strategies to treat <DDF>depressive disorders</DDF> are justified.",
"role": "assistant"
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24103493
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nExcess body weight during pregnancy and offspring obesity: potential mechanisms. The rates of child and adult obesity have increased in most developed countries over the past several decades. The health consequences of obesity affect both physical and mental health, and the excess body weight can be linked to an elevated risk for developing type 2 diabetes, cardiovascular problems, and depression. Among the factors that can influence the development of obesity are higher infant weights and increased weight gain, which are associated with higher risk for excess body weight later in life. In turn, mother's excess body weight during and after pregnancy can be linked to the risk for offspring overweight and obesity through dietary habits, mode of delivery and feeding, breast milk composition, and through the influence on infant gut microbiota. This review considers current knowledge of these potential mechanisms that threaten to create an intergenerational cycle of obesity.",
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"content": "<DDF>Excess body weight during pregnancy</DDF> and <DDF>offspring obesity</DDF>: potential mechanisms. The rates of <DDF>child and adult obesity</DDF> have increased in most developed countries over the past several decades. The health consequences of <DDF>obesity</DDF> affect both physical and mental health, and the <DDF>excess body weight</DDF> can be linked to an elevated risk for developing <DDF>type 2 diabetes</DDF>, <DDF>cardiovascular problems</DDF>, and <DDF>depression</DDF>. Among the factors that can influence the development of <DDF>obesity</DDF> are higher infant weights and increased weight gain, which are associated with higher risk for <DDF>excess body weight</DDF> later in life. In turn, mother's <DDF>excess body weight during and after pregnancy</DDF> can be linked to the risk for <DDF>offspring overweight</DDF> and <DDF>obesity</DDF> through dietary habits, mode of delivery and feeding, breast milk composition, and through the influence on <microbiome>infant gut microbiota</microbiome>. This review considers current knowledge of these potential mechanisms that threaten to create an intergenerational cycle of <DDF>obesity</DDF>.",
"role": "assistant"
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24798884
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPriming for health: gut microbiota acquired in early life regulates physiology, brain and behaviour. The infant gut microbiome is dynamic, and radical shifts in composition occur during the first 3 years of life. Disruption of these developmental patterns, and the impact of the microbial composition of our gut on brain and behaviour, has attracted much recent attention. Integrating these observations is an important new research frontier. Early-life perturbations of the developing gut microbiota can impact on the central nervous system and potentially lead to adverse mental health outcomes.",
"role": "user"
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{
"content": "Priming for health: <microbiome>gut microbiota</microbiome> acquired in early life regulates physiology, <anatomical location>brain</anatomical location> and behaviour. The <microbiome>infant gut microbiome</microbiome> is dynamic, and radical shifts in composition occur during the first 3 years of life. Disruption of these developmental patterns, and the impact of the microbial composition of our <anatomical location>gut</anatomical location> on <anatomical location>brain</anatomical location> and behaviour, has attracted much recent attention. Integrating these observations is an important new research frontier. Early-life perturbations of the <microbiome>developing gut microbiota</microbiome> can impact on the central nervous system and potentially lead to adverse mental health outcomes.",
"role": "assistant"
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24956966
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobiota and neurodevelopmental windows: implications for brain disorders. Gut microbiota is essential to human health, playing a major role in the bidirectional communication between the gastrointestinal tract and the central nervous system. The microbiota undergoes a vigorous process of development throughout the lifespan and establishes its symbiotic rapport with the host early in life. Early life perturbations of the developing gut microbiota can impact neurodevelopment and potentially lead to adverse mental health outcomes later in life. This review compares the parallel early development of the intestinal microbiota and the nervous system. The concept of parallel and interacting microbial-neural critical windows opens new avenues for developing novel microbiota-modulating based therapeutic interventions in early life to combat neurodevelopmental deficits and brain disorders.",
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{
"content": "Microbiota and neurodevelopmental windows: implications for <DDF>brain disorders</DDF>. <microbiome>Gut microbiota</microbiome> is essential to human health, playing a major role in the bidirectional communication between the <anatomical location>gastrointestinal tract</anatomical location> and the central nervous system. The microbiota undergoes a vigorous process of development throughout the lifespan and establishes its symbiotic rapport with the host early in life. Early life perturbations of the developing <microbiome>gut microbiota</microbiome> can impact neurodevelopment and potentially lead to adverse <DDF>mental health outcomes</DDF> later in life. This review compares the parallel early development of the <microbiome>intestinal microbiota</microbiome> and the nervous system. The concept of parallel and interacting microbial-neural critical windows opens new avenues for developing novel microbiota-modulating based therapeutic interventions in early life to combat <DDF>neurodevelopmental deficits</DDF> and <DDF>brain disorders</DDF>.",
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25173628
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nObese-type gut microbiota induce neurobehavioral changes in the absence of obesity. The prevalence of mental illness, particularly depression and dementia, is increased by obesity. Here, we test the hypothesis that obesity-associated changes in gut microbiota are intrinsically able to impair neurocognitive behavior in mice. Conventionally housed, nonobese, adult male C57BL/6 mice maintained on a normal chow diet were subjected to a microbiome depletion/transplantation paradigm using microbiota isolated from donors on either a high-fat diet (HFD) or control diet. Following re-colonization, mice were subjected to comprehensive behavioral and biochemical analyses. The mice given HFD microbiota had significant and selective disruptions in exploratory, cognitive, and stereotypical behavior compared with mice with control diet microbiota in the absence of significant differences in body weight. Sequencing-based phylogenetic analysis confirmed the presence of distinct core microbiota between groups, with alterations in α- and β-diversity, modulation in taxonomic distribution, and statistically significant alterations to metabolically active taxa. HFD microbiota also disrupted markers of intestinal barrier function, increased circulating endotoxin, and increased lymphocyte expression of ionized calcium-binding adapter molecule 1, toll-like receptor 2, and toll-like receptor 4. Finally, evaluation of brain homogenates revealed that HFD-shaped microbiota increased neuroinflammation and disrupted cerebrovascular homeostasis. Collectively, these data reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or pharmacologic manipulation of gut microbiota could attenuate the neurologic complications of obesity.",
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"content": "<microbiome>Obese-type gut microbiota</microbiome> induce <DDF>neurobehavioral changes</DDF> in the absence of <DDF>obesity</DDF>. The prevalence of <DDF>mental illness</DDF>, particularly <DDF>depression</DDF> and <DDF>dementia</DDF>, is increased by <DDF>obesity</DDF>. Here, we test the hypothesis that obesity-associated changes in <microbiome>gut microbiota</microbiome> are intrinsically able to impair neurocognitive behavior in <animal>mice</animal>. <animal>Conventionally housed, nonobese, adult male C57BL/6 mice</animal> maintained on a normal chow diet were subjected to a microbiome depletion/transplantation paradigm using microbiota isolated from <animal>donors</animal> on either a high-fat diet (HFD) or control diet. Following re-colonization, <animal>mice</animal> were subjected to comprehensive <biomedical technique>behavioral and biochemical analyses</biomedical technique>. The <animal>mice</animal> given <microbiome>HFD microbiota</microbiome> had significant and selective disruptions in <DDF>exploratory, cognitive, and stereotypical behavior</DDF> compared with <animal>mice</animal> with <microbiome>control diet microbiota</microbiome> in the absence of significant differences in body weight. <biomedical technique>Sequencing-based phylogenetic analysis</biomedical technique> confirmed the presence of distinct <microbiome>core microbiota</microbiome> between groups, with alterations in α- and β-diversity, modulation in taxonomic distribution, and statistically significant alterations to metabolically active taxa. <microbiome>HFD microbiota</microbiome> also disrupted markers of intestinal barrier function, increased <chemical>circulating endotoxin</chemical>, and increased lymphocyte expression of <gene>ionized calcium-binding adapter molecule 1</gene>, <gene>toll-like receptor 2</gene>, and <gene>toll-like receptor 4</gene>. Finally, evaluation of brain homogenates revealed that <microbiome>HFD-shaped microbiota</microbiome> increased <DDF>neuroinflammation</DDF> and disrupted cerebrovascular homeostasis. Collectively, these data reinforce the link between <DDF>gut dysbiosis</DDF> and <DDF>neurologic dysfunction</DDF> and suggest that dietary and/or pharmacologic manipulation of <microbiome>gut microbiota</microbiome> could attenuate the neurologic complications of <DDF>obesity</DDF>.",
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25231862
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nArtificial sweeteners induce glucose intolerance by altering the gut microbiota. Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.",
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{
"content": "<dietary supplement>Artificial sweeteners</dietary supplement> induce <DDF>glucose intolerance</DDF> by altering the <microbiome>gut microbiota</microbiome>. <dietary supplement>Non-caloric artificial sweeteners</dietary supplement> (<dietary supplement>NAS</dietary supplement>) are among the most widely used food additives worldwide, regularly consumed by <human>lean and obese individuals</human> alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of <DDF>glucose intolerance</DDF> through induction of compositional and functional alterations to the <microbiome>intestinal microbiota</microbiome>. These <DDF>NAS-mediated deleterious metabolic effects</DDF> are abrogated by <drug>antibiotic treatment</drug>, and are fully transferrable to <animal>germ-free mice</animal> upon faecal transplantation of microbiota configurations from <animal>NAS-consuming mice</animal>, or of microbiota anaerobically incubated in the presence of <dietary supplement>NAS</dietary supplement>. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to <DDF>metabolic disease</DDF>, and demonstrate similar <DDF>NAS-induced dysbiosis</DDF> and <DDF>glucose intolerance</DDF> in <human>healthy human subjects</human>. Collectively, our results link NAS consumption, <DDF>dysbiosis</DDF> and <DDF>metabolic abnormalities</DDF>, thereby calling for a reassessment of massive NAS usage.",
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26129950
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAntibiotic-induced imbalances in gut microbiota aggravates cholesterol accumulation and liver injuries in rats fed a high-cholesterol diet. Increasing evidence suggests that maintenance of homeostasis between gut microbiota and host plays an important role in human health. Many diseases, such as those affecting the liver, have been linked to imbalances in gut microbial communities. However, it is not clear whether an imbalance in gut microbiota promotes the onset of liver injury or if the imbalance results from the pathological state. In the current study, antibiotics were used to disturb the gut microbiota of both rats fed a high-cholesterol diet and rats fed a normal diet (controls). The prevalence of Bacteroidetes and Firmicutes were reduced, and Proteobacteria was greatly increased in the guts of rats after antibiotic treatment. The antibiotic-induced perturbation of gut microbiota aggravated cholesterol accumulation and liver injury in rats fed a high-cholesterol diet. This may have been due to an increase in intestinal permeability and plasma lipopolysaccharide (LPS), which lead to an increase in LPS absorption and activation of TLR4 signaling, resulting in the synthesis of pro-inflammatory cytokines and chemokines in liver tissues. This study suggests that imbalances in gut microbiota may be a predisposing factor for the onset of metabolic diseases and liver injuries related to cholesterol and high-cholesterol diets. Modulation of gut microbiota could be a novel target for preventing cholesterol-related metabolic disorders.",
"role": "user"
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{
"content": "<DDF>Antibiotic-induced imbalances</DDF> in <microbiome>gut microbiota</microbiome> aggravates <DDF>cholesterol accumulation</DDF> and <DDF>liver injuries</DDF> in <animal>rats</animal> fed a <food>high-cholesterol diet</food>. Increasing evidence suggests that maintenance of homeostasis between <microbiome>gut microbiota</microbiome> and host plays an important role in human health. Many diseases, such as those affecting the <anatomical location>liver</anatomical location>, have been linked to imbalances in gut microbial communities. However, it is not clear whether an imbalance in <microbiome>gut microbiota</microbiome> promotes the onset of <DDF>liver injury</DDF> or if the imbalance results from the pathological state. In the current study, <drug>antibiotics</drug> were used to disturb the <microbiome>gut microbiota</microbiome> of both <animal>rats</animal> fed a <food>high-cholesterol diet</food> and <animal>rats</animal> fed a <food>normal diet</food> (controls). The prevalence of <bacteria>Bacteroidetes</bacteria> and <bacteria>Firmicutes</bacteria> were reduced, and <bacteria>Proteobacteria</bacteria> was greatly increased in the <anatomical location>guts</anatomical location> of <animal>rats</animal> after antibiotic treatment. The antibiotic-induced perturbation of <microbiome>gut microbiota</microbiome> aggravated <DDF>cholesterol accumulation</DDF> and <DDF>liver injury</DDF> in <animal>rats</animal> fed a <food>high-cholesterol diet</food>. This may have been due to an increase in intestinal permeability and <chemical>plasma lipopolysaccharide</chemical> (<chemical>LPS</chemical>), which lead to an increase in LPS absorption and activation of TLR4 signaling, resulting in the synthesis of <chemical>pro-inflammatory cytokines</chemical> and <chemical>chemokines</chemical> in <anatomical location>liver tissues</anatomical location>. This study suggests that imbalances in <microbiome>gut microbiota</microbiome> may be a predisposing factor for the onset of <DDF>metabolic diseases</DDF> and <DDF>liver injuries</DDF> related to <chemical>cholesterol</chemical> and <food>high-cholesterol diets</food>. Modulation of <microbiome>gut microbiota</microbiome> could be a novel target for preventing <DDF>cholesterol-related metabolic disorders</DDF>.",
"role": "assistant"
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26190966
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRole of neuroinflammation in the emotional and cognitive alterations displayed by animal models of obesity. Obesity is associated with a high prevalence of mood disorders and cognitive dysfunctions in addition to being a significant risk factor for important health complications such as cardiovascular diseases and type 2 diabetes. Identifying the pathophysiological mechanisms underlying these health issues is a major public health challenge. Based on recent findings, from studies conducted on animal models of obesity, it has been proposed that inflammatory processes may participate in both the peripheral and brain disorders associated with the obesity condition including the development of emotional and cognitive alterations. This is supported by the fact that obesity is characterized by peripheral low-grade inflammation, originating from increased adipose tissue mass and/or dysbiosis (changes in gut microbiota environment), both of which contribute to increased susceptibility to immune-mediated diseases. In this review, we provide converging evidence showing that obesity is associated with exacerbated neuroinflammation leading to dysfunction in vulnerable brain regions associated with mood regulation, learning, and memory such as the hippocampus. These findings give new insights to the pathophysiological mechanisms contributing to the development of brain disorders in the context of obesity and provide valuable data for introducing new therapeutic strategies for the treatment of neuropsychiatric complications often reported in obese patients.",
"role": "user"
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"content": "Role of <DDF>neuroinflammation</DDF> in the emotional and cognitive alterations displayed by animal models of <DDF>obesity</DDF>. <DDF>Obesity</DDF> is associated with a high prevalence of <DDF>mood disorders</DDF> and <DDF>cognitive dysfunctions</DDF> in addition to being a significant risk factor for important health complications such as <DDF>cardiovascular diseases</DDF> and <DDF>type 2 diabetes</DDF>. Identifying the pathophysiological mechanisms underlying these health issues is a major public health challenge. Based on recent findings, from studies conducted on animal models of <DDF>obesity</DDF>, it has been proposed that inflammatory processes may participate in both the <DDF>peripheral and brain disorders</DDF> associated with the <DDF>obesity</DDF> condition including the development of <DDF>emotional and cognitive alterations</DDF>. This is supported by the fact that <DDF>obesity</DDF> is characterized by <DDF>peripheral low-grade inflammation</DDF>, originating from increased adipose tissue mass and/or <DDF>dysbiosis</DDF> (changes in gut microbiota environment), both of which contribute to increased susceptibility to <DDF>immune-mediated diseases</DDF>. In this review, we provide converging evidence showing that <DDF>obesity</DDF> is associated with exacerbated <DDF>neuroinflammation</DDF> leading to <DDF>dysfunction</DDF> in <anatomical location>vulnerable brain regions</anatomical location> associated with mood regulation, learning, and memory such as the <anatomical location>hippocampus</anatomical location>. These findings give new insights to the pathophysiological mechanisms contributing to the development of <DDF>brain disorders</DDF> in the context of <DDF>obesity</DDF> and provide valuable data for introducing new therapeutic strategies for the treatment of <DDF>neuropsychiatric complications</DDF> often reported in <human>obese patients</human>.",
"role": "assistant"
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26408987
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAdministration of Lactobacillus helveticus NS8 improves behavioral, cognitive, and biochemical aberrations caused by chronic restraint stress. Increasing numbers of studies have suggested that the gut microbiota is involved in the pathophysiology of stress-related disorders. Chronic stress can cause behavioral, cognitive, biochemical, and gut microbiota aberrations. Gut bacteria can communicate with the host through the microbiota-gut-brain axis (which mainly includes the immune, neuroendocrine, and neural pathways) to influence brain and behavior. It is hypothesized that administration of probiotics can improve chronic-stress-induced depression. In order to examine this hypothesis, the chronic restraint stress depression model was established in this study. Adult specific pathogen free (SPF) Sprague-Dawley rats were subjected to 21 days of restraint stress followed by behavioral testing (including the sucrose preference test (SPT), elevated-plus maze test, open-field test (OFT), object recognition test (ORT), and object placement test (OPT)) and biochemical analysis. Supplemental Lactobacillus helveticus NS8 was provided every day during stress until the end of experiment, and selective serotonin reuptake inhibitor (SSRI) citalopram (CIT) served as a positive control. Results showed that L. helveticus NS8 improved chronic restraint stress-induced behavioral (anxiety and depression) and cognitive dysfunction, showing an effect similar to and better than that of CIT. L. helveticus NS8 also resulted in lower plasma corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels, higher plasma interleukin-10 (IL-10) levels, restored hippocampal serotonin (5-HT) and norepinephrine (NE) levels, and more hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression than in chronic stress rats. Taken together, these results indicate an anti-depressant effect of L. helveticus NS8 in rats subjected to chronic restraint stress depression and that this effect could be due to the microbiota-gut-brain axis. They also suggest the therapeutic potential of L. helveticus NS8 in stress-related and possibly other kinds of depression.",
"role": "user"
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{
"content": "Administration of <bacteria>Lactobacillus helveticus NS8</bacteria> improves <DDF>behavioral, cognitive, and biochemical aberrations</DDF> caused by <DDF>chronic restraint stress</DDF>. Increasing numbers of studies have suggested that the <microbiome>gut microbiota</microbiome> is involved in the pathophysiology of <DDF>stress-related disorders</DDF>. <DDF>Chronic stress</DDF> can cause <DDF>behavioral, cognitive, biochemical, and gut microbiota aberrations</DDF>. Gut bacteria can communicate with the host through the microbiota-gut-brain axis (which mainly includes the immune, neuroendocrine, and neural pathways) to influence <anatomical location>brain</anatomical location> and behavior. It is hypothesized that administration of <dietary supplement>probiotics</dietary supplement> can improve <DDF>chronic-stress-induced depression</DDF>. In order to examine this hypothesis, the chronic restraint stress depression model was established in this study. <animal>Adult specific pathogen free (SPF) Sprague-Dawley rats</animal> were subjected to 21 days of <DDF>restraint stress</DDF> followed by behavioral testing (including the <biomedical technique>sucrose preference test</biomedical technique> (<biomedical technique>SPT</biomedical technique>), <biomedical technique>elevated-plus maze test</biomedical technique>, <biomedical technique>open-field test</biomedical technique> (<biomedical technique>OFT</biomedical technique>), <biomedical technique>object recognition test</biomedical technique> (<biomedical technique>ORT</biomedical technique>), and <biomedical technique>object placement test</biomedical technique> (<biomedical technique>OPT</biomedical technique>)) and <biomedical technique>biochemical analysis</biomedical technique>. <dietary supplement>Supplemental Lactobacillus helveticus NS8</dietary supplement> was provided every day during <DDF>stress</DDF> until the end of experiment, and <drug>selective serotonin reuptake inhibitor (SSRI) citalopram</drug> (<drug>CIT</drug>) served as a positive control. Results showed that <dietary supplement>L. helveticus NS8</dietary supplement> improved <DDF>chronic restraint stress-induced behavioral</DDF> (<DDF>anxiety</DDF> and <DDF>depression</DDF>) and <DDF>cognitive dysfunction</DDF>, showing an effect similar to and better than that of <drug>CIT</drug>. <dietary supplement>L. helveticus NS8</dietary supplement> also resulted in lower plasma corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels, higher plasma <chemical>interleukin-10</chemical> (IL-10) levels, restored <chemical>hippocampal serotonin</chemical> (<chemical>5-HT</chemical>) and <chemical>norepinephrine</chemical> (<chemical>NE</chemical>) levels, and more hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression than in <animal>chronic stress rats</animal>. Taken together, these results indicate an anti-depressant effect of <dietary supplement>L. helveticus NS8</dietary supplement> in <animal>rats</animal> subjected to <DDF>chronic restraint stress depression</DDF> and that this effect could be due to the microbiota-gut-brain axis. They also suggest the therapeutic potential of <dietary supplement>L. helveticus NS8</dietary supplement> in stress-related and possibly other kinds of <DDF>depression</DDF>.",
"role": "assistant"
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26426677
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nNeuroimmune pharmacological approaches. Intestinal inflammation is a major health problem which impairs the quality of life, impacts mental health and is exacerbated by stress and psychiatric disturbances which, in turn, can affect disease prognosis and response to treatment. Accumulating evidence indicates that the immune system is an important interface between intestinal inflammation and the enteric, sensory, central and autonomic nervous systems. In addition, the neuroimmune interactions originating from the gastrointestinal tract are orchestrated by the gut microbiota. This article reviews some major insights into this complex homeostatic network that have been achieved during the past two years and attempts to put these advances into perspective with novel opportunities of pharmacological intervention.",
"role": "user"
},
{
"content": "Neuroimmune pharmacological approaches. <DDF>Intestinal inflammation</DDF> is a major health problem which impairs the quality of life, impacts mental health and is exacerbated by <DDF>stress</DDF> and <DDF>psychiatric disturbances</DDF> which, in turn, can affect disease prognosis and response to treatment. Accumulating evidence indicates that the immune system is an important interface between <DDF>intestinal inflammation</DDF> and the enteric, sensory, central and autonomic nervous systems. In addition, the neuroimmune interactions originating from the <anatomical location>gastrointestinal tract</anatomical location> are orchestrated by the <microbiome>gut microbiota</microbiome>. This article reviews some major insights into this complex homeostatic network that have been achieved during the past two years and attempts to put these advances into perspective with novel opportunities of <drug>pharmacological intervention</drug>.",
"role": "assistant"
}
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26627987
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiome in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. The gut microbiome comprises the collective genome of the trillions of microorganisms residing in our gastrointestinal ecosystem. The interaction between the host and its gut microbiome is a complex relationship whose manipulation could prove critical to preventing or treating not only various gut disorders, like irritable bowel syndrome (IBS) and ulcerative colitis (UC), but also central nervous system (CNS) disorders, such as Alzheimer's and Parkinson's diseases. The purpose of this review is to summarize what is known about the gut microbiome, how it is connected to the development of disease and to identify the bacterial and biochemical targets that should be the focus of future research. Understanding the mechanisms behind the activity and proliferation of the gut microbiome will provide us new insights that may pave the way for novel therapeutic strategies.",
"role": "user"
},
{
"content": "<microbiome>Gut microbiome</microbiome> in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of <DDF>systemic and neurodegenerative diseases</DDF>. The <microbiome>gut microbiome</microbiome> comprises the collective genome of the trillions of microorganisms residing in our gastrointestinal ecosystem. The interaction between the host and its <microbiome>gut microbiome</microbiome> is a complex relationship whose manipulation could prove critical to preventing or treating not only various <DDF>gut disorders</DDF>, like <DDF>irritable bowel syndrome</DDF> (<DDF>IBS</DDF>) and <DDF>ulcerative colitis</DDF> (<DDF>UC</DDF>), but also <DDF>central nervous system (CNS) disorders</DDF>, such as <DDF>Alzheimer's and Parkinson's diseases</DDF>. The purpose of this review is to summarize what is known about the <microbiome>gut microbiome</microbiome>, how it is connected to the development of disease and to identify the bacterial and biochemical targets that should be the focus of future research. Understanding the mechanisms behind the activity and proliferation of the <microbiome>gut microbiome</microbiome> will provide us new insights that may pave the way for novel therapeutic strategies.",
"role": "assistant"
}
] |
27319972
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobes, Immunity, and Behavior: Psychoneuroimmunology Meets the Microbiome. There is now a large volume of evidence to support the view that the immune system is a key communication pathway between the gut and brain, which plays an important role in stress-related psychopathologies and thus provides a potentially fruitful target for psychotropic intervention. The gut microbiota is a complex ecosystem with a diverse range of organisms and a sophisticated genomic structure. Bacteria within the gut are estimated to weigh in excess of 1 kg in the adult human and the microbes within not only produce antimicrobial peptides, short chain fatty acids, and vitamins, but also most of the common neurotransmitters found in the human brain. That the microbial content of the gut plays a key role in immune development is now beyond doubt. Early disruption of the host-microbe interplay can have lifelong consequences, not just in terms of intestinal function but in distal organs including the brain. It is clear that the immune system and nervous system are in continuous communication in order to maintain a state of homeostasis. Significant gaps in knowledge remain about the effect of the gut microbiota in coordinating the immune-nervous systems dialogue. However, studies using germ-free animals, infective models, prebiotics, probiotics, and antibiotics have increased our understanding of the interplay. Early life stress can have a lifelong impact on the microbial content of the intestine and permanently alter immune functioning. That early life stress can also impact adult psychopathology has long been appreciated in psychiatry. The challenge now is to fully decipher the molecular mechanisms that link the gut microbiota, immune, and central nervous systems in a network of communication that impacts behavior patterns and psychopathology, to eventually translate these findings to the human situation both in health and disease. Even at this juncture, there is evidence to pinpoint key sites of communication where gut microbial interventions either with drugs or diet or perhaps fecal microbiota transplantation may positively impact mental health.",
"role": "user"
},
{
"content": "Microbes, Immunity, and Behavior: Psychoneuroimmunology Meets the Microbiome. There is now a large volume of evidence to support the view that the immune system is a key communication pathway between the <anatomical location>gut</anatomical location> and <anatomical location>brain</anatomical location>, which plays an important role in <DDF>stress-related psychopathologies</DDF> and thus provides a potentially fruitful target for psychotropic intervention. The <microbiome>gut microbiota</microbiome> is a complex ecosystem with a diverse range of organisms and a sophisticated genomic structure. Bacteria within the <anatomical location>gut</anatomical location> are estimated to weigh in excess of 1 kg in the <human>adult human</human> and the microbes within not only produce <chemical>antimicrobial peptides</chemical>, <chemical>short chain fatty acids</chemical>, and <chemical>vitamins</chemical>, but also most of the common neurotransmitters found in the <anatomical location>human brain</anatomical location>. That the microbial content of the <anatomical location>gut</anatomical location> plays a key role in immune development is now beyond doubt. Early disruption of the host-microbe interplay can have lifelong consequences, not just in terms of intestinal function but in distal organs including the <anatomical location>brain</anatomical location>. It is clear that the immune system and nervous system are in continuous communication in order to maintain a state of homeostasis. Significant gaps in knowledge remain about the effect of the <microbiome>gut microbiota</microbiome> in coordinating the immune-nervous systems dialogue. However, studies using <animal>germ-free animals</animal>, infective models, <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>probiotics</dietary supplement>, and <drug>antibiotics</drug> have increased our understanding of the interplay. <DDF>Early life stress</DDF> can have a lifelong impact on the microbial content of the <anatomical location>intestine</anatomical location> and permanently alter immune functioning. That <DDF>early life stress</DDF> can also impact <DDF>adult psychopathology</DDF> has long been appreciated in psychiatry. The challenge now is to fully decipher the molecular mechanisms that link the <microbiome>gut microbiota</microbiome>, immune, and central nervous systems in a network of communication that impacts behavior patterns and psychopathology, to eventually translate these findings to the human situation both in health and disease. Even at this juncture, there is evidence to pinpoint key sites of communication where gut microbial interventions either with drugs or diet or perhaps fecal microbiota transplantation may positively impact mental health.",
"role": "assistant"
}
] |
27566465
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAlzheimer's disease and gut microbiota. Alzheimer's disease (AD) is a most common neurodegenerative disorder, which associates with impaired cognition. Gut microbiota can modulate host brain function and behavior via microbiota-gut-brain axis, including cognitive behavior. Germ-free animals, antibiotics, probiotics intervention and diet can induce alterations of gut microbiota and gut physiology and also host cognitive behavior, increasing or decreasing risks of AD. The increased permeability of intestine and blood-brain barrier induced by gut microbiota disturbance will increase the incidence of neurodegeneration disorders. Gut microbial metabolites and their effects on host neurochemical changes may increase or decrease the risk of AD. Pathogenic microbes infection will also increase the risk of AD, and meanwhile, the onset of AD support the \"hygiene hypothesis\". All the results suggest that AD may begin in the gut, and is closely related to the imbalance of gut microbiota. Modulation of gut microbiota through personalized diet or beneficial microbiota intervention will probably become a new treatment for AD.",
"role": "user"
},
{
"content": "<DDF>Alzheimer's disease</DDF> and <microbiome>gut microbiota</microbiome>. <DDF>Alzheimer's disease</DDF> (<DDF>AD</DDF>) is a most common <DDF>neurodegenerative disorder</DDF>, which associates with <DDF>impaired cognition</DDF>. <microbiome>Gut microbiota</microbiome> can modulate host brain function and behavior via microbiota-gut-brain axis, including cognitive behavior. <animal>Germ-free animals</animal>, <drug>antibiotics</drug>, <dietary supplement>probiotics</dietary supplement> intervention and diet can induce alterations of <microbiome>gut microbiota</microbiome> and gut physiology and also host cognitive behavior, increasing or decreasing risks of <DDF>AD</DDF>. The increased permeability of <anatomical location>intestine</anatomical location> and blood-brain barrier induced by <microbiome>gut microbiota</microbiome> disturbance will increase the incidence of <DDF>neurodegeneration disorders</DDF>. <chemical>Gut microbial metabolites</chemical> and their effects on host neurochemical changes may increase or decrease the risk of <DDF>AD</DDF>. <DDF>Pathogenic microbes infection</DDF> will also increase the risk of <DDF>AD</DDF>, and meanwhile, the onset of <DDF>AD</DDF> support the \"hygiene hypothesis\". All the results suggest that <DDF>AD</DDF> may begin in the <anatomical location>gut</anatomical location>, and is closely related to the imbalance of <microbiome>gut microbiota</microbiome>. Modulation of <microbiome>gut microbiota</microbiome> through personalized diet or beneficial microbiota intervention will probably become a new treatment for <DDF>AD</DDF>.",
"role": "assistant"
}
] |
27698624
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nIntegrative Therapies in Anxiety Treatment with Special Emphasis on the Gut Microbiome. Over the past decade, research has shown that diet and gut health affects symptoms expressed in stress related disorders, depression, and anxiety through changes in the gut microbiota. Psycho-behavioral function and somatic health interaction have often been ignored in health care with resulting deficits in treatment quality and outcomes. While mental health care requires the professional training in counseling, psychotherapy and psychiatry, complimentary therapeutic strategies, such as attention to a nutritional and diverse diet and supplementation of probiotic foods, may be integrated alongside psychotherapy treatment models. Development of these alternative strategies is predicated on experimental evidence and diligent research on the biology of stress, fear, anxiety-related behaviors, and the gut-brain connection. This article provides a brief overview on biological markers of anxiety and the expanding nutritional literature relating to brain health and mental disorders. A case study demonstrates an example of a biopsychosocial approach integrating cognitive psychotherapy, dietary changes, and mindfulness activities, in treating symptoms of anxiety. This case study shows a possible treatment protocol to explore the efficacy of targeting the gut-brain-axis that may be used as an impetus for future controlled studies.",
"role": "user"
},
{
"content": "Integrative Therapies in <DDF>Anxiety</DDF> Treatment with Special Emphasis on the <microbiome>Gut Microbiome</microbiome>. Over the past decade, research has shown that diet and gut health affects symptoms expressed in <DDF>stress related disorders</DDF>, <DDF>depression</DDF>, and <DDF>anxiety</DDF> through changes in the <microbiome>gut microbiota</microbiome>. Psycho-behavioral function and somatic health interaction have often been ignored in health care with resulting deficits in treatment quality and outcomes. While mental health care requires the professional training in counseling, psychotherapy and psychiatry, complimentary therapeutic strategies, such as attention to a nutritional and diverse diet and supplementation of <dietary supplement>probiotic foods</dietary supplement>, may be integrated alongside psychotherapy treatment models. Development of these alternative strategies is predicated on experimental evidence and diligent research on the biology of <DDF>stress</DDF>, <DDF>fear</DDF>, <DDF>anxiety-related behaviors</DDF>, and the gut-brain connection. This article provides a brief overview on biological markers of <DDF>anxiety</DDF> and the expanding nutritional literature relating to brain health and <DDF>mental disorders</DDF>. A case study demonstrates an example of a biopsychosocial approach integrating cognitive psychotherapy, dietary changes, and mindfulness activities, in treating symptoms of <DDF>anxiety</DDF>. This case study shows a possible treatment protocol to explore the efficacy of targeting the gut-brain-axis that may be used as an impetus for future controlled studies.",
"role": "assistant"
}
] |
27763700
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEarly life diets with prebiotics and bioactive milk fractions attenuate the impact of stress on learned helplessness behaviours and alter gene expression within neural circuits important for stress resistance. Manipulating gut microbes may improve mental health. Prebiotics are indigestible compounds that increase the growth and activity of health-promoting microorganisms, yet few studies have examined how prebiotics affect CNS function. Using an acute inescapable stressor known to produce learned helplessness behaviours such as failure to escape and exaggerated fear, we tested whether early life supplementation of a blend of two prebiotics, galactooligosaccharide (GOS) and polydextrose (PDX), and the glycoprotein lactoferrin (LAC) would attenuate behavioural and biological responses to stress later in life. Juvenile, male F344 rats were fed diets containing either GOS and PDX alone, LAC alone, or GOS, PDX and LAC. All diets altered gut bacteria, while diets containing GOS and PDX increased Lactobacillus spp. After 4 weeks, rats were exposed to inescapable stress, and either immediately killed for blood and tissues, or assessed for learned helplessness 24 h later. Diets did not attenuate stress effects on spleen weight, corticosterone and blood glucose; however, all diets differentially attenuated stress-induced learned helplessness. Notably, in situ hybridization revealed that all diets reduced stress-evoked cfos mRNA in the dorsal raphe nucleus (DRN), a structure important for learned helplessness behaviours. In addition, GOS, PDX and LAC diet attenuated stress-evoked decreases in mRNA for the 5-HT<sub>1A</sub> autoreceptor in the DRN and increased basal BDNF mRNA within the prefrontal cortex. These data suggest early life diets containing prebiotics and/or LAC promote behavioural stress resistance and uniquely modulate gene expression in corresponding circuits.",
"role": "user"
},
{
"content": "Early life diets with <dietary supplement>prebiotics</dietary supplement> and <dietary supplement>bioactive milk fractions</dietary supplement> attenuate the impact of <DDF>stress</DDF> on <DDF>learned helplessness behaviours</DDF> and alter gene expression within neural circuits important for stress resistance. Manipulating <microbiome>gut microbes</microbiome> may improve mental health. <dietary supplement>Prebiotics</dietary supplement> are indigestible compounds that increase the growth and activity of health-promoting microorganisms, yet few studies have examined how <dietary supplement>prebiotics</dietary supplement> affect CNS function. Using an acute inescapable stressor known to produce <DDF>learned helplessness behaviours</DDF> such as <DDF>failure to escape</DDF> and <DDF>exaggerated fear</DDF>, we tested whether early life supplementation of a blend of two <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>galactooligosaccharide</dietary supplement> (<dietary supplement>GOS</dietary supplement>) and <dietary supplement>polydextrose</dietary supplement> (<dietary supplement>PDX</dietary supplement>), and the glycoprotein <chemical>lactoferrin</chemical> (<chemical>LAC</chemical>) would attenuate behavioural and biological responses to <DDF>stress</DDF> later in life. <animal>Juvenile, male F344 rats</animal> were fed diets containing either <dietary supplement>GOS</dietary supplement> and <dietary supplement>PDX</dietary supplement> alone, <chemical>LAC</chemical> alone, or <dietary supplement>GOS</dietary supplement>, <dietary supplement>PDX</dietary supplement> and <chemical>LAC</chemical>. All diets altered <bacteria>gut bacteria</bacteria>, while diets containing <dietary supplement>GOS</dietary supplement> and <dietary supplement>PDX</dietary supplement> increased <bacteria>Lactobacillus spp.</bacteria> After 4 weeks, <animal>rats</animal> were exposed to <DDF>inescapable stress</DDF>, and either immediately killed for blood and tissues, or assessed for learned helplessness 24 h later. Diets did not attenuate stress effects on spleen weight, <chemical>corticosterone</chemical> and <chemical>blood glucose</chemical>; however, all diets differentially attenuated <DDF>stress-induced learned helplessness</DDF>. Notably, <biomedical technique>in situ hybridization</biomedical technique> revealed that all diets reduced <gene>stress-evoked cfos mRNA</gene> in the dorsal raphe nucleus (DRN), a structure important for <DDF>learned helplessness behaviours</DDF>. In addition, <dietary supplement>GOS</dietary supplement>, <dietary supplement>PDX</dietary supplement> and <chemical>LAC</chemical> diet attenuated <DDF>stress-evoked decreases in mRNA</DDF> for the <chemical>5-HT<sub>1A</sub> autoreceptor</chemical> in the DRN and increased <gene>basal BDNF mRNA</gene> within the <anatomical location>prefrontal cortex</anatomical location>. These data suggest early life diets containing <dietary supplement>prebiotics</dietary supplement> and/or LAC promote behavioural <DDF>stress resistance</DDF> and uniquely modulate gene expression in corresponding circuits.",
"role": "assistant"
}
] |
27793225
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Importance of Diet and Gut Health to the Treatment and Prevention of Mental Disorders. The departure from traditional lifestyles and the rising disease burden of mental disorders are increasing global health concerns. Changes in diet around the world mean that populations are now increasingly reliant on highly processed, poor quality foods, which have been linked to increased risk for mental disorder. Conversely, a nutrient-rich diet is understood to be protective of mental health, and researchers are now aiming to understand the biological underpinnings of this relationship. The gut microbiota has been proposed as a key mediator of this link, given its association with both diet and mental health. Importantly, several critical \"windows of opportunity\" for prevention and intervention have been identified, particularly early life and adolescence; these are periods of rapid development and transition that provide a foundation for future health. Strategies that promote overall diet quality, high in fiber and nutrients, have been linked to increased microbial diversity and gut health. Improving diet quality and subsequent gut health may have benefits for individuals' mental health, as well as the mental health of future generations. Here we discuss specific, targeted dietary and gut focused strategies for the prevention and treatment of mental disorder.",
"role": "user"
},
{
"content": "The Importance of Diet and Gut Health to the Treatment and Prevention of <DDF>Mental Disorders</DDF>. The departure from traditional lifestyles and the rising disease burden of <DDF>mental disorders</DDF> are increasing global health concerns. Changes in diet around the world mean that <human>populations</human> are now increasingly reliant on <food>highly processed, poor quality foods</food>, which have been linked to increased risk for <DDF>mental disorder</DDF>. Conversely, a <food>nutrient-rich diet</food> is understood to be protective of mental health, and researchers are now aiming to understand the biological underpinnings of this relationship. The <microbiome>gut microbiota</microbiome> has been proposed as a key mediator of this link, given its association with both diet and mental health. Importantly, several critical \"windows of opportunity\" for prevention and intervention have been identified, particularly early life and adolescence; these are periods of rapid development and transition that provide a foundation for future health. Strategies that promote overall diet quality, high in <dietary supplement>fiber</dietary supplement> and <food>nutrients</food>, have been linked to increased microbial diversity and gut health. Improving diet quality and subsequent gut health may have benefits for individuals' mental health, as well as the mental health of future generations. Here we discuss specific, targeted dietary and gut focused strategies for the prevention and treatment of <DDF>mental disorder</DDF>.",
"role": "assistant"
}
] |
27900676
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nFunctional Implications of the IL-23/IL-17 Immune Axis in Schizophrenia. The aetiology of schizophrenia seems to stem from complex interactions amongst environmental, genetic, metabolic, immunologic and oxidative components. Chronic low-grade inflammation has been persistently linked to schizophrenia, and this has primarily been based on the findings derived from Th1/Th2 cytokine balance. While the IL-23/IL-17 axis plays crucial role in the pathogenesis of several immune-mediated disorders, it has remained relatively unexplored in neuropsychiatric disorders. Altered levels of cytokines related to IL-23/IL-17 axis have been observed in schizophrenia patients in a few studies. In addition, other indirect factors known to confer schizophrenia risk like complement activation and altered gut microbiota are shown to modulate the IL-23/IL-17 axis. These preliminary observations provide crucial clues about the functional implications of IL-23/IL-17 axis in schizophrenia. In this review, an attempt has been made to highlight the biology of IL-23/IL-17 axis and its relevance to schizophrenia risk and pathogenesis. Given the pathogenic potential of the IL-23/IL-17 axis, therapeutic targeting of this axis may be a promising approach to benefit patients suffering from this devastating disorder.",
"role": "user"
},
{
"content": "Functional Implications of the IL-23/IL-17 Immune Axis in <DDF>Schizophrenia</DDF>. The aetiology of <DDF>schizophrenia</DDF> seems to stem from complex interactions amongst environmental, genetic, metabolic, immunologic and oxidative components. <DDF>Chronic low-grade inflammation</DDF> has been persistently linked to <DDF>schizophrenia</DDF>, and this has primarily been based on the findings derived from Th1/Th2 cytokine balance. While the IL-23/IL-17 axis plays crucial role in the pathogenesis of several <DDF>immune-mediated disorders</DDF>, it has remained relatively unexplored in <DDF>neuropsychiatric disorders</DDF>. Altered levels of <chemical>cytokines</chemical> related to IL-23/IL-17 axis have been observed in <human>schizophrenia patients</human> in a few studies. In addition, other indirect factors known to confer schizophrenia risk like complement activation and altered <microbiome>gut microbiota</microbiome> are shown to modulate the IL-23/IL-17 axis. These preliminary observations provide crucial clues about the functional implications of IL-23/IL-17 axis in <DDF>schizophrenia</DDF>. In this review, an attempt has been made to highlight the biology of IL-23/IL-17 axis and its relevance to schizophrenia risk and pathogenesis. Given the pathogenic potential of the IL-23/IL-17 axis, therapeutic targeting of this axis may be a promising approach to benefit <human>patients</human> suffering from this devastating disorder.",
"role": "assistant"
}
] |
27930574
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nA MeSH-based text mining method for identifying novel prebiotics. Prebiotics contribute to the well-being of their host by altering the composition of the gut microbiota. Discovering new prebiotics is a challenging and arduous task due to strict inclusion criteria; thus, highly limited numbers of prebiotic candidates have been identified. Notably, the large numbers of published studies may contain substantial information attached to various features of known prebiotics that can be used to predict new candidates. In this paper, we propose a medical subject headings (MeSH)-based text mining method for identifying new prebiotics with structured texts obtained from PubMed. We defined an optimal feature set for prebiotics prediction using a systematic feature-ranking algorithm with which a variety of carbohydrates can be accurately classified into different clusters in accordance with their chemical and biological attributes. The optimal feature set was used to separate positive prebiotics from other carbohydrates, and a cross-validation procedure was employed to assess the prediction accuracy of the model. Our method achieved a specificity of 0.876 and a sensitivity of 0.838. Finally, we identified a high-confidence list of candidates of prebiotics that are strongly supported by the literature. Our study demonstrates that text mining from high-volume biomedical literature is a promising approach in searching for new prebiotics.",
"role": "user"
},
{
"content": "A <statistical technique>MeSH-based text mining method</statistical technique> for identifying <dietary supplement>novel prebiotics</dietary supplement>. <dietary supplement>Prebiotics</dietary supplement> contribute to the well-being of their host by altering the composition of the <microbiome>gut microbiota</microbiome>. Discovering new <dietary supplement>prebiotics</dietary supplement> is a challenging and arduous task due to strict inclusion criteria; thus, highly limited numbers of prebiotic candidates have been identified. Notably, the large numbers of published studies may contain substantial information attached to various features of known <dietary supplement>prebiotics</dietary supplement> that can be used to predict new candidates. In this paper, we propose a <statistical technique>medical subject headings (MeSH)-based text mining method</statistical technique> for identifying new <dietary supplement>prebiotics</dietary supplement> with structured texts obtained from PubMed. We defined an optimal feature set for prebiotics prediction using a <statistical technique>systematic feature-ranking algorithm</statistical technique> with which a variety of <chemical>carbohydrates</chemical> can be accurately classified into different clusters in accordance with their chemical and biological attributes. The optimal feature set was used to separate positive <dietary supplement>prebiotics</dietary supplement> from other <chemical>carbohydrates</chemical>, and a <statistical technique>cross-validation procedure</statistical technique> was employed to assess the prediction accuracy of the model. Our method achieved a specificity of 0.876 and a sensitivity of 0.838. Finally, we identified a high-confidence list of candidates of <dietary supplement>prebiotics</dietary supplement> that are strongly supported by the literature. Our study demonstrates that <statistical technique>text mining from high-volume biomedical literature</statistical technique> is a promising approach in searching for new <dietary supplement>prebiotics</dietary supplement>.",
"role": "assistant"
}
] |
28073356
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota disturbance during helminth infection: can it affect cognition and behaviour of children? Bidirectional signalling between the brain and the gastrointestinal tract is regulated at neural, hormonal, and immunological levels. Recent studies have shown that helminth infections can alter the normal gut microbiota. Studies have also shown that the gut microbiota is instrumental in the normal development, maturation and function of the brain. The pathophysiological pathways by which helminth infections contribute to altered cognitive function remain poorly understood. We put forward the hypothesis that gastrointestinal infections with parasitic worms, such as helminths, induce an imbalance of the gut-brain axis, which, in turn, can detrimentally manifest in brain development. Factors supporting this hypothesis are: 1) research focusing on intelligence and school performance in school-aged children has shown helminth infections to be associated with cognitive impairment, 2) disturbances in gut microbiota have been shown to be associated with important cognitive developmental effects, and 3) helminth infections have been shown to alter the gut microbiota structure. Evidence on the complex interactions between extrinsic (parasite) and intrinsic (host-derived) factors has been synthesised and discussed. While evidence in favour of the helminth-gut microbiota-central nervous system hypothesis is circumstantial, it would be unwise to rule it out as a possible mechanism by which gastrointestinal helminth infections induce childhood cognitive morbidity. Further empirical studies are necessary to test an indirect effect of helminth infections on the modulation of mood and behaviour through its effects on the gut microbiota.",
"role": "user"
},
{
"content": "<DDF>Gut microbiota disturbance</DDF> during <DDF>helminth infection</DDF>: can it affect cognition and behaviour of <human>children</human>? Bidirectional signalling between the <anatomical location>brain</anatomical location> and the <anatomical location>gastrointestinal tract</anatomical location> is regulated at neural, hormonal, and immunological levels. Recent studies have shown that <DDF>helminth infections</DDF> can alter the normal <microbiome>gut microbiota</microbiome>. Studies have also shown that the <microbiome>gut microbiota</microbiome> is instrumental in the normal development, maturation and function of the <anatomical location>brain</anatomical location>. The pathophysiological pathways by which <DDF>helminth infections</DDF> contribute to altered cognitive function remain poorly understood. We put forward the hypothesis that <DDF>gastrointestinal infections</DDF> with <animal>parasitic worms</animal>, such as <animal>helminths</animal>, induce an imbalance of the gut-brain axis, which, in turn, can detrimentally manifest in brain development. Factors supporting this hypothesis are: 1) research focusing on intelligence and school performance in <human>school-aged children</human> has shown <DDF>helminth infections</DDF> to be associated with <DDF>cognitive impairment</DDF>, 2) disturbances in <microbiome>gut microbiota</microbiome> have been shown to be associated with important cognitive developmental effects, and 3) <DDF>helminth infections</DDF> have been shown to alter the gut microbiota structure. Evidence on the complex interactions between extrinsic (parasite) and intrinsic (host-derived) factors has been synthesised and discussed. While evidence in favour of the helminth-gut microbiota-central nervous system hypothesis is circumstantial, it would be unwise to rule it out as a possible mechanism by which <DDF>gastrointestinal helminth infections</DDF> induce <DDF>childhood cognitive morbidity</DDF>. Further empirical studies are necessary to test an indirect effect of <DDF>helminth infections</DDF> on the modulation of mood and behaviour through its effects on the <microbiome>gut microbiota</microbiome>.",
"role": "assistant"
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28399458
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe role of maternal anxiety and depressive disorders prior to and during pregnancy and perinatal psychopathological symptoms for early infant diseases and drug administration. Maternal mental health prior to and during pregnancy has been shown to be associated with inflammatory diseases and gastrointestinal complaints in the offspring. Unfortunately, many studies merely focused on perinatal distress without consideration of lifetime anxiety and depressive disorders. To prospectively investigate associations of anxiety and depressive disorders prior to and during pregnancy as well as perinatal distress with infants' inflammatory diseases, gastrointestinal complaints and corresponding drug administration. Prospective-longitudinal study initiated in 2009/2010. N=306 (expectant) mothers with and without DSM-IV lifetime anxiety and depressive disorders (Composite International Diagnostic Interview for Women) and low vs. high severity of psychopathological symptoms during pregnancy (Brief Symptom Inventory) enrolled in early pregnancy and repeatedly assessed during peripartum period. Infant inflammatory diseases, gastrointestinal complaints and drug administration assessed via questionnaire (maternal report) at four months postpartum (n=279). Severe psychopathological symptoms during pregnancy were associated with inflammatory diseases and anti-infective medication, whereas anxiety and depressive disorders prior to and during pregnancy were related to gastrointestinal complaints (diarrhea, colic complaints) and corresponding medication. These results have to be discussed with caution, because information on infants' diseases were based exclusively on maternal self-reports. However, they suggest promising directions regarding our current knowledge about the relevance of maternal perinatal distress for infant inflammatory diseases (e.g. fetal programming). Moreover, the association between maternal anxiety and depressive disorders and infant gastrointestinal complaints may be explained by an anxious misinterpretation of 'normal' infant signals or a transmission of adverse gut microbiota, respectively.",
"role": "user"
},
{
"content": "The role of <DDF>maternal anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy and <DDF>perinatal psychopathological symptoms</DDF> for <DDF>early infant diseases</DDF> and drug administration. Maternal mental health prior to and during pregnancy has been shown to be associated with <DDF>inflammatory diseases</DDF> and <DDF>gastrointestinal complaints</DDF> in the <human>offspring</human>. Unfortunately, many studies merely focused on <DDF>perinatal distress</DDF> without consideration of <DDF>lifetime anxiety</DDF> and <DDF>depressive disorders</DDF>. To prospectively investigate associations of <DDF>anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy as well as <DDF>perinatal distress</DDF> with <DDF>infants' inflammatory diseases</DDF>, <DDF>gastrointestinal complaints</DDF> and corresponding drug administration. Prospective-longitudinal study initiated in 2009/2010. N=306 <human>(expectant) mothers</human> with and without <DDF>DSM-IV lifetime anxiety and depressive disorders</DDF> (<biomedical technique>Composite International Diagnostic Interview for Women</biomedical technique>) and low vs. high severity of psychopathological symptoms during pregnancy (<biomedical technique>Brief Symptom Inventory</biomedical technique>) enrolled in early pregnancy and repeatedly assessed during peripartum period. <DDF>Infant inflammatory diseases</DDF>, <DDF>gastrointestinal complaints</DDF> and drug administration assessed via questionnaire (maternal report) at four months postpartum (n=279). Severe <DDF>psychopathological symptoms</DDF> during pregnancy were associated with <DDF>inflammatory diseases</DDF> and <drug>anti-infective medication</drug>, whereas <DDF>anxiety</DDF> and <DDF>depressive disorders</DDF> prior to and during pregnancy were related to <DDF>gastrointestinal complaints</DDF> (<DDF>diarrhea</DDF>, <DDF>colic complaints</DDF>) and corresponding medication. These results have to be discussed with caution, because information on <DDF>infants' diseases</DDF> were based exclusively on maternal self-reports. However, they suggest promising directions regarding our current knowledge about the relevance of <DDF>maternal perinatal distress</DDF> for <DDF>infant inflammatory diseases</DDF> (e.g. fetal programming). Moreover, the association between <DDF>maternal anxiety</DDF> and <DDF>depressive disorders</DDF> and <DDF>infant gastrointestinal complaints</DDF> may be explained by an anxious misinterpretation of 'normal' infant signals or a transmission of adverse <microbiome>gut microbiota</microbiome>, respectively.",
"role": "assistant"
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28442250
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAnalysis of microbiota in first episode psychosis identifies preliminary associations with symptom severity and treatment response. The effects of gut microbiota on the central nervous system, along its possible role in mental disorders, have received increasing attention. Here we investigated differences in fecal microbiota between 28 patients with first-episode psychosis (FEP) and 16 healthy matched controls and explored whether such differences were associated with response after up to 12months of treatment. Numbers of Lactobacillus group bacteria were elevated in FEP-patients and significantly correlated with severity along different symptom domains. A subgroup of FEP patients with the strongest microbiota differences also showed poorer response after up to 12months of treatment. The present findings support the involvement of microbiota alterations in psychotic illness and may provide the basis for exploring the benefit of their modulation on treatment response and remission.",
"role": "user"
},
{
"content": "Analysis of microbiota in <DDF>first episode psychosis</DDF> identifies preliminary associations with symptom severity and treatment response. The effects of <microbiome>gut microbiota</microbiome> on the central nervous system, along its possible role in <DDF>mental disorders</DDF>, have received increasing attention. Here we investigated differences in <microbiome>fecal microbiota</microbiome> between 28 <human>patients</human> with <DDF>first-episode psychosis</DDF> (<DDF>FEP</DDF>) and 16 <human>healthy matched controls</human> and explored whether such differences were associated with response after up to 12months of treatment. Numbers of <bacteria>Lactobacillus group bacteria</bacteria> were elevated in <human>FEP-patients</human> and significantly correlated with severity along different symptom domains. A subgroup of <human>FEP patients</human> with the strongest microbiota differences also showed poorer response after up to 12months of treatment. The present findings support the involvement of <DDF>microbiota alterations</DDF> in <DDF>psychotic illness</DDF> and may provide the basis for exploring the benefit of their modulation on treatment response and remission.",
"role": "assistant"
}
] |
28629758
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nImplications of the gut microbiota in vulnerability to the social avoidance effects of chronic social defeat in male mice. Appreciable evidence suggests that perturbations within the gut microbiome and the immune system may play a key role in the pathogenesis of depression stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with social avoidance behaviors, a feature of depression, and pro-inflammatory variations among socially stressed mice. Male C57BL/6 mice experienced social defeat or a control condition once a day for 10 consecutive days. Social avoidance behaviors were examined three weeks after the last defeat or control episode and blood, brain, and cecum contents were collected 24h afterward for the determination of corticosterone, pro-inflammatory cytokines, and microbial populations. Mice that were most susceptible to the behavioral effects of chronic social defeat (reflected by severe social avoidance behaviors) displayed the greatest changes within particular sets of bacteria at the phylum and genus taxonomic ranks. Although plasma and brain cytokines were not significantly altered in socially defeated mice, changes in the mRNA expression of interleukin (IL)-1β and IL-6 within the prefrontal cortex were associated with elevated abundance of Flavobacterium spp. and reduced abundance of Turicibacter spp., which were also strongly correlated to social avoidance severity. Although at this time a causal connection cannot be inferred, these results point to the possibility that specific clusters of bacterial communities in cecum contents may be linked to vulnerability to social deficits stemming from prolonged social stressor experiences.",
"role": "user"
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{
"content": "Implications of the <microbiome>gut microbiota</microbiome> in vulnerability to the <DDF>social avoidance effects</DDF> of <DDF>chronic social defeat</DDF> in <animal>male mice</animal>. Appreciable evidence suggests that perturbations within the <microbiome>gut microbiome</microbiome> and the immune system may play a key role in the pathogenesis of <DDF>depression</DDF> stemming from earlier stressful experiences. In the present investigation we examined whether microbial changes in cecum contents were associated with <DDF>social avoidance behaviors</DDF>, a feature of <DDF>depression</DDF>, and <DDF>pro-inflammatory variations</DDF> among <animal>socially stressed mice</animal>. <animal>Male C57BL/6 mice</animal> experienced social defeat or a control condition once a day for 10 consecutive days. <DDF>Social avoidance behaviors</DDF> were examined three weeks after the last defeat or control episode and blood, brain, and cecum contents were collected 24h afterward for the determination of <chemical>corticosterone</chemical>, <chemical>pro-inflammatory cytokines</chemical>, and microbial populations. <animal>Mice</animal> that were most susceptible to the behavioral effects of <DDF>chronic social defeat</DDF> (reflected by <DDF>severe social avoidance behaviors</DDF>) displayed the greatest changes within particular sets of bacteria at the phylum and genus taxonomic ranks. Although <chemical>plasma and brain cytokines</chemical> were not significantly altered in <animal>socially defeated mice</animal>, changes in the mRNA expression of <chemical>interleukin (IL)-1β</chemical> and <chemical>IL-6</chemical> within the <anatomical location>prefrontal cortex</anatomical location> were associated with elevated abundance of <bacteria>Flavobacterium spp.</bacteria> and reduced abundance of <bacteria>Turicibacter spp.</bacteria>, which were also strongly correlated to social avoidance severity. Although at this time a causal connection cannot be inferred, these results point to the possibility that specific clusters of bacterial communities in cecum contents may be linked to vulnerability to <DDF>social deficits</DDF> stemming from prolonged social stressor experiences.",
"role": "assistant"
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28816544
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAnimal inflammation-based models of depression and their application to drug discovery. Depression, anxiety and other affective disorders are globally widespread and severely debilitating human brain diseases. Despite their high prevalence and mental health impact, affective pathogenesis is poorly understood, and often remains recurrent and resistant to treatment. The lack of efficient antidepressants and presently limited conceptual innovation necessitate novel approaches and new drug targets in the field of antidepressant therapy. Areas covered: Herein, the authors discuss the emerging role of neuro-immune interactions in affective pathogenesis, which can become useful targets for CNS drug discovery, including modulating neuroinflammatory pathways to alleviate affective pathogenesis. Expert opinion: Mounting evidence implicates microglia, polyunsaturated fatty acids (PUFAs), glucocorticoids and gut microbiota in both inflammation and depression. It is suggested that novel antidepressants can be developed based on targeting microglia-, PUFAs-, glucocorticoid- and gut microbiota-mediated cellular pathways. In addition, the authors call for a wider application of novel model organisms, such as zebrafish, in studying shared, evolutionarily conserved (and therefore, core) neuro-immune mechanisms of depression.",
"role": "user"
},
{
"content": "Animal inflammation-based models of <DDF>depression</DDF> and their application to drug discovery. <DDF>Depression</DDF>, <DDF>anxiety</DDF> and other <DDF>affective disorders</DDF> are globally widespread and severely debilitating <DDF>human brain diseases</DDF>. Despite their high prevalence and mental health impact, affective pathogenesis is poorly understood, and often remains recurrent and resistant to treatment. The lack of efficient <drug>antidepressants</drug> and presently limited conceptual innovation necessitate novel approaches and new drug targets in the field of antidepressant therapy. Areas covered: Herein, the authors discuss the emerging role of neuro-immune interactions in affective pathogenesis, which can become useful targets for CNS drug discovery, including modulating neuroinflammatory pathways to alleviate <DDF>affective pathogenesis</DDF>. Expert opinion: Mounting evidence implicates microglia, <chemical>polyunsaturated fatty acids</chemical> (<chemical>PUFAs</chemical>), <chemical>glucocorticoids</chemical> and <microbiome>gut microbiota</microbiome> in both <DDF>inflammation</DDF> and <DDF>depression</DDF>. It is suggested that novel <drug>antidepressants</drug> can be developed based on targeting microglia-, PUFAs-, glucocorticoid- and gut microbiota-mediated cellular pathways. In addition, the authors call for a wider application of novel model organisms, such as <animal>zebrafish</animal>, in studying shared, evolutionarily conserved (and therefore, core) neuro-immune mechanisms of <DDF>depression</DDF>.",
"role": "assistant"
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28843021
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behavior disorder. Increasing evidence connects the gut microbiota and the onset and/or phenotype of Parkinson's disease (PD). Differences in the abundances of specific bacterial taxa have been reported in PD patients. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with idiopathic rapid eye movement sleep behavior disorder, a prodromal condition of α-synuclein aggregation disorders including PD. To compare microbiota in carefully preserved nasal wash and stool samples of subjects with idiopathic rapid eye movement sleep behavior disorder, manifest PD, and healthy individuals. Microbiota of flash-frozen stool and nasal wash samples from 76 PD patients, 21 idiopathic rapid eye movement sleep behavior disorder patients, and 78 healthy controls were assessed by 16S and 18S ribosomal RNA amplicon sequencing. Seventy variables, related to demographics, clinical parameters including nonmotor symptoms, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed. Differentially abundant gut microbes, such as Akkermansia, were observed in PD, but no strong differences in nasal microbiota. Eighty percent of the differential gut microbes in PD versus healthy controls showed similar trends in idiopathic rapid eye movement sleep behavior disorder, for example, Anaerotruncus and several Bacteroides spp., and correlated with nonmotor symptoms. Metagenomic sequencing of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms. Our study reveals differential abundances of gut microbial taxa in PD and its prodrome idiopathic rapid eye movement sleep behavior disorder in comparison to the healthy controls, and highlights the potential of metagenomics to identify and characterize microbial taxa, which are enriched or depleted in PD and/or idiopathic rapid eye movement sleep behavior disorder. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.",
"role": "user"
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{
"content": "The <microbiome>nasal and gut microbiome</microbiome> in <DDF>Parkinson's disease</DDF> and <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>. Increasing evidence connects the <microbiome>gut microbiota</microbiome> and the onset and/or phenotype of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). Differences in the abundances of specific bacterial taxa have been reported in <human>PD patients</human>. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, a prodromal condition of <DDF>α-synuclein aggregation disorders</DDF> including <DDF>PD</DDF>. To compare microbiota in carefully preserved nasal wash and stool samples of subjects with <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, <DDF>manifest PD</DDF>, and <human>healthy individuals</human>. Microbiota of flash-frozen stool and nasal wash samples from 76 <human>PD patients</human>, 21 <human>idiopathic rapid eye movement sleep behavior disorder patients</human>, and 78 <human>healthy controls</human> were assessed by <biomedical technique>16S and 18S ribosomal RNA amplicon sequencing</biomedical technique>. Seventy variables, related to demographics, clinical parameters including <DDF>nonmotor symptoms</DDF>, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed. Differentially abundant <bacteria>gut microbes</bacteria>, such as <bacteria>Akkermansia</bacteria>, were observed in <DDF>PD</DDF>, but no strong differences in <microbiome>nasal microbiota</microbiome>. Eighty percent of the differential <bacteria>gut microbes</bacteria> in <human>PD</human> versus <human>healthy controls</human> showed similar trends in <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>, for example, <bacteria>Anaerotruncus</bacteria> and several <bacteria>Bacteroides spp.</bacteria>, and correlated with <DDF>nonmotor symptoms</DDF>. <biomedical technique>Metagenomic sequencing</biomedical technique> of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms. Our study reveals differential abundances of gut microbial taxa in <DDF>PD</DDF> and its <DDF>prodrome idiopathic rapid eye movement sleep behavior disorder</DDF> in comparison to the <human>healthy controls</human>, and highlights the potential of <biomedical technique>metagenomics</biomedical technique> to identify and characterize microbial taxa, which are enriched or depleted in <DDF>PD</DDF> and/or <DDF>idiopathic rapid eye movement sleep behavior disorder</DDF>. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.",
"role": "assistant"
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28852308
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nInfluence of gut microbiota on neuropsychiatric disorders. The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced gut microbiota and its subsequent maintenance for future health of the host. Gut microbiota is currently viewed as a key regulator of a fluent bidirectional dialogue between the gut and the brain (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in neurodevelopmental and neurodegenerative disorders. Furthermore, alterations in the gut microbiota composition in humans have also been linked to a variety of neuropsychiatric conditions, including depression, autism and Parkinson's disease. However, it is not yet clear whether these changes in the microbiome are causally related to such diseases or are secondary effects thereof. In this respect, recent studies in animals have indicated that gut microbiota transplantation can transfer a behavioral phenotype, suggesting that the gut microbiota may be a modifiable factor modulating the development or pathogenesis of neuropsychiatric conditions. Further studies are warranted to establish whether or not the findings of preclinical animal experiments can be generalized to humans. Moreover, although different communication routes between the microbiota and brain have been identified, further studies must elucidate all the underlying mechanisms involved. Such research is expected to contribute to the design of strategies to modulate the gut microbiota and its functions with a view to improving mental health, and thus provide opportunities to improve the management of psychiatric diseases. Here, we review the evidence supporting a role of the gut microbiota in neuropsychiatric disorders and the state of the art regarding the mechanisms underlying its contribution to mental illness and health. We also consider the stages of life where the gut microbiota is more susceptible to the effects of environmental stressors, and the possible microbiota-targeted intervention strategies that could improve health status and prevent psychiatric disorders in the near future.",
"role": "user"
},
{
"content": "Influence of <microbiome>gut microbiota</microbiome> on <DDF>neuropsychiatric disorders</DDF>. The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced <microbiome>gut microbiota</microbiome> and its subsequent maintenance for future health of the host. <microbiome>Gut microbiota</microbiome> is currently viewed as a key regulator of a fluent bidirectional dialogue between the <anatomical location>gut</anatomical location> and the <anatomical location>brain</anatomical location> (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in <DDF>neurodevelopmental and neurodegenerative disorders</DDF>. Furthermore, alterations in the gut microbiota composition in <human>humans</human> have also been linked to a variety of <DDF>neuropsychiatric conditions</DDF>, including <DDF>depression</DDF>, <DDF>autism</DDF> and <DDF>Parkinson's disease</DDF>. However, it is not yet clear whether these changes in the microbiome are causally related to such diseases or are secondary effects thereof. In this respect, recent studies in <animal>animals</animal> have indicated that gut microbiota transplantation can transfer a behavioral phenotype, suggesting that the <microbiome>gut microbiota</microbiome> may be a modifiable factor modulating the development or pathogenesis of <DDF>neuropsychiatric conditions</DDF>. Further studies are warranted to establish whether or not the findings of preclinical animal experiments can be generalized to <human>humans</human>. Moreover, although different communication routes between the <microbiome>microbiota</microbiome> and <anatomical location>brain</anatomical location> have been identified, further studies must elucidate all the underlying mechanisms involved. Such research is expected to contribute to the design of strategies to modulate the <microbiome>gut microbiota</microbiome> and its functions with a view to improving mental health, and thus provide opportunities to improve the management of <DDF>psychiatric diseases</DDF>. Here, we review the evidence supporting a role of the <microbiome>gut microbiota</microbiome> in <DDF>neuropsychiatric disorders</DDF> and the state of the art regarding the mechanisms underlying its contribution to <DDF>mental illness</DDF> and health. We also consider the stages of life where the <microbiome>gut microbiota</microbiome> is more susceptible to the effects of environmental stressors, and the possible microbiota-targeted intervention strategies that could improve health status and prevent <DDF>psychiatric disorders</DDF> in the near future.",
"role": "assistant"
}
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29249803
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPossible role of the gut microbiota-brain axis in the antidepressant effects of (R)-ketamine in a social defeat stress model. Accumulating evidence suggests that the gut microbiota-brain axis plays a role in the pathogenesis of depression, thereby contributing to the antidepressant actions of certain compounds. (R)-ketamine has a greater potency and longer-lasting antidepressant effects than (S)-ketamine. Here, we investigated whether the gut microbiota plays a role in the antidepressant effects of these two ketamine enantiomers. The role of the gut microbiota in the antidepressant effects of ketamine enantiomers in a chronic social defeat stress (CSDS) model of depression was examined using 16S ribosomal RNA gene sequencing of fecal samples. At the phylum level, CSDS-susceptible mice showed alterations in the levels of Tenericutes and Actinobacteria; however, neither ketamine enantiomers influenced these alterations. At the class level, both ketamine enantiomers significantly attenuated the increase in the levels of Deltaproteobacteria in the susceptible mice after CSDS. Furthermore, (R)-ketamine, but not (S)-ketamine, significantly attenuated the reduction in the levels of Mollicutes in the susceptible mice. At the genus level, both ketamine enantiomers significantly attenuated the decrease in the levels of Butyricimonas in the susceptible mice. Notably, (R)-ketamine was more potent than (S)-ketamine at reducing the levels of Butyricimonas in the susceptible mice. In conclusion, this study suggests that the antidepressant effects of two enantiomers of ketamine in CSDS model may be partly mediated by the restoration of the gut microbiota. Furthermore, the specific effect of (R)-ketamine on the levels of Mollicutes and Butyricimonas may explain its robust antidepressant action.",
"role": "user"
},
{
"content": "Possible role of the gut microbiota-brain axis in the antidepressant effects of <drug>(R)-ketamine</drug> in a social defeat stress model. Accumulating evidence suggests that the gut microbiota-brain axis plays a role in the pathogenesis of <DDF>depression</DDF>, thereby contributing to the antidepressant actions of certain compounds. <drug>(R)-ketamine</drug> has a greater potency and longer-lasting antidepressant effects than <drug>(S)-ketamine</drug>. Here, we investigated whether the <microbiome>gut microbiota</microbiome> plays a role in the antidepressant effects of these two <drug>ketamine enantiomers</drug>. The role of the <microbiome>gut microbiota</microbiome> in the antidepressant effects of <drug>ketamine enantiomers</drug> in a chronic social defeat stress (CSDS) model of <DDF>depression</DDF> was examined using <biomedical technique>16S ribosomal RNA gene sequencing</biomedical technique> of fecal samples. At the phylum level, <animal>CSDS-susceptible mice</animal> showed alterations in the levels of <bacteria>Tenericutes</bacteria> and <bacteria>Actinobacteria</bacteria>; however, neither <drug>ketamine enantiomers</drug> influenced these alterations. At the class level, both <drug>ketamine enantiomers</drug> significantly attenuated the increase in the levels of <bacteria>Deltaproteobacteria</bacteria> in the <animal>susceptible mice</animal> after CSDS. Furthermore, <drug>(R)-ketamine</drug>, but not <drug>(S)-ketamine</drug>, significantly attenuated the reduction in the levels of <bacteria>Mollicutes</bacteria> in the <animal>susceptible mice</animal>. At the genus level, both <drug>ketamine enantiomers</drug> significantly attenuated the decrease in the levels of <bacteria>Butyricimonas</bacteria> in the <animal>susceptible mice</animal>. Notably, <drug>(R)-ketamine</drug> was more potent than <drug>(S)-ketamine</drug> at reducing the levels of <bacteria>Butyricimonas</bacteria> in the <animal>susceptible mice</animal>. In conclusion, this study suggests that the antidepressant effects of two enantiomers of <drug>ketamine</drug> in CSDS model may be partly mediated by the restoration of the <microbiome>gut microbiota</microbiome>. Furthermore, the specific effect of <drug>(R)-ketamine</drug> on the levels of <bacteria>Mollicutes</bacteria> and <bacteria>Butyricimonas</bacteria> may explain its robust antidepressant action.",
"role": "assistant"
}
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29955222
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAncient <i>Thali</i> Diet: Gut Microbiota, Immunity, and Health. Diet provides macronutrients (carbohydrates, proteins, and fats), micronutrients (vitamins and minerals), and phytochemicals (non-nutrient bioactive compounds). Emerging evidence suggests that above dietary components can directly impact the composition and metabolic activity of the mammalian gut microbiota and in turn, affect both physical and mental health. There is a growing recognition that rise in chronic disease burden in Western countries may due to progressive loss of beneficial bacteria and microbial diversity. This perspective explores the possibility of using Indian <i>thali</i>, an ancient approach to diet that provides both fiber and different phytochemicals by incorporating a variety of plant foods in different colors. This variety helps to restore diversity in the gut bacteria and may potentially prevent or reverse chronic disease, such as colon cancer or type 2 diabetes.",
"role": "user"
},
{
"content": "Ancient <i>Thali</i> Diet: <microbiome>Gut Microbiota</microbiome>, Immunity, and Health. Diet provides <chemical>macronutrients</chemical> (<chemical>carbohydrates</chemical>, <chemical>proteins</chemical>, and <chemical>fats</chemical>), <chemical>micronutrients</chemical> (<chemical>vitamins</chemical> and <chemical>minerals</chemical>), and <chemical>phytochemicals</chemical> (<chemical>non-nutrient bioactive compounds</chemical>). Emerging evidence suggests that above dietary components can directly impact the composition and metabolic activity of the <microbiome>mammalian gut microbiota</microbiome> and in turn, affect both physical and mental health. There is a growing recognition that rise in chronic disease burden in Western countries may due to progressive loss of beneficial bacteria and microbial diversity. This perspective explores the possibility of using Indian <i>thali</i>, an ancient approach to diet that provides both <chemical>fiber</chemical> and different <chemical>phytochemicals</chemical> by incorporating a variety of <food>plant foods</food> in different colors. This variety helps to restore diversity in the <bacteria>gut bacteria</bacteria> and may potentially prevent or reverse <DDF>chronic disease</DDF>, such as <DDF>colon cancer</DDF> or <DDF>type 2 diabetes</DDF>.",
"role": "assistant"
}
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30033172
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nTowards microbiome-informed dietary recommendations for promoting metabolic and mental health: Opinion papers of the MyNewGut project. The gut microbiota coexists in partnership with the human host through adaptations to environmental and physiological changes that help maintain dynamic homeostatic healthy states. Break-down of this delicate balance under sustained exposure to stressors (e.g. unhealthy diets) can, however, contribute to the onset of disease. Diet is a key modifiable environmental factor that modulates the gut microbiota and its metabolic capacities that, in turn, could impact human physiology. On this basis, the diet and the gut microbiota could act as synergistic forces that provide resilience against disease or that speed the progress from health to disease states. Associations between unhealthy dietary patterns, non-communicable diseases and intestinal dysbiosis can be explained by this hypothesis. Translational studies showing that dietary-induced alterations in microbial communities recapitulate some of the pathological features of the original host further support this notion. In this introductory paper by the European project MyNewGut, we briefly summarize the investigations conducted to better understand the role of dietary patterns and food components in metabolic and mental health and the specificities of the microbiome-mediating mechanisms. We also discuss how advances in the understanding of the microbiome's role in dietary health effects can help to provide acceptable scientific grounds on which to base dietary advice for promoting healthy living.",
"role": "user"
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{
"content": "Towards microbiome-informed dietary recommendations for promoting metabolic and mental health: Opinion papers of the MyNewGut project. The <microbiome>gut microbiota</microbiome> coexists in partnership with the <human>human host</human> through adaptations to environmental and physiological changes that help maintain dynamic homeostatic healthy states. Break-down of this delicate balance under sustained exposure to stressors (e.g. unhealthy diets) can, however, contribute to the onset of disease. Diet is a key modifiable environmental factor that modulates the <microbiome>gut microbiota</microbiome> and its metabolic capacities that, in turn, could impact human physiology. On this basis, the diet and the <microbiome>gut microbiota</microbiome> could act as synergistic forces that provide resilience against disease or that speed the progress from health to disease states. Associations between unhealthy dietary patterns, <DDF>non-communicable diseases</DDF> and <DDF>intestinal dysbiosis</DDF> can be explained by this hypothesis. Translational studies showing that <DDF>dietary-induced alterations</DDF> in microbial communities recapitulate some of the pathological features of the original host further support this notion. In this introductory paper by the European project MyNewGut, we briefly summarize the investigations conducted to better understand the role of dietary patterns and food components in metabolic and mental health and the specificities of the microbiome-mediating mechanisms. We also discuss how advances in the understanding of the microbiome's role in dietary health effects can help to provide acceptable scientific grounds on which to base dietary advice for promoting healthy living.",
"role": "assistant"
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30072879
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEffects of Sub-Chronic MPTP Exposure on Behavioral and Cognitive Performance and the Microbiome of Wild-Type and mGlu8 Knockout Female and Male Mice. Motor dysfunction is a hallmark of Parkinson's disease (PD); however, non-motor symptoms such as gastrointestinal dysfunction often arise prior to motor symptoms. Alterations in the gut microbiome have been proposed as the earliest event in PD pathogenesis. PD symptoms often demonstrate sex differences. Glutamatergic neurotransmission has long been linked to PD pathology. Metabotropic glutamate receptors (mGlu), a family of G protein-coupled receptors, are divided into three groups, with group III mGlu receptors mainly localized presynaptically where they can inhibit glutamate release in the CNS as well as in the gut. Additionally, the gut microbiome can communicate with the CNS via the gut-brain axis. Here, we assessed whether deficiency of metabotropic glutamate receptor 8 (mGlu8), group III mGlu, modulates the effects of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on behavioral and cognitive performance in female and male mice. We studied whether these effects are associated with changes in striatal tyrosine hydroxylase (TH) levels and the gut microbiome. Two-week sub-chronic MPTP increased activity of female and male wild-type (WT) and mGlu8 knockout (KO) mice in the open field. MPTP also showed genotype- and sex-dependent effects. MPTP increased the time WT, but not KO, females and males spent exploring objects. In WT mice, MPTP improved sensorimotor function in males but impaired it in females. Further, MPTP impaired cued fear memory in WT, but not KO, male mice. MPTP reduced striatal TH levels in WT and KO mice but these effects were only pronounced in males. MPTP treatment and genotype affected the diversity of the gut microbiome. In addition, there were significant associations between microbiome α-diversity and sensorimotor performance, as well as microbiome composition and fear learning. These results indicate that specific taxa may directly affect motor and fear learning or that the same physiological effects that enhance both forms of learning also alter diversity of the gut microbiome. MPTP's effect on motor and cognitive performance may then be, at least in part, be mediated by the gut microbiome. These data also support mGlu8 as a novel therapeutic target for PD and highlight the importance of including both sexes in preclinical studies.",
"role": "user"
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{
"content": "Effects of Sub-Chronic MPTP Exposure on Behavioral and Cognitive Performance and the Microbiome of <animal>Wild-Type and mGlu8 Knockout Female and Male Mice</animal>. <DDF>Motor dysfunction</DDF> is a hallmark of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>); however, non-motor symptoms such as <DDF>gastrointestinal dysfunction</DDF> often arise prior to motor symptoms. Alterations in the <microbiome>gut microbiome</microbiome> have been proposed as the earliest event in <DDF>PD pathogenesis</DDF>. PD symptoms often demonstrate sex differences. Glutamatergic neurotransmission has long been linked to <DDF>PD pathology</DDF>. <chemical>Metabotropic glutamate receptors</chemical> (<chemical>mGlu</chemical>), a family of <chemical>G protein-coupled receptors</chemical>, are divided into three groups, with <chemical>group III mGlu receptors</chemical> mainly localized presynaptically where they can inhibit glutamate release in the <anatomical location>CNS</anatomical location> as well as in the <anatomical location>gut</anatomical location>. Additionally, the <microbiome>gut microbiome</microbiome> can communicate with the <anatomical location>CNS</anatomical location> via the gut-brain axis. Here, we assessed whether deficiency of <chemical>metabotropic glutamate receptor 8</chemical> (<chemical>mGlu8</chemical>), <chemical>group III mGlu</chemical>, modulates the effects of the neurotoxin, <chemical>1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine</chemical> (<chemical>MPTP</chemical>), on behavioral and cognitive performance in <animal>female and male mice</animal>. We studied whether these effects are associated with changes in <gene>striatal tyrosine hydroxylase</gene> (<gene>TH</gene>) levels and the <microbiome>gut microbiome</microbiome>. Two-week sub-chronic MPTP increased activity of <animal>female and male wild-type (WT) and mGlu8 knockout (KO) mice</animal> in the open field. <chemical>MPTP</chemical> also showed genotype- and sex-dependent effects. <chemical>MPTP</chemical> increased the time <animal>WT</animal>, but not <animal>KO</animal>, females and males spent exploring objects. In <animal>WT mice</animal>, <chemical>MPTP</chemical> improved sensorimotor function in <animal>males</animal> but impaired it in <animal>females</animal>. Further, <chemical>MPTP</chemical> impaired cued fear memory in <animal>WT</animal>, but not <animal>KO</animal>, male mice. <chemical>MPTP</chemical> reduced striatal TH levels in <animal>WT and KO mice</animal> but these effects were only pronounced in <animal>males</animal>. MPTP treatment and genotype affected the diversity of the <microbiome>gut microbiome</microbiome>. In addition, there were significant associations between microbiome α-diversity and sensorimotor performance, as well as microbiome composition and fear learning. These results indicate that specific taxa may directly affect motor and fear learning or that the same physiological effects that enhance both forms of learning also alter diversity of the <microbiome>gut microbiome</microbiome>. MPTP's effect on motor and cognitive performance may then be, at least in part, be mediated by the <microbiome>gut microbiome</microbiome>. These data also support <chemical>mGlu8</chemical> as a novel therapeutic target for <DDF>PD</DDF> and highlight the importance of including both sexes in preclinical studies.",
"role": "assistant"
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30258234
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicroglia in neurodegeneration. The neuroimmune system is involved in development, normal functioning, aging, and injury of the central nervous system. Microglia, first described a century ago, are the main neuroimmune cells and have three essential functions: a sentinel function involved in constant sensing of changes in their environment, a housekeeping function that promotes neuronal well-being and normal operation, and a defense function necessary for responding to such changes and providing neuroprotection. Microglia use a defined armamentarium of genes to perform these tasks. In response to specific stimuli, or with neuroinflammation, microglia also have the capacity to damage and kill neurons. Injury to neurons in Alzheimer's, Parkinson's, Huntington's, and prion diseases, as well as in amyotrophic lateral sclerosis, frontotemporal dementia, and chronic traumatic encephalopathy, results from disruption of the sentinel or housekeeping functions and dysregulation of the defense function and neuroinflammation. Pathways associated with such injury include several sensing and housekeeping pathways, such as the Trem2, Cx3cr1 and progranulin pathways, which act as immune checkpoints to keep the microglial inflammatory response under control, and the scavenger receptor pathways, which promote clearance of injurious stimuli. Peripheral interference from systemic inflammation or the gut microbiome can also alter progression of such injury. Initiation or exacerbation of neurodegeneration results from an imbalance between these microglial functions; correcting such imbalance may be a potential mode for therapy.",
"role": "user"
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{
"content": "Microglia in <DDF>neurodegeneration</DDF>. The neuroimmune system is involved in development, normal functioning, aging, and injury of the central nervous system. Microglia, first described a century ago, are the main neuroimmune cells and have three essential functions: a sentinel function involved in constant sensing of changes in their environment, a housekeeping function that promotes neuronal well-being and normal operation, and a defense function necessary for responding to such changes and providing neuroprotection. Microglia use a defined armamentarium of genes to perform these tasks. In response to specific stimuli, or with <DDF>neuroinflammation</DDF>, microglia also have the capacity to damage and kill neurons. <DDF>Injury to neurons</DDF> in <DDF>Alzheimer's</DDF>, <DDF>Parkinson's</DDF>, <DDF>Huntington's</DDF>, and prion diseases, as well as in <DDF>amyotrophic lateral sclerosis</DDF>, <DDF>frontotemporal dementia</DDF>, and <DDF>chronic traumatic encephalopathy</DDF>, results from <DDF>disruption of the sentinel or housekeeping functions</DDF> and <DDF>dysregulation of the defense function</DDF> and <DDF>neuroinflammation</DDF>. Pathways associated with such injury include several sensing and housekeeping pathways, such as the <gene>Trem2</gene>, <gene>Cx3cr1</gene> and progranulin pathways, which act as immune checkpoints to keep the <DDF>microglial inflammatory response</DDF> under control, and the scavenger receptor pathways, which promote clearance of injurious stimuli. Peripheral interference from <DDF>systemic inflammation</DDF> or the <microbiome>gut microbiome</microbiome> can also alter progression of such injury. Initiation or exacerbation of <DDF>neurodegeneration</DDF> results from an imbalance between these microglial functions; correcting such imbalance may be a potential mode for therapy.",
"role": "assistant"
}
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30317530
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAn insight into gut microbiota and its functionalities. Gut microbiota has evolved along with their hosts and is an integral part of the human body. Microbiota acquired at birth develops in parallel as the host develops and maintains its temporal stability and diversity through adulthood until death. Recent developments in genome sequencing technologies, bioinformatics and culturomics have enabled researchers to explore the microbiota and in particular their functions at more detailed level than before. The accumulated evidences suggest that though a part of the microbiota is conserved, the dynamic members vary along the gastrointestinal tract, from infants to elderly, primitive tribes to modern societies and in different health conditions. Though the gut microbiota is dynamic, it performs some basic functions in the immunological, metabolic, structural and neurological landscapes of the human body. Gut microbiota also exerts significant influence on both physical and mental health of an individual. An in-depth understanding of the functioning of gut microbiota has led to some very exciting developments in therapeutics, such as prebiotics, probiotics, drugs and faecal transplantation leading to improved health.",
"role": "user"
},
{
"content": "An insight into <microbiome>gut microbiota</microbiome> and its functionalities. <microbiome>Gut microbiota</microbiome> has evolved along with their hosts and is an integral part of the <anatomical location>human body</anatomical location>. Microbiota acquired at birth develops in parallel as the host develops and maintains its temporal stability and diversity through adulthood until death. Recent developments in <biomedical technique>genome sequencing technologies</biomedical technique>, <biomedical technique>bioinformatics</biomedical technique> and <biomedical technique>culturomics</biomedical technique> have enabled researchers to explore the <microbiome>microbiota</microbiome> and in particular their functions at more detailed level than before. The accumulated evidences suggest that though a part of the <microbiome>microbiota</microbiome> is conserved, the dynamic members vary along the <anatomical location>gastrointestinal tract</anatomical location>, from <human>infants</human> to <human>elderly</human>, primitive tribes to modern societies and in different health conditions. Though the <microbiome>gut microbiota</microbiome> is dynamic, it performs some basic functions in the immunological, metabolic, structural and neurological landscapes of the <anatomical location>human body</anatomical location>. <microbiome>Gut microbiota</microbiome> also exerts significant influence on both physical and mental health of an <human>individual</human>. An in-depth understanding of the functioning of <microbiome>gut microbiota</microbiome> has led to some very exciting developments in therapeutics, such as <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>probiotics</dietary supplement>, <drug>drugs</drug> and faecal transplantation leading to improved health.",
"role": "assistant"
}
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30518033
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDifferences in Anxiety Levels of Various Murine Models in Relation to the Gut Microbiota Composition. Psychobiotics are probiotic strains that confer mental health benefits to the host through the modulation of the gut microbial population. Mounting evidence shows that the gut microbiota play an important role in communication within the gut⁻brain axis. However, the relationship between the host genetics and the gut microbiota and their influence on anxiety are still not fully understood. Hence, in our research, we attempted to draw a connection between host genetics, microbiota composition, and anxiety by performing an elevated plus maze (EPM) test on four genetically different mice. Four different breeds of 5-week-old mice were used in this experiment: Balb/c, Orient C57BL/6N, Taconic C57BL/6N, and Taconic C57BL/6J. After 1 week of adaptation, their initial anxiety level was monitored using the EPM test via an EthoVision XT, a standardized software used for behavorial testing. Significant differences in the initial anxiety level and microbial composition were detected. Subsequently, the microbiota of each group was modulated by the administration of either a probiotic, fecal microbiota transplantation, or antibiotics. Changes were observed in host anxiety levels in correlation to the shift of the gut microbiota. Our results suggest that the microbiota, host genetics, and psychological symptoms are strongly related, yet the deeper mechanistic links need further exploration.",
"role": "user"
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{
"content": "Differences in <DDF>Anxiety Levels</DDF> of Various Murine Models in Relation to the <microbiome>Gut Microbiota Composition</microbiome>. <dietary supplement>Psychobiotics</dietary supplement> are <dietary supplement>probiotic strains</dietary supplement> that confer mental health benefits to the host through the modulation of the gut microbial population. Mounting evidence shows that the <microbiome>gut microbiota</microbiome> play an important role in communication within the gut⁻brain axis. However, the relationship between the host genetics and the <microbiome>gut microbiota</microbiome> and their influence on <DDF>anxiety</DDF> are still not fully understood. Hence, in our research, we attempted to draw a connection between host genetics, microbiota composition, and <DDF>anxiety</DDF> by performing an <biomedical technique>elevated plus maze (EPM) test</biomedical technique> on four genetically different <animal>mice</animal>. Four different breeds of <animal>5-week-old mice</animal> were used in this experiment: <animal>Balb/c</animal>, <animal>Orient C57BL/6N</animal>, <animal>Taconic C57BL/6N</animal>, and <animal>Taconic C57BL/6J</animal>. After 1 week of adaptation, their initial <DDF>anxiety level</DDF> was monitored using the <biomedical technique>EPM test</biomedical technique> via an EthoVision XT, a standardized software used for <biomedical technique>behavorial testing</biomedical technique>. Significant differences in the initial <DDF>anxiety</DDF> level and microbial composition were detected. Subsequently, the microbiota of each group was modulated by the administration of either a <dietary supplement>probiotic</dietary supplement>, fecal microbiota transplantation, or <drug>antibiotics</drug>. Changes were observed in <DDF>host anxiety levels</DDF> in correlation to the shift of the <microbiome>gut microbiota</microbiome>. Our results suggest that the microbiota, host genetics, and <DDF>psychological symptoms</DDF> are strongly related, yet the deeper mechanistic links need further exploration.",
"role": "assistant"
}
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30528936
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRole of Actinobacteria and Coriobacteriia in the antidepressant effects of ketamine in an inflammation model of depression. Ketamine, an N-methyl-d-aspartic acid receptor (NMDAR) antagonist, elicits rapid-acting and sustained antidepressant effects in treatment-resistant depressed patients. Accumulating evidence suggests that gut microbiota via the gut-brain axis play a role in the pathogenesis of depression, thereby contributing to the antidepressant actions of certain compounds. Here we investigated the role of gut microbiota in the antidepressant effects of ketamine in lipopolysaccharide (LPS)-induced inflammation model of depression. Ketamine (10 mg/kg) significantly attenuated the increased immobility time in forced swimming test (FST), which was associated with the improvements in α-diversity, consisting of Shannon, Simpson and Chao 1 indices. In addition to α-diversity, β-diversity, such as principal coordinates analysis (PCoA), and linear discriminant analysis (LDA) coupled with effect size measurements (LEfSe), showed a differential profile after ketamine treatment. Furthermore, a total of 30 bacteria were significantly altered in the LPS + saline treated mice and LPS + ketamine treated mice. Interestingly, two bacteria, including the phylum Actinobacteria and the class Coriobacteriia were significantly correlated with the immobility time of FST. Importantly, the receiver operating characteristic (ROC) curves demonstrated that the phylum Actinobacteria and the class Coriobacteriia were potential biomarker for the antidepressant effects of ketamine in an inflammation model. These findings suggest that antidepressant effects of ketamine might be related to the regulation of abnormal composition of gut microbiota, and that the phylum Actinobacteria and the class Coriobacteriia might be potential biomarkers for ketamine's antidepressant efficacy.",
"role": "user"
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{
"content": "Role of <bacteria>Actinobacteria</bacteria> and <bacteria>Coriobacteriia</bacteria> in the antidepressant effects of <drug>ketamine</drug> in an inflammation model of <DDF>depression</DDF>. <drug>Ketamine</drug>, an <chemical>N-methyl-d-aspartic acid receptor</chemical> (<chemical>NMDAR</chemical>) antagonist, elicits rapid-acting and sustained antidepressant effects in <human>treatment-resistant depressed patients</human>. Accumulating evidence suggests that <microbiome>gut microbiota</microbiome> via the gut-brain axis play a role in the pathogenesis of <DDF>depression</DDF>, thereby contributing to the antidepressant actions of certain compounds. Here we investigated the role of <microbiome>gut microbiota</microbiome> in the antidepressant effects of <drug>ketamine</drug> in <DDF>lipopolysaccharide (LPS)-induced inflammation</DDF> model of <DDF>depression</DDF>. <drug>Ketamine</drug> (10 mg/kg) significantly attenuated the increased <DDF>immobility time</DDF> in <biomedical technique>forced swimming test</biomedical technique> (<biomedical technique>FST</biomedical technique>), which was associated with the improvements in α-diversity, consisting of <statistical technique>Shannon, Simpson and Chao 1 indices</statistical technique>. In addition to α-diversity, β-diversity, such as <statistical technique>principal coordinates analysis</statistical technique> (<statistical technique>PCoA</statistical technique>), and <statistical technique>linear discriminant analysis</statistical technique> (<statistical technique>LDA</statistical technique>) coupled with <statistical technique>effect size measurements</statistical technique> (<statistical technique>LEfSe</statistical technique>), showed a differential profile after <drug>ketamine</drug> treatment. Furthermore, a total of 30 bacteria were significantly altered in the <animal>LPS + saline treated mice</animal> and <animal>LPS + ketamine treated mice</animal>. Interestingly, two bacteria, including the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> were significantly correlated with the <DDF>immobility</DDF> time of <biomedical technique>FST</biomedical technique>. Importantly, the <statistical technique>receiver operating characteristic (ROC) curves</statistical technique> demonstrated that the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> were potential biomarker for the antidepressant effects of <drug>ketamine</drug> in an inflammation model. These findings suggest that antidepressant effects of <drug>ketamine</drug> might be related to the regulation of abnormal composition of <microbiome>gut microbiota</microbiome>, and that the phylum <bacteria>Actinobacteria</bacteria> and the class <bacteria>Coriobacteriia</bacteria> might be potential biomarkers for <drug>ketamine</drug>'s antidepressant efficacy.",
"role": "assistant"
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30659564
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nCan microbiology affect psychiatry? A link between gut microbiota and psychiatric disorders. Every single human consists of thousands of genes, billions of neurons and trillions of bacteria. There is a rapidly growing number of data that links the gut microbiome to the development and functioning of the central nervous system, which is a currently proposed paradigm shift in neuroscience. Knowledge on the relationship between gut microbiota and mental disorders is constantly increasing. This phenomenon is known as \"gut-brain axis\". The strongest evidence for the role of microbes in the gut-brain axis comes from animal studies. Nevertheless, the gutbrain crosstalk is a bidirectional communication system that not only provides gastrointestinal homeostasis, but can also affect motivation as well as higher cognitive functions. Moreover, gut microbiome can be associated with obesity and inflammatory gastrointestinal disorders. According to the recent studies, there is a link between the composition of gut microbiota and mental disorders in animals (response to depression and chronic stress). This subject requires further examination, especially taking into consideration potential therapeutic options.",
"role": "user"
},
{
"content": "Can microbiology affect psychiatry? A link between <microbiome>gut microbiota</microbiome> and <DDF>psychiatric disorders</DDF>. Every single human consists of thousands of genes, billions of neurons and trillions of bacteria. There is a rapidly growing number of data that links the <microbiome>gut microbiome</microbiome> to the development and functioning of the central nervous system, which is a currently proposed paradigm shift in neuroscience. Knowledge on the relationship between <microbiome>gut microbiota</microbiome> and <DDF>mental disorders</DDF> is constantly increasing. This phenomenon is known as \"gut-brain axis\". The strongest evidence for the role of microbes in the gut-brain axis comes from animal studies. Nevertheless, the gutbrain crosstalk is a bidirectional communication system that not only provides gastrointestinal homeostasis, but can also affect motivation as well as higher cognitive functions. Moreover, <microbiome>gut microbiome</microbiome> can be associated with <DDF>obesity</DDF> and <DDF>inflammatory gastrointestinal disorders</DDF>. According to the recent studies, there is a link between the composition of <microbiome>gut microbiota</microbiome> and <DDF>mental disorders</DDF> in animals (response to <DDF>depression</DDF> and <DDF>chronic stress</DDF>). This subject requires further examination, especially taking into consideration potential therapeutic options.",
"role": "assistant"
}
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30701194
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAlterations in Gut Glutamate Metabolism Associated with Changes in Gut Microbiota Composition in Children with Autism Spectrum Disorder. Changes in the gut microenvironment may influence the pathogenesis of autism spectrum disorders (ASD). Here, we investigated the composition of the gut microbiota and metabolites in children with ASD. Ninety-two children with ASD and 42 age-matched children exhibiting typical development (TD) were enrolled in the two-stage study. In the discovery stage, shotgun metagenomic sequencing and liquid chromatography-mass spectrometry (LC-MS) were performed simultaneously on fecal samples obtained from 43 children in the ASD group and 31 children in the TD group. Systematic bioinformatic analyses were performed to identify gut metabolites associated with altered gut microbiota composition. At the validation stage, differential metabolites were tested using LC-MS with an additional 49 and 11 children in the ASD and TD groups, respectively. Altered glutamate metabolites were found in the ASD group, along with a decline in 2-keto-glutaramic acid and an abundance of microbiota associated with glutamate metabolism. These changes in glutamate metabolism were correlated with lower levels of the highly abundant bacteria Bacteroides vulgatus and higher levels of the potentially harmful Eggerthella lenta and Clostridium botulinum. Lower gut cortisol levels have also been identified in the ASD group and associated with changes in gut microbiota glutamate metabolism. Finally, gut 2-keto-glutaramic acid was validated as a potential biomarker for ASD. The significant changes in the gut microenvironment in children with ASD may provide new insight into the cause of ASD and aid in the search for diagnostic and therapeutic approaches. <b>IMPORTANCE</b> Multiple lines of evidence suggest that the gut microbiota may play an important role in the pathogenesis of ASD, but the specific mechanism is still unclear. Through a comprehensive gut metagenomic and metabolome study of children with ASD, alterations in gut metabolite composition were found in children with ASD, and these alterations were linked to changes in gut microbiota composition. This may give us a deeper understanding of the role of gut microbiota in the pathogenesis of ASD.",
"role": "user"
},
{
"content": "Alterations in Gut Glutamate Metabolism Associated with Changes in Gut Microbiota Composition in <human>Children</human> with <DDF>Autism Spectrum Disorder</DDF>. Changes in the gut microenvironment may influence the pathogenesis of <DDF>autism spectrum disorders</DDF> (<DDF>ASD</DDF>). Here, we investigated the composition of the <microbiome>gut microbiota</microbiome> and metabolites in <human>children</human> with <DDF>ASD</DDF>. Ninety-two <human>children</human> with <DDF>ASD</DDF> and 42 <human>age-matched children</human> exhibiting <DDF>typical development</DDF> (<DDF>TD</DDF>) were enrolled in the two-stage study. In the discovery stage, <biomedical technique>shotgun metagenomic sequencing</biomedical technique> and <biomedical technique>liquid chromatography-mass spectrometry</biomedical technique> (<biomedical technique>LC-MS</biomedical technique>) were performed simultaneously on fecal samples obtained from 43 <human>children</human> in the <human>ASD group</human> and 31 <human>children</human> in the <human>TD group</human>. Systematic <biomedical technique>bioinformatic analyses</biomedical technique> were performed to identify <chemical>gut metabolites</chemical> associated with altered gut microbiota composition. At the validation stage, differential metabolites were tested using <biomedical technique>LC-MS</biomedical technique> with an additional 49 and 11 <human>children</human> in the <human>ASD and TD groups</human>, respectively. Altered <chemical>glutamate metabolites</chemical> were found in the <human>ASD group</human>, along with a decline in <chemical>2-keto-glutaramic acid</chemical> and an abundance of microbiota associated with glutamate metabolism. These changes in glutamate metabolism were correlated with lower levels of the highly abundant bacteria <bacteria>Bacteroides vulgatus</bacteria> and higher levels of the potentially harmful <bacteria>Eggerthella lenta</bacteria> and <bacteria>Clostridium botulinum</bacteria>. Lower gut cortisol levels have also been identified in the <human>ASD group</human> and associated with changes in gut microbiota glutamate metabolism. Finally, <chemical>gut 2-keto-glutaramic acid</chemical> was validated as a potential biomarker for <DDF>ASD</DDF>. The significant changes in the gut microenvironment in <human>children</human> with <DDF>ASD</DDF> may provide new insight into the cause of <DDF>ASD</DDF> and aid in the search for diagnostic and therapeutic approaches. <b>IMPORTANCE</b> Multiple lines of evidence suggest that the <microbiome>gut microbiota</microbiome> may play an important role in the pathogenesis of <DDF>ASD</DDF>, but the specific mechanism is still unclear. Through a comprehensive <biomedical technique>gut metagenomic and metabolome study</biomedical technique> of <human>children</human> with <DDF>ASD</DDF>, alterations in gut metabolite composition were found in <human>children</human> with <DDF>ASD</DDF>, and these alterations were linked to changes in gut microbiota composition. This may give us a deeper understanding of the role of <microbiome>gut microbiota</microbiome> in the pathogenesis of <DDF>ASD</DDF>.",
"role": "assistant"
}
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30826885
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Relationship Between Perinatal Mental Health and Stress: a Review of the Microbiome. Our current understanding of the underlying mechanisms and etiologies of perinatal mood and anxiety disorders (PMADs) is not clearly identified. The relationship of stress-induced adaptations (i.e., the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), the immune system) and the microbiota are potential contributors to psychopathology exhibited in women during pregnancy and postpartum and should be investigated. The stress response activates the HPA axis and dysregulates the ANS, leading to the inhibition of the parasympathetic system. Sustained high levels of cortisol, reduced heart variability, and modulated immune responses increase the vulnerability to PMAD. Bidirectional communication between the nervous system and the microbiota is an important factor to alter host homeostasis and development of PMAD. Future research in the relationship between the psychoneuroimmune system, the gut microbiota, and PMAD has the potential to be integrated in clinical practice to improve screening, diagnosis, and treatment.",
"role": "user"
},
{
"content": "The Relationship Between Perinatal Mental Health and <DDF>Stress</DDF>: a Review of the Microbiome. Our current understanding of the underlying mechanisms and etiologies of <DDF>perinatal mood and anxiety disorders</DDF> (<DDF>PMADs</DDF>) is not clearly identified. The relationship of stress-induced adaptations (i.e., the hypothalamic-pituitary-adrenal (HPA) axis, the autonomic nervous system (ANS), the immune system) and the microbiota are potential contributors to <DDF>psychopathology</DDF> exhibited in <human>women during pregnancy and postpartum</human> and should be investigated. The stress response activates the HPA axis and dysregulates the ANS, leading to the inhibition of the parasympathetic system. Sustained high levels of <chemical>cortisol</chemical>, reduced heart variability, and modulated immune responses increase the vulnerability to <DDF>PMAD</DDF>. Bidirectional communication between the nervous system and the microbiota is an important factor to alter host homeostasis and development of <DDF>PMAD</DDF>. Future research in the relationship between the psychoneuroimmune system, the <microbiome>gut microbiota</microbiome>, and <DDF>PMAD</DDF> has the potential to be integrated in clinical practice to improve screening, diagnosis, and treatment.",
"role": "assistant"
}
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30828318
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDisentangling What We Know About Microbes and Mental Health. Much has been written in recent years about the gut-brain axis. Exciting pilot studies suggest probiotic applications to the gut can reduce anxiety and depression via the vagus nerve. But not to diminish such findings, much still needs to be considered, including the fact that the vagus nerve links to many other body sites that also host a microbiome. Questions remain that touch the core of being human: (i) Do our microbes influence happiness and to what extent? (ii) What components of the gut microbiota and their function, including as it relates to mental health, are critical and how do they differ between agile, fit hunter gatherers and obese westerners or Danes described as the happiest people on the planet? (iii) What role do environmental pollutants play in this microbes-host ecosystem? While approaching life from a reductionist perspective has a long history in science, we need to try to interrogate these health and disease issues from a wider perspective. For verification of a link between the gut microbiota and brain, and to test new therapies, human studies are needed, and are long overdue.",
"role": "user"
},
{
"content": "Disentangling What We Know About Microbes and Mental Health. Much has been written in recent years about the gut-brain axis. Exciting pilot studies suggest <dietary supplement>probiotic applications</dietary supplement> to the <anatomical location>gut</anatomical location> can reduce <DDF>anxiety</DDF> and <DDF>depression</DDF> via the <anatomical location>vagus nerve</anatomical location>. But not to diminish such findings, much still needs to be considered, including the fact that the <anatomical location>vagus nerve</anatomical location> links to many other body sites that also host a microbiome. Questions remain that touch the core of being human: (i) Do our microbes influence happiness and to what extent? (ii) What components of the <microbiome>gut microbiota</microbiome> and their function, including as it relates to mental health, are critical and how do they differ between <human>agile, fit hunter gatherers</human> and <human>obese westerners</human> or <human>Danes</human> described as the <human>happiest people</human> on the planet? (iii) What role do <chemical>environmental pollutants</chemical> play in this microbes-host ecosystem? While approaching life from a reductionist perspective has a long history in science, we need to try to interrogate these health and disease issues from a wider perspective. For verification of a link between the <microbiome>gut microbiota</microbiome> and <anatomical location>brain</anatomical location>, and to test new therapies, human studies are needed, and are long overdue.",
"role": "assistant"
}
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31132457
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota composition is associated with temperament traits in infants. One of the key behavioral phenotypes in infancy are different temperament traits, and certain early life temperament traits have been shown to precede later mental health problems. Differences in the gut microbiota composition (GMC) have been suggested to link with neurodevelopment. For example, toddler temperament traits have been found to associate with differences in GMC; however, studies in infants are lacking although infancy is a rapid period of neurodevelopment as well as GM development. Thus, we aimed to investigate association between infant GMC and temperament. The study population (n = 301, 53% boys) was drawn from the FinnBrain Birth Cohort Study. Stool samples were collected from the 2.5-month-old infants and sequenced with 16S Illumina MiSeq platform. GMC taxonomic composition (at Genus and OTU level), observed sample clusters, diversity and richness were investigated in relation to the maternal reports of Infant Behavior Questionnaire -Revised (IBQ-R) at the age of 6 months. Three sample clusters (Bifidobacterium/Enterobacteriaceae, Bacteroides, V. Dispar) based on GMC were identified, of which Bifidobacterium/Enterobacteriaceae-cluster presented with higher scores on the IBQ-R main dimension regulation and its subscale duration of orienting compared to Bacteroides-cluster. The clusters associated with temperament in a sex-dependent manner. The IBQ-R main dimension surgency (positive emotionality) was associated positively both with genus Bifidobacterium and Streptococcus. Alpha diversity had a negative association with negative emotionality and fear reactivity. This is the first study demonstrating associations, but not causal connections, between GMC and temperament in young infants in a prospective design.",
"role": "user"
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{
"content": "<microbiome>Gut microbiota composition</microbiome> is associated with temperament traits in <human>infants</human>. One of the key behavioral phenotypes in infancy are different temperament traits, and certain early life temperament traits have been shown to precede later <DDF>mental health problems</DDF>. Differences in the <microbiome>gut microbiota composition</microbiome> (<microbiome>GMC</microbiome>) have been suggested to link with neurodevelopment. For example, <human>toddler</human> temperament traits have been found to associate with differences in <microbiome>GMC</microbiome>; however, studies in <human>infants</human> are lacking although infancy is a rapid period of neurodevelopment as well as GM development. Thus, we aimed to investigate association between <microbiome>infant GMC</microbiome> and temperament. The study population (n = 301, 53% <human>boys</human>) was drawn from the FinnBrain Birth Cohort Study. Stool samples were collected from the <human>2.5-month-old infants</human> and sequenced with 16S Illumina MiSeq platform. <microbiome>GMC</microbiome> taxonomic composition (at Genus and OTU level), observed sample clusters, diversity and richness were investigated in relation to the maternal reports of <biomedical technique>Infant Behavior Questionnaire -Revised</biomedical technique> (<biomedical technique>IBQ-R</biomedical technique>) at the age of 6 months. Three sample clusters (<bacteria>Bifidobacterium/Enterobacteriaceae</bacteria>, <bacteria>Bacteroides</bacteria>, <bacteria>V. Dispar</bacteria>) based on <microbiome>GMC</microbiome> were identified, of which Bifidobacterium/Enterobacteriaceae-cluster presented with higher scores on the <biomedical technique>IBQ-R</biomedical technique> main dimension regulation and its subscale duration of orienting compared to Bacteroides-cluster. The clusters associated with temperament in a sex-dependent manner. The <biomedical technique>IBQ-R</biomedical technique> main dimension surgency (positive emotionality) was associated positively both with genus <bacteria>Bifidobacterium</bacteria> and <bacteria>Streptococcus</bacteria>. Alpha diversity had a negative association with negative emotionality and fear reactivity. This is the first study demonstrating associations, but not causal connections, between <microbiome>GMC</microbiome> and temperament in <human>young infants</human> in a prospective design.",
"role": "assistant"
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31148353
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGutting the brain of inflammation: A key role of gut microbiome in human umbilical cord blood plasma therapy in Parkinson's disease model. Current therapies for Parkinson's disease (PD), including L-3,4-dihydroxyphenylalanine (L-DOPA), and clinical trials investigating dopaminergic cell transplants, have generated mixed results with the eventual induction of dyskinetic side effects. Although human umbilical cord blood (hUCB) stem/progenitor cells present with no or minimal capacity of differentiation into mature dopaminergic neurons, their transplantation significantly attenuates parkinsonian symptoms likely via bystander effects, specifically stem cell graft-mediated secretion of growth factors, anti-inflammatory cytokines, or synaptic function altogether promoting brain repair. Recognizing this non-cell replacement mechanism, we examined here the effects of intravenously transplanted combination of hUCB-derived plasma into the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced rat model of PD. Animals received repeated dosing of either hUCB-derived plasma or vehicle at 3, 5 and 10 days after induction into MPTP lesion, then behaviourally and immunohistochemically evaluated over 56 days post-lesion. Compared to vehicle treatment, transplantation with hUCB-derived plasma significantly improved motor function, gut motility and dopaminergic neuronal survival in the substantia nigra pars compacta (SNpc), which coincided with reduced pro-inflammatory cytokines in both the SNpc and the intestinal mucosa and dampened inflammation-associated gut microbiota. These novel data directly implicate a key pathological crosstalk between gut and brain ushering a new avenue of therapeutically targeting the gut microbiome with hUCB-derived stem cells and plasma for PD.",
"role": "user"
},
{
"content": "Gutting the <anatomical location>brain</anatomical location> of <DDF>inflammation</DDF>: A key role of <microbiome>gut microbiome</microbiome> in human umbilical cord blood plasma therapy in Parkinson's disease model. Current therapies for <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>), including <drug>L-3,4-dihydroxyphenylalanine (L-DOPA)</drug>, and clinical trials investigating dopaminergic cell transplants, have generated mixed results with the eventual induction of <DDF>dyskinetic side effects</DDF>. Although human umbilical cord blood (hUCB) stem/progenitor cells present with no or minimal capacity of differentiation into mature dopaminergic neurons, their transplantation significantly attenuates <DDF>parkinsonian symptoms</DDF> likely via bystander effects, specifically stem cell graft-mediated secretion of growth factors, <chemical>anti-inflammatory cytokines</chemical>, or synaptic function altogether promoting brain repair. Recognizing this non-cell replacement mechanism, we examined here the effects of intravenously transplanted combination of hUCB-derived plasma into the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced rat model of <DDF>PD</DDF>. Animals received repeated dosing of either <chemical>hUCB-derived plasma</chemical> or vehicle at 3, 5 and 10 days after induction into <DDF>MPTP lesion</DDF>, then behaviourally and immunohistochemically evaluated over 56 days post-lesion. Compared to vehicle treatment, transplantation with <chemical>hUCB-derived plasma</chemical> significantly improved motor function, gut motility and dopaminergic neuronal survival in the <anatomical location>substantia nigra pars compacta</anatomical location> (<anatomical location>SNpc</anatomical location>), which coincided with reduced <chemical>pro-inflammatory cytokines</chemical> in both the <anatomical location>SNpc</anatomical location> and the intestinal mucosa and dampened <microbiome>inflammation-associated gut microbiota</microbiome>. These novel data directly implicate a key pathological crosstalk between <anatomical location>gut</anatomical location> and <anatomical location>brain</anatomical location> ushering a new avenue of therapeutically targeting the <microbiome>gut microbiome</microbiome> with hUCB-derived stem cells and plasma for <DDF>PD</DDF>.",
"role": "assistant"
}
] |
31154909
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nUnravelled facets of milk derived opioid peptides: a focus on gut physiology, fractures and obesity. Beyond being a source of key nutrients, bovine milk influences physiological functions by synthesising bioactive peptides during the process of digestion. Some of the claimed negative health outcomes associated with milk consumption, such as cardiovascular diseases and type 1 diabetes may be attributed to an opioid peptide, beta-casomorphin-7 (BCM-7), derived from A1 beta-casein. BCM-7 exerts its function by binding to the μ-opioid receptors in the body. It is hypothesised that activation of the μ-opioid receptors in the gut can alter gut microbial composition, impair gut barrier integrity and bile acid metabolism, in addition to increasing gastrointestinal transit time and gut inflammation. Further, it is hypothesised that BCM-7 may influence fractures and obesity via μ-opioid receptor pathways. In conclusion, it appears that BCM-7 might have multiple functions pertinent to human health; however, the evidence is limited and warrants further pre-clinical and clinical studies for hypothesis confirmation.",
"role": "user"
},
{
"content": "Unravelled facets of <chemical>milk derived opioid peptides</chemical>: a focus on gut physiology, <DDF>fractures</DDF> and <DDF>obesity</DDF>. Beyond being a source of key nutrients, <food>bovine milk</food> influences physiological functions by synthesising <chemical>bioactive peptides</chemical> during the process of digestion. Some of the claimed negative health outcomes associated with milk consumption, such as <DDF>cardiovascular diseases</DDF> and <DDF>type 1 diabetes</DDF> may be attributed to an <chemical>opioid peptide</chemical>, <chemical>beta-casomorphin-7</chemical> (<chemical>BCM-7</chemical>), derived from <chemical>A1 beta-casein</chemical>. <chemical>BCM-7</chemical> exerts its function by binding to the <chemical>μ-opioid receptors</chemical> in the body. It is hypothesised that activation of the <chemical>μ-opioid receptors</chemical> in the <anatomical location>gut</anatomical location> can alter gut microbial composition, impair gut barrier integrity and bile acid metabolism, in addition to increasing gastrointestinal transit time and <DDF>gut inflammation</DDF>. Further, it is hypothesised that <chemical>BCM-7</chemical> may influence <DDF>fractures</DDF> and <DDF>obesity</DDF> via μ-opioid receptor pathways. In conclusion, it appears that <chemical>BCM-7</chemical> might have multiple functions pertinent to human health; however, the evidence is limited and warrants further pre-clinical and clinical studies for hypothesis confirmation.",
"role": "assistant"
}
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31218116
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nA 12-Week Pilot Exercise Program for Inactive Adults With Celiac Disease: Study Protocol. Individuals with celiac disease must follow a strict gluten-free diet (GFD) in order to avoid negative short- and long-term health consequences. Unfortunately, many people with celiac disease report poor quality of life (QoL) despite following a strict GFD, and up to 30% still report negative symptoms (eg, gastrointestinal upset). The purpose of the MOVE-C (understanding the relationship between the <i>M</i>icrobi<i>O</i>me, <i>V</i>itality, and <i>E</i>xercise in <i>C</i>eliac disease) pilot study is to explore the effects of a 12-week supervised progressive high-intensity interval training (HIIT) and lifestyle intervention on physiological, behavioral, and psychosocial outcomes among inactive adults with celiac disease.<b>Methods/Design:</b> Sixty inactive adults diagnosed with celiac disease will be randomized to HIIT+ or waitlist control (WLC). Participants in the HIIT+ will engage in a 12-week HIIT + lifestyle education program. HIIT sessions will be comprised of 2 workouts per week, working up to 14 × 30-second intervals at 90% maximal heart rate (HRmax) followed by 2 minutes recovery at 50% HRmax. The 6 biweekly lifestyle sessions will involve education on the promotion of a whole foods GFD, sleep hygiene, psychosocial coping skills (eg, self-compassion), and self-regulatory skills to master changes in behaviors. Assessments will occur at pre and post 12-week intervention and 3-month follow-up. WLC participants will be offered a 12-week HIIT program + online lifestyle education sessions after completing the final assessment. The primary outcomes are QoL and gut microbiota composition assessed with 16S rRNA sequencing. The secondary outcomes are markers of metabolic syndrome (waist circumference, fasting glucose, serum lipids, blood pressure, and body composition), gastrointestinal symptoms, sleep quality, adherence to a GFD, exercise behavior, self-regulatory efficacy, and self-compassion. It is hypothesized that participants in the HIIT+ will experience improvements in all outcomes when compared to those in the WLC. These improvements are expected to be maintained at the 3-month follow-up. The findings from this study will advance the knowledge regarding the effects of HIIT and lifestyle education on key outcomes for an at-risk chronic disease population. Furthermore, the findings can be used to inform future programs to improve fitness and physical and mental health outcomes for people with celiac disease.",
"role": "user"
},
{
"content": "A 12-Week Pilot Exercise Program for <human>Inactive Adults</human> With <DDF>Celiac Disease</DDF>: Study Protocol. <human>Individuals</human> with <DDF>celiac disease</DDF> must follow a strict gluten-free diet (GFD) in order to avoid negative short- and long-term health consequences. Unfortunately, many <human>people</human> with <DDF>celiac disease</DDF> report poor quality of life (QoL) despite following a strict GFD, and up to 30% still report negative symptoms (eg, <DDF>gastrointestinal upset</DDF>). The purpose of the MOVE-C (understanding the relationship between the <i>M</i>icrobi<i>O</i>me, <i>V</i>itality, and <i>E</i>xercise in <DDF><i>C</i>eliac disease</DDF>) pilot study is to explore the effects of a 12-week supervised progressive high-intensity interval training (HIIT) and lifestyle intervention on physiological, behavioral, and psychosocial outcomes among <human>inactive adults</human> with <DDF>celiac disease</DDF>.<b>Methods/Design:</b> Sixty <human>inactive adults</human> diagnosed with <DDF>celiac disease</DDF> will be randomized to HIIT+ or waitlist control (WLC). Participants in the HIIT+ will engage in a 12-week HIIT + lifestyle education program. HIIT sessions will be comprised of 2 workouts per week, working up to 14 × 30-second intervals at 90% maximal heart rate (HRmax) followed by 2 minutes recovery at 50% HRmax. The 6 biweekly lifestyle sessions will involve education on the promotion of a whole foods GFD, sleep hygiene, psychosocial coping skills (eg, self-compassion), and self-regulatory skills to master changes in behaviors. Assessments will occur at pre and post 12-week intervention and 3-month follow-up. WLC participants will be offered a 12-week HIIT program + online lifestyle education sessions after completing the final assessment. The primary outcomes are QoL and gut microbiota composition assessed with <biomedical technique>16S rRNA sequencing</biomedical technique>. The secondary outcomes are markers of <DDF>metabolic syndrome</DDF> (waist circumference, fasting glucose, <chemical>serum lipids</chemical>, blood pressure, and body composition), <DDF>gastrointestinal symptoms</DDF>, sleep quality, adherence to a GFD, exercise behavior, self-regulatory efficacy, and self-compassion. It is hypothesized that <human>participants</human> in the HIIT+ will experience improvements in all outcomes when compared to those in the WLC. These improvements are expected to be maintained at the 3-month follow-up. The findings from this study will advance the knowledge regarding the effects of HIIT and lifestyle education on key outcomes for an at-risk chronic disease population. Furthermore, the findings can be used to inform future programs to improve fitness and physical and mental health outcomes for <human>people</human> with <DDF>celiac disease</DDF>.",
"role": "assistant"
}
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31255682
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAltered gut microbiota and mucosal immunity in patients with schizophrenia. Evidence shows that gut microbiota may play important roles in schizophrenia pathogenesis via the \"gut-brain\" axis, but the mechanisms remain unclear. Here, eighty-four patients with schizophrenia and 84 sex- and age-matched healthy controls were enrolled. Shotgun metagenomic sequencing and 16S rRNA sequencing were performed, and the gut microbiota-associated epitopes (MEs) were predicted, which, together with IgA content, were used to determine the gut microbiota composition associated with gut immune status. Patients with schizophrenia had significantly reduced gut microbiota richnesses compared with those of the healthy controls, and the gut microbiota compositions clearly distinguished the patients with schizophrenia from the healthy controls. Based on two-stage metagenomic-wide association studies, nineteen gut microbiota taxonomies were associated with schizophrenia, and the microbial dysbiosis (MD) index was calculated based on the abundance of differential taxonomies. We found that MD index was positively correlated with MEs diversity and gut IgA levels, and negatively correlated with gut microbiota richness. Glutamate synthase (GOGAT) was more active in the guts of patients with schizophrenia than in those of healthy controls, and high GOGAT activity was associated with altered gut microbiota taxonomies associated with gut IgA levels. Our results may imply a role of the microbiome in the etiology of schizophrenia and contribute to the development of microbiome targeted interventions for schizophrenia.",
"role": "user"
},
{
"content": "<microbiome>Altered gut microbiota</microbiome> and <DDF>mucosal immunity</DDF> in <human>patients</human> with <DDF>schizophrenia</DDF>. Evidence shows that <microbiome>gut microbiota</microbiome> may play important roles in schizophrenia pathogenesis via the \"gut-brain\" axis, but the mechanisms remain unclear. Here, eighty-four <human>patients</human> with <DDF>schizophrenia</DDF> and 84 <human>sex- and age-matched healthy controls</human> were enrolled. <biomedical technique>Shotgun metagenomic sequencing</biomedical technique> and <biomedical technique>16S rRNA sequencing</biomedical technique> were performed, and the gut microbiota-associated epitopes (MEs) were predicted, which, together with IgA content, were used to determine the gut microbiota composition associated with gut immune status. <human>Patients</human> with <DDF>schizophrenia</DDF> had significantly reduced gut microbiota richnesses compared with those of the <human>healthy controls</human>, and the gut microbiota compositions clearly distinguished the <human>patients</human> with <DDF>schizophrenia</DDF> from the <human>healthy controls</human>. Based on <biomedical technique>two-stage metagenomic-wide association studies</biomedical technique>, nineteen gut microbiota taxonomies were associated with <DDF>schizophrenia</DDF>, and the microbial dysbiosis (MD) index was calculated based on the abundance of differential taxonomies. We found that MD index was positively correlated with MEs diversity and gut IgA levels, and negatively correlated with gut microbiota richness. <gene>Glutamate synthase</gene> (<gene>GOGAT</gene>) was more active in the <anatomical location>guts</anatomical location> of <human>patients</human> with <DDF>schizophrenia</DDF> than in those of <human>healthy controls</human>, and <DDF>high GOGAT activity</DDF> was associated with altered gut microbiota taxonomies associated with gut IgA levels. Our results may imply a role of the microbiome in the etiology of <DDF>schizophrenia</DDF> and contribute to the development of microbiome targeted interventions for <DDF>schizophrenia</DDF>.",
"role": "assistant"
}
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31260640
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMicrobiota-gut brain axis involvement in neuropsychiatric disorders. <b>Introduction</b>: The microbiota-gut brain (MGB) axis is the bidirectional communication between the intestinal microbiota and the brain. An increasing body of preclinical and clinical evidence has revealed that the gut microbial ecosystem can affect neuropsychiatric health. However, there is still a need of further studies to elucidate the complex gene-environment interactions and the role of the MGB axis in neuropsychiatric diseases, with the aim of identifying biomarkers and new therapeutic targets, to allow early diagnosis and improving treatments. <b>Areas covered</b>: To review the role of MGB axis in neuropsychiatric disorders, prediction and prevention of disease through exploitation, integration, and combination of data from existing gut microbiome/microbiota projects and appropriate other International '-Omics' studies. The authors also evaluated the new technological advances to investigate and modulate, through nutritional and other interventions, the gut microbiota. <b>Expert opinion</b>: The clinical studies have documented an association between alterations in gut microbiota composition and/or function, whereas the preclinical studies support a role for the gut microbiota in impacting behaviors which are of relevance to psychiatry and other central nervous system (CNS) disorders. Targeting MGB axis could be an additional approach for treating CNS disorders and all conditions in which alterations of the gut microbiota are involved.",
"role": "user"
},
{
"content": "Microbiota-gut brain axis involvement in <DDF>neuropsychiatric disorders</DDF>. <b>Introduction</b>: The microbiota-gut brain (MGB) axis is the bidirectional communication between the <microbiome>intestinal microbiota</microbiome> and the <anatomical location>brain</anatomical location>. An increasing body of preclinical and clinical evidence has revealed that the <microbiome>gut microbial ecosystem</microbiome> can affect neuropsychiatric health. However, there is still a need of further studies to elucidate the complex gene-environment interactions and the role of the MGB axis in <DDF>neuropsychiatric diseases</DDF>, with the aim of identifying biomarkers and new therapeutic targets, to allow early diagnosis and improving treatments. <b>Areas covered</b>: To review the role of MGB axis in <DDF>neuropsychiatric disorders</DDF>, prediction and prevention of disease through exploitation, integration, and combination of data from existing gut microbiome/microbiota projects and appropriate other International '-Omics' studies. The authors also evaluated the new technological advances to investigate and modulate, through nutritional and other interventions, the <microbiome>gut microbiota</microbiome>. <b>Expert opinion</b>: The clinical studies have documented an association between alterations in gut microbiota composition and/or function, whereas the preclinical studies support a role for the <microbiome>gut microbiota</microbiome> in impacting behaviors which are of relevance to <DDF>psychiatry and other central nervous system (CNS) disorders</DDF>. Targeting MGB axis could be an additional approach for treating <DDF>CNS disorders</DDF> and all conditions in which alterations of the <DDF>gut microbiota</DDF> are involved.",
"role": "assistant"
}
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31302116
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nStress-induced disturbances along the gut microbiota-immune-brain axis and implications for mental health: Does sex matter? Women are roughly twice as likely as men to suffer from stress-related disorders, especially major depression and generalized anxiety. Accumulating evidence suggest that microbes inhabiting the gastrointestinal tract (the gut microbiota) interact with the host brain and may play a key role in the pathogenesis of mental illnesses. Here, the possibility that sexually dimorphic alterations along the gut microbiota-immune-brain axis could play a role in promoting this female bias of mood and anxiety disorders will be discussed. This review will also analyze the idea that gut microbes and sex hormones influence each other, and that this reciprocal crosstalk may come to modulate inflammatory players along the gut microbiota-immune-brain axis and influence behavior in a sex-dependent way.",
"role": "user"
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{
"content": "<DDF>Stress-induced disturbances</DDF> along the gut microbiota-immune-brain axis and implications for mental health: Does sex matter? <human>Women</human> are roughly twice as likely as <human>men</human> to suffer from <DDF>stress-related disorders</DDF>, especially <DDF>major depression</DDF> and <DDF>generalized anxiety</DDF>. Accumulating evidence suggest that microbes inhabiting the <anatomical location>gastrointestinal tract</anatomical location> (the <microbiome>gut microbiota</microbiome>) interact with the <anatomical location>host brain</anatomical location> and may play a key role in the pathogenesis of <DDF>mental illnesses</DDF>. Here, the possibility that sexually dimorphic alterations along the gut microbiota-immune-brain axis could play a role in promoting this female bias of <DDF>mood and anxiety disorders</DDF> will be discussed. This review will also analyze the idea that <microbiome>gut microbes</microbiome> and <chemical>sex hormones</chemical> influence each other, and that this reciprocal crosstalk may come to modulate inflammatory players along the gut microbiota-immune-brain axis and influence behavior in a sex-dependent way.",
"role": "assistant"
}
] |
31330299
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMonocyte mobilisation, microbiota & mental illness. The gastrointestinal microbiome has emerged as a key player in regulating brain and behaviour. This has led to the strategy of targeting the gut microbiota to ameliorate disorders of the central nervous system. Understanding the underlying signalling pathways in which the microbiota impacts these disorders is crucial for the development of future therapeutics for improving CNS functionality. One of the major pathways through which the microbiota influences the brain is the immune system, where there is an increasing appreciation for the role of monocyte trafficking in regulating brain homeostasis. In this review, we will shed light on the role of monocyte trafficking as a relay of microbiota signals in conditions where the central nervous system is in disorder, such as stress, peripheral inflammation, ageing, traumatic brain injury, stroke, multiple sclerosis, Alzheimer's disease and Parkinson's disease. We also cover how the gastrointestinal microbiota is implicated in these mental illnesses. In addition, we aim to discuss how the monocyte system can be modulated by the gut microbiota to mitigate disorders of the central nervous system, which will lead to novel microbiota-targeted strategies.",
"role": "user"
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{
"content": "Monocyte mobilisation, microbiota & <DDF>mental illness</DDF>. The <microbiome>gastrointestinal microbiome</microbiome> has emerged as a key player in regulating <anatomical location>brain</anatomical location> and behaviour. This has led to the strategy of targeting the <microbiome>gut microbiota</microbiome> to ameliorate <DDF>disorders of the central nervous system</DDF>. Understanding the underlying signalling pathways in which the microbiota impacts these disorders is crucial for the development of future therapeutics for improving CNS functionality. One of the major pathways through which the microbiota influences the <anatomical location>brain</anatomical location> is the immune system, where there is an increasing appreciation for the role of monocyte trafficking in regulating brain homeostasis. In this review, we will shed light on the role of monocyte trafficking as a relay of microbiota signals in conditions where the central nervous system is in disorder, such as <DDF>stress</DDF>, <DDF>peripheral inflammation</DDF>, ageing, <DDF>traumatic brain injury</DDF>, <DDF>stroke</DDF>, <DDF>multiple sclerosis</DDF>, <DDF>Alzheimer's disease</DDF> and <DDF>Parkinson's disease</DDF>. We also cover how the <microbiome>gastrointestinal microbiota</microbiome> is implicated in these <DDF>mental illnesses</DDF>. In addition, we aim to discuss how the monocyte system can be modulated by the <microbiome>gut microbiota</microbiome> to mitigate disorders of the central nervous system, which will lead to novel microbiota-targeted strategies.",
"role": "assistant"
}
] |
31377712
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nBiopsychosocial model of resilience in young adults with multiple sclerosis (BPS-ARMS): an observational study protocol exploring psychological reactions early after diagnosis. Multiple sclerosis (MS), the most common neurological disease causing disability in young adults, is widely recognised as a major stress factor. Studies have shown that the first years after the diagnosis are distressing in terms of adjustment to the disease and that MS negatively affects patients' psychological well-being, quality of life (QoL) and social functioning. However, the links between disease-specific variables at diagnosis, resilience and psychological adjustment of patients with MS remain largely unexplored, especially in adolescents and young adults. This observational study aims to fill the gap of knowledge on <u>b</u>io<u>p</u>sycho<u>s</u>ocial characteristics and <u>r</u>esilience of young <u>a</u>dults with MS to evaluate the relationship among these variables and to develop a biopsychosocial model of resilience. Biological and clinical characteristics of young adults newly diagnosed with MS will be investigated by collecting clinical information, performing neurological examinations, MRI and analysing cerebrospinal fluid and blood biomarkers (eg, measures of inflammation), body composition, gut microbiota and movement/perceptual markers. Psychosocial characteristics (eg, psychological distress, coping strategies), QoL, psychological well-being and resilience will be assessed by self-report questionnaires. Comparative statistics (ie, analysis of variance or unpaired samples t-test, correlation and regression analyses) will be applied to evaluate the relationship among biological, psychological and social factors. The results are expected to allow a comprehensive understanding of the determinants of resilience in young patients with MS and to inform resilience interventions, tailored to young patients' specific needs, aiming to reduce the risk of maladaptive reactions to the disease and to improve psychological well-being and QoL. The study has been approved by the Verona University Hospital Ethics Committee (approval number: 2029CESC). The findings will be disseminated through scientific publications in peer-reviewed journals, conference presentations, social media and specific websites. ClinicalTrials.gov (NCT03825055).",
"role": "user"
},
{
"content": "Biopsychosocial model of resilience in <human>young adults</human> with <DDF>multiple sclerosis</DDF> (BPS-ARMS): an observational study protocol exploring psychological reactions early after diagnosis. <DDF>Multiple sclerosis</DDF> (<DDF>MS</DDF>), the most common <DDF>neurological disease</DDF> causing <DDF>disability</DDF> in <human>young adults</human>, is widely recognised as a major stress factor. Studies have shown that the first years after the diagnosis are distressing in terms of adjustment to the disease and that <DDF>MS</DDF> negatively affects patients' psychological well-being, quality of life (QoL) and social functioning. However, the links between disease-specific variables at diagnosis, resilience and psychological adjustment of <human>patients</human> with <DDF>MS</DDF> remain largely unexplored, especially in <human>adolescents</human> and <human>young adults</human>. This observational study aims to fill the gap of knowledge on <u>b</u>io<u>p</u>sycho<u>s</u>ocial characteristics and <u>r</u>esilience of <human>young <u>a</u>dults</human> with <DDF>MS</DDF> to evaluate the relationship among these variables and to develop a biopsychosocial model of resilience. Biological and clinical characteristics of <human>young adults</human> newly diagnosed with <DDF>MS</DDF> will be investigated by collecting clinical information, performing <biomedical technique>neurological examinations</biomedical technique>, <biomedical technique>MRI</biomedical technique> and analysing <biomedical technique>cerebrospinal fluid and blood biomarkers</biomedical technique> (eg, measures of <DDF>inflammation</DDF>), body composition, <microbiome>gut microbiota</microbiome> and movement/perceptual markers. Psychosocial characteristics (eg, psychological distress, coping strategies), QoL, psychological well-being and resilience will be assessed by <biomedical technique>self-report questionnaires</biomedical technique>. <statistical technique>Comparative statistics</statistical technique> (ie, <statistical technique>analysis of variance</statistical technique> or <statistical technique>unpaired samples t-test</statistical technique>, <statistical technique>correlation and regression analyses</statistical technique>) will be applied to evaluate the relationship among biological, psychological and social factors. The results are expected to allow a comprehensive understanding of the determinants of resilience in <human>young patients</human> with <DDF>MS</DDF> and to inform resilience interventions, tailored to young patients' specific needs, aiming to reduce the risk of maladaptive reactions to the disease and to improve psychological well-being and QoL. The study has been approved by the Verona University Hospital Ethics Committee (approval number: 2029CESC). The findings will be disseminated through scientific publications in peer-reviewed journals, conference presentations, social media and specific websites. ClinicalTrials.gov (NCT03825055).",
"role": "assistant"
}
] |
31383280
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nImproving Mental Health for the Mother-Infant Dyad by Nutrition and the Maternal Gut Microbiome. Perinatal mood and anxiety disorders (PMAD) have significant negative impacts on mother and child, yet treatments are limited. Adequate nutrition during the perinatal period is essential to maternal and infant health, including maternal mental health and the child's neurologic and neuropsychiatric development. Nutrition holds promise to improve prevention and treatment of PMAD. The ability to manipulate the gut microbiota composition and structure through host nutrition and to harness the gut microbes for improved individualized nutrition may be an important new direction for prevention and treatment of PMAD, thus improving the mental health of mother and child.",
"role": "user"
},
{
"content": "Improving Mental Health for the <human>Mother-Infant Dyad</human> by Nutrition and the <microbiome>Maternal Gut Microbiome</microbiome>. <DDF>Perinatal mood and anxiety disorders</DDF> (<DDF>PMAD</DDF>) have significant negative impacts on <human>mother</human> and <human>child</human>, yet treatments are limited. Adequate nutrition during the perinatal period is essential to maternal and infant health, including maternal mental health and the child's neurologic and neuropsychiatric development. Nutrition holds promise to improve prevention and treatment of <DDF>PMAD</DDF>. The ability to manipulate the gut microbiota composition and structure through host nutrition and to harness the gut microbes for improved individualized nutrition may be an important new direction for prevention and treatment of <DDF>PMAD</DDF>, thus improving the mental health of <human>mother</human> and <human>child</human>.",
"role": "assistant"
}
] |
31488882
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nSodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer's disease progression. Recently, increasing evidence has suggested the association between gut dysbiosis and Alzheimer's disease (AD) progression, yet the role of gut microbiota in AD pathogenesis remains obscure. Herein, we provide a potential mechanistic link between gut microbiota dysbiosis and neuroinflammation in AD progression. Using AD mouse models, we discovered that, during AD progression, the alteration of gut microbiota composition leads to the peripheral accumulation of phenylalanine and isoleucine, which stimulates the differentiation and proliferation of pro-inflammatory T helper 1 (Th1) cells. The brain-infiltrated peripheral Th1 immune cells are associated with the M1 microglia activation, contributing to AD-associated neuroinflammation. Importantly, the elevation of phenylalanine and isoleucine concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of patients with mild cognitive impairment (MCI) due to AD. Furthermore, GV-971, a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation, harnesses neuroinflammation and reverses the cognition impairment. Together, our findings highlight the role of gut dysbiosis-promoted neuroinflammation in AD progression and suggest a novel strategy for AD therapy by remodelling the gut microbiota.",
"role": "user"
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{
"content": "<dietary supplement>Sodium oligomannate</dietary supplement> therapeutically remodels <microbiome>gut microbiota</microbiome> and suppresses <DDF>gut bacterial amino acids-shaped neuroinflammation</DDF> to inhibit <DDF>Alzheimer's disease progression</DDF>. Recently, increasing evidence has suggested the association between <DDF>gut dysbiosis</DDF> and <DDF>Alzheimer's disease</DDF> (<DDF>AD</DDF>) progression, yet the role of <microbiome>gut microbiota</microbiome> in AD pathogenesis remains obscure. Herein, we provide a potential mechanistic link between <DDF>gut microbiota dysbiosis</DDF> and <DDF>neuroinflammation</DDF> in <DDF>AD progression</DDF>. Using AD mouse models, we discovered that, during <DDF>AD progression</DDF>, the alteration of <microbiome>gut microbiota</microbiome> composition leads to the peripheral accumulation of <chemical>phenylalanine</chemical> and <chemical>isoleucine</chemical>, which stimulates the differentiation and proliferation of pro-inflammatory T helper 1 (Th1) cells. The brain-infiltrated peripheral Th1 immune cells are associated with the M1 microglia activation, contributing to <DDF>AD-associated neuroinflammation</DDF>. Importantly, the elevation of <chemical>phenylalanine</chemical> and <chemical>isoleucine</chemical> concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of <human>patients</human> with <DDF>mild cognitive impairment</DDF> (<DDF>MCI</DDF>) due to <DDF>AD</DDF>. Furthermore, <drug>GV-971</drug>, a <drug>sodium oligomannate</drug> that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses <DDF>gut dysbiosis</DDF> and the associated <chemical>phenylalanine</chemical>/<chemical>isoleucine</chemical> accumulation, harnesses <DDF>neuroinflammation</DDF> and reverses the <DDF>cognition impairment</DDF>. Together, our findings highlight the role of <DDF>gut dysbiosis-promoted neuroinflammation</DDF> in AD progression and suggest a novel strategy for AD therapy by remodelling the <microbiome>gut microbiota</microbiome>.",
"role": "assistant"
}
] |
31493127
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nProbiotics and Psychobiotics: the Role of Microbial Neurochemicals. In light of recent data, microorganisms should be construed as organisms that are capable of communication and collective behaviors. Microbial communication signals are involved both in interactions among microbial cells within microbial social systems, including the human body-inhabiting microconsortium, and the dialog between the microbiota and the host organism. The microbiota inhabits various niches of the host organism, especially the gastrointestinal (GI) tract. Microorganisms release diverse signal molecules and, in addition, specifically respond to host signals. This enables them to constantly interact with the nervous system including the brain and the immune system of the host organism. Evolutionarily conserved signals that are involved in the communication between microbiota and the host include neuroactive substances (neurochemicals) such as peptides, amino acids, biogenic amines, short-chain fatty acids, and gaseous substances. This ongoing dialog may either stabilize the host's physical and mental health state or, alternatively, cause serious health problems. Attempts are made to correct imbalances in the brain-gut-microbiota axis with probiotics including their subgroup called psychobiotics that release neuroactive substances directly influencing the human brain, psyche, and behavior. A number of recent review works address the microbiota-host system and its communication signals. Some of the publications focus on the involvement of neurochemicals in the bidirectional communication within the host-microbiota system. However, this work concentrates on the impact of bacterial cell components, metabolites, and signal molecules as promising alternatives to the currently widespread probiotics that have both advantages and disadvantages. Such biologically active agents of microbial origin are referred to as postbiotics or, alternatively, metabiotics (the term preferred in this work).",
"role": "user"
},
{
"content": "<dietary supplement>Probiotics</dietary supplement> and <dietary supplement>Psychobiotics</dietary supplement>: the Role of <chemical>Microbial Neurochemicals</chemical>. In light of recent data, microorganisms should be construed as organisms that are capable of communication and collective behaviors. Microbial communication signals are involved both in interactions among microbial cells within microbial social systems, including the human body-inhabiting microconsortium, and the dialog between the microbiota and the host organism. The microbiota inhabits various niches of the host organism, especially the gastrointestinal (GI) tract. Microorganisms release diverse signal molecules and, in addition, specifically respond to host signals. This enables them to constantly interact with the nervous system including the <anatomical location>brain</anatomical location> and the immune system of the host organism. Evolutionarily conserved signals that are involved in the communication between microbiota and the host include neuroactive substances (neurochemicals) such as <chemical>peptides</chemical>, <chemical>amino acids</chemical>, <chemical>biogenic amines</chemical>, <chemical>short-chain fatty acids</chemical>, and gaseous substances. This ongoing dialog may either stabilize the host's physical and mental health state or, alternatively, cause serious health problems. Attempts are made to correct imbalances in the brain-gut-microbiota axis with <dietary supplement>probiotics</dietary supplement> including their subgroup called <dietary supplement>psychobiotics</dietary supplement> that release neuroactive substances directly influencing the <anatomical location>human brain</anatomical location>, psyche, and behavior. A number of recent review works address the microbiota-host system and its communication signals. Some of the publications focus on the involvement of neurochemicals in the bidirectional communication within the host-microbiota system. However, this work concentrates on the impact of bacterial cell components, metabolites, and signal molecules as promising alternatives to the currently widespread <dietary supplement>probiotics</dietary supplement> that have both advantages and disadvantages. Such biologically active agents of microbial origin are referred to as postbiotics or, alternatively, metabiotics (the term preferred in this work).",
"role": "assistant"
}
] |
31498131
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nIncreasing Comparability and Utility of Gut Microbiome Studies in Parkinson's Disease: A Systematic Review. Gut microbiota have been studied in relation to the pathophysiology of Parkinson's disease (PD) due to the early gastrointestinal symptomatology and presence of alpha-synuclein pathology in the enteric nervous system, hypothesized to ascend via the vagal nerve to the central nervous system. Accordingly, sixteen human case-control studies have published gut microbiome composition changes in PD and reported over 100 differentially abundant taxa covering all taxonomic levels from phylum to genus or species, depending on methodology. While certain findings were replicated across several studies, various contradictory findings were reported. Here, differences in methodologies and the presence of possible confounders in the study populations are assessed for their potential to confound the results of gut microbiome studies in PD. Gut microbiome studies in PD exhibited considerable variability with respect to the study population, sample transport conditions, laboratory protocols and sequencing, bioinformatics pipelines, and biostatistical methods. To move from the current heterogeneous dataset towards clinically relevant biomarkers and the identification of putative therapeutic targets, recommendations are derived from the limitations of the available studies to increase the future comparability of microbiome studies in PD. In addition, integration of currently available data on the gut microbiome in PD is proposed to identify robust gut microbiome profiles in PD. Furthermore, expansion of the current dataset with atypical parkinsonism cohorts, prodromal and treatment-naïve de novo PD subjects, measurements of fecal microbial concentrations and multi-omics assessments are required to provide clinically relevant biomarkers and reveal therapeutic targets within the gut microbiome of PD.",
"role": "user"
},
{
"content": "Increasing Comparability and Utility of Gut Microbiome Studies in <DDF>Parkinson's Disease</DDF>: A Systematic Review. <microbiome>Gut microbiota</microbiome> have been studied in relation to the pathophysiology of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>) due to the <DDF>early gastrointestinal symptomatology</DDF> and presence of <DDF>alpha-synuclein pathology</DDF> in the enteric nervous system, hypothesized to ascend via the <anatomical location>vagal nerve</anatomical location> to the central nervous system. Accordingly, sixteen human case-control studies have published gut microbiome composition changes in <DDF>PD</DDF> and reported over 100 differentially abundant taxa covering all taxonomic levels from phylum to genus or species, depending on methodology. While certain findings were replicated across several studies, various contradictory findings were reported. Here, differences in methodologies and the presence of possible confounders in the <human>study populations</human> are assessed for their potential to confound the results of gut microbiome studies in <DDF>PD</DDF>. Gut microbiome studies in <DDF>PD</DDF> exhibited considerable variability with respect to the <human>study population</human>, sample transport conditions, laboratory protocols and <biomedical technique>sequencing</biomedical technique>, bioinformatics pipelines, and <statistical technique>biostatistical methods</statistical technique>. To move from the current heterogeneous dataset towards clinically relevant biomarkers and the identification of putative therapeutic targets, recommendations are derived from the limitations of the available studies to increase the future comparability of microbiome studies in <DDF>PD</DDF>. In addition, integration of currently available data on the <microbiome>gut microbiome</microbiome> in <DDF>PD</DDF> is proposed to identify robust gut microbiome profiles in <DDF>PD</DDF>. Furthermore, expansion of the current dataset with <human>atypical parkinsonism cohorts</human>, <human>prodromal and treatment-naïve de novo PD subjects</human>, <biomedical technique>measurements of fecal microbial concentrations</biomedical technique> and <biomedical technique>multi-omics assessments</biomedical technique> are required to provide clinically relevant biomarkers and reveal therapeutic targets within the <microbiome>gut microbiome</microbiome> of <DDF>PD</DDF>.",
"role": "assistant"
}
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31539679
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAntibiotic-induced microbiome depletion is associated with resilience in mice after chronic social defeat stress. The brain-gut axis plays a role in the pathogenesis of stress-related disorders such as depression. However, the role of brain-gut axis in the resilience versus susceptibility after stress remains unclear. Here, we examined the effects of antibiotic-induced microbiome depletion on an anhedonia-like phenotype in adult mice subjected to chronic social defeat stress (CSDS). Using CSDS paradigm, we investigated the effects of antibiotic-induced microbiome depletion on the resilience versus susceptibility in mice. Treatment with an antibiotic cocktail for 14 days significantly decreased the diversity and composition of the microbiota in the host gut. Proteobacteria were markedly increased after treatment with the antibiotic cocktail. At the genus and species levels, the antibiotic-treated group exhibited marked alterations in the microbiota compared with a control group. CSDS was shown to significantly improve the abnormal composition of gut microbiota in the antibiotic-treated group. CSDS did not produce an anhedonia-like phenotype in the antibiotic-treated mice, but did induce an anhedonia-like phenotype in control mice, suggesting that gut bacteria are essential for the development of CSDS-induced anhedonia. CSDS treatment did not alter the plasma levels of interleukin-6 or the expression of synaptic proteins, such as PSD-95 and GluA1, in the prefrontal cortex of antibiotic-treated mice. Specific microbiome were not determined. These findings suggest that antibiotic-induced microbiome depletion contributed to resilience to anhedonia in mice subjected to CSDS. Therefore, it is likely that the brain-gut axis plays a role in resilience versus susceptibility to stress.",
"role": "user"
},
{
"content": "<DDF>Antibiotic-induced microbiome depletion</DDF> is associated with resilience in <animal>mice</animal> after <biomedical technique>chronic social defeat stress</biomedical technique>. The brain-gut axis plays a role in the pathogenesis of <DDF>stress-related disorders</DDF> such as <DDF>depression</DDF>. However, the role of brain-gut axis in the resilience versus susceptibility after <DDF>stress</DDF> remains unclear. Here, we examined the effects of <DDF>antibiotic-induced microbiome depletion</DDF> on an anhedonia-like phenotype in <animal>adult mice</animal> subjected to <DDF>chronic social defeat stress</DDF> (<DDF>CSDS</DDF>). Using CSDS paradigm, we investigated the effects of <DDF>antibiotic-induced microbiome depletion</DDF> on the resilience versus susceptibility in <animal>mice</animal>. Treatment with an <drug>antibiotic cocktail</drug> for 14 days significantly decreased the diversity and composition of the microbiota in the <anatomical location>host gut</anatomical location>. <bacteria>Proteobacteria</bacteria> were markedly increased after treatment with the <drug>antibiotic cocktail</drug>. At the genus and species levels, the <animal>antibiotic-treated group</animal> exhibited marked alterations in the microbiota compared with a <animal>control group</animal>. <DDF>CSDS</DDF> was shown to significantly improve the abnormal composition of <microbiome>gut microbiota</microbiome> in the <animal>antibiotic-treated group</animal>. <DDF>CSDS</DDF> did not produce an <DDF>anhedonia-like phenotype</DDF> in the <animal>antibiotic-treated mice</animal>, but did induce an <DDF>anhedonia-like phenotype</DDF> in <animal>control mice</animal>, suggesting that <bacteria>gut bacteria</bacteria> are essential for the development of <DDF>CSDS-induced anhedonia</DDF>. <DDF>CSDS</DDF> treatment did not alter the plasma levels of <chemical>interleukin-6</chemical> or the expression of <chemical>synaptic proteins</chemical>, such as <chemical>PSD-95</chemical> and <chemical>GluA1</chemical>, in the <anatomical location>prefrontal cortex</anatomical location> of <animal>antibiotic-treated mice</animal>. Specific microbiome were not determined. These findings suggest that <DDF>antibiotic-induced microbiome depletion</DDF> contributed to resilience to <DDF>anhedonia</DDF> in <animal>mice</animal> subjected to <DDF>CSDS</DDF>. Therefore, it is likely that the brain-gut axis plays a role in resilience versus susceptibility to <DDF>stress</DDF>.",
"role": "assistant"
}
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31568686
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe role of the brain-gut-microbiota axis in psychology: The importance of considering gut microbiota in the development, perpetuation, and treatment of psychological disorders. The prevalence of psychological disorders remains stable despite steady increases in pharmacological treatments suggesting the need for auxiliary treatment options. Consideration of the brain-gut-microbiota axis (BGMA) has made inroads into reconceptualizing psychological illness from a more holistic perspective. While our understanding of the precise role of gut microbiota (GM) in psychological illness is in its infancy, it represents an attractive target for novel interventions. An extensive review of relevant literature was undertaken. Gut microbiota are proposed to directly and indirectly influence mood, cognition, and behavior which are key components of mental health. This paper outlines how GM may be implicated in psychological disorders from etiology through to treatment and prevention using the Four P model of case formulation. Moving forward, integration of GM into the conceptualization and treatment of psychological illness will require the discipline of psychology to undergo a significant paradigm shift. While the importance of the GM in psychological well-being must be respected, it is not proposed to be a panacea, but instead, an additional arm to a multidisciplinary approach to treatment and prevention.",
"role": "user"
},
{
"content": "The role of the brain-gut-microbiota axis in psychology: The importance of considering <microbiome>gut microbiota</microbiome> in the development, perpetuation, and treatment of <DDF>psychological disorders</DDF>. The prevalence of <DDF>psychological disorders</DDF> remains stable despite steady increases in pharmacological treatments suggesting the need for auxiliary treatment options. Consideration of the brain-gut-microbiota axis (BGMA) has made inroads into reconceptualizing <DDF>psychological illness</DDF> from a more holistic perspective. While our understanding of the precise role of <microbiome>gut microbiota</microbiome> (<microbiome>GM</microbiome>) in <DDF>psychological illness</DDF> is in its infancy, it represents an attractive target for novel interventions. An extensive review of relevant literature was undertaken. <microbiome>Gut microbiota</microbiome> are proposed to directly and indirectly influence mood, cognition, and behavior which are key components of mental health. This paper outlines how <microbiome>GM</microbiome> may be implicated in <DDF>psychological disorders</DDF> from etiology through to treatment and prevention using the Four P model of case formulation. Moving forward, integration of <microbiome>GM</microbiome> into the conceptualization and treatment of <DDF>psychological illness</DDF> will require the discipline of psychology to undergo a significant paradigm shift. While the importance of the <microbiome>GM</microbiome> in psychological well-being must be respected, it is not proposed to be a panacea, but instead, an additional arm to a multidisciplinary approach to treatment and prevention.",
"role": "assistant"
}
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31596658
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPhotobiomics: Can Light, Including Photobiomodulation, Alter the Microbiome? <b><i>Objective</i>:</b> The objective of this review is to consider the dual effects of microbiome and photobiomodulation (PBM) on human health and to suggest a relationship between these two as a novel mechanism. <b><i>Background</i>:</b> PBM describes the use of low levels of visible or near-infrared (NIR) light to heal and stimulate tissue, and to relieve pain and inflammation. In recent years, PBM has been applied to the head as an investigative approach to treat diverse brain diseases such as stroke, traumatic brain injury (TBI), Alzheimer's and Parkinson's diseases, and psychiatric disorders. Also, in recent years, increasing attention has been paid to the total microbial population that colonizes the human body, chiefly in the gut and the mouth, called the microbiome. It is known that the composition and health of the gut microbiome affects many diseases related to metabolism, obesity, cardiovascular disorders, autoimmunity, and even brain disorders. <b><i>Materials and methods</i>:</b> A literature search was conducted for published reports on the effect of light on the microbiome. <b><i>Results</i>:</b> Recent work by our research group has demonstrated that PBM (red and NIR light) delivered to the abdomen in mice, can alter the gut microbiome in a potentially beneficial way. This has also now been demonstrated in human subjects. <b><i>Conclusions</i>:</b> In consideration of the known effects of PBM on metabolomics, and the now demonstrated effects of PBM on the microbiome, as well as other effects of light on the microbiome, including modulating circadian rhythms, the present perspective introduces a new term \"photobiomics\" and looks forward to the application of PBM to influence the microbiome in humans. Some mechanisms by which this phenomenon might occur are considered.",
"role": "user"
},
{
"content": "Photobiomics: Can Light, Including Photobiomodulation, Alter the Microbiome? <b><i>Objective</i>:</b> The objective of this review is to consider the dual effects of microbiome and <biomedical technique>photobiomodulation</biomedical technique> (<biomedical technique>PBM</biomedical technique>) on human health and to suggest a relationship between these two as a novel mechanism. <b><i>Background</i>:</b> <biomedical technique>PBM</biomedical technique> describes the use of low levels of visible or near-infrared (NIR) light to heal and stimulate tissue, and to relieve <DDF>pain</DDF> and <DDF>inflammation</DDF>. In recent years, <biomedical technique>PBM</biomedical technique> has been applied to the <anatomical location>head</anatomical location> as an investigative approach to treat diverse <DDF>brain diseases</DDF> such as <DDF>stroke</DDF>, <DDF>traumatic brain injury</DDF> (<DDF>TBI</DDF>), <DDF>Alzheimer's and Parkinson's diseases</DDF>, and <DDF>psychiatric disorders</DDF>. Also, in recent years, increasing attention has been paid to the total microbial population that colonizes the human body, chiefly in the <anatomical location>gut</anatomical location> and the <anatomical location>mouth</anatomical location>, called the microbiome. It is known that the composition and health of the <microbiome>gut microbiome</microbiome> affects many diseases related to metabolism, <DDF>obesity</DDF>, <DDF>cardiovascular disorders</DDF>, <DDF>autoimmunity</DDF>, and even <DDF>brain disorders</DDF>. <b><i>Materials and methods</i>:</b> A literature search was conducted for published reports on the effect of light on the <microbiome>microbiome</microbiome>. <b><i>Results</i>:</b> Recent work by our research group has demonstrated that PBM (red and NIR light) delivered to the <anatomical location>abdomen</anatomical location> in <animal>mice</animal>, can alter the <microbiome>gut microbiome</microbiome> in a potentially beneficial way. This has also now been demonstrated in <human>human subjects</human>. <b><i>Conclusions</i>:</b> In consideration of the known effects of PBM on <biomedical technique>metabolomics</biomedical technique>, and the now demonstrated effects of PBM on the <microbiome>microbiome</microbiome>, as well as other effects of light on the <microbiome>microbiome</microbiome>, including modulating circadian rhythms, the present perspective introduces a new term \"photobiomics\" and looks forward to the application of PBM to influence the <microbiome>microbiome</microbiome> in <human>humans</human>. Some mechanisms by which this phenomenon might occur are considered.",
"role": "assistant"
}
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31704402
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nNaturally-diverse airborne environmental microbial exposures modulate the gut microbiome and may provide anxiolytic benefits in mice. Growing epidemiological evidence links natural green space exposure with a range of health benefits, including for mental health. Conversely, greater urbanisation associates with increased risk of mental health disorders. Microbiomes are proposed as an important but understudied link that may help explain many green space-human health associations. However, there remains a lack of controlled experimental evidence testing possible beneficial effects from passive exposure to natural biodiversity via airborne microbiota. Previous mouse model studies have used unrealistic environmental microbial exposures-including excessive soil and organic matter contact, feed supplements and injections-to demonstrate host microbiota, immune biomarker, and behavioural changes. Here, in a randomised controlled experiment, we demonstrate that realistic exposures to trace-level dust from a high biodiversity soil can change mouse gut microbiota, in comparison to dust from low biodiversity soil or no soil (control) (n = 54 total mice, comprising 3 treatments × 18 mice, with 9 females + 9 males per group). Furthermore, we found a nominal soil-derived anaerobic spore-forming butyrate-producer, Kineothrix alysoides, was supplemented to a greater extent in the gut microbiomes of high biodiversity treatment mice. Also, increasing relative abundance of this rare organism correlated with reduced anxiety-like behaviour in the most anxious mice. Our results point to an intriguing new hypothesis: that biodiverse soils may represent an important supplementary source of butyrate-producing bacteria capable of resupplying the mammalian gut microbiome, with potential for gut health and mental health benefits. Our findings have potential to inform cost-effective population health interventions through microbiome-conscious green space design and, ultimately, the mainstreaming of biodiversity into health care.",
"role": "user"
},
{
"content": "Naturally-diverse airborne environmental microbial exposures modulate the <microbiome>gut microbiome</microbiome> and may provide anxiolytic benefits in <animal>mice</animal>. Growing epidemiological evidence links natural green space exposure with a range of health benefits, including for mental health. Conversely, greater urbanisation associates with increased risk of <DDF>mental health disorders</DDF>. Microbiomes are proposed as an important but understudied link that may help explain many green space-human health associations. However, there remains a lack of controlled experimental evidence testing possible beneficial effects from passive exposure to natural biodiversity via <microbiome>airborne microbiota</microbiome>. Previous mouse model studies have used unrealistic environmental microbial exposures-including excessive soil and organic matter contact, feed supplements and injections-to demonstrate <microbiome>host microbiota</microbiome>, immune biomarker, and behavioural changes. Here, in a randomised controlled experiment, we demonstrate that realistic exposures to trace-level dust from a high biodiversity soil can change <microbiome>mouse gut microbiota</microbiome>, in comparison to dust from low biodiversity soil or no soil (control) (n = 54 total <animal>mice</animal>, comprising 3 treatments × 18 <animal>mice</animal>, with 9 <animal>females</animal> + 9 <animal>males</animal> per group). Furthermore, we found a nominal soil-derived anaerobic spore-forming butyrate-producer, <bacteria>Kineothrix alysoides</bacteria>, was supplemented to a greater extent in the <microbiome>gut microbiomes</microbiome> of <animal>high biodiversity treatment mice</animal>. Also, increasing relative abundance of this rare organism correlated with reduced <DDF>anxiety-like behaviour</DDF> in the most <animal>anxious mice</animal>. Our results point to an intriguing new hypothesis: that biodiverse soils may represent an important supplementary source of <bacteria>butyrate-producing bacteria</bacteria> capable of resupplying the <microbiome>mammalian gut microbiome</microbiome>, with potential for gut health and mental health benefits. Our findings have potential to inform cost-effective population health interventions through microbiome-conscious green space design and, ultimately, the mainstreaming of biodiversity into health care.",
"role": "assistant"
}
] |
31722343
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Gut Microbiome in Bipolar Disorder and Pharmacotherapy Management. The gut microbiome is a complex and dynamic community of commensal, symbiotic, and pathogenic microorganisms that exist in a bidirectional relationship with the host. Bacterial functions in the gut play a critical role in healthy host functioning, and its disruption can contribute to many medical conditions. The relationship between gut microbiota and the brain has gained attention in mental health due to the mounting evidence supporting the association of gut bacteria with mood and behavior. Patients with bipolar disorder exhibit an increased frequency of gastrointestinal illnesses such as inflammatory bowel disease, which mechanistically has been linked to microbial community function. While the heterogeneity in microbial communities between individuals might be associated with disease risk, it may also moderate the efficacy or adverse effects associated with the use of medication. The following review highlights published evidence linking the function of gut microbiota both to bipolar disorder risk and to the effect of medications that influence microbiota, inflammation, and mood symptoms.",
"role": "user"
},
{
"content": "The <microbiome>Gut Microbiome</microbiome> in <DDF>Bipolar Disorder</DDF> and Pharmacotherapy Management. The <microbiome>gut microbiome</microbiome> is a complex and dynamic community of commensal, symbiotic, and pathogenic microorganisms that exist in a bidirectional relationship with the host. Bacterial functions in the <anatomical location>gut</anatomical location> play a critical role in healthy host functioning, and its disruption can contribute to many medical conditions. The relationship between <microbiome>gut microbiota</microbiome> and the <anatomical location>brain</anatomical location> has gained attention in mental health due to the mounting evidence supporting the association of <bacteria>gut bacteria</bacteria> with mood and behavior. <human>Patients</human> with <DDF>bipolar disorder</DDF> exhibit an increased frequency of <DDF>gastrointestinal illnesses</DDF> such as <DDF>inflammatory bowel disease</DDF>, which mechanistically has been linked to microbial community function. While the heterogeneity in microbial communities between individuals might be associated with disease risk, it may also moderate the efficacy or adverse effects associated with the use of medication. The following review highlights published evidence linking the function of <microbiome>gut microbiota</microbiome> both to bipolar disorder risk and to the effect of medications that influence microbiota, <DDF>inflammation</DDF>, and <DDF>mood symptoms</DDF>.",
"role": "assistant"
}
] |
31726457
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut Microbiota: A Perspective for Psychiatrists. There is mounting evidence that the trillions of microbes that inhabit our gut are a substantial contributing factor to mental health and, equally, to the progression of neuropsychiatric disorders. The extraordinary complexity of the gut ecosystem, and how it interacts with the intestinal epithelium to manifest physiological changes in the brain to influence mood and behaviour, has been the subject of intense scientific scrutiny over the last 2 decades. To further complicate matters, we each harbour a unique microbiota community that is subject to change by a number of factors including diet, exercise, stress, health status, genetics, medication, and age, amongst others. The microbiota-gut-brain axis is a dynamic matrix of tissues and organs including the gastrointestinal (GI) microbiota, immune cells, gut tissue, glands, the autonomic nervous system (ANS), and the brain that communicate in a complex multidirectional manner through a number of anatomically and physiologically distinct systems. Long-term perturbations to this homeostatic environment may contribute to the progression of a number of disorders by altering physiological processes including hypothalamic-pituitary-adrenal axis activation, neurotransmitter systems, immune function, and the inflammatory response. While an appropriate, co-ordinated physiological response, such as an immune or stress response, is necessary for survival, a dysfunctional response can be detrimental to the host, contributing to the development of a number of central nervous system disorders.",
"role": "user"
},
{
"content": "<microbiome>Gut Microbiota</microbiome>: A Perspective for Psychiatrists. There is mounting evidence that the trillions of microbes that inhabit our <anatomical location>gut</anatomical location> are a substantial contributing factor to mental health and, equally, to the progression of <DDF>neuropsychiatric disorders</DDF>. The extraordinary complexity of the gut ecosystem, and how it interacts with the <anatomical location>intestinal epithelium</anatomical location> to manifest physiological changes in the <anatomical location>brain</anatomical location> to influence mood and behaviour, has been the subject of intense scientific scrutiny over the last 2 decades. To further complicate matters, we each harbour a unique microbiota community that is subject to change by a number of factors including diet, exercise, <DDF>stress</DDF>, health status, genetics, medication, and age, amongst others. The microbiota-gut-brain axis is a dynamic matrix of <anatomical location>tissues</anatomical location> and organs including the <microbiome>gastrointestinal (GI) microbiota</microbiome>, immune cells, <anatomical location>gut tissue</anatomical location>, <anatomical location>glands</anatomical location>, the autonomic nervous system (ANS), and the <anatomical location>brain</anatomical location> that communicate in a complex multidirectional manner through a number of anatomically and physiologically distinct systems. Long-term perturbations to this homeostatic environment may contribute to the progression of a number of disorders by altering physiological processes including hypothalamic-pituitary-adrenal axis activation, neurotransmitter systems, immune function, and the inflammatory response. While an appropriate, co-ordinated physiological response, such as an immune or stress response, is necessary for survival, a dysfunctional response can be detrimental to the host, contributing to the development of a number of <DDF>central nervous system disorders</DDF>.",
"role": "assistant"
}
] |
31750916
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDietary fiber and its associations with depression and inflammation. Dietary fiber is a crucial component of a healthy diet, with benefits that can be attributed to processes in the gut microbiota and the resulting by-products. Observational studies support associations between dietary fiber intake and depression and inflammation, but the potential mechanisms are poorly understood. This review examines evidence of the effects of dietary fiber on depression and inflammation and considers plausible mechanisms linking dietary fiber and depression, including microbiota-driven modification of gene expression and increased production of neurotransmitters. Additionally, inflammation may mediate the relationship between dietary fiber intake and depression. A high-fiber diet potentially lowers inflammation by modifying both the pH and the permeability of the gut. The resultant reduction in inflammatory compounds may alter neurotransmitter concentrations to reduce symptoms of depression. Further research into the link between dietary fiber intake and inflammation and depression is essential, as findings could potentially provide guidance for improvement in or prevention of inflammatory and depressive disorders.",
"role": "user"
},
{
"content": "<dietary supplement>Dietary fiber</dietary supplement> and its associations with <DDF>depression</DDF> and <DDF>inflammation</DDF>. <dietary supplement>Dietary fiber</dietary supplement> is a crucial component of a <food>healthy diet</food>, with benefits that can be attributed to processes in the <microbiome>gut microbiota</microbiome> and the resulting by-products. Observational studies support associations between dietary fiber intake and <DDF>depression</DDF> and <DDF>inflammation</DDF>, but the potential mechanisms are poorly understood. This review examines evidence of the effects of <dietary supplement>dietary fiber</dietary supplement> on <DDF>depression</DDF> and <DDF>inflammation</DDF> and considers plausible mechanisms linking <dietary supplement>dietary fiber</dietary supplement> and <DDF>depression</DDF>, including <DDF>microbiota-driven modification of gene expression</DDF> and <DDF>increased production of neurotransmitters</DDF>. Additionally, <DDF>inflammation</DDF> may mediate the relationship between dietary fiber intake and <DDF>depression</DDF>. A <food>high-fiber diet</food> potentially lowers <DDF>inflammation</DDF> by modifying both the pH and the permeability of the <anatomical location>gut</anatomical location>. The resultant reduction in <chemical>inflammatory compounds</chemical> may alter neurotransmitter concentrations to reduce symptoms of <DDF>depression</DDF>. Further research into the link between dietary fiber intake and <DDF>inflammation</DDF> and <DDF>depression</DDF> is essential, as findings could potentially provide guidance for improvement in or prevention of <DDF>inflammatory and depressive disorders</DDF>.",
"role": "assistant"
}
] |
31769847
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nProbiotics and prebiotics: focus on psychiatric disorders - a systematic review. The gut-brain axis and microbial dysbiosis may play a role in psychiatric diseases. In this view, the gut microbiota has been considered a potential therapeutic target using probiotics and prebiotics. This systematic review aims to find the existing clinical evidence that may justify the use of probiotics or prebiotics in psychiatric patients. PRISMA guidelines were followed for a systematic literature review of randomized controlled trials that assessed the effect of prebiotics or probiotics in patients diagnosed with a classified psychiatric disorder. From a total of 212 studies screened, 11 were included in the final systematic review. Quality assessment of the included trials was assessed by the Jadad scale. Probiotics seem to offer some benefit in major depressive disorder and Alzheimer's disease. One study showed that probiotics reduced rehospitalization in patients with acute mania. In autism spectrum disorders, the results were controversial; however a single study found that early administration of probiotics showed a preventive role. No benefits were found for patients with schizophrenia. In most studies, no major adverse effects were reported. Although recent findings in specific psychiatric disorders are encouraging, the use of prebiotics and probiotics in clinical practice stills lacks sufficiently robust evidence.",
"role": "user"
},
{
"content": "<dietary supplement>Probiotics</dietary supplement> and <dietary supplement>prebiotics</dietary supplement>: focus on <DDF>psychiatric disorders</DDF> - a systematic review. The gut-brain axis and <DDF>microbial dysbiosis</DDF> may play a role in <DDF>psychiatric diseases</DDF>. In this view, the <microbiome>gut microbiota</microbiome> has been considered a potential therapeutic target using <dietary supplement>probiotics</dietary supplement> and <dietary supplement>prebiotics</dietary supplement>. This systematic review aims to find the existing clinical evidence that may justify the use of <dietary supplement>probiotics</dietary supplement> or <dietary supplement>prebiotics</dietary supplement> in <human>psychiatric patients</human>. PRISMA guidelines were followed for a systematic literature review of randomized controlled trials that assessed the effect of <dietary supplement>prebiotics</dietary supplement> or <dietary supplement>probiotics</dietary supplement> in <human>patients</human> diagnosed with a classified <DDF>psychiatric disorder</DDF>. From a total of 212 studies screened, 11 were included in the final systematic review. Quality assessment of the included trials was assessed by the Jadad scale. <dietary supplement>Probiotics</dietary supplement> seem to offer some benefit in <DDF>major depressive disorder</DDF> and <DDF>Alzheimer's disease</DDF>. One study showed that <dietary supplement>probiotics</dietary supplement> reduced rehospitalization in <human>patients</human> with <DDF>acute mania</DDF>. In <DDF>autism spectrum disorders</DDF>, the results were controversial; however a single study found that early administration of <dietary supplement>probiotics</dietary supplement> showed a preventive role. No benefits were found for <human>patients</human> with <DDF>schizophrenia</DDF>. In most studies, no major adverse effects were reported. Although recent findings in specific <DDF>psychiatric disorders</DDF> are encouraging, the use of <dietary supplement>prebiotics</dietary supplement> and <dietary supplement>probiotics</dietary supplement> in clinical practice stills lacks sufficiently robust evidence.",
"role": "assistant"
}
] |
31821833
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe connection between microbiome and schizophrenia. There has been an accumulation of knowledge about the human microbiome, some detailed investigations of the gastrointestinal microbiota and its functions, and the highlighting of complex interactions between the gut, the gut microbiota, and the central nervous system. That assumes the involvement of the microbiome in the pathogenesis of various CNS diseases, including schizophrenia. Given this information and the fact, that the gut microbiota is sensitive to internal and environmental influences, we have speculated that among the factors that influence the formation and composition of gut microbiota during life, possible key elements in the schizophrenia development chain are hidden where gut microbiota is a linking component. This article aims to describe and understand the developmental relationships between intestinal microbiota and the risk of developing schizophrenia.",
"role": "user"
},
{
"content": "The connection between microbiome and <DDF>schizophrenia</DDF>. There has been an accumulation of knowledge about the <microbiome>human microbiome</microbiome>, some detailed investigations of the <microbiome>gastrointestinal microbiota</microbiome> and its functions, and the highlighting of complex interactions between the <anatomical location>gut</anatomical location>, the <microbiome>gut microbiota</microbiome>, and the central nervous system. That assumes the involvement of the microbiome in the pathogenesis of various <DDF>CNS diseases</DDF>, including <DDF>schizophrenia</DDF>. Given this information and the fact, that the <microbiome>gut microbiota</microbiome> is sensitive to internal and environmental influences, we have speculated that among the factors that influence the formation and composition of <microbiome>gut microbiota</microbiome> during life, possible key elements in the schizophrenia development chain are hidden where <microbiome>gut microbiota</microbiome> is a linking component. This article aims to describe and understand the developmental relationships between <microbiome>intestinal microbiota</microbiome> and the risk of developing <DDF>schizophrenia</DDF>.",
"role": "assistant"
}
] |
31917834
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAdolescence and Aging: Impact of Adolescence Inflammatory Stress and Microbiota Alterations on Brain Development, Aging, and Neurodegeneration. Puberty/adolescence is a critical phase during neurodevelopment with numerous structural, neurochemical, and molecular changes occurring in response to genetic and environmental signals. A consequence of this major neuronal reorganizing and remodeling is a heightened level of vulnerability to stressors and immune challenges. The gut microbiota is a fundamental modulator of stress and immune responses and has been found to play a role in mental health conditions and neurodegenerative disorders. Environmental insults (stress, infection, neuroinflammation, and use of antibiotics) during adolescence can result in dysbiosis subsidizing the development of brain disorders later in life. Also, pubertal neuroinflammatory insults can alter neurodevelopment, impact brain functioning in an enduring manner, and contribute to neurological disorders related to brain aging, such as Alzheimer's disease, Parkinson's disease, and depression. Exposure to probiotics during puberty can mitigate inflammation, reverse dysbiosis, and decrease vulnerabilities to brain disorders later in life. The goal of this review is to reveal the consequences of pubertal exposure to stress and immune challenges on the gut microbiota, immune reactivity within the brain, and the risk or resilience to stress-induced mental illnesses and neurodegenerative disorders. We propose that the consumption of probiotics during adolescence contribute to the prevention of brain pathologies in adulthood.",
"role": "user"
},
{
"content": "Adolescence and Aging: Impact of <DDF>Adolescence Inflammatory Stress</DDF> and <DDF>Microbiota Alterations</DDF> on Brain Development, Aging, and <DDF>Neurodegeneration</DDF>. Puberty/adolescence is a critical phase during neurodevelopment with numerous structural, neurochemical, and molecular changes occurring in response to genetic and environmental signals. A consequence of this major neuronal reorganizing and remodeling is a heightened level of vulnerability to stressors and immune challenges. The <microbiome>gut microbiota</microbiome> is a fundamental modulator of <DDF>stress</DDF> and immune responses and has been found to play a role in mental health conditions and <DDF>neurodegenerative disorders</DDF>. Environmental insults (<DDF>stress</DDF>, <DDF>infection</DDF>, <DDF>neuroinflammation</DDF>, and use of <drug>antibiotics</drug>) during adolescence can result in <DDF>dysbiosis</DDF> subsidizing the development of <DDF>brain disorders</DDF> later in life. Also, <DDF>pubertal neuroinflammatory insults</DDF> can alter neurodevelopment, impact brain functioning in an enduring manner, and contribute to <DDF>neurological disorders</DDF> related to brain aging, such as <DDF>Alzheimer's disease</DDF>, <DDF>Parkinson's disease</DDF>, and <DDF>depression</DDF>. Exposure to <dietary supplement>probiotics</dietary supplement> during puberty can mitigate <DDF>inflammation</DDF>, reverse <DDF>dysbiosis</DDF>, and decrease vulnerabilities to <DDF>brain disorders</DDF> later in life. The goal of this review is to reveal the consequences of pubertal exposure to <DDF>stress</DDF> and immune challenges on the <microbiome>gut microbiota</microbiome>, immune reactivity within the <anatomical location>brain</anatomical location>, and the risk or resilience to <DDF>stress-induced mental illnesses</DDF> and <DDF>neurodegenerative disorders</DDF>. We propose that the consumption of <dietary supplement>probiotics</dietary supplement> during adolescence contribute to the prevention of brain pathologies in adulthood.",
"role": "assistant"
}
] |
31940482
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nProbiotic Bacillus subtilis Protects against α-Synuclein Aggregation in C. elegans. Recent discoveries have implicated the gut microbiome in the progression and severity of Parkinson's disease; however, how gut bacteria affect such neurodegenerative disorders remains unclear. Here, we report that the Bacillus subtilis probiotic strain PXN21 inhibits α-synuclein aggregation and clears preformed aggregates in an established Caenorhabditis elegans model of synucleinopathy. This protection is seen in young and aging animals and is partly mediated by DAF-16. Multiple B. subtilis strains trigger the protective effect via both spores and vegetative cells, partly due to a biofilm formation in the gut of the worms and the release of bacterial metabolites. We identify several host metabolic pathways differentially regulated in response to probiotic exposure, including sphingolipid metabolism. We further demonstrate functional roles of the sphingolipid metabolism genes lagr-1, asm-3, and sptl-3 in the anti-aggregation effect. Our findings provide a basis for exploring the disease-modifying potential of B. subtilis as a dietary supplement.",
"role": "user"
},
{
"content": "<dietary supplement>Probiotic Bacillus subtilis</dietary supplement> Protects against α-Synuclein Aggregation in <animal>C. elegans</animal>. Recent discoveries have implicated the <microbiome>gut microbiome</microbiome> in the progression and severity of <DDF>Parkinson's disease</DDF>; however, how gut bacteria affect such <DDF>neurodegenerative disorders</DDF> remains unclear. Here, we report that the <bacteria>Bacillus subtilis probiotic strain PXN21</bacteria> inhibits α-synuclein aggregation and clears preformed aggregates in an established Caenorhabditis elegans model of <DDF>synucleinopathy</DDF>. This protection is seen in <animal>young and aging animals</animal> and is partly mediated by <gene>DAF-16</gene>. <bacteria>Multiple B. subtilis strains</bacteria> trigger the protective effect via both spores and vegetative cells, partly due to a biofilm formation in the <anatomical location>gut</anatomical location> of the <animal>worms</animal> and the release of <chemical>bacterial metabolites</chemical>. We identify several host metabolic pathways differentially regulated in response to probiotic exposure, including sphingolipid metabolism. We further demonstrate functional roles of the <gene>sphingolipid metabolism genes lagr-1</gene>, <gene>asm-3</gene>, and <gene>sptl-3</gene> in the anti-aggregation effect. Our findings provide a basis for exploring the disease-modifying potential of <bacteria>B. subtilis</bacteria> as a dietary supplement.",
"role": "assistant"
}
] |
32056910
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nFeeling down? A systematic review of the gut microbiota in anxiety/depression and irritable bowel syndrome. Background Anxiety/depression and irritable bowel syndrome (IBS) are highly prevalent and burdensome conditions, whose co-occurrence is estimated between 44 and 84%. Shared gut microbiota alterations have been identified in these separate disorders relative to controls; however, studies have not adequately considered their comorbidity. This review set out to identify case-control studies comparing the gut microbiota in anxiety/depression, IBS, and both conditions comorbidly relative to each other and to controls, as well as gut microbiota investigations including measures of both IBS and anxiety/depression. Methods Four databases were systematically searched using comprehensive search terms (OVID Medline, Embase, PsycINFO, and PubMed), following PRISMA guidelines. Results Systematic review identified 17 studies (10 human, 7 animal). Most studies investigated the gut microbiota and anxiety/depression symptoms in IBS cohorts. Participants with IBS and high anxiety/depression symptoms had lower alpha diversity compared to controls and IBS-only cohorts. Machine learning and beta diversity distinguished between IBS participants with and without anxiety/depression by their gut microbiota. Comorbid IBS and anxiety/depression also had higher abundance of Proteobacteria, Prevotella/Prevotellaceae, Bacteroides and lower Lachnospiraceae relative to controls. Limitations A large number of gut microbiota estimation methods and statistical techniques were utilized; therefore, meta-analysis was not possible. Conclusions Well-designed case-control and longitudinal studies are required to disentangle whether the gut microbiota is predicted as a continuum of gastrointestinal and anxiety/depression symptom severity, or whether reported dysbiosis is unique to IBS and anxiety/depression comorbidity. These findings may inform the development of targeted treatment through the gut microbiota for individuals with both anxiety/depression and IBS.",
"role": "user"
},
{
"content": "Feeling down? A systematic review of the <microbiome>gut microbiota</microbiome> in <DDF>anxiety</DDF>/<DDF>depression</DDF> and <DDF>irritable bowel syndrome</DDF>. Background <DDF>Anxiety</DDF>/<DDF>depression</DDF> and <DDF>irritable bowel syndrome</DDF> (<DDF>IBS</DDF>) are highly prevalent and burdensome conditions, whose co-occurrence is estimated between 44 and 84%. Shared gut microbiota alterations have been identified in these separate disorders relative to <human>controls</human>; however, studies have not adequately considered their comorbidity. This review set out to identify case-control studies comparing the <microbiome>gut microbiota</microbiome> in <DDF>anxiety</DDF>/<DDF>depression</DDF>, <DDF>IBS</DDF>, and both conditions comorbidly relative to each other and to <human>controls</human>, as well as gut microbiota investigations including measures of both <DDF>IBS</DDF> and <DDF>anxiety</DDF>/<DDF>depression</DDF>. Methods Four databases were systematically searched using comprehensive search terms (OVID Medline, Embase, PsycINFO, and PubMed), following PRISMA guidelines. Results Systematic review identified 17 studies (10 human, 7 animal). Most studies investigated the <microbiome>gut microbiota</microbiome> and <DDF>anxiety/depression symptoms</DDF> in <human>IBS cohorts</human>. <human>Participants</human> with <DDF>IBS</DDF> and high <DDF>anxiety/depression symptoms</DDF> had lower alpha diversity compared to <human>controls</human> and <human>IBS-only cohorts</human>. Machine learning and beta diversity distinguished between <human>IBS participants</human> with and without <DDF>anxiety</DDF>/<DDF>depression</DDF> by their <microbiome>gut microbiota</microbiome>. Comorbid <DDF>IBS</DDF> and <DDF>anxiety</DDF>/<DDF>depression</DDF> also had higher abundance of <bacteria>Proteobacteria</bacteria>, <bacteria>Prevotella</bacteria>/<bacteria>Prevotellaceae</bacteria>, <bacteria>Bacteroides</bacteria> and lower <bacteria>Lachnospiraceae</bacteria> relative to <human>controls</human>. Limitations A large number of gut microbiota estimation methods and statistical techniques were utilized; therefore, meta-analysis was not possible. Conclusions Well-designed case-control and longitudinal studies are required to disentangle whether the <microbiome>gut microbiota</microbiome> is predicted as a continuum of <DDF>gastrointestinal and anxiety/depression symptom severity</DDF>, or whether reported <DDF>dysbiosis</DDF> is unique to <DDF>IBS</DDF> and anxiety/depression comorbidity. These findings may inform the development of targeted treatment through the <microbiome>gut microbiota</microbiome> for individuals with both <DDF>anxiety</DDF>/<DDF>depression</DDF> and <DDF>IBS</DDF>.",
"role": "assistant"
}
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32155131
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEffects of the probiotic formulation SLAB51 in <i>in vitro</i> and <i>in vivo</i> Parkinson's disease models. Parkinson is a common neurodegenerative disorder, characterized by motor and non-motor symptoms, including abnormalities in the gut function, which may appear before the motor sign. To date, there are treatments that can help relieve Parkinson' disease (PD)-associated symptoms, but there is no cure to control the onset and progression of this disorder. Altered components of the gut could represent a key role in gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Diet can alter the microbiota composition, affecting gut-brain axis function. Gut microbiome restoration through selected probiotics' administration has been reported. In this study, we investigated the effects of the novel formulation SLAB51 in PD. Our findings indicate that this probiotic formulation can counteract the detrimental effect of 6-OHDA <i>in vitro</i> and <i>in vivo</i> models of PD. The results suggest that SLAB51 can be a promising candidate for the prevention or as coadjuvant treatment of PD.",
"role": "user"
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{
"content": "Effects of the <dietary supplement>probiotic formulation SLAB51</dietary supplement> in <i>in vitro</i> and <i>in vivo</i> Parkinson's disease models. <DDF>Parkinson</DDF> is a common <DDF>neurodegenerative disorder</DDF>, characterized by motor and non-motor symptoms, including <DDF>abnormalities in the gut function</DDF>, which may appear before the motor sign. To date, there are treatments that can help relieve Parkinson' disease (PD)-associated symptoms, but there is no cure to control the onset and progression of this disorder. Altered components of the <anatomical location>gut</anatomical location> could represent a key role in gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Diet can alter the microbiota composition, affecting gut-brain axis function. <microbiome>Gut microbiome</microbiome> restoration through selected probiotics' administration has been reported. In this study, we investigated the effects of the novel formulation <dietary supplement>SLAB51</dietary supplement> in <DDF>PD</DDF>. Our findings indicate that this <dietary supplement>probiotic formulation</dietary supplement> can counteract the detrimental effect of <chemical>6-OHDA</chemical> <i>in vitro</i> and <i>in vivo</i> models of PD. The results suggest that <dietary supplement>SLAB51</dietary supplement> can be a promising candidate for the prevention or as coadjuvant treatment of <DDF>PD</DDF>.",
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32163822
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe gut microbiota and mental health in adults. A growing body of evidence point toward the bidirectional gut microbiota-brain axis playing a role in mental health. Most of this research is conducted on animals why we in this review summarize and comment upon recent studies evaluating the gut microbiome in mental health in humans. Further support for the relevance of the bidirectional gut microbiota-brain communication in mood disorders has been presented, such as the effect of probiotics on brain connectivity and mental health outcomes and pregnancy related stress on gut microbiota in the newborn child. However, the heterogeneity between studies precludes conclusions regarding differences in microbiota composition in mental disease and health and many of the studies are limited by a cross-sectional design, small sample sizes and multiple comparisons. Thus, well-designed longitudinal studies with larger sample size, accounting for confounders are needed.",
"role": "user"
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{
"content": "The <microbiome>gut microbiota</microbiome> and mental health in <human>adults</human>. A growing body of evidence point toward the bidirectional gut microbiota-brain axis playing a role in mental health. Most of this research is conducted on <animal>animals</animal> why we in this review summarize and comment upon recent studies evaluating the <microbiome>gut microbiome</microbiome> in mental health in <human>humans</human>. Further support for the relevance of the bidirectional gut microbiota-brain communication in <DDF>mood disorders</DDF> has been presented, such as the effect of <dietary supplement>probiotics</dietary supplement> on brain connectivity and mental health outcomes and <DDF>pregnancy related stress</DDF> on <microbiome>gut microbiota</microbiome> in the <human>newborn child</human>. However, the heterogeneity between studies precludes conclusions regarding differences in microbiota composition in <DDF>mental disease</DDF> and health and many of the studies are limited by a <statistical technique>cross-sectional design</statistical technique>, <statistical technique>small sample sizes</statistical technique> and <statistical technique>multiple comparisons</statistical technique>. Thus, well-designed longitudinal studies with larger sample size, accounting for confounders are needed.",
"role": "assistant"
}
] |
32188376
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDiet and Neurocognition in Mood Disorders - An Overview of the Overlooked. Bipolar disorder and major depression are associated with significant disability, morbidity, and reduced life expectancy. People with mood disorders have shown higher ratios of unhealthy lifestyle choices, including poor diet quality and suboptimal nutrition. Diet and nutrition impact on brain /mental health, but cognitive outcomes have been less researched in psychiatric disorders. Neurocognitive dysfunction is a major driver of social dysfunction and a therapeutic target in mood disorders, although effective cognitive-enhancers are currently lacking. This narrative review aimed to assess the potential cognitive benefits of dietary and nutritional interventions in subjects diagnosed with mood disorders. Eight clinical trials with nutrients were identified, whereas none involved dietary interventions. Efficacy to improve select cognitive deficits has been reported, but results are either preliminary or inconsistent. Methodological recommendations for future cognition trials in the field are advanced. Current evidence and future views are discussed from the perspectives of precision medicine, clinical staging, nutritional psychiatry, and the brain-gut-microbiota axis.",
"role": "user"
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{
"content": "Diet and Neurocognition in <DDF>Mood Disorders</DDF> - An Overview of the Overlooked. <DDF>Bipolar disorder</DDF> and <DDF>major depression</DDF> are associated with significant <DDF>disability</DDF>, <DDF>morbidity</DDF>, and <DDF>reduced life expectancy</DDF>. <human>People</human> with <DDF>mood disorders</DDF> have shown higher ratios of unhealthy lifestyle choices, including poor diet quality and suboptimal nutrition. Diet and nutrition impact on brain /mental health, but cognitive outcomes have been less researched in <DDF>psychiatric disorders</DDF>. <DDF>Neurocognitive dysfunction</DDF> is a major driver of <DDF>social dysfunction</DDF> and a therapeutic target in <DDF>mood disorders</DDF>, although effective cognitive-enhancers are currently lacking. This narrative review aimed to assess the potential cognitive benefits of dietary and nutritional interventions in subjects diagnosed with <DDF>mood disorders</DDF>. Eight clinical trials with nutrients were identified, whereas none involved dietary interventions. Efficacy to improve select <DDF>cognitive deficits</DDF> has been reported, but results are either preliminary or inconsistent. Methodological recommendations for future cognition trials in the field are advanced. Current evidence and future views are discussed from the perspectives of precision medicine, clinical staging, nutritional psychiatry, and the brain-gut-microbiota axis.",
"role": "assistant"
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32379622
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nBetaine supplementation is associated with the resilience in mice after chronic social defeat stress: a role of brain-gut-microbiota axis. The brain-gut-microbiota axis plays a role in the pathogenesis of stress-related psychiatric disorders; however, its role in the resilience versus susceptibility after stress remains unclear. Dietary nutrient betaine is suggested to affect the gut microbiome. Here, we examined whether betaine supplementation can affect anhedonia-like phenotype in mice subjected to chronic social defeat stress (CSDS). CSDS was performed during betaine supplementation. Sucrose preference test and 16S rRNA analysis of fecal samples were performed. CSDS did not produce an anhedonia-like phenotype in the betaine-treated mice, but did induce an anhedonia-like phenotype in water-treated mice. Furthermore, CSDS treatment did not alter the plasma levels of interleukin-6 (IL-6) of betaine-treated mice whereas CSDS caused higher plasma levels of IL-6 in water-treated mice. Betaine supplementation ameliorated the abnormal diversity and composition of the microbiota in the host gut after CSDS. At the genus level, CSDS caused marked increases in the several bacteria of water-treated mice, but not betaine-treated mice. CSDS increased levels of short-chain fatty acids (i.e., succinic acid and acetic acid) in feces from water-treated mice, but not betaine-treated mice. Interestingly, there are positive correlations between short-chain fatty acids (i.e., succinic acid, acetic acid, butyric acid) and several bacteria among the groups. Specific microbiome were not determined. These findings suggest that betaine supplementation contributed to resilience to anhedonia in mice subjected to CSDS through anti-inflammation action. Therefore, it is likely that betaine could be a prophylactic nutrient to prevent stress-related psychiatric disorders.",
"role": "user"
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{
"content": "<dietary supplement>Betaine supplementation</dietary supplement> is associated with the resilience in <animal>mice</animal> after <DDF>chronic social defeat stress</DDF>: a role of brain-gut-microbiota axis. The brain-gut-microbiota axis plays a role in the pathogenesis of <DDF>stress-related psychiatric disorders</DDF>; however, its role in the resilience versus susceptibility after <DDF>stress</DDF> remains unclear. Dietary nutrient <dietary supplement>betaine</dietary supplement> is suggested to affect the <microbiome>gut microbiome</microbiome>. Here, we examined whether <dietary supplement>betaine supplementation</dietary supplement> can affect anhedonia-like phenotype in <animal>mice</animal> subjected to <DDF>chronic social defeat stress</DDF> (<DDF>CSDS</DDF>). <DDF>CSDS</DDF> was performed during <dietary supplement>betaine supplementation</dietary supplement>. <biomedical technique>Sucrose preference test</biomedical technique> and <biomedical technique>16S rRNA analysis</biomedical technique> of fecal samples were performed. <DDF>CSDS</DDF> did not produce an anhedonia-like phenotype in the <animal>betaine-treated mice</animal>, but did induce an anhedonia-like phenotype in <animal>water-treated mice</animal>. Furthermore, <DDF>CSDS</DDF> treatment did not alter the plasma levels of <chemical>interleukin-6</chemical> (<chemical>IL-6</chemical>) of <animal>betaine-treated mice</animal> whereas <DDF>CSDS</DDF> caused higher plasma levels of <chemical>IL-6</chemical> in <animal>water-treated mice</animal>. <dietary supplement>Betaine supplementation</dietary supplement> ameliorated the abnormal diversity and composition of the microbiota in the <anatomical location>host gut</anatomical location> after <DDF>CSDS</DDF>. At the genus level, <DDF>CSDS</DDF> caused marked increases in the several bacteria of <animal>water-treated mice</animal>, but not <animal>betaine-treated mice</animal>. <DDF>CSDS</DDF> increased levels of <chemical>short-chain fatty acids</chemical> (i.e., <chemical>succinic acid</chemical> and <chemical>acetic acid</chemical>) in feces from <animal>water-treated mice</animal>, but not <animal>betaine-treated mice</animal>. Interestingly, there are positive correlations between <chemical>short-chain fatty acids</chemical> (i.e., <chemical>succinic acid</chemical>, <chemical>acetic acid</chemical>, <chemical>butyric acid</chemical>) and several bacteria among the groups. Specific microbiome were not determined. These findings suggest that <dietary supplement>betaine supplementation</dietary supplement> contributed to resilience to <DDF>anhedonia</DDF> in <animal>mice</animal> subjected to <DDF>CSDS</DDF> through anti-inflammation action. Therefore, it is likely that <dietary supplement>betaine</dietary supplement> could be a prophylactic nutrient to prevent <DDF>stress-related psychiatric disorders</DDF>.",
"role": "assistant"
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32431588
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut Microbiome-Modified Polyphenolic Compounds Inhibit α-Synuclein Seeding and Spreading in α-Synucleinopathies. Misfolding, aggregation and deposition of α-synuclein (α-syn) are major pathologic characteristics of Parkinson's disease (PD) and the related synucleinopathy, multiple system atrophy (MSA). The spread of α-syn pathology across brain regions is thought to play a key role in the onset and progression of clinical phenotypes. Thus, there is increasing interest in developing strategies that target and attenuate α-syn aggregation and spread. Recent studies of brain-penetrating polyphenolic acids, namely, 3-hydroxybenzoic acid (3-HBA), 3,4-dihydroxybenzoic acid (3,4-diHBA), and 3-(3-hydroxyphenyl)propionic acid (3-HPPA) that are derived from gut microbiota metabolism of dietary polyphenols, show <i>in vitro</i> ability to effectively modulate α-syn misfolding, oligomerization, and mediate aggregated α-syn neurotoxicity. Here we investigate whether 3-HBA, 4-hydroxybenzoic acid (4-HBA), 3,4-diHBA, or 3-HPPA interfere with α-syn spreading in a cell-based system. Using HEK293 cells overexpressing α-syn-A53T-CFP/YFP, we assessed α-syn seeding activity using Fluorescence Resonance Energy Transfer (FRET) to detect and quantify α-syn aggregation. We demonstrated that 3-HPPA, 3,4-diHBA, 3-HBA, and 4-HBA significantly attenuated intracellular α-syn seeding aggregation. To determine whether our compounds could inhibit brain-derived seeding activity, we utilized insoluble α-syn extracted from post-mortem MSA or PD brain specimens. We found that 3-HPPA effectively attenuated MSA-induced aggregation of monomer into high molecular weight aggregates capable of inducing intracellular aggregation. Outcomes from our studies suggest interactions between gut microbiome and certain dietary factors may form the basis for effective therapies that modulate pathologic α-syn propagation. Collectively, our findings provide the basis for future developments of probiotic, prebiotic, or synbiotic approaches for modulating the onset and/or progression of α-synucleinopathies.",
"role": "user"
},
{
"content": "<chemical>Gut Microbiome-Modified Polyphenolic Compounds</chemical> Inhibit α-Synuclein Seeding and Spreading in <DDF>α-Synucleinopathies</DDF>. Misfolding, aggregation and deposition of <chemical>α-synuclein</chemical> (<chemical>α-syn</chemical>) are major pathologic characteristics of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>) and the related <DDF>synucleinopathy</DDF>, <DDF>multiple system atrophy</DDF> (<DDF>MSA</DDF>). The spread of <DDF>α-syn pathology</DDF> across <anatomical location>brain regions</anatomical location> is thought to play a key role in the onset and progression of clinical phenotypes. Thus, there is increasing interest in developing strategies that target and attenuate α-syn aggregation and spread. Recent studies of brain-penetrating <chemical>polyphenolic acids</chemical>, namely, <chemical>3-hydroxybenzoic acid</chemical> (<chemical>3-HBA</chemical>), <chemical>3,4-dihydroxybenzoic acid</chemical> (<chemical>3,4-diHBA</chemical>), and <chemical>3-(3-hydroxyphenyl)propionic acid</chemical> (<chemical>3-HPPA</chemical>) that are derived from gut microbiota metabolism of <chemical>dietary polyphenols</chemical>, show <i>in vitro</i> ability to effectively modulate <DDF>α-syn misfolding</DDF>, <DDF>oligomerization</DDF>, and mediate <DDF>aggregated α-syn neurotoxicity</DDF>. Here we investigate whether <chemical>3-HBA</chemical>, <chemical>4-hydroxybenzoic acid</chemical> (<chemical>4-HBA</chemical>), <chemical>3,4-diHBA</chemical>, or <chemical>3-HPPA</chemical> interfere with α-syn spreading in a cell-based system. Using <bacteria>HEK293 cells</bacteria> overexpressing <gene>α-syn-A53T-CFP/YFP</gene>, we assessed α-syn seeding activity using <biomedical technique>Fluorescence Resonance Energy Transfer</biomedical technique> (<biomedical technique>FRET</biomedical technique>) to detect and quantify α-syn aggregation. We demonstrated that <chemical>3-HPPA</chemical>, <chemical>3,4-diHBA</chemical>, <chemical>3-HBA</chemical>, and <chemical>4-HBA</chemical> significantly attenuated <DDF>intracellular α-syn seeding aggregation</DDF>. To determine whether our compounds could inhibit brain-derived seeding activity, we utilized <chemical>insoluble α-syn</chemical> extracted from post-mortem <DDF>MSA</DDF> or <DDF>PD</DDF> brain specimens. We found that <chemical>3-HPPA</chemical> effectively attenuated <DDF>MSA-induced aggregation of monomer</DDF> into high molecular weight aggregates capable of inducing intracellular aggregation. Outcomes from our studies suggest interactions between <microbiome>gut microbiome</microbiome> and certain dietary factors may form the basis for effective therapies that modulate pathologic α-syn propagation. Collectively, our findings provide the basis for future developments of <dietary supplement>probiotic</dietary supplement>, <dietary supplement>prebiotic</dietary supplement>, or <dietary supplement>synbiotic</dietary supplement> approaches for modulating the onset and/or progression of <DDF>α-synucleinopathies</DDF>.",
"role": "assistant"
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32517799
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nParkinson's disease-associated alterations of the gut microbiome predict disease-relevant changes in metabolic functions. Parkinson's disease (PD) is a systemic disease clinically defined by the degeneration of dopaminergic neurons in the brain. While alterations in the gut microbiome composition have been reported in PD, their functional consequences remain unclear. Herein, we addressed this question by an analysis of stool samples from the Luxembourg Parkinson's Study (n = 147 typical PD cases, n = 162 controls). All individuals underwent detailed clinical assessment, including neurological examinations and neuropsychological tests followed by self-reporting questionnaires. Stool samples from these individuals were first analysed by 16S rRNA gene sequencing. Second, we predicted the potential secretion for 129 microbial metabolites through personalised metabolic modelling using the microbiome data and genome-scale metabolic reconstructions of human gut microbes. Our key results include the following. Eight genera and seven species changed significantly in their relative abundances between PD patients and healthy controls. PD-associated microbial patterns statistically depended on sex, age, BMI, and constipation. Particularly, the relative abundances of Bilophila and Paraprevotella were significantly associated with the Hoehn and Yahr staging after controlling for the disease duration. Furthermore, personalised metabolic modelling of the gut microbiomes revealed PD-associated metabolic patterns in the predicted secretion potential of nine microbial metabolites in PD, including increased methionine and cysteinylglycine. The predicted microbial pantothenic acid production potential was linked to the presence of specific non-motor symptoms. Our results suggest that PD-associated alterations of the gut microbiome can translate into substantial functional differences affecting host metabolism and disease phenotype.",
"role": "user"
},
{
"content": "<DDF>Parkinson's disease-associated alterations</DDF> of the <microbiome>gut microbiome</microbiome> predict disease-relevant changes in metabolic functions. <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>) is a <DDF>systemic disease</DDF> clinically defined by the degeneration of dopaminergic neurons in the <anatomical location>brain</anatomical location>. While alterations in the <microbiome>gut microbiome</microbiome> composition have been reported in <DDF>PD</DDF>, their functional consequences remain unclear. Herein, we addressed this question by an analysis of stool samples from the Luxembourg Parkinson's Study (n = 147 typical <human>PD cases</human>, n = 162 <human>controls</human>). All individuals underwent detailed clinical assessment, including <biomedical technique>neurological examinations</biomedical technique> and <biomedical technique>neuropsychological tests</biomedical technique> followed by <biomedical technique>self-reporting questionnaires</biomedical technique>. Stool samples from these individuals were first analysed by <biomedical technique>16S rRNA gene sequencing</biomedical technique>. Second, we predicted the potential secretion for 129 <chemical>microbial metabolites</chemical> through personalised <biomedical technique>metabolic modelling</biomedical technique> using the microbiome data and genome-scale metabolic reconstructions of <bacteria>human gut microbes</bacteria>. Our key results include the following. Eight genera and seven species changed significantly in their relative abundances between <human>PD patients</human> and <human>healthy controls</human>. PD-associated microbial patterns statistically depended on sex, age, BMI, and <DDF>constipation</DDF>. Particularly, the relative abundances of <bacteria>Bilophila</bacteria> and <bacteria>Paraprevotella</bacteria> were significantly associated with the Hoehn and Yahr staging after controlling for the disease duration. Furthermore, personalised metabolic modelling of the <microbiome>gut microbiomes</microbiome> revealed PD-associated metabolic patterns in the predicted secretion potential of nine <chemical>microbial metabolites</chemical> in <DDF>PD</DDF>, including increased <chemical>methionine</chemical> and <chemical>cysteinylglycine</chemical>. The predicted microbial pantothenic acid production potential was linked to the presence of specific <DDF>non-motor symptoms</DDF>. Our results suggest that <DDF>PD-associated alterations</DDF> of the <microbiome>gut microbiome</microbiome> can translate into substantial functional differences affecting host metabolism and disease phenotype.",
"role": "assistant"
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32518376
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nA key role of the subdiaphragmatic vagus nerve in the depression-like phenotype and abnormal composition of gut microbiota in mice after lipopolysaccharide administration. The vagus nerve plays a role in the cross talk between the brain and gut microbiota, which could be involved in depression. The subdiaphragmatic vagus nerve serves as a major modulatory pathway between the brain and gut microbiota. Here, we investigated the effects of subdiaphragmatic vagotomy (SDV) on the depression-like phenotype and the abnormal composition of gut microbiota in mice after lipopolysaccharide (LPS) administration. LPS caused a depression-like phenotype, inflammation, increase in spleen weight, and downregulation of synaptic proteins in the medial prefrontal cortex (mPFC) in the sham-operated mice. In contrast, LPS did not produce a depression-like phenotype and downregulated synaptic proteins in the mPFC after SDV. The spleen weight and plasma levels of pro-inflammatory cytokines in the SDV + LPS group were lower than those of the sham + LPS group. Interestingly, there were positive correlations between the plasma levels of pro-inflammatory cytokines and spleen weight, suggesting a relationship between inflammatory events and spleen weight. Furthermore, LPS led to significant alterations in gut microbiota diversity in sham-operated mice, but not SDV-operated mice. In an unweighted UniFrac PCoA, the dots representing the sham + LPS group were located far away from the dots representing the other three groups. Our results suggest that LPS produces a depression-like phenotype, increases spleen weight, triggers inflammation, downregulates synaptic proteins in the mPFC, and leads to abnormal composition of gut microbiota via the subdiaphragmatic vagus nerve. It is likely that the vagus nerve plays a crucial role in the brain-gut-microbiota axis.",
"role": "user"
},
{
"content": "A key role of the <anatomical location>subdiaphragmatic vagus nerve</anatomical location> in the depression-like phenotype and abnormal composition of <microbiome>gut microbiota</microbiome> in <animal>mice</animal> after <chemical>lipopolysaccharide</chemical> administration. The <anatomical location>vagus nerve</anatomical location> plays a role in the cross talk between the <anatomical location>brain</anatomical location> and <microbiome>gut microbiota</microbiome>, which could be involved in <DDF>depression</DDF>. The <anatomical location>subdiaphragmatic vagus nerve</anatomical location> serves as a major modulatory pathway between the <anatomical location>brain</anatomical location> and <microbiome>gut microbiota</microbiome>. Here, we investigated the effects of subdiaphragmatic vagotomy (SDV) on the depression-like phenotype and the abnormal composition of <microbiome>gut microbiota</microbiome> in <animal>mice</animal> after <chemical>lipopolysaccharide</chemical> (<chemical>LPS</chemical>) administration. <chemical>LPS</chemical> caused a depression-like phenotype, <DDF>inflammation</DDF>, increase in spleen weight, and downregulation of <chemical>synaptic proteins</chemical> in the <anatomical location>medial prefrontal cortex</anatomical location> (<anatomical location>mPFC</anatomical location>) in the <animal>sham-operated mice</animal>. In contrast, <chemical>LPS</chemical> did not produce a depression-like phenotype and downregulated <chemical>synaptic proteins</chemical> in the <anatomical location>mPFC</anatomical location> after SDV. The spleen weight and plasma levels of <chemical>pro-inflammatory cytokines</chemical> in the SDV + LPS group were lower than those of the sham + LPS group. Interestingly, there were positive correlations between the plasma levels of <chemical>pro-inflammatory cytokines</chemical> and spleen weight, suggesting a relationship between inflammatory events and spleen weight. Furthermore, <chemical>LPS</chemical> led to significant alterations in gut microbiota diversity in <animal>sham-operated mice</animal>, but not <animal>SDV-operated mice</animal>. In an <biomedical technique>unweighted UniFrac PCoA</biomedical technique>, the dots representing the sham + LPS group were located far away from the dots representing the other three groups. Our results suggest that <chemical>LPS</chemical> produces a depression-like phenotype, increases spleen weight, triggers <DDF>inflammation</DDF>, downregulates <chemical>synaptic proteins</chemical> in the <anatomical location>mPFC</anatomical location>, and leads to abnormal composition of <microbiome>gut microbiota</microbiome> via the <anatomical location>subdiaphragmatic vagus nerve</anatomical location>. It is likely that the <anatomical location>vagus nerve</anatomical location> plays a crucial role in the brain-gut-microbiota axis.",
"role": "assistant"
}
] |
32538869
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nCrosstalk Between Alpha-Synuclein and Other Human and Non-Human Amyloidogenic Proteins: Consequences for Amyloid Formation in Parkinson's Disease. It was recently shown (Sampson et al., Elife9, 2020) that an amyloidogenic protein, CsgA, present in E. coli biofilms in the gut can trigger Parkinson's disease in mice. This study emphasizes the possible role of the gut microbiome in modulation (and even initiation) of human neurodegenerative disorders, such as Parkinson's disease. As the CsgA protein was found to accelerate alpha-synuclein (the key amyloidogenic protein in Parkinson's disease) amyloid formation in vitro, this result suggests that also other amyloidogenic proteins from gut bacteria, and even from the diet (such as stable allergenic proteins), may be able to affect human protein conformations and thereby modulate amyloid-related diseases. In this review, we summarize what has been reported in terms of in vitro cross-reactivity studies between alpha-synuclein and other amyloidogenic human and non-human proteins. It becomes clear from the limited data that exist that there is a fine line between acceleration and inhibition, but that cross-reactivity is widespread, and it is more common for other proteins (among the studied cases) to accelerate alpha-synuclein amyloid formation than to block it. It is of high importance to expand investigations of cross-reactivity between amyloidogenic proteins to both reveal underlying mechanisms and links between human diseases, as well as to develop new treatments that may be based on an altered gut microbiome.",
"role": "user"
},
{
"content": "Crosstalk Between <chemical>Alpha-Synuclein</chemical> and Other <chemical>Human and Non-Human Amyloidogenic Proteins</chemical>: Consequences for Amyloid Formation in <DDF>Parkinson's Disease</DDF>. It was recently shown (Sampson et al., Elife9, 2020) that an <chemical>amyloidogenic protein</chemical>, <chemical>CsgA</chemical>, present in E. coli biofilms in the <anatomical location>gut</anatomical location> can trigger <DDF>Parkinson's disease</DDF> in <animal>mice</animal>. This study emphasizes the possible role of the <microbiome>gut microbiome</microbiome> in modulation (and even initiation) of <DDF>human neurodegenerative disorders</DDF>, such as <DDF>Parkinson's disease</DDF>. As the <chemical>CsgA protein</chemical> was found to accelerate alpha-synuclein (the key <chemical>amyloidogenic protein</chemical> in <DDF>Parkinson's disease</DDF>) amyloid formation in vitro, this result suggests that also other <chemical>amyloidogenic proteins</chemical> from <bacteria>gut bacteria</bacteria>, and even from the diet (such as <chemical>stable allergenic proteins</chemical>), may be able to affect human protein conformations and thereby modulate <DDF>amyloid-related diseases</DDF>. In this review, we summarize what has been reported in terms of in vitro cross-reactivity studies between <chemical>alpha-synuclein</chemical> and other <chemical>amyloidogenic human and non-human proteins</chemical>. It becomes clear from the limited data that exist that there is a fine line between acceleration and inhibition, but that cross-reactivity is widespread, and it is more common for other proteins (among the studied cases) to accelerate alpha-synuclein amyloid formation than to block it. It is of high importance to expand investigations of cross-reactivity between <chemical>amyloidogenic proteins</chemical> to both reveal underlying mechanisms and links between <DDF>human diseases</DDF>, as well as to develop new treatments that may be based on an altered <microbiome>gut microbiome</microbiome>.",
"role": "assistant"
}
] |
32545788
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nFocus on the Role of NLRP3 Inflammasome in Diseases. Inflammation is a protective reaction activated in response to detrimental stimuli, such as dead cells, irritants or pathogens, by the evolutionarily conserved immune system and is regulated by the host. The inflammasomes are recognized as innate immune system sensors and receptors that manage the activation of caspase-1 and stimulate inflammation response. They have been associated with several inflammatory disorders. The NLRP3 inflammasome is the most well characterized. It is so called because NLRP3 belongs to the family of nucleotide-binding and oligomerization domain-like receptors (NLRs). Recent evidence has greatly improved our understanding of the mechanisms by which the NLRP3 inflammasome is activated. Additionally, increasing data in animal models, supported by human studies, strongly implicate the involvement of the inflammasome in the initiation or progression of disorders with a high impact on public health, such as metabolic pathologies (obesity, type 2 diabetes, atherosclerosis), cardiovascular diseases (ischemic and non-ischemic heart disease), inflammatory issues (liver diseases, inflammatory bowel diseases, gut microbiome, rheumatoid arthritis) and neurologic disorders (Parkinson's disease, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis and other neurological disorders), compared to other molecular platforms. This review will provide a focus on the available knowledge about the NLRP3 inflammasome role in these pathologies and describe the balance between the activation of the harmful and beneficial inflammasome so that new therapies can be created for patients with these diseases.",
"role": "user"
},
{
"content": "Focus on the Role of <chemical>NLRP3 Inflammasome</chemical> in Diseases. <DDF>Inflammation</DDF> is a protective reaction activated in response to detrimental stimuli, such as <chemical>dead cells</chemical>, <chemical>irritants</chemical> or <chemical>pathogens</chemical>, by the evolutionarily conserved immune system and is regulated by the host. The inflammasomes are recognized as innate immune system sensors and receptors that manage the activation of <gene>caspase-1</gene> and stimulate inflammation response. They have been associated with several <DDF>inflammatory disorders</DDF>. The <chemical>NLRP3 inflammasome</chemical> is the most well characterized. It is so called because <gene>NLRP3</gene> belongs to the family of <chemical>nucleotide-binding</chemical> and <chemical>oligomerization domain-like receptors</chemical> (<chemical>NLRs</chemical>). Recent evidence has greatly improved our understanding of the mechanisms by which the <chemical>NLRP3 inflammasome</chemical> is activated. Additionally, increasing data in animal models, supported by human studies, strongly implicate the involvement of the inflammasome in the initiation or progression of disorders with a high impact on public health, such as <DDF>metabolic pathologies</DDF> (<DDF>obesity</DDF>, <DDF>type 2 diabetes</DDF>, <DDF>atherosclerosis</DDF>), <DDF>cardiovascular diseases</DDF> (<DDF>ischemic and non-ischemic heart disease</DDF>), <DDF>inflammatory issues</DDF> (<DDF>liver diseases</DDF>, <DDF>inflammatory bowel diseases</DDF>, <microbiome>gut microbiome</microbiome>, <DDF>rheumatoid arthritis</DDF>) and <DDF>neurologic disorders</DDF> (<DDF>Parkinson's disease</DDF>, <DDF>Alzheimer's disease</DDF>, <DDF>multiple sclerosis</DDF>, <DDF>amyotrophic lateral sclerosis</DDF> and other <DDF>neurological disorders</DDF>), compared to other molecular platforms. This review will provide a focus on the available knowledge about the NLRP3 inflammasome role in these pathologies and describe the balance between the activation of the harmful and beneficial inflammasome so that new therapies can be created for <human>patients</human> with these diseases.",
"role": "assistant"
}
] |
32572814
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nButyrate Protects Against Salsolinol-Induced Toxicity in SH-SY5Y Cells: Implication for Parkinson's Disease. Parkinson's disease (PD), a progressive neurodegenerative disorder, is associated with the destruction of dopamine neurons in the substantia nigra (SN) and the formation of Lewy bodies in basal ganglia. Risk factors for PD include aging, as well as environmental and genetic factors. Recent converging reports suggest a role for the gut microbiome and epigenetic factors in the onset and/or progression of PD. Of particular relevance and potential therapeutic targets in this regard are histone deacetylases (HDACs), enzymes that are involved in chromatin remodeling. Butyrate, a short-chain fatty acid (FA) produced in the gut and presumably acting via several G protein-coupled receptors (GPCRs) including FA3 receptors (FA3Rs), is a well-known HDAC inhibitor that plays an important role in maintaining homeostasis of the gut-brain axis. Recently, its significance in regulation of some critical brain functions and usefulness in neurodegenerative diseases such as PD has been suggested. In this study we sought to determine whether butyrate may have protective effects against salsolionl (SALS)-induced toxicity in SH-SY5Y cells. SALS, an endogenous product of aldehyde and dopamine condensation, may be selectively toxic to dopaminergic neurons. SH-SY5Y cells, derived from human neuroblastoma cells, are used as a model of these neurons. Exposure of SH-SY5Y cells for 24 h to 400 μM SALS resulted in approximately 60% cell death, which was concentration-dependently prevented by butyrate. The effects of butyrate in turn were significantly attenuated by beta-hydroxy butyrate (BHB), a selective FA3R antagonist. Moreover, a selective FA3R agonist (AR 420626) also provided protective effects against SALS, which was totally blocked by BHB. These findings provide further support that butyrate or an agonist of FA3R may be of therapeutic potential in PD.",
"role": "user"
},
{
"content": "<chemical>Butyrate</chemical> Protects Against <DDF>Salsolinol-Induced Toxicity</DDF> in SH-SY5Y Cells: Implication for <DDF>Parkinson's Disease</DDF>. <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>), a <DDF>progressive neurodegenerative disorder</DDF>, is associated with the destruction of dopamine neurons in the <anatomical location>substantia nigra</anatomical location> (<anatomical location>SN</anatomical location>) and the formation of Lewy bodies in <anatomical location>basal ganglia</anatomical location>. Risk factors for <DDF>PD</DDF> include aging, as well as environmental and genetic factors. Recent converging reports suggest a role for the <microbiome>gut microbiome</microbiome> and epigenetic factors in the onset and/or progression of <DDF>PD</DDF>. Of particular relevance and potential therapeutic targets in this regard are <chemical>histone deacetylases</chemical> (<chemical>HDACs</chemical>), enzymes that are involved in chromatin remodeling. <chemical>Butyrate</chemical>, a <chemical>short-chain fatty acid</chemical> (<chemical>FA</chemical>) produced in the <anatomical location>gut</anatomical location> and presumably acting via several <chemical>G protein-coupled receptors</chemical> (<chemical>GPCRs</chemical>) including <chemical>FA3 receptors</chemical> (<chemical>FA3Rs</chemical>), is a well-known <chemical>HDAC</chemical> inhibitor that plays an important role in maintaining homeostasis of the gut-brain axis. Recently, its significance in regulation of some critical brain functions and usefulness in <DDF>neurodegenerative diseases</DDF> such as <DDF>PD</DDF> has been suggested. In this study we sought to determine whether <chemical>butyrate</chemical> may have protective effects against <DDF>salsolionl (SALS)-induced toxicity</DDF> in SH-SY5Y cells. <chemical>SALS</chemical>, an endogenous product of aldehyde and dopamine condensation, may be selectively toxic to dopaminergic neurons. SH-SY5Y cells, derived from human neuroblastoma cells, are used as a model of these neurons. Exposure of SH-SY5Y cells for 24 h to 400 μM <chemical>SALS</chemical> resulted in approximately 60% cell death, which was concentration-dependently prevented by <chemical>butyrate</chemical>. The effects of <chemical>butyrate</chemical> in turn were significantly attenuated by <drug>beta-hydroxy butyrate</drug> (<drug>BHB</drug>), a selective <chemical>FA3R</chemical> antagonist. Moreover, a selective <chemical>FA3R</chemical> agonist (<drug>AR 420626</drug>) also provided protective effects against <chemical>SALS</chemical>, which was totally blocked by <drug>BHB</drug>. These findings provide further support that <chemical>butyrate</chemical> or an agonist of <chemical>FA3R</chemical> may be of therapeutic potential in <DDF>PD</DDF>.",
"role": "assistant"
}
] |
32600151
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRapid improvement in Alzheimer's disease symptoms following fecal microbiota transplantation: a case report. Alzheimer's disease (AD), the most common form of dementia, is a leading cause of death and a major cause of morbidity in older people. The disease is characterized by progressive memory loss, cognitive impairment, and the cerebral accumulation of amyloid-β peptide. Given the health and economic impacts of AD, treatments that target the underlying etiology of AD or modify the course of the disease are of significant interest. The gut microbiome has been increasingly implicated in the pathogenesis of several neurological diseases, including multiple sclerosis and Parkinson's disease. Furthermore, emerging evidence has demonstrated that there are alterations in gut microbiome composition in patients with AD, suggesting involvement of the microbiome-gut-brain axis. We present symptom improvement in a patient with AD following fecal microbiota transplantation for a <i>Clostridioides difficile</i> infection.",
"role": "user"
},
{
"content": "Rapid improvement in <DDF>Alzheimer's disease symptoms</DDF> following fecal microbiota transplantation: a case report. <DDF>Alzheimer's disease</DDF> (<DDF>AD</DDF>), the most common form of <DDF>dementia</DDF>, is a leading cause of death and a major cause of morbidity in <human>older people</human>. The disease is characterized by <DDF>progressive memory loss</DDF>, <DDF>cognitive impairment</DDF>, and the cerebral accumulation of <chemical>amyloid-β peptide</chemical>. Given the health and economic impacts of <DDF>AD</DDF>, treatments that target the underlying etiology of <DDF>AD</DDF> or modify the course of the disease are of significant interest. The <microbiome>gut microbiome</microbiome> has been increasingly implicated in the pathogenesis of several <DDF>neurological diseases</DDF>, including <DDF>multiple sclerosis</DDF> and <DDF>Parkinson's disease</DDF>. Furthermore, emerging evidence has demonstrated that there are alterations in <microbiome>gut microbiome</microbiome> composition in <human>patients</human> with <DDF>AD</DDF>, suggesting involvement of the microbiome-gut-brain axis. We present symptom improvement in a <human>patient</human> with <DDF>AD</DDF> following fecal microbiota transplantation for a <i><DDF>Clostridioides difficile</i> infection</DDF>.",
"role": "assistant"
}
] |
32605552
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe study protocol for a pseudo-randomised pre-post designed controlled intervention trial to study the effects of a 7-week cooking program on self-efficacy and biomarkers of health: the ECU lifestyle and biomarkers get connected study (ECULABJMOF) including the Jamie's Ministry of Food WA participant experience. Australia, like other nations, has experienced a shift in dietary patterns away from home cooking of nutritious foods, towards a reliance on pre-prepared convenience meals. These are typically energy-dense, nutrient-poor and contribute to the rising prevalence of obesity and chronic disease burden. The aims of this study were to evaluate whether a community-based cooking program instigated a change to participants' skills, attitudes, knowledge, enjoyment and satisfaction of cooking and cooking confidence (self-efficacy). The pseudo-random, pre-post study design consisted of an intervention and a control group. Participant recruitment and group allocation was based on their program start dates. Intervention participants were surveyed three times (baseline, 7 weeks and 6 months) and the control group were surveyed at baseline and 5 weeks. All participants were registered via an online website and were 18 years or over. Upon consent, participants were offered four levels of commitment, defined by different assessments. The minimum participation level included an online survey and levels 2, 3 and 4 involved attendance at a clinic with increasing functional, anthropometric and biomarker measurements. Primary endpoints were participants' cooking confidence as a proxy for self-efficacy. Secondary endpoints were dietary intake, physical activity levels, body composition, anthropometry, blood, urine and faecal biomarkers of systemic, physical and mental health. The community cooking program provided participants with information and advice on food sourcing, preparation and nutrition to improve home cooking skills. The study was designed to explore whether food literacy programs are efficacious in improving participant physical health and well-being in order to combat the rise in obesity and diet-related disease. It will support future use of public health cooking program initiatives aimed at improving food literacy, self-efficacy and physical and mental health. The extensive data collected will inform future research into the relationship between diet, the gut-microbiota and human health. Retrospectively registered on 16.08.2019 with the Australian New Zealand Clinical Trials Registry (ANZCTR). ACTRN12619001144101 . Protocol version 4.",
"role": "user"
},
{
"content": "The study protocol for a <statistical technique>pseudo-randomised pre-post designed controlled intervention trial</statistical technique> to study the effects of a 7-week cooking program on self-efficacy and biomarkers of health: the ECU lifestyle and biomarkers get connected study (ECULABJMOF) including the Jamie's Ministry of Food WA participant experience. Australia, like other nations, has experienced a shift in dietary patterns away from home cooking of <food>nutritious foods</food>, towards a reliance on <food>pre-prepared convenience meals</food>. These are typically energy-dense, nutrient-poor and contribute to the rising prevalence of <DDF>obesity</DDF> and <DDF>chronic disease burden</DDF>. The aims of this study were to evaluate whether a community-based cooking program instigated a change to participants' skills, attitudes, knowledge, enjoyment and satisfaction of cooking and cooking confidence (self-efficacy). The pseudo-random, pre-post study design consisted of an intervention and a control group. Participant recruitment and group allocation was based on their program start dates. Intervention participants were surveyed three times (baseline, 7 weeks and 6 months) and the control group were surveyed at baseline and 5 weeks. All <human>participants</human> were registered via an online website and were 18 years or over. Upon consent, <human>participants</human> were offered four levels of commitment, defined by different assessments. The minimum participation level included an online survey and levels 2, 3 and 4 involved attendance at a clinic with increasing functional, anthropometric and biomarker measurements. Primary endpoints were participants' cooking confidence as a proxy for self-efficacy. Secondary endpoints were dietary intake, physical activity levels, body composition, anthropometry, blood, urine and faecal biomarkers of systemic, physical and mental health. The community cooking program provided <human>participants</human> with information and advice on food sourcing, preparation and nutrition to improve home cooking skills. The study was designed to explore whether food literacy programs are efficacious in improving participant physical health and well-being in order to combat the rise in <DDF>obesity</DDF> and <DDF>diet-related disease</DDF>. It will support future use of public health cooking program initiatives aimed at improving food literacy, self-efficacy and physical and mental health. The extensive data collected will inform future research into the relationship between diet, the <microbiome>gut-microbiota</microbiome> and human health. Retrospectively registered on 16.08.2019 with the Australian New Zealand Clinical Trials Registry (ANZCTR). ACTRN12619001144101 . Protocol version 4.",
"role": "assistant"
}
] |
32667590
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe role of the microbiota-gut-brain axis in neuropsychiatric disorders. The microbiota-gut-brain axis is a bidirectional signaling mechanism between the gastrointestinal tract and the central nervous system. The complexity of the intestinal ecosystem is extraordinary; it comprises more than 100 trillion microbial cells that inhabit the small and large intestine, and this interaction between microbiota and intestinal epithelium can cause physiological changes in the brain and influence mood and behavior. Currently, there has been an emphasis on how such interactions affect mental health. Evidence indicates that intestinal microbiota are involved in neurological and psychiatric disorders. This review covers evidence for the influence of gut microbiota on the brain and behavior in Alzheimer disease, dementia, anxiety, autism spectrum disorder, bipolar disorder, major depressive disorder, Parkinson's disease, and schizophrenia. The primary focus is on the pathways involved in intestinal metabolites of microbial origin, including short-chain fatty acids, tryptophan metabolites, and bacterial components that can activate the host's immune system. We also list clinical evidence regarding prebiotics, probiotics, and fecal microbiota transplantation as adjuvant therapies for neuropsychiatric disorders.",
"role": "user"
},
{
"content": "The role of the microbiota-gut-brain axis in <DDF>neuropsychiatric disorders</DDF>. The microbiota-gut-brain axis is a bidirectional signaling mechanism between the gastrointestinal tract and the central nervous system. The complexity of the intestinal ecosystem is extraordinary; it comprises more than 100 trillion microbial cells that inhabit the <anatomical location>small and large intestine</anatomical location>, and this interaction between microbiota and intestinal epithelium can cause physiological changes in the <anatomical location>brain</anatomical location> and influence mood and behavior. Currently, there has been an emphasis on how such interactions affect mental health. Evidence indicates that <microbiome>intestinal microbiota</microbiome> are involved in <DDF>neurological and psychiatric disorders</DDF>. This review covers evidence for the influence of <microbiome>gut microbiota</microbiome> on the <anatomical location>brain</anatomical location> and behavior in <DDF>Alzheimer disease</DDF>, <DDF>dementia</DDF>, <DDF>anxiety</DDF>, <DDF>autism spectrum disorder</DDF>, <DDF>bipolar disorder</DDF>, <DDF>major depressive disorder</DDF>, <DDF>Parkinson's disease</DDF>, and <DDF>schizophrenia</DDF>. The primary focus is on the pathways involved in <chemical>intestinal metabolites of microbial origin</chemical>, including <chemical>short-chain fatty acids</chemical>, <chemical>tryptophan metabolites</chemical>, and bacterial components that can activate the host's immune system. We also list clinical evidence regarding <dietary supplement>prebiotics</dietary supplement>, <dietary supplement>probiotics</dietary supplement>, and fecal microbiota transplantation as adjuvant therapies for <DDF>neuropsychiatric disorders</DDF>.",
"role": "assistant"
}
] |
32739746
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nColonization with the commensal fungus Candida albicans perturbs the gut-brain axis through dysregulation of endocannabinoid signaling. Anxiety disorders are the most prevalent mental health disorder worldwide, with a lifetime prevalence of 5-7 % of the human population. Although the etiology of anxiety disorders is incompletely understood, one aspect of host health that affects anxiety disorders is the gut-brain axis. Adolescence is a key developmental window in which stress and anxiety disorders are a major health concern. We used adolescent female mice in a gastrointestinal (GI) colonization model to demonstrate that the commensal fungus Candida albicans affects host health via the gut-brain axis. In mice, bacterial members of the gut microbiota can influence the host gut-brain axis, affecting anxiety-like behavior and the hypothalamus-pituitary-adrenal (HPA) axis which produces the stress hormone corticosterone (CORT). Here we showed that mice colonized with C. albicans demonstrated increased anxiety-like behavior and increased basal production of CORT as well as dysregulation of CORT production following acute stress. The HPA axis and anxiety-like behavior are negatively regulated by the endocannabinoid N-arachidonoylethanolamide (AEA). We demonstrated that C. albicans-colonized mice exhibited changes in the endocannabinoidome. Further, increasing AEA levels using the well-characterized fatty acid amide hydrolase (FAAH) inhibitor URB597 was sufficient to reverse both neuroendocrine phenotypes in C. albicans-colonized mice. Thus, a commensal fungus that is a common colonizer of humans had widespread effects on the physiology of its host. To our knowledge, this is the first report of microbial manipulation of the endocannabinoid (eCB) system that resulted in neuroendocrine changes contributing to anxiety-like behavior.",
"role": "user"
},
{
"content": "Colonization with the <bacteria>commensal fungus Candida albicans</bacteria> perturbs the gut-brain axis through <DDF>dysregulation of endocannabinoid signaling</DDF>. <DDF>Anxiety disorders</DDF> are the most prevalent <DDF>mental health disorder</DDF> worldwide, with a lifetime prevalence of 5-7 % of the <human>human population</human>. Although the etiology of <DDF>anxiety disorders</DDF> is incompletely understood, one aspect of host health that affects <DDF>anxiety disorders</DDF> is the gut-brain axis. Adolescence is a key developmental window in which <DDF>stress</DDF> and <DDF>anxiety disorders</DDF> are a major health concern. We used <animal>adolescent female mice</animal> in a gastrointestinal (GI) colonization model to demonstrate that the commensal fungus <bacteria>Candida albicans</bacteria> affects host health via the gut-brain axis. In <animal>mice</animal>, bacterial members of the <microbiome>gut microbiota</microbiome> can influence the host gut-brain axis, affecting <DDF>anxiety-like behavior</DDF> and the hypothalamus-pituitary-adrenal (HPA) axis which produces the <chemical>stress hormone corticosterone</chemical> (<chemical>CORT</chemical>). Here we showed that <animal>mice</animal> colonized with <bacteria>C. albicans</bacteria> demonstrated increased <DDF>anxiety-like behavior</DDF> and increased basal production of <chemical>CORT</chemical> as well as <DDF>dysregulation of CORT production</DDF> following <DDF>acute stress</DDF>. The HPA axis and <DDF>anxiety-like behavior</DDF> are negatively regulated by the <chemical>endocannabinoid N-arachidonoylethanolamide</chemical> (<chemical>AEA</chemical>). We demonstrated that <animal>C. albicans-colonized mice</animal> exhibited changes in the <chemical>endocannabinoidome</chemical>. Further, increasing AEA levels using the well-characterized <chemical>fatty acid amide hydrolase (FAAH) inhibitor URB597</chemical> was sufficient to reverse both neuroendocrine phenotypes in <animal>C. albicans-colonized mice</animal>. Thus, a commensal fungus that is a common colonizer of <human>humans</human> had widespread effects on the physiology of its host. To our knowledge, this is the first report of microbial manipulation of the endocannabinoid (eCB) system that resulted in neuroendocrine changes contributing to <DDF>anxiety-like behavior</DDF>.",
"role": "assistant"
}
] |
32772900
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbes in neurocognitive and mental health disorders. As individuals age, the prevalence of neurocognitive and mental health disorders increases. Current biomedical treatments do not completely address the management of these conditions. Despite new pharmacological therapy the challenges of managing these diseases remain.There is increasing evidence that the Gut Microbiome (GM) and microbial dysbiosis contribute to some of the more prevalent mental health and neurocognitive disorders, such as depression, anxiety, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), schizophrenia, bipolar disorder (BP), and dementia as well as the behavioural and psychological symptoms of dementia (BPSD) through the microbiota-gut-brain axis. <b>Methodology:</b> Scoping review about the effect of gut microbiota on neurocognitive and mental health disorders. This scoping review found there is an evolving evidence of the involvement of the gut microbiota in the pathophysiology of neurocognitive and mental health disorders. This manuscript also discusses how the psychotropics used to treat these conditions may have an antimicrobial effect on GM, and the potential for new strategies of management with probiotics and faecal transplantation. This understanding can open up the need for a gut related approach in these disorders as well as unlock the door for the role of gut related microbiota management. KEY MESSAGES Challenges of managing mental health conditions remain in spite of new pharmacological therapy. Gut dysbiosis is seen in various mental health conditions. Various psychotropic medications can have an influence on the gut microbiota by their antimicrobial effect.",
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"content": "<microbiome>Gut microbes</microbiome> in <DDF>neurocognitive and mental health disorders</DDF>. As <human>individuals</human> age, the prevalence of <DDF>neurocognitive and mental health disorders</DDF> increases. Current biomedical treatments do not completely address the management of these conditions. Despite new pharmacological therapy the challenges of managing these diseases remain.There is increasing evidence that the <microbiome>Gut Microbiome</microbiome> (<microbiome>GM</microbiome>) and <DDF>microbial dysbiosis</DDF> contribute to some of the more prevalent <DDF>mental health and neurocognitive disorders</DDF>, such as <DDF>depression</DDF>, <DDF>anxiety</DDF>, <DDF>obsessive-compulsive disorder</DDF> (<DDF>OCD</DDF>), <DDF>post-traumatic stress disorder</DDF> (<DDF>PTSD</DDF>), <DDF>schizophrenia</DDF>, <DDF>bipolar disorder</DDF> (<DDF>BP</DDF>), and <DDF>dementia</DDF> as well as the <DDF>behavioural and psychological symptoms of dementia</DDF> (<DDF>BPSD</DDF>) through the microbiota-gut-brain axis. <b>Methodology:</b> Scoping review about the effect of <microbiome>gut microbiota</microbiome> on <DDF>neurocognitive and mental health disorders</DDF>. This scoping review found there is an evolving evidence of the involvement of the <microbiome>gut microbiota</microbiome> in the pathophysiology of <DDF>neurocognitive and mental health disorders</DDF>. This manuscript also discusses how the <drug>psychotropics</drug> used to treat these conditions may have an antimicrobial effect on <microbiome>GM</microbiome>, and the potential for new strategies of management with <dietary supplement>probiotics</dietary supplement> and faecal transplantation. This understanding can open up the need for a gut related approach in these disorders as well as unlock the door for the role of gut related microbiota management. KEY MESSAGES Challenges of managing mental health conditions remain in spite of new pharmacological therapy. <DDF>Gut dysbiosis</DDF> is seen in various mental health conditions. Various <drug>psychotropic medications</drug> can have an influence on the <microbiome>gut microbiota</microbiome> by their antimicrobial effect.",
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32816830
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDoes Fibre-fix provided to people with irritable bowel syndrome who are consuming a low FODMAP diet improve their gut health, gut microbiome, sleep and mental health? A double-blinded, randomised controlled trial. A diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) is an effective way to reduce gut symptoms in people with irritable bowel syndrome (IBS). This diet reduces the intake of fermentable fibres, leading to changes of the gut microbiota and insufficient fermentation in the large bowel, resulting in reduced production of short-chain fatty acids (SCFAs), such as butyrate, which has unfavourable implications for gut health, sleep and mental health. This study will examine the effect of Fibre-fix, a supplement containing a mix of dietary fibres, on the human gut microbiome composition, fermentative capacity, sleep, quality of life (QOL) and mental health of people with IBS who consume a low FODMAP diet (LFD). A randomised, double-blind, placebo-controlled, study design is proposed to examine whether Fibre-fix added to an existing LFD may help modulate gastrointestinal function, improve markers of sleep, mental health and promote QOL in patients with IBS. Participants will provide stool and blood samples, daily bowel symptoms diaries and 3-day diet records. Additionally, they will complete validated questionnaires relating to FODMAP intake, sleep, mental health and QOL before and after a 3-week intervention. Gut health will be assessed via faecal microbiome composition, faecal pH and SCFA levels. Alteration of sleep will be recorded using an actigraphy device worn by all participants over the whole study. Multivariate analysis will be used to examine the gut microbiome and repeated measures Analysis of variance (ANOVA) will be used for dependent variables from questionnaires related to bowel symptoms, stool type, sleep, mental health and QOL to assess the differences between intervention and control groups after adjustment for confounding variables. Ethics approval was obtained from the Human Research Ethics Committee of Edith Cowan University (2019-00619-YAN). Results will be disseminated in peer-review journal publications, and conference presentations. Participants will be provided with a summary of findings once the study is completed. If Fibre-fix is shown to result in favourable changes in gut microbial composition, SCFA production, sleep and mental well-being without exacerbating symptoms, this will provide additional dietary management options for those with IBS following an LFD. ACTRN12620000032954.",
"role": "user"
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{
"content": "Does <dietary supplement>Fibre-fix</dietary supplement> provided to <human>people</human> with <DDF>irritable bowel syndrome</DDF> who are consuming a low FODMAP diet improve their gut health, <microbiome>gut microbiome</microbiome>, sleep and mental health? A <statistical technique>double-blinded, randomised controlled trial</statistical technique>. A diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) is an effective way to reduce <DDF>gut symptoms</DDF> in <human>people</human> with <DDF>irritable bowel syndrome</DDF> (<DDF>IBS</DDF>). This diet reduces the intake of fermentable fibres, leading to changes of the <microbiome>gut microbiota</microbiome> and insufficient fermentation in the <anatomical location>large bowel</anatomical location>, resulting in reduced production of <chemical>short-chain fatty acids</chemical> (<chemical>SCFAs</chemical>), such as <chemical>butyrate</chemical>, which has unfavourable implications for gut health, sleep and mental health. This study will examine the effect of <dietary supplement>Fibre-fix</dietary supplement>, a supplement containing a mix of dietary fibres, on the human <microbiome>gut microbiome</microbiome> composition, fermentative capacity, sleep, quality of life (QOL) and mental health of <human>people</human> with <DDF>IBS</DDF> who consume a low FODMAP diet (LFD). A randomised, double-blind, placebo-controlled, study design is proposed to examine whether <dietary supplement>Fibre-fix</dietary supplement> added to an existing LFD may help modulate gastrointestinal function, improve markers of sleep, mental health and promote QOL in <human>patients</human> with <DDF>IBS</DDF>. <human>Participants</human> will provide stool and blood samples, daily bowel symptoms diaries and 3-day diet records. Additionally, they will complete validated questionnaires relating to FODMAP intake, sleep, mental health and QOL before and after a 3-week intervention. Gut health will be assessed via <microbiome>faecal microbiome</microbiome> composition, faecal pH and <chemical>SCFA</chemical> levels. Alteration of sleep will be recorded using an actigraphy device worn by all <human>participants</human> over the whole study. <statistical technique>Multivariate analysis</statistical technique> will be used to examine the <microbiome>gut microbiome</microbiome> and <statistical technique>repeated measures Analysis of variance (ANOVA)</statistical technique> will be used for dependent variables from questionnaires related to <DDF>bowel symptoms</DDF>, stool type, sleep, mental health and QOL to assess the differences between intervention and control groups after adjustment for confounding variables. Ethics approval was obtained from the Human Research Ethics Committee of Edith Cowan University (2019-00619-YAN). Results will be disseminated in peer-review journal publications, and conference presentations. <human>Participants</human> will be provided with a summary of findings once the study is completed. If <dietary supplement>Fibre-fix</dietary supplement> is shown to result in favourable changes in <microbiome>gut microbial composition</microbiome>, SCFA production, sleep and mental well-being without exacerbating symptoms, this will provide additional dietary management options for those with IBS following an LFD. ACTRN12620000032954.",
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32819434
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe gut microbiota regulates autism-like behavior by mediating vitamin B<sub>6</sub> homeostasis in EphB6-deficient mice. Autism spectrum disorder (ASD) is a developmental disorder, and the effective pharmacological treatments for the core autistic symptoms are currently limited. Increasing evidence, particularly that from clinical studies on ASD patients, suggests a functional link between the gut microbiota and the development of ASD. However, the mechanisms linking the gut microbiota with brain dysfunctions (gut-brain axis) in ASD have not yet been full elucidated. Due to its genetic mutations and downregulated expression in patients with ASD, EPHB6, which also plays important roles in gut homeostasis, is generally considered a candidate gene for ASD. Nonetheless, the role and mechanism of EPHB6 in regulating the gut microbiota and the development of ASD are unclear. Here, we found that the deletion of EphB6 induced autism-like behavior and disturbed the gut microbiota in mice. More importantly, transplantation of the fecal microbiota from EphB6-deficient mice resulted in autism-like behavior in antibiotic-treated C57BL/6J mice, and transplantation of the fecal microbiota from wild-type mice ameliorated the autism-like behavior in EphB6-deficient mice. At the metabolic level, the disturbed gut microbiota in EphB6-deficient mice led to vitamin B<sub>6</sub> and dopamine defects. At the cellular level, the excitation/inhibition (E/I) balance in the medial prefrontal cortex was regulated by gut microbiota-mediated vitamin B<sub>6</sub> in EphB6-deficient mice. Our study uncovers a key role for the gut microbiota in the regulation of autism-like social behavior by vitamin B<sub>6</sub>, dopamine, and the E/I balance in EphB6-deficient mice, and these findings suggest new strategies for understanding and treating ASD. Video abstract.",
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"content": "The <microbiome>gut microbiota</microbiome> regulates <DDF>autism-like behavior</DDF> by mediating <chemical>vitamin B<sub>6</sub></chemical> homeostasis in <animal>EphB6-deficient mice</animal>. <DDF>Autism spectrum disorder</DDF> (<DDF>ASD</DDF>) is a <DDF>developmental disorder</DDF>, and the effective pharmacological treatments for the <DDF>core autistic symptoms</DDF> are currently limited. Increasing evidence, particularly that from clinical studies on <human>ASD patients</human>, suggests a functional link between the <microbiome>gut microbiota</microbiome> and the development of <DDF>ASD</DDF>. However, the mechanisms linking the <microbiome>gut microbiota</microbiome> with <DDF>brain dysfunctions</DDF> (gut-brain axis) in <DDF>ASD</DDF> have not yet been full elucidated. Due to its genetic mutations and downregulated expression in <human>patients</human> with <DDF>ASD</DDF>, <gene>EPHB6</gene>, which also plays important roles in gut homeostasis, is generally considered a candidate gene for <DDF>ASD</DDF>. Nonetheless, the role and mechanism of <gene>EPHB6</gene> in regulating the <microbiome>gut microbiota</microbiome> and the development of <DDF>ASD</DDF> are unclear. Here, we found that the deletion of <gene>EphB6</gene> induced <DDF>autism-like behavior</DDF> and disturbed the <microbiome>gut microbiota</microbiome> in <animal>mice</animal>. More importantly, transplantation of the <microbiome>fecal microbiota</microbiome> from <animal>EphB6-deficient mice</animal> resulted in <DDF>autism-like behavior</DDF> in antibiotic-treated <animal>C57BL/6J mice</animal>, and transplantation of the <microbiome>fecal microbiota</microbiome> from <animal>wild-type mice</animal> ameliorated the <DDF>autism-like behavior</DDF> in <animal>EphB6-deficient mice</animal>. At the metabolic level, the disturbed <microbiome>gut microbiota</microbiome> in <animal>EphB6-deficient mice</animal> led to <chemical>vitamin B<sub>6</sub></chemical> and <chemical>dopamine</chemical> defects. At the cellular level, the excitation/inhibition (E/I) balance in the <anatomical location>medial prefrontal cortex</anatomical location> was regulated by <chemical>gut microbiota-mediated vitamin B<sub>6</sub></chemical> in <animal>EphB6-deficient mice</animal>. Our study uncovers a key role for the <microbiome>gut microbiota</microbiome> in the regulation of <DDF>autism-like social behavior</DDF> by <chemical>vitamin B<sub>6</sub></chemical>, <chemical>dopamine</chemical>, and the E/I balance in <animal>EphB6-deficient mice</animal>, and these findings suggest new strategies for understanding and treating <DDF>ASD</DDF>. Video abstract.",
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32834004
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nPredictive analysis methods for human microbiome data with application to Parkinson's disease. Microbiome data consists of operational taxonomic unit (OTU) counts characterized by zero-inflation, over-dispersion, and grouping structure among samples. Currently, statistical testing methods are commonly performed to identify OTUs that are associated with a phenotype. The limitations of statistical testing methods include that the validity of p-values/q-values depend sensitively on the correctness of models and that the statistical significance does not necessarily imply predictivity. Predictive analysis using methods such as LASSO is an alternative approach for identifying associated OTUs and for measuring the predictability of the phenotype variable with OTUs and other covariate variables. We investigate three strategies of performing predictive analysis: (1) LASSO: fitting a LASSO multinomial logistic regression model to all OTU counts with specific transformation; (2) screening+GLM: screening OTUs with q-values returned by fitting a GLMM to each OTU, then fitting a GLM model using a subset of selected OTUs; (3) screening+LASSO: fitting a LASSO to a subset of OTUs selected with GLMM. We have conducted empirical studies using three simulation datasets generated using Dirichlet-multinomial models and a real gut microbiome data related to Parkinson's disease to investigate the performance of the three strategies for predictive analysis. Our simulation studies show that the predictive performance of LASSO with appropriate variable transformation works remarkably well on zero-inflated data. Our results of real data analysis show that Parkinson's disease can be predicted based on selected OTUs after the binary transformation, age, and sex with high accuracy (Error Rate = 0.199, AUC = 0.872, AUPRC = 0.912). These results provide strong evidences of the relationship between Parkinson's disease and the gut microbiome.",
"role": "user"
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"content": "<statistical technique>Predictive analysis methods</statistical technique> for human microbiome data with application to <DDF>Parkinson's disease</DDF>. Microbiome data consists of operational taxonomic unit (OTU) counts characterized by zero-inflation, over-dispersion, and grouping structure among samples. Currently, <statistical technique>statistical testing methods</statistical technique> are commonly performed to identify OTUs that are associated with a phenotype. The limitations of <statistical technique>statistical testing methods</statistical technique> include that the validity of p-values/q-values depend sensitively on the correctness of models and that the statistical significance does not necessarily imply predictivity. Predictive analysis using methods such as <statistical technique>LASSO</statistical technique> is an alternative approach for identifying associated OTUs and for measuring the predictability of the phenotype variable with OTUs and other covariate variables. We investigate three strategies of performing predictive analysis: (1) <statistical technique>LASSO</statistical technique>: fitting a <statistical technique>LASSO multinomial logistic regression model</statistical technique> to all OTU counts with specific transformation; (2) <statistical technique>screening+GLM</statistical technique>: screening OTUs with q-values returned by fitting a <statistical technique>GLMM</statistical technique> to each OTU, then fitting a <statistical technique>GLM model</statistical technique> using a subset of selected OTUs; (3) screening+<statistical technique>LASSO</statistical technique>: fitting a <statistical technique>LASSO</statistical technique> to a subset of OTUs selected with <statistical technique>GLMM</statistical technique>. We have conducted empirical studies using three simulation datasets generated using <statistical technique>Dirichlet-multinomial models</statistical technique> and a real gut microbiome data related to <DDF>Parkinson's disease</DDF> to investigate the performance of the three strategies for predictive analysis. Our simulation studies show that the predictive performance of <statistical technique>LASSO</statistical technique> with appropriate variable transformation works remarkably well on zero-inflated data. Our results of real data analysis show that <DDF>Parkinson's disease</DDF> can be predicted based on selected OTUs after the binary transformation, age, and sex with high accuracy (Error Rate = 0.199, AUC = 0.872, AUPRC = 0.912). These results provide strong evidences of the relationship between <DDF>Parkinson's disease</DDF> and the <microbiome>gut microbiome</microbiome>.",
"role": "assistant"
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32890382
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nFrom Family Surroundings to Intestinal Flora, A Literature Review Concerning Epigenetic Processes in Psychiatric Disorders. Some behaviors or psychiatric conditions seem to be inherited from parents or explain by family environment. We hypothesized interactions between epigenetic processes, inflammatory response and gut microbiota with family surroundings or environmental characteristics. We searched in literature interactions between epigenetic processes and psychiatric disorders with a special interest for environmental factors such as traumatic or stress events, family relationships and also gut microbiota. We searched on Pubmed, PsycINFO, PsycARTICLES and Sciencedirect articles with the keywords psychiatric disorders, epigenome, microbiome and family relationships. Some gene polymorphisms interact with negative environment and lead to psychiatric disorders. Negative environment is correlated with different epigenetic modifications in genes implicated in mental health. Gut microbiota diversity affect host epigenetic. Animal studies showed evidences for a transgenerational transmission of epigenetic characteristics. Our findings support the hypothesis that epigenetic mediate gene-environment interactions and psychiatric disorders. Several environmental characteristics such as traumatic life events, family adversity, psychological stress or internal environment such as gut microbiota diversity and diet showed an impact on epigenetic. These epigenetic modifications are also correlated with neurophysiological, inflammatory or hypothalamic-pituitary-adrenal axis dysregulations.",
"role": "user"
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{
"content": "From Family Surroundings to <microbiome>Intestinal Flora</microbiome>, A Literature Review Concerning Epigenetic Processes in <DDF>Psychiatric Disorders</DDF>. Some behaviors or <DDF>psychiatric conditions</DDF> seem to be inherited from <human>parents</human> or explain by family environment. We hypothesized interactions between <DDF>epigenetic processes</DDF>, <DDF>inflammatory response</DDF> and <microbiome>gut microbiota</microbiome> with family surroundings or environmental characteristics. We searched in literature interactions between <DDF>epigenetic processes</DDF> and <DDF>psychiatric disorders</DDF> with a special interest for environmental factors such as <DDF>traumatic or stress events</DDF>, family relationships and also <microbiome>gut microbiota</microbiome>. We searched on Pubmed, PsycINFO, PsycARTICLES and Sciencedirect articles with the keywords <DDF>psychiatric disorders</DDF>, epigenome, microbiome and family relationships. Some gene polymorphisms interact with negative environment and lead to <DDF>psychiatric disorders</DDF>. Negative environment is correlated with different epigenetic modifications in genes implicated in mental health. Gut microbiota diversity affect host epigenetic. Animal studies showed evidences for a transgenerational transmission of epigenetic characteristics. Our findings support the hypothesis that epigenetic mediate gene-environment interactions and <DDF>psychiatric disorders</DDF>. Several environmental characteristics such as traumatic life events, family adversity, <DDF>psychological stress</DDF> or internal environment such as gut microbiota diversity and diet showed an impact on epigenetic. These epigenetic modifications are also correlated with <DDF>neurophysiological, inflammatory or hypothalamic-pituitary-adrenal axis dysregulations</DDF>.",
"role": "assistant"
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32983561
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nRetracted: Exploring the microbiome and mindfulness connection. Mental health and its impact on overall well-being is a topic that is at the forefront of consideration in most industrialized countries. Ironically in the expansive world of the microbiome, gut microbes are most affected by modern, fast paced, westernized lifestyles, indicating a significant correlation based on geography, and physical and mental habits. The gut–brain axis is an established axis demonstrating the effect of the gut microbiota on the biochemical processes in the brain. With the existence of mindfulness initiatives such as adoption of a ‘yogic lifestyle’ aimed at creating a sense of harmony and balance within the individual, this special report considers the available evidence base, asking whether the harmony created by adopting this lifestyle can be related to establishing harmony in the gut–brain axis.",
"role": "user"
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{
"content": "Retracted: Exploring the microbiome and mindfulness connection. Mental health and its impact on overall well-being is a topic that is at the forefront of consideration in most industrialized countries. Ironically in the expansive world of the microbiome, <microbiome>gut microbes</microbiome> are most affected by modern, fast paced, westernized lifestyles, indicating a significant correlation based on geography, and physical and mental habits. The gut–brain axis is an established axis demonstrating the effect of the <microbiome>gut microbiota</microbiome> on the biochemical processes in the <anatomical location>brain</anatomical location>. With the existence of mindfulness initiatives such as adoption of a ‘yogic lifestyle’ aimed at creating a sense of harmony and balance within the <human>individual</human>, this special report considers the available evidence base, asking whether the harmony created by adopting this lifestyle can be related to establishing harmony in the gut–brain axis.",
"role": "assistant"
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32987656
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Pathology of Parkinson's Disease and Potential Benefit of Dietary Polyphenols. Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by a loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction, impaired sleep, fatigue, and behavioral changes. The pathogenesis of PD is believed to involve oxidative stress, disruption to mitochondria, alterations to the protein α-synuclein, and neuroinflammatory processes. There is currently no cure for the disease. Polyphenols are secondary metabolites of plants, which have shown benefit in several experimental models of PD. Intake of polyphenols through diet is also associated with lower PD risk in humans. In this review, we provide an overview of the pathology of PD and the data supporting the potential neuroprotective capacity of increased polyphenols in the diet. Evidence suggests that the intake of dietary polyphenols may inhibit neurodegeneration and the progression of PD. Polyphenols appear to have a positive effect on the gut microbiome, which may decrease inflammation that contributes to the disease. Therefore, a diet rich in polyphenols may decrease the symptoms and increase quality of life in PD patients.",
"role": "user"
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{
"content": "The Pathology of <DDF>Parkinson's Disease</DDF> and Potential Benefit of <chemical>Dietary Polyphenols</chemical>. <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>) is a <DDF>progressive neurodegenerative disorder</DDF> that is characterized by a loss of dopaminergic neurons, leading to <DDF>bradykinesia</DDF>, <DDF>rigidity</DDF>, <DDF>tremor at rest</DDF>, and <DDF>postural instability</DDF>, as well as <DDF>non-motor symptoms</DDF> such as <DDF>olfactory impairment</DDF>, <DDF>pain</DDF>, <DDF>autonomic dysfunction</DDF>, <DDF>impaired sleep</DDF>, <DDF>fatigue</DDF>, and <DDF>behavioral changes</DDF>. The pathogenesis of <DDF>PD</DDF> is believed to involve <DDF>oxidative stress</DDF>, <DDF>disruption to mitochondria</DDF>, <DDF>alterations to the protein α-synuclein</DDF>, and <DDF>neuroinflammatory processes</DDF>. There is currently no cure for the disease. <chemical>Polyphenols</chemical> are secondary metabolites of plants, which have shown benefit in several experimental models of <DDF>PD</DDF>. Intake of <chemical>polyphenols</chemical> through diet is also associated with lower PD risk in <human>humans</human>. In this review, we provide an overview of the pathology of <DDF>PD</DDF> and the data supporting the potential neuroprotective capacity of increased <chemical>polyphenols</chemical> in the diet. Evidence suggests that the intake of <anatomical location>dietary polyphenols</anatomical location> may inhibit <DDF>neurodegeneration</DDF> and the <DDF>progression of PD</DDF>. <chemical>Polyphenols</chemical> appear to have a positive effect on the <microbiome>gut microbiome</microbiome>, which may decrease <DDF>inflammation</DDF> that contributes to the disease. Therefore, a diet rich in <chemical>polyphenols</chemical> may decrease the symptoms and increase quality of life in <human>PD patients</human>.",
"role": "assistant"
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33063712
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe emerging role of probiotics in neurodegenerative diseases: new hope for Parkinson's disease? Neurodegenerative disease etiology is still unclear, but different contributing factors, such as lifestyle and genetic factors are involved. Altered components of the gut could play a key role in the gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Variations in the composition of the gut microbiota and its function between healthy people and patients have been reported for a variety of human disorders comprising metabolic, autoimmune, cancer, and, notably, neurodegenerative disorders. Diet can alter the microbiota composition, affecting the gut-brain axis function. Different nutraceutical interventions have been devoted to normalizing gut microbiome dysbiosis and to improving biological outcomes in neurological conditions, including the use of probiotics. Preclinical and clinical investigations discussed in this review strengthen the correlation between intestinal microbiota and brain and the concept that modifying the microbiome composition may improve brain neurochemistry, modulating different pathways. This review will discuss the potential use of probiotics for Parkinson's disease prevention or treatment or as adjuvant therapy, confirming that gut microbiota modulation influences different pro-survival pathways. Future investigations in Parkinson's disease should consider the role of the gut-brain axis and additional comprehension of the underlying mechanisms is extremely necessary.",
"role": "user"
},
{
"content": "The emerging role of <dietary supplement>probiotics</dietary supplement> in <DDF>neurodegenerative diseases</DDF>: new hope for <DDF>Parkinson's disease</DDF>? Neurodegenerative disease etiology is still unclear, but different contributing factors, such as lifestyle and genetic factors are involved. Altered components of the <anatomical location>gut</anatomical location> could play a key role in the gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Variations in the composition of the <microbiome>gut microbiota</microbiome> and its function between <human>healthy people</human> and <human>patients</human> have been reported for a variety of <DDF>human disorders</DDF> comprising metabolic, autoimmune, <DDF>cancer</DDF>, and, notably, <DDF>neurodegenerative disorders</DDF>. Diet can alter the microbiota composition, affecting the gut-brain axis function. Different nutraceutical interventions have been devoted to normalizing <DDF>gut microbiome dysbiosis</DDF> and to improving biological outcomes in <DDF>neurological conditions</DDF>, including the use of <dietary supplement>probiotics</dietary supplement>. Preclinical and clinical investigations discussed in this review strengthen the correlation between <microbiome>intestinal microbiota</microbiome> and <anatomical location>brain</anatomical location> and the concept that modifying the microbiome composition may improve brain neurochemistry, modulating different pathways. This review will discuss the potential use of <dietary supplement>probiotics</dietary supplement> for <DDF>Parkinson's disease</DDF> prevention or treatment or as adjuvant therapy, confirming that <microbiome>gut microbiota</microbiome> modulation influences different pro-survival pathways. Future investigations in <DDF>Parkinson's disease</DDF> should consider the role of the gut-brain axis and additional comprehension of the underlying mechanisms is extremely necessary.",
"role": "assistant"
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33076930
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut bacterial deamination of residual levodopa medication for Parkinson's disease. Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by both motor and non-motor symptoms. Gastrointestinal tract dysfunction is one of the non-motor features, where constipation is reported as the most common gastrointestinal symptom. Aromatic bacterial metabolites are attracting considerable attention due to their impact on gut homeostasis and host's physiology. In particular, Clostridium sporogenes is a key contributor to the production of these bioactive metabolites in the human gut. Here, we show that C. sporogenes deaminates levodopa, the main treatment in Parkinson's disease, and identify the aromatic aminotransferase responsible for the initiation of the deamination pathway. The deaminated metabolite from levodopa, 3-(3,4-dihydroxyphenyl)propionic acid, elicits an inhibitory effect on ileal motility in an ex vivo model. We detected 3-(3,4-dihydroxyphenyl)propionic acid in fecal samples of Parkinson's disease patients on levodopa medication and found that this metabolite is actively produced by the gut microbiota in those stool samples. Levodopa is deaminated by the gut bacterium C. sporogenes producing a metabolite that inhibits ileal motility ex vivo. Overall, this study underpins the importance of the metabolic pathways of the gut microbiome involved in drug metabolism not only to preserve drug effectiveness, but also to avoid potential side effects of bacterial breakdown products of the unabsorbed residue of medication.",
"role": "user"
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{
"content": "<biomedical technique>Gut bacterial deamination</biomedical technique> of <drug>residual levodopa medication</drug> for <DDF>Parkinson's disease</DDF>. <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>) is a <DDF>progressive neurodegenerative disorder</DDF> characterized by both motor and non-motor symptoms. <DDF>Gastrointestinal tract dysfunction</DDF> is one of the non-motor features, where <DDF>constipation</DDF> is reported as the most common gastrointestinal symptom. <chemical>Aromatic bacterial metabolites</chemical> are attracting considerable attention due to their impact on gut homeostasis and host's physiology. In particular, <bacteria>Clostridium sporogenes</bacteria> is a key contributor to the production of these bioactive metabolites in the <anatomical location>human gut</anatomical location>. Here, we show that <bacteria>C. sporogenes</bacteria> deaminates <drug>levodopa</drug>, the main treatment in <DDF>Parkinson's disease</DDF>, and identify the <chemical>aromatic aminotransferase</chemical> responsible for the initiation of the deamination pathway. The deaminated metabolite from <drug>levodopa</drug>, <chemical>3-(3,4-dihydroxyphenyl)propionic acid</chemical>, elicits an inhibitory effect on ileal motility in an ex vivo model. We detected <chemical>3-(3,4-dihydroxyphenyl)propionic acid</chemical> in fecal samples of <human>Parkinson's disease patients</human> on <drug>levodopa medication</drug> and found that this metabolite is actively produced by the <microbiome>gut microbiota</microbiome> in those stool samples. <drug>Levodopa</drug> is deaminated by the <bacteria>gut bacterium C. sporogenes</bacteria> producing a metabolite that inhibits ileal motility ex vivo. Overall, this study underpins the importance of the metabolic pathways of the <microbiome>gut microbiome</microbiome> involved in drug metabolism not only to preserve drug effectiveness, but also to avoid potential side effects of bacterial breakdown products of the unabsorbed residue of medication.",
"role": "assistant"
}
] |
33092203
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nClustering on Human Microbiome Sequencing Data: A Distance-Based Unsupervised Learning Model. Modeling and analyzing human microbiome allows the assessment of the microbial community and its impacts on human health. Microbiome composition can be quantified using 16S rRNA technology into sequencing data, which are usually skewed and heavy-tailed with excess zeros. Clustering methods are useful in personalized medicine by identifying subgroups for patients stratification. However, there is currently a lack of standardized clustering method for the complex microbiome sequencing data. We propose a clustering algorithm with a specific beta diversity measure that can address the presence-absence bias encountered for sparse count data and effectively measure the sample distances for sample stratification. Our distance measure used for clustering is derived from a parametric based mixture model producing sample-specific distributions conditional on the observed operational taxonomic unit (OTU) counts and estimated mixture weights. The method can provide accurate estimates of the true zero proportions and thus construct a precise beta diversity measure. Extensive simulation studies have been conducted and suggest that the proposed method achieves substantial clustering improvement compared with some widely used distance measures when a large proportion of zeros is presented. The proposed algorithm was implemented to a human gut microbiome study on Parkinson's diseases to identify distinct microbiome states with biological interpretations.",
"role": "user"
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{
"content": "<statistical technique>Clustering on Human Microbiome Sequencing Data</statistical technique>: A Distance-Based Unsupervised Learning Model. Modeling and analyzing <microbiome>human microbiome</microbiome> allows the assessment of the microbial community and its impacts on human health. Microbiome composition can be quantified using <biomedical technique>16S rRNA technology</biomedical technique> into sequencing data, which are usually skewed and heavy-tailed with excess zeros. <statistical technique>Clustering methods</statistical technique> are useful in personalized medicine by identifying subgroups for patients stratification. However, there is currently a lack of <statistical technique>standardized clustering method for the complex microbiome sequencing data</statistical technique>. We propose a <statistical technique>clustering algorithm with a specific beta diversity measure</statistical technique> that can address the presence-absence bias encountered for sparse count data and effectively measure the sample distances for sample stratification. Our distance measure used for clustering is derived from a parametric based mixture model producing sample-specific distributions conditional on the observed operational taxonomic unit (OTU) counts and estimated mixture weights. The method can provide accurate estimates of the true zero proportions and thus construct a precise beta diversity measure. Extensive simulation studies have been conducted and suggest that the proposed method achieves substantial clustering improvement compared with some widely used distance measures when a large proportion of zeros is presented. The proposed algorithm was implemented to a human gut microbiome study on <DDF>Parkinson's diseases</DDF> to identify distinct microbiome states with biological interpretations.",
"role": "assistant"
}
] |
33144709
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nDiet and depression: exploring the biological mechanisms of action. The field of nutritional psychiatry has generated observational and efficacy data supporting a role for healthy dietary patterns in depression onset and symptom management. To guide future clinical trials and targeted dietary therapies, this review provides an overview of what is currently known regarding underlying mechanisms of action by which diet may influence mental and brain health. The mechanisms of action associating diet with health outcomes are complex, multifaceted, interacting, and not restricted to any one biological pathway. Numerous pathways were identified through which diet could plausibly affect mental health. These include modulation of pathways involved in inflammation, oxidative stress, epigenetics, mitochondrial dysfunction, the gut microbiota, tryptophan-kynurenine metabolism, the HPA axis, neurogenesis and BDNF, epigenetics, and obesity. However, the nascent nature of the nutritional psychiatry field to date means that the existing literature identified in this review is largely comprised of preclinical animal studies. To fully identify and elucidate complex mechanisms of action, intervention studies that assess markers related to these pathways within clinically diagnosed human populations are needed.",
"role": "user"
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{
"content": "<food>Diet</food> and <DDF>depression</DDF>: exploring the biological mechanisms of action. The field of nutritional psychiatry has generated observational and efficacy data supporting a role for healthy dietary patterns in depression onset and symptom management. To guide future clinical trials and targeted dietary therapies, this review provides an overview of what is currently known regarding underlying mechanisms of action by which diet may influence mental and brain health. The mechanisms of action associating diet with health outcomes are complex, multifaceted, interacting, and not restricted to any one biological pathway. Numerous pathways were identified through which diet could plausibly affect mental health. These include modulation of pathways involved in <DDF>inflammation</DDF>, <DDF>oxidative stress</DDF>, epigenetics, <DDF>mitochondrial dysfunction</DDF>, the <microbiome>gut microbiota</microbiome>, tryptophan-kynurenine metabolism, the HPA axis, neurogenesis and <chemical>BDNF</chemical>, epigenetics, and <DDF>obesity</DDF>. However, the nascent nature of the nutritional psychiatry field to date means that the existing literature identified in this review is largely comprised of preclinical animal studies. To fully identify and elucidate complex mechanisms of action, intervention studies that assess markers related to these pathways within <human>clinically diagnosed human populations</human> are needed.",
"role": "assistant"
}
] |
33240722
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut-Brain Axis and its Neuro-Psychiatric Effects: A Narrative Review. The gut microbiota regulates the function and health of the human gut. Preliminary evidence suggests its impact on multiple human systems including the nervous and immune systems. A major area of research has been the directional relationship between intestinal microbiota and the central nervous system (CNS), called the microbiota-gut-brain axis. It is hypothesized that the intestinal microbiota affects brain activity and behavior via endocrine, neural, and immune pathways. An alteration in the composition of the gut microbiome has been linked to a variety of neurodevelopmental and neurodegenerative disorders. The connection between gut microbiome and several CNS disorders indicates that the focus of research in the future should be on the bacterial and biochemical targets. Through this review, we outline the established knowledge regarding the gut microbiome and gut-brain axis. In addition to gut microbiome in neurological and psychiatry diseases, we have briefly discussed microbial metabolites affecting the blood-brain barrier (BBB), immune dysregulation, modification of autonomic sensorimotor connections, and hypothalamus-pituitary-adrenal axis.",
"role": "user"
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{
"content": "Gut-Brain Axis and its Neuro-Psychiatric Effects: A Narrative Review. The <microbiome>gut microbiota</microbiome> regulates the function and health of the <anatomical location>human gut</anatomical location>. Preliminary evidence suggests its impact on multiple human systems including the nervous and immune systems. A major area of research has been the directional relationship between <microbiome>intestinal microbiota</microbiome> and the central nervous system (CNS), called the microbiota-gut-brain axis. It is hypothesized that the <microbiome>intestinal microbiota</microbiome> affects brain activity and behavior via endocrine, neural, and immune pathways. An alteration in the composition of the <microbiome>gut microbiome</microbiome> has been linked to a variety of <DDF>neurodevelopmental and neurodegenerative disorders</DDF>. The connection between <microbiome>gut microbiome</microbiome> and several <DDF>CNS disorders</DDF> indicates that the focus of research in the future should be on the bacterial and biochemical targets. Through this review, we outline the established knowledge regarding the <microbiome>gut microbiome</microbiome> and gut-brain axis. In addition to <microbiome>gut microbiome</microbiome> in <DDF>neurological and psychiatry diseases</DDF>, we have briefly discussed <chemical>microbial metabolites</chemical> affecting the blood-brain barrier (BBB), immune dysregulation, modification of autonomic sensorimotor connections, and hypothalamus-pituitary-adrenal axis.",
"role": "assistant"
}
] |
33244049
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEmotional well-being and gut microbiome profiles by enterotype. With increasing attention being paid to improving emotional well-being, recent evidence points to gut microbiota as a key player in regulating mental and physical health via bidirectional communication between the brain and gut. Here, we examine the association between emotional well-being and gut microbiome profiles (i.e., gut microbiome composition, diversity, and the moderating role of the enterotypes) among healthy Korean adults (n = 83, mean age = 48.9, SD = 13.2). The research was performed using high-throughput 16S rRNA gene sequencing to obtain gut microbiome profiles, as well as a self-report survey that included the Positive Affect Negative Affect Schedule (PANAS). The cluster-based analysis identified two enterotypes dominated by the genera Bacteroides (n = 49) and Prevotella (n = 34). Generalized linear regression analysis reveals significant associations between positive emotion and gut microbiome diversity (Shannon Index) among participants in the Prevotella dominant group, whereas no such relationship emerged among participants in the Bacteroides group. Moreover, a novel genus from the family Lachnospiraceae is associated with emotional well-being scores, both positive and negative. Together, the current findings highlight the enterotype-specific links between the gut microbiota community and emotion in healthy adults and suggest the possible roles of the gut microbiome in promoting mental health.",
"role": "user"
},
{
"content": "Emotional well-being and gut microbiome profiles by enterotype. With increasing attention being paid to improving emotional well-being, recent evidence points to <microbiome>gut microbiota</microbiome> as a key player in regulating mental and physical health via bidirectional communication between the <anatomical location>brain</anatomical location> and <anatomical location>gut</anatomical location>. Here, we examine the association between emotional well-being and gut microbiome profiles (i.e., gut microbiome composition, diversity, and the moderating role of the enterotypes) among <human>healthy Korean adults</human> (n = 83, mean age = 48.9, SD = 13.2). The research was performed using <biomedical technique>high-throughput 16S rRNA gene sequencing</biomedical technique> to obtain gut microbiome profiles, as well as a self-report survey that included the <statistical technique>Positive Affect Negative Affect Schedule</statistical technique> (<statistical technique>PANAS</statistical technique>). The <statistical technique>cluster-based analysis</statistical technique> identified two enterotypes dominated by the genera <bacteria>Bacteroides</bacteria> (n = 49) and <bacteria>Prevotella</bacteria> (n = 34). <statistical technique>Generalized linear regression analysis</statistical technique> reveals significant associations between positive emotion and gut microbiome diversity (Shannon Index) among <human>participants in the Prevotella dominant group</human>, whereas no such relationship emerged among <human>participants in the Bacteroides group</human>. Moreover, a novel genus from the family <bacteria>Lachnospiraceae</bacteria> is associated with emotional well-being scores, both positive and negative. Together, the current findings highlight the enterotype-specific links between the <microbiome>gut microbiota community</microbiome> and emotion in <human>healthy adults</human> and suggest the possible roles of the <microbiome>gut microbiome</microbiome> in promoting mental health.",
"role": "assistant"
}
] |
33287442
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nThe Gut Microbiota: A Potential Gateway to Improved Health Outcomes in Breast Cancer Treatment and Survivorship. Breast cancer is the most frequently diagnosed cancer in women worldwide. The disease and its treatments exert profound effects on an individual's physical and mental health. There are many factors that impact an individual's risk of developing breast cancer, their response to treatments, and their risk of recurrence. The community of microorganisms inhabiting the gastrointestinal tract, the gut microbiota, affects human health through metabolic, neural, and endocrine signaling, and immune activity. It is through these mechanisms that the gut microbiota appears to influence breast cancer risk, response to treatment, and recurrence. A disrupted gut microbiota or state of 'dysbiosis' can contribute to a biological environment associated with higher risk for cancer development as well as contribute to negative treatment side-effects. Many cancer treatments have been shown to shift the gut microbiota toward dysbiosis; however, the microbiota can also be positively manipulated through diet, prebiotic and probiotic supplementation, and exercise. The objective of this review is to provide an overview of the current understanding of the relationship between the gut microbiota and breast cancer and to highlight potential strategies for modulation of the gut microbiota that could lead to improved clinical outcomes and overall health in this population.",
"role": "user"
},
{
"content": "The <microbiome>Gut Microbiota</microbiome>: A Potential Gateway to Improved Health Outcomes in Breast Cancer Treatment and Survivorship. <DDF>Breast cancer</DDF> is the most frequently diagnosed <DDF>cancer</DDF> in <human>women</human> worldwide. The disease and its treatments exert profound effects on an individual's physical and mental health. There are many factors that impact an individual's risk of developing <DDF>breast cancer</DDF>, their response to treatments, and their risk of recurrence. The community of microorganisms inhabiting the <anatomical location>gastrointestinal tract</anatomical location>, the <microbiome>gut microbiota</microbiome>, affects human health through metabolic, neural, and endocrine signaling, and immune activity. It is through these mechanisms that the <microbiome>gut microbiota</microbiome> appears to influence breast cancer risk, response to treatment, and recurrence. A disrupted <microbiome>gut microbiota</microbiome> or state of '<DDF>dysbiosis</DDF>' can contribute to a biological environment associated with higher risk for cancer development as well as contribute to negative treatment side-effects. Many cancer treatments have been shown to shift the <microbiome>gut microbiota</microbiome> toward <DDF>dysbiosis</DDF>; however, the microbiota can also be positively manipulated through diet, <dietary supplement>prebiotic</dietary supplement> and <dietary supplement>probiotic supplementation</dietary supplement>, and exercise. The objective of this review is to provide an overview of the current understanding of the relationship between the <microbiome>gut microbiota</microbiome> and <DDF>breast cancer</DDF> and to highlight potential strategies for modulation of the <microbiome>gut microbiota</microbiome> that could lead to improved clinical outcomes and overall health in this population.",
"role": "assistant"
}
] |
33301807
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nSpinal cord injury and gut microbiota: A review. After spinal cord injury (SCI), intestinal dysfunction has a serious impact on physical and mental health, quality of life, and social participation. Recent data from rodent and human studies indicated that SCI causes gut dysbiosis. Remodeling gut microbiota could be beneficial for the recovery of intestinal function and motor function after SCI. However, few studies have explored SCI with focus on the gut microbiota and \"microbiota-gut-brain\" axis. In this review, the complications following SCI, including intestinal dysfunction, anxiety and depression, metabolic disorders, and neuropathic pain, are directly or indirectly related to gut dysbiosis, which may be mediated by \"gut-brain\" interactions. Furthermore, we discuss the research strategies that can be beneficial in this regard, including germ-free animals, fecal microbiota transplantation, probiotics, phages, and brain imaging techniques. The current microbial research has shifted from descriptive to mechanismal perspective, and future research using new technologies may further demonstrate the pathophysiological mechanism of association of SCI with gut microbiota, elucidate the mode of interaction of gut microbiota and hosts, and help develop personalized microbiota-targeted therapies and drugs based on microbiota or corresponding metabolites.",
"role": "user"
},
{
"content": "<DDF>Spinal cord injury</DDF> and <microbiome>gut microbiota</microbiome>: A review. After <DDF>spinal cord injury</DDF> (<DDF>SCI</DDF>), <DDF>intestinal dysfunction</DDF> has a serious impact on physical and mental health, quality of life, and social participation. Recent data from rodent and human studies indicated that <DDF>SCI</DDF> causes <DDF>gut dysbiosis</DDF>. Remodeling <microbiome>gut microbiota</microbiome> could be beneficial for the recovery of intestinal function and motor function after <DDF>SCI</DDF>. However, few studies have explored <DDF>SCI</DDF> with focus on the <microbiome>gut microbiota</microbiome> and \"microbiota-gut-brain\" axis. In this review, the complications following <DDF>SCI</DDF>, including <DDF>intestinal dysfunction</DDF>, <DDF>anxiety and depression</DDF>, <DDF>metabolic disorders</DDF>, and <DDF>neuropathic pain</DDF>, are directly or indirectly related to <DDF>gut dysbiosis</DDF>, which may be mediated by \"gut-brain\" interactions. Furthermore, we discuss the research strategies that can be beneficial in this regard, including <animal>germ-free animals</animal>, fecal microbiota transplantation, <dietary supplement>probiotics</dietary supplement>, <chemical>phages</chemical>, and <biomedical technique>brain imaging techniques</biomedical technique>. The current microbial research has shifted from descriptive to mechanismal perspective, and future research using new technologies may further demonstrate the pathophysiological mechanism of association of <DDF>SCI</DDF> with <microbiome>gut microbiota</microbiome>, elucidate the mode of interaction of <microbiome>gut microbiota</microbiome> and hosts, and help develop personalized microbiota-targeted therapies and drugs based on microbiota or corresponding metabolites.",
"role": "assistant"
}
] |
33318317
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMental awareness improved mild cognitive impairment and modulated gut microbiome. There is ample scientific and clinical evidence of the effects of gut microbiota on the brain but no definitive evidence that the brain can affect changes in gut microbiota under the bi-directional gut-brain axis concept. As there is no pharmacotherapeutic intervention for the early stages of cognitive decline, research has focused on cognitive stimulation in reversing or slowing the impairment. Elderly patients diagnosed with mild cognitive impairment underwent a randomized-control trial of mindful awareness practice. Neuropsychological assessments, inflammatory markers, and gut microbiota profiles were tested. Here, we report that their cognitive impairment was improved and associated with changes in gut bacterial profile. A cognition-score-dependent-abundance was observed in <i>Ruminococcus</i> vs Recognition Trials (RT), Digit Span Backward (DSB), Semantic Fluency Span (SFS) and Memory Domain (MD); <i>Coprococcus</i> vs DSB, Color Trails Test 2 (CTT2) and Block Design (BD); <i>Parabacteroides</i> vs DSB and SFS; <i>Fusobacterium</i> vs DSB and CTT2; <i>Enterobacteriaceae</i> vs BD and SFS; <i>Ruminococcaceae</i> vs DSB; <i>Phascolarctobacterium</i> vs MD. The study showed for the first-time, alteration in the cognitive capacity leading to the corresponding changes in microbiota profiles. This strongly suggests that signals from the different segments of brain could dictate directly or indirectly the abundances of specific gut microbes.",
"role": "user"
},
{
"content": "Mental awareness improved <DDF>mild cognitive impairment</DDF> and modulated <microbiome>gut microbiome</microbiome>. There is ample scientific and clinical evidence of the effects of <microbiome>gut microbiota</microbiome> on the <anatomical location>brain</anatomical location> but no definitive evidence that the <anatomical location>brain</anatomical location> can affect changes in <microbiome>gut microbiota</microbiome> under the bi-directional gut-brain axis concept. As there is no pharmacotherapeutic intervention for the early stages of <DDF>cognitive decline</DDF>, research has focused on cognitive stimulation in reversing or slowing the <DDF>impairment</DDF>. <human>Elderly patients</human> diagnosed with <DDF>mild cognitive impairment</DDF> underwent a <biomedical technique>randomized-control trial of mindful awareness practice</biomedical technique>. <biomedical technique>Neuropsychological assessments</biomedical technique>, <biomedical technique>inflammatory markers</biomedical technique>, and gut microbiota profiles were tested. Here, we report that their <DDF>cognitive impairment</DDF> was improved and associated with changes in gut bacterial profile. A cognition-score-dependent-abundance was observed in <i><bacteria>Ruminococcus</bacteria></i> vs <biomedical technique>Recognition Trials</biomedical technique> (<biomedical technique>RT</biomedical technique>), <biomedical technique>Digit Span Backward</biomedical technique> (<biomedical technique>DSB</biomedical technique>), <biomedical technique>Semantic Fluency Span</biomedical technique> (<biomedical technique>SFS</biomedical technique>) and <biomedical technique>Memory Domain</biomedical technique> (<biomedical technique>MD</biomedical technique>); <i><bacteria>Coprococcus</bacteria></i> vs <biomedical technique>DSB</biomedical technique>, <biomedical technique>Color Trails Test 2</biomedical technique> (<biomedical technique>CTT2</biomedical technique>) and <biomedical technique>Block Design</biomedical technique> (<biomedical technique>BD</biomedical technique>); <i><bacteria>Parabacteroides</bacteria></i> vs <biomedical technique>DSB</biomedical technique> and <biomedical technique>SFS</biomedical technique>; <i><bacteria>Fusobacterium</bacteria></i> vs <biomedical technique>DSB</biomedical technique> and <biomedical technique>CTT2</biomedical technique>; <i><bacteria>Enterobacteriaceae</bacteria></i> vs <biomedical technique>BD</biomedical technique> and <biomedical technique>SFS</biomedical technique>; <i><bacteria>Ruminococcaceae</bacteria></i> vs <biomedical technique>DSB</biomedical technique>; <i><bacteria>Phascolarctobacterium</bacteria></i> vs <biomedical technique>MD</biomedical technique>. The study showed for the first-time, <DDF>alteration in the cognitive capacity</DDF> leading to the corresponding changes in microbiota profiles. This strongly suggests that signals from the different segments of <anatomical location>brain</anatomical location> could dictate directly or indirectly the abundances of specific <microbiome>gut microbes</microbiome>.",
"role": "assistant"
}
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33406628
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut Microbiota Dysbiosis Is Associated with Elevated Bile Acids in Parkinson's Disease. The gut microbiome can impact brain health and is altered in Parkinson's disease (PD). The vermiform appendix is a lymphoid tissue in the cecum implicated in the storage and regulation of the gut microbiota. We sought to determine whether the appendix microbiome is altered in PD and to analyze the biological consequences of the microbial alterations. We investigated the changes in the functional microbiota in the appendix of PD patients relative to controls (<i>n</i> = 12 PD, 16 C) by metatranscriptomic analysis. We found microbial dysbiosis affecting lipid metabolism, including an upregulation of bacteria responsible for secondary bile acid synthesis. We then quantitatively measure changes in bile acid abundance in PD relative to the controls in the appendix (<i>n</i> = 15 PD, 12 C) and ileum (<i>n</i> = 20 PD, 20 C). Bile acid analysis in the PD appendix reveals an increase in hydrophobic and secondary bile acids, deoxycholic acid (DCA) and lithocholic acid (LCA). Further proteomic and transcriptomic analysis in the appendix and ileum corroborated these findings, highlighting changes in the PD gut that are consistent with a disruption in bile acid control, including alterations in mediators of cholesterol homeostasis and lipid metabolism. Microbially derived toxic bile acids are heightened in PD, which suggests biliary abnormalities may play a role in PD pathogenesis.",
"role": "user"
},
{
"content": "<DDF>Gut Microbiota Dysbiosis</DDF> Is Associated with Elevated <chemical>Bile Acids</chemical> in <DDF>Parkinson's Disease</DDF>. The <microbiome>gut microbiome</microbiome> can impact brain health and is altered in <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). The <anatomical location>vermiform appendix</anatomical location> is a lymphoid tissue in the <anatomical location>cecum</anatomical location> implicated in the storage and regulation of the <microbiome>gut microbiota</microbiome>. We sought to determine whether the <microbiome>appendix microbiome</microbiome> is altered in <DDF>PD</DDF> and to analyze the biological consequences of the microbial alterations. We investigated the changes in the <microbiome>functional microbiota</microbiome> in the <anatomical location>appendix</anatomical location> of <human>PD patients</human> relative to <human>controls</human> (<i>n</i> = 12 PD, 16 C) by <biomedical technique>metatranscriptomic analysis</biomedical technique>. We found <DDF>microbial dysbiosis</DDF> affecting lipid metabolism, including an upregulation of <bacteria>bacteria responsible for secondary bile acid synthesis</bacteria>. We then quantitatively measure changes in bile acid abundance in <DDF>PD</DDF> relative to the <human>controls</human> in the <anatomical location>appendix</anatomical location> (<i>n</i> = 15 PD, 12 C) and <anatomical location>ileum</anatomical location> (<i>n</i> = 20 PD, 20 C). <biomedical technique>Bile acid analysis</biomedical technique> in the <anatomical location>PD appendix</anatomical location> reveals an increase in <chemical>hydrophobic and secondary bile acids</chemical>, <chemical>deoxycholic acid</chemical> (<chemical>DCA</chemical>) and <chemical>lithocholic acid</chemical> (<chemical>LCA</chemical>). Further <biomedical technique>proteomic and transcriptomic analysis</biomedical technique> in the <anatomical location>appendix</anatomical location> and <anatomical location>ileum</anatomical location> corroborated these findings, highlighting changes in the <anatomical location>PD gut</anatomical location> that are consistent with a <DDF>disruption in bile acid control</DDF>, including <DDF>alterations in mediators of cholesterol homeostasis and lipid metabolism</DDF>. <chemical>Microbially derived toxic bile acids</chemical> are heightened in <DDF>PD</DDF>, which suggests <DDF>biliary abnormalities</DDF> may play a role in <DDF>PD pathogenesis</DDF>.",
"role": "assistant"
}
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33416892
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[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nEffects of dietary restriction on neuroinflammation in neurodegenerative diseases. Recent and accumulating work in experimental animal models and humans shows that diet has a much more pervasive and prominent role than previously thought in modulating neuroinflammatory and neurodegenerative mechanisms leading to some of the most common chronic central nervous system (CNS) diseases. Chronic or intermittent food restriction has profound effects in shaping brain and peripheral metabolism, immunity, and gut microbiome biology. Interactions among calorie intake, meal frequency, diet quality, and the gut microbiome modulate specific metabolic and molecular pathways that regulate cellular, tissue, and organ homeostasis as well as inflammation during normal brain aging and CNS neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis, among others. This review discusses these findings and their potential application to the prevention and treatment of CNS neuroinflammatory diseases and the promotion of healthy brain aging.",
"role": "user"
},
{
"content": "Effects of dietary restriction on <DDF>neuroinflammation</DDF> in <DDF>neurodegenerative diseases</DDF>. Recent and accumulating work in experimental animal models and <human>humans</human> shows that diet has a much more pervasive and prominent role than previously thought in modulating neuroinflammatory and neurodegenerative mechanisms leading to some of the most common <DDF>chronic central nervous system (CNS) diseases</DDF>. Chronic or intermittent food restriction has profound effects in shaping brain and peripheral metabolism, immunity, and <microbiome>gut microbiome</microbiome> biology. Interactions among calorie intake, meal frequency, diet quality, and the <microbiome>gut microbiome</microbiome> modulate specific metabolic and molecular pathways that regulate cellular, tissue, and organ homeostasis as well as <DDF>inflammation</DDF> during normal brain aging and <DDF>CNS neurodegenerative diseases</DDF>, including <DDF>Alzheimer's disease</DDF>, <DDF>Parkinson's disease</DDF>, <DDF>amyotrophic lateral sclerosis</DDF>, and <DDF>multiple sclerosis</DDF>, among others. This review discusses these findings and their potential application to the prevention and treatment of <DDF>CNS neuroinflammatory diseases</DDF> and the promotion of healthy brain aging.",
"role": "assistant"
}
] |
33454868
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota homeostasis restoration may become a novel therapy for breast cancer. Breast cancer is the most diagnosed cancer in women. It significantly impairs a patient's physical and mental health. Gut microbiota comprise the bacteria residing in a host's gastrointestinal tract. Through studies over the last decade, we now know that alterations in the composition of the gut microbiome are associated with protection against colonization by pathogens and other diseases, such as diabetes and cancer. This review focuses on how gut microbiota can affect breast cancer development through estrogen activity and discusses the types of bacteria that may be involved in the onset and the progression of breast cancer. We also describe potential therapies to curtail the risk of breast cancer by restoring gut microbiota homeostasis and reducing systemic estrogen levels. This review will further explore the relationship between intestinal microbes and breast cancer and propose a method to treat breast cancer by improving intestinal microbes. We aimed at discovering new methods to prevent or treat BC by changing intestinal microorganisms.",
"role": "user"
},
{
"content": "Gut microbiota homeostasis restoration may become a novel therapy for <DDF>breast cancer</DDF>. <DDF>Breast cancer</DDF> is the most diagnosed <DDF>cancer</DDF> in <human>women</human>. It significantly impairs a patient's physical and mental health. <microbiome>Gut microbiota</microbiome> comprise the bacteria residing in a host's gastrointestinal tract. Through studies over the last decade, we now know that alterations in the composition of the <microbiome>gut microbiome</microbiome> are associated with protection against colonization by pathogens and other diseases, such as <DDF>diabetes</DDF> and <DDF>cancer</DDF>. This review focuses on how <microbiome>gut microbiota</microbiome> can affect breast cancer development through <chemical>estrogen</chemical> activity and discusses the types of <bacteria>bacteria</bacteria> that may be involved in the onset and the progression of <DDF>breast cancer</DDF>. We also describe potential therapies to curtail the risk of <DDF>breast cancer</DDF> by restoring gut microbiota homeostasis and reducing systemic estrogen levels. This review will further explore the relationship between <microbiome>intestinal microbes</microbiome> and <DDF>breast cancer</DDF> and propose a method to treat <DDF>breast cancer</DDF> by improving <microbiome>intestinal microbes</microbiome>. We aimed at discovering new methods to prevent or treat <DDF>BC</DDF> by changing intestinal microorganisms.",
"role": "assistant"
}
] |
33467657
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nMechanisms Underlying the Cognitive and Behavioural Effects of Maternal Obesity. The widespread consumption of 'western'-style diets along with sedentary lifestyles has led to a global epidemic of obesity. Epidemiological, clinical and preclinical evidence suggests that maternal obesity, overnutrition and unhealthy dietary patterns programs have lasting adverse effects on the physical and mental health of offspring. We review currently available preclinical and clinical evidence and summarise possible underlying neurobiological mechanisms by which maternal overnutrition may perturb offspring cognitive function, affective state and psychosocial behaviour, with a focus on (1) neuroinflammation; (2) disrupted neuronal circuities and connectivity; and (3) dysregulated brain hormones. We briefly summarise research implicating the gut microbiota in maternal obesity-induced changes to offspring behaviour. In animal models, maternal obesogenic diet consumption disrupts CNS homeostasis in offspring, which is critical for healthy neurodevelopment, by altering hypothalamic and hippocampal development and recruitment of glial cells, which subsequently dysregulates dopaminergic and serotonergic systems. The adverse effects of maternal obesogenic diets are also conferred through changes to hormones including leptin, insulin and oxytocin which interact with these brain regions and neuronal circuits. Furthermore, accumulating evidence suggests that the gut microbiome may directly and indirectly contribute to these maternal diet effects in both human and animal studies. As the specific pathways shaping abnormal behaviour in offspring in the context of maternal obesogenic diet exposure remain unknown, further investigations are needed to address this knowledge gap. Use of animal models permits investigation of changes in neuroinflammation, neurotransmitter activity and hormones across global brain network and sex differences, which could be directly and indirectly modulated by the gut microbiome.",
"role": "user"
},
{
"content": "Mechanisms Underlying the <DDF>Cognitive and Behavioural Effects</DDF> of <DDF>Maternal Obesity</DDF>. The widespread consumption of 'western'-style diets along with sedentary lifestyles has led to a global epidemic of <DDF>obesity</DDF>. Epidemiological, clinical and preclinical evidence suggests that <DDF>maternal obesity</DDF>, <DDF>overnutrition</DDF> and unhealthy dietary patterns programs have lasting adverse effects on the physical and mental health of <human>offspring</human>. We review currently available preclinical and clinical evidence and summarise possible underlying neurobiological mechanisms by which <DDF>maternal overnutrition</DDF> may perturb offspring cognitive function, affective state and psychosocial behaviour, with a focus on (1) <DDF>neuroinflammation</DDF>; (2) <DDF>disrupted neuronal circuities and connectivity</DDF>; and (3) <DDF>dysregulated brain hormones</DDF>. We briefly summarise research implicating the <microbiome>gut microbiota</microbiome> in maternal <DDF>obesity-induced changes</DDF> to offspring behaviour. In animal models, maternal obesogenic diet consumption disrupts CNS homeostasis in <human>offspring</human>, which is critical for healthy neurodevelopment, by altering hypothalamic and hippocampal development and recruitment of glial cells, which subsequently dysregulates dopaminergic and serotonergic systems. The adverse effects of maternal obesogenic diets are also conferred through changes to hormones including <chemical>leptin</chemical>, <chemical>insulin</chemical> and <chemical>oxytocin</chemical> which interact with these brain regions and neuronal circuits. Furthermore, accumulating evidence suggests that the <microbiome>gut microbiome</microbiome> may directly and indirectly contribute to these maternal diet effects in both human and animal studies. As the specific pathways shaping <DDF>abnormal behaviour</DDF> in <human>offspring</human> in the context of maternal obesogenic diet exposure remain unknown, further investigations are needed to address this knowledge gap. Use of animal models permits investigation of changes in <DDF>neuroinflammation</DDF>, neurotransmitter activity and hormones across global brain network and sex differences, which could be directly and indirectly modulated by the <microbiome>gut microbiome</microbiome>.",
"role": "assistant"
}
] |
33505487
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nAcupoint Massage Therapy Alters the Composition of Gut Microbiome in Functional Constipation Patients. Results showed the overall structure of gut microbiome has no significant difference between experimental and control groups. In the genus level, the abundance of <i>Pseudobutyrivibrio</i> and <i>Ruminiclostridium</i> is higher in the experiment group than in the control, whereas that of <i>Fusicatenibacter</i> is less. The 16S KEGG function prediction suggested that Parkinson disease, retinol metabolism, and arachidonic acid metabolism could explain the biological function of different gut microbiome. Furthermore, cytokines in the serum showed a correlation with the abundance of <i>Pseudobutyrivibrio</i> in CFC. AMT could change the composition of gut microbiome which is associated with cytokines in CFC patients.",
"role": "user"
},
{
"content": "Acupoint Massage Therapy Alters the Composition of <microbiome>Gut Microbiome</microbiome> in <human>Functional Constipation Patients</human>. Results showed the overall structure of <microbiome>gut microbiome</microbiome> has no significant difference between <human>experimental and control groups</human>. In the genus level, the abundance of <i><bacteria>Pseudobutyrivibrio</bacteria></i> and <i><bacteria>Ruminiclostridium</bacteria></i> is higher in the <human>experiment group</human> than in the <human>control</human>, whereas that of <i><bacteria>Fusicatenibacter</bacteria></i> is less. The <biomedical technique>16S KEGG function prediction</biomedical technique> suggested that <DDF>Parkinson disease</DDF>, retinol metabolism, and arachidonic acid metabolism could explain the biological function of different <microbiome>gut microbiome</microbiome>. Furthermore, <chemical>cytokines</chemical> in the serum showed a correlation with the abundance of <i><bacteria>Pseudobutyrivibrio</bacteria></i> in <DDF>CFC</DDF>. AMT could change the composition of <microbiome>gut microbiome</microbiome> which is associated with <chemical>cytokines</chemical> in <human>CFC patients</human>.",
"role": "assistant"
}
] |
33514545
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nHuman physiomimetic model integrating microphysiological systems of the gut, liver, and brain for studies of neurodegenerative diseases. Slow progress in the fight against neurodegenerative diseases (NDs) motivates an urgent need for highly controlled in vitro systems to investigate organ-organ- and organ-immune-specific interactions relevant for disease pathophysiology. Of particular interest is the gut/microbiome-liver-brain axis for parsing out how genetic and environmental factors contribute to NDs. We have developed a mesofluidic platform technology to study gut-liver-cerebral interactions in the context of Parkinson's disease (PD). It connects microphysiological systems (MPSs) of the primary human gut and liver with a human induced pluripotent stem cell-derived cerebral MPS in a systemically circulated common culture medium containing CD4<sup>+</sup> regulatory T and T helper 17 cells. We demonstrate this approach using a patient-derived cerebral MPS carrying the PD-causing A53T mutation, gaining two important findings: (i) that systemic interaction enhances features of in vivo-like behavior of cerebral MPSs, and (ii) that microbiome-associated short-chain fatty acids increase expression of pathology-associated pathways in PD.",
"role": "user"
},
{
"content": "Human physiomimetic model integrating microphysiological systems of the <anatomical location>gut</anatomical location>, <anatomical location>liver</anatomical location>, and <anatomical location>brain</anatomical location> for studies of <DDF>neurodegenerative diseases</DDF>. Slow progress in the fight against <DDF>neurodegenerative diseases</DDF> (<DDF>NDs</DDF>) motivates an urgent need for highly controlled in vitro systems to investigate organ-organ- and organ-immune-specific interactions relevant for disease pathophysiology. Of particular interest is the gut/microbiome-liver-brain axis for parsing out how genetic and environmental factors contribute to <DDF>NDs</DDF>. We have developed a mesofluidic platform technology to study gut-liver-cerebral interactions in the context of <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). It connects microphysiological systems (MPSs) of the <anatomical location>primary human gut</anatomical location> and <anatomical location>liver</anatomical location> with a <biomedical technique>human induced pluripotent stem cell-derived cerebral MPS</biomedical technique> in a systemically circulated common culture medium containing <chemical>CD4<sup>+</sup> regulatory T</chemical> and <chemical>T helper 17</chemical> cells. We demonstrate this approach using a patient-derived cerebral MPS carrying the <gene>PD-causing A53T mutation</gene>, gaining two important findings: (i) that systemic interaction enhances features of in vivo-like behavior of cerebral MPSs, and (ii) that <chemical>microbiome-associated short-chain fatty acids</chemical> increase expression of pathology-associated pathways in <DDF>PD</DDF>.",
"role": "assistant"
}
] |
33651324
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nGut microbiota dysbiosis is associated with worse emotional states in HIV infection. The biological mechanisms underlying emotional distress in HIV infection are likely to be complex but remain understudied. We investigated whether dysbiotic signatures in the gut microbiome of persons living with HIV (PLWH) are associated with their emotional status. We retrospectively examined the gut microbiome and clinical evaluation of 129 adults (94 PLWH and 35 HIV-) enrolled at UC San Diego's HIV Neurobehavioral Research Program. A subset of participants (32 PLWH vs. 13 HIV-) underwent an emotional assessment using the NIH Toolbox Emotion Battery summarized by three composite scores (negative affect, social satisfaction, and psychological well-being). We then sequenced the 16S rDNA V3-V4 regions from stool and performed taxonomic assignment using CLC Microbial Genomics Module. The gut microbiota profiles were evaluated in relation to participants' emotional assessment. All analyses were done in R statistical software. We found that the relative abundance of aerotolerant bacteria was significantly higher in PLWH (p < 0.01) and was associated with a lifetime major depression diagnosis independently of HIV status (p = 0.05). Moreover, PLWH experienced significantly worse psychological well-being (p = 0.02), less social satisfaction (p = 0.03), and more negative affect (p = 0.02). Higher levels of aerotolerant bacteria were associated with worse psychological well-being (rho = -0.35, p = 0.02), less social satisfaction (r = - 0.42, p < 0.01), and more negative affect (rho = 0.46, p < 0.01). The association of aerotolerant bacteria with social satisfaction and negative affect was independent of HIV status (p < 0.05, for both). The over-representation of aerotolerant bacteria in the gut may reflect worse oxidative stress and barrier defects and may contribute to emotional distress during HIV infection.",
"role": "user"
},
{
"content": "<DDF>Gut microbiota dysbiosis</DDF> is associated with worse emotional states in <DDF>HIV infection</DDF>. The biological mechanisms underlying <DDF>emotional distress</DDF> in <DDF>HIV infection</DDF> are likely to be complex but remain understudied. We investigated whether dysbiotic signatures in the <microbiome>gut microbiome</microbiome> of <human>persons</human> living with <DDF>HIV</DDF> (<human>PLWH</human>) are associated with their emotional status. We retrospectively examined the <microbiome>gut microbiome</microbiome> and clinical evaluation of 129 <human>adults</human> (94 <human>PLWH</human> and 35 HIV-) enrolled at UC San Diego's HIV Neurobehavioral Research Program. A subset of <human>participants</human> (32 <human>PLWH</human> vs. 13 HIV-) underwent an emotional assessment using the NIH Toolbox Emotion Battery summarized by three composite scores (negative affect, social satisfaction, and psychological well-being). We then sequenced the 16S rDNA V3-V4 regions from stool and performed taxonomic assignment using CLC Microbial Genomics Module. The <microbiome>gut microbiota</microbiome> profiles were evaluated in relation to participants' emotional assessment. All analyses were done in R statistical software. We found that the relative abundance of <bacteria>aerotolerant bacteria</bacteria> was significantly higher in <human>PLWH</human> (p < 0.01) and was associated with a lifetime major depression diagnosis independently of HIV status (p = 0.05). Moreover, <human>PLWH</human> experienced significantly worse psychological well-being (p = 0.02), less social satisfaction (p = 0.03), and more negative affect (p = 0.02). Higher levels of <bacteria>aerotolerant bacteria</bacteria> were associated with worse psychological well-being (rho = -0.35, p = 0.02), less social satisfaction (r = - 0.42, p < 0.01), and more negative affect (rho = 0.46, p < 0.01). The association of <bacteria>aerotolerant bacteria</bacteria> with social satisfaction and negative affect was independent of HIV status (p < 0.05, for both). The over-representation of <bacteria>aerotolerant bacteria</bacteria> in the <anatomical location>gut</anatomical location> may reflect worse oxidative stress and barrier defects and may contribute to <DDF>emotional distress</DDF> during <DDF>HIV infection</DDF>.",
"role": "assistant"
}
] |
33664475
|
[
{
"content": "You are an expert biomedical NER annotator.\nIdentify every mention of these entity types:\n chemical, microbiome, DDF, gene, animal, dietary supplement,\n human, statistical technique, anatomical location, bacteria,\n biomedical technique, food, drug\n\nFocus on tagging each entire noun or noun phrase that denotes one coherent biological entity.\nDo not split, nest, or overlap tags. Preserve all punctuation and spacing; only insert tags.\n\nTEXT:\nSialylated human milk oligosaccharides program cognitive development through a non-genomic transmission mode. Breastmilk contains bioactive molecules essential for brain and cognitive development. While sialylated human milk oligosaccharides (HMOs) have been implicated in phenotypic programming, their selective role and underlying mechanisms remained elusive. Here, we investigated the long-term consequences of a selective lactational deprivation of a specific sialylated HMO in mice. We capitalized on a knock-out (KO) mouse model (B6.129-St6gal1<sup>tm2Jxm</sup>/J) lacking the gene responsible for the synthesis of sialyl(alpha2,6)lactose (6'SL), one of the two sources of sialic acid (Neu5Ac) to the lactating offspring. Neu5Ac is involved in the formation of brain structures sustaining cognition. To deprive lactating offspring of 6'SL, we cross-fostered newborn wild-type (WT) pups to KO dams, which provide 6'SL-deficient milk. To test whether lactational 6'SL deprivation affects cognitive capabilities in adulthood, we assessed attention, perseveration, and memory. To detail the associated endophenotypes, we investigated hippocampal electrophysiology, plasma metabolomics, and gut microbiota composition. To investigate the underlying molecular mechanisms, we assessed gene expression (at eye-opening and in adulthood) in two brain regions mediating executive functions and memory (hippocampus and prefrontal cortex, PFC). Compared to control mice, WT offspring deprived of 6'SL during lactation exhibited consistent alterations in all cognitive functions addressed, hippocampal electrophysiology, and in pathways regulating the serotonergic system (identified through gut microbiota and plasma metabolomics). These were associated with a site- (PFC) and time-specific (eye-opening) reduced expression of genes involved in central nervous system development. Our data suggest that 6'SL in maternal milk adjusts cognitive development through a short-term upregulation of genes modulating neuronal patterning in the PFC.",
"role": "user"
},
{
"content": "<dietary supplement>Sialylated human milk oligosaccharides</dietary supplement> program cognitive development through a non-genomic transmission mode. <food>Breastmilk</food> contains bioactive molecules essential for brain and cognitive development. While <dietary supplement>sialylated human milk oligosaccharides</dietary supplement> (<dietary supplement>HMOs</dietary supplement>) have been implicated in phenotypic programming, their selective role and underlying mechanisms remained elusive. Here, we investigated the long-term consequences of a selective lactational deprivation of a specific <dietary supplement>sialylated HMO</dietary supplement> in <animal>mice</animal>. We capitalized on a knock-out (KO) mouse model (B6.129-St6gal1<sup>tm2Jxm</sup>/J) lacking the gene responsible for the synthesis of <chemical>sialyl(alpha2,6)lactose</chemical> (<chemical>6'SL</chemical>), one of the two sources of <chemical>sialic acid</chemical> (<chemical>Neu5Ac</chemical>) to the <animal>lactating offspring</animal>. <chemical>Neu5Ac</chemical> is involved in the formation of brain structures sustaining cognition. To deprive <animal>lactating offspring</animal> of <chemical>6'SL</chemical>, we cross-fostered <animal>newborn wild-type (WT) pups</animal> to <animal>KO dams</animal>, which provide <food>6'SL-deficient milk</food>. To test whether lactational 6'SL deprivation affects cognitive capabilities in adulthood, we assessed attention, perseveration, and memory. To detail the associated endophenotypes, we investigated hippocampal electrophysiology, <biomedical technique>plasma metabolomics</biomedical technique>, and gut microbiota composition. To investigate the underlying molecular mechanisms, we assessed gene expression (at eye-opening and in adulthood) in two brain regions mediating executive functions and memory (<anatomical location>hippocampus</anatomical location> and <anatomical location>prefrontal cortex</anatomical location>, <anatomical location>PFC</anatomical location>). Compared to <animal>control mice</animal>, <animal>WT offspring</animal> deprived of <chemical>6'SL</chemical> during lactation exhibited consistent alterations in all cognitive functions addressed, hippocampal electrophysiology, and in pathways regulating the serotonergic system (identified through <microbiome>gut microbiota</microbiome> and <biomedical technique>plasma metabolomics</biomedical technique>). These were associated with a site- (PFC) and time-specific (eye-opening) reduced expression of genes involved in central nervous system development. Our data suggest that <chemical>6'SL</chemical> in <food>maternal milk</food> adjusts cognitive development through a short-term upregulation of genes modulating neuronal patterning in the <anatomical location>PFC</anatomical location>.",
"role": "assistant"
}
] |
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