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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:\nChronic intestinal pseudo-obstruction: associations with gut microbiota and genes expression of intestinal serotonergic pathway. Pediatric chronic intestinal pseudo-obstruction (PIPO) is a rare disease characterized by symptoms and radiological signs suggestive of intestinal obstruction, in the absence of lumen-occluding lesions. It results from an extremely severe impairment of propulsive motility. The intestinal endocrine system (IES) jointly with the enteric nervous system (ENS) regulates secreto-motor functions via different hormones and bioactive messengers/neurotransmitters. The neurotransmitter 5-hydroxytryptamine (5-HT) (or serotonin) is linked to intestinal peristalsis and secretory reflexes. Gut microbiota and its interplay with ENS affect 5-HT synthesis, release, and the subsequent serotonin receptor activation. To date, the interplay between 5-HT and gut microbiota in PIPO remains largely unclear. This study aimed to assess correlations between mucosa associated microbiota (MAM), intestinal serotonin-related genes expression in PIPO. To this purpose, biopsies of the colon, ileum and duodenum have been collected from 7 PIPO patients, and 7 age-/sex-matched healthy controls. After DNA extraction, the MAM was assessed by next generation sequencing (NGS) of the V3-V4 region of the bacterial RNA 16 S, on an Illumina Miseq platform. The expression of genes implicated in serotoninergic pathway (TPH1, SLC6A4, 5-HTR3 and 5-HTR4) was established by qPCR, and correlations with MAM and clinical parameters of PIPO have been evaluated. Our results revealed that PIPO patients exhibit a MAM with a different composition and with dysbiosis, i.e. with a lower biodiversity and fewer less connected species with a greater number of non-synergistic relationships, compared to controls. qPCR results revealed modifications in the expression of serotonin-related intestinal genes in PIPO patients, when compared to controls. Correlation analysis do not reveal any kind of connection. For the first time, we report in PIPO patients a specific MAM associated to underlying pathology and an altered intestinal serotonin pathway. A possible dysfunction of the serotonin pathway, possibly related to or triggered by an altered microbiota, may contribute to dysmotility in PIPO patients. The results of our pilot study provide the basis for new biomarkers and innovative therapies targeting the microbiota or serotonin pathways in PIPO patients.",
"role": "user"
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"content": "<DDF>Chronic intestinal pseudo-obstruction</DDF>: associations with <microbiome>gut microbiota</microbiome> and genes expression of intestinal serotonergic pathway. <DDF>Pediatric chronic intestinal pseudo-obstruction</DDF> (<DDF>PIPO</DDF>) is a rare disease characterized by <DDF>symptoms and radiological signs suggestive of intestinal obstruction</DDF>, in the absence of <DDF>lumen-occluding lesions</DDF>. It results from an <DDF>extremely severe impairment of propulsive motility</DDF>. The intestinal endocrine system (IES) jointly with the enteric nervous system (ENS) regulates secreto-motor functions via <chemical>different hormones</chemical> and <chemical>bioactive messengers/neurotransmitters</chemical>. The <chemical>neurotransmitter 5-hydroxytryptamine</chemical> (<chemical>5-HT</chemical>) (or <chemical>serotonin</chemical>) is linked to intestinal peristalsis and secretory reflexes. <microbiome>Gut microbiota</microbiome> and its interplay with ENS affect 5-HT synthesis, release, and the subsequent serotonin receptor activation. To date, the interplay between <chemical>5-HT</chemical> and <microbiome>gut microbiota</microbiome> in <DDF>PIPO</DDF> remains largely unclear. This study aimed to assess correlations between <microbiome>mucosa associated microbiota</microbiome> (<microbiome>MAM</microbiome>), intestinal serotonin-related genes expression in <DDF>PIPO</DDF>. To this purpose, biopsies of the <anatomical location>colon</anatomical location>, <anatomical location>ileum</anatomical location> and <anatomical location>duodenum</anatomical location> have been collected from 7 <human>PIPO patients</human>, and 7 <human>age-/sex-matched healthy controls</human>. After <biomedical technique>DNA extraction</biomedical technique>, the <microbiome>MAM</microbiome> was assessed by <biomedical technique>next generation sequencing (NGS) of the V3-V4 region of the bacterial RNA 16 S</biomedical technique>, on an Illumina Miseq platform. The expression of genes implicated in serotoninergic pathway (<gene>TPH1</gene>, <gene>SLC6A4</gene>, <gene>5-HTR3</gene> and <gene>5-HTR4</gene>) was established by <biomedical technique>qPCR</biomedical technique>, and correlations with <microbiome>MAM</microbiome> and clinical parameters of <DDF>PIPO</DDF> have been evaluated. Our results revealed that <human>PIPO patients</human> exhibit a <microbiome>MAM</microbiome> with a different composition and with <DDF>dysbiosis</DDF>, i.e. with a lower biodiversity and fewer less connected species with a greater number of non-synergistic relationships, compared to <human>controls</human>. <biomedical technique>qPCR</biomedical technique> results revealed modifications in the expression of <gene>serotonin-related intestinal genes</gene> in <human>PIPO patients</human>, when compared to <human>controls</human>. <statistical technique>Correlation analysis</statistical technique> do not reveal any kind of connection. For the first time, we report in <human>PIPO patients</human> a <microbiome>specific MAM associated to underlying pathology</microbiome> and an <DDF>altered intestinal serotonin pathway</DDF>. A possible <DDF>dysfunction of the serotonin pathway, possibly related to or triggered by an altered microbiota</DDF>, may contribute to <DDF>dysmotility</DDF> in <human>PIPO patients</human>. The results of our pilot study provide the basis for new biomarkers and innovative therapies targeting the microbiota or serotonin pathways in <human>PIPO patients</human>.",
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38331354
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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:\nDepression-like phenotypes in mice following common bile duct ligation: Insights into the gut-liver-brain axis via the vagus nerve. Depression frequently occurs in patients with liver cirrhosis, yet the reasons for this correlation are not fully understood. Dysbiosis of gut microbiota has been implicated in depression through the gut-brain axis via the vagus nerve. This study explored the potential role of the gut-liver-brain axis via the vagus nerve in depression-like phenotypes in mice with liver cirrhosis. These mice underwent common bile duct ligation (CBDL), a method used to stimulate liver cirrhosis. To assess depression-like behaviors, behavioral tests were conducted 10 days following either sham or CBDL surgeries. The mice with CBDL displayed symptoms such as splenomegaly, elevated plasma levels of interleukin-6 and tumor necrosis factor-α, depression-like behaviors, decreased levels of synaptic proteins in the prefrontal cortex (PFC), disrupted gut microbiota balance, and changes in blood metabolites (or lipids). Additionally, there were positive or negative correlations between the relative abundance of microbiome and behavioral data or blood metabolites (or lipids). Significantly, these changes were reversed in CBDL mice by performing a subdiaphragmatic vagotomy. Intriguingly, depression-like phenotypes in mice with CBDL were improved after a single injection of arketamine, a new antidepressant. These results suggest that CBDL-induced depression-like phenotypes in mice are mediated through the gut-liver-brain axis via the subdiaphragmatic vagus nerve, and that arketamine might offer a new treatment approach for depression in liver cirrhosis patients.",
"role": "user"
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{
"content": "Depression-like phenotypes in <animal>mice</animal> following common bile duct ligation: Insights into the gut-liver-brain axis via the <anatomical location>vagus nerve</anatomical location>. <DDF>Depression</DDF> frequently occurs in <human>patients</human> with <DDF>liver cirrhosis</DDF>, yet the reasons for this correlation are not fully understood. <DDF>Dysbiosis</DDF> of <microbiome>gut microbiota</microbiome> has been implicated in <DDF>depression</DDF> through the gut-brain axis via the <anatomical location>vagus nerve</anatomical location>. This study explored the potential role of the gut-liver-brain axis via the <anatomical location>vagus nerve</anatomical location> in depression-like phenotypes in <animal>mice</animal> with <DDF>liver cirrhosis</DDF>. These <animal>mice</animal> underwent common bile duct ligation (CBDL), a method used to stimulate <DDF>liver cirrhosis</DDF>. To assess <DDF>depression-like behaviors</DDF>, behavioral tests were conducted 10 days following either sham or CBDL surgeries. The <animal>mice</animal> with CBDL displayed symptoms such as <DDF>splenomegaly</DDF>, elevated plasma levels of <chemical>interleukin-6</chemical> and <chemical>tumor necrosis factor-α</chemical>, <DDF>depression-like behaviors</DDF>, decreased levels of <chemical>synaptic proteins</chemical> in the <anatomical location>prefrontal cortex</anatomical location> (<anatomical location>PFC</anatomical location>), disrupted <microbiome>gut</microbiome> microbiota balance, and changes in <chemical>blood metabolites</chemical> (or <chemical>lipids</chemical>). Additionally, there were positive or negative correlations between the relative abundance of <microbiome>microbiome</microbiome> and behavioral data or <chemical>blood metabolites</chemical> (or <chemical>lipids</chemical>). Significantly, these changes were reversed in <animal>CBDL mice</animal> by performing a subdiaphragmatic vagotomy. Intriguingly, depression-like phenotypes in <animal>mice</animal> with CBDL were improved after a single injection of <drug>arketamine</drug>, a new <drug>antidepressant</drug>. These results suggest that CBDL-induced depression-like phenotypes in <animal>mice</animal> are mediated through the gut-liver-brain axis via the <anatomical location>subdiaphragmatic vagus nerve</anatomical location>, and that <drug>arketamine</drug> might offer a new treatment approach for <DDF>depression</DDF> in <human>liver cirrhosis patients</human>.",
"role": "assistant"
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38401573
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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 role of gut-brain axis on prophylactic actions of arketamine in male mice exposed to chronic restrain stress. The gut-brain axis, which includes gut microbiota and microbiome-derived metabolites, might be implicated in depression. We reported the sustained prophylactic effects of a new antidepressant arketamine in chronic restrain stress (CRS) model of depression. In this study, we investigated the role of gut-brain axis on the prophylactic effects of arketamine in the CRS (7 days) model. Pretreatment with arketamine (10 mg/kg, 1 day prior to the CRS onset) significantly prevented CRS-induced body weight loss, increased immobility time of forced swimming test, decreased sucrose preference of sucrose preference test, and reduced expressions of synaptic proteins (GluA1 and PSD-95) in the prefrontal cortex (PFC) in the male mice. Gut microbiota analysis showed that pretreatment with arketamine might restore altered abundance of gut microbiota in CRS-exposed mice. An untargeted metabolomics analysis revealed four metabolites (e.g., L-leucine, N-acetyl-l-glutamine, 2-(2,4-dichlorophenyl)-3-[4-(dimethylamino)phenyl]acrylonitrile, L-threonine amide) that were altered between control and CRS group; however, there were found to be altered between the saline + CRS group and the arketamine + CRS group. Network analysis demonstrated correlations among synaptic proteins in the PFC and certain microbiota, and blood metabolites. These findings suggest that gut-brain axis, including its metabolites, might partially contribute to the persistent prophylactic effects of arketamine in the CRS model.",
"role": "user"
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{
"content": "A role of gut-brain axis on prophylactic actions of <drug>arketamine</drug> in <animal>male mice</animal> exposed to <DDF>chronic restrain stress</DDF>. The gut-brain axis, which includes <microbiome>gut microbiota</microbiome> and <chemical>microbiome-derived metabolites</chemical>, might be implicated in <DDF>depression</DDF>. We reported the sustained prophylactic effects of a new antidepressant <drug>arketamine</drug> in <DDF>chronic restrain stress</DDF> (<DDF>CRS</DDF>) model of <DDF>depression</DDF>. In this study, we investigated the role of gut-brain axis on the prophylactic effects of <drug>arketamine</drug> in the CRS (7 days) model. Pretreatment with <drug>arketamine</drug> (10 mg/kg, 1 day prior to the <DDF>CRS</DDF> onset) significantly prevented <DDF>CRS-induced body weight loss</DDF>, increased immobility time of forced swimming test, decreased sucrose preference of sucrose preference test, and reduced expressions of synaptic proteins (<chemical>GluA1</chemical> and <chemical>PSD-95</chemical>) in the <anatomical location>prefrontal cortex</anatomical location> (<anatomical location>PFC</anatomical location>) in the <animal>male mice</animal>. Gut microbiota analysis showed that pretreatment with <drug>arketamine</drug> might restore altered abundance of <microbiome>gut microbiota</microbiome> in <animal>CRS-exposed mice</animal>. An <biomedical technique>untargeted metabolomics</biomedical technique> analysis revealed four metabolites (e.g., <chemical>L-leucine</chemical>, <chemical>N-acetyl-l-glutamine</chemical>, <chemical>2-(2,4-dichlorophenyl)-3-[4-(dimethylamino)phenyl]acrylonitrile</chemical>, <chemical>L-threonine amide</chemical>) that were altered between <human>control</human> and <human>CRS group</human>; however, there were found to be altered between the <human>saline + CRS group</human> and the <human>arketamine + CRS group</human>. <statistical technique>Network analysis</statistical technique> demonstrated correlations among <chemical>synaptic proteins</chemical> in the <anatomical location>PFC</anatomical location> and certain microbiota, and <chemical>blood metabolites</chemical>. These findings suggest that gut-brain axis, including its metabolites, might partially contribute to the persistent prophylactic effects of <drug>arketamine</drug> in the CRS model.",
"role": "assistant"
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38432867
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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 and thyroid-associated ophthalmopathy. Thyroid-associated ophthalmopathy (TAO) is a multifactorial-mediated autoimmune orbital disease with the highest incidence of orbital disease in adults. Due to the complex clinical manifestations and prolonged course,TAO seriously affect the physical and mental health of patients.The pathogenesis of TAO has not been fully elucidated and the treatment lacks specificity. Therefore, in-depth research on the pathogenesis of TAO is to find effective treatments. In recent years, studies have suggested that there is gut microbiota disorder in TAO, and the risk factors of TAO can promote gut microbiota disorder. Disordered gut microbiota can participate in the occurrence and development of TAO via influencing T cell differentiation, mimicking autoantigens, and influencing host non-coding RNA expression. Modulating the gut microbiota also has therapeutic effects on TAO and is a promising therapeutic approach.",
"role": "user"
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{
"content": "<microbiome>Gut microbiota</microbiome> and <DDF>thyroid-associated ophthalmopathy</DDF>. <DDF>Thyroid-associated ophthalmopathy</DDF> (<DDF>TAO</DDF>) is a <DDF>multifactorial-mediated autoimmune orbital disease</DDF> with the highest incidence of <DDF>orbital disease</DDF> in <human>adults</human>. Due to the complex clinical manifestations and prolonged course,<DDF>TAO</DDF> seriously affect the physical and mental health of <human>patients</human>.The pathogenesis of <DDF>TAO</DDF> has not been fully elucidated and the treatment lacks specificity. Therefore, in-depth research on the pathogenesis of <DDF>TAO</DDF> is to find effective treatments. In recent years, studies have suggested that there is <DDF>gut microbiota disorder</DDF> in <DDF>TAO</DDF>, and the risk factors of <DDF>TAO</DDF> can promote <DDF>gut microbiota disorder</DDF>. <microbiome>Disordered gut microbiota</microbiome> can participate in the occurrence and development of <DDF>TAO</DDF> via influencing T cell differentiation, mimicking <chemical>autoantigens</chemical>, and influencing host non-coding RNA expression. Modulating the <microbiome>gut microbiota</microbiome> also has therapeutic effects on <DDF>TAO</DDF> and is a promising therapeutic approach.",
"role": "assistant"
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38606411
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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:\nMarkers of intestinal barrier damage in patients with chronic insomnia disorder. Insomnia disorder stands out as one of the prevalent clinical sleep and psychiatric disorders. Prior research has unequivocally demonstrated variations in the diversity and abundance of gut microbiota among individuals with insomnia disorder. These alterations may play a direct or indirect role in the onset and progression of insomnia disorder by compromising the integrity of the intestinal barrier. This study aims to evaluate the impairment of the intestinal barrier in individuals with insomnia disorder by scrutinizing the serum functionality of this barrier. 45 patients with chronic insomnia disorder and 30 matched healthy volunteers were meticulously selected based on inclusion criteria. ELISA technology was employed to measure serum levels of diamine oxidase (DAO), D-lactic acid (D-LA), intestinal fatty acid binding protein (I-FABP), and endothelin (ET). Spearman correlation analysis was used to explore the relationship between intestinal mucosal markers and clinical characteristics. Data were analyzed using SPSS 26.0. Compared to the healthy control group, the insomnia disorder group exhibited significantly elevated scores on subjective mood and sleep scales (GAD-7, PHQ-9, HAMA, HAMD, PSQI, and ISI) (P < 0.05). Overnight PSG indicated a notable increase in bed time, total wake time, sleep onset latency, and wake after sleep onset in individuals with insomnia disorder. Additionally, there was a decrease in sleep efficiency and alterations in sleep structure (increased proportion of N1 and N3 stages, prolonged N1 stage) (P < 0.05). The chronic insomnia disorder group displayed significantly reduced concentrations of serum DAO, D-LA, I-FABP, and ET (P < 0.05). Furthermore, significant positive correlations were identified between intestinal epithelial barrier markers and sleep efficiency, while negative correlations were found with wake after sleep onset, total wake time, PSQI, HAMA, and HAMD. Additionally, D-LA levels were significantly positively correlated with ET concentrations. Individuals with chronic insomnia disorder manifest disruptions in sleep structure, heightened susceptibility to anxiety and depressive moods, and impaired intestinal barrier function. These findings suggest that the occurrence and development of insomnia disorder may be linked to the impairment of the intestinal barrier.",
"role": "user"
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"content": "Markers of <DDF>intestinal barrier damage</DDF> in <human>patients</human> with <DDF>chronic insomnia disorder</DDF>. <DDF>Insomnia disorder</DDF> stands out as one of the prevalent <DDF>clinical sleep and psychiatric disorders</DDF>. Prior research has unequivocally demonstrated variations in the diversity and abundance of <microbiome>gut microbiota</microbiome> among <human>individuals</human> with <DDF>insomnia disorder</DDF>. These alterations may play a direct or indirect role in the onset and progression of <DDF>insomnia disorder</DDF> by compromising the integrity of the intestinal barrier. This study aims to evaluate the impairment of the <anatomical location>intestinal barrier</anatomical location> in <human>individuals</human> with <DDF>insomnia disorder</DDF> by scrutinizing the serum functionality of this barrier. 45 <human>patients</human> with <DDF>chronic insomnia disorder</DDF> and 30 matched <human>healthy volunteers</human> were meticulously selected based on inclusion criteria. <biomedical technique>ELISA technology</biomedical technique> was employed to measure serum levels of <chemical>diamine oxidase</chemical> (<chemical>DAO</chemical>), <chemical>D-lactic acid</chemical> (<chemical>D-LA</chemical>), <chemical>intestinal fatty acid binding protein</chemical> (<chemical>I-FABP</chemical>), and <chemical>endothelin</chemical> (<chemical>ET</chemical>). <statistical technique>Spearman correlation analysis</statistical technique> was used to explore the relationship between intestinal mucosal markers and clinical characteristics. Data were analyzed using SPSS 26.0. Compared to the <human>healthy control group</human>, the <human>insomnia disorder group</human> exhibited significantly elevated scores on subjective mood and sleep scales (GAD-7, PHQ-9, HAMA, HAMD, PSQI, and ISI) (P < 0.05). Overnight PSG indicated a notable increase in bed time, total wake time, sleep onset latency, and wake after sleep onset in <human>individuals</human> with <DDF>insomnia disorder</DDF>. Additionally, there was a decrease in sleep efficiency and alterations in sleep structure (increased proportion of N1 and N3 stages, prolonged N1 stage) (P < 0.05). The <human>chronic insomnia disorder group</human> displayed significantly reduced concentrations of <chemical>serum DAO</chemical>, <chemical>D-LA</chemical>, <chemical>I-FABP</chemical>, and <chemical>ET</chemical> (P < 0.05). Furthermore, significant positive correlations were identified between intestinal epithelial barrier markers and sleep efficiency, while negative correlations were found with wake after sleep onset, total wake time, PSQI, HAMA, and HAMD. Additionally, D-LA levels were significantly positively correlated with ET concentrations. <human>Individuals</human> with <DDF>chronic insomnia disorder</DDF> manifest disruptions in sleep structure, heightened susceptibility to <DDF>anxiety</DDF> and depressive moods, and <DDF>impaired intestinal barrier function</DDF>. These findings suggest that the occurrence and development of insomnia disorder may be linked to the impairment of the intestinal barrier.",
"role": "assistant"
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38664425
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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 microbiome-based interventions on neurodegenerative diseases: a systematic review and meta-analysis. Neurodegenerative diseases (NDDs) are characterized by neuronal damage and progressive loss of neuron function. Microbiome-based interventions, such as dietary interventions, biotics, and fecal microbiome transplant, have been proposed as a novel approach to managing symptoms and modulating disease progression. Emerging clinical trials have investigated the efficacy of interventions modulating the GM in alleviating or reversing disease progression, yet no comprehensive synthesis have been done. A systematic review of the literature was therefore conducted to investigate the efficacy of microbiome-modulating methods. The search yielded 4051 articles, with 15 clinical trials included. The overall risk of bias was moderate in most studies. Most microbiome-modulating interventions changed the GM composition. Despite inconsistent changes in GM composition, the meta-analysis showed that microbiome-modulating interventions improved disease burden (SMD, - 0.57; 95% CI - 0.93 to - 0.21; I<sup>2</sup> = 42%; P = 0.002) with a qualitative trend of improvement in constipation. However, current studies have high methodological heterogeneity and small sample sizes, requiring more well-designed and controlled studies to elucidate the complex linkage between microbiome, microbiome-modulating interventions, and NDDs.",
"role": "user"
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{
"content": "Effects of microbiome-based interventions on <DDF>neurodegenerative diseases</DDF>: a systematic review and <statistical technique>meta-analysis</statistical technique>. <DDF>Neurodegenerative diseases</DDF> (<DDF>NDDs</DDF>) are characterized by <DDF>neuronal damage</DDF> and <DDF>progressive loss of neuron function</DDF>. Microbiome-based interventions, such as dietary interventions, <biomedical technique>biotics</biomedical technique>, and fecal microbiome transplant, have been proposed as a novel approach to managing symptoms and modulating disease progression. Emerging clinical trials have investigated the efficacy of interventions modulating the <microbiome>GM</microbiome> in alleviating or reversing disease progression, yet no comprehensive synthesis have been done. A systematic review of the literature was therefore conducted to investigate the efficacy of microbiome-modulating methods. The search yielded 4051 articles, with 15 clinical trials included. The overall risk of bias was moderate in most studies. Most microbiome-modulating interventions changed the GM composition. Despite inconsistent changes in GM composition, the <statistical technique>meta-analysis</statistical technique> showed that microbiome-modulating interventions improved disease burden (SMD, - 0.57; 95% CI - 0.93 to - 0.21; I<sup>2</sup> = 42%; P = 0.002) with a qualitative trend of improvement in <DDF>constipation</DDF>. However, current studies have high methodological heterogeneity and small sample sizes, requiring more well-designed and controlled studies to elucidate the complex linkage between microbiome, microbiome-modulating interventions, and <DDF>NDDs</DDF>.",
"role": "assistant"
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38679353
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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:\nAssociation between increased and decreased gut microbiota abundance and Parkinson's disease: A systematic review and subgroup meta-analysis. The objective of the study was to systematically investigate the association between gut microbiota (GM) abundance and Parkinson's disease (PD). PubMed, Medline, Cochrane Library and other literature datebase platforms were searched for eligible studies in the English-language from conception to March 1, 2024. Studies evaluating the association between GM and PD were included. The results of the included studies were analyzed using a random effects model with calculation of the mean difference (MD) with the 95 % confidence interval to quantify the incidence of differences in abundance of various bacterial families in PD patients. Continuous models were used to analyze the extracted data. A total of 14 studies with 1045 PD cases and 821 healthy controls were included for data extraction and meta-analysis. All the included studies exhibited reasonable quality. The included studies reported the data on the ratios of 10 families of GM. Of these 10 microbiota families, Bifidobacteriaceae, Ruminococcaceae, Rikenellaceae, Lactobacillaceae, Verrucomicrobiaceae and Christensenellaceae were found to have increased ratios according to the pooled ratios, while Prevotellaceae, Lachnospiraceae, Erysipelotrichaceae and Faecalibacterium were decreased in PD cases. Patients in the PD cohort exhibited distinctive microbiota compositions compared to healthy individuals, with unique differential patterns in gut microbiome abundance at the phylum, family, and genus levels that may be associated wtih PD pathogenesis.",
"role": "user"
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{
"content": "Association between increased and decreased gut microbiota abundance and <DDF>Parkinson's disease</DDF>: A systematic review and <statistical technique>subgroup meta-analysis</statistical technique>. The objective of the study was to systematically investigate the association between <microbiome>gut microbiota</microbiome> (<microbiome>GM</microbiome>) abundance and <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). PubMed, Medline, Cochrane Library and other literature datebase platforms were searched for eligible studies in the English-language from conception to March 1, 2024. Studies evaluating the association between <microbiome>GM</microbiome> and <DDF>PD</DDF> were included. The results of the included studies were analyzed using a <statistical technique>random effects model</statistical technique> with calculation of the <statistical technique>mean difference (MD)</statistical technique> with the 95 % confidence interval to quantify the incidence of differences in abundance of various bacterial families in <human>PD patients</human>. <statistical technique>Continuous models</statistical technique> were used to analyze the extracted data. A total of 14 studies with 1045 <human>PD cases</human> and 821 <human>healthy controls</human> were included for data extraction and meta-analysis. All the included studies exhibited reasonable quality. The included studies reported the data on the ratios of 10 families of <microbiome>GM</microbiome>. Of these 10 microbiota families, <bacteria>Bifidobacteriaceae</bacteria>, <bacteria>Ruminococcaceae</bacteria>, <bacteria>Rikenellaceae</bacteria>, <bacteria>Lactobacillaceae</bacteria>, <bacteria>Verrucomicrobiaceae</bacteria> and <bacteria>Christensenellaceae</bacteria> were found to have increased ratios according to the pooled ratios, while <bacteria>Prevotellaceae</bacteria>, <bacteria>Lachnospiraceae</bacteria>, <bacteria>Erysipelotrichaceae</bacteria> and <bacteria>Faecalibacterium</bacteria> were decreased in PD cases. <human>Patients</human> in the PD cohort exhibited distinctive microbiota compositions compared to <human>healthy individuals</human>, with unique differential patterns in <microbiome>gut microbiome</microbiome> abundance at the phylum, family, and genus levels that may be associated wtih <DDF>PD</DDF> pathogenesis.",
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38686220
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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:\nSafety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial. Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD. The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. Participants (aged 50-65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. Computer-generated randomisation was done in a 1:1 ratio through permutated-block scheduling. Treatment allocation was concealed for participants and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. Intention-to-treat analysis was performed using a mixed model for repeated measures analysis. This completed trial is registered on ClinicalTrials.gov (NCT03808389). Between December 2020 and December 2021, FMT procedures were conducted on 46 patients with PD: 22 in the healthy donor group and 24 in the placebo group. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 participants in the healthy donor group and 22 in the placebo group. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI -11.4 to -0.2) in the healthy donor group and by 2.7 points (-8.3 to 2.9) in the placebo group (p = 0.0235). Adverse events were limited to temporary abdominal discomfort. Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on motor symptoms in patients with early-stage PD. These findings highlight the potential of modulating the gut microbiome as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of patients with PD in various disease stages. Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.",
"role": "user"
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{
"content": "Safety and efficacy of faecal microbiota transplantation in <human>patients</human> with <DDF>mild to moderate Parkinson's disease</DDF> (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial. Dysregulation of the <microbiome>gut microbiome</microbiome> has been implicated in <DDF>Parkinson's disease</DDF> (<DDF>PD</DDF>). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in <human>patients</human> with <DDF>early-stage PD</DDF>. The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. <human>Participants</human> (aged 50-65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. <statistical technique>Computer-generated randomisation</statistical technique> was done in a 1:1 ratio through <statistical technique>permutated-block scheduling</statistical technique>. Treatment allocation was concealed for <human>participants</human> and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. <statistical technique>Intention-to-treat analysis</statistical technique> was performed using a <statistical technique>mixed model for repeated measures analysis</statistical technique>. This completed trial is registered on ClinicalTrials.gov (NCT03808389). Between December 2020 and December 2021, FMT procedures were conducted on 46 <human>patients</human> with <DDF>PD</DDF>: 22 in the <human>healthy donor group</human> and 24 in the <human>placebo group</human>. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 <human>participants</human> in the <human>healthy donor group</human> and 22 in the <human>placebo group</human>. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI -11.4 to -0.2) in the <human>healthy donor group</human> and by 2.7 points (-8.3 to 2.9) in the <human>placebo group</human> (p = 0.0235). Adverse events were limited to temporary <DDF>abdominal discomfort</DDF>. Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on <DDF>motor symptoms</DDF> in <human>patients</human> with <DDF>early-stage PD</DDF>. These findings highlight the potential of modulating the <microbiome>gut microbiome</microbiome> as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of <human>patients</human> with <DDF>PD</DDF> in various disease stages. Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.",
"role": "assistant"
}
] |
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