Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Input: Consider Input: Context: For many decades, the debate on children's competence to give informed consent in medical settings concentrated on ethical and legal aspects, with little empirical underpinnings. Recently, data from empirical research became available to advance the discussion. It was shown that children's competence to consent to clinical research could be accurately assessed by the modified MacArthur Competence Assessment Tool for Clinical Research. Age limits for children to be deemed competent to decide on research participation have been studied: generally children of 11.2 years and above were decision-making competent, while children of 9.6 years and younger were not. Age was pointed out to be the key determining factor in children's competence. In this article we reflect on policy implications of these findings, considering legal, ethical, developmental and clinical perspectives.
Answer: Although assessment of children's competence has a normative character, ethics, law and clinical practice can benefit from research data. The findings may help to do justice to the capacities children possess and challenges they may face when deciding about treatment and research options. We discuss advantages and drawbacks of standardized competence assessment in children on a case-by-case basis compared to application of a fixed age limit, and conclude that a selective implementation of case-by-case competence assessment in specific populations is preferable. We recommend the implementation of age limits based on empirical evidence. Furthermore, we elaborate on a suitable model for informed consent involving children and parents that would do justice to developmental aspects of children and the specific characteristics of the parent-child dyad. Previous research outcomes showed that children's medical decision-making capacities could be operationalized into a standardized assessment instrument. Recommendations for policies include a dual consent procedure, including both child as well as parents, for children from the age of 12 until they reach majority. For children between 10 and 12 years of age, and in case of children older than 12 years in special research populations of mentally compromised patients, we suggest a case-by-case assessment of children's competence to consent. Since such a dual consent procedure is fundamentally different from a procedure of parental permission and child assent, and would imply a considerable shift regarding some current legislations, practical implications are elaborated.

Output: Is informed consent instead of assent appropriate in children from the age of twelve : Policy implications of new findings on children 's competence to consent to clinical research?


Input: Consider Input: Context: Diabetic cardiomyopathy (DCM) is associated with suppressed autophagy and augmented apoptosis in the heart although the interplay between the two remains elusive. The ability of mammalian sterile 20-like kinase 1 to regulate both autophagy and apoptosis prompted us to investigate it as a possible candidate in the progression of DCM.', 'Wild-type, Mst1 (also known as Stk4) transgenic and Mst1-knockout mice were challenged with streptozotocin to induce experimental diabetes. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated diabetes to probe mechanisms.', 'Mst1 knockout alleviated while Mst1 overexpression aggravated cardiac dysfunction in diabetes. Diabetic Mst1 transgenic mice exhibited decreased LC3 expression and enhanced protein aggregation. In contrast, typical autophagosomes were observed in diabetic Mst1-knockout mice with increased LC3 expression and reduced protein aggregation. Mst1 downregulation promoted autophagic flux as demonstrated by increased LC3-II and decreased p62 expression in the presence of bafilomycin A1. Furthermore, Mst1 overexpression increased, while Mst1 knockout decreased, cardiomyocyte apoptosis both in vivo and in vitro. Co-immunoprecipitation assays showed that Mst1 overexpression promoted Beclin1 binding to B cell lymphoma 2 (Bcl-2) and induced dissociation of Bcl-2 from Bax in diabetic mice. Conversely, Mst1 knockout disrupted the Beclin1-Bcl-2 complex and enhanced the interaction between Bcl-2 and Bax.
Answer: Mst1 knockout restores autophagy and protects against apoptosis in cardiomyocytes, en route to the rescue against DCM.

Output: Does mST1 coordinately regulate autophagy and apoptosis in diabetic cardiomyopathy in mice?


Input: Consider Input: Context: Exposure to hypoxia has been suggested to acutely alter glucose regulation. However, the effects of successive exposure to moderate hypoxia on postprandial glucose regulation and substrate oxidation pattern after multiple meals have not been elucidated.', 'We examined the effects of successive exposure to moderate hypoxia on metabolic responses and substrate oxidation pattern.', 'Eight healthy men (21.0\u2009±\u20090.6\xa0yrs, 173\u2009±\u20092.3\xa0cm, 70.6\u2009±\u20095.0\xa0kg, 23.4\u2009±\u20091.1\xa0kg/m(2)) completed two experimental trials on separate days: a rest trial under normoxic conditions (FiO2\u2009=\u200920.9%) and a rest trial under hypoxic conditions (FiO2\u2009=\u200915.0%). Experimental trials were performed over 7\xa0h in an environmental chamber. Blood and respiratory gas samples were collected over 7\xa0h. Standard meals were provided 1\xa0h (745\xa0kcal) and 4\xa0h (731\xa0kcal) after entering the chamber.', 'Although each meal significantly increased blood glucose and serum insulin concentrations (P\u2009<\u20090.05), these responses did not differ significantly between the trials. There were no significant differences in areas under the curves for glucose or insulin concentrations over 7\xa0h between the trials. No significant differences were observed in blood lactate, serum cortisol, free fatty acid, or glycerol concentrations over 7\xa0h between the trials. The oxygen consumption ( [Formula: see text]) and carbon dioxide production ( [Formula: see text]) 3\xa0h after entering the chamber were significantly higher in the hypoxic trial than in the normoxic trial (P\u2009<\u20090.05). However, the differences did not affect respiratory exchange ratio (RER). The average values of [Formula: see text], [Formula: see text], and RER did not differ between the trials.
Answer: Seven hours of moderate hypoxia did not alter postprandial glucose responses or substrate oxidation in young healthy men.


Output: Does successive exposure to moderate hypoxia affect glucose metabolism and substrate oxidation in young healthy men?


