Given a passage, 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.

Q: Previous results have shown that mice lacking in the group 1B phospholipase A(2) (Pla2g1b) are resistant to obesity and diabetes induced by feeding a diabetogenic high-fat/high-carbohydrate diet. This study examined the potential of using the Pla2g1b inhibitor methyl indoxam as therapy to suppress diet-induced obesity and diabetes.', 'Male C57BL/6 mice were fed the diabetogenic diet with or without methyl indoxam supplementation. Body weight gain, fasting plasma glucose levels, glucose tolerance and postprandial lysophospholipid absorption were compared.', 'Wild-type C57BL/6 mice fed the diabetogenic diet without Pla2g1b inhibitor showed 31 and 69% body weight gain after 4 and 10 weeks respectively. These animals also showed elevated plasma glucose levels and were glucose intolerant. In contrast, C57BL/6 mice fed the diabetogenic diet with 90 mg.kg(-1) of methyl indoxam gained only 5% body weight after 10 weeks. These animals were also euglycaemic and displayed normal glucose excursion rates in glucose tolerance test. Methyl indoxam suppression of diet-induced body weight gain and glucose intolerance was correlated with the inhibition of Pla2g1b-mediated postprandial lysophospholipid absorption.

A: Does the phospholipase A ( 2 ) inhibitor methyl indoxam suppress diet-induced obesity and glucose intolerance in mice?
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Q: There is insufficient knowledge of infectious risk in patients after splenectomy; minimal data exists specifically for trauma patients. This study evaluated patient knowledge and practices regarding infection risk after traumatic splenectomy. Our hypothesis was that patients with poor knowledge regarding their asplenic state would be less likely to pursue medical care in the event of an illness than those with good knowledge.', 'Non-randomized, cohort study of all posttraumatic splenectomy patients < or =11 years after injury in 2 rural trauma centers. Patients received a validated questionnaire; weighted responses determined knowledge about infection risks and appropriate follow-up actions.', 'Fifty-four percent of patients responded to the questionnaire. Overall, 47% of responders were identified as having adequate knowledge regarding infectious risk, and only 28% would pursue appropriate medical care. Of patients with adequate knowledge, 42% were more likely to pursue appropriate care versus 15% of patients with inadequate knowledge (p = 0.06). Patients with adequate knowledge were more likely to receive an annual influenza vaccine (p = 0.03) and contact their provider with fewer symptoms (p = 0.03). Logistic regression revealed significant interactions between knowledge and presence of comorbidities (p = 0.04). Focusing on patients with poor knowledge and absence of comorbidities, none would engage in appropriate action in the event of illness (p < 0.01). A longer time since injury, >3 years, was associated with a diminished likelihood of appropriate action (p = 0.03). The relationship between knowledge and action was not accounted for by other potential confounders.

A: Do time lapse and comorbidities influence patient knowledge and pursuit of medical care after traumatic splenectomy?
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Q: Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.', 'We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.

A:
Is altered gene expression in early atherosclerosis blocked by low level apolipoprotein E?
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