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?


[Q]: Our previous in-vivo and in-vitro studies demonstrated that inflammation accelerated the progression of atherosclerosis via the dysregulation of the low-density lipoprotein receptor (LDLr) pathway. The current study aimed to investigate the effects and their underlying mechanisms of inflammation on lipid accumulation in the radial arteries of endstage renal disease (ESRD) patients with arteriovenostomy.', '30 ESRD patients with arteriovenostomy were included. The patients were divided into two groups based on their plasma levels of C-reactive protein: a control (n = 16) and an inflamed group (n = 14). The expression of tumor necrosis factor-alpha (TNF-alpha) and monocyte chemotactic protein-1 of the radial arteries were increased in the inflamed group. Foam cell formation and lipid droplet accumulation were examined by hematoxylin and eosin (H & E) and Oil Red O staining. Intracellular cholesterol trafficking-related proteins were examined by immunohistochemistry and immunofluorescent staining.', 'There was significant lipid accumulation in the radial arteries of the inflamed group compared with the control. Further analysis demonstrated that this accumulation was correlated with the increased protein expression of LDLr, sterol regulatory element-binding protein-2 (SREBP-2), and SREBP cleavageactivating protein (SCAP). Confocal microscopy showed that inflammation enhanced the translocation of SCAP escorting SREBP-2 from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Interestingly, upregulated LDLr expression was positively associated with the increased protein expression of mammalian target of rapamycin (mTOR), which had enhanced coexpression with SREBP-2. This finding suggests that the activation of mTOR may be involved in LDLr pathway disruption through the upregulation of SREBP-2 expression.
[A]: Does activation of mTOR contribute to foam cell formation in the radial arteries of patients with end-stage renal disease?


[Q]: The aim of the present study was to evaluate baseline regional cerebral oxygen saturation (rSO2) values and identify factors influencing preoperative rSO2 in elective minor surgery.', 'Observational analysis post-hoc.', 'Observational post-hoc analysis of data for the patient sample (n=50) of a previously conducted clinical trial in patients undergoing tumourectomy for breast cancer or inguinal hernia repair. Exclusion criteria included pre-existing cerebrovascular diseases, anaemia, baseline pulse oximetry <97% and low quality rSO2 sensor signals. Demographic data, comorbidities, and ASA physical status as well as height and weight were collected prospectively from all patients. Baseline rSO2 values were recorded while the patient breathed room air, using the INVOS 5100C monitor™ (Covidien, Dublin, Ireland).', 'Thirty-seven women (72%) and 13 men (28%) 48 ± 13 years of age were enrolled in this study. Baseline rSO2 was 62.01 ± 10.38%. Baseline rSO2 was significantly different between men (67.6 ± 11.2%) and women (60 ± 9.4%), (P=0.023). There were also differences between baseline rSO2 and ASA physical status (ASA I: 67.6 ± 10.7%, ASA II: 61.6 ± 8.4%, ASA III: 55.8 ± 13.9%, P=0.045). Baseline rSO2 had a positive correlation with body weight (r=0.347, P=0.014) and height (r=0.345, P=0.014). We also found significant differences in baseline rSO2 among patients with and without chronic renal failure (P=0.005). No differences were found in any other studied variables.
[A]:
Do baseline cerebral oximetry values depend on non-modifiable patient characteristics?