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.

Input: Consider Input: Bone and antler collagen δ(13) C and δ(15) N values are often assumed to be equivalent when measured in palaeodietary, palaeoclimate and palaeocological studies. Although compositionally similar, bone grows slowly and is remodelled whereas antler growth is rapid and remodelling does not occur. These different patterns of growth could result in isotopic difference within antler and between the two tissue types. Here we test whether red deer (Cervus elaphus) bone and antler δ(13) C and δ(15) N values are equivalent, and whether intra-antler isotopic values are uniform.', 'Bone and antler were isotopically analysed from six stags that lived in a temperate maritime climate on the Isle of Rum, Scotland. Multiple antlers from different years were sampled per individual, together with a single bone sample per individual. Up to 12 samples were taken along the length of each antler (total of 25 antlers, 259 samples) so that a chronological record of the isotopic composition during antler growth could be obtained. Collagen was extracted and its δ(13) C and δ(15) N values were measured by continuous-flow isotope ratio mass spectrometry.', 'Intra-antler collagen isotope signatures vary, and show that not all antlers from an individual or a growth year are equivalent in carbon and nitrogen isotopic ratios. δ(15) N values typically increase with distance along antler length, but no overall trend is observed in δ(13) C values. An isotopic offset is visible between bone and antler, with bone δ(13) C and δ(15) N values being higher in most cases.

Output: Are red deer bone and antler collagen isotopically equivalent in carbon and nitrogen?


Input: Consider Input: Visfatin is an insulin-mimicking adipokine. Visfatin is elevated in obesity and type 2 diabetes. However, its role in glucose and lipid metabolism in healthy humans is unclear.', 'The objective was to investigate the correlations of visfatin with phenotypes of glucose, lipids, and body composition and the responses of visfatin to short-term overfeeding in healthy young men.', 'Sixty-one healthy young men were recruited from the Newfoundland population. Serum visfatin, interleukin 6, glucose, insulin, total cholesterol, HDL cholesterol, LDL cholesterol, and triacylglycerol concentrations were measured with an autoanalyzer, and percentage body fat (%BF) and percentage trunk fat (%TF) were measured with dual-energy X-ray absorptiometry. Insulin resistance and beta cell function were assessed with the homeostasis model. All measurements were completed at baseline and after a 7-d overfeeding protocol exceeding the baseline requirement by 70%. Subjects were classified on the basis of %BF as lean (<21%), overweight (21-25.9%), or obese (>or=26%).', 'Multiple regression analysis showed that triacylglycerols correlated with fasting serum visfatin (P < 0.001). Moreover, serum visfatin decreased 19% overall-23% in lean, 9% in overweight, and 18% in obese subjects (P < 0.0001)-after the overfeeding protocol. None of the variables measured, including interleukin 6, were associated with the reduction in visfatin. In contrast with the findings in mice, visfatin concentrations before and after overfeeding did not correlate with glucose, insulin, insulin resistance, beta cell function, %BF, or %TF.

Output: Are serum visfatin concentrations positively correlated with serum triacylglycerols and down-regulated by overfeeding in healthy young men?


Input: Consider Input: Volatile anesthetic postconditioning has been documented to provide neuroprotection in adult animals. Our aim was to investigate whether sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage (HIBD) rats, and whether the PI3K/Akt pathway and mitochondrial permeability transition pore (mPTP) opening participate in the effect.', 'Seven-day-old Sprague-Dawley rats were subjected to brain HI and randomly allocated to 10 groups (n=24 each group) and treated as follows: (1) Sham, without hypoxia-ischemia; (2) HI/Control, received cerebral hypoxia-ischemia; (3) HI+Atractyloside (Atr), (4) HI+Cyclosporin A (CsA), (5) HI+sevoflurane (Sev), (6) HI+Sev+ LY294002 (LY), (7) HI+Sev+ L-NAME (L-N), (8) HI+Sev+ SB216763 (SB), (9) HI+Sev+Atr, and (10) HI+Sev+CsA. Twelve rats in each group underwent behavioral testing and their brains were harvested for hippocampus neuron count and morphology study. Brains of the other 12 animals were harvested 24h after intervention to examine the expression of Akt, p-Akt, eNOS, p-eNOS, GSK-3β, p-GSK-3β by Western bolting and mPTP opening.', 'Sevoflurane postconditioning significantly improved the long-term cognitive performance of the rats, increased the number of surviving neurons in CA1 and CA3 hippocampal regions, and protected the histomorphology of the left hippocampus. These effects were abolished by inhibitors of PI3K/eNOS/GSK-3β. Although blocking mPTP opening simulated sevoflurane postconditioning-induced neuroprotection, it failed to enhance it.


Output: Does sevoflurane postconditioning improve long-term learning and memory of neonatal hypoxia-ischemia brain damage rats via the PI3K/Akt-mPTP pathway?