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.

Example Input: Corticosteroid treatment affects muscle protein and glutamine metabolism. In the present study we aimed to clarify to what extent anorexia, weight loss and corticosteroids determine protein and glutamine metabolism in muscle.', 'The study was performed in Wistar rats (300-350 g, n = 40) given triamcinolone (0.25 mg/kg/day i.m.) treatment (CS group) for 14 days, sham treated free fed (FF group), sham treated pair fed (PF group) and sham treated pair weight (PW group). In vivo protein and glutamine turnover were measured using L-[2,6-3H]phenylalanine and L-[3,4-3H]glurtamine as tracer in a three compartment model across the hindquarter.', 'Corticosteroid treatment decreased total body weight to a greater extent than can be explained by decreased food intake only, justifying the need for pair weight controls. Muscle weight loss was relatively greater in the corticosteroid treated rats than in the pair weight controls indicating specific corticosteroid induced changes in muscle protein metabolism. Pair weight rats increased muscle net protein breakdown rates from -5 +/- 3 nmol x 100 g body weight(-1) x min(-1) to -15 +/- 3 nmol x 100 g body weight(-1) x min(-1) (P < 0.05 vs FF). In the corticosteroid treated rats net protein breakdown rates increased to -22 +/- 4 nmol x 100 g body weight(-1) x min(-1) (P < 0.01 CS vs FF/PF) Net protein breakdown in corticosteroid treated rats was accompanied by increased glutamine efflux from the hindquarter (P < 0.05, CS vs FF/PF/PW). The latter could predominantly be explained by de novo synthesis. Furthermore, corticosteroid treatment induced a loss of plasma to free muscle glutamine gradient indicating down regulation of glutamine membrane transport rates into muscle. This effect was, however, similar in the pair weight control group and can thus be fully accounted for by the muscle weight loss.
Example Output: Is de novo glutamine synthesis induced by corticosteroids in vivo in rats secondary to weight loss?

Example Input: The local anesthetic properties of tetrodotoxin, a potent naturally occurring sodium channel blocker, have been recently reexamined. It was found that sciatic nerve block duration could be greatly increased and systemic toxicity greatly decreased if epinephrine was injected with tetrodotoxin. The mechanism that underlies epinephrine-mediated prolongation of tetrodotoxin nerve blocks is not known, but indirect evidence suggests that epinephrine may slow the clearance of tetrodotoxin from the site of injection. The authors hypothesized that tetrodotoxin causes vasodilatation at its injection site, which accelerates its systemic uptake, and that this vasodilatation is attenuated by coinjected epinephrine.', 'The radiolabeled microsphere technique was used to measure tissue blood flow in anesthetized rats before and after perisciatic injection of tetrodotoxin alone and in combination with epinephrine.', 'Tetrodotoxin, in a dose of 0.1 ml of a 60 microM solution, significantly increased blood flow in perisciatic muscle at the injected side compared with simultaneous contralateral control and ipsilateral preinjection baseline. Tetrodotoxin did not increase blood flow in the sciatic nerve. Coinjection of epinephrine with tetrodotoxin prevented tetrodotoxin-induced increases in perisciatic muscle blood flow over time and did not alter sciatic nerve blood flow. Arterial blood pressure was maintained with this dose of tetrodotoxin, although brain blood flow decreased. Coinjection of epinephrine with tetrodotoxin prevented decreases in brain blood flow. Higher doses of tetrodotoxin produced hypotension.
Example Output: Does epinephrine prevent muscle blood flow increases after perineural injection of tetrodotoxin?

Example Input: Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by severe joint erosion and systemic osteoporosis. Chronic T cell activation is a hallmark of RA, and agents that target the CD28 receptor on T cells, which is required for T cell activation, are being increasingly used as therapies for RA and other inflammatory diseases. Lymphocytes play complex roles in the regulation of the skeleton, and although activated T cells and B cells secrete cytokines that promote skeletal decline, under physiologic conditions lymphocytes also have key protective roles in the stabilization of skeletal mass. Consequently, disruption of T cell costimulation may have unforeseen consequences for physiologic bone turnover. This study was undertaken to investigate the impact of pharmacologic CD28 T cell costimulation blockade on physiologic bone turnover and structure.', 'C57BL6 mice were treated with CTLA-4Ig, a pharmacologic CD28 antagonist or with irrelevant control antibody (Ig), and serum biochemical markers of bone turnover were quantified by enzyme-linked immunosorbent assay. Bone mineral density and indices of bone structure were further measured by dual x-ray absorptiometry and micro-computed tomography, respectively, and static and dynamic indices of bone formation were quantified using bone histomorphometry.', 'Pharmacologic disruption of CD28 T cell costimulation in mice significantly increased bone mass and enhanced indices of bone structure, a consequence of enhanced bone formation, concurrent with enhanced secretion of the bone anabolic factor Wnt-10b by T cells.
Example Output:
Does cTLA-4Ig-induced T cell anergy promote Wnt-10b production and bone formation in a mouse model?