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.

Ex Input:
One variant of multiple endocrine neoplasia type 1 (MEN1) is defined by sporadic tumors of both the parathyroids and pituitary. The prevalence of identified MEN1 mutations in this variant is lower than in familial MEN1 (7% vs. 90%), suggesting different causes. Recently, one case of this variant had a germline mutation of p27(Kip1)/CDKN1B.', 'The objective was to test p27 in germline DNA from cases with tumors of both the parathyroids and pituitary.', 'Medical record review and sequence analysis in DNA were performed.', 'This study involved an inpatient and outpatient referral program for cases of endocrine tumors.', 'Sixteen index cases had sporadic tumors of two organs, both the parathyroids and the pituitary. There were 18 additional index cases with related features of familial tumors. Five subjects were normal controls. No case had an identified MEN1 mutation.', 'Clinical status of endocrine tumors was tabulated. Sequencing of germline DNA from index cases and control cases for the p27 gene was performed by PCR.', 'Endocrine tumor types and their expressions were measured, as were sequence changes in the p27 gene.', 'Tumor features were documented in index cases and families. One p27 germline single nucleotide change was identified. This predicted a silent substitution of Thr142Thr. Furthermore, there was a normal prevalence of heterozygosity for a common p27 polymorphism, making a large p27 deletion unlikely in all or most of these cases.

Ex Output:
Does the parathyroid/pituitary variant of multiple endocrine neoplasia type 1 usually have causes other than p27Kip1 mutations?

Ex 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.

Ex Output:
Is de novo glutamine synthesis induced by corticosteroids in vivo in rats secondary to weight loss?

Ex Input:
Repeat positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) and chest computed tomography (CT) are used to assess the effectiveness of chemoradiotherapy in patients with non-small cell lung cancer (NSCLC); however, the change in the standardized uptake values (SUV) has not been correlated with the pathologic change of the primary tumor.', 'This is a retrospective cohort study of a prospective database of 56 patients who had NSCLC, FDG-PET, and chest CT scans both before and after neoadjuvant therapy, followed by complete resection of their cancer. Maximum SUVs (maxSUV) and tumor size were measured, and the percentage of change was compared with the percentage of nonviable tumor cells. The primary objective was to measure the degree of correlation between these values.', "The change in the maxSUV has a near linear relationship to the percent of nonviable tumor cells in the resected tumors. FDG-PET's maxSUV is better correlated to pathology than the change in size on CT scan (r2 = 0.75, r2 = 0.03, p < 0.001). When the maxSUV decreased by 80% or more, a complete pathologic response could be predicted with a sensitivity of 90%, specificity of 100%, and accuracy of 96%.

Ex Output:
Is repeat FDG-PET after neoadjuvant therapy a predictor of pathologic response in patients with non-small cell lung cancer?