Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

[EX Q]: Single nucleotide polymorphisms (SNPs) in approximately 40 genes have been associated with an increased risk for type 2 diabetes (T2D) in genome-wide association studies. It is not known whether a similar genetic impact on the risk of prediabetes (impaired glucose tolerance [IGT] or impaired fasting glycemia [IFG]) exists.', 'In our cohort of 1442 non-diabetic subjects of European origin (normal glucose tolerance [NGT] n\u200a=\u200a1046, isolated IFG n\u200a=\u200a142, isolated IGT n\u200a=\u200a140, IFG+IGT n\u200a=\u200a114), an impact on glucose homeostasis has been shown for 9 SNPs in previous studies in this specific cohort. We analyzed these SNPs (within or in the vicinity of the genes TCF7L2, KCNJ11, HHEX, SLC30A8, WFS1, KCNQ1, MTNR1B, FTO, PPARG) for association with prediabetes.', 'The genetic risk load was significantly associated with the risk for IGT (p\u200a=\u200a0.0006) in a model including gender, age, BMI and insulin sensitivity. To further evaluate potential confounding effects, we stratified the population on gender, BMI and insulin sensitivity. The association of the risk score with IGT was present in female participants (p\u200a=\u200a0.008), but not in male participants. The risk score was significantly associated with IGT (p\u200a=\u200a0.008) in subjects with a body mass index higher than 30 kg/m(2) but not in non-obese individuals. Furthermore, only in insulin resistant subjects a significant association between the genetic load and the risk for IGT (p\u200a=\u200a0.01) was found.
[EX A]: 0

[EX Q]: Studies on the safety of aprotinin in coronary artery surgery have given conflicting results. Therefore, we studied the possible link between perioperative aprotinin treatment and renal dysfunction in patients undergoing first-time coronary surgery with a high risk of bleeding.', 'We performed a matched cohort study, comparing 200 patients receiving high-dose aprotinin with 200 patients receiving tranexamic acid during primary isolated coronary surgery. Patients were matched according to age, sex, and presence of acute coronary syndrome. Primary outcome was fractional change in creatinine clearance. Secondary outcomes were other evaluations of postoperative renal function, mortality, stroke, reoperation for bleeding, and transfusion requirements.', 'The groups were similar in baseline characteristics except that triple-vessel disease and history of myocardial infarction were more prevalent in the aprotinin group. No significant differences were found in fractional change in creatinine clearance (-11% versus -12%, medians, p = 0.75) or any other assessments of postoperative renal function between the tranexamic acid and the aprotinin group. Adverse event rates were similar: early mortality (3.5% versus 4.5%, p = 0.80), stroke (1.5% versus 2%, p = 1.0), reoperation for bleeding (3.5% versus 2.5%, p = 0.77), and 5-year survival (87% versus 84%, p = 0.17). Patients in the aprotinin group received fewer transfusions (48% versus 60.5%, p = 0.02), fewer units of packed red blood cells (2.0 versus 1.4, p = 0.02) and plasma (1.3 versus 0.5, p < 0.001), but more units of platelets (0.1 versus 0.2, p = 0.02).
[EX A]: 0

[EX Q]: A growing body of evidence supports the notion that MicroRNAs (miRNAs) function as key regulators of tumorigenesis. In the present study, the expression and roles of miRNA-361-5p were explored in hepatocellular carcinoma (HCC).', 'Quantitative real-time PCR was used to detect the expression miR-361-5p in HCC tissues and pair-matched adjacent normal tissues. MTT and BrdU assays were used to identify the role of miR-361-5p in the regulation of proliferation and invasion of HCC cells. Using bioinformatics analysis, luciferase reporter assays and Western blots were used to identify the molecular target of miR-361-5p. nude mice were used to detect the anti-tumor role of miR-361-5p in vivo.', 'miR-361-5p was down-regulated in HCC tissues in comparison to adjacent normal tissues, due to hypermethylation at its promoter region. Overexpression of miR-361-5p suppressed proliferation and invasion of HCC cells. Chemokine (C-X-C Motif) receptor 6 (CXCR6) was identified as a target of miR-361-5p. Indeed, knockdown of CXCR6 photocopied, while overexpression of CXCR6 largely attenuated the anti-proliferative effect of miR-361-5p. More importantly, in vivo studies demonstrated that forced expression of miR-361-5p significantly inhibited tumor growth in the nude mice.
[EX A]:
1