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.

[Q]: To determine the association of ethanol intoxication with hypoglycemia in ED patients.', 'Retrospective, laboratory log review of 953 consecutive patients who were evaluated for ethanol intoxication in an urban university hospital ED over a three-month period. Simultaneous serum glucose determination was carried out for each patient and associations between ethanol level and glucose were sought.', 'Glucose concentrations were unavailable for 16 patients (1.7%). Of the remaining patients, 584 patients had detectable ethanol concentrations (ethanol-positive), and 353 had no detectable ethanol (ethanol-negative). Ethanol concentrations (mean +/- SD) in the ethanol-positive group were 50.11 +/- 24.08 mmol/L (231 +/- 111 mg/dL), and glucose concentrations were 5.83 +/- 1.94 mmol/L (105 +/- 35 mg/dL). Hypoglycemia [glucose < 3.72 mmol/L (67 mg/dL)] was observed for five (0.9%) ethanol-positive patients. It was classified as mild-moderate [2.78-3.66 mmol/L (50-66 mg/dL)] for four patients (0.7%) and severe [< 2.78 mmol/L (50 mg/dL)] for one (0.2%). Ethanol concentrations ranged from 25.60 to 68.33 mmol/L (118 to 315 mg/dL). There was no correlation between ethanol and glucose concentrations in any subset of the ethanol-positive patients population. In the ethanol-positive group, patients who had several ethanol-positive visits (56 patients, mean 3.6 visits/patient) accounted for four of the five episodes of hypoglycemia, including the one episode of severe hypoglycemia. The frequency of hypoglycemia in repeat visitors (2.0%) was higher than that in the group of patients without repeat visits (0.2%). In the ethanol-negative group, there were four (1.1%) episodes of mild-moderate hypoglycemia and no severely hypoglycemic patients. Hypoglycemia was not more likely to occur among ethanol-positive patients than it was among ethanol-negative patients.
[A]: 1


[Q]: The aim of this study was to assess the relationship between cardiomyopathy and recipient twin (RT) outcome in twin-twin transfusion syndrome (TTTS).', 'Fetal echocardiography and outcomes data in 62 consecutive pregnancies with TTTS were reviewed. The primary outcome was neonatal RT survival. The severity of RT cardiomyopathy at presentation was assessed by the cardiovascular profile score (CVPS). RT outcomes and odds of survival were compared between groups stratified by CVPS.', 'Overall neonatal survival for all fetuses was 61% (76 of 124). RT survival was 58% (36 of 62). Grouped by CVPS, RT survival was greater (50%) for those with CVPS > or = 9 and even higher (74%) for CVPS of 10. Among the components of the CVPS, atrioventricular valve regurgitation was associated with negative RT outcome. Other factors at presentation were not predictive of RT outcome.
[A]: 0


[Q]: Insulin resistance is a central feature of type 2 diabetes. Salicylates prevent lipid-induced insulin resistance in rodents by interrupting inflammatory pathways. We therefore investigated whether salicylates reduce lipid-induced insulin resistance in humans by affecting inflammatory pathways as reflected by serum adipocytokines.', 'Ten healthy men were included in a crossover intervention study. Four euglycemic-hyperinsulinemic clamps were performed, one without pretreatment, one with prior 2-h lipid infusion, one after pretreatment with 4 g acetylsalicylic acid (ASA), and one with ASA pretreatment and prior lipid infusion.', 'Lipid-induced insulin resistance was quantified by the euglycemic-hyperinsulinemic clamp technique running at least 2 h. Repeated-measures ANOVA on two factors was used for comparison, and results were Bonferroni adjusted for multiple measurements. ASA effects on serum adipocytokines were addressed by comparing the areas under the curves.', "Glucose infusion rate (M value) of the control clamp without pretreatment was 6.3 (+/- 0.6) mg/kg.min. ASA pretreatment did not change glucose infusion rates (P = 0.6). Lipid infusion significantly decreased the M value to 4.1 (+/- 0.6) mg/kg.min (P = 0.008). After ASA pretreatment and lipid infusion, the M value was 4.8 (+/- 0.7) mg/kg.min and was significantly improved, compared with the lipid-only clamp (P = 0.036 after Bonferroni's adjustment). General biomarkers of inflammatory processes (IL-6, C-reactive protein), the insulin-sensitizing mediator adiponectin, and circulating adiponectin oligomers were unchanged by ASA pretreatment.
[A]:
1