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]: To analyze whether peroxisome proliferator-activated receptor gamma (PPARγ2) rs1801282 (Pro12Ala) polymorphism is associated with the response to pegylated-interferon-alpha plus ribavirin treatment in HIV/hepatitis C virus (HCV)-coinfected patients, and whether it is able to predict the outcome of HCV treatment.', 'Retrospective follow-up study.', 'Two hundred eighty-five naive patients, who started HCV-treatment, were genotyped for PPARγ2 and interleukin 28B polymorphisms. Genetic data were analyzed under dominant inheritance model. Sustained virological response (SVR) was defined as undetectable HCV viremia through 24 weeks after the end of HCV treatment.', 'The variables significantly associated with SVR in a multivariate analysis were HCV-genotype (GT) 3 {adjusted odds ratio [aOR] = 7.66 [95% of confidence interval (95% CI): 3.96 to 14.81] P < 0.001}, HCV-viremia <500,000 IU/mL [aOR = 2.20 (95% CI: 1.16 to 4.15] P = 0.015), no/mild liver fibrosis (F < 2) [aOR = 1.92 (95% CI: 1.08 to 3.42) P = 0.026], IL28B rs12980275 AA genotype [aOR = 2.70 (95% CI: 1.54 to 4.71) P < 0.001], and PPARγ2 rs1801282 CG/GG genotype [aOR = 2.93 (95% CI: 1.27 to 6.72) P = 0.011]. When PPARγ2 rs1801282 genotype was included in a decision tree analysis, HCV-GT3 patients with CG/GG genotype had increased SVR from 80.3% to 100%. In GT1/4 patients, rs12980275 AA carriers had increased SVR from 58.7% to 78.6%, and rs12980275 AG/GG carriers had increased SVR from 28.7% to 35.7%. The overall percentage of patients correctly classified was 71.6% and the area under the receiver operating characteristic curves was 0.766 ± 0.028.
[EX A]: 1

[EX Q]: With advances in medicine, the subjective assessment of patients on hemodialysis regarding their quality of life (QOL) is gaining importance. Clinicians cannot rely solely on objective markers, such as the rates of complications and mortality, when evaluating responses to dialysis. In clinical settings, laboratory values are used as measures of patients' health. However, the relationship between clinical laboratory values and QOL has not been elucidated yet. Therefore, the present study aimed to define the relationship of laboratory values and patient attributes to the QOL of outpatients on hemodialysis in order to obtain basic data for reevaluating nursing support for patients on hemodialysis in the future.", 'The participants were 44 outpatients receiving hemodialysis at Hospital B. The QOL was surveyed using a self-administered questionnaire, the Kidney Disease Quality of Life Short Form. The following patient attributes and laboratory values were taken from the medical records: age; sex; primary disease; number of years on hemodialysis; complications; number of hours of hemodialysis per session; percentage weight gain; cardiothoracic ratio; blood pressure; hematocrit; and the serum levels of albumin, potassium, phosphorus, and calcium.', 'The serum potassium level significantly affected mental health, social functioning, symptoms, and the effect of kidney disease, with the 3.5-5.0 mEq/L target range group scoring higher than the > or =5.1 mEq/L group.
[EX A]: 1

[EX Q]: Viral fulminant hepatitis (FH) remains a serious clinical problem with very high mortality. Lacking understanding of FH pathogenesis has in essence hindered efficient clinical treatment. Inferring from a correlation observed between the genetic differences in the complement component 5 (C5) and the susceptibility of mouse strains to murine hepatitis virus strain-3 (MHV-3) infections, we propose that excessive complement activation plays a critical role in the development of FH. We show that MHV-3 infection causes massive complement activation, along with a rapid increase in serum C5a levels and quick development of FH in susceptible strains. Mice deficient in the C5a receptor (C5aR) or the susceptible strains treated with C5aR antagonists (C5aRa) exhibit significant attenuation of the disease, accompanied by a remarkable reduction of hepatic fibrinogen-like protein 2 (Fgl2), a hallmark protein that causes necrosis of infected livers. In accordance, biopsy of FH patients shows a dramatic increase of Fgl2 expression, which correlates with C5aR up-regulation in the liver. In vitro C5a administration accelerates MHV-3-induced Fgl2 secretion by macrophages. Furthermore, inhibiting ERK1/2 and p38 efficiently blocks C5a-mediated Fgl2 production during viral infections.
[EX A]:
0