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.

Input: Consider Input: Patients with frequent premature ventricular complexes (PVCs) might be at risk for the developing or exacerbation of left ventricular (LV) dysfunction. However, some patients with a high-PVC burden do not develop cardiomyopathy, while other patients with low-PVC burden can develop cardiomyopathy. The purpose of this study was to evaluate the positive predictors of idiopathic PVCs-induced cardiomyopathy.', 'We investigated 214 patients undergoing successful ablation of PVCs who had no other causes of cardiomyopathy. We divided the study cohort into 2 groups: ejection fraction (EF) ≥ 50% (normal LV) and EF < 50% (LV dysfunction). We analyzed the clinical characteristics, including the electrocardiogram and findings at electrophysiology study. Among these patients, 51 (24%) had reduced LVEF and 163 (76%) had normal LV function. Patients with LV dysfunction had significantly longer coupling interval (CI) dispersion (maximum-CI-minimum-CI) and had significantly higher PVC burden compared to those with normal LV function (CI-dispersion: 115 ± 25 milliseconds vs. 94 ± 19 milliseconds; P < 0.001; PVC burden: 19% vs. 15%; P = 0.04). Furthermore, patients with LV dysfunction had significantly higher body mass index (BMI) compared to those with normal LV function (BMI > 30 kg/m(2) ; 37% vs. 13%; P = 0.001). Logistic regression analysis showed that CI-dispersion, PVC burden, and BMI (>30\xa0kg/m(2) ) are independent predictors of PVC-induced cardiomyopathy.

Output: 0


Input: Consider Input: Disseminated intravascular coagulation (DIC) is a complex systemic thrombohemorrhagic disorder involving intravascular coagulation and hemorrhage. The aim of this study is to test whether static magnetic field (SMF) is effective in attenuating lipopolysaccharide (LPS)-induced DIC.', 'In vivo experiments were performed in this study using male BALB/cByJ mice. An intraperitoneal injection of 50 mg/kg LPS was shown to lead to approximately 50% mortality and this dose was used in subsequent experiments. To test the effects of SMF on the survival rate of LPS-induced animals, the mice were exposed to 0.25-T SMF for 2 h before LPS injection. In addition, the effect of a 2-h SMF treatment on the production of anti-inflammatory cytokines was evaluated.', 'In the first set of experiments, we found that the survival rate was higher in the SMF-exposed group than in the sham-exposed group. The circulating platelet (PLT) counts in the SMF-exposed mice were significantly higher than in the unexposed animals. However, no significant changes in inflammatory cytokine, including tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1), in plasma were found after SMF treatment. The results from the second experiment showed that the plasma levels of interleukin-1 receptor antagonist (IL-1ra) were higher in the SMF-exposed group than in the sham group.

Output: 1


Input: Consider Input: Approximately 30% to 40% of all patients with osteosarcomas ultimately experience recurrence. The study investigated the hypothesis that the resistance of osteosarcoma to chemotherapy may be related to the expression of a pregnane xenobiotic receptor (PXR) variant protein and its role as the major inducer of P450 3A4 in these tumors.', 'Polymerase chain reaction (PCR) and Western blot analysis were used to determine PXR mRNA and protein expression, respectively. Real-time PCR and CYP3A catalytic activity using 7-benzyl-trifluoromethyl coumarin (BFC) as the probe substrate were used to measure the induction of P450 3A4 or MDR1. siRNA transfections were performed for PXR and cytotoxicity determined by a colorimetric based assay or Annexin v-Fitc staining.', 'Differences were observed in the molecular size of the PXR protein expressed in sarcoma cell lines when compared with the wildtype PXR expressed in normal liver, kidney, or small intestine. A polyclonal PXR antibody raised against the N-terminus of the wildtype PXR did not detect PXR expressed in these sarcoma cell lines. In the osteosarcoma cell lines, etoposide and doxorubicin were better inducers of P450 3A4 and MDR1 than rifampin. siRNA against PXR down-regulated P450 3A4 expression only in the osteosarcoma cell line. Cytotoxicity assays showed that the resistance of the osteosarcoma cell lines to etoposide correlated with PXR protein expression levels and activation of P450 3A4 and could be prevented by ketoconazole.


Output: 0