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 Input:
Infarct heterogeneity has been shown to be independently associated with adverse outcomes in previous smaller studies. However, it is unknown whether infarct characterization is an independent predictor of all-cause mortality in patients with advanced ischemic cardiomyopathy, after adjusting for clinical risk factors, severity of ischemic mitral regurgitation, incomplete revascularization, and device therapy.', 'A total of 362 patients with ischemic cardiomyopathy (left ventricular dysfunction with >70% stenosis in ≥1 epicardial coronary artery) underwent delayed hyperenhancement-magnetic resonance imaging and coronary angiography between 2002 and 2006. Total myocardial scar and peri-infarct (PI) area were measured using various threshold techniques. Multivariate survival analysis (primary end point of all-cause mortality) was conducted. One hundred fifty-seven deaths occurred during a mean 5.4-year follow-up (mean left ventricular ejection fraction, 23±9%; mean end-systolic volume index, 113±48 mL; mean total myocardial scar %, 25.5±16.0%; mean PI%, 5.7±2.9%). PI% (β=2.07; P<0.001) was an independent predictor of survival, independent of age, end-systolic volume, sex, mitral regurgitation, diabetes mellitus, dyslipidemia, coronary artery disease severity, implantable cardioverter defibrillator, and incomplete revascularization. PI% using 2 to 3 SD technique yielded the highest incremental prognostic power (χ(2) score 149).

Ex Output:
0


Ex Input:
We designed and tested an innovative transitional care program, involving cardiac surgery nurse practitioners, to improve care continuity after patient discharge home from coronary artery bypass graft (CABG) operations and decrease the composite end point of 30-day readmission and death.', 'A total of 401 consecutive CABG patients were eligible between May 1, 2010, and August 31, 2011, for analysis. Patient data were entered prospectively into The Society of Thoracic Surgeons database and the New York State Cardiac Surgery Reporting System and retrospectively analyzed with Institutional Review Board approval. The "Follow Your Heart" program enrolled 169 patients, and 232 controls received usual care. Univariate and multivariate analyses were used to identify readmission predictors, and propensity score matching was performed with 13 covariates.', 'Binary logistic regression analysis identified "Follow Your Heart" as the only independently significant variable in preventing the composite outcome (p=0.015). Odds ratios for readmission were 3.11 for dialysis patients, 2.17 for Medicaid recipients, 1.87 for women, 1.86 for non-Caucasians, 1.78 for chronic obstructive pulmonary disease, 1.26 for diabetes, and 1.09 for congestive heart failure. Propensity score matching yielded matches for 156 intervention patients (92%). The intervention showed a significantly lower 30-day readmission/death rate of 3.85% (6 of 156) compared with 11.54% (18 of 156) for the usual care matched group (p=0.023).

Ex Output:
0


Ex Input:
Dexmedetomidine (DEX) has been implicated in modulating the inflammatory response in central nervous system (CNS). However, the mechanism is still poorly understood. In this study, we evaluate the effects of DEX on lipopolysaccharide (LPS)-induced microglia activation and elucidate its possible signaling pathway involved in its anti-inflammatory effects.', 'BV2 and primary microglia were pretreated with various concentrations of DEX (0·01, 0·1, 1, and 10 μM) and/or PD98059 for 1 hour, then microglia were incubated with LPS (1 μg/ml) for 24 hours. Nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression were measured by Griess reagent and real-time polymerase chain reaction. Furthermore, two intracellular signaling cascades including extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) were investigated by western blot analysis.', 'Dexmedetomidine significantly attenuated LPS-induced NO production and iNOS expression in both BV2 cells and primary microglial cells. Lipopolysaccharide activated both ERK1/2 and JNK signal pathways; however, DEX exerted a specific inhibitory effect on ERK1/2 rather than JNK. Intriguingly, treatment of primary microglia and BV2 cells with DEX in combination with ERK1/2 inhibitor (PD98059) enhanced attenuation of LPS-induced NO production and iNOS expression.

Ex Output:

1