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:
Most patients are admitted to the hospital through the emergency department (ED), and ED waiting times partly reflect the availability of inpatient beds. We test whether the balance between daily hospital admissions and discharges affects next-day ED length of stay.', 'We conducted a cross-sectional study of hospitals in metropolitan Toronto, served by a single emergency medical services provider in a publicly funded system. During a 3-year period, we evaluated the daily ratio of admissions to discharges at each hospital and the next-day median ED length of stay in the same hospital by using linear regression.', 'Across hospitals, the daily mean (SD) 50th percentile ED length of stay averaged 218 (51) minutes. As the inpatient admission-discharge ratio increased or decreased, next-day ED length of stay changed accordingly. Compared with ratios of 1.0, those less than 0.6 were associated with an 11-minute (95% confidence interval [CI] 5 to 16 minutes) shorter next-day median ED length of stay; at admission-discharge ratios of 1.3 to 1.4, ED length of stay was significantly prolonged by 5 minutes (95% CI 3 to 6 minutes). Admission-discharge ratios on weekends and among medical inpatients had a stronger influence on next-day ED length of stay; effects were also greater among higher-acuity and admitted ED patients.

Ex Output:
1


Ex Input:
Sinonasal epithelial cells are recognized as drivers of inflammation in chronic sinusitis with nasal polyps (CRSwNP) through secretion of T helper 2 (Th2)-promoting cytokines. P-glycoprotein (P-gp) is overexpressed in nasal polyps and modulates epithelial cytokine secretion in healthy mucosa. The objective of this study is to determine whether P-gp overactivity promotes Th2-associated cytokine secretion in CRSwNP.', 'Polyp explants (n = 4) and primary epithelial cell cultures (n = 5) were cultivated from patients with CRSwNP. Explant P-gp activity was determined using a calcein assay. In culture, P-gp was quantified by enzyme-linked immunosorbent assay (ELISA) and sensitivity to PSC-833 inhibition was determined using a calcein assay. Lipopolysaccharide (LPS)-stimulated cytokine secretion of interleukin 6 (IL-6), IL-8, IL-25, and granulocyte macrophage colony stimulating factor (GM-CSF) were quantified by ELISA and compared to secretion following P-gp inhibition. Differences in P-gp expression and cytokine secretion were compared using a Mann-Whitney U test. Secretion was correlated with P-gp expression using a Pearson correlation coefficient.', 'Calcein retention is increased in P-gp inhibited vs uninhibited polyp explants (mean ± standard deviation [SD]; 5.17 ± 1.76 vs 2.55 ± 0.62; p < 0.05) but not in controls, indicating increased nasal polyp P-gp activity. P-gp is sensitive to dose-dependent P-gp inhibition with PSC-833 in vitro. LPS-stimulated secretion of normalized GM-CSF (45.21 ± 41.39) and IL-6 (63.16 ± 36.37) were significantly reduced following P-gp inhibition (8.47 ± 3.28; p < 0.01, and 39.94 ± 31.07; p < 0.05; respectively) and secretion was highly correlated with P-gp expression(r = 0.824, p < 0.05, and r = 0.833, p < 0.05; respectively).

Ex Output:
0


Ex Input:
Cervical cancer continues to threaten women's health worldwide, and the incidence of cervical adenocarcinoma (AD) is rising in the developed countries. Previously, we showed that glucose-regulated protein 58 (Grp58) served as an independent factor predictive of poor prognosis of patients with cervical AD. However, the molecular mechanism underlying the involvement of Grp58 in cervical carcinogenesis is currently unknown.", 'DNA microarray and enrichment analysis were used to identify the pathways disrupted by knockdown of Grp58 expression.', 'Among the pathway identified, the WNT signaling pathway was one of those that were significantly associated with knockdown of Grp58 expression in HeLa cells. Our experiments showed that β-catenin, a critical effector of WNT signaling, was stabilized thereby accumulated in stable Grp58 knockdown cells. Membrane localization of β-catenin was observed in Grp58 knockdown, but not control cells. Using a transwell assay, we found that accumulated β-catenin induced by Grp58 knockdown or lithium chloride treatment inhibited the migration ability of HeLa cells. Furthermore, an inverse expression pattern of Grp58 and β-catenin was observed in cervical tissues.

Ex Output:

0