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]: Transfusion of packed erythrocytes stored for a long duration is associated with increased pulmonary arterial pressure and vascular resistance. Prolonged storage decreases erythrocyte deformability, and older erythrocytes are rapidly removed from the circulation after transfusion. The authors studied whether treating stored packed ovine erythrocytes with NO before transfusion could prevent pulmonary vasoconstriction, enhance erythrocyte deformability, and prolong erythrocyte survival after transfusion.', 'Ovine leukoreduced packed erythrocytes were treated before transfusion with either NO gas or a short-lived NO donor. Sheep were transfused with autologous packed erythrocytes, which were stored at 4°C for either 2 ("fresh blood") or 40 days ("stored blood"). Pulmonary and systemic hemodynamic parameters were monitored before, during, and after transfusion. Transfused erythrocytes were labeled with biotin to measure their circulating lifespan. Erythrocyte deformability was assessed before and after NO treatment using a microfluidic device.', 'NO treatment improved the deformability of stored erythrocytes and increased the number of stored erythrocytes circulating at 1 and 24\u2009h after transfusion. NO treatment prevented transfusion-associated pulmonary hypertension (mean pulmonary arterial pressure at 30\u2009min of 21\u2009±\u20091 vs. 15\u2009±\u20091 mmHg in control and NO-treated packed erythrocytes, P < 0.0001). Washing stored packed erythrocytes before transfusion did not prevent pulmonary hypertension.
[A]: 0


[Q]: In dialysis patients, volume overhydration is common and is related to increased risk of cardiovascular morbidity and mortality. However, it remains unclear whether volume overload imposes those detrimental effects through endothelial dysfunction.', 'In this cross-sectional study, 81 stable patients on continuous ambulatory peritoneal dialysis in a single center were recruited. Volume status was evaluated by extracellular water, assessed by bioimpedance analysis, and normalized to individual height (nECW). Endothelial function was estimated by endothelial-dependent flow-mediated dilatation (FMD) of the brachial artery and expressed as percentage change relative to baseline diameter.', 'There were 37 male and 44 female patients (mean age 61 +/- 12 years, dialysis vintage 20 +/- 23 months). FMD in female patients was significantly higher than that in male patients (9.17% +/- 6.23% vs 6.31% +/- 5.01%, p < 0.05). FMD was negatively correlated with weight (r = -0.308, p < 0.01), body mass index (r = -0.242, p < 0.05), systolic blood pressure (r = -0.228, p < 0.05), ECW (r = -0.404, p < 0.001), and nECW (r = -0.418, p < 0.001). No correlation was found between FMD and other variables. In multiple stepwise regression analysis, calcium x phosphate product (beta = 0.422, p < 0.001), nECW (beta = -0.343, p < 0.01), and dialysis vintage (beta = -0.237, p < 0.05) were independent determinants of FMD (adjusted R(2) = 0.327 for this model).
[A]: 1


[Q]: Increased rates of apoptosis have been reported to play a role in the pathophysiology of many disorders, including liver diseases. Conversely, genetic mutations that result in impairment of programmed cell death have been associated with cancer development. However, apoptosis resistance can also be the result of nongenetic stress adaptation, as seen in the cancer-prone metabolic liver disease hereditary tyrosinemia. To clarify whether stress-induced apoptosis resistance is a general feature of chronic liver diseases, an animal model of chronic cholestasis was examined.', 'Studies were performed with mice before and 2 weeks following bile duct ligation and with Fah-/- and Fah/p21-/- mice before and after NTBC withdrawal.', 'Here we show that bile duct ligation induced profound resistance against Fas monoclonal antibody-mediated hepatocyte death. The apoptosis signaling pathway was blocked downstream of caspase-8 activation and proximal to mitochondrial cytochrome c release. In controls, activation of the Fas receptor resulted in rapid dephosphorylation of Bid and its subsequent cleavage, whereas Bid remained phosphorylated and uncleaved in chronic cholestasis and other models of hepatic apoptosis resistance.
[A]:
1