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: Endothelin receptor antagonists improve pulmonary arterial hypertension (PAH). Mutations in the bone morphogenetic protein (BMP) type 2 receptor (BMPR2) predispose to PAH. Here, we sought to determine whether there might exist interactions between these 2 signaling pathways and their effect on the acquisition of the altered phenotype of pulmonary artery smooth muscle cells (PA-SMCs) observed in PAH.', 'Expression of BMPR2, of the BMP agonist BMP4, and of the BMP antagonists gremlin1 and gremlin2 was evaluated in lungs and in PA-SMCs from 6 PAH patients and 14 controls treated with endothelin-1. Endothelin-1 pre-treated PA-SMCs were assessed for proliferation, apoptosis, and downstream signaling activation of Smad1/5/8 and p38 mitogen-activated protein kinase (p38(MAPK)) after BMP2 treatment.', 'In PA-SMCs from PAH patients, expression of BMPR2 and BMP4 decreased, whereas expression of gremlin1 and gremlin2 increased compared with controls. Treatment of control PA-SMCs with endothelin-1 induced a dose-dependent increase in gremlin1 and gremlin2, whereas BMPR2 and BMP4 expression decreased, reaching similar levels as those observed in PAH cells. In control PA-SMCs, endothelin-1 pre-treatment reduced inhibitor of DNA binding 1 (Id1) expression and Smad1/5/8 activation induced by BMP2, whereas it enhanced p38(MAPK) activation. Moreover, BMP2 decreased serum-induced proliferation and increased the pro-apoptotic Bax/Bcl-2 ratio. These effects were attenuated by endothelin-1 pre-treatment. Endothelin-1 did not alter BMPR2 signaling in PA-SMCs from PAH patients.

Output: 0

Input: Consider Input: Epinephrine is a component of all resuscitation algorithms. Vasopressin is a pulmonary vasodilator and systemic vasopressor. We investigated the effect of epinephrine vs. vasopressin on survival and hemodynamics after neonatal porcine cardiac arrest (CA).', 'A 4-min asphyxial CA was induced, after which cardiopulmonary resuscitation (CPR) was commenced. Animals were randomized to low- (LDE: 0.01 mg/kg) or high-dose epinephrine (HDE: 0.03 mg/kg), low- (LDV: 0.2 U/kg) or high-dose vasopressin (HDV: 0.4 U/kg), or control (saline). Clinical and echocardiography indexes were monitored.', 'Sixty-nine animals were randomized. Survival was greater in HDV (n = 8 (89%); P < 0.05 ANOVA) vs. control (n = 7 (43%)) and LDE (n = 5 (36%)) but not vs. HDE (n = 7 (64%)) or LDV (n = 6 (75%)). Animals resuscitated with LDE required more shocks (2.5 (interquartile range: 2-6); P < 0.05) and higher doses of energy (15 J (interquartile range: 10-20); P < 0.05). Left ventricular output was comparable between groups, but a greater increase in superior vena caval flow was seen after HDV (P < 0.001 vs. control, LDE, and HDE). Plasma troponin was greatest in the HDE group (P < 0.05 vs. control and HDV).

Output: 0

Input: Consider Input: Uracil DNA glycosylase (UDG) plays a major role in repair of uracil formed due to deamination of cytosine. UDG in human cells is present in both the nucleus and mitochondrial compartments. Although, UDG's role in the nucleus is well established its role in mitochondria is less clear.", "In order to identify UDG's role in the mitochondria we expressed UGI (uracil glycosylase inhibitor) a natural inhibitor of UDG in the mitochondria. Our studies suggest that inhibition of UDG by UGI in the mitochondria does not lead to either spontaneous or induced mutations in mtDNA. Our studies also suggest that UGI expression has no affect on cellular growth or cytochrome c-oxidase activity.
Output: 0