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: Oxidants are believed to play a major role in the development of emphysema.', 'This study aimed to determine if the expression of human copper-zinc superoxide dismutase (CuZnSOD) within the lungs of mice protects against the development of emphysema.', 'Transgenic CuZnSOD and littermate mice were exposed to cigarette smoke (6 h/d, 5 d/wk, for 1 yr) and compared with nonexposed mice. A second group was treated with intratracheal elastase to induce emphysema.', 'Lung inflammation was measured by cell counts and myeloperoxidase levels. Oxidative damage was assessed by immunofluorescence for 3-nitrotyrosine and 8-hydroxydeoxyguanosine and lipid peroxidation levels. The development of emphysema was determined by measuring the mean linear intercept (Lm).', 'Smoke exposure caused a fourfold increase in neutrophilic inflammation and doubled lung myeloperoxidase activity. This inflammatory response did not occur in the smoke-exposed CuZnSOD mice. Similarly, CuZnSOD expression prevented the 58% increase in lung lipid peroxidation products that occurred after smoke exposure. Most important, CuZnSOD prevented the onset of emphysema in both the smoke-induced model (Lm, 68 exposed control vs. 58 exposed transgenic; p < 0.04) and elastase-generated model (Lm, 80 exposed control vs. 63 exposed transgenic; p < 0.03). These results demonstrate for the first time that antioxidants can prevent smoke-induced inflammation and can counteract the proteolytic cascade that leads to emphysema formation in two separate animal models of the disease.

Output: 1


Input: Consider Input: Endothelial junctions control functions such as permeability, angiogenesis and contact inhibition. VE-Cadherin (VECad) is essential for the maintenance of intercellular contacts. In confluent endothelial monolayers, N-Cadherin (NCad) is mostly expressed on the apical and basal membrane, but in the absence of VECad it localizes at junctions. Both cadherins are required for vascular development. The intercellular adhesion molecule (ICAM)-2, also localized at endothelial junctions, is involved in leukocyte recruitment and angiogenesis.', 'In human umbilical vein endothelial cells (HUVEC), both VECad and NCad were found at nascent cell contacts of sub-confluent monolayers, but only VECad localized at the mature junctions of confluent monolayers. Inhibition of ICAM-2 expression by siRNA caused the appearance of small gaps at the junctions and a decrease in NCad junctional staining in sub-confluent monolayers. Endothelioma lines derived from WT or ICAM-2-deficient mice (IC2neg) lacked VECad and failed to form junctions, with loss of contact inhibition. Re-expression of full-length ICAM-2 (IC2 FL) in IC2neg cells restored contact inhibition through recruitment of NCad at the junctions. Mutant ICAM-2 lacking the binding site for ERM proteins (IC2 ΔERM) or the cytoplasmic tail (IC2 ΔTAIL) failed to restore junctions. ICAM-2-dependent Rac-1 activation was also decreased in these mutant cell lines. Barrier function, measured in vitro via transendothelial electrical resistance, was decreased in IC2neg cells, both in resting conditions and after thrombin stimulation. This was dependent on ICAM-2 signalling to the small GTPase Rac-1, since transendothelial electrical resistance of IC2neg cells was restored by constitutively active Rac-1. In vivo, thrombin-induced extravasation of FITC-labeled albumin measured by intravital fluorescence microscopy in the mouse cremaster muscle showed that permeability was increased in ICAM-2-deficient mice compared to controls.

Output: 0


Input: Consider Input: The perineum stretches naturally during obstetrical labor, but it is unknown whether this stretch has a negative impact on pelvic floor outcomes after a vaginal birth (VB). We aimed to evaluate whether perineal stretch was associated with postpartum pelvic floor dysfunction, and we hypothesized that greater perineal stretch would correlate with worsened outcomes.', 'This was a prospective cohort study of primiparous women who had a VB. Perineal body (PB) length was measured antepartum, during labor, and 6\xa0months postpartum. We determined the maximum PB (PBmax) measurements during the second stage of labor and PB change (ΔPB) between time points. Women completed functional questionnaires and had a Pelvic Organ Prolapse Quantification (POP-Q) system exam 6\xa0months postpartum. We analyzed the relationship of PB measurements to perineal lacerations and postpartum outcomes, including urinary, anal, and fecal incontinence, sexual activity and function, and POP-Q measurements.', 'Four hundred and forty-eight women with VB and a mean age of 24\u2009±\u20095.0\xa0years with rare (5\xa0%) third- or fourth-degree lacerations were assessed. During the second stage of labor, 270/448 (60\xa0%) had perineal measurements. Mean antepartum PB length was 3.7\u2009±\u20090.8\xa0cm, with a maximum mean PB length (PBmax) during the second stage of 6.1\u2009±\u20091.5\xa0cm, an increase of 65\xa0%. The change in PB length (ΔPB) from antepartum to 6\xa0months postpartum was a net decrease (-0.39\u2009±\u20091.02\xa0cm). PB change and PBmax were not associated with perineal lacerations or outcomes postpartum (all p\u2009>\u20090.05).


Output: 1