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 Q]: Arteriogenesis represents the maturation of preformed vascular connections in response to flow changes and shear stress. These collateral vessels can restore up to 60% of the native blood flow. Shear stress and vascular injury can induce the release of nucleotides from vascular smooth muscle cells and platelets that can serve as signaling ligands, suggesting they may be involved in mediating arteriogenesis. The P2Y2 nucleotide receptor (P2Y2R) has also been shown to mediate smooth muscle migration and arterial remodeling. Thus, we hypothesize that P2Y2R mediates arteriogenesis in response to ischemia.', 'Hind limb ischemia was induced by femoral artery ligation (FAL) in C57Bl/6NJ or P2Y2R negative mice (P2Y2(-/-)). Hind limb perfusion was measured with laser Doppler perfusion imaging and compared with the sham-operated contralateral limb immediately and at 3, 7, 14, 21, and 28 days after ligation. Collateral vessel size was measured by Microfil casting. Muscle specimens were harvested and analyzed with immunohistochemistry for Ki67, vascular cell adhesion molecule, macrophages, and muscle viability by hematoxylin and essoin stain.', 'Hind limb ischemia induced by FAL in C57Bl/6NJ mice resulted in significant ischemia as measured by laser Doppler perfusion imaging. There was rapid recovery to nearly normal levels of perfusion by 2 weeks. FAL in P2Y2(-/-) mice resulted in severe ischemia with greater tissue loss. Recovery of perfusion was impaired, achieving only 40% compared with wild-type mice by 28 days. Collateral vessels in the P2Y2(-/-) mice were underdeveloped, with reduced vascular cell proliferation and smaller vessel size. The collaterals were 65% the size of wild-type collateral vessels (P = .011). Angiogenesis at 28 days in the ischemic muscle, however, was greater in the P2Y2(-/-) mice (P < .001), possibly related to persistent ischemia leading and angiogenic drive. Early macrophage recruitment was reduced by nearly 70% in P2Y2(-/-) despite significantly more myocyte necrosis. However, inflammation was greater at 28 days in the P2Y2(-/-) mice.
[EX A]: 1

[EX Q]: To determine the association of ethanol intoxication with hypoglycemia in ED patients.', 'Retrospective, laboratory log review of 953 consecutive patients who were evaluated for ethanol intoxication in an urban university hospital ED over a three-month period. Simultaneous serum glucose determination was carried out for each patient and associations between ethanol level and glucose were sought.', 'Glucose concentrations were unavailable for 16 patients (1.7%). Of the remaining patients, 584 patients had detectable ethanol concentrations (ethanol-positive), and 353 had no detectable ethanol (ethanol-negative). Ethanol concentrations (mean +/- SD) in the ethanol-positive group were 50.11 +/- 24.08 mmol/L (231 +/- 111 mg/dL), and glucose concentrations were 5.83 +/- 1.94 mmol/L (105 +/- 35 mg/dL). Hypoglycemia [glucose < 3.72 mmol/L (67 mg/dL)] was observed for five (0.9%) ethanol-positive patients. It was classified as mild-moderate [2.78-3.66 mmol/L (50-66 mg/dL)] for four patients (0.7%) and severe [< 2.78 mmol/L (50 mg/dL)] for one (0.2%). Ethanol concentrations ranged from 25.60 to 68.33 mmol/L (118 to 315 mg/dL). There was no correlation between ethanol and glucose concentrations in any subset of the ethanol-positive patients population. In the ethanol-positive group, patients who had several ethanol-positive visits (56 patients, mean 3.6 visits/patient) accounted for four of the five episodes of hypoglycemia, including the one episode of severe hypoglycemia. The frequency of hypoglycemia in repeat visitors (2.0%) was higher than that in the group of patients without repeat visits (0.2%). In the ethanol-negative group, there were four (1.1%) episodes of mild-moderate hypoglycemia and no severely hypoglycemic patients. Hypoglycemia was not more likely to occur among ethanol-positive patients than it was among ethanol-negative patients.
[EX A]: 1

[EX Q]: Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis.', 'Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.227.6 and 150.131.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.81.7 and 1.00.2%, P<0.01, 76.227.5 and 32.77.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1 positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1 was significantly increased in the PAB group than that in the control group (2.310.84 and 1.00.18 arbitrary units, P<0.05).
[EX A]:
0