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.

Example Input: One-fifth of patients with seemingly 'curable' pancreatic ductal adenocarcinoma (PDA) experience an early recurrence and death, receiving no definable benefit from a major operation. Some patients with advanced stage tumors are deemed 'unresectable' by conventional staging criteria (e.g. liver metastasis), yet progress slowly. Effective biomarkers that stratify PDA based on biologic behavior are needed. To help researchers sort through the maze of biomarker data, a compendium of 2500 published candidate biomarkers in PDA was compiled (PLoS Med, 2009. 6(4) p. e1000046).", 'Building on this compendium, we constructed a survival tissue microarray (termed s-TMA) comprised of short-term (cancer-specific death <12 months, n=58) and long-term survivors (>30 months, n=79) who underwent resection for PDA (total, n=137). The s-TMA functions as a biological filter to identify bona fide prognostic markers associated with survival group extremes (at least 18 months separate survival groups). Based on a stringent selection process, 13 putative PDA biomarkers were identified from the public biomarker repository. Candidates were tested against the s-TMA by immunohistochemistry to identify the best markers of tumor biology. In a multivariate model, MUC1 (odds ratio, OR=28.95, 3+ vs. negative expression, p=0.004) and MSLN (OR=12.47, 3+ vs. negative expression, p=0.01) were highly predictive of early cancer-specific death. By comparison, pathologic factors (size, lymph node metastases, resection margin status, and grade) had ORs below three, and none reached statistical significance. ROC curves were used to compare the four pathologic prognostic features (ROC area=0.70) to three univariate molecular predictors (MUC1, MSLN, MUC2) of survival group (ROC area=0.80, p=0.07).
Example Output: 0

Example Input: Biliary tract carcinoma is a deadly disease, accounting for nearly 4500 malignancy-related deaths each year in the United States. Early detection has the potential to improve survival for patients with biliary tract malignancies, enabling curative surgical resection. Early detection approaches would benefit from an accurate, minimally invasive diagnostic test. To identify novel diagnostic markers, the authors recently completed a comprehensive proteomic study of bile samples from patients with biliary carcinoma. One of the proteins identified by tandem mass spectrometry was Mac-2-binding protein (Mac-2BP). The authors evaluated the performance of Mac-2BP and its ligand, galectin-3, as diagnostic markers for patients with biliary carcinoma.', 'Levels of Mac-2BP, galectin-3, and CA19-9 were measured using an enzyme-linked immunosorbent assay (ELISA) in bile samples from patients with biliary tract carcinoma (n = 26), benign biliary conditions (n = 32), and primary sclerosing cholangitis (n = 20). Serum levels of Mac-2BP and galectin-3 also were determined using ELISA. Mac-2BP tissue expression was investigated by immunohistochemical methods using a biliary carcinoma tissue microarray.', 'Biliary Mac-2BP levels were elevated by a factor of approximately 3 in the biliary carcinoma group compared with the group of patients who had PSC or another type of nonneoplastic biliary disease. In contrast, Mac-2BP levels were not elevated in serum samples from patients with biliary carcinoma. According to the immunohistochemical analysis, Mac-2BP was expressed in 34 of 36 patients (94.4%) with biliary tract carcinoma. As a diagnostic marker for biliary carcinoma, Mac-2BP levels were as accurate as biliary CA19-9 levels, with an area under the curve (AUC) of 0.70 on receiver operator characteristic analysis. The use of both of these bile markers in combination, however, led to significantly better diagnostic accuracy compared with the accuracy achieved using CA19-9 alone (AUC, 0.75; P < 0.001). Serum and biliary galectin-3 levels did not differ in the biliary carcinoma group relative to the control groups.
Example Output: 0

Example Input: The peptidyl-proline isomerase, Protein Never in Mitosis Gene A Interacting-1 (PIN1), regulates turnover of inducible nitric oxide synthase (iNOS) in murine aortic endothelial cells (MAEC) stimulated with E. coli endotoxin (LPS) and interferon-gamma (IFN). Degradation of iNOS was reduced by a calpain inhibitor, suggesting that PIN1 may affect induction of other calpain-sensitive inflammatory proteins, such as cyclooxygenase (COX)-2, in MAEC.', 'MAEC, transduced with lentivirus encoding an inactive control short hairpin (sh) RNA or one targeting PIN1 that reduced PIN1 by 85%, were used. Cells were treated with LPS/IFN, calpain inhibitors (carbobenzoxy-valinyl-phenylalaninal (zVF), PD150606), cycloheximide and COX inhibitors to determine the effect of PIN1 depletion on COX-2 and calpain.', 'LPS or IFN alone did not induce COX-2. However, treatment with 10 mug LPS plus 20 ng IFN per ml induced COX-2 protein 10-fold in Control shRNA MAEC. Induction was significantly greater (47-fold) in PIN1 shRNA cells. COX-2-dependent prostaglandin E2 production increased 3-fold in KD MAEC, but did not increase in Control cells. The additional increase in COX-2 protein due to PIN1 depletion was post-transcriptional, as induction of COX-2 mRNA by LPS/IFN was the same in cells containing or lacking PIN1. Instead, the loss of COX-2 protein, after treatment with cycloheximide to block protein synthesis, was reduced in cells lacking PIN1 in comparison with Control cells, indicating that degradation of the enzyme was reduced. zVF and PD150606 each enhanced the induction of COX-2 by LPS/IFN. zVF also slowed the loss of COX-2 after treatment with cycloheximide, and COX-2 was degraded by exogenous mu-calpain in vitro. In contrast to iNOS, physical interaction between COX-2 and PIN1 was not detected, suggesting that effects of PIN1 on calpain, rather than COX-2 itself, affect COX-2 degradation. While cathepsin activity was unaltered, depletion of PIN1 reduced calpain activity by 55% in comparison with Control shRNA cells.
Example Output:
0