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: Treatment of rheumatoid arthritis (RA) with tumor necrosis factor (TNF)-blocking agents, including etanercept and infliximab, has resulted in reductions in the radiographic progression of RA. However, the exact mechanism by which this protection occurs has not been determined. In order to add to such knowledge, we investigated the effect of anti-TNF therapy on the expression of osteoprotegerin (OPG) and receptor activator of NF-kappaB ligand (RANKL) in synovial tissue.', "The expression of OPG and RANKL in synovial biopsy specimens was evaluated by immunohistochemistry. Serial synovial biopsy specimens were obtained from 18 patients with RA, before and after treatment with etanercept (9 patients) or infliximab (9 patients). Biopsy specimens were evaluated by double-blind semiquantitative analysis and image analysis. The in vitro effect of TNF antagonists on the RANKL/OPG expression in osteoblasts and endothelial cells was evaluated by Western blotting. Statistical analysis was performed using Wilcoxon's signed rank test, followed by the Bonferroni correction for multiple comparisons of paired samples. The results of in vitro experiments were evaluated by one-way analysis of variance, with Tukey's post hoc test.", 'Treatment with both infliximab and etanercept increased the expression of OPG in synovial tissue. After 8 weeks of treatment, neither infliximab nor etanercept influenced RANKL expression. In both groups of patients, the RANKL:OPG ratio decreased following therapy. In vitro, both of the TNF antagonists mimicked the in vivo effect, inducing a decrease in the RANKL:OPG ratio in TNF-primed osteoblasts and endothelial cells.
Example Output: 1

Example Input: Single nucleotide polymorphisms (SNPs) in approximately 40 genes have been associated with an increased risk for type 2 diabetes (T2D) in genome-wide association studies. It is not known whether a similar genetic impact on the risk of prediabetes (impaired glucose tolerance [IGT] or impaired fasting glycemia [IFG]) exists.', 'In our cohort of 1442 non-diabetic subjects of European origin (normal glucose tolerance [NGT] n\u200a=\u200a1046, isolated IFG n\u200a=\u200a142, isolated IGT n\u200a=\u200a140, IFG+IGT n\u200a=\u200a114), an impact on glucose homeostasis has been shown for 9 SNPs in previous studies in this specific cohort. We analyzed these SNPs (within or in the vicinity of the genes TCF7L2, KCNJ11, HHEX, SLC30A8, WFS1, KCNQ1, MTNR1B, FTO, PPARG) for association with prediabetes.', 'The genetic risk load was significantly associated with the risk for IGT (p\u200a=\u200a0.0006) in a model including gender, age, BMI and insulin sensitivity. To further evaluate potential confounding effects, we stratified the population on gender, BMI and insulin sensitivity. The association of the risk score with IGT was present in female participants (p\u200a=\u200a0.008), but not in male participants. The risk score was significantly associated with IGT (p\u200a=\u200a0.008) in subjects with a body mass index higher than 30 kg/m(2) but not in non-obese individuals. Furthermore, only in insulin resistant subjects a significant association between the genetic load and the risk for IGT (p\u200a=\u200a0.01) was found.
Example Output: 0

Example Input: Hypothalamic orexinergic neurons play a critical role in the promotion and maintenance of wakefulness in mammals. Previous studies have demonstrated that activities of orexinergic neurons were inhibited by isoflurane and sevoflurane, and microinjection of orexin facilitated the emergence from volatile anesthesia. In this study we first examined the hypothesis that the activity of orexin neurons is inhibited by propofol anesthesia. Moreover, the role of the orexinergic signals in basal forebrain in regulating the anesthesia-arousal cycle of propofol anesthesia is also elucidated.', 'Rats were killed at 0, 30, 60, and 120 minutes of propofol infusion as well as at the time the righting reflex returned after the termination of anesthesia. Activated orexinergic neurons were detected by c-Fos expression. The plasma concentrations of orexin-A were measured by radioimmunoassay. Orexin-A (30 or 100 pmol) or the orexin-1 receptor antagonist, SB-334867A (5 or 20 μg), was microinjected into the basal forebrain 15 minutes before propofol infusion, or 15 minutes before the termination of propofol infusion. The loss and the return of the righting reflex time were recorded as the induction and the emergence time.', 'Propofol anesthesia resulted in an inhibition of orexinergic neuron activity as demonstrated by the reduced numbers of c-Fos-immunoreactive orexinergic neurons. The activities of orexinergic neurons were restored when rats emerged from anesthesia. Propofol anesthesia decreased plasma orexin-A concentrations. Intrabasalis microinjection of orexin-A had no effect on the induction time but facilitated the emergence from propofol anesthesia. Inversely, intrabasalis microinjection of the orexin-1 receptor antagonist SB-334867A delayed the emergence from propofol anesthesia.
Example Output:
0