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]: Immune dysregulation can affect insulin resistance (IR) and -cell function and hence contribute to development of type 2 diabetes mellitus (T2DM). The complement system, as a regulator of immune and inflammatory homeostasis, may be a relevant contributor therein. However, longitudinal studies focusing on complement as a determinant of T2DM and IR are scarce. Therefore, we prospectively investigated the association of plasma complement factor 3 (C3) with (estimates of) IR in muscle, liver, and adipocytes, as well as with glucose tolerance, including incident T2DM.', 'Fasting C3, nonesterified fatty acids, glucose, and insulin (the latter two during oral glucose tolerance tests) were measured at baseline (n = 545) and after 7 years of follow-up (n = 394) in a prospective cohort study.', 'Over the 7-year period, C3 levels (per 0.1 g/L) were longitudinally associated with higher homeostasis model assessment of IR (HOMA2-IR; = 15.2% [95% CI 12.9-17.6]), hepatic IR ( = 6.1% [95% CI 4.7-7.4]), adipocyte IR ( = 16.0% [95% CI 13.0-19.1]), fasting glucose ( = 1.8% [95% CI 1.2-2.4]), 2-h glucose ( = 5.2% [95% CI 3.7-6.7]), and area under the curve for glucose ( = 3.6% [95% CI 2.7-4.6]). In addition, greater changes in C3 (per 0.1 g/L) were associated with greater changes in HOMA2-IR ( = 0.08 [95% CI 0.02-0.15]) and greater changes in hepatic IR ( = 0.87 [95% CI 0.12-1.61]) over 7 years, but not glucose tolerance. Moreover, baseline C3 was associated with the 7-year incidence of T2DM (odds ratio 1.5 [95% CI 1.1-2.0]).
[EX A]: 1

[EX Q]: Effective therapeutic interventions for chronic, idiopathic lung diseases remain elusive. Normalized T-cell function is an important contributor to spontaneous resolution of pulmonary sarcoidosis. Up-regulation of inhibitor receptors, such as programmed death-1 (PD-1) and its ligand, PD-L1, are important inhibitors of T-cell function.', 'To determine the effects of PD-1 pathway blockade on sarcoidosis CD4(+) T-cell proliferative capacity.', 'Gene expression profiles of sarcoidosis and healthy control peripheral blood mononuclear cells were analyzed at baseline and follow-up. Flow cytometry was used to measure ex vivo expression of PD-1 and PD-L1 on systemic and bronchoalveolar lavage-derived cells of subjects with sarcoidosis and control subjects, as well as the effects of PD-1 pathway blockade on cellular proliferation after T-cell receptor stimulation. Immunohistochemistry analysis for PD-1/PD-L1 expression was conducted on sarcoidosis, malignant, and healthy control lung specimens.', 'Microarray analysis demonstrates longitudinal increase in PDCD1 gene expression in sarcoidosis peripheral blood mononuclear cells. Immunohistochemistry analysis revealed increased PD-L1 expression within sarcoidosis granulomas and lung malignancy, but this was absent in healthy lungs. Increased numbers of sarcoidosis PD-1(+) CD4(+) T cells are present systemically, compared with healthy control subjects (P < 0.0001). Lymphocytes with reduced proliferative capacity exhibited increased proliferation with PD-1 pathway blockade. Longitudinal analysis of subjects with sarcoidosis revealed reduced PD-1(+) CD4(+) T cells with spontaneous clinical resolution but not with disease progression.
[EX A]: 1

[EX Q]: Earlier studies regarding the risk of colorectal cancer in women with a prior diagnosis of breast cancer yielded conflicting results.', 'A retrospective cohort study was performed using the General Practitioner Research Database of the United Kingdom. Women with a prior diagnosis of breast cancer were compared with female control patients without a prior history of breast cancer. The primary outcome was an incident diagnosis of colorectal cancer. Poisson regression analysis was utilized to assess the effects of potential confounder variables.', 'The study included 17,415 breast cancer patients and 69,660 matched control patients with follow-up time in person years of 52,914 and 331,480, respectively. The relative rate of colorectal cancer among breast cancer patients was 0.80 (95% CI 0.56-1.15). The relative rate of colorectal cancer among women exposed and unexposed to tamoxifen were 0.73 (95% CI 0.49-1.08) and 1.81 (95% CI 0.85-3.85), respectively.
[EX A]:
0