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.

[Q]: To compensate for the lack of haptic feedback by surgical robots, limitation of exerted forces could be implemented. The limits should be based on the observed relationship between tissue load and induced damage. This study examines whether age-related changes influence this relationship.', 'Descending thoracic aortas of male C57BL/6J mice of 10, 25 and 40 weeks were clamped in vivo (no clamp, 0.5N or 2.0N) for 2 min. Functional integrity was tested in vitro by studying endothelium-dependent and -independent vasoreactivity.', 'Endothelium-dependent relaxation deteriorated with increased clamping force at all ages. Clamping did not influence endothelium-independent vasodilation. Age (10, 25 and 40 weeks) did not significantly impact on the effect of clamping on endothelium-dependent and independent vasoreactivity.
[A]: 1

[Q]: The regulatory mechanisms of IL-5 gene transcription in human peripheral T cells are unclear because the transfection efficiency of plasmid constructs into nontransformed T cells is very low.', 'Concanavalin A (ConA)-stimulated blastocytes derived from peripheral blood lymphocytes of asthmatic subjects were transiently transfected with the human IL-5 gene promoter/enhancer-luciferase gene construct, pIL-5 (-511)Luc, and cultured with THP-1 cells (human monocytoid cells) and anti-CD3 monoclonal antibody (mAb). IL-5 level in the culture medium was determined by an enzyme-linked immunosorbent assay. Transcriptional activity of the IL-5 gene was measured by luciferase reporter analysis.', "ConA-blast lymphocytes of asthmatic patients produced a significant amount of IL-5 upon combined stimulation with anti-CD3 mAb and THP-1 cells, but not with anti-CD3 mAb alone. Costimulation with anti-CD28 mAb also enhanced the anti-CD3 mAb- induced IL-5 production. Accordingly, luciferase activity induced by anti-CD3 mAb stimulation in pIL-5(-511)Luc-transfected ConA-blast lymphocytes was increased 1.9- and 3.4-fold by the addition of anti-CD28 mAb and THP-1 cells, respectively. Serial 5' deletion analysis of the reporter gene demonstrated that the cis-regulatory element located at -119 to -80 is critical for anti-CD3 mAb-induced IL-5 gene transcription.
[A]: 0

[Q]: We previously reported that the intimal endothelium of the rat aorta switches to a microvascular phenotype during angiogenesis in vitro. The microvessels formed by the rat aortic endothelium are coated with pericytes. The purpose of this study was to evaluate the relation of the pericytes to the angiogenic process and to identify the site of origin of these cells in the aortic wall.', 'Rings of rat aorta were cultured in collagen gel under serum-free conditions. The formation of a pericyte coating around aorta-derived microvessels was evaluated by counting pericytes and microvessels in the living cultures. Pericytes and endothelial cells were studied by immunohistochemistry, lectin labeling, electron microscopy, 3H-thymidine labeling followed by autoradiography, and time-lapse video microscopy. The capacity of aortic smooth muscle cells to differentiate into pericytes was studied by coculturing intimal- or medial-derived smooth muscle cells with endothelial cells in a collagen gel overlay assay that induced reorganization of endothelial cells into microvessels.', 'Microvessels during the early stages of angiogenesis were composed primarily of endothelial cells. As vascular proliferation decreased, the microvessels became coated with pericytes. The pericytes migrated from the root to the tip of the microvessels using the endothelium as a surface for attachment, proliferation, and contact guidance. The pericytes were continuous with the myointimal endothelial cells of the cultured aorta. Pericytes and myointimal cells were positive for alpha-smooth muscle actin and vimentin and were actively engaged in DNA synthesis. Treatment of the cultures with heparin caused a marked reduction in the number of pericytes. Smooth muscle cells isolated from the intimal aspect of the rat aorta migrated toward the endothelium and differentiated into pericytes when cocultured with microvessels formed by isolated endothelial cells in a collagen gel overlay assay. Conversely, smooth muscle cells isolated from the deep layers of the media had no significant endothelial tropism and failed to differentiate into pericytes.
[A]:
0