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.

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is a devastating complication, yet despite multiple lines of investigation an effective treatment remains lacking. Cytokine-mediated inflammation has been implicated as a causative factor in the development of posthemorrhagic vasospasm. In previous experiments using the rat femoral artery model of vasospasm, we demonstrated that elevated levels of the proinflammatory cytokine interleukin (IL)-6 are present after hemorrhage and that a polyclonal antibody against IL-6 is capable of attenuating experimental vasospasm.', 'In the present study, we tested the ability of a novel selective proinflammatory cytokine inhibitor (CNI-1493) to protect against the occurrence of experimental vasospasm in the same rat femoral artery model. CNI-1493 was administered by injection directly into the blood-filled femoral pouches of animals at the time of their initial surgery (hemorrhage). Control animals received an equal volume of vehicle alone. Animals were killed at 8 days posthemorrhage and degree of vasospasm was assessed by image analysis of artery cross-sectional area. In a separate series of experiments, enzyme-linked immunosorbent assay (ELISA) was used to assess levels of the proinflammatory cytokine IL-6 and the prototypical antiinflammatory cytokine transforming growth factor (TGF)-beta1 after treatment with CNI-1493.', 'Pretreatment with CNI-1493 provided dose-dependent attenuation of posthemorrhagic vasospasm, with the highest dose (200 microg in 8 microL dH2O) causing complete reversal of vasospasm (vessel cross-sectional area ratio 1.06 +/- 0.04 versus 0.87 +/- 0.06, p < 0.05, one-way analysis of variance). Assessment of cytokine levels by ELISA confirmed the selectivity of CNI-1493 by demonstrating significant reductions in IL-6 levels, but no suppression of TGF-beta1 levels.
0