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.

The extent to which tolerance acquired in one motion environment can be transferred to another has not been fully elucidated. This study compares three provocative motion stimuli and whether tolerance acquired from cross-coupled motion and torso rotation can be transferred to simulated aircraft motion.', "There were 18 healthy subjects (9 men and 9 women), 18-44 yr of age, who were divided into 3 groups. Each group was exposed to the following desensitization procedure in a pseudo-random repeated measures design. In condition D1, subjects were exposed to 4 consecutive days of cross-coupling and on the 5th d they were exposed to simulated aircraft motion. In D2, subjects were exposed to 4 consecutive days of torso rotation and on the 5th day they were exposed to the simulated aircraft motion as in D1. In D3, subjects were exposed to 5 consecutive days of simulated aircraft motion. Based on Graybiel's diagnostic criteria, severity of motion sickness on the 1st and 5th day in D1, D2, and D3 were compared.", 'Cross-coupled motion was the most provocative stimulus followed by torso rotation and simulated aircraft motion. Within each motion stimulus, there was evidence of desensitization (p < 0.001) within 4 d. There were no significant differences in the severity of motion sickness observed on the 5th day regardless of the desensitization stimuli.
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We hypothesized that preconditioning (PC) with a short exposure to isoflurane (ISO) would reduce neurodegeneration induced by prolonged exposure to ISO in neonatal rats, as previously shown in neuronal cell culture.', 'We randomly divided 7-day-old Sprague-Dawley rats into 3 groups: control, 1.5% ISO, and PC + 1.5% ISO. The control group was exposed to carrier gas (30% oxygen balanced in nitrogen) for 30 minutes and then to carrier gas again for 6 hours the following day. The 1.5% ISO group was exposed to carrier gas for 30 minutes and then to 1.5% ISO for 6 hours the following day. The PC + 1.5% ISO group was preconditioned with a 30-minute 1.5% ISO exposure and then exposed to 1.5% ISO for 6 hours the following day. Blood and brain samples were collected 2 hours after the exposures for determination of neurodegenerative biomarkers, including caspase-3, S100β, caspase-12, and an autophagy biomarker Beclin-1.', 'Prolonged exposure to ISO significantly increased cleaved caspase-3 expression in the cerebral cortex of 7-day-old rats compared with the group preconditioned with ISO and the controls using Western blot assays. However, significant differences were not detected for other markers of neuronal injury.
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Recent studies indicate that a1-adrenergic receptors (a1-ARs) are cardioprotective by preventing cardiac myocyte death and augmenting contractility in heart failure. Although G-protein-coupled receptors are assumed to localize to and signal at the plasma membrane, we previously demonstrated that endogenous a1-ARs localize to the nuclei in adult cardiac myocytes. However, the functional consequence of this nuclear localization remains unclear. Here, we attempted to reconcile nuclear localization of a1-ARs with their physiologic function by examining a1-AR-induced contractility in adult cardiac myocytes.', 'By measuring shortening in unloaded, cultured adult cardiac myocytes, we found that the a1A-subtype regulated contractility through phosphorylation of cardiac troponin I (cTnI) at the protein kinase C (PKC) site, threonine 144. Reconstitution of an a1A-subtype nuclear localization mutant in cardiac myocytes lacking a1-ARs failed to rescue nuclear a1A-mediated phosphorylation of cTnI and myocyte contractility. Leptomycin B, the nuclear export inhibitor, also blocked a1A-mediated phosphorylation of cTnI. These data indicate that a1-AR signaling originates in the nucleus. Consistent with these observations, we localized the a1A-subtype to the inner nuclear membrane, identified PKCa, d, and e in the nucleus, and found that a1-ARs activate PKCd in nuclei isolated from adult cardiac myocytes. Finally, we found that a PKCd nuclear localization mutant blunted a1-induced phosphorylation of cTnI.

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