4,656 research outputs found
Manual control analysis of drug effects on driving performance
The effects of secobarbital, diazepam, alcohol, and marihuana on car-driver transfer functions obtained using a driving simulator were studied. The first three substances, all CNS depressants, reduced gain, crossover frequency, and coherence which resulted in poorer tracking performance. Marihuana also impaired tracking performance but the only effect on the transfer function parameters was to reduce coherence
Hyperfine Structure Constants for Eu Isotopes: Is The Empirical Formula of HFS Anomaly Universal ?
We calculate the hyperfine structure constant for the Eu isotopes with shell
model wave functions. The calculated results are compared with those predicted
by the Moskowitz-Lombardi (M-L) empirical formula. It turns out that the two
approaches give the very different behaviors of the hfs constants in the
isotope dependence. This should be easily measured by experiment, which may
lead to the universality check of the M-L formula.Comment: 18 pages, Latex, two figure
Function of BID - a molecule of the bcl-2 family - in ischemic cell death in the brain
Mitochondrial mechanisms, particularly the release of cytochrome c, play a role in the death of nerve and glial cells in cerebral ischemia. We have currently investigated whether BID, a proapoptotic molecule of the bcl-2 family and promoter of the release of cytochrome c is expressed in the brain, activated by cerebral ischemia in vivo, and contributes to ischemic cell death. We found BID in the cytosol of mouse brain and of primary cultured mouse neurons and showed that neuronal BID is a substrate for caspase 8. BID was cleaved in vivo 4 h after transitory occlusion of the middle cerebral artery. Further, BID-/- mice had a significant attenuation of infarction (-67%) and significantly lower release of cytochrome c (-41 %). The findings indicate that the proapoptotic molecule BID may contribute to the demise of nerve cells from cerebral ischemia by release of cytochrome c and activation of caspase. Copyright (C) 2002 S. Karger AG, Basel
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