Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-Naphthoxyacetic acid (alpha-NOAA), one of the retching-inducers, elicited a dose-dependent jumping behavior shortly after i.p. administration in doses ranging from 250 to 700 mg/kg in ddY mice, the incidence of jumping being 97% at a dose of 700 mg/kg. alpha-NOAA also induced hypothermia, retching, head shaking, salivation and lacrimation. Phentolamine, reserpine, disulfiram, tranylcypromine, haloperidol, scopolamine, bicuculline, diazepam and lithium among the drugs tested inhibited to a certain degree but not markedly the alpha-NOAA-induced jumping behavior. However, the behavior was markedly inhibited by a dopaminergic agonist, apomorphine (1 mg/kg, i.p.), and this inhibitory effect was significantly antagonized by a dopaminergic antagonist, haloperidol (2 mg/kg, i.p.). These findings suggest that the jumping behavior elicited by alpha-NOAA may be due to the inhibition of dopaminergic neuron activity.
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PMID:Dopaminergic inhibition involved in the alpha-naphthoxyacetic acid-induced jumping behavior in mice. 738 15

Mild hypothermia, applied either during or soon after cerebral ischemia, has been shown to confer robust neuroprotection against brain injury in experimental stroke and in patients recovering from cardiac arrest. However, the mechanism underlying hypothermic neuroprotection is not completely understood. In this study, the effect of mild hypothermia on the induction of oxidative DNA damage, an early harmful event during post-ischemic reperfusion that triggers both necrotic and apoptotic cell death in the brain, was studied using the rat model of middle cerebral artery occlusion (MCAO) and reperfusion. Rats were subjected to 2-hr MCAO and reperfusion of various durations up to 3 days. Selective brain hypothermia (33 degrees C) was induced at the onset of ischemia and terminated at the beginning of reperfusion, and this significantly decreased infarct volume 72 hr later. Correlated with this protective effect, intraischemic mild hypothermia markedly attenuated the nuclear accumulations of several oxidative DNA lesions, including 8-oxodG, AP sites, and DNA single-strand breaks, after 2-hr MCAO. Consequently, harmful DNA damage-dependent signaling events, including NAD depletion, p53 activation, and mitochondrial translocation of PUMA and NOXA, were reduced during post-ischemic reperfusion in hypothermia-treated brains. These results suggest that the attenuation of oxidative DNA damage and DNA damage-triggered pro-death signaling events may be an important mechanism underlying the neuroprotective effect of mild hypothermia against ischemic brain injury.
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PMID:Mild hypothermia diminishes oxidative DNA damage and pro-death signaling events after cerebral ischemia: a mechanism for neuroprotection. 1712 18