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decarboxylase/stroke
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 64 tuloksia
Mevalonate pyrophosphate decarboxylase in stroke-prone spontaneously hypertensive rat is reduced from the age of two weeks.
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We carried out a comparison of tissue distribution of mevalonate pyrophosphate decarboxylase (MPD) between normotensive Wistar Kyoto rat (WKY) and stroke-prone spontaneously hypertensive rat (SHRSP) using Western blotting. However, there was no difference in tissue distribution of MPD between WKY
[Comparison of biochemical properties and protein level of mevalonate pyrophosphate decarboxylase between stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats].
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The spontaneously hypertensive rat (stroke-prone) (SHRSP) experiences severe hypertension and cerebral hemorrhage. The serum cholesterol level in this rat is lower than that in the normotensive Wistar-Kyoto rat. Epidemiologic studies have indicated a negative association between serum cholesterol
Involvement of microRNA214 and transcriptional regulation in reductions in mevalonate pyrophosphate decarboxylase mRNA levels in stroke-prone spontaneously hypertensive rat livers.
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Hypocholesterolemia has been epidemiologically identified as one of the causes of stroke (cerebral hemorrhage). We previously reported that lower protein levels of mevalonate pyrophosphate decarboxylase (MPD), which is responsible for reducing serum cholesterol levels in stroke-prone spontaneously
Comparison of subcellular distribution of mevalonate pyrophosphate decarboxylase between stroke-prone spontaneously hypertensive rat and Wistar Kyoto rat.
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We previously reported that the lower activity of mevalonate pyrophosphate decarboxylase (MPD) was caused by the reduced amount of this enzyme in stroke-prone spontaneously hypertensive rat (SHRSP) by immunoblot analysis using 20,000 x g supernatant containing cytosol and microsomes. A recent study
Lower mevalonate pyrophosphate decarboxylase activity is caused by the reduced amount of enzyme in stroke-prone spontaneously hypertensive rat.
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Spontaneously hypertensive rat (stroke-prone) (SHRSP) has a low serum cholesterol level as compared with the normotensive Wistar Kyoto rat (WKY). We previously indicated that the lower activity of mevalonate pyrophosphate decarboxylase (MPD) was responsible for the reduced cholesterol biosynthesis
Liver mevalonate 5-pyrophosphate decarboxylase is responsible for reduced serum cholesterol in stroke-prone spontaneously hypertensive rat.
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Spontaneously hypertensive rat (stroke-prone) (SHRSP) has an interestingly low serum cholesterol level due to a reduced biosynthesis of cholesterol in the liver (Iritani, N., Fukuda, E., Nara, Y., and Yamori, Y. (1977) Atherosclerosis 28, 217-222). In this study, we examined the mechanism underlying
Nifedipine and nimodipine competitively inhibit uridine kinase and orotidine-phosphate decarboxylase: theoretical relevance to poor outcome in stroke.
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Nifedipine and nimodipine, dihydropyridine calcium channel blockers, are commonly used as antihypertensive and antianginal agents in patients at risk for stroke. At least one stroke trial suggests that patients receiving calcium channel blockers at the time of an acute stroke have worse outcomes
Neuroprotective role of ornithine decarboxylase activation in transient focal cerebral ischaemia: a study using ornithine decarboxylase-overexpressing transgenic rats.
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Nuclear magnetic resonance imaging (MRI) was used to study dynamics of maturation and the size of ischaemic stroke lesions in rats with greatly increased activity of ornithine decarboxylase (ODC). Syngenic rats, either with or without chronic pre-ischaemic treatment with an ODC inhibitor,
Brain neurons express ornithine decarboxylase-activating antizyme inhibitor 2 with accumulation in Alzheimer's disease.
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Polyamines are small cationic molecules that in adult brain are connected to neuronal signaling by regulating inward-rectifier K(+)-channels and different glutamate receptors. Antizyme inhibitors (AZINs) regulate the cellular uptake of polyamines and activate ornithine decarboxylase (ODC), the
Evidence for nuclear ornithine decarboxylase activity in different brain regions of the male rat.
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The subcellular distribution of ornithine decarboxylating activity in nucleus caudatus putamen, hippocampus, parietal cerebral cortex, cerebellum and hypothalamus of male rat brain has been investigated. The 7000 g supernatant (cytosolic fraction), the 7000 g sediment and the 700 g sediment (nuclear
Transgenic rats as models for studying the role of ornithine decarboxylase expression in permanent middle cerebral artery occlusion.
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OBJECTIVE
Cerebral ischemia causes activation of ornithine decarboxylase (ODC) gene and subsequent accumulation of putrescine, which might either directly or indirectly affect the outcome of cerebral infarct. We developed a transgenic rat overexpressing human ODC, which was used to explore the
Neuroprotective actions of FK506 in experimental stroke: in vivo evidence against an antiexcitotoxic mechanism.
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The cellular mechanisms underlying the neuroprotective action of the immunosuppressant FK506 in experimental stroke remain uncertain, although in vitro studies have implicated an antiexcitotoxic action involving nitric oxide and calcineurin. The present in vivo study demonstrates that
Abolished perineuronal nets and altered parvalbumin-immunoreactivity in the nucleus reticularis thalami of wildtype and 3xTg mice after experimental stroke.
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Treatment strategies for ischemic stroke are still limited, since numerous attempts were successful only in preclinical research but failed under clinical condition. To overcome this translational roadblock, clinical relevant stroke models should consider co-morbidities, age-related effects and the
Effect of NC-1100 [1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl) ethanol dihydrochloride] on gamma-aminobutyric acid (GABA) metabolism in rat brain: analysis using stroke-prone spontaneously hypertensive rat.
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Effects of oral administration of NC-1100 on the metabolism of neuroactive amino acids in rat brain were studied using stroke-prone spontaneously hypertensive (SHR-SP) and Wistar Kyoto rats. The repeated administration of NC-1100 induced a significant increase of gamma-aminobutyric acid (GABA)
Purification and characterization of two mevalonate pyrophosphate decarboxylases from rat liver: a novel molecular species of 37 kDa.
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The biosynthesis of cholesterol is regulated mainly by HMG-CoA reductase, however, recent studies indicated the pivotal role of another enzyme in cholesterol homeostasis. A previous report showed a marked decrease in the activity of mevalonate pyrophosphate decarboxylase (MPD) in stroke-prone
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