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Sida 1 från 46 resultat
Enhanced ornithine decarboxylase activity is associated with attenuated rate of damage evolution and reduction of infarct volume in transient middle cerebral artery occlusion in the rat.
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Ornithine decarboxylase (ODC) transgenic and alpha-difluoromethyl ornithine (DFMO)-treated rats were exposed to transient middle cerebral occlusion (MCAO) to examine the role of intraischaemic ODC-activity on the evolution of ischaemia-reperfusion damage. Magnetic resonance imaging (MRI) data show
[The serum Ornithine-Carbamyl-Transferase activity after myocardial infarction].
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[On the behavior of ornithine carbamoyl-transferase (OCT) in myocardial infarct].
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Liver cell affection in myocardial infarction revealed by elevated serum ornithine carbamoyl transferase.
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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,
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
Akt and Erk1/2 activate the ornithine decarboxylase/polyamine system in cardioprotective ischemic preconditioning in rats: the role of mitochondrial permeability transition pores.
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Ornithine decarboxylase (ODC) is the first rate-limiting enzyme in polyamine biosynthesis, which is essential for cell survival. We hypothesized that the ODC/polyamine system is involved in ischemic preconditioning (IPC)-mediated cardioprotection through the activation of Erk1/2 and Akt and through
Amino acid concentrations in cerebrospinal fluid in presenile and senile dementia of Alzheimer type and multi-infarct dementia.
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Free amino acid levels were measured in cerebrospinal fluid (CSF) from demented patients (D, n = 30) suffering from presenile and senile dementia of Alzheimer type (PDAT, n = 7; SDAT, n = 9), multi-infarct dementia (MID, n = 14) and a reference sample group consisting of young neurotic patients (R,
A female carrier of ornithine carbamoyltransferase deficiency masquerading as attention deficit-hyperactivity disorder.
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Many females who are heterozygous for ornithine carbamoyltransferase (OTC) deficiency are asymptomatic or intermittently symptomatic with great phenotypic variability. Therefore, the diagnosis of this condition is occasionally a challenge and is often delayed. A 12-year-old girl who was initially
Involvement of the ornithine decarboxylase/polyamine system in precondition-induced cardioprotection through an interaction with PKC in rat hearts.
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Polyamines (putrescine, spermidine, and spermine) play an essential role in cell growth, differentiation, and apoptosis. Protein kinase C (PKC) stimulates polyamine biosynthesis through the induction of ornithine decarboxylase (ODC), a rate-limiting enzyme in polyamine biosynthesis. Activation of
Urea cycle defect: a case with MR and CT findings resembling infarct.
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A 2 1/2 year old girl was admitted to the hospital because of recurrent vomitting, impaired consciousness, and hyperammonemia. MR and CT findings resembled an infarct, but she was found to have a defect in the urea cycle, partial ornithine transcarbamylase deficiency.
Inherited metabolic disorders and cerebral infarction.
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The association of genetic factors and cerebral infarction (CI) has long been established. A positive family history alone is a recognized risk factor for CI and vascular events in general. However, there are certain inherited conditions that further increase the risk of stroke. These conditions are
DFMO reduces cortical infarct volume after middle cerebral artery occlusion in the rat.
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Ornithine decarboxylase (ODC), a key enzyme in polyamine biosynthesis, is induced in ischemic tissue and may mediate vasogenic edema and delayed neuronal death. We determined the effects of alpha-difluoromethylornithine (DFMO), a specific inhibitor of ODC, on infarct size and ODC activity in a rat
Differing effects of alpha-difluoromethylornithine and CGP 40116 on polyamine levels and infarct volume in a rat model of focal cerebral ischaemia.
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Focal cerebral ischaemia was induced in rats by occlusion of the left middle cerebral artery. Two days later, infarct volume was determined by magnetic resonance imaging and the concentrations of the polyamines putrescine (PU), spermine and spermidine by HPLC. In control (occluded) animals, PU
Decrease in myocardial polyamine concentration in rats with myocardial infarction.
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Cardiac polyamines are thought to protect the myocardium against harmful stimuli and to be regulated by sympathetic nerve activation. In the present study, polyamines concentrations in non-infarcted myocardium were investigated. Myocardial polyamines contents decreased significantly in the
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