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glutamate dehydrogenase/мождани удар

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ЧланциКлиничка испитивањаПатенти
6 резултати

Glutamate Dehydrogenase as a Neuroprotective Target Against Neurodegeneration.

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Regulation of glutamate metabolism via glutamate dehydrogenase (GDH) might be the promising therapeutic approach for treating neurodegenerative disorders. In the central nervous system, glutamate functions both as a major excitatory neurotransmitter and as a key intermediate metabolite for neurons.

Neuroprotection by lowering cholesterol: a decrease in membrane cholesterol content reduces transporter-mediated glutamate release from brain nerve terminals.

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BACKGROUND In our earlier work, a reduction of cholesterol content increased the extracellular glutamate level in rat brain nerve terminals (synaptosomes) that was a result of the lack of transporter-mediated glutamate uptake. The aim of this study was to assess transporter-mediated release of

An amperometric glutamate biosensor for monitoring glutamate release from brain nerve terminals and in blood plasma.

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An excess of the excitatory neurotransmitter, glutamate, in the synaptic cleft during hypoxia/ischemia provokes development of neurotoxicity and originates from the reversal of Na+-dependent glutamate transporters located in the plasma membrane of presynaptic brain nerve terminals. Here, we have

Transduction of enzyme-ligand binding energy into catalytic driving force.

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We propose a testable general mechanism by which ligand binding energy can be used to drive a catalytic step in an enzyme catalyzed reaction or to do other forms of work involving protein molecules. This energy transduction theory is based on our finding of the widespread occurrence of ligand

Combined Gene Therapy to Reduce the Neuronal Damage in the Mouse Model of Focal Ischemic Injury.

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Research into stroke is driven by frustration over the limited available therapeutics. Targeting a single aspect of this multifactorial disease contributes to the therapeutic boundaries. To overcome this, we devised a novel multifactorial-cocktail treatment, using lentiviruses encoding excitatory

Effects of exercise-training on cardiac performance and muscle enzymes in rainbow trout,Oncorhynchus mykiss.

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Rainbow trout,Oncorhynchus mykiss, were exercise-trained for 18 hours per day over 28 days at water velocities up to 60% of their measured Ucrit. Anin situ perfused heart preparation was used to compare maximum cardiac performance between control and trained fish. Trained fish had a larger stroke
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