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Mitochondrial inner membrane depolarization is one of the major alterations observed in apoptotic cells.
Membrane depolarization is mediated by the mitochondrial permeability transition pore.
Abnormal motor nerve membrane depolarization is a general finding in critically ill patients and is correlated with illness severity.
Abnormal motor nerve membrane depolarization is a general finding in critically ill patients whereas voltage-gated sodium channel dysfunction is a characteristic of CIP patients.
In the cortex, the initial membrane depolarization is associated with a large efflux of potassium, influx of sodium and calcium and release of glutamate.
This study tested the hypothesis that membrane depolarization is a general feature of critically ill patients, whereas inactivation of voltage-gated sodium channels is related to loss of membrane excitability in CIP patients, developing muscle weakness.
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The degree of mitochondrial membrane depolarization was calculated as the ratio of depolarized (green) to polarized (red) signals from the dot plots.
The magnitude of the membrane depolarization was positively correlated with the amplitude of the stimulus-evoked EPSP.
The OXT-induced membrane depolarization was not observed in CA3 pyramidal neurons from Oxtr −/− mice (0.98 ± 0.21 mV, n = 10; Fig. 7d, e) and was prevented by the selective OXTR antagonist L-371257 (1 μM, Supplementary Fig. 5a, b), indicating that such action is mediated by the OXTR.
DNA damage was observed only in cancer cells whereas membrane depolarization was observed in normal cells.
On the other hand, faulty membrane depolarization was reported in various tissues of critically ill patients including muscle fibers, monocytes, and platelet mitochondria [6 8].
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