cytochrome c/stroke

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MiR-34a Interacts with Cytochrome c and Shapes Stroke Outcomes.

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Blood-brain barrier (BBB) dysfunction occurs in cerebrovascular diseases and neurodegenerative disorders such as stroke. Opening of the BBB during a stroke has a negative impact on acute outcomes. We have recently demonstrated that miR-34a regulates the BBB by targeting cytochrome c (CYC) in vitro.

Retraction statement: Dynamics of Cytochrome C Oxidase Activity in Acute Ischemic Stroke' by Selaković, V.M., Jovanović, M.D., Mihajlović, R.R. and Radenović, L.L.J.

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The above article from Acta Neurologica Scandinavica, published online on 7 April 2005 in Wiley Online Library (wileyonlinelibrary.com) and in Volume 111, pp. 329-332, has been retracted by agreement between the journal Editor in Chief, Professor Elinor Ben-Menachem, and John Wiley & Sons Ltd. The

High cytochrome c oxidase expression links to severe skeletal energy failure by (31)P-MRS spectroscopy in mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.

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OBJECTIVE The purpose of this study was to evaluate the energy metabolism and mitochondrial function in skeletal muscle from patients with Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) or chronic progressive external ophthalmoplegia (CPEO) using phosphorus

[A case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) with progressive cytochrome c oxidase deficiency].

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We report a 9 year-old boy with MELAS. High dosed oral thiamine administration and high fat diet induced remarkable neurological and biochemical improvement. His mother had episodic headaches and hemiplegia, probably MELAS. He complained muscle weakness and repeated episodes of vomiting started from

Glutathione peroxidase overexpression inhibits cytochrome C release and proapoptotic mediators to protect neurons from experimental stroke.

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OBJECTIVE Ischemic injury and reperfusion increases superoxide (O2-) production and reduces the ability of neurons to scavenge free radicals, leading to the release of cytochrome c and apoptosis. Here we test whether overexpression with the use of gene therapy of the antioxidant glutathione

Bcl-2 overexpression protects against neuron loss within the ischemic margin following experimental stroke and inhibits cytochrome c translocation and caspase-3 activity.

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Bcl-2 protects against both apoptotic and necrotic death induced by several cerebral insults. We and others have previously demonstrated that defective herpes simplex virus vectors expressing Bcl-2 protect against various insults in vitro and in vivo, including cerebral ischemia. Because the infarct

Mild hypothermia attenuates cytochrome c release but does not alter Bcl-2 expression or caspase activation after experimental stroke.

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Mild hypothermia protects the brain from ischemia, but the underlying mechanisms of this effect are not well known. The authors previously found that hypothermia reduces the density of apoptotic cells, but it is not certain whether temperature alters associated biochemical events. Mitochondrial

Dynamics of cytochrome c oxidase activity in acute ischemic stroke.

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We have investigated the dynamics of cytochrome c oxidase (COX) activity in the cerebrospinal fluid (CSF) and the erythrocyte haemolysate (EH) in 85 patients suffering from brain infarction (BI), reversible (RIA), or transient (TIA) ischemic attack from the perspective of mitochondrial affection in

[Cytochrome C in the treatment of patients in the acute stage of ischemic strokes].

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Mechanism of proton translocation by cytochrome c oxidase: a new four-stroke histidine cycle.

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Proton exit channels in bovine cytochrome c oxidase.

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Cytochrome c oxidase (CcO) is the terminal transmembrane enzyme of the respiratory electron transport chain in aerobic cells. It catalyzes the reduction of oxygen to water and utilizes the free energy of the reduction reaction for proton pumping, a process which results in a membrane electrochemical

TAT-Ngn2 Enhances Cognitive Function Recovery and Regulates Caspase-Dependent and Mitochondrial Apoptotic Pathways After Experimental Stroke.

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Neurogenin-2 (Ngn2) is a basic helix-loop-helix (bHLH) transcription factor that contributes to the identification and specification of neuronal fate during neurogenesis. In our previous study, we found that Ngn2 plays an important role in alleviating neuronal apoptosis, which may be viewed as an

Potential Role of Cytochrome c and Tryptase in Psoriasis and Psoriatic Arthritis Pathogenesis: Focus on Resistance to Apoptosis and Oxidative Stress.

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Psoriasis (PsO) is an autoimmune disease characterized by keratinocyte proliferation, chronic inflammation and mast cell activation. Up to 42% of patients with PsO may present psoriatic arthritis (PsA). PsO and PsA share common pathophysiological mechanisms: keratinocytes and fibroblast-like

Platelet mitochondrial evaluation during cytochrome c and dichloroacetate treatments of MELAS.

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We hypothesized that serial changes in platelet (PLT) mitochondrial enzyme (ME) activities might correspond to the effects of medications for mitochondrial encephalomyopathy and stroke-like episodes (MELAS). Cytochrome c and sodium dichloroacetate (DCA) were given to a 7-year-old girl with MELAS who

Neuroprotective Effects of Purple Sweet Potato Balinese Cultivar in Wistar Rats With Ischemic Stroke.

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BACKGROUND

Purple sweet potato (Ipomoea Batatas L.) is one of the sources for anthocyanin, which promotes the health through antioxidant, anti-inflammatory, anti-cancer, neuroprotection, and anti-apoptosis activities. Oxidative stress has been shown to be the cause of

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