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Mitochondrial Encephalomyopathy Lactic Acidosis and Stroke-Like Episodes (MELAS): A Case Report and Critical Reappraisal of Treatment Options.

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OBJECTIVE Stroke-like episodes signal progression and significant disability in the mitochondrial encephalomyopathy lactic acidosis and stroke-like episodes syndrome. Arginine is widely used as a treatment for stroke-like episode, although there is little evidence for this intervention. We discuss

Noble gas xenon is a novel adenosine triphosphate-sensitive potassium channel opener.

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BACKGROUND Adenosine triphosphate-sensitive potassium (KATP) channels in brain are involved in neuroprotective mechanisms. Pharmacologic activation of these channels is seen as beneficial, but clinical exploitation by using classic K channel openers is hampered by their inability to cross the

Inducible glutamate oxaloacetate transaminase as a therapeutic target against ischemic stroke.

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CONCLUSIONS Glutamate serves multi-faceted (patho)physiological functions in the central nervous system as the most abundant excitatory neurotransmitter and under pathological conditions as a potent neurotoxin. Regarding the latter, elevated extracellular glutamate is known to play a central role in

Apolipoprotein-E controls adenosine triphosphate-binding cassette transporters ABCB1 and ABCC1 on cerebral microvessels after methamphetamine intoxication.

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OBJECTIVE Methamphetamine is a powerful addictive, which has been associated with ischemic stroke and brain hemorrhage in humans. Whether and how methamphetamine influences the expression of tight junctions and adenosine triphosphate-binding cassette transporters, which have previously been shown to

Hyperthermia depletes adenosine triphosphate and decreases glutamate uptake in rat hippocampal slices.

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The central nervous system is especially vulnerable to hyperthermia-induced dysfunction, yet the mechanism for this susceptibility is poorly understood. High levels of adenosine triphosphate are necessary to maintain normal re-uptake of glutamate and aspartate, the major excitatory amino acids, by

Effects of prostaglandin E1 on left ventricular performance in dogs; comparisons with trinitroglycerin and adenosine triphosphate.

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To examine the cardiovascular response to prostaglandin E1 infusion, we observed hemodynamic changes including left ventricular diameter (an ultrasonic crystal pair) during PGE(1)-induced hypotension in anesthetized open-chest dogs. Left ventricular contractility was assessed primarily by measuring

CeeTox™ Analysis of CNB-001 a Novel Curcumin-Based Neurotrophic/Neuroprotective Lead Compound to Treat Stroke: Comparison with NXY-059 and Radicut.

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In the present study, we used a comprehensive cellular toxicity (CeeTox) analysis panel to determine the toxicity profile for CNB-001 [4-((1E)-2-(5-(4-hydroxy-3-methoxystyryl-)-1-phenyl-1H-pyrazoyl-3-yl)vinyl)-2-methoxy-phenol)], which is a hybrid molecule created by combining cyclohexyl bisphenol

Calcium-channel blockers: effects on cerebral blood flow and potential uses for acute stroke.

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Current research suggests that ischemia induces a massive shift of calcium from the extracellular fluid to the intracellular space. This is associated with a precipitous decrease in the concentration of adenosine triphosphate, the energy source required to drive the ion pumps of the calcium channels

Platelet ultrastructure and secretion in acute ischemic stroke.

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We used transmission electron microscopy to count the organelles (dense bodies, alpha granules, and mitochondria) contained within platelets from 11 acute ischemic stroke patients and 12 healthy controls. We randomly selected for evaluation 25 platelet profiles in ultrathin sections cut from three

The association between early neurological deterioration and whole blood purine concentration during acute stroke.

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Early neurological deterioration (END) is common after stroke. Prediction could identify patients requiring additional monitoring and intervention. Purines, breakdown products of adenosine triphosphate which accumulate during acute hypoxia, may reflect the subclinical presence of

Repression of adenosine triphosphate-binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury.

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The adenosine triphosphate-binding cassette efflux transporter ABCG2, which is located in the blood-brain barrier limits the entry of endogenous compounds and xenobiotics into the brain, and its expression and activity are regulated by estrogen. This study was aimed to define the role of ABCG2 in

Fluctuating hearing loss, episodic headache, and stroke with platelet hyperaggregability: coexistence of auditory neuropathy and cochlear hearing loss.

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We encountered a 10-year-old girl with fluctuating sensorineural hearing loss, episodic headache, and white matter stroke. Strenuous exercise, febrile illness, and general anesthesia all temporarily worsened hearing. Audiologic findings were asymmetric: left-sided retrocochlear dysfunction

The forces applied by cilia depend linearly on their frequency due to constant geometry of the effective stroke.

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Mucus propelling cilia are excitable by many stimulants, and have been shown to increase their beating frequency up to threefold, by physiological extracellular stimulants, such as adenosine-triphosphate, acetylcholine, and others. This is thought to represent the evolutionary adaptation of

Biochemical studies: failure of tissue adenosine triphosphate levels to predict recovery of contractile function after controlled reperfusion.

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This study tests the hypotheses that postischemic adenosine triphosphate levels are unreliable predictors of functional recovery, myocardial adenosine triphosphate concentration of less than 2 mumol/gm does not indicate irreversible damage, mitochondrial adenosine triphosphate generating capacity

The modulation of hepatic adenosine triphosphate and inflammation by eicosapentaenoic acid during severe fibrotic progression in the SHRSP5/Dmcr rat model.

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OBJECTIVE Eicosapentaenoic acid (EPA) can ameliorate certain liver lesions involved in non-alcoholic steatohepatitis (NASH). A previous study has found that stroke-prone spontaneously hypertensive 5/Dmcr (SHRSP5/Dmcr) rats fed a high fat-cholesterol (HFC) diet developed fibrotic steatohepatitis with

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