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2 3 dihydroxybenzoic acid/hemorragia

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Time course of production of hydroxyl free radical after subarachnoid hemorrhage in dogs.

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Vasospasm after subarachnoid hemorrhage (SAH) is associated with lipid peroxidation. However, lipid peroxides increase in a delayed fashion after SAH and may be a byproduct of but not a cause of vasospasm. This study correlated vasospasm with hydroxyl free radical and lipid peroxide levels. 24 dogs

U74389G prevents vasospasm after subarachnoid hemorrhage in dogs.

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OBJECTIVE Oxygen-derived free radicals may contribute to vasospasm after the rupture of an intracranial aneurysm through direct vasoconstricting effects occurring within the arterial wall or, secondarily, by causing lipid peroxidation in the subarachnoid erythrocytes with secondary induction of

Oxidative stress causes nuclear factor-kappaB activation in acute hypovolemic hemorrhagic shock.

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Nuclear Factor kappaB (NFkappaB) is an ubiquitous rapid response transcription factor involved in inflammatory reactions and exerts its action by expressing cytokines, chemokines, and cell adhesion molecules. We investigated the role of NF-kappaB in acute hypovolemic hemorrhagic (Hem) shock. Hem

Melatonin reduces acute lung inflammation, edema, and hemorrhage in heatstroke rats.

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OBJECTIVE To assess the therapeutic effect of melatonin on heat-induced acute lung inflammation and injury in rats. METHODS Heatstroke was induced by exposing anesthetized rats to heat stress (36 °C, 100 min). Rats were treated with vehicle or melatonin (0.2, 1, 5 mg/kg) by intravenous
Blood-borne biomarkers are a mainstay of diagnosis and follow-up in many diseases. For stroke, however, no reliable biomarkers have thus far been identified. To remedy this situation, we investigated the usefulness of a modified in situ isolated brain perfusion (IBP) technique for screening

Oxyradical generation after resuscitation of hemorrhagic shock with blood or stroma-free hemoglobin solution.

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Hypovolemic states are characterized by inadequate tissue perfusion; when this state is reversed, the reintroduction of oxygen is accompanied by the excess generation of oxyradicals and these, in turn, may cause "reperfusion injury" in susceptible tissues. When hemoglobin solution is used to
HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the

Complete sequence of virulence plasmid pJM1 from the marine fish pathogen Vibrio anguillarum strain 775.

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The virulence plasmid pJM1 enables the fish pathogen Vibrio anguillarum, a gram-negative polarly flagellated comma-shaped rod bacterium, to cause a highly fatal hemorrhagic septicemic disease in salmonids and other fishes, leading to epizootics throughout the world. The pJM1 plasmid
Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry imaging (MALDI-TOF-MSI) has received considerable attention in recent years since it allows molecular mapping of diverse bimolecular in animal/plant tissue sections, although some barriers still exist in absolute

Mitochondrial generation of reactive oxygen species after brain ischemia in the rat.

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OBJECTIVE Brain mitochondria have a substantial capacity to generate reactive oxygen species after ischemia when the components of the respiratory chain are reduced and molecular oxygen is present. We tested the hypothesis that brain mitochondria in vivo produce reactive oxygen species after

Methamphetamine-induced striatal dopamine release, behavior changes and neurotoxicity in BALB/c mice.

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The behaviors associated with the neurotoxic effects of methamphetamine were evaluated in BALB/c mice. Hyperthermia and behavioral observations were measured 60 min after each subcutaneous injection of methamphetamine (4x4 or 8 mg/kg) or saline, each given 2 h apart. The behavioral observations

Postischemic hypothermia inhibits the generation of hydroxyl radical following transient forebrain ischemia in rats.

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A small reduction of body temperature during reperfusion following cerebral ischemia has been known to ameliorate neuronal injury. However, the mechanisms underlying postischemic hypothermia-induced neuroprotection are poorly understood. The burst of reactive oxygen species (ROS) formation that

Brain temperature alters hydroxyl radical production during cerebral ischemia/reperfusion in rats.

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Selective neuronal cell death in the CA1 pyramidal cells of the hippocampus and neurons of the dorsolateral striatum as a consequence of brain ischemia/reperfusion (IR) can be ameliorated with brain hypothermia. Since postischemic injury is mediated partially by chemical production of reactive
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