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peroxidase/hémorragie

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Glutathione peroxidase 1 C593T polymorphism is associated with lobar intracerebral hemorrhage.

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BACKGROUND Oxidative stress plays an important role in vascular pathology and contributes to the pathophysiology of primary intracerebral hemorrhage (PICH). Glutathione peroxidase 1 (GPX1) is a key enzyme of the antioxidant system. Here, we investigated whether a functional C593T polymorphism of

Vasospasm after subarachnoid hemorrhage in haptoglobin 2-2 mice can be prevented with a glutathione peroxidase mimetic.

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Vasospasm after subarachnoid hemorrhage (SAH) is attributable to inflammation and oxidative stress associated with extracellular hemoglobin (Hb). Haptoglobin (Hp) binds free Hb and the Hp-Hb complex is cleared by macrophages, and the Hp-2 isoform of Hp is associated with more oxidative stress and

Glutathione peroxidase and subarachnoid hemorrhage: implications for the role of oxidative stress in cerebral vasospasm.

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OBJECTIVE Worldwide, cerebral vasospasm after subarachnoid hemorrhage (SAH) has an estimated morbidity and mortality of 1.2 million annually. While it has long been suspected that reactive oxygen species play a major role in the etiology of cerebral vasospasm after SAH, promising results in animal
Titers of hemorrhagic fever with renal syndrome virus were estimated by counting foci stained with peroxidase-antiperoxidase or by using immunofluorescence methods. Foci stained with PAP were clearer and easier to count. The peroxidase-antiperoxidase method showed a linear relationship between virus
BHK-21 cells infected with dengue virus type 1 were stained by a newly developed 4 step PAP (peroxidase-anti-peroxidase) technique using sera from patients with dengue hemorrhagic fever as anti-virus antibody. The intensity of staining of the sera was proportional to the hemagglutination inhibition
BACKGROUND Malondialdehyde (MDA) is a marker of lipid peroxidation. Glutathione peroxidase (GPX) and superoxide dismutase (SOD) are the main enzymes responsible for the detoxification of superoxide anion. The aim was to assess whether serum MDA, erythrocyte GPX, and erythrocyte SOD levels altered

Neuroprotective role of glutathione peroxidase 4 in experimental subarachnoid hemorrhage models

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Background and purpose: Early brain injury is an essential pathological process after subarachnoid hemorrhage (SAH), with many cell death modalities. Ferroptosis is a newly discovered regulated cell death caused by the iron-dependent
We determined the differential expression levels of proteins in peripheral blood mononuclear cells of patients with dengue fever (DF) and dengue hemorrhagic fever (DHF). Proteins were subjected to two-dimensional electrophoresis, mass spectrometry and Western blot analysis. We identified 8 proteins

Glutathione peroxidase 4 participates in secondary brain injury through mediating ferroptosis in a rat model of intracerebral hemorrhage.

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Oxidative stress plays an important role in secondary brain injury (SBI) after intracerebral hemorrhage (ICH), but the underling mechanism has not been fully elucidated. Recently, the antioxidant enzyme glutathione peroxidase 4 (GPX4), has attracted increasing attention due to its ability to degrade

Barrier disruption in the major cerebral arteries following experimental subarachnoid hemorrhage.

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The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the major cerebral arteries were studied in 20 normotensive dogs. Horseradish peroxidase (HRP) was given intravenously before the animals were sacrificed to assess the integrity of the barrier. Transient
Intracerebral hemorrhage (ICH) is a subtype of stroke with high disability and mortality. Dexmedetomidine (Dex) has been shown to provide neuroprotection in several neurological diseases. The aim of present study was to investigate the effects of Dex on ICH-induced neurological

Prevalence of occult gastrointestinal bleeding in celiac disease.

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OBJECTIVE By using colorimetric tests, reports have indicated that occult gastrointestinal bleeding is common in celiac disease. These results suggest that bleeding is a significant contributor to iron deficiency in this disorder and imply a significant inflammatory hemorrhagic component. Both these
SS31 has been shown to have neuroprotective effects in a number of neurological degenerative diseases. However, the mechanisms and its role of neuroprotection after subarachnoid hemorrhage (SAH) remain unexplored. The aim of the present study is to evaluate the neuroprotective effects

Astragaloside IV alleviates early brain injury following experimental subarachnoid hemorrhage in rats.

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Astragaloside IV, one of the main effective components isolated from Astragalus membranaceus, has multiple neuroprotective properties, while the effects of astragaloside IV on the attenuation of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) and its possible mechanisms are unknown.
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