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encephalitis/hypoxia
Veza se sprema u međuspremnik
Stranica 1 iz 125 rezultatima
Possible role of local hypoxia in the de novo formation of dural and osteodural arteriovenous fistulas after encephalitis. A case report.
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A rare case of de novo formation of dural and osteodural arteriovenous fistulas after encephalitis is presented. We review and discuss the etiological angiogenetic factors and processes in intracranial dural arteriovenous fistulas formation. Local tissue hypoxia may have played a role in the initial
Characterization of Brain Inflammation, Apoptosis, Hypoxia, Blood-Brain Barrier Integrity and Metabolism in Venezuelan Equine Encephalitis Virus (VEEV TC-83) Exposed Mice by In Vivo Positron Emission Tomography Imaging.
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Traditional pathogenesis studies of alphaviruses involves monitoring survival, viremia, and pathogen dissemination via serial necropsies; however, molecular imaging shifts this paradigm and provides a dynamic assessment of pathogen infection. Positron emission tomography (PET) with PET tracers
Repetitive administration of acetylcholine receptor agonist rescues brain inflammation and brain damage after hypoxia-ischemia in newborn rat.
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OBJECTIVE
We examined the effect of repetitive administration of acetylcholine receptor agonist (carbachol) on brain damage and microglial accumulation in three brain regions after hypoxia-ischemia (HI) in newborn rat.
METHODS
Seven-day-old Wistar rats were divided into two groups, one receiving a
Nitric oxide, hypoxia and brain inflammation.
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NO (nitric oxide) acutely and potently inhibits mitochondrial cytochrome oxidase in competition with oxygen, thereby raising the apparent K(M) for oxygen of mitochondria and neurons into the physiological or pathological range. We find that NO from an NO donor or glial inducible NOS (nitric oxide
[Organic bases of the difficult child. II. Mechanical injury and anoxia of the brain, encephalitis].
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[Respiratory syncytial virus brainstem encephalitis in a 7-year-old boy].
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The literature reports that neurological complications of childhood respiratory diseases due to respiratory syncytial virus (RSV) fluctuate between 1 and 40% of cases. They mostly involve central apnea - often the first symptom of infection - anoxia, and ischemic brain damage due to severe sudden
Neuropathological studies of patients with possible non-herpetic acute limbic encephalitis and so-called acute juvenile female non-herpetic encephalitis.
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OBJECTIVE
This study was to clarify the neuropathological findings of non-herpetic acute limbic encephalitis (NHALE) and so-called acute juvenile female non-herpetic encephalitis (AJFNHE).
METHODS
We examined three rare autopsied cases consisting of probable one NHALE and two AJFNHLE. For
MR and CT imaging patterns in post-varicella encephalitis.
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The aim of the investigation was to determine the patterns of cerebral involvement on computed tomography (CT) and magnetic resonance (MR) imaging in post-varicella encephalitis. Four children between the ages of 2 and 11 years presented over a 5-year period with a diagnosis of post-varicella
Production of macrophage inflammatory protein-2 following hypoxia/reoxygenation in glial cells.
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Polymorphonuclear neutrophils (PMNs) are known to mediate brain inflammation following hypoxia/reoxygenation (H/R), but the precise mechanisms leading to PMN recruitment are undefined. The alpha-chemokine macrophage inflammatory protein-2 (MIP-2) has specificity for the recruitment of PMNs. In this
A case of antirabies inoculation encephalitis with a long clinical course.
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In 1950, a 24-year-old man developed gait disturbance, incontinence of urine and increasing lethargy a week after a course of antirabies vaccination. He was diagnosed as having post-rabies vaccination encephalitis and had been in hospital for 37 years before he died in 1987. This is one of the rare
Who's failure? encephalitis kills!
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Encephalitis continues to be one of the most dreaded diagnoses because a high rate of morbidity and mortality are accepted even before starting the treatment. Most encephalitis cases occur in rural areas due to poor environmental sanitation, high-vector density, shortage of protected water supplies
[Brain thermo-pooling is the major problem in pediatric influenza encephalitis].
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The prognosis of pediatric encephalitides, such as infantile influenza encephalitis, is still poor because of the rapid progression, severe brain edema, selective bilateral basal ganglia necrosis, and a poor immune function, the mechanism of which is still unknown. Especially, little is known about
Avian pox infection with secondary Candida albicans encephalitis in a juvenile golden eagle (Aquila chrysaetos).
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Abstract: A juvenile golden eagle (Aquila chrysaetos) was presented with proliferative epithelial lesions, consistent with avian poxvirus infection, around the eyes, on commissures of the beak, and on both feet. Despite treatment, the eagle declined clinically, and, 15 days after presentation, the
The anti-inflammatory agent N-acetyl cysteine exacerbates endotoxin-induced hypoxemia and hypotension and induces polycythemia in the ovine fetus.
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BACKGROUND
Lipopolysaccharide (LPS) delivered acutely to the ovine fetus induces cerebral white matter injury and brain inflammation. N-acetyl cysteine (NAC) is potentially neuroprotective as it blocks the production of inflammatory cytokines and increases glutathione levels; however, it is unknown
Perinatal hypoxia-ischemia reduces α 7 nicotinic receptor expression and selective α 7 nicotinic receptor stimulation suppresses inflammation and promotes microglial Mox phenotype.
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Inflammation plays a central role in neonatal brain injury. During brain inflammation the resident macrophages of the brain, the microglia cells, are rapidly activated. In the periphery, α 7 nicotinic acetylcholine receptors ( α 7R) present on macrophages can regulate inflammation by suppressing
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