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neurodegenerative diseases/edema
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 340 risultati
Thrombin inhibition attenuates neurodegeneration and cerebral edema formation following transient forebrain ischemia.
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The disturbance of microcirculation following cerebral ischemia leads to an enlargement of cerebral infarct volume. Endogenous thrombin may play a role in this disturbance of microcirculation following cerebral ischemia. Therefore, the inhibition of thrombin may improve neurodegeneration and the
Small interfering RNA-mediated xCT silencing in gliomas inhibits neurodegeneration and alleviates brain edema.
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Neurodegeneration and brain edema are hallmarks of human malignant brain tumors. Here we show that genetic or pharmacological inhibition of the glutamate transporter xCT (X(c-) system, encoded by SLC7a11) in vivo leads to abrogated neurodegeneration, attenuated perifocal edema and prolonged
Quantification of retinal microvasculature and neurodegeneration changes in branch retinal vein occlusion after resolution of cystoid macular edema on optical coherence tomography angiography.
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Cardiac arrest-induced regional blood-brain barrier breakdown, edema formation and brain pathology: a light and electron microscopic study on a new model for neurodegeneration and neuroprotection in porcine brain.
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Brief cardiac arrest and survival is often associated with marked neurological alterations related to cognitive and sensory motor functions. However, detail studies using selective vulnerability of brain after cardiac arrest in animal models are still lacking. We examined selective vulnerability of
Tissue-type transglutaminase and the effects of cystamine on intracerebral hemorrhage-induced brain edema and neurological deficits.
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Neurodegeneration occurs after intracerebral hemorrhage (ICH) and tissue-type transglutaminase (tTG) has a role in neurodegenerative disorders. The present study investigated tTG expression after ICH and the effects of a tTG inhibitor, cystamine, on ICH-induced brain edema and neurological deficits.
COMPARISON OF GANGLION CELL INNER PLEXIFORM LAYER THICKNESS BY CIRRUS AND SPECTRALIS OPTICAL COHERENCE TOMOGRAPHY IN DIABETIC MACULAR EDEMA.
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OBJECTIVE
Reduced thickness of the ganglion cell inner plexiform layer indicates diabetic neurodegeneration and can be assessed by spectral domain optical coherence tomography. The authors investigated the comparability of ganglion cell inner plexiform layer measurements from two spectral domain
Idiopathic remitting seronegative symmetrical synovitis with pitting edema syndrome associated with bilateral pleural and pericardial effusions: a case report.
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BACKGROUND
Remitting seronegative symmetrical synovitis with pitting edema syndrome is characterized by symmetrical synovitis with pitting edema in the dorsum of the hands or feet. Most cases of remitting seronegative symmetrical synovitis with pitting edema syndrome are idiopathic, but some are
Reliability of diagnostic imaging for degenerative diseases with osseous changes in the temporomandibular joint with special emphasis on subchondral cyst.
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High-resolution en face images of microcystic macular edema in patients with autosomal dominant optic atrophy.
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The purpose of this study was to investigate the characteristics of microcystic macular edema (MME) determined from the en face images obtained by an adaptive optics (AO) fundus camera in patients with autosomal dominant optic atrophy (ADOA) and to try to determine the mechanisms underlying the
Application of magnetic resonance imaging to the measurement of neurodegeneration in rat brain: MRI data correlate strongly with histology and enzymatic analysis.
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Focal brain ischemia was induced by middle cerebral artery occlusion in the rat. The volume of cerebral damage was determined 2 days later by MRI in vivo and in the same animals histologically. The edema volume as measured by MRI and the histologically determined infarction was highly correlated. As
Brain damage due to episodic alcohol exposure in vivo and in vitro: furosemide neuroprotection implicates edema-based mechanism.
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Adult rats intubated with a single dose of ethanol (alcohol; approximately 5 g/kg) for 5 to 10 successive days incur neurodegeneration in the entorhinal cortex, dentate gyrus, and olfactory bulbs accompanied by cerebrocortical edema and electrolyte (Na+, K+) accumulation. The brain damage is not
Cerebral edema induced in mice by a convulsive dose of soman. Evaluation through diffusion-weighted magnetic resonance imaging and histology.
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OBJECTIVE
In the present study, diffusion-weighted magnetic resonance imaging (DW-MRI) and histology were used to assess cerebral edema and lesions in mice intoxicated by a convulsive dose of soman, an organophosphate compound acting as an irreversible cholinesterase inhibitor.
METHODS
Three hours
Delayed neurodegeneration and early astrogliosis after excitotoxicity to the aged brain.
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Excitotoxicity is well recognised as a mechanism underlying neuronal cell death in several brain injuries. To investigate age-dependent differences in neurodegeneration, edema formation and astrogliosis, intrastriatal N-methyl-d-aspartate injections were performed in young (3 months) and aged (22-24
Disturbances of cerebrospinal fluid flow attributable to arachnoid scarring cause interstitial edema of the cat spinal cord.
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OBJECTIVE
Spinal arachnoid scarring may be caused by trauma, inflammation, surgery, spinal instability, degenerative diseases, or malformations and may lead to progressive neurological deficits and syringomyelia. We wanted to investigate the effects of focal arachnoid scarring in the cervical spinal
Linking binge alcohol-induced neurodamage to brain edema and potential aquaporin-4 upregulation: evidence in rat organotypic brain slice cultures and in vivo.
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Brain edema and derived oxidative stress potentially are critical events in the hippocampal-entorhinal cortical (HEC) neurodegeneration caused by binge alcohol (ethanol) intoxication and withdrawal in adult rats. Edema's role is based on findings that furosemide diuretic antagonizes binge
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