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brain edema/phosphatase
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Seite 1 von 35 Ergebnisse
Ultrastructural observations on the transvascular route of protein removal in vasogenic brain edema.
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Micro-blood vessels (MBVs), located in the area of edema, were studied in cat brain at various time intervals (1 h, 24 h, 7 days) after cold-lesion injury. Both cold-injured and adjacent gyri were examined for blood-brain barrier (BBB) permeability to i. v. injected horseradish peroxidase (HRP) with
Tristetraprolin attenuates brain edema in a rat model of cerebral hemorrhage.
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Biochemical changes in the rat brain associated with dinitrophenol-induced brain edema.
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The present paper was designed to the study of cerebral edema induced by intracarotid infusion of dinitrophenol. The determinations included variations in three lysosomal enzymes (acid phosphatase, cathepsin C and beta-glucuronidase), Na+-K+-ATP-ase, changes in cerebral RNA and protein
Phosphatases and cathepsin D activities after vasogenic oedema: an experimental study.
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The role of two phosphatases (acid and alkaline phosphatase) and a lysosomal aspartyl endopeptidase (cathepsin D) in producing rat brain oedema was studied in 3 different rat cerebral areas (i.e. frontal cortex, hippocampus and striatum) at 1, 2 and 3 d after vasogenic brain oedema induction. The
Neuroprotective Effect of Protein Phosphatase 2A/Tristetraprolin Following Subarachnoid Hemorrhage in Rats.
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Early brain injury (EBI) following subarachnoid hemorrhage (SAH) can lead to inflammation and neuronal dysfunction. There is a need for effective strategies to mitigate these effects and improve the outcome of patients who experience SAH. The mRNA-destabilizing protein tristetraprolin (TTP) is an
Recombinant Alkaline Phosphatase Prevents Acute on Chronic Liver Failure.
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The lipopolysaccharide (LPS)- toll-like receptor-4 (TLR4) pathway plays an important role in liver failure. Recombinant alkaline phosphatase (recAP) deactivates LPS. The aim of this study was to determine whether recAP prevents the progression of acute and acute-on-chronic liver failure (ACLF).
Causative role of lysosomal enzymes in the pathogenesis of cerebral lesions due to brain edema under chronic hypertension.
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In order to clarify the role of lysosomal enzymes in the developmental mechanisms of cerebral lesions under chronic hypertensive conditions, we histochemically and biochemically investigated acid phosphatase, N-acetyl-beta-glucosaminidase, and cathepsin B in the cerebral cortex and subcortical white
[Activity of lysosomal enzymes in rabbit brain during the development of edema].
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Liberation and consequent activation of lysosomal enzymes seems to play significant role in the development of brain edema. In the present experiment with adult rabbits, anesthetized with urethane we investigated in the brain tissue homogenates the activity of four lysosomal enzymes, such as
[Evaluation of acute hepatic failure treated at the Department of Medicine III, Kyushu University Hospital: indications for living-donor liver transplantation].
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To evaluate indications for living-donor liver transplantation (LDLT), we examined 25 consecutive patients with acute hepatic failure admitted to the Department of Medicine III, Kyushu University Hospital between November 2001 and July 2004. These cases were diagnosed as fluminant hepatitis (n=13),
[Studies on ultrastructural changes in perivascular cells (F.G.P.) of small cerebral vessels at the initial stage after cold injury--chronological observations on F.G.P. within 24 hours].
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As the potentiated cells in reaction to cerebral edema and damage, microglia, astrocytes and macrophages had been listed. Recent neuropathological study elucidated that most of cerebral macrophages were derived from blood leucocytes including monocytes. Several years ago, one of the authors reported
Neurotoxic and teratogenic effects of an organophosphorus insecticide (phenyl phosphonothioic acid-O-ethyl-O-[4-nitrophenyl] ester) on mallard development.
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Phenyl phosphonothioic acid-O-ethyl-O-[4-nitrophenyl] ester (EPN) is one of the 10 most frequently used organophosphorus insecticides and causes delayed neurotoxicity in adult chickens and mallards. Small amounts of organophosphorus insecticides placed on birds' eggs are embryotoxic and teratogenic.
Dexamethasone selectively regulates the activity of enzymatic markers of cerebral endothelial cell lines.
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Two endothelial cell lines were derived from grafts of the central nervous system using retrovirus mediated gene transfer to introduce the polyoma middle-T oncogene into fetal rat brain endothelial cells and transplantation of these cells into adult rat brain. In this report, we further characterize
Over-expression of DSCR1 protects against post-ischemic neuronal injury.
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OBJECTIVE
The Down syndrome candidate region 1 (DSCR1) gene is located on human chromosome 21 and its protein is over-expressed in brains of Down syndrome individuals. DSCR1 can modulate the activity of calcineurin, a phosphatase abundant in the brain, but its influence on stroke outcome is not
Enzyme cytochemistry of blood-brain barrier (BBB) disturbances.
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Alkaline phosphatase (AP) is one of the enzymes which is highly active in the plasmalemma of endothelial cells (ECs) of BBB-type microvessels. In the ECs of non-BBB type vessels, the reaction for AP (and other phosphatases) is negative (e.g. choroid plexus, area postrema, hypophysis). After BBB
A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy.
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Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72h period of alcohol
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