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Side 1 fra 132 resultater
A gamma methionine-310 to threonine substitution and consequent N-glycosylation at gamma asparagine-308 identified in a congenital dysfibrinogenemia associated with posttraumatic bleeding, fibrinogen Asahi.
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In an abnormal fibrinogen with severely impaired polymerization of fibrin monomers, we identified a methionine-to-threonine substitution at position 310 of the gamma chain. Furthermore, asparagine at position 308 was found to be N-glycosylated due to a newly formed consensus sequence,
Granulocyte colony-stimulating factor improves neurological function and angiogenesis in intracerebral hemorrhage rats.
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OBJECTIVE
Granulocyte colony-stimulating factor (G-CSF) plays a role in regulating phosphatidylinositol-3-kinase/serine/threonine kinase (PI3K/AKT) pathway, affecting cell proliferation and apoptosis, and inducing vascular endothelial growth factor (VEGF) expression. This study investigated the
Difference in protein substrate specificity between hemorrhagic toxin and lethal toxin from Clostridium sordellii.
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The hemorrhagic toxin (HT) from Clostridium sordellii is pharmacologically related to Clostridium difficile toxins A and B and Clostridium sordellii lethal toxin which have been recently identified as mono-glucosyl-transferases. Here we report that HT, which is coexpressed with lethal toxin, is also
[Phylogenetic analysis of South American sequences of the nonstructural protein-1 (ns1) of dengue serotype 2 associated with severe clinical bleeding].
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Objective The objective of this in silico study was to compare nucleotide and amino acids DENV-2-NS1 sequences isolated from febrile patients, with and without disease severity, from different South American countries. Matherials and Methods A bayesian MCMC phylogenetic analysis was carried out
The alanine/threonine polymorphism of the alpha-1-antichymotrypsin (SERPINA3) gene and ruptured intracranial aneurysms in the Japanese population.
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BACKGROUND
Serine protease inhibitor member 3 of clade A (SERPINA3), also known as alpha-1-antichymotrypsin, inhibits the activity of cathepsin G. The release of neutrophil cathepsin G (proteolytic enzyme) can destroy the vascular matrix through degradation, platelet aggregation and coagulation
Inhibition of mammalian target of rapamycin improves neurobehavioral deficit and modulates immune response after intracerebral hemorrhage in rat.
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BACKGROUND
Mammalian target of rapamycin (mTOR), a serine/threonine kinase, regulates many processes, including cell growth and the immune response. mTOR is also dysregulated in several neurological diseases, such as traumatic brain injury (TBI), stroke, and neurodegenerative disease. However, the
Ciglitazone, a novel inhibitor of lung apoptosis following hemorrhagic shock.
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Apoptosis or programmed cell death has been demonstrated to play a role in the development of lung injury following hemorrhagic shock. A major pathway modulating the apoptotic response is the phosphatidylinositol 3-kinase/serine/threonine kinase (PI3K/Akt) pathway. Ciglitazone, a peroxisome
Inhibition of Let7c microRNA is neuroprotective in a rat intracerebral hemorrhage model.
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Intracerebral hemorrhage (ICH) is a devastating neurological disease with a grave prognosis. We evaluated microRNA (miRNA) expression after ICH and evaluated Let7c as a therapeutic target. We harvested hemorrhagic brain 24 hours after collagenase induced ICH in the rat. Microarray analysis was
Discovery of a ROCK inhibitor, FPND, which prevents cerebral hemorrhage through maintaining vascular integrity by interference with VE-cadherin.
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Hemorrhagic stroke occurs when a weakened vessel ruptures and bleeds into the surrounding brain, leading to high rates of death and disability worldwide. A series of complex pathophysiological cascades contribute to the risk of hemorrhagic stroke, and no therapies have proven effective to prevent
Hepatic apoptosis after hemorrhagic shock in rats can be reduced through modifications of conventional Ringer's solution.
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BACKGROUND
Resuscitation with racemic lactated Ringer's solution induces cellular apoptosis. This study was conducted to determine if the elimination of D-lactate isomer would attenuate apoptosis in the liver, and to investigate the possible mechanisms.
METHODS
Sprague Dawley rats (n=30, 5 per
Bax inhibitor-1 suppresses early brain injury following experimental subarachnoid hemorrhage in rats.
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Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is an important cause of high mortality and poor prognosis in SAH. B‑cell lymphoma 2‑associated X protein inhibitor‑1 (BI‑1) is an evolutionarily conserved antiapoptotic protein that is primarily located in the membranes of endoplasmic
Novel serine/threonine kinase 11 gene mutations in Peutz-Jeghers syndrome patients and endoscopic management.
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OBJECTIVE
To explore mutations in serine/threonine kinase 11 (STK11) gene in Peutz-Jeghers syndrome (PJS) with gastrointestinal (GI) hamartomatous polyps.
METHODS
Six Japanese PJS patients in 3 families were enrolled in this study. Each of the cases had hamartomatous polyposis in the
Inhibition of glycogen synthase kinase (GSK)-3-β improves liver microcirculation and hepatocellular function after hemorrhagic shock.
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Ischemia and reperfusion may cause liver injury and are characterized by hepatic microperfusion failure and a decreased hepatocellular function. Inhibition of glycogen synthase kinase (GSK)-3β, a serine-threonine kinase that has recently emerged as a key regulator in the modulation of the
Novel molecular defect in the platelet ADP receptor P2Y12 of a patient with haemorrhagic diathesis.
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BACKGROUND
The platelet adenosine 5'-diphosphate (ADP) receptor P2Y(12) plays a crucial role in haemostasis. Only a few patients with haemorrhagic diathesis due to molecular defects in the P2Y(12) receptor have been described so far. We report a novel molecular defect in the gene coding for P2Y(12)
Glycogen synthase kinase-3beta inhibitors protect against the organ injury and dysfunction caused by hemorrhage and resuscitation.
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Glycogen synthase kinase 3beta (GSK-3beta) is a serine/threonine protein kinase that has recently emerged as a key regulatory switch in the modulation of the inflammatory response. Dysregulation of GSK-3beta has been implicated in the pathogenesis of several diseases including sepsis. Here we
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