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s adenosylmethionine/blutung
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10 Ergebnisse
[Prostaglandin E1 (misoprostol) and S-adenosylmethionine in the prevention of hemorrhagic gastritis induced by aspirin in the human. Endoscopic, histologic and histochemical study].
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On 58 healthy subjects, it was evaluated in endoscopic and histopathologic form, the cytoprotective effect on the gastroduodenal mucosa, such of T.G.E 1 (misoprostol) as of SAMe, in the present of acute bleeding gastritis induced by 1300 mg aspirin in a single dose and during 2 hours. SAMe was given
Folate deficiency inhibits pancreatic amylase secretion in rats.
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Previous studies have suggested that the metabolism of methyl groups is an important factor in the function of the exocrine pancreas. Ethionine, an inhibitor of cellular methylation reactions, produces hemorrhagic pancreatitis when administered to mice fed a choline-deficient diet. Glycine
Abnormal methyl metabolism in pancreatic toxicity and diabetes.
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Several experimental studies suggest that disturbed methylation can influence cellular differentiation in the pancreas and contribute to toxic injury in ways that enhance the pathogenesis of pancreatitis and carcinogenesis. In vitro development of fetal rat pancreas requires a basal level of
Modulation of tumor necrosis factor-alpha-mediated cytotoxicity by changes of the cellular methylation state: mechanism and in vivo relevance.
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A combination of adenosine (Ado) and homocysteine (Homo) enhances tumor necrosis factor (TNF)-alpha cytotoxicity in vitro and in vivo in several tumor cells. Ado and Homo at concentrations that enhanced TNF-alpha-mediated cytotoxicity accumulated S-adenosylhomocysteine (AdoHcy) and as consequence
Construction of plasmid, bacterial expression, purification, and assay of dengue virus type 2 NS5 methyltransferase.
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Dengue virus (DENV), a member of mosquito-borne flavivirus, causes self-limiting dengue fever as well as life-threatening dengue hemorrhagic fever and dengue shock syndrome. Its positive sense RNA genome has a cap at the 5'-end and no poly(A) tail at the 3'-end. The viral RNA encodes a single
Massive transfusion and surgical management of iatrogenic aortic laceration associated with cystocentesis in a dog.
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METHODS
A 4-year-old 29-kg (63.8-lb) spayed female Husky crossbred was referred for emergency treatment because of catastrophic hemorrhagic shock following attempts at cystocentesis for investigation of suspected urinary tract infection.
RESULTS
On arrival at the hospital, clinicopathologic
A novel transgenic mouse model of CBS-deficient homocystinuria does not incur hepatic steatosis or fibrosis and exhibits a hypercoagulative phenotype that is ameliorated by betaine treatment.
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Cystathionine beta-synthase (CBS) catalyzes the condensation of homocysteine (Hcy) and serine to cystathionine, which is then hydrolyzed to cysteine by cystathionine gamma-lyase. Inactivation of CBS results in CBS-deficient homocystinuria more commonly referred to as classical homocystinuria, which,
Alternate reasons for atherogenesis in uremia.
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The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent
Nitric oxide synthase inhibitors and cerebral vasospasm.
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L-arginine is a source of nitric oxide (NO) that is cleaved from the terminal guanidino nitrogen atom by nitric oxide synthase (NOS). NO evokes, because of its free radical properties and affinity to heme, ferrous iron and cysteine, a wide spectrum of physiological and pathophysiological effects.
A diet rich in taurine, cysteine, folate, B12 and betaine may lessen risk for Alzheimer's disease by boosting brain synthesis of hydrogen sulfide.
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The gaseous physiological modulator hydrogen sulfide (H2S) has recently been shown to exert a variety of neuroprotective effects. In particular, the treatment of transgenic mouse models of Alzheimer's disease (AD) with agents that release H2S aids preservation of cognitive
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