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stomach diseases/phosphatase
A hivatkozás a vágólapra kerül
Oldal 1 tól től 21 eredmények
Aging gastropathy-novel mechanisms: hypoxia, up-regulation of multifunctional phosphatase PTEN, and proapoptotic factors.
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OBJECTIVE
Aging gastric mucosa has impaired mucosal defense and increased susceptibility to injury. Our aims were to determine the mechanisms responsible for above abnormalities.
METHODS
We used Fisher F-344 rats, 3 and 24 months of age. We measured gastric mucosal blood flow; visualized mucosal
[Clinical significance of results in determination of alkaline phosphatase and peroxidase in peripheral blood leukocytes in some gastric diseases].
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Gastropathy and defense mechanisms in common bile duct ligated portal hypertensive rats.
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Portal hypertensive gastropathy is associated with a broad spectrum of gastric mucosal damage inspite of decreased gastric acid secretion, suggestive of compromised endogenous protective mechanisms. To determine the mechanisms of damage in portal hypertensive gastropathy we measured lipid
[Lipid peroxidation, the enzyme antioxidative system and acid phosphatase content of the gastric mucosa in stomach ulcer].
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Lipid peroxidation, a state of the antioxidative system and activity of acid phosphatase were studied in mucosal membrane of 53 patients with ulcerous disease of stomach. Increase of the acid phosphatase activity in cytoplasm, activation of lipid peroxidation and inhibition of the antioxidative
Deregulation of SHP-2 tyrosine phosphatase by the Helicobacter pylori virulence factor CagA.
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Helicobacter pylori (H. pylori) is estimated to infect about half of the world population. It causes gastric diseases ranging from gastritis to cancer and has been classified as a class I carcinogen by WHO. However, little is known about the molecular mechanisms by which H. pylori induces
Development and progression of portal hypertensive gastropathy in patients with chronic hepatitis C.
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OBJECTIVE
The objective of this study was to determine the incidence and risk factors associated with new-onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC).
METHODS
A total of 831 CHC patients with bridging fibrosis or cirrhosis at the time of entry
Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy.
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OBJECTIVE
Portal hypertension (PHI) is a clinical syndrome characterized by increases of the blood flow and/or of the vascular resistance in the portal system. A direct consequence of PHI can appearance different lesions on the gastric mucosa and submucosa, cumulatively termed portal hypertensive
[Light and electron microscopic histochemical studies of alkaline phosphatase (ALP) isoenzymes in gastric cancer].
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By using light and electron microscopic histochemical techniques, the activities and distributions of ALP isoenzymes in gastric cancers and benign gastric diseases were examined. The results showed: Nagao, Regan and Kasahara isoenzymes, which were not expressed in normal gastric mucosae and
Malignant Helicobacter pylori-Associated Diseases: Gastric Cancer and MALT Lymphoma.
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Helicobacter pylori is the first bacterium formally recognized to play a causative role in human malignancies, gastric cancer and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Evidence accumulates that H. pylori cagA-positive strains play a crucial role in the neoplastic transformation
Aesculin modulates bone metabolism by suppressing receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis and transduction signals.
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Aesculin (AES), a coumarin compound derived from Aesculus hippocasanum L, is reported to exert protective role against inflammatory diseases, gastric disease and cancer. However, direct effect of AES in bone metabolism is deficient. In this study, we examined the effects of AES on osteoclast (OC)
Helicobacter pylori-related host gene polymorphisms associated with susceptibility of gastric carcinogenesis: a two-stage case-control study in Chinese.
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Stomach carcinogenesis progresses stepwise from normal mucosa/superficial gastritis, atrophic gastritis (GA) to gastric cancer (GC). Host factors independent of or combined with Helicobacter pylori infection may modulate the carcinogenesis process. In this two-stage study, we selected 24 putative
Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D production in renal tubules.
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A 60-year-old man with portal hypertensive gastropathy due to type C liver cirrhosis developed severe bone pains, marked hypophosphatemia with inappropriately increased urinary excretion of phosphate (%TRP; 9.6%), and hyperalkaline phosphatasia, after intravenous administration of saccharated ferric
Isolation of Campylobacter pyloridis from human gastric mucosa and characterization of the isolates.
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Biopsy specimens of human gastric mucosa of patients with gastric complaints and subjected to endoscopic examination were cultured microaerobically, and Campylobacter pyloridis was detected in 46 out of 80 cases (57.5%). The organism was found in 13 out of 22 patients with gastritis, 11 out of 16
Increased susceptibility of aging gastric mucosa to injury: the mechanisms and clinical implications.
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This review updates the current views on aging gastric mucosa and the mechanisms of its increased susceptibility to injury. Experimental and clinical studies indicate that gastric mucosa of aging individuals-"aging gastropathy"-has prominent structural and functional abnormalities vs young gastric
Helicobacter pylori causes gastric cancer by hijacking cell growth signaling.
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Extract: Infection with certain strains (carrying the cagA gene) of the bacterium Helicobacter pylori (H. pylori) is associated with the development of gastric carcinoma. Upon introduction into the gastric epithelial cells and its subsequent modification by phosphorylation (adding a phosphate group)
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