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stomach ulcer/tyrosine
L'enllaç es desa al porta-retalls
Pàgina 1 des de 99 resultats
Identification of cagA tyrosine phosphorylation DNA motifs in Helicobacter pylori isolates from peptic ulcer patients by novel PCR-restriction fragment length polymorphism and real-time fluorescence PCR assays.
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Cag pathogenicity island-containing Helicobacter pylori (type I) induces signal transduction pathways resulting in tyrosine phosphorylation of proteins adjacent to the site of bacterial adhesion on host gastric epithelial cells. Conventional block PCR-restriction fragment length polymorphism (RFLP)
Mice deficient in protein tyrosine phosphatase receptor type Z are resistant to gastric ulcer induction by VacA of Helicobacter pylori.
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The vacuolating cytotoxin VacA produced by Helicobacter pylori causes massive cellular vacuolation in vitro and gastric tissue damage in vivo, leading to gastric ulcers, when administered intragastrically. Here we report that mice deficient in protein tyrosine phosphatase receptor type Z (Ptprz,
[Effect of DOPA and tyrosine on the healing of stomach ulcers and on the content of norepinephrine in the stomach].
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Protective role of β-patchoulene from Pogostemon cablin against indomethacin-induced gastric ulcer in rats: Involvement of anti-inflammation and angiogenesis.
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BACKGROUND
Non-steroidal anti-inflammatory drugs (NSAIDs) are most widely used as effective anti-inflammatory agents. However, their clinical application brings about inevasible gastrointestinal side effects. Pogostemon cablin is a traditional herbal medicine used for the treatment of
In vitro inhibitory effects of bergenin and norbergenin on bovine adrenal tyrosine hydroxylase.
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The aqueous extract of Mallotus japonicus (Euphorbiaceae) showed an inhibitory effect on bovine adrenal tyrosine hydroxylase (TH), the rate-limiting enzyme in the biosynthesis of catecholamine. The present study was undertaken to investigate the effects of bergenin and norbergenin, constituents of
Increased expression of inducible nitric oxide synthase and peroxynitrite in Helicobacter pylori gastric ulcer.
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The role of nitric oxide in ulcer formation remains unknown. Accordingly, we assessed local expression of inducible nitric oxide synthase (NOS) and nitration of tyrosine as an indicator of peroxynitrite formation in patients with Helicobacter pylori (HP)-associated gastric ulcers compared with
Aging diminishes gastric mucosal regeneration: relationship to tyrosine kinases.
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BACKGROUND
Increased incidence of gastric ulcer observed in the aged could be partly attributed to increased susceptibility of the mucosa to various damaging agents together with impediment of the repair process. The present investigation was undertaken to compare the rate of mucosal regeneration
Tyrosine and glycine derivatives as potential prodrugs: design, synthesis, and pharmacological evaluation of amide derivatives of mefenamic acid.
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This study deals with the synthesis, pharmacological activity, and kinetic studies of mefenamic acid (MA) prodrugs of tyrosine and glycine. The synthesis involved a series of protection and deprotection reactions. The hydrolysis of these prodrugs in the intestine was confirmed by hydrolysis kinetics
NSAID, aspirin delays gastric ulcer healing with reduced accumulation of CXCR4(+)VEGFR1(+) cells to the ulcer granulation tissues.
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BACKGROUND
Ulcer healing is a complex process, which involves cell migration, proliferation, angiogenesis and re-epithelialization. Several growth factors have been implicated in this process but the precise mechanism is not well understood. This study examined the involvement of VEGFR1 signaling in
Protein tyrosine phosphatase beta, a receptor for Helicobacter pylori vacA toxin.
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Helicobacter pylori is the leading bacterial cause of food-borne illness worldwide and plays a major role in the development of chronic gastritis, peptic ulcer, and gastric cancer. Strains isolated from patients contain the cagA gene (cytotoxin-associated gene A) and produce the vacuolating
Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wv mice.
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c-Kit is a receptor tyrosine kinase, and it is encoded by the mouse W locus. Mutant W/Wv mice develop spontaneous gastric antral ulcers. The aim of the present study was to investigate the pathogenesis of these gastric ulcers and to examine the effects of two antiulcer drugs; a proton pump inhibitor
The cationic host defense peptide rCRAMP promotes gastric ulcer healing in rats.
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Cathelicidin, a cationic host defense peptide, has been shown to promote cutaneous wound repair and reaches high levels in the gastric mucosa during infection and inflammation. Therefore, we investigated whether this peptide contributes to gastric ulcer healing in rats. Ulcer induction increased the
A tyrosine-based signal targets H/K-ATPase to a regulated compartment and is required for the cessation of gastric acid secretion.
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Gastric acid secretion is mediated by the H/K-ATPase of parietal cells. Activation of acid secretion involves insertion of H/K-ATPase into the parietal cell plasmalemma, while its cessation is associated with reinternalization of the H/K-ATPase into an intracellular storage compartment. The
Expression of midkine and receptor-like protein tyrosine phosphatase (RPTP)-beta genes in the rat stomach and the influence of rebamipide.
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Midkine has been reported to bind to receptor-like protein tyrosine phosphatase (RPTP)-beta and to play important roles in growth and differentiation of various cells. Midkine is expressed in rat stomach during experimental ulcer healing, suggesting that the midkine-RPTP-beta system has
[Receptor for VacA toxin and pathogenesis of gastric ulcer].
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The vacuolating cytotoxin VacA produced by Helicobacter pylori causes massive cellular vacuolation in vitro, and gastric tissue damage in vivo leading to gastric ulcers when administered intragastrically. We found that mice deficient in protein tyrosine phosphatase receptor type Z(Ptprz) do not show
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