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This assists in identifying new virulence factors for the infectivity of H. pylori on the molecular level. [57] [58] 2001 Chan et al. show in a randomized control trial that eradication of H. pylori even prevents bleeding from ulcers that is caused by aspirin and non-steroidal anti-inflammatory drugs. [59] 2002
H. pylori is able to adhere to the surface of the phagocytes and impede their action. This is responded to by the phagocyte in the generation and release of oxygen metabolites into the surrounding space. H. pylori can survive this response by the activity of catalase at its attachment to the phagocytic cell surface. Catalase decomposes hydrogen ...
The success of H. pylori cure depends on the type and duration of therapy, patient compliance and bacterial factors such as antibiotic resistance. Patients most often fail to respond to initial H. pylori eradication therapy because of noncompliance or antibiotic resistance. Patients should be queried about any side effects, missed doses, and ...
Marshall did not develop antibodies to H. pylori, suggesting that innate immunity can sometimes eradicate acute H. pylori infection. Marshall's illness and recovery, based on a culture of organisms extracted from a patient, fulfilled Koch's postulates for H. pylori and gastritis, but not for peptic ulcers.
Patients swallow urea labelled with an uncommon isotope, either radioactive carbon-14 (nowadays preferred in many countries) or non-radioactive carbon-13.In the subsequent 10–30 minutes, the detection of isotope-labelled carbon dioxide in exhaled breath indicates that the urea was split; this indicates that urease (the enzyme that H. pylori uses to metabolize urea to produce ammonia) is ...
H. pylori can infect the stomach of some people without causing stomach ulcers. In investigating asymptomatic carriers of H. pylori, researchers identified a genetic trait called Interleuik-1 beta-31 which causes increased production of stomach acid, resulting in ulcers if patients become infected with H. pylori. Patients without the trait do ...
The disulfide binding of the inhibitor takes place in the luminal sector of the H + /K + ATPase were 2 mol of inhibitor is bound per 1 mol of active site H + /K + ATPase. [19] [20] All PPIs react with cysteine 813 in the loop between TM5 and TM6 on the H + /K + ATPase, fixing the enzyme in the E2 configuration. Omeprazole reacts with cysteine ...
Helicobacter heilmannii sensu lato (i.e. H. heilmanni s.l.) is a grouping of non-H. pylori Helicobacter species that take as part of their definition a similarity to H. pylori in being associated with the development of stomach inflammation, stomach ulcers, [11] duodenum ulcers, [12] stomach cancers that are not lymphomas, and extranodal ...