Peptic Ulcer Disease

dc.contributor.advisorJuhász, Béla
dc.contributor.advisordeptDebreceni Egyetem::Általános Orvostudományi Kar::Farmakológiai és Farmakoterápiai Intézethu_HU
dc.contributor.authorSadeghi, Parichehr
dc.contributor.departmentDE--Általános Orvostudományi Karhu_HU
dc.contributor.opponentMajoros, László
dc.contributor.opponentGesztelyi, Rudolf
dc.contributor.opponentdeptDebreceni Egyetem::Általános Orvostudományi Kar::Orvosi Mikrobiológiai Intézethu_HU
dc.contributor.opponentdeptDebreceni Egyetem::Általános Orvostudományi Kar::Farmakológiai és Farmakoterápiai Intézethu_HU
dc.date.accessioned2018-11-19T12:44:49Z
dc.date.available2018-11-19T12:44:49Z
dc.date.created2018-06-22
dc.description.abstractPUD is mostly associated with Helicobacter Pylori (H. pylori) and non-steroidal anti-inflammatory drugs (NSAIDs).H. pylori are class one carcinogen causing chronic gastritis, gastric/duodenal ulcer, and may associate with coronary artery disease, stroke, vitamin B12 and iron deficiency. The pathogenicity of H. pylori in development of PUD mainly belong two major virulence factors namely cytotoxin-associated gene A (CagA) and vacuolating cytotoxin gene A(VacA). CagA is associated with a more severe form of the disease as well as gastric carcinoma. Cag A via activation of the ERK/MAPK pathway will lead to increase cellular proliferation and giving rise to cancer. VacA secretes vacuolating cytotoxin, which will result in vacuolation of epithelial cells and damage of mucosal tight junction, causing leakage of ions and acid into the gastric lumen.hu_HU
dc.description.courseáltalános orvoshu_HU
dc.description.courselangangolhu_HU
dc.description.degreeegységes, osztatlanhu_HU
dc.format.extent41hu_HU
dc.identifier.urihttp://hdl.handle.net/2437/259310
dc.language.isoenhu_HU
dc.subjectPeptic Ulcer Diseasehu_HU
dc.subject.dspaceDEENK Témalista::Orvostudományhu_HU
dc.titlePeptic Ulcer Diseasehu_HU
dc.title.translatedFormation of ulcer within stomach and duodenumhu_HU
Fájlok