onr:"swepub:oai:DiVA.org:uu-5898"
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03956nam a2200517 4500 | |
| 001 | oai:DiVA.org:uu-5898 | |
| 003 | SwePub | |
| 008 | 050909s2005 | |||||||||||000 ||eng| | |
| 020 | a 9155463134q print | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-58982 URI |
| 040 | a (SwePub)uu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a vet2 swepub-contenttype |
| 072 | 7 | a dok2 swepub-publicationtype |
| 100 | 1 | a Henriksnäs, Johanna,d 1973-u Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut |
| 245 | 1 0 | a Helicobacter pylori and Gastric Protection Mechanisms :b An in vivo Study in Mice and Rats |
| 264 | 1 | a Uppsala :b Acta Universitatis Upsaliensis,c 2005 |
| 300 | a 67 s. | |
| 338 | a electronic2 rdacarrier | |
| 490 | 0 | a Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,x 1651-6206 ;v 60 |
| 520 | a The stomach is frequently exposed to hazardous agents and to resist this harsh environment, several protective mechanisms exist. Of special interest is the gastric pathogen Helicobacter pylori which causes gastritis, ulcers and cancer but the mechanism leading to these diseases are still unclear. However it is very likely that H. pylori negatively influence the protection mechanisms that exist in the stomach. The aims of the present investigation were first to develop an in vivo mouse model in which different protection mechanisms could be studied, and second to investigate the influence of H. pylori on these mechanisms. An in vivo preparation of the gastric mucosa in mice was developed. This preparation allows studies of different gastric mucosal variables and can also be applied for studies in other gastro-intestinal organs. Mice chronically infected with H. pylori, were shown to have a reduced ability of the mucosa to maintain a neutral pH at the epithelial cell surface. This could be due to the thinner inner, firmly adherent mucus gel layer, and/or to defective bicarbonate transport across the epithelium. The Cl-/HCO3- exchanger SLC26A9 was inhibited by NH4+, which also is produced by H. pylori. The mRNA levels of SLC26A9 were upregulated in infected mice, suggesting a way to overcome the inhibition of the transporter. Furthermore, the hyperemic response to acid pH 2 and 1.5 was abolished in these mice. The mechanisms by which the bacteria could alter the blood flow response might involve inhibition of the epithelial iNOS.Water extracts of H. pylori (HPE) reduces the blood flow acutely through an iNOS and nerve-mediated pathway, possibly through the endogenous iNOS inhibitor ADMA. Furthermore, HPE alters the blood flow response to acid as the hyperemic response to acid pH 0.8 is accentuated in mice treated with HPE. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Fysiologi0 (SwePub)301062 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Physiology0 (SwePub)301062 hsv//eng |
| 653 | a Physiology | |
| 653 | a mucus gel layer | |
| 653 | a mucosal blood flow | |
| 653 | a mucus thickness | |
| 653 | a intra-vital microscopy | |
| 653 | a laser-Doppler flowmetry | |
| 653 | a pH-sensitive microelectrode | |
| 653 | a nitric oxide | |
| 653 | a Helicobacter pylori | |
| 653 | a bicarbonate secretion | |
| 653 | a mouse model | |
| 653 | a Fysiologi | |
| 653 | a Physiology | |
| 653 | a Fysiologi | |
| 700 | 1 | a Holm, Lena4 ths |
| 700 | 1 | a Engstrand, Lars4 ths |
| 700 | 1 | a Persson, Erik4 ths |
| 700 | 1 | a Fändriks, Lars,c Professoru Avd för gastroforskning, Göteborg4 opn |
| 710 | 2 | a Uppsala universitetb Institutionen för medicinsk cellbiologi4 org |
| 856 | 4 | u https://uu.diva-portal.org/smash/get/diva2:166791/FULLTEXT01.pdfx primaryx Raw objecty fulltext |
| 856 | 4 | u https://uu.diva-portal.org/smash/get/diva2:166791/COVER01.pdfy cover |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5898 |
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