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Article: Epidermal growth factor and its receptor in chronic active gastritis and gastroduodenal ulcer before and after Helicobacter pylori eradication

TitleEpidermal growth factor and its receptor in chronic active gastritis and gastroduodenal ulcer before and after Helicobacter pylori eradication
Authors
Issue Date2001
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2001, v. 15 n. 9, p. 1459-1465 How to Cite?
AbstractBackground: Helicobacteria pylori infection of gastroduodenal mucosa is strongly associated with gastritis and peptic ulcer disease. The aims of the present study were to compare the gastroduodenal mucosal levels of epidermal growth factor (EGF) and its receptor (EGFR) among H. pylori-negative controls and H. pylori infected patients with chronic active gastritis or gastroduodenal ulcer before and after H. pylori eradication. Methods: The protein levels of EGF in mucosal tissues and saliva were determined by a solid-phase enzyme-linked immunosorbent assay (ELISA). Repeat transcription-polymerase chain reaction and the following polymerase chain reaction ELISA were employed to examine the mucosal EGFR mRNA expression. Results: Mucosal injury and H. pylori infection increased EGF protein levels and EGFR mRNA expression in the antral mucosa. The concentration of EGF in saliva was not affected by mucosal damage or H. pylori infection. Successful H. pylori eradication normalized the EGFR mRNA back to its basal level 6 weeks after treatment. However, after unsuccessful eradication their high levels in the antrum persisted. All patients experienced ulcer healing after drug treatment, regardless of H. pylori eradication. Conclusions: Mucosal damage increased the expression of EGF protein and EGFR mRNA in the gastric mucosa. H. pylori could induce the expression of EGFR but not the EGF in the antral mucosa. The expression of EGFR could be a contributing factor for ulcer healing in patients with H. pylori infection.
Persistent Identifierhttp://hdl.handle.net/10722/77515
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorWang, WPen_HK
dc.contributor.authorSo, WHLen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorFung, FMYen_HK
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorHiu, WMen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T07:32:44Z-
dc.date.available2010-09-06T07:32:44Z-
dc.date.issued2001en_HK
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2001, v. 15 n. 9, p. 1459-1465en_HK
dc.identifier.issn0269-2813en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77515-
dc.description.abstractBackground: Helicobacteria pylori infection of gastroduodenal mucosa is strongly associated with gastritis and peptic ulcer disease. The aims of the present study were to compare the gastroduodenal mucosal levels of epidermal growth factor (EGF) and its receptor (EGFR) among H. pylori-negative controls and H. pylori infected patients with chronic active gastritis or gastroduodenal ulcer before and after H. pylori eradication. Methods: The protein levels of EGF in mucosal tissues and saliva were determined by a solid-phase enzyme-linked immunosorbent assay (ELISA). Repeat transcription-polymerase chain reaction and the following polymerase chain reaction ELISA were employed to examine the mucosal EGFR mRNA expression. Results: Mucosal injury and H. pylori infection increased EGF protein levels and EGFR mRNA expression in the antral mucosa. The concentration of EGF in saliva was not affected by mucosal damage or H. pylori infection. Successful H. pylori eradication normalized the EGFR mRNA back to its basal level 6 weeks after treatment. However, after unsuccessful eradication their high levels in the antrum persisted. All patients experienced ulcer healing after drug treatment, regardless of H. pylori eradication. Conclusions: Mucosal damage increased the expression of EGF protein and EGFR mRNA in the gastric mucosa. H. pylori could induce the expression of EGFR but not the EGF in the antral mucosa. The expression of EGFR could be a contributing factor for ulcer healing in patients with H. pylori infection.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_HK
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_HK
dc.rightsAlimentary Pharmacology and Therapeutics. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshDuodenal Ulcer - drug therapy - metabolismen_HK
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_HK
dc.subject.meshEpidermal Growth Factor - isolation & purification - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGastric Mucosa - drug effects - metabolismen_HK
dc.subject.meshGastritis - drug therapy - metabolismen_HK
dc.subject.meshHelicobacter Infections - drug therapy - metabolismen_HK
dc.subject.meshHelicobacter pylorien_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - isolation & purification - metabolismen_HK
dc.titleEpidermal growth factor and its receptor in chronic active gastritis and gastroduodenal ulcer before and after Helicobacter pylori eradicationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0269-2813&volume=15&issue=9&spage=1459&epage=1465&date=2001&atitle=Epidermal+growth+factor+and+its+receptor+in+chronic+active+gastritis+and+gastroduodenal+ulcer+before+and+after+Helicobacter+pylori+eradicationen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2036.2001.01051.xen_HK
dc.identifier.pmid11552919-
dc.identifier.scopuseid_2-s2.0-0034853251en_HK
dc.identifier.hkuros72116en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034853251&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1459en_HK
dc.identifier.epage1465en_HK
dc.identifier.isiWOS:000171126900026-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridWang, WP=7501765704en_HK
dc.identifier.scopusauthoridSo, WHL=7004974020en_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridFung, FMY=7003833944en_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridHiu, WM=6506527812en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK

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