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AuthorRösch, Danieladc.contributor.author
Date of accession2016-03-14T13:40:47Zdc.date.accessioned
Available in OPARU since2016-03-14T13:40:47Zdc.date.available
Year of creation2005dc.date.created
AbstractPatients with diabetes mellitus exhibit an increased propensity to develop arteriosclerosis with its sequelae acute myocardial infarction and stroke. Besides various associated metabolic disorders the presence of advanced glycation endproducts, AGEs, and its interaction with the respective receptor RAGE (receptor for advanced glycation endproducts) is considered a major contributor to vascular disease in these patients. RAGE is a member of the immunoglobulin superfamily of cell surface molecules, known to be expressed in vascular cells such as endothelial cells and monocytes. Activation of RAGEs on these cells activates the transcription factor NFkB, subsequently leading to increased expression of pro-inflammatory mediators such as TNF-alpha, thus furnishing lesion development. Clinical data suggest that monocyte RAGE expression is increased in diabetic patients, but to date nothing is known about the underlying mechanisms of this observation. Given that TNF-alpha serum levels are increased in diabetic patients, the present study seeks to investigate the regulation of RAGE expression in human monocytes by the pro-inflammatory cytokine TNF-a.dc.description.abstract
Languagededc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseStandard (Fassung vom 03.05.2003)dc.rights
Link to license texthttps://oparu.uni-ulm.de/xmlui/license_v1dc.rights.uri
KeywordRAGEdc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
TitleRegulation der Expression der Rezeptoren für advanced glycation end products (RAGE) auf humanen Monozytendc.title
Resource typeDissertationdc.type
DOIhttp://dx.doi.org/10.18725/OPARU-709dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-vts-56739dc.identifier.urn
GNDArteriosklerosedc.subject.gnd
GNDDiabetes mellitusdc.subject.gnd
GNDMonozytdc.subject.gnd
GNDTumor-Nekrose-Faktor <alpha>dc.subject.gnd
FacultyMedizinische Fakultätuulm.affiliationGeneral
Date of activation2006-08-03T08:47:43Zuulm.freischaltungVTS
Peer reviewneinuulm.peerReview
Shelfmark print versionZ: J-H 11.238 ; W: W-H 9.352uulm.shelfmark
DCMI TypeTextuulm.typeDCMI
VTS-ID5673uulm.vtsID
CategoryPublikationenuulm.category
University Bibliographyjauulm.unibibliographie


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