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dc.contributor.authorHançer, V. Sabri
dc.contributor.authorGüvenç, Serkan
dc.contributor.authorHindilerden, Fehmi
dc.contributor.authorBüyükdoğan, Murat
dc.contributor.authorDiz-Küçükkaya, Reyhan
dc.date.accessioned2015-01-23T08:40:42Z
dc.date.available2015-01-23T08:40:42Z
dc.date.issued2014
dc.identifier.citationHancer VS, Guvenc S, Hindilerden F, Buyukdogan M, Diz-Kucukkaya R. (2014). Analysis of the complement pathway mutations in atypical hemolytic uremic syndrome (AHUS). Thrombosis Research. 2014: S35–S123. 23rd MLTD Biennial International Congress on Thrombosis. Valencia, May 14-17, 2014en_US
dc.identifier.issn0049-3848
dc.identifier.urihttps://hdl.handle.net/11446/676en_US
dc.identifier.urihttps://www.clinicalkey.com/#!/content/journal/1-s2.0-S0049384814502642en_US
dc.descriptionİstanbul Bilim Üniversitesi, Tıp Fakültesi.en_US
dc.description.abstractBackground: HUS is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. Typical HUS is triggered by infectious agents such as strains of E. coli that produce powerful Shiga-like exotoxins, whereas AHUS can be genetic, acquired, or idiopathic.en_US
dc.language.isoengen_US
dc.publisherElsevier Ltd.en_US
dc.rightsinfo:eu-repo/semantics/embargoedAccessen_US
dc.titleAnalysis of the complement pathway mutations in atypical hemolytic uremic syndrome (AHUS)en_US
dc.typeconferenceObjecten_US
dc.relation.journalThrombosis Researchen_US
dc.departmentDBÜ, Tıp Fakültesien_US
dc.identifier.issueS3
dc.identifier.volume133
dc.identifier.startpageS81
dc.identifier.endpageS81
dc.contributor.authorIDTR43513en_US
dc.contributor.authorIDTR181051en_US
dc.contributor.authorIDTR165522en_US
dc.contributor.authorIDTR116136en_US
dc.relation.publicationcategoryBelirsizen_US


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