Maas, Jens-Holger

[["dc.bibliographiccitation.firstpage","327"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Leukemia Research"],["dc.bibliographiccitation.lastpage","332"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Hartmann, Julia"],["dc.contributor.author","Braulke, Friederike"],["dc.contributor.author","Sinzig, Ursula"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Maas, Jens Holger"],["dc.contributor.author","Konietschke, Frank"],["dc.contributor.author","Haase, Detlef"],["dc.date.accessioned","2018-11-07T09:27:53Z"],["dc.date.available","2018-11-07T09:27:53Z"],["dc.date.issued","2013"],["dc.description.abstract","In patients with myelodysplastic syndromes (MDS) iron overload caused by long-term red blood cell transfusions is an important factor for comorbidity especially in low-risk MDS. In this report we present the results of a comparative study based on colony formation assays of hematopoietic cells in MDS patients with and without iron overload. We demonstrate that iron overload suppresses the proliferation of erythroid progenitors cells (BFU-E), while the myeloid compartment (CFU-GM) was not found to be affected. Even patients with slightly elevated ferritin values show an impaired proliferation capacity in comparison to patients with normal ferritin levels. Furthermore, we show that this negative impact is reversible by sufficient iron chelation therapy. (C) 2012 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.leukres.2012.11.005"],["dc.identifier.isi","000314871500018"],["dc.identifier.pmid","23259989"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30643"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0145-2126"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Iron overload impairs proliferation of erythroid progenitors cells (BFU-E) from patients with myelodysplastic syndromes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3051"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lipphardt, Mark"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Maas, Jens-Holger"],["dc.contributor.author","Schäfer, Ann-Kathrin"],["dc.contributor.author","Amlaz, Saskia I."],["dc.contributor.author","Ratliff, Brian B."],["dc.contributor.author","Koziolek, Michael J."],["dc.contributor.author","Wallbach, Manuel"],["dc.date.accessioned","2021-04-14T08:32:33Z"],["dc.date.available","2021-04-14T08:32:33Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/jcm9093051"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83944"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Syndecan-4 as a Marker of Endothelial Dysfunction in Patients with Resistant Hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]