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dc.contributor.author Tőkési, Natália
dc.contributor.author Kozák, Eszter Zita
dc.contributor.author Fülöp, Krisztina
dc.contributor.author Dedinszki, Dóra
dc.contributor.author Hegedűs, Nikolett
dc.contributor.author Király, Bálint
dc.contributor.author Szigeti, K
dc.contributor.author Ajtay, Kitti
dc.contributor.author Jakus, Zoltán
dc.contributor.author Zaworski, J
dc.contributor.author Letavernier, E
dc.contributor.author Pomozi, Viola
dc.contributor.author Váradi, András
dc.date.accessioned 2021-09-07T07:56:04Z
dc.date.available 2021-09-07T07:56:04Z
dc.date.issued 2020
dc.identifier 85090113867
dc.identifier.citation journalVolume=24;journalIssueNumber=20;journalTitle=JOURNAL OF CELLULAR AND MOLECULAR MEDICINE;pagerange=11791-11799;journalAbbreviatedTitle=J CELL MOL MED;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/8470
dc.identifier.uri doi:10.1111/jcmm.15793
dc.description.abstract Trauma-induced calcification is the pathological consequence of complex injuries which often affect the central nervous system and other parts of the body simultaneously. We demonstrated by an animal model recapitulating the calcification of the above condition that adrenaline transmits the stress signal of brain injury to the calcifying tissues. We have also found that although the level of plasma pyrophosphate, the endogenous inhibitor of calcification, was normal in calcifying animals, it could not counteract the acute calcification. However, externally added pyrophosphate inhibited calcification even when it was administered after the complex injuries. Our finding suggests a potentially powerful clinical intervention of calcification triggered by polytrauma injuries which has no effective treatment. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd
dc.relation.ispartof urn:issn:1582-1838
dc.title Pyrophosphate therapy prevents trauma-induced calcification in the mouse model of neurogenic heterotopic ossification
dc.type Journal Article
dc.date.updated 2020-09-14T12:07:58Z
dc.language.rfc3066 en
dc.rights.holder NULL
dc.identifier.mtmt 31600074
dc.contributor.department SE/AOK/I/Biofizikai és Sugárbiológiai Intézet
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Semmelweis Egyetem


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