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Sökning: onr:"swepub:oai:DiVA.org:uu-160343" > The Plasma Contact ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004271nam a2200457 4500
001oai:DiVA.org:uu-160343
003SwePub
008111021s2011 | |||||||||||000 ||eng|
020 a 9789155482008q print
024a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1603432 URI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a vet2 swepub-contenttype
072 7a dok2 swepub-publicationtype
100a Bäck, Jennie,d 1981-u Uppsala universitet,Klinisk immunologi,Bo Nilsson4 aut0 (Swepub:uu)jenba617
2451 0a The Plasma Contact System :b New Functional Insights from a Hemostatic and Thrombotic Perspective
264 1a Uppsala :b Acta Universitatis Upsaliensis,c 2011
300 a 65 s.
338 a electronic2 rdacarrier
490a Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,x 1651-6206 ;v 718
520 a The physiological role of the plasma contact system still remains a partial enigma. The aim of the presented work was to expand our understanding of the plasma contact system, focusing on its physiological activation and function, principally from a hemostatic perspective. It also explored contact system activation under pathological conditions. We found that when human platelets become activated in blood, plasma proteins of the contact system bind to platelets and initiate contact activation. The platelet-triggered contact activation contributed to clot formation by shortening the clotting time and enhancing clot stability. We demonstrated that the regulation of contact activation elicited by activated platelets differed from the previously described contact activation elicited by negatively charged material surfaces. Platelet-triggered contact activation and activation propelled by clotting blood were found to be regulated by antithrombin, whereas material-induced activation was regulated by C1 inhibitor. We also showed that the fibrin fibers that are formed during the clot process further enhance and propagate the contact activation initially induced by activated platelets. Fibrin not only activated factor XII but also seemed to increase the affinity of antithrombin for the proteases of the contact system, leading to the generation of contact enzyme-antithrombin complexes during clot formation. To determine whether the contact system might be involved in the inflammation and vascular disease associated with systemic lupus erythematosus (SLE), we analyzed plasma samples from SLE patients. These patients were found to have altered levels of contact enzyme-serpin complexes, supporting the concept that the contact system may be involved in the pathophysiology of SLE. The contact enzyme-antithrombin complexes were clearly linked to platelet activation in vivo. Altered levels of both FXIIa-antithrombin and FXIIa-C1 inhibitor were found to be correlated with previous vascular disease and may therefore be potential biomarkers for assessing the risk of thrombotic events in SLE patients. These findings add to our knowledge of how the plasma contact system is activated and functions in vivo and will help us to understand the role of the contact system, not only in hemostasis but also in vascular disease and thrombotic conditions.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng
653 a Contact activation
653 a factor XII
653 a platelets
653 a coagulation
653 a antithrombin
653 a C1 inhibitor
653 a hemostasis
653 a biomarkers
653 a vascular disease.
653 a Klinisk immunologi
653 a Clinical Immunology
700a Nilsson, Bo,c Prof.u Uppsala universitet,Klinisk immunologi4 ths
700a Nilsson Ekdahl, Kristina,c Prof.u Uppsala universitet,Klinisk immunologi4 ths
700a Hedner, Ulla,c Prof.u Lund University4 opn
710a Uppsala universitetb Klinisk immunologi4 org
856u https://uu.diva-portal.org/smash/get/diva2:450654/FULLTEXT02.pdfx primaryx Raw objecty fulltext
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-160343

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