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Sökning: WFRF:(Ten Cate Hugo) > Linköpings universitet

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1.
  • Maas, Angela H E M, et al. (författare)
  • Red alert for womens heart: the urgent need for more research and knowledge on cardiovascular disease in women
  • 2011
  • Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 32:11, s. 1362-1368
  • Forskningsöversikt (refereegranskat)abstract
    • A recent report of the EuroHeart project has shown that women are still underrepresented in many cardiovascular clinical trials, while important gender differences are present within most areas of heart disease. As the burden of cardiovascular disease is increasing in middle-aged women relative to men, a more profound understanding is needed of the fundamental biological differences that exist between men and women. In the current review, we aim to address the need for more explanatory sex-specific cardiovascular research to be able to adapt existing guidelines for a better heart health in women.
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2.
  • Maas, Coen, et al. (författare)
  • Misfolded proteins activate Factor XII in humans, leading to kallikrein formation without initiating coagulation
  • 2008
  • Ingår i: Journal of Clinical Investigation. - 0021-9738 .- 1558-8238. ; 118:9, s. 3208-3218
  • Tidskriftsartikel (refereegranskat)abstract
    • When blood is exposed to negatively charged surface materials such as glass, an enzymatic cascade known as the contact system becomes activated. This cascade is initiated by autoactivation of Factor XII and leads to both coagulation (via Factor XI) and an inflammatory response (via the kallikrein-kinin system). However, while Factor XII is important for coagulation in vitro, it is not important for physiological hemostasis, so the physiological role of the contact system remains elusive. Using patient blood samples and isolated proteins, we identified a novel class of Factor XII activators. Factor XII was activated by misfolded protein aggregates that formed by denaturation or by surface adsorption, which specifically led to the activation of the kallikreinkinin system without inducing coagulation. Consistent with this, we found that Factor XII, but not Factor XI, was activated and kallikrein was formed in blood from patients with systemic amyloidosis, a disease marked by the accumulation and deposition of misfolded plasma proteins. These results show that the kallikrein-kinin system can be activated by Factor XII, in a process separate from the coagulation cascade, and point to a protective role for Factor XII following activation by misfolded protein aggregates.
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