Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Mia Golder"'
Autor:
Samantha K. Sarkar, Angela Matyas, Ikhuosho Asikhia, Zhenkun Hu, Mia Golder, Kaitlyn Beehler, Tanja Kosenko, Thomas A. Lagace
Publikováno v:
Frontiers in Physiology, Vol 13 (2022)
Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds and mediates endo-lysosomal degradation of low-density lipoprotein receptor (LDLR), limiting plasma clearance of cholesterol-rich LDL particles in liver. Gain-of-f
Externí odkaz:
https://doaj.org/article/5b011592ba30443bbae7dc2981011534
Autor:
Ziad Solh, Andrew W. Shih, Peter Schubert, William P. Sheffield, Mia Golder, Geraldine M. Walsh, Margaret Fearon
Publikováno v:
Transfusion Medicine Reviews
Testing donations for pathogens and deferring selected blood donors have reduced the risk of transmission of known pathogens by transfusion to extremely low levels in most developed countries. Protecting the blood supply from emerging infectious thre
Publikováno v:
Transfusion Medicine Reviews. 29:181-194
Plasma obtained via whole blood donation processing or via apheresis technology can either be transfused directly to patients or pooled and fractionated into plasma protein products that are concentrates of 1 or more purified plasma protein. The evid
Autor:
Lin Yang, David S. Allan, Mark Walker, Cherie Mastronardi, Heidi Elmoazzen, Mia Golder, Mike Halpenny, Sophie Chargé, Rosario Isasi
Publikováno v:
TransfusionREFERENCES. 58(7)
BACKGROUND Research is needed to enhance cord blood (CB) transplantation outcomes and to develop new clinical applications. Based on quality criteria for transplantation, CB collected by public CB banks (CBBs) is often unsuitable for banking, but may
Publikováno v:
Thrombosis and Haemostasis. 109:53-60
SummaryFactor VIII (FVIII), a procoagulant cofactor, plays a crucial role in the intrinsic coagulation cascade. A causal association between elevated FVIII levels and venous thrombosis incidence has been established; no such association has been conf
Autor:
Andrea Bryant, Sandra L. Haberichter, Mia Golder, Kate Sponagle, Cynthia M. Pruss, Kimberly Laverty, Erin Burnett, Colleen Notley, Carol Hegadorn, David Lillicrap, Aly S. Dhala
Publikováno v:
Blood. 117:4358-4366
Type 1 VWD is the mild to moderate reduction of VWF levels. This study examined the mechanisms underlying 2 common type 1 VWD mutations, the severe R1205H and more moderate Y1584C. In vitro biosynthesis was reduced for both mutations in human and mou
Autor:
Kimberly Laverty, Kate Sponagle, David Lillicrap, Mia Golder, Cynthia M. Pruss, Jeffrey Mewburn, Carol Hegadorn
Publikováno v:
Blood. 115:4862-4869
Type 2B von Willebrand disease (2B VWD) results from von Willebrand factor (VWF) A1 mutations that enhance VWF-GPIbα binding. These “gain of function” mutations lead to an increased affinity of the mutant VWF for platelets and the binding of mut
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 34
Rationale: We have previously shown that a substantial proportion of plasma PCSK9 (30-40%) is associated with LDL particles in normolipidemic subjects. Cellular assays show that LDL-bound PCSK9 is less active for binding to cell surface LDLRs. Theref
Publikováno v:
The Journal of Biological Chemistry
Background: Secreted PCSK9 regulates LDL levels in plasma by mediating degradation of hepatic LDL receptors. Results: LDL binds to PCSK9 in human plasma and in vitro and inhibits PCSK9 binding to cell surface LDL receptors. Conclusion: A large propor
Autor:
Mia Golder, Sandra L. Haberichter, David Lillicrap, Carol Hegadorn, Andrea Bryant, Cynthia M. Pruss
Publikováno v:
Journal of thrombosis and haemostasis : JTH. 10(5)
Summary. Background: von Willebrand Factor (VWF) is tightly regulated by the metalloproteinase ADAMTS13, which cleaves VWF to reduce VWF multimer size and binding affinity for collagen and platelets. Objective: This study examines two VWF mutations,