Zobrazeno 1 - 10
of 27
pro vyhledávání: '"Judith S. Greengard"'
Autor:
Szilárd Kiss, Ruslan Grishanin, Aivan Nguyen, Romeo Rosario, Judith S. Greengard, Julio Nieves, Claire M. Gelfman, Mehdi Gasmi
Publikováno v:
Molecular Therapy: Methods & Clinical Development, Vol 18, Iss , Pp 345-353 (2020)
Several standard-of-care therapies for the treatment of retinal disease, including aflibercept, inhibit vascular endothelial growth factor (VEGFA). The main shortcoming of these therapies is potential undertreatment due to a lack of compliance result
Externí odkaz:
https://doaj.org/article/90238570e14b4903b4cc336b4e25c2c6
Autor:
Lois M. Fisher, Simona Zannetti, Jenna M. Weidman, Malhar Desai, Richard L.S. Thomas, Judith S. Greengard, Kevin Boyle, Arif Iftekhar
Publikováno v:
Progress in Cardiovascular Diseases. 56:92-102
Endovascular treatments for catastrophic aortic conditions have gained increasing popularity over the past 20 years. Originally developed for abdominal aortic aneurysms (EVAR), treatment has been modified for use in thoracic aortic repair (TEVAR). As
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 20:2689-2695
Abstract —Although it is known that factor VIII (FVIII) plasma levels increase rapidly in response to a number of stimuli, the biological stimuli behind this release is less clear. Previously, we showed that FVIII can traffic together with von Will
Autor:
Douglas J. Jolly, Judith S. Greengard
Publikováno v:
Thrombosis and Haemostasis. 82:555-561
IntroductionHemophilia A results from the plasma deficiency of factor VIII, a gene carried on the X chromosome. Bleeding results from a lack of coagulation factor VIII, a large and complex protein that circulates in complex with its carrier, von Will
Autor:
Naomi Lanir, Uri Seligsohn, Ariella Zivelin, Benjamin Brenner, John H. Griffin, Judith S. Greengard
Publikováno v:
Blood. 88:877-880
It is remarkable that certain patients with heterozygous protein C (PC) deficiency manifest venous thromboembolism (VTE), whereas others, particularly those belonging to families with homozygous PC deficiency, remain asymptomatic. The goals of the pr
Publikováno v:
Thrombosis and Haemostasis. 75:062-069
SummarycDNAs for protein C inhibitor (PCI), prepared from human liver RNA, contained two forms of PCI, designated PCI*A and PCPB 1 . While PCI*A is identical to the published PCI sequence, PCPB differs in 4 of 1221 bp and two amino acids, A36V and K8
Activated protein C resistance: molecular mechanisms based on studies using purified Gln506-factor V
Publikováno v:
Blood. 85:3405-3411
Gln506-factor V (FV) was purified from plasma of an individual homozygous for an Arg506Gln mutation in FV that is associated with activated protein C (APC) resistance. Purified Gln506-FV, as well as Gln506-FVa generated by either thrombin or FXa, con
Autor:
John H. Griffin, José A. Fernández, Judith S. Greengard, Tilman M. Hackeng, Mary J. Heeb, Kazuhisa Kojima, Yumi Kojima
Publikováno v:
Thrombosis and Haemostasis. 74:444-448
Activated protein C (APC) resistance is usually associated with a single DNA mutation predicting replacement of Arg506 by Gln in factor V (FV). Studies using synthetic peptides suggest that FV residues 493-506 provide factor Xa (FXa) and protein S bi
Publikováno v:
Thrombosis and Haemostasis. 74:1079-1087
SummarycDNAs for protein C inhibitor (PCI) were cloned from human and rhesus monkey 1 liver RNAs by reverse transcription and polymerase chain reaction (PCR) amplification. Sequencing showed that rhesus monkey and human PCI cDNAs were 93% identical.
Publikováno v:
New England Journal of Medicine. 331:1559-1562
The most frequent laboratory abnormality in patients with idiopathic deep-vein thrombosis is resistance to activated protein C1. Depending on the selection criteria, in vitro resistance to activated protein C can be identified in 20 to 50 percent of