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carotid stenosis/protease

Povezava se shrani v odložišče
ČlankiKliničnih preskušanjPatenti
Stran 1 iz 33 rezultatov

Marburg I polymorphism of factor VII--activating protease: a prominent risk predictor of carotid stenosis.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
BACKGROUND Atherothrombosis is a main pathomechanism in the evolution of vessel stenosis and is counteracted by endogenous fibrinolysis. Recently, the plasmatic serine protease "factor seven-activating protease" (FSAP) was recognized as a potent activator of prourokinase in vitro. The Marburg I
The myxoma virus protein Serp-1 is a member of the serine protease inhibitor superfamily. Serp-1 potently inhibits human serum proteases including plasmin, urokinase-type plasminogen activator (uPA), and tissue-type plasminogen activator (tPA). Serp-1 also displays a high antiinflammatory activity,

Factor VII-activating protease promotes the proteolysis and inhibition of tissue factor pathway inhibitor.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
OBJECTIVE Factor VII-activating protease (FSAP) activates both factor VII and pro-urokinase and inhibits platelet-derived growth factor-BB, thus regulating hemostasis- and remodeling-associated processes in the vasculature. A genetic variant of FSAP (Marburg I polymorphism) results in low enzymatic

Factor VII activating protease. Single nucleotide polymorphisms light the way.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Factor VII activating protease (FSAP) is a circulating serine protease with high homology to fibrinolytic enzymes. A role in the regulation of coagulation and fibrinolysis is suspected based on in vitro studies demonstrating activation of FVII or pro-urokinase plasminogen activator (uPA). However,

Factor VII-activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Essentials Factor VII-activating protease (FSAP) is a plasma protease involved in vascular processes. Neointima formation was investigated after vascular injury in FSAP-/- mice. The neointimal lesion size and the accumulation of macrophages were increased in FSAP-/- mice. This was due to an

Factor VII activating protease.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Factor VII activating protease (FSAP) is a circulating serine protease with high homology to fibrinolytic enzymes. A role in the regulation of coagulation and fibrinolysis is suspected based on in vitro studies demonstrating activation of FVII or pro-urokinase plasminogen activator (uPA). However,
BACKGROUND The single nucleotide Marburg I (MRI) polymorphism of the factor VII-activating protease (FSAP) gene, the prourokinase-activating activity of FSAP, and antigen levels of FSAP in plasma have been associated with incidence and progression of carotid stenosis and venous thromboembolism.
BACKGROUND The Marburg I (MRI) single nucleotide polymorphism (SNP) of the factor VII-activating protease (FSAP) gene has been associated with thrombophilia, thromboembolism, atherosclerosis, and the incidence and progression of carotid stenosis. At present, MRI SNP testing is mainly performed using

Factor VII Activating Protease Expression in Human Platelets and Accumulation in Symptomatic Carotid Plaque

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Background Factor VII activating protease (FSAP) is of interest as a marker for vascular inflammation and plaque destabilization. The aim of this study was to analyze the expression profile of FSAP in endarterectomy specimens that were taken from patients with asymptomatic and symptomatic carotid

Factor VII-activating protease in patients with acute deep venous thrombosis.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Factor VII-activating protease (FSAP) is involved in haemostasis and inflammation. FSAP cleaves single chain urokinase-type plasminogen activator (scu-PA). The 1601GA genotype of the 1601G/A polymorphism in the FSAP gene leads to the expression of a FSAP variant with reduced ability to activate

Marburg I polymorphism of factor VII-activating protease is associated with idiopathic venous thromboembolism.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
The factor VII-activating protease (FSAP) variant Marburg I is known to attenuate the profibrinolytic system in vitro and was recently shown to be a significant predictor for the evolution and progression of carotid stenosis. The objective of this case-control study was to assess FSAP Marburg I's

Deficiency of Factor VII activating protease alters the outcome of ischemic stroke in mice.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Factor VII activating protease (FSAP) is a circulating protease with a putative role in hemostasis, remodeling and inflammation. A polymorphism giving rise to low proteolytic activity has been associated with an increased risk of stroke and carotid stenosis. To date, no in vivo studies or
OBJECTIVE The factor VII activating protease (FSAP) knockout mice have a bigger neointima after vascular injury and a larger infarct volume after stroke. The Marburg I (MI) single nucleotide polymorphism (SNP) in the FSAP-encoding gene is associated with an increased risk of stroke and carotid
The factor VII activating protease (FSAP) is a serine-protease present in human plasma that serves to activate single-chain plasminogen activators, as well as coagulation factor VII. FSAP was localized within atherosclerotic lesions, and a genetic polymorphism in FSAP is associated with carotid
OBJECTIVE There is hope that molecular imaging can identify vulnerable atherosclerotic plaques. However, there is a paucity of clinical translational data to guide the future development of this field. Here, we cross-correlate cathepsin-B or matrix metalloproteinase-2/-9 molecular optical imaging
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