zymogen/infarction

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Эрэмбэлэх төрлийг сонгоно уу

Хуудас 1 -аас 29 үр дүн

[Combined pathology of the pancreas and myocardium in myocardial infarction and acute destructive pancreatitis].

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Pancreas was studied in 30 patients who died of myocardial infarction (MI). Total pancreonecrosis was found in 1 case (recurring MI), diffuse focal pancreonecrosis in 3 cases (the second MI). Local microcirculation disturbances, thrombosis of some interlobular veins, degenerative changes of the

TAFI polymorphisms at amino acids 147 and 325 are not risk factors for cerebral infarction.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Thrombin-activatable fibrinolysis inhibitor (TAFI) was reported as an anaphylatoxin-inactivating enzyme generated by proteolytic cleavage of its zymogen, and is the same enzyme as that first designated by our group as procarboxypeptidase R (proCPR). Its level in plasma appears to influence vascular

[Carotid artery thrombosis and myocardial infarction in nephrotic syndrome].

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

The authors report the case of a 18 year old man with a chronic corticosteroid-refractory nephrotic syndrome complicated by carotid artery thrombosis and myocardial infarction. Thromboembolism is one of the most serious complications of the nephrotic syndrome. Serious clotting factor disturbances

[Protein C dynamics in peripheral arterial occlusive diseases and myocardial infarction: association of homozygous protein C deficiency with heterozygous dysplasminogenemia found among patients with deep vein thrombosis].

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Protein C(PC) is the zymogen of a serine protease which regulates blood coagulation by inactivating activated blood coagulation factors V and VIII. We investigated the plasma level of PC in patients with deep vein thrombosis (DVT, n = 50), Buerger's disease (n = 34), arteriosclerosis obliterans (n =

Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

MMPs are implicated in LV remodeling after acute myocardial infarction (MI). To analyze the role of MMP-2, we generated MI by ligating the left coronary artery of MMP-2-KO and WT mice, the latter of which were administered orally an MMP-2-selective inhibitor or vehicle (TISAM). The survival rate was

A history of late and very late stent thrombosis is not associated with increased activation of the contact system, a case control study.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

BACKGROUND The pathophysiological pathways resulting in Late Stent Thrombosis (LST) remain uncertain. Findings from animal studies indicate a role of the intrinsic coagulation pathway in arterial thrombus formation, while clinical studies support an association with ischemic cardiovascular disease.

A potential basis for the thrombotic risks associated with lipoprotein(a).

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Lipoprotein(a) (Lp(a)) has been strongly linked with atherosclerosis and is an independent risk factor for myocardial infarction. Distinguishing Lp(a) from other low-density lipoprotein particles is its content of a unique apoprotein, apo(a). The recently described sequence of apo(a) indicates a

Therapeutic potential of matrix metalloproteinase inhibitors in atherosclerosis.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

The activity of matrix-degrading metalloproteinases (MMPs) is essential for many of the processes involved in atherosclerotic plaque formation, for example, infiltration of inflammatory cells, smooth muscle cell migration and proliferation and angiogenesis. Furthermore, matrix degradation by MMPs

Examining thrombin hydrolysis of the factor XIII activation peptide segment leads to a proposal for explaining the cardioprotective effects observed with the factor XIII V34L mutation.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

In the blood coagulation cascade, thrombin cleaves fibrinopeptides A and B from fibrinogen revealing sites for fibrin polymerization that lead to insoluble clot formation. Factor XIII stabilizes this clot by catalyzing the formation of intermolecular cross-links in the fibrin network. Thrombin

Elevation of factor VII activity and mass in coronary artery disease of varying severity.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

The present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial

Factor XI and contact activation as targets for antithrombotic therapy.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

The most commonly used anticoagulants produce therapeutic antithrombotic effects either by inhibiting thrombin or factor Xa (FXa) or by lowering the plasma levels of the precursors of these key enzymes, prothrombin and FX. These drugs do not distinguish between thrombin generation contributing to

Aggregation of washed platelets by plasminogen and plasminogen activators is mediated by plasmin and is inhibited by a synthetic peptide disulfide.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Plasmin is known to activate platelets. However, it is not clear whether plasminogen activators as used in thrombolytic therapy can aggregate platelets and how this relates to the ability of each activator to convert plasminogen to plasmin. Urokinase (UK) and streptokinase (SK) activated purified

Potential approaches for therapeutic intervention of thrombosis by fibrinolytic agents.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Fibrin-specific thrombolytic agents are being developed based on a better understanding of the molecular mechanisms that regulate in vivo fibrinolysis. These agents may be more effective than those available currently and may induce less systemic fibrinolysis. In this respect, t-PA has been

[Tissue-type plasminogen activator].

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Tissue-type plasminogen activator (t-PA) is a serine protease that converts a zymogen plasminogen into an active serine protease, namely, plasmin. Plasmin is the proteolytic enzyme that degrades fibrin. In the absence of fibrin, e.g., in circulating plasma, t-PA activates plasminogen at a very slow

Extensive heterogeneity of human urokinase, as detected by two-dimensional mapping.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой

Нэвтрэх / Бүртгүүлэх

Urokinase (uPA, urinary plasminogen activator) is a serine protease belonging to the peptidase S1 family. Specifically, uPA cleaves the zymogen plasminogen into the active form (plasmin), which then degrades the fibrin clots. It is widely used as a fibrinolytic agent in thrombolytic therapy and it

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