The natural enzymatic dissolution of FIBRIN.
A metallocarboxypeptidase that removes C-terminal lysine and arginine from biologically active peptides and proteins thereby regulating their activity. It is a zinc enzyme with no preference shown for lysine over arginine. Pro-carboxypeptidase U in human plasma is activated by thrombin or plasmin during clotting to form the unstable carboxypeptidase U.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
A member of the serpin superfamily found in plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin.
A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.
Precursor of plasmin (FIBRINOLYSIN). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent.
A product of the lysis of plasminogen (profibrinolysin) by PLASMINOGEN activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins.
Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.
Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.
A heterogeneous group of proteolytic enzymes that convert PLASMINOGEN to FIBRINOLYSIN. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation.
A ZINC-dependent carboxypeptidase primary found in the DIGESTIVE SYSTEM. The enzyme catalyzes the preferential cleavage of a C-terminal peptidyl-L-lysine or arginine. It was formerly classified as EC 3.4.2.2 and EC 3.4.12.3.
A proteolytic enzyme that converts PLASMINOGEN to FIBRINOLYSIN where the preferential cleavage is between ARGININE and VALINE. It was isolated originally from human URINE, but is found in most tissues of most VERTEBRATES.
All blood proteins except albumin ( = SERUM ALBUMIN, which is not a globulin) and FIBRINOGEN (which is not in the serum). The serum globulins are subdivided into ALPHA-GLOBULINS; BETA-GLOBULINS; and GAMMA-GLOBULINS on the basis of their electrophoretic mobilities. (From Dorland, 28th ed)
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.
Important modulators of the activity of plasminogen activators. The inhibitors belong to the serpin family of proteins and inhibit both the tissue-type and urokinase-type plasminogen activators.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Laboratory tests for evaluating the individual's clotting mechanism.
A fibrin-stabilizing plasma enzyme (TRANSGLUTAMINASES) that is activated by THROMBIN and CALCIUM to form FACTOR XIIIA. It is important for stabilizing the formation of the fibrin polymer (clot) which culminates the coagulation cascade.
Formation and development of a thrombus or blood clot in the blood vessel.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.
Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.
Enzymes that act at a free C-terminus of a polypeptide to liberate a single amino acid residue.
Antifibrinolytic hemostatic used in severe hemorrhage.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.
Streptococcal fibrinolysin . An enzyme produced by hemolytic streptococci. It hydrolyzes amide linkages and serves as an activator of plasminogen. It is used in thrombolytic therapy and is used also in mixtures with streptodornase (STREPTODORNASE AND STREPTOKINASE). EC 3.4.-.
Double-layered inflatable suits which, when inflated, exert pressure on the lower part of the wearer's body. The suits are used to improve or stabilize the circulatory state, i.e., to prevent hypotension, control hemorrhage, and regulate blood pressure. The suits are also used by pilots under positive acceleration.
An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.
Amino derivatives of caproic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the amino caproic acid structure.
Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Low-molecular-weight fragment of heparin, having a 4-enopyranosuronate sodium structure at the non-reducing end of the chain. It is prepared by depolymerization of the benzylic ester of porcine mucosal heparin. Therapeutically, it is used as an antithrombotic agent. (From Merck Index, 11th ed)
Stable blood coagulation factor activated by contact with the subendothelial surface of an injured vessel. Along with prekallikrein, it serves as the contact factor that initiates the intrinsic pathway of blood coagulation. Kallikrein activates factor XII to XIIa. Deficiency of factor XII, also called the Hageman trait, leads to increased incidence of thromboembolic disease. Mutations in the gene for factor XII that appear to increase factor XII amidolytic activity are associated with HEREDITARY ANGIOEDEMA TYPE III.
Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
A member of the annexin family that is a substrate for a tyrosine kinase, ONCOGENE PROTEIN PP60(V-SRC). Annexin A2 occurs as a 36-KDa monomer and in a 90-KDa complex containing two subunits of annexin A2 and two subunits of S100 FAMILY PROTEIN P11. The monomeric form of annexin A2 was formerly referred to as calpactin I heavy chain.
Endogenous factors and drugs that directly inhibit the action of THROMBIN, usually by blocking its enzymatic activity. They are distinguished from INDIRECT THROMBIN INHIBITORS, such as HEPARIN, which act by enhancing the inhibitory effects of antithrombins.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Elements of limited time intervals, contributing to particular results or situations.
A protease nexin and serpin subtype that is specific for several SERINE PROTEASES including UROKINASE; THROMBIN; TRYPSIN; and PLASMINOGEN ACTIVATORS.
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.
Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.
Agents that prevent clotting.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
Shock produced as a result of trauma.
Proteins prepared by recombinant DNA technology.
A deficiency or absence of FIBRINOGEN in the blood.
Formation or presence of a blood clot (THROMBUS) in a blood vessel within the SKULL. Intracranial thrombosis can lead to thrombotic occlusions and BRAIN INFARCTION. The majority of the thrombotic occlusions are associated with ATHEROSCLEROSIS.
Retraction of a clot resulting from contraction of PLATELET pseudopods attached to FIBRIN strands. The retraction is dependent on the contractile protein thrombosthenin. Clot retraction is used as a measure of platelet function.
Bleeding or escape of blood from a vessel.
Stable blood coagulation factor involved in the intrinsic pathway. The activated form XIa activates factor IX to IXa. Deficiency of factor XI is often called hemophilia C.
Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The time required by whole blood to produce a visible clot.
Forms of hereditary angioedema that occur due to mutations in the gene for COMPLEMENT C1 INHIBITOR PROTEIN. Type I hereditary angioedema is associated with reduced serum levels of complement C1 inhibitor protein. Type II hereditary angioedema is associated with the production of a non-functional complement C1 inhibitor protein.
A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.
Inflammation of a vein associated with a blood clot (THROMBUS).
A measurement of the time needed for FIBRINOLYSIS to occur.
Physiologically inactive substances that can be converted to active enzymes.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
A single-chain polypeptide derived from bovine tissues consisting of 58 amino-acid residues. It is an inhibitor of proteolytic enzymes including CHYMOTRYPSIN; KALLIKREIN; PLASMIN; and TRYPSIN. It is used in the treatment of HEMORRHAGE associated with raised plasma concentrations of plasmin. It is also used to reduce blood loss and transfusion requirements in patients at high risk of major blood loss during and following open heart surgery with EXTRACORPOREAL CIRCULATION. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
A procedure in which fluid is withdrawn from a body cavity or organ via a trocar and cannula, needle, or other hollow instrument.
A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.

Coagulation and fibrinolysis in intact hydatidiform molar pregnancy. (1/1717)

Tests of coagulation, fibrinolysis, and platelet function were performed in 17 patients with intact molar pregnancies. Women with intact molar pregnancies had higher fibrinogen factor VIII, and fibrinogen degradation products, concentrations and lower prothrombin, factor X, plasminogen, and plasminogen activator concentrations than controls with normal pregnancies. They also had reduced platelet counts and thromboelastographic values, which indicated hypocoagulability. These results suggest that intravascular coagulation occurs in intact hydatidiform molar pregnancies.  (+info)

Isolation of SMTP-3, 4, 5 and -6, novel analogs of staplabin, and their effects on plasminogen activation and fibrinolysis. (2/1717)

Four novel triprenyl phenol metabolites, designated SMTP-3, -4, -5, and -6, have been isolated from cultures of Stachybotrys microspora IFO 30018 by solvent extraction and successive chromatographic fractionation using silica gel and silica ODS columns. A combination of spectroscopic analyses showed that SMTP-3, -4, -5, and -6 are staplabin analogs, containing a serine, a phenylalanine, a leucine or a tryptophan moiety in respective molecules in place of the N-carboxybutyl portion of the staplabin molecule. SMTP-4, -5, and -6 were active at 0.15 to 0.3 mM in enhancing urokinase-catalyzed plasminogen activation and plasminogen binding to fibrin, as well as plasminogen- and urokinase-mediated fibrinolysis. On the other hand, the concentration of staplabin required to exert such effects was 0.4 to 0.6 mM, and SMTP-3 was inactive at concentrations up to 0.45 mM.  (+info)

Regulation of the activities of thrombin and plasmin by cholesterol sulfate as a physiological inhibitor in human plasma. (3/1717)

Thrombin and plasmin, both of which are serine proteases in the plasma of vertebrates, play essential roles in blood clotting and fibrinolysis, respectively, and regulation of their activities is important to suppress the excessive reactions within the vascular network and to prevent tissue injury. Along with the peptidic inhibitors belonging to the serpin family, we found that cholesterol sulfate (CS), which is present at the concentration of 2.0+/-1.2 nmol/ml in human plasma, was a potent inhibitor of both plasma thrombin and plasmin. Thrombin, as determined both using a chromogenic substrate and the natural substrate, fibrinogen, was inactivated upon reaction with CS in a dose-dependent manner, but not in the presence of the structurally related steroid sulfates, I3SO3-GalCer and II3NAalpha-LacCer, suggesting that both the sulfate group and the hydrophobic side chain of CS are necessary for the inhibitory activity of CS. Preincubation of thrombin with CS at 37 degrees C for 10 min was required to achieve maximum inhibition, and virtually complete inhibition was achieved at a molar ratio of CS to thrombin of 18:1. CS-treated thrombin had the same Km and a lower Vmax than the original enzyme, and a higher molecular weight. The molecular weight and activity of the original enzyme were not observed on the attempted separation of the CS-treated enzyme by gel permeation chromatography and native PAGE, indicating that the inactivation of thrombin by CS is irreversible. In contrast, CS was readily liberated from the enzyme by SDS-PAGE, suggesting that hydrophobic interactions are involved in the CS-mediated inactivation of thrombin. When acidic lipids were reacted with thrombin after dissolving them in DMSO, I3SO3-GalCer, steroid sulfates and II3NAalpha-LacCer, as well as CS, but not SDS and sodium taurocholate, exhibited inhibitory activity, probably due to micellar formation facilitating interaction between thrombin and negatively charged lipids. On the other hand, plasmin, as determined using a chromogenic substrate, was more susceptible to acidic lipids than thrombin. CS, I3SO3-GalCer and II3NAalpha-LacCer, all of which are present in serum, inhibited the activity of plasmin in aqueous media, as well as in DMSO-mediated lipid solutions. Thus, acidic lipids in plasma were demonstrated to possess regulatory activity as endogenous detergents toward both enzymes for blood clotting and fibrinolysis.  (+info)

Distinct contributions of residue 192 to the specificity of coagulation and fibrinolytic serine proteases. (4/1717)

Archetypal members of the chymotrypsin family of serine proteases, such as trypsin, chymotrypsin, and elastase, exhibit relatively broad substrate specificity. However, the successful development of efficient proteolytic cascades, such as the blood coagulation and fibrinolytic systems, required the evolution of proteases that displayed restricted specificity. Tissue-type plasminogen activator (t-PA), for example, possesses exquisitely stringent substrate specificity, and the molecular basis of this important biochemical property of t-PA remains obscure. Previous investigations of related serine proteases, which participate in the blood coagulation cascade, have focused attention on the residue that occupies position 192 (chymotrypsin numbering system), which plays a pivotal role in determining both the inhibitor and substrate specificity of these enzymes. Consequently, we created and characterized the kinetic properties of new variants of t-PA that contained point mutations at position 192. These studies demonstrated that, unlike in coagulation serine proteases, Gln-192 does not contribute significantly to the substrate or inhibitor specificity of t-PA in physiologically relevant reactions. Replacement of Gln-192 with a glutamic acid residue did, however, decrease the catalytic efficiency of mature, two-chain t-PA toward plasminogen in the absence of a fibrin co-factor.  (+info)

Age-related changes in blood coagulation and fibrinolysis in mice fed on a high-cholesterol diet. (5/1717)

To investigate the pathogenesis of hyperlipidemia-induced atherosclerosis, we examined age-dependent changes in platelet activity, blood coagulation and fibrinolysis in susceptibility to a high cholesterol diet (HCD) feeding in male ICR mice. Pretreatment of platelet-rich-plasma from HCD feeding mice for 3 days with epinephrine (300 microM) resulted in a marked enhancement of adenosine 5'-diphosphate (ADP: 0.1 microM) or collagen (0.7 microgram/ml)-stimulated aggregation compared with the same in control mice. Yohimbine as alpha 2-adrenergic blocker antagonized these aggregations in a dose-dependent manner. A significant increase in plasma total cholesterol and VLDL (very low-density lipoprotein)-LDL (low-density lipoprotein)-cholesterol and the liver/body weight ratio was observed in mice fed on HCD for 3 months (3-month HCD mice). In the early phase of this experiment, a significant increase in fibrinogen was observed. In the middle phase, increases in the activity of antithrombin III (ATIII) and alpha 2-plasmin inhibitor (alpha 2-Pl) followed. Plasminogen content gradually decreased in both normal diet and HCD mice throughout the experiment. The activity of plasminogen activator inhibitor (PAI) decreased in 3-month HCD mice. Morphological observation of the aortic arch from 3-month HCD mice revealed apparent atheromatous plaques not seen in control mice. These results suggest that 3-month HCD mice can be a convenient hyperlipidemia-induced atherosclerotic model and the changes in platelet activity, coagulation and fibrinolysis in the early phase may be a cause of pathologic changes in this model.  (+info)

Fibrinolytic activation markers predict myocardial infarction in the elderly. The Cardiovascular Health Study. (6/1717)

Coagulation factor levels predict arterial thrombosis in epidemiological studies, but studies of older persons are needed. We studied 3 plasma antigenic markers of fibrinolysis, viz, plasminogen activator inhibitor-1 (PAI-1), fibrin fragment D-dimer, and plasmin-antiplasmin complex (PAP) for the prediction of arterial thrombosis in healthy elderly persons over age 65. The study was a nested case-control study in the Cardiovascular Health Study cohort of 5201 men and women >/=65 years of age who were enrolled from 1989 to 1990. Cases were 146 participants without baseline clinical vascular disease who developed myocardial infarction, angina, or coronary death during a follow-up of 2.4 years. Controls remained free of cardiovascular events and were matched 1:1 to cases with respect to sex, duration of follow-up, and baseline subclinical vascular disease status. With increasing quartile of D-dimer and PAP levels but not of PAI-1, there was an independent increased risk of myocardial infarction or coronary death, but not of angina. The relative risk for D-dimer above versus below the median value (>/=120 microg/L) was 2.5 (95% confidence interval, 1.1 to 5.9) and for PAP above the median (>/=5.25 nmol/L), 3.1 (1.3 to 7.7). Risks were independent of C-reactive protein and fibrinogen concentrations. There were no differences in risk by sex or presence of baseline subclinical disease. D-dimer and PAP, but not PAI-1, predicted future myocardial infarction in men and women over age 65. Relationships were independent of other risk factors, including inflammation markers. Results indicate a major role for these markers in identifying a high risk of arterial disease in this age group.  (+info)

Relationship of plasmin generation to cardiovascular disease risk factors in elderly men and women. (7/1717)

Plasmin-alpha2-antiplasmin complex (PAP) marks plasmin generation and fibrinolytic balance. We recently observed that elevated levels of PAP predict acute myocardial infarction in the elderly, yet little is known about the correlates of PAP. We measured PAP in 800 elderly subjects who were free of clinical cardiovascular disease in 2 cohort studies: the Cardiovascular Health Study and the Honolulu Heart Program. Median PAP levels did not differ between the Cardiovascular Health Study (6.05+/-1.46 nmol/L) and the Honolulu Heart Program (6.11+/-1.44 nmol/L), and correlates of PAP were similar in both cohorts. In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37). PAP was associated with increased atherosclerosis as measured by the ankle-arm index (AAI) (P for trend, +info)

Relative contribution of insulin and its precursors to fibrinogen and PAI-1 in a large population with different states of glucose tolerance. The Insulin Resistance Atherosclerosis Study (IRAS). (8/1717)

Hyperinsulinemia is associated with the development of coronary heart disease. However, the underlying mechanisms are still poorly understood. Hypercoagulability and impaired fibrinolysis are possible candidates linking hyperinsulinism with atherosclerotic disease, and it has been suggested that proinsulin rather than insulin is the crucial pathophysiological agent. The aim of this study was to investigate the relationship of insulin and its precursors to markers of coagulation and fibrinolysis in a large triethnic population. A strong and independent relationship between plasminogen activator inhibitor-1 (PAI-1) antigen and insulin and its precursors (proinsulin, 32-33 split proinsulin) was found consistently across varying states of glucose tolerance (PAI-1 versus fasting insulin [proinsulin], r=0.38 [r=0.34] in normal glucose tolerance; r=0.42 [r=0.43] in impaired glucose tolerance; and r=0.38 [r=0.26] in type 2 diabetes; all P<0.001). The relationship remained highly significant even after accounting for insulin sensitivity as measured by a frequently sampled intravenous glucose tolerance test. In a stepwise multiple regression model after adjusting for age, sex, ethnicity, and clinic, both insulin and its precursors were significantly associated with PAI-1 levels. The relationship between fibrinogen and insulin and its precursors was significant in the overall population (r=0.20 for insulin and proinsulin; each P<0.001) but showed a more inconsistent pattern in subgroup analysis and after adjustments for demographic and metabolic variables. Stepwise multiple regression analysis showed that proinsulin (split products) but not fasting insulin significantly contributed to fibrinogen levels after adjustment for age, sex, clinic, and ethnicity. Decreased insulin sensitivity was independently associated with higher PAI-1 and fibrinogen levels. In summary, we were able to demonstrate an independent relationship of 2 crucial factors of hemostasis, fibrinogen and PAI-1, to insulin and its precursors. These findings may have important clinical implications in the risk assessment and prevention of macrovascular disease, not only in patients with overt diabetes but also in nondiabetic subjects who are hyperinsulinemic.  (+info)

TY - JOUR. T1 - Fibrinolysis és érbetegségek.. AU - Udvardy, M.. AU - Boda, Z.. PY - 1996/8/25. Y1 - 1996/8/25. N2 - A wide array of in vitro fibrinolysis tests had been performed for a long period, suggesting defective fibrinolysis, mainly impaired tPA response and reserve as major, frequent abnormality, predecessor or causative factor of venous thromboembolism. However, these abnormalities were troublesome to reproduce, and more recently fibrinolytic activators and inhibitors received growing attention as rather atherogenic and less thrombogenic risk factors. Even if it is still not settled, lipoprotein(a) may interfere with fibrinolysis, and seems to carry atherogenic risk, too. The genetic polymorphism of fibrinogen, plasminogen, PAI-1 and some other compounds modifying circulating fibrinogen levels are also discussed in this review.. AB - A wide array of in vitro fibrinolysis tests had been performed for a long period, suggesting defective fibrinolysis, mainly impaired tPA response and ...
Smoking is associated with endothelial dysfunction and abnormalities in thrombosis/fibrinolysis system, possibly through increased oxidative stress. In this study we investigated the effect of combined antioxidant treatment with vitamins C and E on endothelial function and plasma levels of plasminogen activator inhibitor (PAI-1), von Willebrand factor (vWF), tissue plasminogen activator (tPA) and factor VII (fVII), in smokers. Forty-one healthy smokers were randomly divided into 4 groups receiving vitamin C 2g/day (group A), vitamin C 2g/day plus vitamin E 400 IU/day (group B), vitamin C 2g/day plus vitamin E 800 IU/day (group C) or no antioxidants (controls, group D), for 4 weeks. Forearm blood flow was measured using venous occlusion strain-gauge plethysmography. Forearm vasodilatory response to reactive hyperemia (RH%) or to sublingual nitroglycerin administration (NTG%) were considered as indexes of endothelium dependent or independent dilation respectively. After treatment, RH% was increased only
Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. This process has two types: primary fibrinolysis and secondary fibrinolysis. The primary type is a normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause. In fibrinolysis, a fibrin clot, the product of coagulation, is broken down. Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Plasmin is produced in an inactive form, plasminogen, in the liver. Although plasminogen cannot cleave fibrin, it still has an affinity for it, and is incorporated into the clot when it is formed. Tissue plasminogen activator (t-PA) and urokinase are the agents that convert plasminogen to the active plasmin, thus allowing fibrinolysis to occur. t-PA is released into the blood very slowly by the damaged endothelium of the ...
Serial changes in coagulation and fibrinolysis studied among 42 patients admitted to hospital with a wide variety of injuries are reported. The first hours after trauma are dominated by an acceleration of fibrinolysis (clot lysis) and clotting time which are often followed by an abrupt rebound to prolonged fibrinolysis and normal clotting. Evidence is presented that acceleration of fibrinolysis is due to flooding of the circulation by plasminogen activator and that prolongation is probably due to an inhibitor. A prolonged prothrombin time, increased prothrombin consumption index, an acceleration of the heparin-retarded clotting time, and a fall in the platelet count are also frequent during the first hours after injury. There is evidence also of an early deficiency in factor V and the onset of a fall in factor VII and prothrombin.. The following days are characterized by continued prolongation of fibrinolysis, a lengthening of clotting time, and an increased prothrombin consumption index ...
TY - JOUR. T1 - Hypercholesterolaemia and lipid lowering treatment do not affect the acute endogenous fibrinolytic capacity in vivo. AU - Newby, D.E.. AU - Witherow, F.N.. AU - Wright, R.A.. AU - Bloomfield, P.. AU - Boon, N.A.. AU - Fox, K.A.A.. AU - Ludlam, C.A.. AU - Webb, D.J.. PY - 2002/1/1. Y1 - 2002/1/1. N2 - OBJECTIVE: To assess acute tissue plasminogen activator (t-PA) release in vivo in patients with hypercholesterolaemia in the presence and absence of lipid lowering treatment and in matched normocholesterolaemic controls.DESIGN: Parallel group comparison and double blind randomised crossover.SETTING: University hospital.PATIENTS: Eight patients with hypercholesterolaemia (, 7.8 mmol/l) and eight matched normocholesterolaemic controls (, 5.5 mmol/l).METHODS: Blood flow and plasma fibrinolytic factors were measured in both forearms during unilateral brachial artery infusions of the endothelium dependent vasodilator substance P (2-8 pmol/min) and the endothelium independent vasodilator ...
D.K. Nagi, S. Jain, S. Garvey, S. Walji, J.S. Yudkin; Defective Fibrinolysis in Non-Insulin-Dependent Diabetics Relates to Plasma Insulin Concentrations. Clin Sci (Lond) 1 March 1991; 80 (s24): 25P. doi: https://doi.org/10.1042/cs080025Pb. Download citation file:. ...
The local fibrinolytic activity generated in the leg and arm veins during venous occlusion (fibrinolytic capacity) and the systemic fibrinolytic activity were measured at intervals in 11 patients after fracture of the femoral shaft and in 11 patients after acute myocardial infarction. In both groups the fibrinolytic capacity of the leg veins and the systemic fibrinolytic activity were significantly reduced two days after the onset of tissue injury. The fibrinolytic capacity of the arm veins was not altered. These results provide a possible explanation for the predilection of venous thrombosis for the leg veins after accidental trauma and acute myocardial infarction. ...
Abstract. High plasma levels of lipoprotein(a) [Lp(a)] are considered to be an independent risk factor for premature cardiovascular disease and are inversely as
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Impaired fibrinolysis is believed to promote atherosclerosis and contribute to myocardial infarction. The major triggering factor for fibrinolysis is vascular tissue plasminogen activator (t-PA), and the aim of this study was to evaluate the capacity of human arterial smooth muscle cells (SMC) for induction of fibrinolysis. SMC were plated on labeled fibrin gels, and lysis was measured as release of label. Fibrinolytic capacity was dependent on the phenotypic state of SMC. The multilayered phenotype to which SMC modulate after cellular injury had a much lower fibrinolysis-inducing capacity than the more ordinary monolayered SMC type. Fibrinolysis was mediated by activation of plasminogen. In long-term experiments under conditions imitating thrombolysis, platelet-derived growth factor promoted fibrinolysis indirectly by increase of SMC number, and a direct effect on cellular production of t-PA was not detected. SMC from atherosclerotic intima had a much lower capacity for induction of ...
TY - JOUR. T1 - Reduced fibrinolytic activity in glomeruli isolated from rabbits infused with tumor necrosis factor. AU - Colucci, Mario. AU - Zoja, A.. AU - Remuzzi, E.. AU - Semeraro, N.. PY - 1993. Y1 - 1993. N2 - Glomerular fibrin deposition may result from local activation of blood coagulation and/or impaired removal by the fibrinolytic system. We evaluated the fibrinolytic activity of glomeruli isolated from rabbits infused for 5 h with tumor necrosis factor (TNF) at the doses of 0.8 μg/kg/h (n = 5) and 8 μg/kg/h (n = 3) or with endotoxin (8 μg/kg/h, n = 7). Animals infused with vehicle (n = 11) served as control group. Plasminogen activator (PA) activity of glomerular extracts from rabbits infused with 8 μg/kg/h of TNF or endotoxin was significantly lower than that of samples from control animals (p = 0.013 and p = 0.003, respectively). At the dose of 0.8 μg/kg/h, TNF caused a reduction in glomerular PA activity which, however, did not reach statistical significance. Neither ...
activities of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1), using a bio-functional immunosorbent assay (BIA). Although the walking capacity was increased significantly after 12 weeks of training (p,0.01), the activities of t-PA (pre 1.04±0.68, post 0.93±0.71 UI/ml), and PAI-1 (pre 18.43±17.19, post 23.08±20.01 UI/ml) did not show significant changes. The results suggest that 12 weeks of supervised exercise training did not increase, while there was a trend of decrease in the resting fibrinolytic function in this group of patients. The reason of this change needs to be studied in the future.. ...
TY - JOUR. T1 - Plasmin catalyzed fibrinolysis as quantified by a new kinetic method. AU - Sazonova, I. V.. AU - Sirovskava, S. F.. AU - Aisina, R. B.. AU - Varfolomevev, S. D.. PY - 1996/12/1. Y1 - 1996/12/1. N2 - Kinetics fibrinolysis by plasmin (Pro) was studied by a new method which allowed to describe quantitatively the clot lysis reaction. Cylindrical fibrin (Fn) clots (0.9 ml) were formed in glass tubes of different diameters. After addition of Pm (5 nM1 μM) in buffer over the clots, the lysis kinetics at 37°C was traced by decrease of clot column height with catetometer. Linear rate of lysis (VI) was measured as tangent of the clot boundary movement in time (mm/min). Because of fibrin surface square (S) did not change during the lysis, the mass rates of lysis (VM, M/min) were calculated from equation: VM=vI·S·[Fn]/v, where [Fn] was Fn concentration in clot, v was liquid phase volume. Dependences of VM on the Pm and Fn concentrations, as well as on S and shaking rate were obtained. It ...
If the thrombotic tendency plays a significant role in the etiology of psychosis, one would expect to find ischemic brain injuries in neuroimaging studies, but it does not happen. Therefore, if there is a correlation between thrombotic tendency-hypofibrinolysis and psychosis it is likely to occur at the biochemical level, such as in neuronal transmission.. The investigators hypothesis is that mechanisms that inhibit tissue plasminogen activator (t-PA) and therefore promote hypofibrinolysis, are directly or indirectly involved in the genesis of psychosis, because t-PA participates in neuronal plasticity and low t-PA levels are related to dementia.. Hypofibrinolysis due to t-PA inhibition can be seen in:. ...
A two-stage assay for canine profibrinolysin plasminogen is described. This assay is suitable for following in vivo changes in profibrinolysin titer induced by various experimental procedures. Plasma profibrinolysin is concentrated by a low ionic strength, protamine sulfate precipitation technic and activated with staphylokinase. Diluted aliquots of the activated solution are then assayed for fibrinolytic activity. One unit is that amount of activity which at 37 degrees C. and pH 7.25 will bring about lysis of 0.4 ml. of a 0.1 percent bovine fibrin clot in 300 seconds. The average dog plasma contains 19.4 units per milliliter. In general, increases in circulating fibrinolytic activity are associated with decreases in profibrinolysin.
Methods: Twenty patients undergoing endovascular stenting for abdominal aortic aneurysm were randomized to receive 100 mL of 10% dextran-40. orsalinc, over I hour, during their operation in addition to heparin. Mood samples were taken preoperatively, intraoperatively (immediately after operative procedure), and 24 hours postoperatively. Thrombi were formed in a Chandler loop and used to assess endogenous fibrinolysis over 24 hours, measured as the fall in thrombus weight, and the release of fluorescently labelled fibrinogen from the thrombus. Plasma samples were analyzed for markers of fibrinolysis; plasmin-antiplasmin (PAP), PAI-1, and t-PA, and for functional von Willebrand factor (vWF). Platelet response to thrombin and other agonists was measured by flow cytometry.. Results: S63845 supplier Thrombi formed ex vivo front the intraoperative blood samples from the dextran-treated patients. exhibited significantly greater fibrinolysis vs preoperative samples, seen both as a significantly greater ...
Summary. Background: Activated factor XIII (FXIIIa), a transglutaminase, introduces fibrin-fibrin and fibrin-inhibitor cross-links, resulting in more mechanically stable clots. The impact of cross-linking on resistance to fibrinolysis has proved challenging to evaluate quantitatively. Methods: We used a whole blood model thrombus system to characterize the role of cross-linking in resistance to fibrinolytic degradation. Model thrombi, which mimic arterial thrombi formed in vivo, were prepared with incorporated fluorescently labeled fibrinogen, in order to allow quantification of fibrinolysis as released fluorescence units per minute. Results: A site-specific inhibitor of transglutaminases, added to blood from normal donors, yielded model thrombi that lysed more easily, either spontaneously or by plasminogen activators. This was observed both in the cell/platelet-rich head and fibrin-rich tail. Model thrombi from an FXIII-deficient patient lysed more quickly than normal thrombi; replacement ...
A case-control comparison within the framework of the prospective, multidisciplinary PLAT Study was performed to assess whether altered baseline fibrinolytic variables were associated with an elevated risk of ischemic thrombotic events in patients with documented coronary, cerebral, and/or peripheral atherosclerotic disease. Fibrinogen, D-dimer, tissue plasminogen activator (t-PA) antigen, and fibrinolytic activity before and after venous stasis (delta = difference between the two values), t-PA inhibitor, and lipid levels in 60 atherosclerotic patients with a thrombotic event during the first year of follow-up were compared with those in 94 atherosclerotic patients without such events, who were matched for age, sex, and diagnosis at enrollment. Events were associated with a higher release of delta t-PA antigen (P = .047), higher D-dimer (P = .024), and higher t-PA inhibitor (P = .001) levels. delta Fibrinolytic activity was correlated inversely with t-PA inhibitor (P , .01) and triglycerides (P ...
Bambakidis, T., Dekker, S. E., Halaweish, I., Liu, B., Nikolian, V. C., Georgoff, P. E., Piascik, P., Li, Y., Sillesen, M. & Alam, H. B., sep. 2017, I: Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis. 28, 6, s. 479-484 6 s.. Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review ...
The coagulation-fibrinolysis system is considered to be an important factor in the growth and spread of tumors (Kodama, 1974; Kinjo, 1978). At the advancing border of the tumors, deposition of fibrin...
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INTRODUCTION: Pulse pressure is a potent risk factor for atherosclerotic disease. The purpose of this cross-sectional study was to determine whether pulse pressure is associated with blood coagulation and fibrinolysis in patients with diabetes. MATER
In this case, because the patient is hemodynamically stable and has no heart failure or contraindications to fibrinoysis, and because transfer for PCI would impose a further treatment delay, largely exceeding 60 minutes, fibrinolysis is the preferred option.3. Question: What if your community hospital is within 30 minutes from a centre that could perform a PCI and therefore both fibrinolysis and angioplasty are possible within appropriate time frames? What treatment option should be favoured?. Comment: We believe that both options would be acceptable and that it is reasonable in this case to select immediate on-site fibrinolysis because (a) the patient is not at very high risk in terms of her clinical presentation (no evidence of heart failure or hemodynamic instability; (b) the ischemic time is less than 3 hours, a time frame when fibrinolysis is most effective;2,3 and (c) the fibrinolytic risk of major bleeding is low. Commonly used fibrinolytics in Canada are the bolus agents tenecteplase and ...
Severe infectious diseases, including sepsis, remain a serious medical challenge worldwide. Clinical symptoms of patients suffering from sepsis are a culmination of complex interactions between the infecting microorganism and host immune responses, such as the induction of overwhelming inflammatory reactions, systemic activation of the coagulation system, and impaired fibrinolysis. These alarming findings prompted many research groups, including my own, to search for novel strategies to treat severe infectious diseases. Many of these approaches are focused on so-called host effector systems, since evidence has accumulated that complications from an infection are caused by an over-stimulation of host defense systems that are modulated by bacteria or bacterial products. In severe infections, such as sepsis and septic shock, vascular leakage, increased cytokine levels, and coagulation/fibrinolysis dysfunction are often observed.. My research projects aim to identify and characterize molecular ...
The introduction of highly effective combined antiretroviral therapy (cART) in 1996 resulted in effective, long-term suppression of HIV with consequent recovery of the patients immune system. Although the enthusiasm about the effectiveness of current cART remains strong, the ongoing work in the area of HIV disease and treatment complications appears ... read more to reflect concerns that these clinical problems will continue to be important and possibly increase over time in the current therapeutic area. There is growing interest in the pathogenesis, treatment and prevention of long-term complications of HIV disease and its therapies. This thesis describes some of the long-term complications of HIV-infection since the introduction of cART. Cardiac and vascular complications are one of the most frequently occurring complications in long-term surviving HIV-infected patients in different ethnical populations. In the first part markers of coagulation, anticoagulation and fibrinolysis are studied to ...
The existence of a potent fibrinolytic enzyme (nattokinase, NK) in the traditional fermented food called natto, was reported by us previously. It was confirmed that oral administration of NK (or nat
The liver is the primary site of synthesis of coagulation, anticoagulant, and fibrinolytic proteins. In fact, only five blood clotting factors are not produced there. Therefore, liver diseases that cause clotting issues in dogs can be very serious and sometimes life-threatening.
The reduction of MS relapses in preganancy is a well documented phenomenon and the reasons for it are not known. I propose that it is secondary to increased fibrinolytic activity during pregnancy. Fibrinolytic activity is the bloods ability to break ...
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Affiliation:福岡大学,薬学部,教授, Research Field:Biological pharmacy, Keywords:セラミド,Ceramide,Sulfated polysaccharide,情報伝達因子,Endotoxin,虚血性心疾患,Fibrinolytic factor,血管内皮,Vascular endothelium,Vascular endothelial cells, # of Research Projects:2, # of Research Products:0
Plasminogen, Apolipoprotein, Apolipoprotein(a), Atherosclerosis, Binding Sites, Cardiovascular Disease, Disease, Fibrin, Fibrinogen, Fibrinolysis, Human, Inhibition, Lipoprotein, Lipoprotein(a), Lysine, Measure, Oxidative Stress, Patients, Plasma, Plasminogen Activator
For many years it has been known that abnormal coagulation and fibrinolytic activity existed in the environs of malignant tumours. Whether these activities affected the invasiveness and metastatic...
Title: Thrombin-Activatable Fibrinolysis Inhibitor. VOLUME: 11 ISSUE: 17. Author(s):Pauline F. Marx. Affiliation:Dept. Vascular Medicine, G1-114, Academic Medical Center, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands.. Keywords:tafi, cpu, cpr, cpb, carboxypeptidase, coagulation, fibrinolysis. Abstract: The coagulation system is a potent mechanism that prevents blood loss after vascular injury. It consists of a number of linked enzymatic reactions resulting in thrombin generation. Thrombin converts soluble fibrinogen into a fibrin clot. The clot is subsequently removed by the fibrinolytic system upon wound healing. Thrombin-activatable fibrinolysis inhibitor (TAFI), which is identical to the previously identified proteins procarboxypeptidase B, R, and U, forms a link between blood coagulation and fibrinolysis. TAFI circulates as an inactive proenzyme in the bloodstream, and becomes activated during blood clotting. The active form, TAFIa, inhibits fibrinolysis by cleaving off C-terminal ...
We investigated clot lysis time, thrombin activatable fibrinolysis inhibitor antigen (TAFI) levels and TAFI gene polymorphisms in pregnant patients with severe preeclampsia, with or without associated antiphospholipid syndrome (APS). The study groups
The thrombin-catalysed conversion of plasma fibrinogen into fibrin and the development of an insoluble fibrin clot are the final steps of the coagulation cascade during haemostasis. A delicate balance between coagulation and fibrinolysis determines the stability of the fibrin clot. Thrombin Activatable Fibrinolysis Inhibitor (TAFI) plays an important role in this process. TAFI is activated by thrombin and protects the fibrin clot against lysis. The role of TAFI in bleeding and thrombotic disorders is discussed as well as its novel emerging role in wound healing and inflammation ...
Thrombin-activatable fibrinolysis inhibitor (TAFI) is a metallocarboxypeptidase (MCP) that links blood coagulation and fibrinolysis. TAFI hampers fibrin-clot lysis and is a pharmacological target for the treatment of thrombotic conditions. TAFI is transformed through removal of its prodomain by thrombin-thrombomodulin into TAFIa, which is intrinsically unstable and has a short half-life in vivo. Here we show that purified bovine TAFI activated in the presence of a proteinaceous inhibitor renders a stable enzyme-inhibitor complex. Its crystal structure reveals that TAFIa conforms to the α/β-hydrolase fold of MCPs and displays two unique flexible loops on the molecular surface, accounting for structural instability and susceptibility to proteolysis. In addition, point mutations reported to enhance protein stability in vivo are mainly located in the first loop and in another surface region, which is a potential heparin-binding site. The protein inhibitor contacts both the TAFIa active site and an ...
Background Mortality and morbidity in patients with bacterial meningitis result from the proinflammatory response and dysregulation of coagulation and fibrinolysis. Thrombin-activatable fibrinolysis inhibitor (TAFI) is activated by free thrombin or thrombin in complex with thrombomodulin, and plays an antifibrinolytic role during fibrin clot degradation, but also has an anti-inflammatory role by inactivating proinflammatory mediators, such as complement activation products. Objective To assess the role of TAFI in pneumococcal meningitis. Methods We performed a prospective nationwide genetic association study in patients with bacterial meningitis, determined TAFI and complement levels in cerebrospinal fluid (CSF), and assessed the function of TAFI in a pneumococcal meningitis mouse model by using Cpb2 (TAFI) knockout mice. Results Polymorphisms (reference sequences: rs1926447 and rs3742264) in the CPB2 gene, coding for TAFI, were related to the development of systemic complications in patients ...
Objective: Inflammation and migration of leukocytes to the brain parenchyma play a role in atherosclerosis and cerebral ischemic stroke. Migration occurs with the help of adhesion molecules on the surface of cerebral endothelial cells and leukocytes. P-selectin, an adhesion molecule, is present on the platelet and endothelial surface and allows leukocytes to loosely adhere to the endothelium, and its increase has been shown in acute ischemic stroke (AIS). Thrombin-activatable fibrinolysis inhibitor (TAFI) is a procarboxypeptidase molecule that can be another marker of AIS, which has been shown to increase the risk of thromboembolism and stroke 6-fold. Intima-media thickness (IMT) is thought to be associated with atherosclerotic diseases in carotid ultrasonography (USG) and increased risk of ischemic stroke has been found to be associated with increased carotid IMT. In this study, we investigated the relationship between P-selectin and TAFI levels, which have been shown to be effective for AIS ...
Inhibition of Fibrinolysis. For maintaining high fidelity regulation between coagulatory clotting and proteolytic fibrinolysis TAFI (Thrombin activatable fibrinolysis inhibitor) plays an important inhibitory role. Apart from this, four different forms of plasminogen activator inhibitors, denoted PAI-1 to PAI-4, are also known.. PAI-1, which is the most prominent form, is mainly synthesized in endothelial cells and stored in thrombocytes. Its release is concentrated to platelet rich clots leading to an increased thrombus resistance to fibrinolysis. Another fibrinolysis inhibitor is the plasmin inhibitor (α2-antiplasmin). FXIIIa makes it an initial clot stabilizer by rapidly and covalently binding this inhibitor to fibrin. The role of inhibiting plasmin is made directly by a 1:1-complex formation between plasmin and antiplasmin (PAP). PAP can be immunologically detected in plasma, and is therefore used as a diagnostic parameter for proving thrombosis.. Function of plasmin. The fibrinogen molecule ...
Thrombin activatable fibrinolysis inhibitor (TAFI) is a human plasma-derived zymogen that is activated through proteolytic cleavage by thrombin, thrombin in complex with thrombomodulin, or plasmin. Active TAFI attenuates fibrinolysis by removing carboxyl-terminal lysine residues from partially degraded fibrin, thereby inhibiting a potent positive feedback loop in the fibrinolytic cascade. In addition to the plasma pool of TAFI arising from expression in the liver, a distinct pool of TAFI has been reported to be present in platelets. While the antifibrinolytic effect of plasma-derived TAFI has been well-documented by in vitro and in vivo clot lysis assays, characterization of the platelet-derived form has been limited. Here, we not only confirm the presence of TAFI in the medium of washed, thrombin-stimulated platelets, but also that platelet-derived TAFI is capable of attenuating platelet-rich thrombus lysis in vitro independently of plasma TAFI using a novel thrombus lysis assay. Fluorescent ...
AIMS: To determine whether circulating tissue plasminogen activator (t-PA) antigen concentrations are prospectively related to risk of coronary heart disease (CHD) in the general population. METHODS AND RESULTS: We measured baseline concentrations of t-PA antigen in the stored serum samples of 606 CHD cases and 1227 controls nested in a prospective cohort of 5661 men monitored for 16 years, and conducted a meta-analysis of previous relevant studies to place our findings in context. Tissue plasminogen activator antigen values were strongly correlated with several vascular risk factors, including serum lipids, body mass index, alcohol consumption, and markers of systemic inflammation. In a comparison of men in the top third compared with those in the bottom third of baseline t-PA antigen values, the odds ratio for CHD was 2.20 (95% confidence interval (CI) 1.70-2.85) after adjustment for age and town only, but this fell to 1.48 (1.09-2.01) after further adjustment. Analysis of t-PA as a continuous
TY - CHAP. T1 - Plasmin-antiplasmin system. AU - Mutch, Nicola J.. AU - Booth, Nuala A.. PY - 2016/4/19. Y1 - 2016/4/19. N2 - Plasmin is the key enzyme involved in the dissolution of fibrin. It is produced from plasminogen, which is activated by a plasminogen activator; the two primary activators are tissue-type plasminogen activator (tPA) and urinary-type plasminogen activator (uPA), also called urokinase. The process is regulated by inhibitors, principally plasminogen activator inhibitor 1 (PAI-1), α2-antiplasmin (α2AP) and thrombin-activatable fibrinolysis inhibitor (TAFI). Crucial control is exerted by surfaces, such as fibrin or cells, with plasminogen activation not normally occurring in the circulation. Here we will consider the individual players of the fibrinolytic cascade and their specific locations and potential interactions. Key questions considered are the initiation of fibrinolysis and the most appropriate ways to measure abnormalities in disease situations.. AB - Plasmin is the ...
TAFI is a plasma protein assumed to be an important link between coagulation and fibrinolysis. The three-dimensional crystal structures of authentic mature bovine TAFI (TAFIa) in complex with tick carboxypeptidase inhibitor, authentic full lenght bovine plasma thrombin-activatable fibrinolysis inhibitor (TAFI), and recombinant human TAFI have recently been solved. In light of these recent advances, we have characterized authentic bovine TAFI biochemically and compared it to human TAFI. The four N-linked glycosylation sequons within the activation peptide were all occupied in bovine TAFI, similar to human TAFI, while the sequon located within the enzyme moiety of the bovine protein was non-glycosylated. The enzymatic stability and the kinetic constants of TAFIa differed somewhat between the two proteins, as did the isoelectric point of TAFI, but not TAFIa. Equivalent to human TAFI, bovine TAFI was a substrate for transglutaminases and could be proteolytically cleaved by trypsin or thrombin/solulin
TY - JOUR. T1 - Fibrinolysis resistant fibrin deposits in lymph nodes with Hodgkins disease. AU - Adany, R.. AU - Szegedi, A.. AU - Ablin, R. J.. AU - Muszbek, L.. PY - 1988/1/1. Y1 - 1988/1/1. N2 - Extravasal fibrin deposition is frequently observed within and around tumorous tissues and has been implicated in various aspects of tumor growth. However, no adequate information has been available on the mechanism how intratumoral interstitial fibrin deposits escape a prompt elimination by the fibrinolytic system. In this study we provide immunomorphological evidence showing that fibrin deposits in lymph nodes with Hodgkins disease are stabilized and made resistant to fibrinolysis by factor XIII (FXIII) of blood coagulation. By double immunofluorescent labelling systems fibrin deposits were simultaneously stained for α2-antiplasmin (α2-AP), the main physiological inhibitor of fibrinolysis and in a number of nodular areas they were also labelled for plasmin(ogen). The detection of ...
Free Online Library: Assay of procarboxypeptidase U, a novel determinant of the fibrinolytic cascade, in human plasma.(Enzymes and Protein Markers) by Clinical Chemistry; Fibrin Lysine
ECLT provides an overall assessment of the fibrinolysis system by measuring the time for an in vitro clot to dissolve in the absence of the normal plasmin inhibitors. ECLT is useful in assessing the fibrinolytic system and monitoring patients on urokinase or streptokinase fibrinolytic therapy ...
Abstract The present study was designed to investigate whether medium-term, low-dose heparin treatment is able to affect the fibrinolytic system. In a randomized cross-over study 10 asymptomatic patients with previous (1-6 years) myocardial infarction underwent two sequential 15-day treatments, respectively, on heparin and on placebo (saline solution), preceded and separated by 10-day wash-out periods. Heparin (as calcium heparin, 12,500 IU in 0.5 ml) and saline (0.5 ml) were subcutaneously administered once a day at 8 a.m. Blood samples for fibrinolysis studies were withdrawn on the first and 15th day of each period immediately before and 4 h after heparin or saline administration before and after 10 min venous occlusion (VO) respectively. Four hours after the first heparin administration tissue plasminogen activator antigen (t-PA ag) levels significantly increased with respect to saline administration (p , 0.01 and p , 0.05, respectively). After 15-day heparin treatment a decrease in ...
PubMed journal article: Effect of second- and third-generation oral contraceptives on fibrinolysis in the absence or presence of the factor V Leiden mutation. Download Prime PubMed App to iPhone, iPad, or Android
Anti-Human TAFI Clone 1 - Detects Human Thrombin Activatable Fibrinolysis Inhibitor (TAFI) and activated TAFI. Mouse monoclonal of isotype IgG1.
Anti-Human TAFI Clone 3 - Detects Human Thrombin Activatable Fibrinolysis Inhibitor (TAFI) and activated TAFI. Mouse monoclonal of isotype IgG3.
OBJECTIVE: To examine the effect of vitamin C on forearm vasodilatory response to reactive hyperemia and on plasma level of plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF), tissue plasminogen activator (tPA), antithrombin III (ATIII), proteins C and S, and factors V (fV) and VII (fVII) in patients with both type 2 diabetes and CAD. RESEARCH DESIGN AND METHODS: A total of 39 patients with type 2 diabetes and CAD were divided into two groups and received vitamin C (2 g/day) or no antioxidant for 4 weeks. Forearm blood flow was determined using venous occlusion gauge-strain plethysmography at baseline and after treatment. Forearm vasodilatory response to reactive hyperemia (RH%) or nitrate (NTG%) was defined as the percent change of flow from baseline to the maximum flow during reactive hyperemia or after administration of nitrate, respectively. Biochemical markers were determined by enzyme-linked immunosorbent assay (ELISA) or other standard methods. RESULTS: RH% was significantly
Fibrin provides a temporary matrix at the site of vascular injury. The aims of the present work were (1) to follow fibrin formation and lysis onto the surface of human dermal microvascular endothelial cells (HMEC-1), and (2) to quantify the secretion of fibrinolytic components in the presence of fibrin. Fibrin clots at different fibrinogen concentrations were formed on top of (model 1) or beneath (model 2) the endothelial cells. Fibrin formation or lysis onto the surface of HMEC-1 cells, was followed by turbidity. Clot structure was visualized by laser scanning confocal microscopy (LSCM). The secretion of uPA and PAI-1 by HMEC-1 cells was quantified by ELISA. The rate of fibrin formation increased approximately 1.5-fold at low fibrinogen content (0.5 and 1 mg/mL; p | 0.05) compared to the condition without cells; however, it was decreased at 2 mg/mL fibrinogen (p | 0.05) and no differences were found at higher fibrinogen concentrations (3 and 5 mg/mL). HMEC-1 retarded dissolution of clots formed onto
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Impaired fibrinolytic activity is known to play an integral role in the development of vascular disease.19 20 The degree of fibrinolytic dysfunction may be determined in vivo by analyzing levels and/or activity of fibrinolytic proteins (PAI-1, TPA) in plasma samples or by in situ analysis of tissue samples taken from diseased vessels. When detected in the plasma, impaired fibrinolytic activity correlates best with the occurrence of clinical events such as myocardial infarction and stroke but not clearly with angiographic or histological extent of atherosclerosis.19 21 In contrast, in situ evidence of impaired fibrinolytic activity clearly correlates with the extent of histological atherosclerosis. This may also be true for Tx CAD. In a recent study, allografts with depleted levels of arteriolar TPA (possibly as a result of complex formation with PAI-1) were at greater risk of developing earlier and more severe disease than those grafts with normal arteriolar TPA.4 In the case of the transplanted ...
According to the recently described immunothrombosis concept [8], adequate and controlled coagulation activation would stand for an essential innate immune defense mechanism. When over-activated, coagulation pathways however switch from a beneficial to an uncontrolled noxious response. Similarly, excessive neutrophil activation could have deleterious consequences, notably by sustaining coagulation through NETs formation. In the present study, we report that rhTM both impact coagulation and neutrophil activation, two main actors of immunothrombosis.. Sepsis is indeed always associated with the activation of the coagulation cascade [28], resulting in excessive thrombin formation, defective fibrinolysis and consumption of natural anticoagulant proteins, ultimately leading to DIC. Nevertheless, impairment of fibrinolysis plays a key role in microvascular thrombosis, responsible for multiple organ failure syndrome and death [29]. Delayed fibrinolysis might therefore also contribute to septic ...
P8 We have studied the effect of valsartan treatment (3 and 10 mg/kg/day) on plasma fibrinolytic balance in normo- and hypercholesterolemic rabbits. Animals were fed a normal chow or an experimental diet containing 1% cholesterol for 10 weeks. Systolic blood pressure, as well as plasma cholesterol, dimer D, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) were measured. Plasma cholesterol concentrations were higher in rabbits fed the experimental diet compared with control ones. None of the doses of valsartan were able to affect either plasma cholesterol or blood pressure levels in any group.As compared with control animals hypercholesterolemic rabbits presented lower dimer D (0.37±0.07 mg/ml vs 0.96±0.13, p,0.05) and tPA levels (0.27±0.003 ng/ml vs 0.31±0.007, p,0.05) but higher PAI-1 levels (11.1±0.9 ng/ml vs 8.84±0.04, p,0.05). In cholesterol-fed rabbits, valsartan treatment (3 or 10 mg/kg/day) significantly increased both dimer D (0.73±0.1 mg/ml and, ...
Changes in the fibrinolytic system may lead to coagulation disorders in acute trauma patients. This study examined fibrin degradation by measuring D-dimer crosslinked fibrin degradation products (indicates hypercoagulability), plasminogen activators (fibrinolysis), and antithrombin III in 42 adult t...
This article reports the crystal structures of inhibitors of the functional form of thrombin-activatable fibrinolysis inhibitor (TAFIa). In vivo experiments ind
TY - JOUR. T1 - Effects of recombinant human activated protein C on the fibrinolytic system of patients undergoing conventional or tight glycemic control. AU - Polli, F.. AU - Savioli, M.. AU - Cugno, M.. AU - Taccone, R.. AU - Bellani, G.. AU - Spanu, R.. AU - Pesenti, A.. AU - Iapichino, G.. AU - Gattinoni, L.. PY - 2009/7. Y1 - 2009/7. N2 - Aim. Recombinant human activated protein C (rh-APC) and tight glycemic control (TGC) have been shown to reduce mortality in septic patients. Both interventions can reduce the plasma concentration and/or activity of the most powerful suppressor of fibrinolysis, plasminogen activator inhibitor-1 (PAI-I). Our aim was to evaluate the effects on the fibrinolytic system after the administration of rh-APC in septic patients undergoing conventional or TGC. Methods. Posthoc analysis of data was collected from 90 patients with severe sepsis/septic shock, randomized to either conventional or TGC groups. Independent of these treatments, patients with at least two ...
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Blood coagulation and fibrinolytic factors have been measured in 13 patients treated by liver transplantation. During operation intravascular coagulation and fibrinolysis were increased, but seldom to a degree which would cause abnormal bleeding. Measurement of the catabolism of radioactive fibrinogen showed that increased intravascular coagulation continued for long periods after the operation. Despite secondarily increased fibrinolysis, there was a high incidence of thrombosis. Treatment with anticoagulants or with fibrinolysis inhibitors may be valuable in these patients.. ...
Fingerprint Dive into the research topics of Simultaneous thrombin and plasmin generation capacities in normal and abnormal states of coagulation and fibrinolysis in children and adults. Together they form a unique fingerprint. ...
Following treatment of Syrian hamster embryo cells with benzo(a)pyrene, the time required for the expression of enhanced fibrinolytic activity was examined. For this study, the fibrin-agarose overlay method was developed to distinguish the activity of normal and transformed colonies of hamster cells. Colonies possessing enhanced fibrinolytic activity were not observed 8 days after treatment, but they were observed following one passage (2 weeks after treatment). Morphologically transformed colonies, which exhibited no enhanced fibrinolytic activity, were observed 8 days following treatment. In contrast to these two early changes, cells capable of growth in soft agar were observed much later (6 to 8 weeks after treatment). Untreated Syrian hamster embryo cells generally senesced and did not exhibit enhanced fibrinolytic activity. Approximately 1 of 10 untreated cultures escaped senescence and evolved as a continuous cell line; such cultures frequently exhibited enhanced fibrinolytic activity. ...
Behcets disease (BD) is a widespread occlusive-type vasculitis with life-threatening manifestations. The vasculopathy of BD is unique and any type of vessel can be involved. Moreover, vascular lesions in BD represent an occlusive nature suggesting a hypercoagulable/prothrombotic state. The data concerning the genetic defects of the coagulation cascade are expanding. There is evidence of universal activation of haemostatic system in BD. Procoagulant markers of thrombosis are elevated reflecting intravenous excessive thrombin formation. Defective fibrinolysis with impaired fibrinolytic kinetics may have a role in the hypercoagulable/prothrombotic state of BD. Endothelial cell injury and/or pathological activation is well documented in BD. The aim of this paper is to review current literature knowledge and our experience regarding the unresolved complicated issues of genetic thrombotic defects, in vivo haemostatic markers, coagulation inhibitors, impaired fibrinolysis, and endothelial ...
MJ Underwood, RS More, N Weeresena, RK Firmin, DP De Bono; Distention during Surgical Preparation Impairs the Intrinsic Fibrinolytic Activity of Human Saphenous Vein. Clin Sci (Lond) 1 July 1993; 85 (s29): 15P. doi: https://doi.org/10.1042/cs085015Pa. Download citation file:. ...
E. Bonnefoy-Cudraz, P-G. Steg, F. Boutitie, P-Y. Dubien, F. Lapostolle, et al.. Comparison of primary angioplasty and pre-hospital fibrinolysis in acute myocardial infarction (CAPTIM) trial: a 5-year follow-up. European Heart Journal, 2009, 30, pp.1598-1606. ⟨10.1093/eurheartj/ehp156⟩. ⟨hal-02307192⟩ ...
The PhD studentship jointly funded by the BSH, Lifeblood and the BSHT has been awarded to Dr Nicola Mutch and Dr Claire Whyte from the University of Aberdeen for the following project:. The impact of thrombus composition on regulation of fibrinolysis under flow. Fibrin structure profoundly impacts a clots susceptibility to fibrinolysis with compact networks linked to early onset of coronary heart disease. Shear stress modulates the structure and cellular composition of thrombi in vivo, but most models of fibrinolysis do not account for flow. This project will develop a novel flow model which allows thrombus formation and lysis to be visualized in a single system. Using this novel model and our established Chandler model thrombi system, we will assess how shear rates that mimic venous and arterial circulation affect thrombus structure, composition and susceptibility to lysis. Using fluorescent confocal microscopy we will monitor movement of fibrinolytic proteases through thrombi of different ...
This study has investigated the effects of clamped hyperinsulinemic euglycemia and acute and repeated 2-h episodes of moderate hyperinsulinemic hypoglycemia (2.9 mmol/L) on endothelial function, fibrinolytic balance, and proinflammatory and proatherothrombotic mechanisms in healthy man. Our results demonstrate that acute hypoglycemia reduces endogenous NO-mediated endothelial vasodilation, activates inflammatory processes, impairs fibrinolytic balance, and increases proatherothrombotic mechanisms. Secondly, repeated episodes of hypoglycemia can further impair vascular function by additionally reducing both endogenous and exogenous NO-mediated endothelial function and increasing TAT complex formation.. Recent large randomized controlled trials investigating the effects of intensifying glucose control both in hospitals and in outpatient settings have demonstrated an association with hypoglycemia and severe cardiovascular outcomes and even death (5,8). The in vivo vascular pathophysiologic ...
From NCBI Gene:. This gene encodes tissue-type plasminogen activator, a secreted serine protease that converts the proenzyme plasminogen to plasmin, a fibrinolytic enzyme. The encoded preproprotein is proteolytically processed by plasmin or trypsin to generate heavy and light chains. These chains associate via disulfide linkages to form the heterodimeric enzyme. This enzyme plays a role in cell migration and tissue remodeling. Increased enzymatic activity causes hyperfibrinolysis, which manifests as excessive bleeding, while decreased activity leads to hypofibrinolysis, which can result in thrombosis or embolism. Alternative splicing of this gene results in multiple transcript variants, at least one of which encodes an isoform that is proteolytically processed. [provided by RefSeq, Jan 2016]. From UniProt: ...
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TY - THES. T1 - Fibrin structure and mechanics. T2 - A journey across scales. AU - Vos, B.E.. PY - 2018. Y1 - 2018. M3 - PhD Thesis - Research VU, graduation VU. SN - 9789492323217. ER - ...
VTE is a common complication in patients undergoing elective hip or knee surgery. Over the past 25 years several anticoagulant regimens have been shown to be effective, though no regimen offers complete protection.. Previous studies have suggested that the incidence of deep VTE in patients with RA undergoing hip or knee surgery is three to 10 times less than in patients with osteoarthritis.3 4 The explanation is likely to be multifactorial: patients with RA are on average younger, their body weight is lower, their haemoglobin is lower, and reports have been published indicating that their fibrinolytic activity is higher4 8; however, recent publications also seem to find the lower fibrinolytic activity. Another explanation for the lower rate of thromboembolic complications in patients with RA may be the frequent use of NSAIDs, with their antiplatelet activity.4 In 1994 an overview of randomised trials of antiplatelet treatment showed a significant, clinically important reduction in thrombosis and ...
The liver is vital for the synthesis of anticoagulant, coagulation, and fibrinolytic proteins. In fact, only five blood clotting factors are not produced there. Therefore, liver diseases that cause clotting issues in cats can be very serious and sometimes life-threatening.
10. Cerneca F., Ricci G., Simeone R. et al. Coagulation and fibrinolysis changes in normalpregnancy. Increased levels of procoagulants and reduced levels of inhibitors duringpregnancy induce a hypercoagulable state, combined with a reactive fibrinolysis //Eur. J. Obstet. Gynecol. Reprod. Biol. - 1997. - May; 73(1). - P.31-36. Значимість деяких показників фібринолітичної системиA. V. Palladins Institute of biochemistry National Academy of Sciences of ...
Annexin II is thought to serve as a profibrinolytic coreceptor for both plasminogen and tissue plasminogen activator on the surface
Cardiovascular disease (CVD) is the major cause of death worldwide. Underlying causes, such as atherosclerosis and hypertension, are associated with remodeling of the vessel wall ultimately leading to loss of structural integrity. There are a number of factors that can influence vascular remodeling and hence structural integrity. The overall aim of this thesis was to investigate aortic wall integrity in relation to genetics and blood flow.. The influence of SNPs within the currently most robust susceptibility locus identified for CVD (chromosome 9p21.3) on abdominal aortic integrity was studied in elderly individuals. In men, risk-variants were associated with a decreased abdominal aortic stiffness, independent of other factors related to arterial stiffness. Impaired mechanical properties of the abdominal aortic wall may explain the association between chromosome 9p21.3 and vascular disease.. Plasminogen activator inhibitor 1 (PAI-1) is the key inhibitor of fibrinolysis, and involved in several ...
Endovan increases the fibrinolytic activity (fibrin-degrading) in the blood by encouraging increased plasmin production as well as by mimicking the function of plasmin.. With a more robust plasmin response, the body is better able to break down accumulated fibrin allowing the immune system to clean up the site and direct the debris to be processed as waste.. Try Endovan Today. ...
Introduction to Antithromboticthrombotic Monitoring 1 Topics What is thrombosis, and why is it significant? Coagulation Cascade Pathways of coagulation, anticoagulation, and fibrinolysis Thrombophilia
Fibrinolysis. 5 (4): 551-9. PMID 7841311. v t e. ...
Fibrinolysis. 4 Suppl 1: S55-8, discussion S59-60. PMID 8180331. Karsch KR, Preisack MB, Baildon R, Eschenfelder V, Foley D, ...
Fibrinolysis. 19 (6): 543-55. doi:10.1097/MBC.0b013e3283068859. PMID 18685438. S2CID 31127950. Llorca J, Rodríguez-Rodríguez E ... Fibrinolysis. 19 (2): 166-77. doi:10.1097/MBC.0b013e3282f5457b. PMID 18277139. S2CID 10380641. Ananyeva NM, Makogonenko YM, ...
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Impaired fibrinolysis. Severe liver disease. Manifest or impending shock. I.M.-Injection : Ancrod should not be injected i.m., ... acts as cofactor for the tPA-induced plasminogen activation and an increased fibrinolysis results in return (profibrinolytic ... viscoelastic analyses of the effects of Calloselasma rhodostoma venom on plasma coagulation and fibrinolysis". Journal of ...
Todd AS (February 1958). "Fibrinolysis autographs". Nature. 181 (4607): 495-6. Bibcode:1958Natur.181..495T. doi:10.1038/ ... thrombosis and fibrinolysis). The endothelium normally provides a surface on which blood does not clot, because it contains and ...
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Blood Coagul Fibrinolysis. 17 (7): 557-61. doi:10.1097/01.mbc.0000245300.10387.ca. PMID 16988551. Sharp MK, Mohammad SF (Sep ...
Blood Coagul Fibrinolysis. 15 (8): 673-6. doi:10.1097/00001721-200412000-00007. PMID 15613922. S2CID 19214006. Lengyel M; ...
Budzynski, A. Z. (February 1991). "Interaction of hementin with fibrinogen and fibrin". Blood Coagulation & Fibrinolysis. 2 (1 ... Fibrinolysis. DOI: 10.1097/00001721-199102000-00023 (1): 153-9. doi:10.1097/00001721-199102000-00023. PMID 1772983. "UniProtKB ...
Fibrinolysis. 16 (1): 1-7. doi:10.1097/00001721-200501000-00001. PMID 15650539. S2CID 44664652. Melzer C, Richter C, Rogalla P ...
Fibrinolysis. 19 (7): 709-718. doi:10.1097/MBC.0b013e32830b2891. PMC 2713681. PMID 18832915. "Genomatix: Annotation & Analysis ...
Fibrinolysis. 19 (7): 709-18. doi:10.1097/MBC.0b013e32830b2891. PMC 2713681. PMID 18832915. Lee, J; Zheng, Y; -von Bornstadt, D ...
Franco, David; Everett, George; Manoucheri, Manoucher (2013). "I smell a rat". Blood Coagulation & Fibrinolysis. 24 (2): 202-4 ...
Marsh, NA (July 1998). "Use of snake venom fractions in the coagulation laboratory". Blood Coagulation & Fibrinolysis. 9 (5): ... Fibrinolysis. 1 (3): 259-66. doi:10.1097/00001721-199008000-00002. PMID 2129412. Laboratory testing for the lupus anticoagulant ...
Fibrinolysis. 14 Suppl 1: S59-64. doi:10.1097/00001721-200306001-00014. PMID 14567539. Du X (May 2007). "Signaling and ...
The circulating enzyme plasmin, the main enzyme of fibrinolysis, cleaves the fibrin gel in a number of places. The resultant ... a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it ... Fibrinolysis. 27 (5): 542-50. doi:10.1097/MBC.0000000000000453. PMC 4935535. PMID 26656897. Olson JD, Cunningham MT, Higgins RA ...
Suzuki K (1 March 2000). "Protein C inhibitor (PAI-3): structure and multi-function". Fibrinolysis and Proteolysis. 14 (2): 133 ... Fibrinolysis. 4 (1): 153-8. doi:10.1097/00001721-199304010-00027. PMID 8384496. Moore A, Penfold LM, Johnson JL, Latchman DS, ... Fibrinolysis. 6 (5): 382-7. doi:10.1097/00001721-199507000-00003. PMID 8589203. The MEROPS online database for peptidases and ... Fibrinolysis. 4 (6): 921-6. doi:10.1097/00001721-199304060-00009. PMID 8148485. Hayashi T, Suzuki K (October 1993). "Gene ...
Blood Coagul Fibrinolysis. 2009; 20: 517-23. Delgado J, Jiménez-Yuste V, Hernández-Navarro F, Villar A. Acquired haemophilia: ...
Vanderschueren S, Van de Werf F, Collen D (August 1997). "Recombinant staphylokinase for thrombolytic therapy". Fibrinolysis ...
Fibrinolysis. 27 (3): 242-245. doi:10.1097/MBC.0000000000000427. ISSN 0957-5235. PMID 27023878. S2CID 33380206. "Avocado: ...
Blood Coagul Fibrinolysis. 5 (5): 671-8. PMID 7507361. Rasmus KBJKJER and Inger SCHOUSBOE (1997). "The surface-dependent ...
This is due to excessive consumption of coagulation factors and subsequent activation of fibrinolysis using all of the body's ... Budzynski, A. Z. (1991). "Interaction of hementin with fibrinogen and fibrin". Blood Coagulation & Fibrinolysis. 2 (1): 149-52 ...
Fibrinolysis. 25 (5): 507-511. doi:10.1097/MBC.0000000000000057. ISSN 1473-5733. PMID 24553060. Chinsakchai, Khamin; ten Duis, ... Fibrinolysis. 25 (5): 507-511. doi:10.1097/MBC.0000000000000057. ISSN 1473-5733. PMID 24553060. Gardella, Layne; Faulk, JimBob ... Fibrinolysis. 25 (5): 507-511. doi:10.1097/MBC.0000000000000057. ISSN 1473-5733. PMID 24553060. Gardella, Layne; Faulk, JimBob ...
Fibrinolysis. 24 (5): 484-8. doi:10.1097/MBC.0b013e32835e4230. PMID 23348429. S2CID 31284130. Kornerup KN, Page CP (August 2007 ...
Fibrinolysis. 19 (7): 709-18. doi:10.1097/MBC.0b013e32830b2891. PMC 2713681. PMID 18832915. Park J, Chun KH (5 May 2020). " ...
FibrinolysisEdit. Main article: Fibrinolysis. Eventually, blood clots are reorganised and resorbed by a process termed ... Tranexamic acid and aminocaproic acid inhibit fibrinolysis and lead to a de facto reduced bleeding rate. Before its withdrawal ... fibrinolysis. The main enzyme responsible for this process (plasmin) is regulated by various activators and inhibitors.[12] ...
Blood Coagulation and Fibrinolysis. 12 (2): 123-8. doi:10.1097/00001721-200103000-00006. PMID 11302474. S2CID 28411589. ...
Blood Coagulation and Fibrinolysis. 22(2): 110-7 (2011). Ignjatovic V, Straka E, Summerhayes R, Monagle P. Age-specific ...
... primary fibrinolysis and secondary fibrinolysis. The primary type is a normal body process, whereas secondary fibrinolysis is ... Testing of overall fibrinolysis can be measured by a euglobulin lysis time (ELT) assay. The ELT measures fibrinolysis by ... In this assay, increased fibrinolysis is assessed by comparing the TEM profile in the absence or presence of the fibrinolysis ... In fibrinolysis, a fibrin clot, the product of coagulation, is broken down.[2] Its main enzyme plasmin cuts the fibrin mesh at ...
Exercise and Fibrinolysis. Br Med J 1966; 2 doi: https://doi.org/10.1136/bmj.2.5520.1011 (Published 22 October 1966) Cite this ...
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Fibrinolysis syndrome is characterized by an acute hemorrhagic state brought about by inability of the blood to clot, with ... The cause for Fibrinolysis syndrome, is the inability of the body to produce blood-coagulates to stop bleeding. What causes the ...
Cite this: Fibrinolysis for Pulmonary Embolism Effective but Risky - Medscape - Apr 10, 2014. ... The findings also reflect the relative safety of withholding fibrinolysis unless hemodynamic decompensation occurs. ...
Fibrinolysis is a normal body process. It prevents blood clots that occur naturally from growing and causing problems. ... Primary fibrinolysis refers to the normal breakdown of clots.. Secondary fibrinolysis is the breakdown of blood clots due to a ... Fibrinolysis is a normal body process. It prevents blood clots that occur naturally from growing and causing problems. ... Hemostasis, thrombosis, fibrinolysis, and cardiovascular disease. In: Zipes DP, Libby P, Bonow RO, Mann DL, Tomaselli GF, ...
New subscriptions to Blood Coagulation & Fibrinolysis are managed through Lippincott Williams & Wilkins (LWW) online store. If ... Subscription renewals for Blood Coagulation & Fibrinolysis are managed through Lippincott Williams & Wilkins online store. If ...
A heparinoid cream and tissue fibrinolysis. Br Med J 1976; 2 :1297 ... A heparinoid cream and tissue fibrinolysis.. Br Med J 1976; 2 doi: https://doi.org/10.1136/bmj.2.6047.1297 (Published 27 ...
Urokinase versus Alteplase for intraventricular hemorrhage fibrinolysis.. Gaberel T1, Montagne A2, Lesept F2, Gauberti M2, ... Our study provides evidence supporting the use of uPA for fibrinolysis of IVH. A clinical trial could be warranted if tPA ... Intraventricular hemorrhage (IVH) is the most severe form of stroke with intraventricular fibrinolysis (IVF) as a hopeful ...
B. Wiman and D. Collen, Molecular mechanism of physiological fibrinolysis, Nature 272:549 (1978).PubMedCrossRefGoogle Scholar ... Collen D. (1984) Impairment of Fibrinolysis as a Risk Factor for Thrombosis. In: Chazov E.I., Smirnov V.N., Oganov R.G. (eds) ... T. Astrup, Biological significance of fibrinolysis, Lancet 2:565 (1956).CrossRefGoogle Scholar ... D. Collen, On the regulation and control of fibrinolysis, Thrombos.Haemostas. 43:77 (1980).Google Scholar ...
... Lead Guest Editor: Zsuzsa Bagoly. Guest Editors: Robert A. S. ... Inhibition of Fibrinolysis by Coagulation Factor XIII, Dingeman C. Rijken and Shirley Uitte de Willige Review Article (6 pages ... Clot Structure and Fibrinolysis in Thrombosis and Hemostasis, Zsuzsa Bagoly, Robert A. S. Ariëns, Dingeman C. Rijken, Marlien ... Intracardiac Hemostasis and Fibrinolysis Parameters in Patients with Atrial Fibrillation, Noémi Klára Tóth, Zoltán Csanádi, ...
2018 Laboratory Corporation of America® Holdings and Lexi-Comp Inc. All Rights Reserved.. CPT Statement/Profile Statement. The LOINC® codes are copyright © 1994-2018, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee. Permission is granted in perpetuity, without payment of license fees or royalties, to use, copy, or distribute the LOINC® codes for any commercial or non-commercial purpose, subject to the terms under the license agreement found at https://loinc.org/license/. Additional information regarding LOINC® codes can be found at LOINC.org, including the LOINC Manual, which can be downloaded at LOINC.org/downloads/files/LOINCManual.pdf. ...
Fibrinolysis Before Cardiopulmonary Bypass?. The safety and scientific validity of this study is the responsibility of the ... The investigators want to show that there is no proof of fibrinolysis in standard sternotomy cardiac surgery patients before ... Value of Thromboelastography as Monitor of Fibrinolysis [ Time Frame: 6 months ]. Thromboelastography may display if ...
... fibrinolysis, and platelets. [M -C Shen; C -M Teng; Akikazu Takada;] ... Fibrinolysis--congresses. a schema:Intangible ;. schema:name "Fibrinolysis--congresses"@en ;. schema:name "Fibrinolysis-- ... fibrinolysis_and_platelets_2nd_1992_taipei_taiwan> ; # Sino-Japanese Symposium on Coagulation, Fibrinolysis, and Platelets (2nd ... Current aspects of blood coagulation, fibrinolysis, and platelets. Author:. 高田, 明和, ; ; M -C Shen; C -M Teng; Akikazu Takada. ...
... Noémi Klára Tóth,1 Zoltán Csanádi,2 ... L. Drabik, P. Wołkow, and A. Undas, "Denser plasma clot formation and impaired fibrinolysis in paroxysmal and persistent atrial ... Fibrinolysis, vol. 3, no. 4, pp. 469-473, 1992. View at Publisher · View at Google Scholar · View at Scopus ...
Primary fibrinogenolysis is an uncommon acquired bleeding disorder which should be distinguished from DIC with secondary fibrin lysis.. Review clinical features; Full blood count, Platelet count, Blood film, APTT, INR, Prothrombin time, Thrombin time, Fibrinogen, D Dimer.. ...
Fibrin is therefore not essential for fracture repair, but inefficient fibrinolysis decreases endochondral angiogenesis and ...
Clinical indicators results for Memorial Hermann hospitals when compared to the current benchmarks for fibrinolysis therapy ... Fibrinolysis therapy received within 30 min of arrival. Primary PCI within 90 minutes of arrival ...
... on fibrinolysis, blood coagulation and lipids was evaluated in 12 healthy male volunteers. Significantly increased plasminogen ... The effect of intramuscular stanozolol on fibrinolysis and blood lipids Thromb Res. 1982 Oct 1;28(1):27-36. doi: 10.1016/0049- ... The effects of a single 50 mg intramuscular injection of the anabolic steroid stanozolol (Stromba) on fibrinolysis, blood ...
Fibrinolysis / physiology*. Humans. Intermittent Claudication / blood, complications, physiopathology*. Leg / blood supply. ... 7667817 - Early markers of blood coagulation and fibrinolysis activation in argentine hemorrhagic.... 23168017 - Targeting ... the activator of fibrinolysis) and its inhibitor plasminogen activator inhibitor-1 (PAI-1).. METHODS: The study group consisted ... suggesting that the progression to more severe levels of PAD may be associated with worsening endogenous fibrinolysis.. ...
Intra-Arterial Fibrinolysis for Acute Ischemic Stroke. The Message of Melt. Jeffrey L. Saver ... Meta-analysis: IA fibrinolysis for acute ischemic stroke, death or dependency at longterm follow-up. ... An updated meta-analysis of intra-arterial fibrinolysis trials incorporating MELT is shown in the Figure. Stopped early because ... In US national practice guidelines, intra-arterial fibrinolysis occupied a gray zone, receiving a Level B recommendation, ...
C.S. Grace and R.B. Goldrick, Fibrinolysis and body build. Interrelationships between blood, fibrinolysis, body composition and ... 1984) Fibrinolysis and Body Weight: Fibrinolytic Response to Venous Occlusion in Obese Children. In: Strano A. (eds) Thrombosis ... Fibrinolysis and Body Weight: Fibrinolytic Response to Venous Occlusion in Obese Children. ...
Hyperinsulinemia inhibits fibrinolysis irrespective of glucose levels. Mean ± SD plasma concentrations of tPA antigen (A), ... Hyperglycemia Stimulates Coagulation, Whereas Hyperinsulinemia Impairs Fibrinolysis in Healthy Humans. Michiel E. Stegenga, ... Hyperglycemia Stimulates Coagulation, Whereas Hyperinsulinemia Impairs Fibrinolysis in Healthy Humans. Michiel E. Stegenga, ... Hyperglycemia Stimulates Coagulation, Whereas Hyperinsulinemia Impairs Fibrinolysis in Healthy Humans Message Subject (Your ...
Vitronectin deficiency is associated with increased wound fibrinolysis and decreased microvascular angiogenesis in mice.. Jang ...
Expression of Coagulase and Mechanism of Fibrinolysis. E. D. Beesley, R. R. Brubaker, W. A. Janssen, M. J. Surgalla ... Expression of Coagulase and Mechanism of Fibrinolysis Message Subject (Your Name) has forwarded a page to you from Journal of ...
... Supervisors. J.C.M. Meijers. ... Chantal Verkleij bestudeerde de rol van Thrombin-activatable fibrinolysis inhibitor - een eiwit dat bloedstolsels beschermt ...
2010) The Effects of Age on Inflammatory and Coagulation-Fibrinolysis Response in Patients Hospitalized for Pneumonia. PLoS ONE ... The differences in coagulation-fibrinolysis response that exist do not explain the large differences in outcome observed ... 1997) Interleukin-10 inhibits activation of coagulation and fibrinolysis during human endotoxemia. Blood 89: 2701-2705. * View ... We hypothesized that age-related increases in circulating inflammatory and coagulation-fibrinolysis response would occur ...
Different coagulation and fibrinolysis parameters were investigated in 149 patients with metastatic and non-metastatic tumours ... Clotting activation and impairment of fibrinolysis in malignancy. Jun 15, 1989 , Magazine: Thrombosis Research ... This study demonstrates clotting activation, at the level of fibrinogen to fibrin conversion, and impairment of fibrinolysis in ...
Inhibition of Coagulation and Fibrinolysis Inhibition of Coagulation and Fibrinolysis. Chapter:. (p. 641) Nomenclature. Author( ...
... of this cross-sectional study was to determine whether pulse pressure is associated with blood coagulation and fibrinolysis in ... RESULTS: Pulse pressure was found to be significantly correlated with blood fibrinolysis markers, such as plasmin-alpha2- ... CONCLUSIONS: Pulse pressure is associated with blood fibrinolysis as well as atherosclerotic progression in patients with type ... including blood coagulation and fibrinolysis markers, were investigated in subjects with type 2 diabetes. ...
  • In this ancillary study, we will measure plasma levels of inflammatory, coagulation, and fibrinolysis proteins and genotype DNA for polymorphisms among patients enrolled in the HALF PINT trial. (clinicaltrials.gov)
  • We will measure plasma levels of selected markers of coagulation and fibrinolysis and genotype DNA for polymorphisms in the corresponding genes. (clinicaltrials.gov)
  • We will correlate changes over time in the biomarkers with allocation to treatment arm to test whether the beneficial effects of TGC-NL are achieved via normalization of coagulation and fibrinolysis. (clinicaltrials.gov)
  • Different coagulation and fibrinolysis parameters were investigated in 149 patients with metastatic and non-metastatic tumours and results were compared with those obtained in a healthy population. (cun.es)
  • The purpose of this cross-sectional study was to determine whether pulse pressure is associated with blood coagulation and fibrinolysis in patients with diabetes. (biomedsearch.com)
  • MATERIALS AND METHODS: The relationships between pulse pressure and atherosclerotic risk factors, including blood coagulation and fibrinolysis markers, were investigated in subjects with type 2 diabetes. (biomedsearch.com)
  • Disequilibrium between coagulation and fibrinolysis can lead to severe haemostatic disorders such as thrombosis and hemophilia. (queensu.ca)
  • Coagulation and fibrinolysis are essential processes that ensure a rapid, localized response to vascular damage and subsequent removal once the damage is repaired. (queensu.ca)
  • Thrombin-activatable fibrinolysis inhibitor (TAFI), which is identical to the previously identified proteins procarboxypeptidase B, R, and U, forms a link between blood coagulation and fibrinolysis. (eurekaselect.com)
  • Serial changes in coagulation and fibrinolysis studied among 42 patients admitted to hospital with a wide variety of injuries are reported. (bmj.com)
  • Anticoagulated COVID-19 patients have persistent in vivo activation of coagulation and fibrinolysis, but no evidence of excessive platelet activation. (unboundmedicine.com)
  • TY - JOUR T1 - In vitro hypercoagulability and ongoing in vivo activation of coagulation and fibrinolysis in COVID-19 patients on anticoagulation. (unboundmedicine.com)
  • Many investigators are interested in the relationship between mental stress and platelet function, coagulation and fibrinolysis [1, 2], since several lines of evidence suggest that atherosclerotic cardiovascular events may be related to mental stress. (springer.com)
  • The initial observation that the fear of impending surgery increased fibrinolytic activitymade by Macfarlane and Biggs [10] Recently Jern et al [11] reported y the effects of mental stress on plasma coagulation and fibrinolysis. (springer.com)
  • Jern C, Eriksson E, Tengborn L, Risberg B, Wadenvik H, Jern S (1989) Changes of plasma coagulation and fibrinolysis in response to mental stress. (springer.com)
  • Blood coagulation and fibrinolysis of the newborn viewed äs perinatal factors. (hu-berlin.de)
  • It is believed that abnormal coagulation and fibrinolysis is a frequent complication in patients with head injury, and this abnormality is initiated by the released of thromboplastin (tissue factor) from damaged brain. (biomedcentral.com)
  • But some authors [ 1 , 2 ] reported that the activation of coagulation and fibrinolysis after head injury is not the specific phenomenon comparing with the population of trauma victim. (biomedcentral.com)
  • Recently, we have been able to measure some molecular markers of coagulation and fibrinolysis system in clinical setting. (biomedcentral.com)
  • We compared coagulation and fibrinolysis activity of trauma and head injury patients using the molecular markers. (biomedcentral.com)
  • HI and TR had significantly activation of coagulation and fibrinolysis compared with CVD, but there were no evidence that HI had significantly activation of coagulation and fibrinolysis compared with TR. (biomedcentral.com)
  • Gando S, Tedo I, Kubota M: Posttrauma coagulation and fibrinolysis. (biomedcentral.com)
  • Arthritis is linked to local and systemic activation of coagulation and fibrinolysis pathways. (semanticscholar.org)
  • BACKGROUND Activation of coagulation and fibrinolysis play a role in the pathophysiology of experimental arthritis. (semanticscholar.org)
  • Hankey, C.R. , Lean, M.E.J. , Lowe, G.D.O. , Rumley, A. and Woodward, M. (2002) Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris. (gla.ac.uk)
  • For more information see ADIC / Disseminated Intravascular Coagulation/Intravascular Coagulation and Fibrinolysis (DIC/ICF) Profile, Plasma. (testcatalog.org)
  • Plasmin activity is also reduced by thrombin-activatable fibrinolysis inhibitor (TAFI), which modifies fibrin to make it more resistant to the tPA-mediated plasminogen. (wikipedia.org)
  • Thrombin-activable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like pro-enzyme that, once activated, attenuates fibrinolysis. (queensu.ca)
  • Abstract -Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently described fibrinolysis inhibitor that circulates in plasma as a procarboxypeptidase and is converted into an active form during coagulation. (ahajournals.org)
  • Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently described fibrinolysis inhibitor cloned from human liver. (ahajournals.org)
  • D-Dimers, thrombin-activatable fibrinolysis inhibitor (TAFI) and the clot lysis time in the absence (LYSmin) or the presence (LYSplus) of a blocking anti-factor XI antibody were determined in plasmas of the participating women, and the mean difference in changes between the OC were calculated. (unboundmedicine.com)
  • The aim of the present study is to investigate the effect of gestational diabetes on plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen levels. (endocrine-abstracts.org)
  • The purpose of this study was to investigate plasma levels of thrombin activatable fibrinolysis inhibitor (TAFI) and TAFI's relationship with coagulation markers (prothrombin fragment 1 + 2) in gastric cancer patients. (springermedizin.de)
  • Bajzar L, Manuel R, Nesheim ME: Purification and characterization of TAFI, a thrombin-activable fibrinolysis inhibitor. (springermedizin.de)
  • Impaired fibrinolysis in subjects with hypertriglyceridemia/low HDL-cholesterol is associated with increased serum levels of PAI-1 whereas enhanced thrombin generation and TAFI hyperactivity are the main findings in hypercholesterolemia. (mysciencework.com)
  • For maintaining high fidelity regulation between coagulatory clotting and proteolytic fibrinolysis TAFI (Thrombin activatable fibrinolysis inhibitor) plays an important inhibitory role. (diapharma.com)
  • Hyperglycemia is known to result in a pro-thrombotic state via activation of coagulation and impairment of fibrinolysis. (clinicaltrials.gov)
  • Patients with SC had more impaired fibrinolytic activity than those with MC and the control subjects, suggesting that the progression to more severe levels of PAD may be associated with worsening endogenous fibrinolysis. (biomedsearch.com)
  • Impaired endogenous fibrinolysis at high shear using a point-of-care test in STEMI is associated with alterations in clot architecture. (bioportfolio.com)
  • Impaired endogenous fibrinolysis is an adverse prognostic biomarker in acute coronary syndrome (ACS). (bioportfolio.com)
  • In contrast, endogenous fibrinolysis, using one-thousandth of the t-PA concentration, is regularly lysing fibrin and induced Thrombolysis In Myocardial Infarction flow grade 3 patency in 15% of patients with acute myocardial infarction. (onlinejacc.org)
  • Endogenous fibrinolysis may provide a paradigm that is relevant for therapeutic fibrinolysis. (onlinejacc.org)
  • Improved endogenous fibrinolysis and endothelial function may represent important mechanisms through which ω-3 fatty acids confer potential cardiovascular benefits. (bmj.com)
  • Inhibition of PN-1 is thus predicted to promote endogenous and exogenous tissue plasminogen activator-mediated fibrinolysis and may enhance the therapeutic efficacy of thrombolytic agents. (inserm.fr)
  • The endogenous plasmin-mediated process of dissolving a formed thrombus is denoted fibrinolysis. (diapharma.com)
  • In conclusion, anti-plasminogen and anti-tPA antibodies occur in AAV and associate with functional inhibition of fibrinolysis in vitro . (asnjournals.org)
  • Wang W, Boffa MB, Bajzar L, Walker JB, Nesheim ME: A study of the mechanism of inhibition of fibrinolysis by activated thrombin-activable fibrinolysis inhibitor. (springermedizin.de)
  • It goes on to discuss local fibrinolytic potential in thrombi, both venous and arterial, and in the diseased vessel wail, presenting evidence that increased local inhibition of fibrinolysis by PAI-1, PAI-2 and alpha(2)-antiplasmin is intimately involved in thrombus stability and in the generation of fibrin-rich vessel wall lesions. (elsevier.com)
  • The journal is devoted to publishing significant developments worldwide in the field of blood coagulation, fibrinolysis, thrombosis, platelets and the kininogen-kinin system, as well as dealing with those aspects of blood rheology relevant to haemostasis and the effects of drugs on haemostatic components. (ovid.com)
  • Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis, vol. 13, no. 5, 2002, pp. 373-81. (unboundmedicine.com)
  • This study demonstrates clotting activation, at the level of fibrinogen to fibrin conversion, and impairment of fibrinolysis in patients with malignancy. (cun.es)
  • This study examined fibrin degradation by measuring D-dimer crosslinked fibrin degradation products (indicates hypercoagulability), plasminogen activators (fibrinolysis), and antithrombin III in 42 adult trauma patients and correlated these data with injury severity, types of injury, complications, and clinical tests of coagulation. (ovid.com)
  • There are 2 plasminogen activators in the blood responsible for fibrinolysis: tissue-type plasminogen activator (t-PA) and urokinase plasminogen activator (uPA). (onlinejacc.org)
  • We work with several global collaborators to study fundamental questions around the regulation of enzymes used as plasminogen activators that promote fibrinolysis. (nibsc.org)
  • Increased plasma thrombin-activatable fibrinolysis inhibitor levels in young obese women with polycystic ovary syndrome. (semanticscholar.org)
  • Doppler sonography enhances rtPA-induced fibrinolysis in an in vitro clot model of spontaneous intracerebral hemorrhages. (bioportfolio.com)
  • The aim of this study was to assess the potential of TCD to enhance rtPA-induced fibrinolysis in an in vitro clot system. (bioportfolio.com)
  • Eighteen of 74 AAV-IgG (but no control IgG) retarded fibrinolysis in vitro , and this associated with anti-plasminogen and/or anti-tPA antibody positivity. (asnjournals.org)
  • In conclusion, human arterial SMC in vitro induce fibrinolysis by activation of plasminogen. (ahajournals.org)
  • The in vitro and in vivo hematological effects of puff adder (Bitis arietans) venom in the baboon (Papio ursinus) with regard to its effect on coagulation, fibrinolysis and platelet aggregation were studied. (sun.ac.za)
  • There is a delay in the intrinsic coagulation mechanism with fibrinolysis and in vitro fibrinogenolysis. (sun.ac.za)
  • A wide array of in vitro fibrinolysis tests had been performed for a long period, suggesting defective fibrinolysis, mainly impaired tPA response and reserve as major, frequent abnormality, predecessor or causative factor of venous thromboembolism. (elsevier.com)
  • Both in vitro and in vivo, tPA and prouPA have complementary modes of action in fibrinolysis are synergistic when combined. (heraldopenaccess.us)
  • The first Sino-Japanese symposium on Coagulation, Fibrinolysis and Platelets, originating from the Hamamatsu symposium, held in early 1990, was held in Hanchow, Mainland China in October, 1990. (worldcat.org)
  • RESULTS: Pulse pressure was found to be significantly correlated with blood fibrinolysis markers, such as plasmin-alpha2-antiplasmin complex (PAP) and D-dimer, but not with platelets and blood coagulation markers, such as fibrinogen and thrombin-antithrombin III complex (TAT). (biomedsearch.com)
  • The body is often accompanied by hypoxia and injury of small blood vessel endothelial cells, as well as abnormalities in functions such as coagulation, fibrinolysis, and platelets. (scirp.org)
  • Thrombin has been the primary target to attenuate the procoagulant response associated with fibrinolysis, because it activates platelets, converts fibrinogen to fibrin, and binds to clots. (aspetjournals.org)
  • Methods and Results- In this study, the role of platelet PN-1 in fibrinolysis was investigated with the use of human platelets incubated with a blocking antibody and platelets from PN-1-deficient mice. (inserm.fr)
  • CONCLUSIONS: Pulse pressure is associated with blood fibrinolysis as well as atherosclerotic progression in patients with type 2 diabetes. (biomedsearch.com)
  • At the time, there was limited experience using fibrinolytic agents other than urokinase for local intraarterial fibrinolysis in cases of basilar thrombosis or acute thromboembolic stroke (11-19) . (ajnr.org)
  • Several open-label clinical studies using continuous infusion of thrombolytic agents have suggested that local intraarterial fibrinolysis (LIF) is efficacious in the treatment of central retinal artery occlusion. (ahajournals.org)
  • The deep veins of both lower limbs were examined by Rili Erlangshen's color Doppler ultrasound diagnostic instrument (CDU), and the fibrinolysis system was tested by enzyme-linked immunosorbent assay (ELISA) method and automatic hemagglutination analyzer. (scirp.org)
  • Clinically, the TEM is useful for near real-time measurement of activated fibrinolysis for at-risk patients, such as those experiencing significant blood loss during surgery. (wikipedia.org)
  • The investigators want to show that there is no proof of fibrinolysis in standard sternotomy cardiac surgery patients before cardiopulmonary bypass, and that antifibrinolytic agents should only be started on cardiopulmonary bypass. (clinicaltrials.gov)
  • Association of pulse pressure with fibrinolysis in patients with type 2 diabetes. (biomedsearch.com)
  • Hypercoagulability and suppression of fibrinolysis were seen in most patients and were not correlated with severity of injury. (ovid.com)
  • Latex agglutination of D-dimer provides a rapid test of fibrinolysis that may be clinically useful in the management of trauma patients who cannot be easily studied for thrombosis. (ovid.com)
  • Fibrinolysis with local intraarterial urokinase infusion for basilar artery thrombosis has been associated with a low rate of spontaneous symptomatic cerebral hemorrhage, even when patients have been treated late in the course of symptoms. (ajnr.org)
  • 0.001) in the group of patients when compared to controls, indicating a degree of fibrinolysis/proteolysis activation. (cun.es)
  • We conclude that there is a disturbance of the plasma fibrinolysis/proteolysis in patients with stable angina not related to the extent of atherosclerosis. (cun.es)
  • Objective To understand more about the individual variation in the time course of fibrinolysis following major injury and to assess the potential for stratification of trauma patients for tranexamic acid (TXA) therapy. (bmj.com)
  • However, it is unknown whether TCD would be suitable to enhance rtPA-induced fibrinolysis in patients with ICH. (bioportfolio.com)
  • Borzak S. Early transfer for angiography after fibrinolysis reduced ischemic events in patients with STEMI. (annals.org)
  • Longitudinally Measured Fibrinolysis Factors are Strong Predictors of Clinical Outcome in Patients with Chronic Heart Failure: The Bio-SHiFT Study. (medworm.com)
  • Conceivably, therapies that enhance fibrinolysis might benefit a subset of AAV patients. (asnjournals.org)
  • 7 , 8 Under these circumstances, down-regulation of fibrinolysis by anti-plasminogen antibodies in AAV patients would promote persistent or extensive fibrinoid necrosis. (asnjournals.org)
  • We show that Ig from AAV patients retards fibrinolysis and that seropositivity for these antibodies correlates with reduced renal function and the presence of hallmark histopathologic renal lesions. (asnjournals.org)
  • We studied 24 patients who were diagnosed to have F1GO stage Ill/IV ovarian cancer compared to nine subjects with FIGO Stage I/II disease for their systemic levels of fibrinolysis and inhibitors. (nus.edu.sg)
  • Effects of atorvastatin on reactive hyperaemia and the thrombosis-fibrinolysis system in patients with heart failure. (ox.ac.uk)
  • OBJECTIVE: To investigate the effects of short term atorvastatin treatment on forearm vasodilatory response to reactive hyperaemia (RH%) and on components of the thrombosis-fibrinolysis system (antithrombin III, proteins and S, factors V and VII, von Willebrand factor, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1)) in patients with heart failure. (ox.ac.uk)
  • Therefore, short term treatment with atorvastatin may affect the expression of both endothelium and liver derived components of the thrombosis-fibrinolysis system in patients with heart failure. (ox.ac.uk)
  • Since these are among the commonest causes of morbidity and mortality worldwide, for the majority of patients only more effective and safer fibrinolysis can provide sufficiently timely reperfusion. (heraldopenaccess.us)
  • as a natural inhibitor of fibrinolysis) and D-dimer (as a marker of the extent of fibrinolysis). (bmj.com)
  • By double immunofluorescent labelling systems fibrin deposits were simultaneously stained for α 2 -antiplasmin (α 2 -AP), the main physiological inhibitor of fibrinolysis and in a number of nodular areas they were also labelled for plasmin(ogen). (elsevier.com)
  • The current study was performed to determine whether peripheral arterial disease (PAD) and its progression are also associated with impaired fibrinolysis, by measurement of tissue plasminogen activator (tPA, the activator of fibrinolysis) and its inhibitor plasminogen activator inhibitor-1 (PAI-1). (biomedsearch.com)
  • In this study we provide immunomorphological evidence showing that fibrin deposits in lymph nodes with Hodgkin's disease are stabilized and made resistant to fibrinolysis by factor XIII (FXIII) of blood coagulation. (elsevier.com)
  • The impact of cross-linking on resistance to fibrinolysis has proved challenging to evaluate quantitatively. (wiley.com)
  • Although very low levels of FXIII are known to produce mechanical clot stability, and to achieve γ-dimerization, they appear to be suboptimal in conferring full resistance to fibrinolysis. (wiley.com)
  • Its release is concentrated to platelet rich clots leading to an increased thrombus resistance to fibrinolysis. (diapharma.com)
  • Fibrinolysis is the enzymatic breakdown of fibrin in blood clots. (diapharma.com)
  • What concentration of tranexamic acid is needed to inhibit fibrinolysis? (bioportfolio.com)
  • Therapeutic fibrinolysis has been dominated by the experience with tissue-type plasminogen activator (t-PA), which proved little better than streptokinase in acute myocardial infarction. (onlinejacc.org)
  • We present the first documented case of intraosseous systemic fibrinolysis in a patient with ST-segment elevation myocardial infarction. (ivteam.com)
  • Rescue angioplasty or repeat fibrinolysis after failed fibrinolytic therapy for ST-segment myocardial infarction: a meta-analysis of randomized trials. (acpjc.org)
  • Impaired fibrinolysis is believed to promote atherosclerosis and contribute to myocardial infarction. (ahajournals.org)
  • The ELT measures fibrinolysis by clotting the euglobulin fraction (primarily the important fibrinolytic factors fibrinogen , PAI-1 , tPA , alpha 2-antiplasmin , and plasminogen ) from plasma and then observing the time required for clot dissolution. (wikipedia.org)
  • Model thrombi, which mimic arterial thrombi formed in vivo , were prepared with incorporated fluorescently labeled fibrinogen, in order to allow quantification of fibrinolysis as released fluorescence units per minute. (wiley.com)
  • Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. (bioportfolio.com)
  • The only pharmacological means to remove the thrombus is fibrinolysis. (onlinejacc.org)
  • Hence, this jet is expected to promote fibrinolysis by means of injecting fibrinolytics deeply into the thrombus . (curehunter.com)
  • This effect can be seen in the thrombin clotting time (TCT) test, which is prolonged in a person that has active fibrinolysis. (wikipedia.org)
  • A prematurely active fibrinolysis could endanger the important acute clot stability. (diapharma.com)
  • Hyperinsulinemia inhibits fibrinolysis irrespective of glucose levels. (diabetesjournals.org)
  • The active form, TAFIa, inhibits fibrinolysis by cleaving off C-terminal lysine residues from partially degraded fibrin that stimulates the tissue-type plasminogen activator-mediated conversion of plasminogen to plasmin. (eurekaselect.com)
  • [1] This process has two types: primary fibrinolysis and secondary fibrinolysis. (wikipedia.org)
  • The primary type is a normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause. (wikipedia.org)
  • The major triggering factor for fibrinolysis is vascular tissue plasminogen activator (t-PA), and the aim of this study was to evaluate the capacity of human arterial smooth muscle cells (SMC) for induction of fibrinolysis. (ahajournals.org)
  • Fibrinolysis is the body's natural defense that prevents physiological fibrin, needed for the repair of wear and tear vascular injuries, from building up and interfering with blood flow. (heraldopenaccess.us)
  • Tissue plasminogen activator (t-PA) [3] and urokinase are the agents that convert plasminogen to the active plasmin, thus allowing fibrinolysis to occur. (wikipedia.org)
  • A heparinoid cream and tissue fibrinolysis. (bmj.com)
  • Risberg B , Peterson H I . A heparinoid cream and tissue fibrinolysis. (bmj.com)
  • Because urokinase is presently unavailable in the United States, this study was undertaken to determine the frequency of spontaneous cerebral hemorrhage in basilar artery fibrinolysis performed with tissue plasminogen activator (tPA). (ajnr.org)
  • Fibrinolysis was induced with recombinant human tissue-type plasminogen activator (1.0 mg/kg i.v. over 1 h), and patency was monitored continuously for 24 h with an implanted Doppler probe. (aspetjournals.org)
  • 6 RCTs ( n = 908, mean age range 57 to 63 y, 76% men) of rescue PCI and 3 RCTs ( n = 410, mean age range 56 to 63 y, 75% men) of repeated fibrinolysis (with tissue-type plasminogen activator) met the selection criteria. (acpjc.org)
  • Fibrinolysis initiation is mainly dependent on the tissue-type plasminogen activator ( t-PA ). (diapharma.com)
  • Fibrinolysis plays a role as well in other biological processes such as tissue repair, macrophage activation and function, ovulation, and embryo implantation. (perfusion.com)
  • Tissue plasminogen activator (tPA) is a serine protease found on endothelial cells (cells that line the blood vessels) involved in the breakdown of blood clots ( fibrinolysis ). (diapharma.com)
  • Thrombin activatable fibrinolysis inhibitor (TAFIa) suppresses fibrinolysis by removing carboxyl-terminal lysine residues exposed by plasmin (Pn) on fibrin. (queensu.ca)
  • These data identified new mechanisms in which TAFIa can attenuate fibrinolysis. (queensu.ca)
  • An update on the role of carboxypeptidase U (TAFIa) in fibrinolysis. (semanticscholar.org)
  • Urokinase versus Alteplase for intraventricular hemorrhage fibrinolysis. (nih.gov)
  • Despite delays in diagnosis and treatment common in this condition, fibrinolysis with urokinase has had an acceptable safety profile, especially in view of the high mortality rate associated with conservative treatment. (ajnr.org)
  • Beginning in April 1999, tPA was substituted for urokinase for intraarterial fibrinolysis in cases of acute thromboembolic stroke. (ajnr.org)
  • Reocclusion occurred in all control and heparin/aspirin-treated dogs within 1 h after fibrinolysis. (aspetjournals.org)
  • In minimal amounts there is evidence of consumption of blood coagulation factors with sustained thrombocytopenia, but no fibrinolysis, where heparin therapy might have a beneficial effect. (sun.ac.za)
  • The first hours after trauma are dominated by an acceleration of fibrinolysis (clot lysis) and clotting time which are often followed by an abrupt rebound to prolonged fibrinolysis and normal clotting. (bmj.com)
  • We have investigated the effects of DNA and histones on fibrinolysis and proposed that these highly charged molecules are able to hold the fibrin network together and retard clot lysis. (nibsc.org)
  • Fingerprint Dive into the research topics of 'Fibrinolysis és érbetegségek. (elsevier.com)
  • Primary fibrinolysis refers to the normal breakdown of clots. (medlineplus.gov)
  • Primary fibrinolysis is a normal body process. (diapharma.com)
  • As a result, t-PA became essentially equated with fibrinolysis, as shown by it frequently not being identified specifically in publications on clinical fibrinolysis. (onlinejacc.org)
  • These new actors and concepts in plasminogen activation represent hitherto unknown pathways in our comprehension of fibrinolysis and potential novel biomarkers in clinical practice. (inserm.fr)
  • Booth, NA 1999, ' Fibrinolysis and thrombosis ', Best Practice & Research Clinical Obstetrics & Gynaecology , vol. 12, pp. 423-433. (elsevier.com)
  • OBJECTIVE To evaluate carotid intima-media thickness and thrombin-activatable fibrinolysis inhibitor levels in young women with polycystic ovary syndrome (PCOS) and age-matched healthy controls, and to investigate their relationship with each other and with clinical, metabolic, and hormonal parameters. (semanticscholar.org)
  • The fibrinolytic clinical experience has been with tPA monotherapy almost exclusively and this has been sufficiently disappointing that fibrinolysis has become discredited. (heraldopenaccess.us)
  • Fibrinolysis involves dissolution of polymeric fibrin networks that is required to restore blood flow through vessels obstructed by thrombi. (bioportfolio.com)
  • Fibrinolysis Fibrinolysis is the dissolution of the clot formation process involving the plasma protein plasminogen. (perfusion.com)
  • There are two pathways in the fibrinolysis system: the intrinsic pathway initiates upon the activation of a coagulation factor XII to XIIa in its interaction with a negatively charged foreign surface in the presence of high molecular weight kininogen and prekallikrein, and the other pathway, extrinsic pathway, initiates by PAs introduced in the blood exogenously from endothelial cells or upon the addition of bacterial activators such as streptokinase (SK). (springer.com)
  • Objective The effects of ω-3 fatty acids on endothelial function, fibrinolysis and platelet function are uncertain. (bmj.com)
  • Prothrombin fragment F1 + 2 and thrombin-antithrombin III complex are useful markers of the hypercoagulable state in atrial fibrillation," Blood Coagulation & Fibrinolysis , vol. 3, no. 4, pp. 469-473, 1992. (hindawi.com)
  • Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. (wikipedia.org)
  • Fibrinolysis syndrome is characterized by an acute hemorrhagic state brought about by inability of the blood to clot, with massive hemorrhages into the skin producing blackish, purplish swellings and sloughing. (wikipedia.org)
  • The cause for Fibrinolysis syndrome, is the inability of the body to produce blood-coagulates to stop bleeding. (wikipedia.org)
  • New subscriptions to Blood Coagulation & Fibrinolysis are managed through Lippincott Williams & Wilkins (LWW) online store. (lww.com)
  • Subscription renewals for Blood Coagulation & Fibrinolysis are managed through Lippincott Williams & Wilkins online store. (lww.com)
  • S. Isacson and I. M. Nilsson, Defective fibrinolysis in blood and vein walls in recurrent "idiopathic" venous thrombosis, Acta Chir.Scand. (springer.com)
  • The effects of a single 50 mg intramuscular injection of the anabolic steroid stanozolol (Stromba) on fibrinolysis, blood coagulation and lipids was evaluated in 12 healthy male volunteers. (nih.gov)
  • Interrelationships between blood, fibrinolysis, body composition and parameters of lipid and carbohydrate metabolism. (springer.com)
  • Blood clot contraction differentially modulates internal and external fibrinolysis. (bioportfolio.com)
  • Deep vein CDU examination of both lower extremities combined with blood fibrinolysis monitoring is of great value in the prevention and treatment of hypertension during pregnancy. (scirp.org)
  • Fibrinolysis is a system in which fibrin clot dissolves due to the degradation of fibrin by plasmin, which is present in the blood as a precursor form, plasminogen (plg). (springer.com)
  • Fibrinolysis is a normal body process that keeps naturally occurring blood clots from growing and causing problems. (drugster.info)
  • D-dimer (D dimer, DDimer) is a specific fibrin degradation product (FDP) generated after a blood clot is degraded by fibrinolysis . (diapharma.com)
  • By contrast to tPA mono-therapy, natural fibrinolysis uses a sequential combination of both biological activators, tPA and uPA, the native form of which is a proenzyme, prouPA. (heraldopenaccess.us)
  • Finally, it reviews the evidence that defective plasma fibrinolysis has a causal role in venous and arterial thrombosis. (elsevier.com)
  • Animal and human experimental models of infection also suggest that older subjects have higher circulating levels of inflammatory and coagulation-fibrinolysis response. (plos.org)
  • Two parallel lines of investigation elucidating novel mechanisms by which iron (scanning electron microscopy-based) and carbon monoxide (viscoelastic-based) enhance coagulation and diminish fibrinolysis have emerged over the past few years. (up.ac.za)