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)

Fibrinolysis is the natural process in the body that leads to the dissolution of blood clots. It is a vital part of hemostasis, the process that regulates bleeding and wound healing. Fibrinolysis occurs when plasminogen activators convert plasminogen to plasmin, an enzyme that breaks down fibrin, the insoluble protein mesh that forms the structure of a blood clot. This process helps to prevent excessive clotting and maintains the fluidity of the blood. In medical settings, fibrinolysis can also refer to the therapeutic use of drugs that stimulate this process to dissolve unwanted or harmful blood clots, such as those that cause deep vein thrombosis or pulmonary embolism.

Carboxypeptidase U is also known as thiol protease or thiol carboxypeptidase. It is a type of enzyme that belongs to the peptidase family, specifically the serine proteases. This enzyme plays a role in the regulation of blood pressure by cleaving and inactivating bradykinin, a potent vasodilator peptide. Carboxypeptidase U is primarily produced in the kidneys and is released into the circulation in response to various stimuli, such as renin and angiotensin II. It functions by removing the C-terminal arginine residue from bradykinin, thereby reducing its biological activity and helping to maintain blood pressure homeostasis.

Fibrin is defined as a protein that is formed from fibrinogen during the clotting of blood. It plays an essential role in the formation of blood clots, also known as a clotting or coagulation cascade. When an injury occurs and bleeding starts, fibrin threads form a net-like structure that entraps platelets and red blood cells to create a stable clot, preventing further loss of blood.

The process of forming fibrin from fibrinogen is initiated by thrombin, another protein involved in the coagulation cascade. Thrombin cleaves fibrinogen into fibrin monomers, which then polymerize to form long strands of fibrin. These strands cross-link with each other through a process catalyzed by factor XIIIa, forming a stable clot that protects the wound and promotes healing.

It is important to note that abnormalities in fibrin formation or breakdown can lead to bleeding disorders or thrombotic conditions, respectively. Proper regulation of fibrin production and degradation is crucial for maintaining healthy hemostasis and preventing excessive clotting or bleeding.

Blood coagulation, also known as blood clotting, is a complex process that occurs in the body to prevent excessive bleeding when a blood vessel is damaged. This process involves several different proteins and chemical reactions that ultimately lead to the formation of a clot.

The coagulation cascade is initiated when blood comes into contact with tissue factor, which is exposed after damage to the blood vessel wall. This triggers a series of enzymatic reactions that activate clotting factors, leading to the formation of a fibrin clot. Fibrin is a protein that forms a mesh-like structure that traps platelets and red blood cells to form a stable clot.

Once the bleeding has stopped, the coagulation process is regulated and inhibited to prevent excessive clotting. The fibrinolytic system degrades the clot over time, allowing for the restoration of normal blood flow.

Abnormalities in the blood coagulation process can lead to bleeding disorders or thrombotic disorders such as deep vein thrombosis and pulmonary embolism.

Tissue Plasminogen Activator (tPA) is a thrombolytic enzyme, which means it dissolves blood clots. It is naturally produced by the endothelial cells that line the interior surface of blood vessels. tPA activates plasminogen, a zymogen, to convert it into plasmin, a protease that breaks down fibrin, the structural protein in blood clots. This enzyme is used medically as a thrombolytic drug under various brand names, such as Activase and Alteplase, to treat conditions like acute ischemic stroke, pulmonary embolism, and deep vein thrombosis by dissolving the clots and restoring blood flow.

Alpha-2-antiplasmin (α2AP) is a protein found in the blood plasma that inhibits fibrinolysis, the process by which blood clots are broken down. It does this by irreversibly binding to and inhibiting plasmin, an enzyme that degrades fibrin clots.

Alpha-2-antiplasmin is one of the most important regulators of fibrinolysis, helping to maintain a balance between clot formation and breakdown. Deficiencies or dysfunction in alpha-2-antiplasmin can lead to an increased risk of bleeding due to uncontrolled plasmin activity.

Plasminogen Activator Inhibitor 1 (PAI-1) is a protein involved in the regulation of fibrinolysis, which is the body's natural process of breaking down blood clots. PAI-1 inhibits tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), two enzymes that convert plasminogen to plasmin, which degrades fibrin clots. Therefore, PAI-1 acts as a natural antagonist of the fibrinolytic system, promoting clot formation and stability. Increased levels of PAI-1 have been associated with thrombotic disorders, such as deep vein thrombosis and pulmonary embolism.

Plasminogen is a glycoprotein that is present in human plasma, and it is the inactive precursor of the enzyme plasmin. Plasmin is a serine protease that plays a crucial role in the dissolution of blood clots by degrading fibrin, one of the major components of a blood clot.

Plasminogen can be activated to form plasmin through the action of various activators, such as tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Once activated, plasmin can break down fibrin and other proteins, helping to prevent excessive clotting and promoting the normal turnover of extracellular matrix components.

Abnormalities in plasminogen activation have been implicated in various diseases, including thrombosis, fibrosis, and cancer. Therefore, understanding the regulation and function of plasminogen is important for developing therapies to treat these conditions.

Fibrinolysin is defined as a proteolytic enzyme that dissolves or breaks down fibrin, a protein involved in the clotting of blood. This enzyme is produced by certain cells, such as endothelial cells that line the interior surface of blood vessels, and is an important component of the body's natural mechanism for preventing excessive blood clotting and maintaining blood flow.

Fibrinolysin works by cleaving specific bonds in the fibrin molecule, converting it into soluble degradation products that can be safely removed from the body. This process is known as fibrinolysis, and it helps to maintain the balance between clotting and bleeding in the body.

In medical contexts, fibrinolysin may be used as a therapeutic agent to dissolve blood clots that have formed in the blood vessels, such as those that can occur in deep vein thrombosis or pulmonary embolism. It is often administered in combination with other medications that help to enhance its activity and specificity for fibrin.

Antifibrinolytic agents are a class of medications that inhibit the breakdown of blood clots. They work by blocking the action of enzymes called plasminogen activators, which convert plasminogen to plasmin, the main enzyme responsible for breaking down fibrin, a protein that forms the framework of a blood clot.

By preventing the conversion of plasminogen to plasmin, antifibrinolytic agents help to stabilize existing blood clots and prevent their premature dissolution. These medications are often used in clinical settings where excessive bleeding is a concern, such as during or after surgery, childbirth, or trauma.

Examples of antifibrinolytic agents include tranexamic acid, aminocaproic acid, and epsilon-aminocaproic acid. While these medications can be effective in reducing bleeding, they also carry the risk of thromboembolic events, such as deep vein thrombosis or pulmonary embolism, due to their pro-coagulant effects. Therefore, they should be used with caution and only under the close supervision of a healthcare provider.

Fibrin(ogen) degradation products (FDPs) are a group of proteins that result from the breakdown of fibrinogen and fibrin, which are key components of blood clots. This process occurs during the normal physiological process of fibrinolysis, where clots are dissolved to maintain blood flow.

FDPs can be measured in the blood as a marker for the activation of the coagulation and fibrinolytic systems. Elevated levels of FDPs may indicate the presence of a disorder that causes abnormal clotting or bleeding, such as disseminated intravascular coagulation (DIC), deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of cancer.

It is important to note that FDPs are not specific to any particular disorder and their measurement should be interpreted in conjunction with other clinical and laboratory findings.

Fibrinolytic agents are medications that dissolve or break down blood clots by activating plasminogen, which is converted into plasmin. Plasmin is a proteolytic enzyme that degrades fibrin, the structural protein in blood clots. Fibrinolytic agents are used medically to treat conditions such as acute ischemic stroke, deep vein thrombosis, pulmonary embolism, and myocardial infarction (heart attack) by restoring blood flow in occluded vessels. Examples of fibrinolytic agents include alteplase, reteplase, and tenecteplase. It is important to note that these medications carry a risk of bleeding complications and should be administered with caution.

Thrombomodulin is a protein that is found on the surface of endothelial cells, which line the interior surface of blood vessels. It plays an important role in the regulation of blood coagulation (clotting) and the activation of natural anticoagulant pathways. Thrombomodulin binds to thrombin, a protein involved in blood clotting, and changes its function from promoting coagulation to inhibiting it. This interaction also activates protein C, an important anticoagulant protein, which helps to prevent the excessive formation of blood clots. Thrombomodulin also has anti-inflammatory properties and is involved in the maintenance of the integrity of the endothelial cell lining.

Fibrinogen is a soluble protein present in plasma, synthesized by the liver. It plays an essential role in blood coagulation. When an injury occurs, fibrinogen gets converted into insoluble fibrin by the action of thrombin, forming a fibrin clot that helps to stop bleeding from the injured site. Therefore, fibrinogen is crucial for hemostasis, which is the process of stopping bleeding and starting the healing process after an injury.

Hemostasis is the physiological process that occurs to stop bleeding (bleeding control) when a blood vessel is damaged. This involves the interaction of platelets, vasoconstriction, and blood clotting factors leading to the formation of a clot. The ultimate goal of hemostasis is to maintain the integrity of the vascular system while preventing excessive blood loss.

Plasminogen activators are a group of enzymes that play a crucial role in the body's fibrinolytic system, which is responsible for breaking down and removing blood clots. These enzymes activate plasminogen, a zymogen (inactive precursor) found in circulation, converting it into plasmin - a protease that degrades fibrin, the insoluble protein mesh that forms the structural basis of a blood clot.

There are two main types of plasminogen activators:

1. Tissue Plasminogen Activator (tPA): This is a serine protease primarily produced by endothelial cells lining blood vessels. tPA has a higher affinity for fibrin-bound plasminogen and is therefore more specific in activating plasmin at the site of a clot, helping to localize fibrinolysis and minimize bleeding risks.
2. Urokinase Plasminogen Activator (uPA): This is another serine protease found in various tissues and body fluids, including urine. uPA can be produced by different cell types, such as macrophages and fibroblasts. Unlike tPA, uPA does not have a strong preference for fibrin-bound plasminogen and can activate plasminogen in a more general manner, which might contribute to its role in processes like tissue remodeling and cancer progression.

Plasminogen activators are essential for maintaining vascular homeostasis by ensuring the proper removal of blood clots and preventing excessive fibrin accumulation. They have also been implicated in various pathological conditions, including thrombosis, hemorrhage, and tumor metastasis.

Carboxypeptidase B is a type of enzyme that belongs to the peptidase family. It is also known as carboxypeptidase B1 or CpB. This enzyme plays a crucial role in the digestion of proteins by cleaving specific amino acids from the carboxyl-terminal end of polypeptides.

Carboxypeptidase B preferentially removes basic arginine and lysine residues from protein substrates, making it an essential enzyme in various physiological processes, including blood clotting, hormone processing, and neuropeptide metabolism. It is synthesized as an inactive zymogen, procarboxypeptidase B, which is converted to its active form upon proteolytic activation.

In addition to its physiological functions, carboxypeptidase B has applications in research and industry, such as protein sequencing, peptide synthesis, and food processing.

Urokinase-type plasminogen activator (uPA) is a serine protease enzyme that plays a crucial role in the degradation of the extracellular matrix and cell migration. It catalyzes the conversion of plasminogen to plasmin, which then breaks down various proteins in the extracellular matrix, leading to tissue remodeling and repair.

uPA is synthesized as a single-chain molecule, pro-uPA, which is activated by cleavage into two chains, forming the mature and active enzyme. uPA binds to its specific receptor, uPAR, on the cell surface, where it exerts its proteolytic activity.

Abnormal regulation of uPA and uPAR has been implicated in various pathological conditions, including cancer, where they contribute to tumor invasion and metastasis. Therefore, uPA is a potential target for therapeutic intervention in cancer and other diseases associated with excessive extracellular matrix degradation.

Serum globulins are a group of proteins present in the liquid portion of blood, known as serum. They are produced by the immune system in response to foreign substances such as bacteria, viruses, and allergens. Serum globulins include several types of immunoglobulins (antibodies), complement components, and other proteins involved in the immune response.

The serum globulin level is often measured as part of a complete blood count (CBC) or a protein electrophoresis test. An elevated serum globulin level may indicate an ongoing infection, inflammation, or an autoimmune disorder. Conversely, a decreased level may suggest a liver or kidney disease, or a malnutrition condition. It is important to note that the interpretation of serum globulin levels should be done in conjunction with other laboratory and clinical findings.

Thrombolytic therapy, also known as thrombolysis, is a medical treatment that uses medications called thrombolytics or fibrinolytics to dissolve or break down blood clots (thrombi) in blood vessels. These clots can obstruct the flow of blood to vital organs such as the heart, lungs, or brain, leading to serious conditions like myocardial infarction (heart attack), pulmonary embolism, or ischemic stroke.

The goal of thrombolytic therapy is to restore blood flow as quickly and efficiently as possible to prevent further damage to the affected organ and potentially save lives. Commonly used thrombolytic drugs include alteplase (tPA), reteplase, and tenecteplase. It's essential to administer these medications as soon as possible after the onset of symptoms for optimal treatment outcomes. However, there are risks associated with thrombolytic therapy, such as an increased chance of bleeding complications, which must be carefully weighed against its benefits in each individual case.

Antithrombin III is a protein that inhibits the formation of blood clots (thrombi) in the body. It does this by inactivating several enzymes involved in coagulation, including thrombin and factor Xa. Antithrombin III is produced naturally by the liver and is also available as a medication for the prevention and treatment of thromboembolic disorders, such as deep vein thrombosis and pulmonary embolism. It works by binding to and neutralizing excess clotting factors in the bloodstream, thereby reducing the risk of clot formation.

Plasminogen inactivators are substances that inhibit the activity of plasminogen, a proenzyme that is converted into the active enzyme plasmin. Plasmin plays a crucial role in the breakdown of blood clots by cleaving fibrin, the protein that forms the structural framework of a clot.

There are two main types of plasminogen activators: tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). These enzymes convert plasminogen into plasmin, thereby promoting fibrinolysis, or the dissolution of blood clots. Plasminogen inactivators, on the other hand, inhibit this process by blocking the conversion of plasminogen to plasmin.

Plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) are two main types of plasminogen inactivators. PAI-1 is a serine protease inhibitor that inactivates tPA and uPA by forming covalent complexes with them. PAI-1 is produced by various cells, including endothelial cells, hepatocytes, and adipocytes. Elevated levels of PAI-1 have been associated with an increased risk of thrombosis and cardiovascular disease.

PAI-2 is another serine protease inhibitor that primarily inhibits uPA. It is produced by various cells, including monocytes, macrophages, and trophoblasts. PAI-2 has been shown to play a role in pregnancy, immune response, and cancer.

Overall, plasminogen inactivators are important regulators of the fibrinolytic system, which helps maintain blood flow and prevent excessive clotting or bleeding. Dysregulation of this system can lead to various pathological conditions, such as thrombosis, hemorrhage, and cancer.

Thrombin is a serine protease enzyme that plays a crucial role in the coagulation cascade, which is a complex series of biochemical reactions that leads to the formation of a blood clot (thrombus) to prevent excessive bleeding during an injury. Thrombin is formed from its precursor protein, prothrombin, through a process called activation, which involves cleavage by another enzyme called factor Xa.

Once activated, thrombin converts fibrinogen, a soluble plasma protein, into fibrin, an insoluble protein that forms the structural framework of a blood clot. Thrombin also activates other components of the coagulation cascade, such as factor XIII, which crosslinks and stabilizes the fibrin network, and platelets, which contribute to the formation and growth of the clot.

Thrombin has several regulatory mechanisms that control its activity, including feedback inhibition by antithrombin III, a plasma protein that inactivates thrombin and other serine proteases, and tissue factor pathway inhibitor (TFPI), which inhibits the activation of factor Xa, thereby preventing further thrombin formation.

Overall, thrombin is an essential enzyme in hemostasis, the process that maintains the balance between bleeding and clotting in the body. However, excessive or uncontrolled thrombin activity can lead to pathological conditions such as thrombosis, atherosclerosis, and disseminated intravascular coagulation (DIC).

Blood coagulation tests, also known as coagulation studies or clotting tests, are a series of medical tests used to evaluate the blood's ability to clot. These tests measure the functioning of various clotting factors and regulatory proteins involved in the coagulation cascade, which is a complex process that leads to the formation of a blood clot to prevent excessive bleeding.

The most commonly performed coagulation tests include:

1. Prothrombin Time (PT): Measures the time it takes for a sample of plasma to clot after the addition of calcium and tissue factor, which activates the extrinsic pathway of coagulation. The PT is reported in seconds and can be converted to an International Normalized Ratio (INR) to monitor anticoagulant therapy.
2. Activated Partial Thromboplastin Time (aPTT): Measures the time it takes for a sample of plasma to clot after the addition of calcium, phospholipid, and a contact activator, which activates the intrinsic pathway of coagulation. The aPTT is reported in seconds and is used to monitor heparin therapy.
3. Thrombin Time (TT): Measures the time it takes for a sample of plasma to clot after the addition of thrombin, which directly converts fibrinogen to fibrin. The TT is reported in seconds and can be used to detect the presence of fibrin degradation products or abnormalities in fibrinogen function.
4. Fibrinogen Level: Measures the amount of fibrinogen, a protein involved in clot formation, present in the blood. The level is reported in grams per liter (g/L) and can be used to assess bleeding risk or the effectiveness of fibrinogen replacement therapy.
5. D-dimer Level: Measures the amount of D-dimer, a protein fragment produced during the breakdown of a blood clot, present in the blood. The level is reported in micrograms per milliliter (µg/mL) and can be used to diagnose or exclude venous thromboembolism (VTE), such as deep vein thrombosis (DVT) or pulmonary embolism (PE).

These tests are important for the diagnosis, management, and monitoring of various bleeding and clotting disorders. They can help identify the underlying cause of abnormal bleeding or clotting, guide appropriate treatment decisions, and monitor the effectiveness of therapy. It is essential to interpret these test results in conjunction with a patient's clinical presentation and medical history.

Factor XIII, also known as fibrin stabilizing factor, is a protein involved in the clotting process of blood. It is a transglutaminase enzyme that cross-links fibrin molecules to form a stable clot. Factor XIII becomes activated during the coagulation cascade, and its activity helps strengthen the clot and protect it from premature degradation by proteolytic enzymes. A deficiency in Factor XIII can lead to a bleeding disorder characterized by prolonged bleeding after injury or surgery.

Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.

Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.

Thromboelastography (TEG) is a viscoelastic method used to assess the kinetics of clot formation, clot strength, and fibrinolysis in whole blood. It provides a global assessment of hemostasis by measuring the mechanical properties of a clot as it forms and dissolves over time. The TEG graph displays several parameters that reflect the different stages of clotting, including reaction time (R), clot formation time (K), angle of clot formation (α), maximum amplitude (MA), and percentage lysis at 30 minutes (LY30). These parameters can help guide transfusion therapy and inform decisions regarding the management of coagulopathy in various clinical settings, such as trauma, cardiac surgery, liver transplantation, and obstetrics.

Protein C is a vitamin K-dependent protease that functions as an important regulator of coagulation and inflammation. It is a plasma protein produced in the liver that, when activated, degrades clotting factors Va and VIIIa to limit thrombus formation and prevent excessive blood clotting. Protein C also has anti-inflammatory properties by inhibiting the release of pro-inflammatory cytokines and reducing endothelial cell activation. Inherited or acquired deficiencies in Protein C can lead to an increased risk of thrombosis, a condition characterized by abnormal blood clot formation within blood vessels.

Blood coagulation disorders, also known as bleeding disorders or clotting disorders, refer to a group of medical conditions that affect the body's ability to form blood clots properly. Normally, when a blood vessel is injured, the body's coagulation system works to form a clot to stop the bleeding and promote healing.

In blood coagulation disorders, there can be either an increased tendency to bleed due to problems with the formation of clots (hemorrhagic disorder), or an increased tendency for clots to form inappropriately even without injury, leading to blockages in the blood vessels (thrombotic disorder).

Examples of hemorrhagic disorders include:

1. Hemophilia - a genetic disorder that affects the ability to form clots due to deficiencies in clotting factors VIII or IX.
2. Von Willebrand disease - another genetic disorder caused by a deficiency or abnormality of the von Willebrand factor, which helps platelets stick together to form a clot.
3. Liver diseases - can lead to decreased production of coagulation factors, increasing the risk of bleeding.
4. Disseminated intravascular coagulation (DIC) - a serious condition where clotting and bleeding occur simultaneously due to widespread activation of the coagulation system.

Examples of thrombotic disorders include:

1. Factor V Leiden mutation - a genetic disorder that increases the risk of inappropriate blood clot formation.
2. Antithrombin III deficiency - a genetic disorder that impairs the body's ability to break down clots, increasing the risk of thrombosis.
3. Protein C or S deficiencies - genetic disorders that lead to an increased risk of thrombosis due to impaired regulation of the coagulation system.
4. Antiphospholipid syndrome (APS) - an autoimmune disorder where the body produces antibodies against its own clotting factors, increasing the risk of thrombosis.

Treatment for blood coagulation disorders depends on the specific diagnosis and may include medications to manage bleeding or prevent clots, as well as lifestyle changes and monitoring to reduce the risk of complications.

Carboxypeptidases are a group of enzymes that catalyze the cleavage of peptide bonds at the carboxyl-terminal end of polypeptides or proteins. They specifically remove the last amino acid residue from the protein chain, provided that it has a free carboxyl group and is not blocked by another chemical group. Carboxypeptidases are classified into two main types based on their catalytic mechanism: serine carboxypeptidases and metallo-carboxypeptidases.

Serine carboxypeptidases, also known as chymotrypsin C or carboxypeptidase C, use a serine residue in their active site to catalyze the hydrolysis of peptide bonds. They are found in various organisms, including animals and bacteria.

Metallo-carboxypeptidases, on the other hand, require a metal ion (usually zinc) for their catalytic activity. They can be further divided into several subtypes based on their structure and substrate specificity. For example, carboxypeptidase A prefers to cleave hydrophobic amino acids from the carboxyl-terminal end of proteins, while carboxypeptidase B specifically removes basic residues (lysine or arginine).

Carboxypeptidases have important roles in various biological processes, such as protein maturation, digestion, and regulation of blood pressure. Dysregulation of these enzymes has been implicated in several diseases, including cancer, neurodegenerative disorders, and cardiovascular disease.

Tranexamic acid is an antifibrinolytic medication that is used to reduce or prevent bleeding. It works by inhibiting the activation of plasminogen to plasmin, which is a protease that degrades fibrin clots. By preventing the breakdown of blood clots, tranexamic acid helps to reduce bleeding and promote clot formation.

Tranexamic acid is available in various forms, including tablets, capsules, and injectable solutions. It is used in a variety of clinical settings, such as surgery, trauma, and heavy menstrual bleeding. The medication can be taken orally or administered intravenously, depending on the severity of the bleeding and the patient's medical condition.

Common side effects of tranexamic acid include nausea, vomiting, diarrhea, and headache. Less commonly, the medication may cause allergic reactions, visual disturbances, or seizures. It is important to follow the prescribing physician's instructions carefully when taking tranexamic acid to minimize the risk of side effects and ensure its safe and effective use.

Blood coagulation factors, also known as clotting factors, are a group of proteins that play a crucial role in the blood coagulation process. They are essential for maintaining hemostasis, which is the body's ability to stop bleeding after injury.

There are 13 known blood coagulation factors, and they are designated by Roman numerals I through XIII. These factors are produced in the liver and are normally present in an inactive form in the blood. When there is an injury to a blood vessel, the coagulation process is initiated, leading to the activation of these factors in a specific order.

The coagulation cascade involves two pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is activated when there is damage to the blood vessel itself, while the extrinsic pathway is activated by tissue factor released from damaged tissues. Both pathways converge at the common pathway, leading to the formation of a fibrin clot.

Blood coagulation factors work together in a complex series of reactions that involve activation, binding, and proteolysis. When one factor is activated, it activates the next factor in the cascade, and so on. This process continues until a stable fibrin clot is formed.

Deficiencies or abnormalities in blood coagulation factors can lead to bleeding disorders such as hemophilia or thrombosis. Hemophilia is a genetic disorder that affects one or more of the coagulation factors, leading to excessive bleeding and difficulty forming clots. Thrombosis, on the other hand, occurs when there is an abnormal formation of blood clots in the blood vessels, which can lead to serious complications such as stroke or pulmonary embolism.

Disseminated Intravascular Coagulation (DIC) is a complex medical condition characterized by the abnormal activation of the coagulation cascade, leading to the formation of blood clots in small blood vessels throughout the body. This process can result in the consumption of clotting factors and platelets, which can then lead to bleeding complications. DIC can be caused by a variety of underlying conditions, including sepsis, trauma, cancer, and obstetric emergencies.

The term "disseminated" refers to the widespread nature of the clotting activation, while "intravascular" indicates that the clotting is occurring within the blood vessels. The condition can manifest as both bleeding and clotting complications, which can make it challenging to diagnose and manage.

The diagnosis of DIC typically involves laboratory tests that evaluate coagulation factors, platelet count, fibrin degradation products, and other markers of coagulation activation. Treatment is focused on addressing the underlying cause of the condition while also managing any bleeding or clotting complications that may arise.

Streptokinase is a thrombolytic or clot-busting enzyme produced by certain strains of streptococcus bacteria. It functions by converting plasminogen to plasmin, which then degrades fibrin, a protein that forms the structural framework of blood clots. This activity helps in dissolving blood clots and restoring blood flow in areas obstructed by them. In a medical context, streptokinase is often used as a medication to treat conditions associated with abnormal blood clotting, such as heart attacks, pulmonary embolisms, and deep vein thromboses. However, its use carries the risk of bleeding complications due to excessive fibrinolysis or clot dissolution.

"Gravity suits" is not a recognized medical term. However, in the context of space medicine and space travel, gravity suits, also known as g-suits or anti-G suits, are specialized garments worn by pilots and astronauts to prevent or reduce the negative effects of high gravitational forces (G-forces) on their bodies during high-speed maneuvers or while re-entering the Earth's atmosphere.

These suits work by applying pressure to specific areas of the body, typically around the lower abdomen and legs, to prevent the pooling of blood in those areas due to the increased G-forces. This helps maintain adequate blood flow to the brain and other vital organs, reducing the risk of loss of consciousness (G-induced Loss of Consciousness or G-LOC) and other symptoms associated with high G-forces such as blackouts, vision impairment, and disorientation.

It's important to note that gravity suits are not used as a medical treatment for any specific condition but rather as a protective measure during space travel and high-performance aviation.

Aminocaproic acid is an antifibrinolytic medication, which means it helps to prevent the breakdown of blood clots. It works by blocking plasmin, an enzyme in your body that dissolves blood clots.

This drug is used for the treatment of bleeding conditions due to various causes, such as:

1. Excessive menstrual bleeding (menorrhagia)
2. Bleeding after tooth extraction or surgery
3. Hematuria (blood in urine) due to certain medical procedures or conditions like kidney stones
4. Intracranial hemorrhage (bleeding inside the skull)
5. Hereditary angioedema, a genetic disorder that causes swelling of various parts of the body

Aminocaproic acid is available in oral and injectable forms. Common side effects include nausea, vomiting, diarrhea, and headache. Serious side effects are rare but may include allergic reactions, seizures, or vision changes. It's essential to use this medication under the supervision of a healthcare professional, as improper usage might lead to blood clots, stroke, or other severe complications.

Aminocaproates are a group of chemical compounds that contain an amino group and a carboxylic acid group, as well as a straight or branched alkyl chain with 6-10 carbon atoms. They are often used in medical settings as anti-fibrinolytic agents, which means they help to prevent the breakdown of blood clots.

One example of an aminocaproate is epsilon-aminocaproic acid (EACA), which is a synthetic analogue of the amino acid lysine. EACA works by inhibiting the activation of plasminogen to plasmin, which is an enzyme that breaks down blood clots. By doing so, EACA can help to reduce bleeding and improve clot stability in certain medical conditions, such as hemophilia or following surgery.

Other aminocaproates include tranexamic acid (TXA) and 4-aminoethylbenzoic acid (AEBA), which also have anti-fibrinolytic properties and are used in similar clinical settings. However, it's important to note that these medications can increase the risk of thrombosis (blood clots) if not used properly, so they should only be administered under the close supervision of a healthcare provider.

Prothrombin time (PT) is a medical laboratory test that measures the time it takes for blood to clot. It's often used to evaluate the functioning of the extrinsic and common pathways of the coagulation system, which is responsible for blood clotting. Specifically, PT measures how long it takes for prothrombin (a protein produced by the liver) to be converted into thrombin, an enzyme that converts fibrinogen into fibrin and helps form a clot.

Prolonged PT may indicate a bleeding disorder or a deficiency in coagulation factors, such as vitamin K deficiency or the use of anticoagulant medications like warfarin. It's important to note that PT is often reported with an international normalized ratio (INR), which allows for standardization and comparison of results across different laboratories and reagent types.

Prothrombin is a protein present in blood plasma, and it's also known as coagulation factor II. It plays a crucial role in the coagulation cascade, which is a complex series of reactions that leads to the formation of a blood clot.

When an injury occurs, the coagulation cascade is initiated to prevent excessive blood loss. Prothrombin is converted into its active form, thrombin, by another factor called factor Xa in the presence of calcium ions, phospholipids, and factor Va. Thrombin then catalyzes the conversion of fibrinogen into fibrin, forming a stable clot.

Prothrombin levels can be measured through a blood test, which is often used to diagnose or monitor conditions related to bleeding or coagulation disorders, such as liver disease or vitamin K deficiency.

Heparin is defined as a highly sulfated glycosaminoglycan (a type of polysaccharide) that is widely present in many tissues, but is most commonly derived from the mucosal tissues of mammalian lungs or intestinal mucosa. It is an anticoagulant that acts as an inhibitor of several enzymes involved in the blood coagulation cascade, primarily by activating antithrombin III which then neutralizes thrombin and other clotting factors.

Heparin is used medically to prevent and treat thromboembolic disorders such as deep vein thrombosis, pulmonary embolism, and certain types of heart attacks. It can also be used during hemodialysis, cardiac bypass surgery, and other medical procedures to prevent the formation of blood clots.

It's important to note that while heparin is a powerful anticoagulant, it does not have any fibrinolytic activity, meaning it cannot dissolve existing blood clots. Instead, it prevents new clots from forming and stops existing clots from growing larger.

Enoxaparin is a low molecular weight heparin (LMWH) medication that is used as an anticoagulant to prevent and treat blood clots. It works by binding to and inhibiting the activity of factor Xa, a clotting factor in the blood. This helps to reduce the risk of clot formation and can help to prevent conditions such as deep vein thrombosis (DVT) and pulmonary embolism (PE). Enoxaparin is typically given by injection under the skin (subcutaneously) and is available under the brand names Lovenox and Clexane, among others. It is important to follow the instructions of a healthcare professional when using enoxaparin, as it can increase the risk of bleeding.

Factor XII, also known as Hageman factor, is a protein that plays a role in the coagulation cascade, which is the series of events that leads to the formation of a blood clot. It is one of the zymogens, or inactive precursor proteins, that becomes activated and helps to trigger the coagulation process.

When Factor XII comes into contact with negatively charged surfaces, such as damaged endothelial cells or artificial surfaces like those found on medical devices, it undergoes a conformational change and becomes activated. Activated Factor XII then activates other proteins in the coagulation cascade, including Factor XI, which ultimately leads to the formation of a fibrin clot.

Deficiencies in Factor XII are generally not associated with bleeding disorders, as the coagulation cascade can still proceed through other pathways. However, excessive activation of Factor XII has been implicated in certain thrombotic disorders, such as deep vein thrombosis and disseminated intravascular coagulation (DIC).

Thromboplastin is a substance that activates the coagulation cascade, leading to the formation of a clot (thrombus). It's primarily found in damaged or injured tissues and blood vessels, as well as in platelets (thrombocytes). There are two types of thromboplastin:

1. Extrinsic thromboplastin (also known as tissue factor): This is a transmembrane glycoprotein that is primarily found in subendothelial cells and released upon injury to the blood vessels. It initiates the extrinsic pathway of coagulation by binding to and activating Factor VII, ultimately leading to the formation of thrombin and fibrin clots.
2. Intrinsic thromboplastin (also known as plasma thromboplastin or factor III): This term is used less frequently and refers to a labile phospholipid component present in platelet membranes, which plays a role in the intrinsic pathway of coagulation.

In clinical settings, the term "thromboplastin" often refers to reagents used in laboratory tests like the prothrombin time (PT) and activated partial thromboplastin time (aPTT). These reagents contain a source of tissue factor and calcium ions to initiate and monitor the coagulation process.

Partial Thromboplastin Time (PTT) is a medical laboratory test that measures the time it takes for blood to clot. It's more specifically a measure of the intrinsic and common pathways of the coagulation cascade, which are the series of chemical reactions that lead to the formation of a clot.

The test involves adding a partial thromboplastin reagent (an activator of the intrinsic pathway) and calcium to plasma, and then measuring the time it takes for a fibrin clot to form. This is compared to a control sample, and the ratio of the two times is calculated.

The PTT test is often used to help diagnose bleeding disorders or abnormal blood clotting, such as hemophilia or disseminated intravascular coagulation (DIC). It can also be used to monitor the effectiveness of anticoagulant therapy, such as heparin. Prolonged PTT results may indicate a bleeding disorder or an increased risk of bleeding, while shortened PTT results may indicate a hypercoagulable state and an increased risk of thrombosis.

Myocardial infarction (MI), also known as a heart attack, is a medical condition characterized by the death of a segment of heart muscle (myocardium) due to the interruption of its blood supply. This interruption is most commonly caused by the blockage of a coronary artery by a blood clot formed on the top of an atherosclerotic plaque, which is a buildup of cholesterol and other substances in the inner lining of the artery.

The lack of oxygen and nutrients supply to the heart muscle tissue results in damage or death of the cardiac cells, causing the affected area to become necrotic. The extent and severity of the MI depend on the size of the affected area, the duration of the occlusion, and the presence of collateral circulation.

Symptoms of a myocardial infarction may include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and sweating. Immediate medical attention is necessary to restore blood flow to the affected area and prevent further damage to the heart muscle. Treatment options for MI include medications, such as thrombolytics, antiplatelet agents, and pain relievers, as well as procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

Annexin A2 is a protein found in various types of cells, including those that line the inside of blood vessels. It is a member of the annexin family of proteins, which are characterized by their ability to bind to calcium ions and membranes. Annexin A2 is involved in several cellular processes, including the regulation of ion channels, the modulation of enzyme activity, and the promotion of cell adhesion and migration. It also plays a role in the coagulation of blood, and has been implicated in the development and progression of various diseases, including cancer and cardiovascular disease.

Antithrombins are substances that prevent the formation or promote the dissolution of blood clots (thrombi). They include:

1. Anticoagulants: These are medications that reduce the ability of the blood to clot. Examples include heparin, warfarin, and direct oral anticoagulants (DOACs) such as apixaban, rivaroxaban, and dabigatran.
2. Thrombolytic agents: These are medications that break down existing blood clots. Examples include alteplase, reteplase, and tenecteplase.
3. Fibrinolytics: These are a type of thrombolytic agent that specifically target fibrin, a protein involved in the formation of blood clots.
4. Natural anticoagulants: These are substances produced by the body to regulate blood clotting. Examples include antithrombin III, protein C, and protein S.

Antithrombins are used in the prevention and treatment of various thromboembolic disorders, such as deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, and myocardial infarction (heart attack). It is important to note that while antithrombins can help prevent or dissolve blood clots, they also increase the risk of bleeding, so their use must be carefully monitored.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Serpin E2, also known as Neuroserpin, is a member of the serine protease inhibitor (Serpin) superfamily. It is primarily expressed in neuronal cells and plays a crucial role in regulating tissue plasminogen activator (tPA), a protein involved in the breakdown of blood clots. Serpin E2 helps to prevent excessive proteolytic activity, which can lead to neurodegeneration and other neurological disorders. Mutations in the SERPINE2 gene have been associated with certain forms of dementia and cerebral amyloid angiopathy (CAA), a condition characterized by the accumulation of beta-amyloid protein in the walls of blood vessels in the brain.

Hemorrhagic disorders are medical conditions characterized by abnormal bleeding due to impaired blood clotting. This can result from deficiencies in coagulation factors, platelet dysfunction, or the use of medications that interfere with normal clotting processes. Examples include hemophilia, von Willebrand disease, and disseminated intravascular coagulation (DIC). Treatment often involves replacing the missing clotting factor or administering medications to help control bleeding.

Peptide hydrolases, also known as proteases or peptidases, are a group of enzymes that catalyze the hydrolysis of peptide bonds in proteins and peptides. They play a crucial role in various biological processes such as protein degradation, digestion, cell signaling, and regulation of various physiological functions. Based on their catalytic mechanism and the specificity for the peptide bond, they are classified into several types, including serine proteases, cysteine proteases, aspartic proteases, and metalloproteases. These enzymes have important clinical applications in the diagnosis and treatment of various diseases, such as cancer, viral infections, and inflammatory disorders.

Thrombin time (TT) is a medical laboratory test that measures the time it takes for a clot to form after thrombin, an enzyme that converts fibrinogen to fibrin in the final step of the coagulation cascade, is added to a plasma sample. This test is used to evaluate the efficiency of the conversion of fibrinogen to fibrin and can be used to detect the presence of abnormalities in the coagulation system, such as the presence of heparin or dysfibrinogenemia. Increased thrombin time may indicate the presence of a systemic anticoagulant or a deficiency in fibrinogen.

Anticoagulants are a class of medications that work to prevent the formation of blood clots in the body. They do this by inhibiting the coagulation cascade, which is a series of chemical reactions that lead to the formation of a clot. Anticoagulants can be given orally, intravenously, or subcutaneously, depending on the specific drug and the individual patient's needs.

There are several different types of anticoagulants, including:

1. Heparin: This is a naturally occurring anticoagulant that is often used in hospitalized patients who require immediate anticoagulation. It works by activating an enzyme called antithrombin III, which inhibits the formation of clots.
2. Low molecular weight heparin (LMWH): LMWH is a form of heparin that has been broken down into smaller molecules. It has a longer half-life than standard heparin and can be given once or twice daily by subcutaneous injection.
3. Direct oral anticoagulants (DOACs): These are newer oral anticoagulants that work by directly inhibiting specific clotting factors in the coagulation cascade. Examples include apixaban, rivaroxaban, and dabigatran.
4. Vitamin K antagonists: These are older oral anticoagulants that work by inhibiting the action of vitamin K, which is necessary for the formation of clotting factors. Warfarin is an example of a vitamin K antagonist.

Anticoagulants are used to prevent and treat a variety of conditions, including deep vein thrombosis (DVT), pulmonary embolism (PE), atrial fibrillation, and prosthetic heart valve thrombosis. It is important to note that anticoagulants can increase the risk of bleeding, so they must be used with caution and regular monitoring of blood clotting times may be required.

Factor VII, also known as proconvertin, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor VII is synthesized in the liver and is activated when it comes into contact with tissue factor, which is exposed when blood vessels are damaged. Activated Factor VII then activates Factor X, leading to the formation of thrombin and ultimately a fibrin clot.

Inherited deficiencies or dysfunctions of Factor VII can lead to an increased risk of bleeding, while elevated levels of Factor VII have been associated with an increased risk of thrombosis (blood clots).

Traumatic shock is a type of physiological response that occurs when an individual experiences a severe physical trauma, such as severe injury, burns, or bleeding. This condition is characterized by inadequate tissue perfusion and oxygenation, which can lead to cellular damage and organ dysfunction. The primary cause of traumatic shock is a significant decrease in blood volume due to hemorrhage, which reduces the amount of oxygen and nutrients delivered to tissues and organs.

The symptoms of traumatic shock include:

1. Hypotension (low blood pressure)
2. Tachycardia (rapid heart rate)
3. Altered mental status (confusion, agitation, or lethargy)
4. Cool, clammy skin
5. Weak or absent peripheral pulses
6. Rapid, shallow breathing
7. Decreased urine output
8. Lactic acidosis (elevated levels of lactic acid in the blood)
9. Metabolic disturbances

Traumatic shock is a medical emergency that requires immediate treatment to prevent further tissue damage and organ dysfunction. Treatment typically involves fluid resuscitation, blood transfusion, and surgery to control bleeding. In some cases, medications such as vasopressors may be necessary to maintain blood pressure and perfusion to vital organs.

Recombinant proteins are artificially created proteins produced through the use of recombinant DNA technology. This process involves combining DNA molecules from different sources to create a new set of genes that encode for a specific protein. The resulting recombinant protein can then be expressed, purified, and used for various applications in research, medicine, and industry.

Recombinant proteins are widely used in biomedical research to study protein function, structure, and interactions. They are also used in the development of diagnostic tests, vaccines, and therapeutic drugs. For example, recombinant insulin is a common treatment for diabetes, while recombinant human growth hormone is used to treat growth disorders.

The production of recombinant proteins typically involves the use of host cells, such as bacteria, yeast, or mammalian cells, which are engineered to express the desired protein. The host cells are transformed with a plasmid vector containing the gene of interest, along with regulatory elements that control its expression. Once the host cells are cultured and the protein is expressed, it can be purified using various chromatography techniques.

Overall, recombinant proteins have revolutionized many areas of biology and medicine, enabling researchers to study and manipulate proteins in ways that were previously impossible.

Afibrinogenemia is a rare genetic disorder characterized by the complete absence or severely decreased levels of fibrinogen, a protein involved in blood clotting. This condition leads to an increased risk of excessive bleeding due to the inability to form proper blood clots. It is caused by mutations in the genes that provide instructions for making the three chains (Aα, Bβ, and γ) that make up the fibrinogen protein. Inheritance is autosomal recessive, meaning an individual must inherit two copies of the defective gene, one from each parent, to have the condition.

Intracranial thrombosis refers to the formation of a blood clot (thrombus) within the intracranial vessels, which supply blood to the brain. This condition can occur in any of the cerebral arteries or veins and can lead to serious complications such as ischemic stroke, transient ischemic attack (TIA), or venous sinus thrombosis.

The formation of an intracranial thrombus can be caused by various factors, including atherosclerosis, cardiac embolism, vasculitis, sickle cell disease, hypercoagulable states, and head trauma. Symptoms may vary depending on the location and extent of the thrombosis but often include sudden onset of headache, weakness or numbness in the face or limbs, difficulty speaking or understanding speech, vision changes, and loss of balance or coordination.

Diagnosis of intracranial thrombosis typically involves imaging studies such as computed tomography (CT) angiography, magnetic resonance angiography (MRA), or digital subtraction angiography (DSA). Treatment options may include anticoagulation therapy, thrombolysis, endovascular intervention, or surgical intervention, depending on the underlying cause and severity of the condition.

Clot retraction is the process that occurs during blood clotting where the platelets in the blood contract and pull together the edges of the clot, causing it to shrink. This process helps to seal off injured blood vessels and prevent further bleeding. Clot retraction also aids in the healing process by helping to remove damaged tissue and debris from the wound site. The proteins in the blood, called fibrin, form a mesh that traps red and white blood cells and platelets, creating a clot. As the platelets contract, they pull on the fibrin mesh, causing it to tighten and the clot to shrink. This process is an important part of the body's natural healing response to injury.

Hemorrhage is defined in the medical context as an excessive loss of blood from the circulatory system, which can occur due to various reasons such as injury, surgery, or underlying health conditions that affect blood clotting or the integrity of blood vessels. The bleeding may be internal, external, visible, or concealed, and it can vary in severity from minor to life-threatening, depending on the location and extent of the bleeding. Hemorrhage is a serious medical emergency that requires immediate attention and treatment to prevent further blood loss, organ damage, and potential death.

Factor XI, also known as plasma thromboplastin antecedent (PTA) or antihemophilic factor C, is a protein involved in blood coagulation. It is one of the factors in the intrinsic pathway of coagulation, which is activated when blood comes into contact with negatively charged surfaces, such as damaged blood vessels.

When Factor XI is activated (usually by thrombin or activated Factor XII), it activates more Factor XI and also activates Factor IX, leading to the formation of a complex that converts Factor X to its active form, Factor Xa. This ultimately leads to the formation of a fibrin clot and helps to stop bleeding.

Deficiencies in Factor XI can lead to an increased risk of bleeding, although the severity of the bleeding disorder can vary widely among individuals with Factor XI deficiency. Treatment for Factor XI deficiency typically involves replacement therapy with fresh frozen plasma or recombinant Factor XI concentrate.

Myocardial reperfusion is the restoration of blood flow to the heart muscle (myocardium), usually after a period of ischemia or reduced oxygen supply, such as during a myocardial infarction (heart attack). This can be achieved through various medical interventions, including thrombolytic therapy, percutaneous coronary intervention (PCI), or coronary artery bypass surgery (CABG). The goal of myocardial reperfusion is to salvage the jeopardized myocardium, preserve cardiac function, and reduce the risk of complications like heart failure or arrhythmias. However, it's important to note that while reperfusion is crucial for treating ischemic heart disease, it can also lead to additional injury to the heart muscle, known as reperfusion injury.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Whole Blood Coagulation Time (WBCT) is not a standard term used in medical literature. However, I believe you may be referring to "bleeding time" or "coagulation time" which are tests used to evaluate the function of the blood's clotting system.

Bleeding time is a measure of how long it takes for bleeding to stop after a small cut is made in the skin. It helps assess the function of the platelets and the smaller blood vessels.

Coagulation time, on the other hand, measures the time it takes for a larger clot to form in whole blood. This test is not commonly used in clinical practice.

It's important to note that these tests have largely been replaced by more specific coagulation tests, such as prothrombin time (PT) and activated partial thromboplastin time (aPTT), which provide more detailed information about the different components of the clotting system.

Hereditary angioedema (HAE) is a rare genetic disorder that affects the body's immune system and causes recurring episodes of swelling (angioedema). The two most common types of HAE are Type I and Type II, which are caused by mutations in the SERPING1 gene.

Type I HAE: This is the most common form of HAE, accounting for about 85% of cases. In Type I HAE, there is a deficiency of C1 inhibitor (C1-INH), a protein that helps regulate the immune system and prevent inflammation. As a result, levels of bradykinin, a peptide that causes blood vessels to dilate and leads to swelling, are increased. This can cause episodes of swelling in various parts of the body, including the face, hands, feet, and airways.

Type II HAE: This form of HAE is less common than Type I, accounting for about 15% of cases. In Type II HAE, there are normal or even elevated levels of C1-INH in the blood, but the protein is dysfunctional and cannot properly regulate the immune system. This also leads to increased levels of bradykinin and episodes of angioedema.

Both types of HAE can be serious and potentially life-threatening if swelling occurs in the airways and obstructs breathing. Treatment typically involves medications that help control the production of bradykinin or block its effects, as well as measures to prevent and manage symptoms during an acute attack.

Thrombophlebitis is a medical condition characterized by the inflammation and clotting of blood in a vein, usually in the legs. The term thrombophlebitis comes from two words: "thrombo" which means blood clot, and "phlebitis" which refers to inflammation of the vein.

The condition can occur in superficial or deep veins. Superficial thrombophlebitis affects the veins just below the skin's surface, while deep vein thrombophlebitis (DVT) occurs in the deeper veins. DVT is a more serious condition as it can lead to complications such as pulmonary embolism if the blood clot breaks off and travels to the lungs.

Symptoms of thrombophlebitis may include redness, warmth, pain, swelling, or discomfort in the affected area. In some cases, there may be visible surface veins that are hard, tender, or ropy to touch. If left untreated, thrombophlebitis can lead to chronic venous insufficiency and other long-term complications. Treatment typically involves medications such as anticoagulants, antiplatelet agents, or thrombolytics, along with compression stockings and other supportive measures.

Fibrin clot lysis time, also known as fibrinolytic time, is the measurement of the amount of time it takes for a blood clot to dissolve or lyse. This is typically measured in a laboratory setting using specialized tests such as the thromboelastography (TEG) or rotational thromboelastometry (ROTEM) assays. These tests measure the viscoelastic properties of a clot and can provide information about the rate of fibrinolysis, which is the natural process by which the body breaks down and removes blood clots.

Increased fibrin clot lysis time may indicate an impaired fibrinolytic system, which can lead to an increased risk of thrombosis or blood clot formation. Decreased fibrin clot lysis time may indicate an overactive fibrinolytic system, which can lead to an increased risk of bleeding.

It's important to note that the fibrin clot lysis time is just one factor among many that are considered when evaluating a patient's coagulation status and risk of thrombosis or bleeding. Other factors, such as platelet function, coagulation factor levels, and the presence of inhibitors or anticoagulants, must also be taken into account.

Enzyme precursors are typically referred to as zymogens or proenzymes. These are inactive forms of enzymes that can be activated under specific conditions. When the need for the enzyme's function arises, the proenzyme is converted into its active form through a process called proteolysis, where it is cleaved by another enzyme. This mechanism helps control and regulate the activation of certain enzymes in the body, preventing unwanted or premature reactions. A well-known example of an enzyme precursor is trypsinogen, which is converted into its active form, trypsin, in the digestive system.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

Aprotinin is a medication that belongs to a class of drugs called serine protease inhibitors. It works by inhibiting the activity of certain enzymes in the body that can cause tissue damage and bleeding. Aprotinin is used in medical procedures such as heart bypass surgery to reduce blood loss and the need for blood transfusions. It is administered intravenously and its use is typically stopped a few days after the surgical procedure.

Aprotinin was first approved for use in the United States in 1993, but its use has been restricted or withdrawn in many countries due to concerns about its safety. In 2006, a study found an increased risk of kidney damage and death associated with the use of aprotinin during heart bypass surgery, leading to its withdrawal from the market in Europe and Canada. However, it is still available for use in the United States under a restricted access program.

It's important to note that the use of aprotinin should be carefully considered and discussed with the healthcare provider, taking into account the potential benefits and risks of the medication.

Von Willebrand factor (vWF) is a large multimeric glycoprotein that plays a crucial role in hemostasis, the process which leads to the cessation of bleeding and the formation of a blood clot. It was named after Erik Adolf von Willebrand, a Finnish physician who first described the disorder associated with its deficiency, known as von Willebrand disease (vWD).

The primary functions of vWF include:

1. Platelet adhesion and aggregation: vWF mediates the initial attachment of platelets to damaged blood vessel walls by binding to exposed collagen fibers and then interacting with glycoprotein Ib (GPIb) receptors on the surface of platelets, facilitating platelet adhesion. Subsequently, vWF also promotes platelet-platelet interactions (aggregation) through its interaction with platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptors under high shear stress conditions found in areas of turbulent blood flow, such as arterioles and the capillary bed.

2. Transport and stabilization of coagulation factor VIII: vWF serves as a carrier protein for coagulation factor VIII (FVIII), protecting it from proteolytic degradation and maintaining its stability in circulation. This interaction between vWF and FVIII is essential for the proper functioning of the coagulation cascade, particularly in the context of vWD, where impaired FVIII function can lead to bleeding disorders.

3. Wound healing: vWF contributes to wound healing by promoting platelet adhesion and aggregation at the site of injury, which facilitates the formation of a provisional fibrin-based clot that serves as a scaffold for tissue repair and regeneration.

In summary, von Willebrand factor is a vital hemostatic protein involved in platelet adhesion, aggregation, coagulation factor VIII stabilization, and wound healing. Deficiencies or dysfunctions in vWF can lead to bleeding disorders such as von Willebrand disease.

Paracentesis is a medical procedure in which a thin needle or catheter is inserted through the abdominal wall to remove excess fluid from the peritoneal cavity. This procedure is also known as abdominal tap or paracentesis aspiration. The fluid removed, called ascites, can be analyzed for infection, malignant cells, or other signs of disease. Paracentesis may be performed to relieve symptoms caused by the buildup of excess fluid in the abdomen, such as pain, difficulty breathing, or loss of appetite. It is commonly used to diagnose and manage conditions such as liver cirrhosis, cancer, heart failure, and kidney failure.

Platelet activation is the process by which platelets (also known as thrombocytes) become biologically active and change from their inactive discoid shape to a spherical shape with pseudopodia, resulting in the release of chemical mediators that are involved in hemostasis and thrombosis. This process is initiated by various stimuli such as exposure to subendothelial collagen, von Willebrand factor, or thrombin during vascular injury, leading to platelet aggregation and the formation of a platelet plug to stop bleeding. Platelet activation also plays a role in inflammation, immune response, and wound healing.

Primary fibrinolysis is a normal body process, while secondary fibrinolysis is the breakdown of clots due to a medicine, a ... 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. Its main enzyme plasmin cuts the fibrin mesh at ...
... 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 ...
Term thrombin-activatable fibrinolysis inhibitor may refer to: Carboxypeptidase B2, an enzyme that in humans is encoded by the ... an enzyme class This disambiguation page lists articles associated with the title Thrombin-activatable fibrinolysis inhibitor. ...
Fibrinolysis. 5 (4): 551-9. PMID 7841311. v t e (Articles with short description, Short description is different from Wikidata ...
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, ...
Fibrinolysis. 19 (8): 743-755. doi:10.1097/MBC.0b013e3283104093. PMID 19002040. S2CID 45231920. Ovanesov M.V.; Krasotkina J.V ... 2012). "Predicting prothrombotic tendencies in sepsis using spatial clot growth dynamics". Blood Coagul Fibrinolysis. 23 (6): ...
Fibrinolysis. 13 (5): 433-41. doi:10.1097/00001721-200207000-00008. PMID 12138371. S2CID 39490260. Wang KK, Liu N, Radulovich N ...
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): 495-496. 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 ...
Fibrinolysis. 16 (4): 231-8. doi:10.1097/01.mbc.0000169214.62560.a5. PMID 15870541. S2CID 23922781. Seligsohn U (Jul 2007). " ...
Fibrinolysis. 23 (1): 45-50. doi:10.1097/mbc.0b013e32834d7ce3. PMID 22024796. S2CID 3327902. Keane C, Nourse JP, Crooks P, ...
Blood Coagul Fibrinolysis. 17 (7): 557-61. doi:10.1097/01.mbc.0000245300.10387.ca. PMID 16988551. S2CID 25135810. Sharp MK, ...
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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 ...
... or fibrinolysis.[citation needed] In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is ... Simultaneously, excess circulating thrombin assists in the conversion of plasminogen to plasmin, resulting in fibrinolysis. The ... which prevents fibrinolysis. Excess circulating thrombin results from the excess activation of the coagulation cascade. The ... Blood Coagul Fibrinolysis. 18 (7): 589-93. doi:10.1097/MBC.0b013e32822d2a3c. PMID 17890943. S2CID 37247533. Becker, Joseph U ...
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. S2CID 33601129. Hayashi T, Suzuki K (October ...
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. 4 (5): 671-8. doi:10.1097/00001721-199310000-00002. PMID 7507361. Rasmus KBJKJER and Inger SCHOUSBOE ...
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. S2CID 10642849. Chinsakchai, ... Fibrinolysis. 25 (5): 507-511. doi:10.1097/MBC.0000000000000057. ISSN 1473-5733. PMID 24553060. S2CID 10642849. Chinsakchai, ... Fibrinolysis. 25 (5): 507-511. doi:10.1097/MBC.0000000000000057. ISSN 1473-5733. PMID 24553060. S2CID 10642849. Chinsakchai, ...
Primary fibrinolysis is a normal body process, while secondary fibrinolysis is the breakdown of clots due to a medicine, a ... 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. Its main enzyme plasmin cuts the fibrin mesh at ...
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: Libby P, Bonow RO, Mann DL, Tomaselli GF, Bhatt DL, ...
The journal is devoted to publishing significant developments worldwide in the field of blood coagulation, fibrinolysis, ... Fibrinolysis is an international fully refereed journal that features review and original research articles on all clinical, ... Blood Coagulation & Fibrinolysis. You may be trying to access this site from a secured browser on the server. Please enable ...
The effect of ultrasound on the rate of fibrinolysis has been investigated using an in vitro system. Plasma or blood clots ... We conclude that ultrasound at 1 MHz potentiates enzymatic fibrinolysis by a nonthermal mechanism at energies that can ... which could not explain the enhancement of fibrinolysis. Ultrasound exposure did not cause mechanical fragmentation of the clot ...
Fibrinolysis shutdown, as evidenced by elevated d-dimer and complete failure of clot lysis at 30 minutes on thromboelastography ... Fibrinolysis Shutdown Correlation with Thromboembolic Events in Severe COVID-19 Infection J Am Coll Surg. 2020 Aug;231(2):193- ... Conclusions: Fibrinolysis shutdown, as evidenced by elevated d-dimer and complete failure of clot lysis at 30 minutes on ... to ascertain the need for early therapeutic anticoagulation or fibrinolytic therapy to address this state of fibrinolysis ...
... the thrombosis/fibrinolysis system, and forearm hyperemic response were investigated. It was shown that smokers with ... The combined effects of smoking and hypercholesterolemia on the inflammatory process, the thrombosis/fibrinolysis system, and ... Combined effects of smoking and hypercholesterolemia on inflammatory process, thrombosis/fibrinolysis system, and forearm ... phenomenon was associated with a respective increase in the inflammatory process and changes in the thrombosis/fibrinolysis ...
The combination of severe thrombocytopenia and increased fibrinolysis appeared to be a determinant in the production of a ...
Increased plasma thrombin-activatable fibrinolysis inhibitor levels in young obese women with polycystic ovary syndrome. ... Impaired fibrinolysis may be responsible for the increased risk of cardiovascular diseases in women with PCOS. SN - 1556-5653 ... Plasma thrombin-activatable fibrinolysis inhibitor levels in the overweight or obese PCOS group were significantly higher than ... Plasma thrombin-activatable fibrinolysis inhibitor, serum FSH, LH, DHEAS, total T, E(2), total cholesterol, high-density ...
The role of fibrinolysis in vascular diseases in UK biobank. *Mark. Zöller, Bengt LU ; Manderstedt, Eric LU ; Lind-Halldén, ... Cardiovascular disease, Fibrinolysis, Mutation, Venous thromboembolism, Whole exome sequencing. in Journal of Thrombosis and ... Fibrinolysis; Mutation; Venous thromboembolism; Whole exome sequencing}}, language = {{eng}}, number = {{4}}, pages = {{635-- ... 638}}, publisher = {{Springer}}, series = {{Journal of Thrombosis and Thrombolysis}}, title = {{The role of fibrinolysis in ...
Cardiovascular diseases (CVD) cause more deaths per year than the next six leading causes of death combined. There is also strong evidence for a role of oxidative stress, a key focus at Oxford Biomedical Research, in the development of CVD. Emerging risk factors for CVD include isoprostanes, C-reactive proteins, fibrinogen and plasminogen activator inhibitor 1 (PAI-1). Fibrinogen and PAI-1 are key components of the highly regulated coagulation process. Elevated PAI-1 transcription has been reported to be caused by oxidative stress activation of the AP-1 response element. Vascular endothelial cells also play a key role in cancer by limiting the access of circulating cells to sub-endothelial space and thereby reducing tumor metastasis. We offer a wide range of antibodies, purified and recombinant proteins, and immunoassay kits for studies of proteins involved in cardiovascular biology - including those that play key roles in coagulation and its regulation, as well as other proteins that have been
Is chest drain insertion and fibrinolysis therapy equivalent to video-assisted thoracoscopic surgery to treat children with ... Is chest drain insertion and fibrinolysis therapy equivalent to video-assisted thoracoscopic surgery to treat children with ... Is chest drain insertion and fibrinolysis therapy equivalent to video-assisted thoracoscopic surgery to treat children with ...
Dive into the research topics of SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: Implications for ... SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: Implications for microclot formation in COVID-19. ...
Surgical decortication had a slightly lower cost than fibrinolysis ($13,345 vs $13,965), but fibrinolysis had marginally higher ... Sensitivity analyses found that fibrinolysis as the initial therapy was more cost-effective when the probability of success was ... Surgical decortication is recommended by national guidelines for management of early empyema, but intrapleural fibrinolysis is ... Surgical decortication and intrapleural fibrinolysis have nearly equivalent cost-effectiveness for early empyema in patients ...
VM 531-Hemostasis 3 - Anticoagulants Fibrinolysis and Endothelium From cvmlect CVM Information Technology Center ...
Fibrinolysis (simplified). Blue arrows denote stimulation, and red arrows inhibition.. WikiDoc Resources for Fibrinolysis ... Fibrinolysis is the process where a fibrin clot, the product of coagulation, is broken down. Its main enzyme, plasmin, cuts the ... This is more specific than the TCT, and virtually confirms that fibrinolysis has occurred. It is therefore used to indicate ... Antifibrinolytics, such as aminocaproic acid (ε-aminocaproic acid) and tranexamic acid are used as inhibitors of fibrinolysis ...
TRANSFER AMI Trial Summary: Early Angioplasty after Fibrinolysis for Acute MI. Posted by admin on July 17, 2022. , Featured ... 2009 TRANSFER-AMI trial: Routine Early Angioplasty after Fibrinolysis for Acute Myocardial Infarction Multicenter, randomized, ...
... is an international fully refereed journal that features review and original research articles ... The journal is devoted to publishing significant developments worldwide in the field of blood coagulation, fibrinolysis, ...
This presentation is for medical professionals and may have content not suitable for minors or non-medical viewers.. Trauma Induced Coagulopathy was presented by Denis Bensard, MD, FACS on November 16, 2017 at the 9th annual Southwest Trauma & Acute Care Symposium. Dr. Bensard is a Professor, Surgery-Pediatric Surgery with University of Colorado School of Medicine and a pediatric trauma surgeon at Colorado Childrens Hospital in Denver, CO.. ...
Fibrinolysis. Alterations in fibrinolysis (through increased plasminogen activator inhibitor activity) and the production of ...
Fibrinogenolysis and fibrinolysis in Vaccine-induced Immune Thrombocytopenia and Thrombosis (VITT). 2023 - E-pub ahead of print ... Claire is currently working on the role of platelet-derived plasmiongen in driving local fibrinolysis. ... The impact of thrombus composition on regulation of fibrinolysis under flow ... Platelet plasminogen as a driver of local fibrinolysis ... The Fibrinolysis Renaissance. 2023 - Published. Mutch, N. J., ...
Our central focus is fibrinolysis, thrombolysis, proteolysis of the blood and cells. ... Home of International Society for Fibrinolysis and Proteolysis (ISFP). Meetings, events, funding opportunities, membership, and ... International Society for Fibrinolysis & Proteolysis. The ISFP was founded to stimulate scientific research on proteolysis ... the objectives include the furtherance of scientific research relating to fundamental and medical aspects of fibrinolysis, ...
FDPs will increase in any state of accelerated fibrinolysis such as advanced liver disease, DIC, or in situations following ... The traditional fibrinolysis tests include fibrin degradation products and D-dimer levels. ...
2017 Anesthesia Sensitivity/Fibrinolysis Projects. Dr. Michael Court at Washington State University Veterinary School needs a ... Court needs to test for both anesthesia sensitivities and fibrinolysis (post-operative bleeding), so we expect to know, one way ... to help rule out other potential gene mutations involved in excessive fibrinolysis that we havent tested for yet, as well as ...
Reply To: What petrified tadalafil tops imaging fibrinolysis.. Your information:. Name (required):. ...
The study identifies a reduction in fibrinolysis as an important mechanism in COVID-19-associated coagulopathy. The combination ... Acute fibrinolysis shutdown occurs early in septic shock and is associated with increased morbidity and mortality: results of ... noted markedly reduced fibrinolysis in COVID-19 patients; however, no distinction with respect to the presence of ... c A physiological fibrinolysis pattern in a healthy person, reflected by the subtle decrease of the MCF during the measurement ...
Moore in examining the temporal changes in fibrinolysis over time in the recipient, as well as the complex interactions between ... Moore will investigate the association of low fibrinolysis and microvascular clots in the organs of donors for Aim 1, followed ... Aim 3 will assess the donor organ local proteomes effect on forming fibrinolysis resistant clots. These aims will provide ... Moore is establishing himself as a young investigator in patient-oriented research with a translational focus on fibrinolysis ...
Coagulation and Fibrinolysis. 1151 Choi, Sun Young; Kim, Moo Hyun; Lee, Kwang Min; Cho, Young-Rak; Park, Jong Sung; Yun, Sung- ...
Coagulation and Fibrinolysis. 039 Langsted, Anne; Nordestgaard, Børge G.: Smoking is Associated with Increased Risk of Major ...
Effect on Blood Coagulation and Fibrinolysis. Fibrinolysis is the enzymatic breakdown of fibrin in blood clots and secure ... Fibrinolysis 2016, 27, 441-449. [Google Scholar] [CrossRef] [PubMed]. *Kelly, G.S. Bromelain: A literature review and ... and increasing fibrinolysis. It also reduces prekallikrein (PK), and thus, inhibits the generation of bradykinin at the site of ... clearance of clot fragments [81]. Bromelain effectively performs fibrinolysis and restricts coagulation of blood [82]. It ...
  • Fibrinolysis is the process where a fibrin clot , the product of coagulation , is broken down. (wikidoc.org)
  • Blood Coagulation & Fibrinolysis is an international fully refereed journal that features review and original research articles on all clinical, laboratory and experimental aspects of haemostasis and thrombosis. (wkadcenter.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. (wkadcenter.com)
  • In addition to conventional laboratory parameters, rotational thromboelastometry (ROTEM) provides evidence for net coagulation capacity and insight into clot formation time, clot firmness and fibrinolysis in the critically ill patients [ 12 ]. (biomedcentral.com)
  • Mishchenko V.P., Gol'denberg Iu.M., Novosel'tseva T.V. (1980) Effect of the antioxidant ionol on blood coagulation and fibrinolysis. (msk.ru)
  • Our aim is to evaluate the effects of rhC1INH on coagulation and fibrinolysis in symptomatic HAE patients. (chaen-rcah.ca)
  • Prior to rhC1INH treatment, the majority of patients had low to normal activated partial thromboplastin times (aPTT) and increased levels of prothrombin fragment 1+2, thrombin-antithrombin complexes, D-dimers and plasmin-antiplasmin complexes, all of which indicate activation of both coagulation and fibrinolysis. (chaen-rcah.ca)
  • Natural oestrogen in the female climacteric--influence on blood coagulation and fibrinolysis. (herbal-organic.com)
  • The aim of the present study was to investigate the effect on blood coagulation and fibrinolysis of a natural oestrogen preparation, piperazine oestrone sulphate, prospectively in menopausal women. (herbal-organic.com)
  • In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
  • Instead of the inhibition of bloodstream coagulation, you can also activate the break down of bloodstream clots, an activity known as fibrinolysis. (cell-signaling-pathways.com)
  • There is limited information about coagulation and fibrinolysis status in infected PwHA treated with emicizumab and the use of anti-coagulant agents in such cases. (isth.org)
  • In this study, we investigated how anti-coagulant agents affect the balance of coagulation and fibrinolysis in PwHA plasma spiked with emicizumab. (isth.org)
  • These results showed a tendency similar to the inhibitory effect of anti-coagulant agents on coagulation and fibrinolysis function in normal reference plasma. (isth.org)
  • Onishi T, Harada S, Shimo H, Tashiro Y, Soeda T, Nogami K. The effect of anti-coagulant agents against in vitro hemophilia A plasma coagulation and fibrinolysis potential in the presence of emicizumab [abstract]. (isth.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)
  • Thrombolysis refers to the dissolution of the thrombus due to various agents while fibrinolysis refers specifically to the agents causing fibrin breakdown in the clot. (wikipedia.org)
  • The traditional fibrinolysis tests include fibrin degradation products and D-dimer levels. (openanesthesia.org)
  • Fibrinolysis appears to be associated with altered fibrin structure during early clot formation and elongation. (edu.au)
  • Mature thrombin activatable fibrinolysis inhibitor (TAFIa) is a carboxypeptidase that stabilizes fibrin clots by detatching C-terminal arginines and lysines from partially degraded fibrin. (cell-signaling-pathways.com)
  • The combined effects of smoking and hypercholesterolemia on the inflammatory process, the thrombosis/fibrinolysis system, and forearm hyperemic response were investigated. (nih.gov)
  • This phenomenon was associated with a respective increase in the inflammatory process and changes in the thrombosis/fibrinolysis system. (nih.gov)
  • Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. (wikipedia.org)
  • Primary fibrinolysis is a normal body process, while secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause. (wikipedia.org)
  • Primary fibrinolysis refers to the normal breakdown of clots. (medlineplus.gov)
  • The maximum temperature increase of plasma clots exposed to 4 W/cm2 ultrasound was only 1.7 degrees C, which could not explain the enhancement of fibrinolysis. (jci.org)
  • Dr. Moore will investigate the association of low fibrinolysis and microvascular clots in the organs of donors for Aim 1, followed by Aim 2, defining the association between low fibrinolysis and impaired early graft function in liver transplant recipients. (ucdenver.edu)
  • Aim 3 will assess the donor organ local proteomes effect on forming fibrinolysis resistant clots. (ucdenver.edu)
  • The DASH diet did not affect markers of fibrinolysis. (johnshopkins.edu)
  • In contrast, the DASH diet had no significant effect on markers of fibrinolysis in whites or African-Americans. (johnshopkins.edu)
  • Because this would have the effect of enhancing endogenous fibrinolysis, we explored this effect of dextran-40 on fibrinolysis in man. (reading.ac.uk)
  • 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. (reading.ac.uk)
  • This suggests that dextran exerts a combined therapeutic effect, enhancing endogenous fibrinolysis, whilst also reducing platelet adhesion to vWF and platelet activation by thrombin. (reading.ac.uk)
  • Is chest drain insertion and fibrinolysis therapy equivalent to video-assisted thoracoscopic surgery to treat children with parapneumonic effusions? (bmj.com)
  • This study compared the cost-effectiveness of video-assisted thoracoscopic surgery (VATS) decortication with intrapleural fibrinolysis for early empyema. (nih.gov)
  • The study identifies a reduction in fibrinolysis as an important mechanism in COVID-19-associated coagulopathy. (biomedcentral.com)
  • Results: After hemorrhagic shock, 7.5% NaCl failed to resuscitate and exacerbated coagulopathy and fibrinolysis. (edu.au)
  • Conclusions: Small-volume 7.5% NaCl resuscitation exacerbated coagulopathy and fibrinolysis that was not corrected by APTEM test. (edu.au)
  • The ELT measures fibrinolysis by clotting the euglobulin fraction (primarily the fibrinolytic factors fibrinogen, PAI-1, tPA, α2-antiplasmin, and plasminogen) from plasma and then observing the time required for clot dissolution. (wikipedia.org)
  • Fibrinolysis shutdown, as evidenced by elevated d-dimer and complete failure of clot lysis at 30 minutes on thromboelastography predicts thromboembolic events and need for hemodialysis in critically ill patients with COVID-19. (nih.gov)
  • The coagulable and fibrinolytic status of plasma was measured by Thrombin/Plasmin-Generation Assay (T/P-GA) and Clot-Fibrinolysis Waveform Analysis (CFWA). (isth.org)
  • Plasminogen activator inhibitor (PAI)-1 is an inhibitor of fibrinolysis, the physiological process involved in blood clot degradation. (cdc.gov)
  • Impaired fibrinolysis may be responsible for the increased risk of cardiovascular diseases in women with PCOS. (unboundmedicine.com)
  • To check the hypothesis that excitement of fibrinolysis via TAFIa inhibition is certainly associated with a lesser risk of blood loss compared to set up anticoagulants, we targeted at finding little molecule inhibitors of TAFIa as novel antithrombotic agencies. (cell-signaling-pathways.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)
  • 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. (unboundmedicine.com)
  • Plasma thrombin-activatable fibrinolysis inhibitor levels in the overweight or obese PCOS group were significantly higher than those in the nonobese PCOS and control groups. (unboundmedicine.com)
  • Obesity and insulin resistance were associated positively with plasma thrombin-activatable fibrinolysis inhibitor levels, but there was no association between carotid intima-media thickness and thrombin-activatable fibrinolysis inhibitor. (unboundmedicine.com)
  • Young overweight or obese women with PCOS have increased plasma thrombin-activatable fibrinolysis inhibitor levels. (unboundmedicine.com)
  • Affinity's TAFI - Thrombin Activatable Fibrinolysis Inhibitor Polyclonal Antibody - HRP Conjugated is a whole IgG purified from antiserum conjugated to horseradish peroxidase. (affinitybiologicals.com)
  • CONCLUSIONS: These data are consistent with a rise in plasmin due to dextran blockade of tPA uptake in vivo, leading to enhanced fibrinolysis, cleavage of vWF and of the platelet protease-activated receptor-1 (PAR-1) thrombin receptor. (reading.ac.uk)
  • The carboxypeptidase TAFIa (triggered thrombin activatable fibrinolysis inhibitor) is usually a central participant in fibrinolysis (Assisting Information, Body S1)4,5. (cell-signaling-pathways.com)
  • The decrease in fibrinolysis might be due to an increase in thrombin-activatable fibrinolysis inhibitor and an increase in factor XIIIa. (medscape.com)
  • In this assay, increased fibrinolysis is assessed by comparing the TEM profile in the absence or presence of the fibrinolysis inhibitor aprotinin. (wikipedia.org)
  • At 15 and 60 min, the activation as extrinsically-activated test using tissue factor (EXTEM) with aprotinin to inhibit fibrinolysis (APTEM) test showed little or no correction of fibrinolysis, indicating a plasmin-independent fibrinolysis. (edu.au)
  • Additional clinical trials are required to ascertain the need for early therapeutic anticoagulation or fibrinolytic therapy to address this state of fibrinolysis shutdown. (nih.gov)
  • The combination of severe thrombocytopenia and increased fibrinolysis appeared to be a determinant in the production of a haemorrhagic tendency in leukaemia. (bmj.com)
  • Tissue plasminogen activator (t-PA) and urokinase are the agents that convert plasminogen to the active plasmin, thus allowing fibrinolysis to occur. (wikipedia.org)
  • 1) Establishing a prospective outcome registry to identify variables associated with graft dysfunction, 2) Training in advanced basic science methodologies of quantifying fibrinolysis, 3) Integration of clinical and translation data to form a mechanistic hypothesis for factors driving low fibrinolysis 4) Concurrent success in clinical training with maturation as a physician scientist. (ucdenver.edu)
  • We conclude that ultrasound at 1 MHz potentiates enzymatic fibrinolysis by a nonthermal mechanism at energies that can potentially be applied and tolerated in vivo to accelerate therapeutic fibrinolysis. (jci.org)
  • Sensitivity analyses found that fibrinolysis as the initial therapy was more cost-effective when the probability of success was greater than 60% or the initial cost was less than $13,000. (nih.gov)
  • We are also developing a more comprehensive bleeding/anesthesia sensitivity/malignant hyperthermia multigene testing panel (through Next-Gen sequencing) to help rule out other potential gene mutations involved in excessive fibrinolysis that we haven't tested for yet, as well as genes related to other bleeding, anesthesia, and malignant hyperthermia. (deerhoundhealth.org)
  • Testing of overall fibrinolysis can be measured by a euglobulin lysis time (ELT) assay. (wikipedia.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)
  • Surgical decortication and intrapleural fibrinolysis have nearly equivalent cost-effectiveness for early empyema in patients who can tolerate both procedures. (nih.gov)
  • We compared the outcome of endovascular mechanical thrombectomy (EMT) versus intra-arterial fibrinolysis (IAF)-based ERT in patients with acute BAO. (j-stroke.org)
  • Enhancement of fibrinolysis in vitro by ultrasound. (jci.org)
  • The effect of ultrasound on the rate of fibrinolysis has been investigated using an in vitro system. (jci.org)
  • Our aim was to examine the effect of small-volume 7.5% NaCl adenosine, lidocaine, and Mg2+ (ALM) on fibrinolysis in the rat model of hemorrhagic shock. (edu.au)
  • Her expertise in analyzing longitudinal data and variable reduction techniques will be critical for training Dr. Moore in examining the temporal changes in fibrinolysis over time in the recipient, as well as the complex interactions between the donor and recipient. (ucdenver.edu)
  • Another study demonstrated a trend towards reduction in 30-day mortality with fibrinolysis when initiated within 2 hours of symptom onset compared to PPCI (2.2% vs. 5.7%, P=0.058) [2] . (wikidoc.org)
  • Fibrinolysis has been the main stay of treatment for patients with acute ST segment elevation myocardial infarction over 30 years. (wikidoc.org)
  • For patients who present within 2 hours of symptom onset, a previous study demonstrated that there was no significant difference in the in-hospital mortality between fibrinolysis and PPCI treatment groups (5.1% vs. 7.8%, p=0.37) [1] . (wikidoc.org)
  • These include the inability of fibrinolysis to restore normal TIMI flow grade 3 in 50-60% of patients, the occurrence of intracerebral hemorrhage in 0.9% of cases [3] and recurrent ischemia and reinfarction in 3-5% cases. (wikidoc.org)
  • Les concentrations sériques de sCD40L circulant et d'interleukine 10 circulante ont été analysées à l'aide de la méthode immuno-enzymatique chez 30 patients positifs pour le VHC avec un CHC, chez 30 patients patients positifs pour le VHC avec une cirrhose du foie, et chez 30 volontaires d'âge correspondant en bonne santé avec des anticorps anti-VHC négatifs servant de groupe témoin. (who.int)
  • 05). Fibrinolysis returned to baseline levels the next day. (reading.ac.uk)
  • Surgical decortication is recommended by national guidelines for management of early empyema, but intrapleural fibrinolysis is frequently used as a first-line therapy in clinical practice. (nih.gov)
  • Over the past 60 years, due to the advancement of hemo- the Work Group and tasked it with planning, developing, dialysis (HD) technology and the introduction of medical reviewing, and disseminating appropriate HD treatment insurance, dialysis treatment has become widespread, en- guidelines in accordance with international standards. (bvsalud.org)
  • There was no significant change towards hypercoagulability or decreased fibrinolysis in any group. (herbal-organic.com)