Substances, usually endogenous, that act as inhibitors of blood coagulation. They may affect one or multiple enzymes throughout the process. As a group, they also inhibit enzymes involved in processes other than blood coagulation, such as those from the complement system, fibrinolytic enzyme system, blood cells, and bacteria.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
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.
Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).
Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.
Activated form of factor X that participates in both the intrinsic and extrinsic pathways of blood coagulation. It catalyzes the conversion of prothrombin to thrombin in conjunction with other cofactors.
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.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
Activated form of factor XI. In the intrinsic pathway, Factor XI is activated to XIa by factor XIIa in the presence of cofactor HMWK; (HIGH MOLECULAR WEIGHT KININOGEN). Factor XIa then activates factor IX to factor IXa in the presence of calcium.
Laboratory tests for evaluating the individual's clotting mechanism.
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.
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
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.
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.
Activated form of factor IX. This activation can take place via the intrinsic pathway by the action of factor XIa and calcium, or via the extrinsic pathway by the action of factor VIIa, thromboplastin, and calcium. Factor IXa serves to activate factor X to Xa by cleaving the arginyl-leucine peptide bond in factor X.
Agents that cause clotting.
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
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 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.
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.
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.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
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.
Activated form of factor V. It is an essential cofactor for the activation of prothrombin catalyzed by factor Xa.
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.
Activated form of factor VIII. The B-domain of factor VIII is proteolytically cleaved by thrombin to form factor VIIIa. Factor VIIIa exists as a non-covalent dimer in a metal-linked (probably calcium) complex and functions as a cofactor in the enzymatic activation of factor X by factor IXa. Factor VIIIa is similar in structure and generation to factor Va.
Found in various tissues, particularly in four blood-clotting proteins including prothrombin, in kidney protein, in bone protein, and in the protein present in various ectopic calcifications.
A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (Also known as Christmas Disease, after the first patient studied in detail, not the holy day.) Historical and clinical features resemble those in classic hemophilia (HEMOPHILIA A), but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. (From Cecil Textbook of Medicine, 19th ed, p1008)
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Transglutaminases catalyze cross-linking of proteins at a GLUTAMINE in one chain with LYSINE in another chain. They include keratinocyte transglutaminase (TGM1 or TGK), tissue transglutaminase (TGM2 or TGC), plasma transglutaminase involved with coagulation (FACTOR XIII and FACTOR XIIIa), hair follicle transglutaminase, and prostate transglutaminase. Although structures differ, they share an active site (YGQCW) and strict CALCIUM dependence.
The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.
A subclass of tumor necrosis family receptors that lack cell signaling domains. They bind to specific TNF RECEPTOR LIGANDS and are believed to play a modulating role in the TNF signaling pathway. Some of the decoy receptors are products of distinct genes, while others are products of ALTERNATIVE SPLICING of the MRNA for the active receptor.
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.
Inhibitor of differentiation proteins are negative regulators of BASIC HELIX-LOOP-HELIX TRANSCRIPTION FACTORS. They inhibit CELL DIFFERENTIATION and induce CELL PROLIFERATION by modulating different CELL CYCLE regulators.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
A family of ark shell mollusks, in the class BIVALVIA. They have soft bodies with platelike GILLS enclosed within two shells hinged together.
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.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
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.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
Agents that prevent clotting.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Antibodies produced by a single clone of cells.
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.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A nutritional condition produced by a deficiency of VITAMIN K in the diet, characterized by an increased tendency to hemorrhage (HEMORRHAGIC DISORDERS). Such bleeding episodes may be particularly severe in newborn infants. (From Cecil Textbook of Medicine, 19th ed, p1182)
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
An absence or reduced level of blood coagulation factor XII. It normally occurs in the absence of patient or family history of hemorrhagic disorders and is marked by prolonged clotting time.
The natural enzymatic dissolution of FIBRIN.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
Activated form of factor XII. In the initial event in the intrinsic pathway of blood coagulation, kallikrein (with cofactor HIGH MOLECULAR WEIGHT KININOGEN) cleaves factor XII to XIIa. Factor XIIa is then further cleaved by kallikrein, plasmin, and trypsin to yield smaller factor XII fragments (Hageman-Factor fragments). These fragments increase the activity of prekallikrein to kallikrein but decrease the procoagulant activity of factor XII.

Identification and purification of vitamin K-dependent proteins and peptides with monoclonal antibodies specific for gamma -carboxyglutamyl (Gla) residues. (1/55)

Novel monoclonal antibodies that specifically recognize gamma-carboxyglutamyl (Gla) residues in proteins and peptides have been produced. As demonstrated by Western blot and time-resolved immunofluorescence assays the antibodies are pan-specific for most or all of the Gla-containing proteins tested (factors VII, IX, and X, prothrombin, protein C, protein S, growth arrest-specific protein 6, bone Gla protein, conantokin G from a cone snail, and factor Xa-like proteins from snake venom). Only the Gla-containing light chain of the two-chain proteins was bound. Decarboxylation destroyed the epitope(s) on prothrombin fragment 1, and Ca(2+) strongly inhibited binding to prothrombin. In Western blot, immunofluorescence, and surface plasmon resonance assays the antibodies bound peptides conjugated to bovine serum albumin that contained either a single Gla or a tandem pair of Gla residues. Binding was maintained when the sequence surrounding the Gla residue(s) was altered. Replacement of Gla with glutamic acid resulted in a complete loss of the epitope. The utility of the antibodies was demonstrated in immunochemical methods for detecting Gla-containing proteins and in the immunopurification of a factor Xa-like protein from tiger snake venom. The amino acid sequences of the Gla domain and portions of the heavy chain of the snake protein were determined.  (+info)

The role of coagulation abnormalities in the development of Perthes' disease. (2/55)

Recent reports have suggested an association between Perthes' disease and an underlying thrombophilic or hypofibrinolytic tendency. In Northern Ireland there is a high incidence of Perthes' disease (11.7 per 100,000 or 1 in 607 children) in a stable paediatric population. We reviewed 139 children with Perthes' disease and compared them with a control group of 220 aged- and gender-matched healthy primary schoolchildren with similar racial and ethnic backgrounds. There were no significant deficiencies of antithrombotic factors protein C, protein S, antithrombin III or resistance to activated protein C. A total of 53 (38.1%) of the children with Perthes' disease had a prolonged activated partial thromboplastin time (>38) compared with 13 (5.9%) of the control group (p < 0.001). Our findings have shown that using standard assays, thrombophilia secondary to antithrombotic factor deficiency or resistance to activated protein does not appear to be an aetiological factor for Perthes' disease. The cause of the prolonged activated partial thromboplastin time, usually associated with a clotting factor deficiency, is under further investigation.  (+info)

Factor V Leiden mutation, prothrombin gene mutation, and deficiencies in coagulation inhibitors associated with Budd-Chiari syndrome and portal vein thrombosis: results of a case-control study. (3/55)

In a collaborative multicenter case-control study, we investigated the effect of factor V Leiden mutation, prothrombin gene mutation, and inherited deficiencies of protein C, protein S, and antithrombin on the risk of Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT). We compared 43 BCS patients and 92 PVT patients with 474 population-based controls. The relative risk of BCS was 11.3 (95% CI 4.8-26.5) for individuals with factor V Leiden mutation, 2.1(95% CI 0.4-9.6) for those with prothrombin gene mutation, and 6.8 (95% CI 1.9-24.4) for those with protein C deficiency. The relative risk of PVT was 2.7 (95% CI 1.1-6.9) for individuals with factor V Leiden mutation, 1.4 (95% CI 0.4-5.2) for those with prothrombin gene mutation, and 4.6 (95% CI 1.5-14.1) for those with protein C deficiency. The relative risk of BCS or PVT was not increased in the presence of inherited protein S or antithrombin deficiency. Concurrence of either acquired or inherited thrombotic risk factors was observed in 26% of the BCS patients and 37% of the PVT patients. We conclude that factor V Leiden mutation and hereditary protein C deficiency appear to be important risk factors for BCS and PVT. Although the prevalence of the prothrombin gene mutation was increased, it was not found to be a significant risk factor for BCS and PVT. The coexistence of thrombogenic risk factors in many patients indicates that BCS and PVT can be the result of a combined effect of different pathogenetic mechanisms.  (+info)

Structural basis for inhibition promiscuity of dual specific thrombin and factor Xa blood coagulation inhibitors. (4/55)

BACKGROUND: A major current focus of pharmaceutical research is the development of selective inhibitors of the blood coagulation enzymes thrombin or factor Xa to be used as orally bioavailable anticoagulant drugs in thromboembolic disorders and in the prevention of venous and arterial thrombosis. Simultaneous direct inhibition of thrombin and factor Xa by synthetic proteinase inhibitors as a novel approach to antithrombotic therapy could result in potent anticoagulants with improved pharmacological properties. RESULTS: The binding mode of such dual specific inhibitors of thrombin and factor Xa was determined for the first time by comparative crystallography using human alpha-thrombin, human des-Gla (1--44) factor Xa and bovine trypsin as the ligand receptors. The benzamidine-based inhibitors utilize two different conformations for the interaction with thrombin and factor Xa/trypsin, which are evoked by the steric requirements of the topologically different S2 subsites of the enzymes. Compared to the unliganded forms of the proteinases, ligand binding induces conformational adjustments of thrombin and factor Xa active site residues indicative of a pronounced induced fit mechanism. CONCLUSION: The structural data reveal the molecular basis for a desired unselective inhibition of the two key components of the blood coagulation cascade. The 4-(1-methyl-benzimidazole-2-yl)-methylamino-benzamidine moieties of the inhibitors are able to fill both the small solvent accessible as well as the larger hydrophobic S2 pockets of factor Xa and thrombin, respectively. Distal fragments of the inhibitors are identified which fit into both the cation hole/aromatic box of factor Xa and the hydrophobic aryl binding site of thrombin. Thus, binding constants in the medium-to-low nanomolar range are obtained against both enzymes.  (+info)

The dynamics of thrombin formation. (5/55)

The central event of the hemostatic process is the generation of thrombin through the tissue factor pathway. This is a highly regulated, dynamic process in which thrombin itself plays many roles, positively and negatively its production and destruction. The hemostatic process is essential to normal physiology and is also the Achilles heel of our aging population. The inappropriate generation of thrombin may lead to vascular occlusion with the consequence of myocardial infarction, stroke, pulmonary embolism, or venous thrombosis. In this review, we summarize our present views regarding the tissue factor pathway by which thrombin is generated and the roles played by extrinsic and intrinsic factor Xa generating complexes in hemostasis and the roles of the stoichiometric and dynamic inhibitors that regulate thrombin generation.  (+info)

Thrombotic risk factors and extent of liver fibrosis in chronic viral hepatitis. (6/55)

BACKGROUND AND AIMS: Thrombosis of the small intrahepatic veins has been suggested to trigger liver tissue remodelling. We evaluated the prevalence of multiple thrombotic risk factors and their association with the extent of fibrosis in chronic viral hepatitis. METHODS: Ninety consecutive patients with chronic hepatitis B or C without malignancy, a history of venous thrombosis, or antiviral/immunosuppressive therapy within the last six months were included. Thrombophilic and coagulation factors were evaluated on the liver biopsy day. RESULTS: One or more thrombotic risk factors were found in 68% and > or =2 factors in 37% of patients. Higher necroinflammatory activity was independently associated with higher prothrombin time (p=0.003), alanine aminotransferase level (p=0.011), and histological staging (p=0.018). Patients with staging scores of 4-6 compared with those with scores of 0-3 more frequently had deficiency of protein C (24% v 3%; p=0.007), antithrombin III (28% v 5%; p=0.005), and plasminogen (19% v 2%; p=0.03), and a trend for more frequent activated protein C resistance (8% v 0%; p=0.075). The presence of > or =1 significant thrombotic risk factor was observed in 11/25 (44%) patients with staging scores of 4-6 and in 6/65 (9%) patients with scores of 0-3 (p<0.001), being the only variable independently associated with advanced staging (odds ratio 2.4, p=0.02). CONCLUSIONS: Thrombotic risk factors are frequently detected in patients with chronic viral hepatitis and the presence of > or =1 significant factor is associated with more advanced fibrosis. Whether the association of such thrombophilic conditions with advanced fibrosis is a primary or secondary phenomenon and whether their development in combination with local inflammation accelerate the progression of liver fibrosis need further evaluation.  (+info)

Mikamo Lecture: a radical view on the 'superfamily' of cardiovascular risk factors. (7/55)

Many risk factors for cardiovascular disease generate superoxide in the blood vessels and thereby impair endothelial function. To emphasize the critical role of oxygen radicals, this is a 'radical view' of those risk factors. It will be useful to organize risk factors into a 'superfamily', with consideration of mediators, mechanisms, and target organs. Studies are summarized which suggest that, in parallel with the impairment of endothelial vasomotor function, the thrombin/thrombomodulin/activated protein C anticoagulant mechanism, which requires endothelial thrombomodulin, is also impaired by atherosclerosis and improves during regression of atherosclerosis. Impairment of the anticoagulant mechanism may contribute to thrombosis in atherosclerotic arteries, and improvement of the anticoagulant mechanism during regression of atherosclerosis may reduce the risk of cardiovascular events.  (+info)

Time course of coagulation parameters, cytokines and adhesion molecules in Plasmodium falciparum malaria. (8/55)

We studied 38 patients with malaria tropica over a period of 5 days during antiparasitic therapy. Serum or plasma levels of interleukin (IL) 1beta, IL-6, IL-10, tumour necrosis factor-alpha (TNF-alpha), the soluble vascular adhesion molecule (sVCAM) and the soluble intracellular adhesion molecule (sICAM) were determined by enzyme-linked immunosorbent assay. Protein C and antithrombin III activity were analysed by chromogenic tests and protein S activity by a clotting test. Antithrombin III, protein C and protein S activity was significantly lower in patients with severe malaria and displayed a highly significant increase in activity over the time of evaluation. Levels of sVCAM and sICAM were increased for the whole study period, but no significant differences were found between severe and mild malaria cases. Serum IL-1beta, IL-6 and IL-10 levels were significantly higher in patients with severe malaria, whereas no significant differences were found for TNF-alpha. IL-6 and IL-10 decreased significantly over 5 days during schizontocidal therapy. Our data show an impairment of the coagulation system which correlates with pro-inflammatory cytokines and therefore with the severity of the disease.  (+info)

Blood coagulation factor inhibitors are substances that interfere with the normal blood clotting process by inhibiting the function of coagulation factors. These inhibitors can be either naturally occurring or artificially produced.

Naturally occurring coagulation factor inhibitors include antithrombin, protein C, and tissue factor pathway inhibitor (TFPI). These inhibitors play a crucial role in regulating the coagulation cascade and preventing excessive clot formation.

Artificially produced coagulation factor inhibitors are used as therapeutic agents to treat thrombotic disorders. Examples include direct oral anticoagulants (DOACs) such as apixaban, rivaroxaban, and dabigatran, which selectively inhibit specific coagulation factors (factor Xa or thrombin).

Additionally, there are also antibodies that can act as coagulation factor inhibitors. These include autoantibodies that develop in some individuals and cause bleeding disorders such as acquired hemophilia A or antiphospholipid syndrome.

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.

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.

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.

Factor IX is also known as Christmas factor, which is a protein that plays a crucial role in the coagulation cascade, a series of chemical reactions that leads to the formation of a blood clot. It is one of the essential components required for the proper functioning of the body's natural blood-clotting mechanism.

Factor IX is synthesized in the liver and activated when it comes into contact with an injured blood vessel. Once activated, it collaborates with other factors to convert factor X to its active form, which then converts prothrombin to thrombin. Thrombin is responsible for converting fibrinogen to fibrin, forming a stable fibrin clot that helps stop bleeding and promote healing.

Deficiencies in Factor IX can lead to hemophilia B, a genetic disorder characterized by prolonged bleeding and an increased risk of spontaneous bleeding. Hemophilia B is inherited in an X-linked recessive pattern, meaning it primarily affects males, while females serve as carriers of the disease. Treatment for hemophilia B typically involves replacing the missing or deficient Factor IX through infusions to prevent or manage bleeding episodes.

Factor X is a protein that is essential for blood clotting, also known as coagulation. It is an enzyme that plays a crucial role in the coagulation cascade, which is a series of chemical reactions that lead to the formation of a blood clot. Factor X is activated by one of two pathways: the intrinsic pathway, which is initiated by damage to the blood vessels, or the extrinsic pathway, which is triggered by the release of tissue factor from damaged cells. Once activated, Factor X converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.

Inherited deficiencies in Factor X can lead to bleeding disorders, while increased levels of Factor X have been associated with an increased risk of thrombosis or blood clots. Therefore, maintaining appropriate levels of Factor X is important for the proper balance between bleeding and clotting in the body.

Factor Xa is a serine protease that plays a crucial role in the coagulation cascade, which is a series of reactions that lead to the formation of a blood clot. It is one of the activated forms of Factor X, a pro-protein that is converted to Factor Xa through the action of other enzymes in the coagulation cascade.

Factor Xa functions as a key component of the prothrombinase complex, which also includes calcium ions, phospholipids, and activated Factor V (also known as Activated Protein C or APC). This complex is responsible for converting prothrombin to thrombin, which then converts fibrinogen to fibrin, forming a stable clot.

Inhibitors of Factor Xa are used as anticoagulants in the prevention and treatment of thromboembolic disorders such as deep vein thrombosis and pulmonary embolism. These drugs work by selectively inhibiting Factor Xa, thereby preventing the formation of the prothrombinase complex and reducing the risk of clot formation.

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).

Factor VIII is a protein in the blood that is essential for normal blood clotting. It is also known as antihemophilic factor (AHF). Deficiency or dysfunction of this protein results in hemophilia A, a genetic disorder characterized by prolonged bleeding and easy bruising. Factor VIII works together with other proteins to help form a clot and stop bleeding at the site of an injury. It acts as a cofactor for another clotting factor, IX, in the so-called intrinsic pathway of blood coagulation. Intravenous infusions of Factor VIII concentrate are used to treat and prevent bleeding episodes in people with hemophilia A.

Factor XIa is a serine protease enzyme that plays a crucial role in blood coagulation. It is formed through the activation of Factor XI, which is one of the key components in the intrinsic pathway of the coagulation cascade. The activation of Factor XI to Factor XIa occurs via either autoactivation or through the action of thrombin. Once activated, Factor XIa can cleave and activate Factor IX, leading to the formation of Factor IXa, which further amplifies the coagulation cascade.

In summary, Factor XIa is a vital enzyme in the blood coagulation process, contributing to the formation of a stable fibrin clot that helps prevent excessive bleeding during injury or trauma.

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.

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.

Factor VIIa 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 VIIa is the activated form of factor VII, which is normally activated by tissue factor (TF) when there is damage to the blood vessels. Together, TF and Factor VIIa convert Factor X to its active form, Factor Xa, which then converts prothrombin to thrombin, leading to the formation of a fibrin clot.

In summary, Factor VIIa is an important protein in the coagulation cascade that helps to initiate the formation of a blood clot in response to injury.

Antirheumatic agents are a class of drugs used to treat rheumatoid arthritis, other inflammatory types of arthritis, and related conditions. These medications work by reducing inflammation in the body, relieving symptoms such as pain, swelling, and stiffness in the joints. They can also help slow down or prevent joint damage and disability caused by the disease.

There are several types of antirheumatic agents, including:

1. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen and naproxen, reduce inflammation and relieve pain. They are often used to treat mild to moderate symptoms of arthritis.
2. Corticosteroids: These powerful anti-inflammatory drugs, such as prednisone and cortisone, can quickly reduce inflammation and suppress the immune system. They are usually used for short-term relief of severe symptoms or in combination with other antirheumatic agents.
3. Disease-modifying antirheumatic drugs (DMARDs): These medications, such as methotrexate and hydroxychloroquine, work by slowing down the progression of rheumatoid arthritis and preventing joint damage. They can take several weeks or months to become fully effective.
4. Biologic response modifiers (biologics): These are a newer class of DMARDs that target specific molecules involved in the immune response. They include drugs such as adalimumab, etanercept, and infliximab. Biologics are usually used in combination with other antirheumatic agents for patients who have not responded to traditional DMARD therapy.
5. Janus kinase (JAK) inhibitors: These medications, such as tofacitinib and baricitinib, work by blocking the action of enzymes called JAKs that are involved in the immune response. They are used to treat moderate to severe rheumatoid arthritis and can be used in combination with other antirheumatic agents.

It is important to note that antirheumatic agents can have significant side effects and should only be prescribed by a healthcare provider who is experienced in the management of rheumatoid arthritis. Regular monitoring and follow-up are essential to ensure safe and effective treatment.

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.

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.

Factor IXa is a protein that plays a crucial role in the coagulation cascade, which is a series of biochemical reactions involved in blood clotting. It is an activated form of Factor IX, which is one of the coagulation factors that help convert prothrombin to thrombin, leading to the formation of a fibrin clot and stopping bleeding at the site of injury.

Factor IXa works by activating Factor X in the presence of calcium ions, phospholipids, and Factor VIIIa, which is another activated coagulation factor. This complex is called the tenase complex. The activation of Factor X leads to the formation of thrombin, which then converts fibrinogen to fibrin, forming a stable clot.

Deficiencies or dysfunctions in Factor IXa can lead to bleeding disorders such as hemophilia B, also known as Christmas disease, which is characterized by prolonged bleeding times and spontaneous bleeding episodes.

Coagulants are substances that promote the process of coagulation or clotting. They are often used in medical settings to help control bleeding and promote healing. Coagulants work by encouraging the formation of a clot, which helps to stop the flow of blood from a wound or cut.

There are several different types of coagulants that may be used in medical treatments. Some coagulants are naturally occurring substances, such as vitamin K, which is essential for the production of certain clotting factors in the body. Other coagulants may be synthetic or semi-synthetic compounds, such as recombinant activated factor VII (rFVIIa), which is used to treat bleeding disorders and prevent excessive bleeding during surgery.

Coagulants are often administered through injection or infusion, but they can also be applied topically to wounds or cuts. In some cases, coagulants may be used in combination with other treatments, such as compression or cauterization, to help control bleeding and promote healing.

It is important to note that while coagulants can be helpful in controlling bleeding and promoting healing, they can also increase the risk of blood clots and other complications. As a result, they should only be used under the guidance and supervision of a qualified healthcare professional.

Factor V, also known as proaccelerin or labile factor, 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 V acts as a cofactor for the activation of Factor X to Factor Xa, which is a critical step in the coagulation cascade.

When blood vessels are damaged, the coagulation cascade is initiated to prevent excessive bleeding. During this process, Factor V is activated by thrombin, another protein involved in coagulation, and then forms a complex with activated Factor X and calcium ions on the surface of platelets or other cells. This complex converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.

Deficiency or dysfunction of Factor V can lead to bleeding disorders such as hemophilia B or factor V deficiency, while mutations in the gene encoding Factor V can increase the risk of thrombosis, as seen in the Factor V Leiden mutation.

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.

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.

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.

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.

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).

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).

Factor V, also known as proaccelerin or labile factor, 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 V acts as a cofactor for the conversion of prothrombin to thrombin, which is a critical step in the coagulation process.

Inherited deficiencies or abnormalities in Factor V can lead to bleeding disorders. For example, Factor V Leiden is a genetic mutation that causes an increased risk of blood clots, while Factor V deficiency can cause a bleeding disorder.

It's worth noting that "Factor Va" is not a standard medical term. Factor V becomes activated and turns into Factor Va during the coagulation cascade. Therefore, it is possible that you are looking for the definition of "Factor Va" in the context of its role as an activated form of Factor V in the coagulation process.

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.

Factor VIIIa is a protein that plays a crucial role in the coagulation cascade, which is the series of biochemical reactions involved in blood clotting. Specifically, Factor VIIIa is an activated form of Factor VIII, which is one of the essential clotting factors required for normal hemostasis (the process that stops bleeding).

Factor VIIIa functions as a cofactor for another protein called Factor IXa, and together they form the "tenase complex." This complex activates Factor X to Factor Xa, which ultimately leads to the formation of a fibrin clot.

Deficiencies or dysfunctions in Factor VIII or Factor VIIIa can result in bleeding disorders such as hemophilia A, a genetic condition characterized by prolonged bleeding and spontaneous hemorrhages.

1-Carboxyglutamic acid, also known as γ-carboxyglutamic acid, is a post-translational modification found on certain blood clotting factors and other calcium-binding proteins. It is formed by the carboxylation of glutamic acid residues in these proteins, which enhances their ability to bind to calcium ions. This modification is essential for the proper functioning of many physiological processes, including blood coagulation, bone metabolism, and wound healing.

Hemophilia B is a genetic disorder that affects the body's ability to control blood clotting, also known as coagulation. This condition is caused by a deficiency or dysfunction in Factor IX, one of the proteins essential for normal blood clotting. As a result, people with Hemophilia B experience prolonged bleeding and bruising after injuries, surgeries, or spontaneously, particularly in joints and muscles.

There are different degrees of severity, depending on how much Factor IX is missing or not functioning properly. Mild cases may only become apparent after significant trauma, surgery, or tooth extraction, while severe cases can lead to spontaneous bleeding into joints and muscles, causing pain, swelling, and potential long-term damage. Hemophilia B primarily affects males, as it is an X-linked recessive disorder, but females can be carriers of the condition and may experience mild symptoms.

Tumor Necrosis Factor (TNF) Receptors are cell surface receptors that bind to tumor necrosis factor cytokines. They play crucial roles in the regulation of a variety of immune cell functions, including inflammation, immunity, and cell survival or death (apoptosis).

There are two major types of TNF receptors: TNFR1 (also known as p55 or CD120a) and TNFR2 (also known as p75 or CD120b). TNFR1 is widely expressed in most tissues, while TNFR2 has a more restricted expression pattern and is mainly found on immune cells.

TNF receptors have an intracellular domain called the death domain, which can trigger signaling pathways leading to apoptosis when activated by TNF ligands. However, they can also activate other signaling pathways that promote cell survival, differentiation, and inflammation. Dysregulation of TNF receptor signaling has been implicated in various diseases, including cancer, autoimmune disorders, and neurodegenerative conditions.

Vitamin K is a fat-soluble vitamin that plays a crucial role in blood clotting and bone metabolism. It is essential for the production of several proteins involved in blood clotting, including factor II (prothrombin), factor VII, factor IX, and factor X. Additionally, Vitamin K is necessary for the synthesis of osteocalcin, a protein that contributes to bone health by regulating the deposition of calcium in bones.

There are two main forms of Vitamin K: Vitamin K1 (phylloquinone), which is found primarily in green leafy vegetables and some vegetable oils, and Vitamin K2 (menaquinones), which is produced by bacteria in the intestines and is also found in some fermented foods.

Vitamin K deficiency can lead to bleeding disorders such as hemorrhage and excessive bruising. While Vitamin K deficiency is rare in adults, it can occur in newborns who have not yet developed sufficient levels of the vitamin. Therefore, newborns are often given a Vitamin K injection shortly after birth to prevent bleeding problems.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects the joints. It is characterized by persistent inflammation, synovial hyperplasia, and subsequent damage to the articular cartilage and bone. The immune system mistakenly attacks the body's own tissues, specifically targeting the synovial membrane lining the joint capsule. This results in swelling, pain, warmth, and stiffness in affected joints, often most severely in the hands and feet.

RA can also have extra-articular manifestations, affecting other organs such as the lungs, heart, skin, eyes, and blood vessels. The exact cause of RA remains unknown, but it is believed to involve a complex interplay between genetic susceptibility and environmental triggers. Early diagnosis and treatment are crucial in managing rheumatoid arthritis to prevent joint damage, disability, and systemic complications.

Transglutaminases are a family of enzymes that catalyze the post-translational modification of proteins by forming isopeptide bonds between the carboxamide group of peptide-bound glutamine residues and the ε-amino group of lysine residues. This process is known as transamidation or cross-linking. Transglutaminases play important roles in various biological processes, including cell signaling, differentiation, apoptosis, and tissue repair. There are several types of transglutaminases, such as tissue transglutaminase (TG2), factor XIII, and blood coagulation factor XIIIA. Abnormal activity or expression of these enzymes has been implicated in various diseases, such as celiac disease, neurodegenerative disorders, and cancer.

Hemophilia A is a genetic bleeding disorder caused by a deficiency in clotting factor VIII. This results in impaired blood clotting and prolonged bleeding, particularly after injuries or surgeries. Symptoms can range from mild to severe, with the most severe form resulting in spontaneous bleeding into joints and muscles, leading to pain, swelling, and potential joint damage over time. Hemophilia A primarily affects males, as it is an X-linked recessive disorder, and is usually inherited from a carrier mother. However, about one third of cases result from a spontaneous mutation in the gene for factor VIII. Treatment typically involves replacement therapy with infusions of factor VIII concentrates to prevent or control bleeding episodes.

Tumor Necrosis Factor (TNF) Decoy Receptors are soluble forms of TNF receptors that act as decoy molecules to neutralize the activity of TNF-α, a pro-inflammatory cytokine. They function by binding to TNF-α and preventing it from interacting with its cell surface receptors (TNFR1 and TNFR2), thereby inhibiting the downstream signaling cascades that lead to inflammation and tissue damage.

There are two main types of TNF decoy receptors:

1. TNF Receptor 1 (TNFR1, also known as p55 or p60) - This type of decoy receptor is produced by alternative splicing of the TNFR1 gene and can be found in both membrane-bound and soluble forms. The soluble form of TNFR1 acts as a decoy receptor for TNF-α, preventing it from binding to its cell surface receptors.
2. TNF Receptor 2 (TNFR2, also known as p75 or p80) - This type of decoy receptor is primarily found in the soluble form and is produced by proteolytic cleavage of the membrane-bound TNFR2. Soluble TNFR2 can bind to TNF-α with higher affinity than TNFR1, making it a more effective decoy receptor.

TNF decoy receptors have been implicated in various physiological and pathological processes, including inflammation, immune regulation, and cancer. They are being investigated as potential therapeutic targets for the treatment of various inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis.

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.

Inhibitors of Differentiation (ID) proteins are a family of transcriptional regulators that play crucial roles in controlling cell growth, differentiation, and survival. They belong to the basic helix-loop-helix (bHLH) protein family and function as negative regulators of differentiation in various cell types.

ID proteins lack the DNA-binding domain required for specific interactions with DNA, but they contain a highly conserved HLH region that enables them to form heterodimers with other bHLH transcription factors. By doing so, ID proteins prevent these partner bHLH factors from binding to their target DNA sequences and thus inhibit the differentiation programs driven by those factors.

There are four members in the ID protein family: ID1, ID2, ID3, and ID4. These proteins exhibit distinct expression patterns during embryonic development and in adult tissues, reflecting their diverse roles in regulating cell fate decisions and homeostasis. Dysregulation of ID protein function has been implicated in several pathological conditions, including cancer and neurodevelopmental disorders.

Tumor Necrosis Factor-alpha (TNF-α) is a cytokine, a type of small signaling protein involved in immune response and inflammation. It is primarily produced by activated macrophages, although other cell types such as T-cells, natural killer cells, and mast cells can also produce it.

TNF-α plays a crucial role in the body's defense against infection and tissue injury by mediating inflammatory responses, activating immune cells, and inducing apoptosis (programmed cell death) in certain types of cells. It does this by binding to its receptors, TNFR1 and TNFR2, which are found on the surface of many cell types.

In addition to its role in the immune response, TNF-α has been implicated in the pathogenesis of several diseases, including autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as cancer, where it can promote tumor growth and metastasis.

Therapeutic agents that target TNF-α, such as infliximab, adalimumab, and etanercept, have been developed to treat these conditions. However, these drugs can also increase the risk of infections and other side effects, so their use must be carefully monitored.

Arcidae is a family of marine bivalves, commonly known as ark clams or angel wings. These bivalves are characterized by their triangular or elongated shells, which are often sculptured with radial ribs and concentric growth lines. They are filter feeders, living buried in the sand or mud and feeding on plankton and organic matter in the water. Arcidae species can be found in both shallow and deep waters, ranging from tropical to polar regions. Some examples of genera within this family include Barbatia, Arca, and Anadara.

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.

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.

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.

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.

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.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

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.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Vitamin K deficiency is a condition that occurs when the body lacks adequate amounts of Vitamin K, a fat-soluble vitamin essential for blood clotting and bone metabolism. This can lead to an increased risk of excessive bleeding (hemorrhage) and calcification of tissues.

Vitamin K is required for the activation of several proteins involved in blood clotting, known as coagulation factors II, VII, IX, and X. A deficiency in Vitamin K can result in these factors remaining in their inactive forms, leading to impaired blood clotting and an increased risk of bleeding.

Vitamin K deficiency can occur due to several reasons, including malnutrition, malabsorption disorders (such as cystic fibrosis or celiac disease), liver diseases, use of certain medications (such as antibiotics or anticoagulants), and prolonged use of warfarin therapy.

In newborns, Vitamin K deficiency can lead to a serious bleeding disorder known as hemorrhagic disease of the newborn. This is because newborns have low levels of Vitamin K at birth, and their gut bacteria, which are responsible for producing Vitamin K, are not yet fully developed. Therefore, it is recommended that newborns receive a dose of Vitamin K within the first few days of life to prevent this condition.

Symptoms of Vitamin K deficiency can include easy bruising, nosebleeds, bleeding gums, blood in urine or stools, and excessive menstrual bleeding. In severe cases, it can lead to life-threatening hemorrhage. Treatment typically involves administering Vitamin K supplements or injections to replenish the body's levels of this essential nutrient.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Monoclonal antibodies are laboratory-produced proteins that mimic the immune system's ability to fight off harmful antigens such as viruses and cancer cells. They are created by fusing a single B cell (the type of white blood cell responsible for producing antibodies) with a tumor cell, resulting in a hybrid cell called a hybridoma. This hybridoma can then be cloned to produce a large number of identical cells, all producing the same antibody, hence "monoclonal."

Humanized monoclonal antibodies are a type of monoclonal antibody that have been genetically engineered to include human components. This is done to reduce the risk of an adverse immune response in patients receiving the treatment. In this process, the variable region of the mouse monoclonal antibody, which contains the antigen-binding site, is grafted onto a human constant region. The resulting humanized monoclonal antibody retains the ability to bind to the target antigen while minimizing the immunogenicity associated with murine (mouse) antibodies.

In summary, "antibodies, monoclonal, humanized" refers to a type of laboratory-produced protein that mimics the immune system's ability to fight off harmful antigens, but with reduced immunogenicity due to the inclusion of human components in their structure.

Benzamidines are a group of organic compounds that contain a benzene ring linked to an amidine functional group. They are commonly used as antimicrobial agents, particularly in the treatment of various gram-negative bacterial infections. Benzamidines work by inhibiting the enzyme bacterial dehydrogenases, which are essential for the bacteria's survival.

Some examples of benzamidine derivatives include:

* Tempanamine hydrochloride (Tembaglanil): used to treat urinary tract infections caused by susceptible strains of Escherichia coli and Klebsiella pneumoniae.
* Chlorhexidine: a broad-spectrum antimicrobial agent used as a disinfectant and preservative in various medical and dental applications.
* Prothiobenzamide: an anti-inflammatory and analgesic drug used to treat gout and rheumatoid arthritis.

It is important to note that benzamidines have a narrow therapeutic index, which means that the difference between an effective dose and a toxic dose is small. Therefore, they should be used with caution and under the supervision of a healthcare professional.

In the context of medical and biological sciences, a "binding site" refers to a specific location on a protein, molecule, or cell where another molecule can attach or bind. This binding interaction can lead to various functional changes in the original protein or molecule. The other molecule that binds to the binding site is often referred to as a ligand, which can be a small molecule, ion, or even another protein.

The binding between a ligand and its target binding site can be specific and selective, meaning that only certain ligands can bind to particular binding sites with high affinity. This specificity plays a crucial role in various biological processes, such as signal transduction, enzyme catalysis, or drug action.

In the case of drug development, understanding the location and properties of binding sites on target proteins is essential for designing drugs that can selectively bind to these sites and modulate protein function. This knowledge can help create more effective and safer therapeutic options for various diseases.

Factor XII deficiency, also known as Hageman factor deficiency, is a rare genetic disorder characterized by a lack or dysfunction of coagulation factor XII. This protein is involved in the initiation of the coagulation cascade, which leads to the formation of a blood clot. People with Factor XII deficiency may have an increased risk of bleeding, but it is typically mild and not life-threatening. The diagnosis is usually made through blood tests that measure the level and function of Factor XII. Treatment is generally not necessary unless there is significant bleeding, in which case fresh frozen plasma or cryoprecipitate may be given to provide temporary correction of the deficiency. It's important to note that Factor XII deficiency is not a common cause of bleeding disorders and it doesn't increase the risk of thrombosis.

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.

Immunologic factors refer to the elements of the immune system that contribute to the body's defense against foreign substances, infectious agents, and cancerous cells. These factors include various types of white blood cells (such as lymphocytes, neutrophils, monocytes, and eosinophils), antibodies, complement proteins, cytokines, and other molecules involved in the immune response.

Immunologic factors can be categorized into two main types: innate immunity and adaptive immunity. Innate immunity is the non-specific defense mechanism that provides immediate protection against pathogens through physical barriers (e.g., skin, mucous membranes), chemical barriers (e.g., stomach acid, enzymes), and inflammatory responses. Adaptive immunity, on the other hand, is a specific defense mechanism that develops over time as the immune system learns to recognize and respond to particular pathogens or antigens.

Abnormalities in immunologic factors can lead to various medical conditions, such as autoimmune disorders, immunodeficiency diseases, and allergies. Therefore, understanding immunologic factors is crucial for diagnosing and treating these conditions.

Factor XIIa is a protease enzyme that plays a role in the coagulation cascade, which is the series of events that leads to blood clotting. It is formed when Factor XII, also known as Hageman factor, is activated by contact with negatively charged surfaces such as damaged endothelial cells or artificial surfaces like medical devices.

Once activated, Factor XIIa can activate other components of the coagulation cascade, including Factor XI, which ultimately leads to the formation of a fibrin clot. While Factor XIIa is an important part of the coagulation system, it is not essential for normal hemostasis (the process that stops bleeding) in humans, as people with deficiencies in Factor XII do not have an increased risk of bleeding. However, excessive activation of Factor XIIa has been implicated in several pathological conditions, including thrombosis and inflammation.

TAP and antistasin were used to estimate factor Xa as a drug target. Blood coagulation is a complex process by which the blood ... and orally bioavailable inhibitor of blood coagulation factor Xa". J Med Chem. 50 (22): 5339-56. doi:10.1021/jm070245n. PMID ... and Orally Bioavailable Inhibitor of Blood Coagulation Factor Xa". Journal of Medicinal Chemistry. 50 (22): 5339-56. doi: ... and Orally Bioavailable Inhibitor of Blood Coagulation Factor Xa". Journal of Medicinal Chemistry. 50 (22): 5339-56. doi: ...
TEM investigates the interaction of coagulation factors, their inhibitors, anticoagulant drugs, blood cells, specifically ... Prolongation of CT may be a result of coagulation deficiencies, primarily coagulation factors, or heparin (dependent on the ... Whole blood coagulation thrombelastographic profiles employing minimal tissue factor activation. J Thromb Haemost. 2003;1:551-8 ... Whole blood thrombelastographic coagulation profiles using minimal tissue factor activation can display hypercoagulation in ...
Xarelto (rivaroxaban) is a small molecule inhibitor of Factor Xa, a key enzyme involved in blood coagulation. In the United ... Factor VIII, a clotting agent used to treat hemophilia, was produced, at the time, by processing donated blood. In the early ... In the mid-1980s, when Bayer's Cutter Laboratories realized that their blood products, the clotting agents Factor VIII and IX, ... Khoshnood, M.; McHenry, L. (2014). "Blood money: Bayer's inventory of HIV-contaminated blood products and third world ...
Rao LV, Rapaport SI (1987). "Studies of a mechanism inhibiting the initiation of the extrinsic pathway of coagulation". Blood. ... "The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: ... "The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: ... "The effect of leukocyte elastase on tissue factor pathway inhibitor". Blood. 79 (7): 1712-9. doi:10.1182/blood.V79.7.1712.1712 ...
This situation is analogous to the low levels of clotting factors found in disseminated intravascular coagulation (DIC). Blood- ... C1-inhibitor is contained in the human blood; it can, therefore, be isolated from donated blood. Risks of infectious disease ... C1-inhibitor (C1-inh, C1 esterase inhibitor) is a protease inhibitor belonging to the serpin superfamily. Its main function is ... Note that C1-inhibitor is the most important physiological inhibitor of plasma kallikrein, FXIa, and FXIIa. C1-inhibitor is the ...
This is a highly selective inhibitor of factor Xa in the blood coagulation pathways. TAP molecules are highly dipolar, and are ... and tissue factor pathway inhibitor (TFPI). Kunitz STI protease inhibitor, the trypsin inhibitor initially studied by Moses ... tissue factor pathway inhibitor precursor; and Kunitz STI protease inhibitor contained in legume seeds. Kunitz domains are ... Salier JP (1990). "Inter-alpha-trypsin inhibitor: emergence of a family within the Kunitz-type protease inhibitor superfamily ...
... is a protein circulating in the blood which inhibits factors Xa and XIa of the coagulation cascade. It is a member of the class ... doi:10.1182/blood.V96.9.3049. PMID 11049983. The MEROPS online database for peptidases and their inhibitors: I04.005 (Genes on ... Han X, Fiehler R, Broze GJ (November 2000). "Characterization of the protein Z-dependent protease inhibitor". Blood. 96 (9): ... Han X, Fiehler R, Broze GJ (August 1998). "Isolation of a protein Z-dependent plasma protease inhibitor". Proceedings of the ...
... inhibiting several blood coagulation enzymes counting thrombin and factor Xa. In the beginning, protein C inhibitor(PCI) was ... Protein C inhibitor (PCI) is serine protease inhibitor of serpin type that is found in most tissues and fluids, including blood ... doi:10.1182/blood-2009-04-217240. PMID 19855083. Pratt CW, Church FC (May 1992). "Heparin binding to protein C inhibitor" (PDF ... Hayashi S, Wakizaka A (July 1995). "Urinary protein C inhibitor binding region in the A alpha-chain of human fibrinogen". Blood ...
... factor VII comes into contact with tissue factors which starts a process called the blood coagulation cascade. Its purpose is ... but the research focus has shifted towards factor Xa inhibitors, or even dual thrombin and fXa inhibitors that have a broader ... Direct thrombin inhibitors (DTIs) are a class of anticoagulant drugs that can be used to prevent and treat embolisms and blood ... Most of those drugs are in the class of direct factor Xa inhibitors, but there is one DTI called AZD0837, which is a follow-up ...
"The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: ... Leytus SP, Foster DC, Kurachi K, Davie EW (September 1986). "Gene for human factor X: a blood coagulation factor whose gene ... "Kcentra- prothrombin, coagulation factor vii human, coagulation factor ix human, coagulation factor x human, protein c, protein ... "The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: ...
... aldosterone inhibitors. Coagulation: anticoagulants, heparin, antiplatelet drugs, fibrinolytics, anti-hemophilic factors, ... Affecting blood pressure/(antihypertensive drugs): ACE inhibitors, angiotensin receptor blockers, beta-blockers, α blockers, ... HMG-CoA reductase inhibitors (statins) for lowering LDL cholesterol inhibitors: hypolipidaemic agents. Drugs affecting the ... Cytotoxic drugs, therapeutic antibodies, sex hormones, aromatase inhibitors, somatostatin inhibitors, recombinant interleukins ...
When endothelium of a blood vessel is damaged, the endothelial cells stop secretion of coagulation and aggregation inhibitors ... Coagulation reinforces the platelet plug with fibrin threads that act as a "molecular glue". Platelets are a large factor in ... This involves coagulation, which changes blood from a liquid to a gel. Intact blood vessels are central to moderating blood's ... vasoconstriction temporary blockage of a hole in a damaged blood vessel by a platelet plug blood coagulation (formation of ...
... a blood coagulation factor (ATC code: B02BD08). Eptacog beta is almost identical to, and functions like, coagulation factor VII ... These inhibitors often increase over time and inhibit the action of coagulation in the body. Recombinant factor VIIa, which is ... This treatment results in activation of the extrinsic pathway of blood coagulation. Coagulation factor VIIa (recombinant)-jncw ... It can't be given without inhibitor.[citation needed] It is important for some patients to shift to proper blood factors ...
Studies show that DM1 and DM2 cause a change in balancing of metabolites such as carbohydrates, blood coagulation factors,[ ... P. Zaoui, et al, (2000) "Role of Metalloproteases and Inhibitors in the Occurrence and Prognosis of Diabetic Renal Lesions," ... Chronic elevation of blood glucose level leads to damage of blood vessels called angiopathy. The endothelial cells lining the ... While feeling unwell, Start with regular monitoring of blood glucose levels. In addition to measuring blood or urine ketone ...
"Recombinant Antidote for Reversal of Anticoagulation by Factor Xa Inhibitors". Blood. 112 (11): 983. doi:10.1182/blood.V112.11. ... April 2013). "A specific antidote for reversal of anticoagulation by direct and indirect inhibitors of coagulation factor Xa". ... "Reversing factor Xa inhibitors - clinical utility of andexanet alfa". Journal of Blood Medicine. 8: 141-149. doi:10.2147/JBM. ... It has not been found to be useful for other factor Xa inhibitors. It is given by injection into a vein. Common side effects ...
Inhibition of Factor Xa interrupts the intrinsic and extrinsic pathway of the blood coagulation cascade, inhibiting both ... Rivaroxaban inhibits both free and bound Factor Xa in the prothrombinase complex. It is a selective direct factor Xa inhibitor ... decreasing a number of coagulation factors, including factor X. Rivaroxaban has predictable pharmacokinetics across a wide ... "U.S. FDA Approves Portola Pharmaceuticals' Andexxa, First and Only Antidote for the Reversal of Factor Xa Inhibitors" (Press ...
... reversible and competitive inhibitor of human factor Xa, with an inhibitory constant (Ki) value of 0.561 nM. In coagulation, ... Thrombins turn blood-soluble fibrinogens to insoluble fibrins, which are the main components of blood clots. In human, 15-150 ... Edoxaban, sold under the brand name Lixiana among others, is an anticoagulant medication and a direct factor Xa inhibitor. It ... uninhibited factor Xa forms a prothrombinase complex with factor Va on platelet surfaces. Prothrombinases turn prothrombins to ...
Fibrin is then cross linked by factor XIII (Fibrin Stabilizing Factor) to form a blood clot. The principal inhibitor of ... Factor Xa along with Factor Va as a cofactor), in the final states of coagulation. ... A key event in the final stages of blood coagulation is the conversion of fibrinogen into fibrin by the serine protease enzyme ... On the action of a secretion obtained from the medicinal leech on the coagulation of the blood". Proceedings of the Royal ...
The activation of factor X is a common point between the intrinsic and extrinsic pathway of blood coagulation. Activated factor ... the anticoagulant factor in vampire bat saliva, is a tight-binding, noncompetitive inhibitor of activated factor X". Biochimica ... These two processes inhibit blood coagulation thus keeping the blood of the bitten victim from clotting while the bat is ... inhibiting coagulation factors IX (IXa) and X (Xa) by establishing rapid equilibrium with factor Xa, and is the first natural ...
Previously, to monitor coagulation effects, blood was placed in a glass tube, kept at 37 degrees Celsius, and manually ... It measures the seconds needed for whole blood to clot upon activation of the intrinsic pathway by the addition of factor XII ... Clotting time measurements can be affected by drugs such as warfarin, aprotinin, and GpIIb/IIIa inhibitors, and physiologic ... Typically a sample of blood is put in a vial or cartridge along with coagulation activators. The sample is maintained at a ...
Chapter 38 Coagulation Factors V and VIII by GC White and GE Gilbert Archived 2017-09-11 at the Wayback Machine in Blood: ... If a person becomes refractory to replacement coagulation factor as a result of high levels of circulating inhibitors, this may ... Factor VIII is used in haemophilia A and factor IX in haemophilia B. Factor replacement can be either isolated from human blood ... Franchini, M; Mannucci, PM (October 2011). "Inhibitors of propagation of coagulation (factors VIII, IX and XI): a review of ...
While warfarin and heparin have their major effects on coagulation factors, an increased bleeding time is sometimes seen with ... Lind, S. E. (1991). "The bleeding time does not predict surgical bleeding". Blood. 77 (12): 2547-2552. doi:10.1182/blood.V77.12 ... Aspirin and other cyclooxygenase inhibitors can significantly prolong bleeding time. ... certain vascular disorders and von Willebrand Disease-not by other coagulation factors such as haemophilia. Diseases that cause ...
MASP-1 can cleave coagulation pathway proteins such as PAR-4, fibrinogen, and factor XIII which leads to high clot and fibrin ... A spliced variant of this gene, which lacks the serine protease domain, functions as an inhibitor of the complement pathway. ... However, MASP-1 is useful for biological pathways other than the complement pathway, such as blood clots. ... "A new member of the C1s family of complement proteins found in a bactericidal factor, Ra-reactive factor, in human serum". ...
The inhibitor also inactivates kallikrein and plasmin[citation needed], also involved in blood coagulation. However it ... Factor XI (XIa), Factor XII (XIIa) and, to a greater extent, Factor II (thrombin) (IIa), and also the activated form of Factor ... Antithrombin IV (AT IV) refers to an antithrombin that becomes activated during and shortly after blood coagulation. Only AT ... Yin ET, Wessler S, Stoll PJ (1971). "Identity of plasma-activated factor X inhibitor with antithrombin 3 and heparin cofactor ...
... functions to inhibit blood coagulation by binding to an inhibitor. It is a GLA domain protein and thus Vitamin K- ... The main role of Protein Z appears to be the degradation of Factor Xa. This is done by Protein Z-related protease inhibitor ( ... Protein Z is a member of the coagulation cascade, the group of blood proteins that leads to the formation of blood clots. It is ... Blood. 114 (17): 3662-3667. doi:10.1182/blood-2009-04-210021. PMC 2766681. PMID 19528533. Wei Z, Yan Y, Carrell RW, Zhou A ( ...
... an antithrombin-III variant that acts as a substrate but not an inhibitor of alpha-thrombin and factor Xa". Blood. 77 (10): ... which is able to inhibit trypsin and chymotrypsin as well as several blood coagulation factors. However, close relatives of ... a more effective inhibitor of thrombin and factor Xa. Furthermore, both of these coagulation proteases also contain binding ... Miao RQ, Agata J, Chao L, Chao J (November 2002). "Kallistatin is a new inhibitor of angiogenesis and tumor growth". Blood. 100 ...
A Bethesda unit (BU) is a measure of blood coagulation inhibitor activity. It is the amount of inhibitor that will inactivate ... human factor Xa decoy that reverses the effect of factor Xa inhibitors by binding at the active sites of factor Xa inhibitor ... The activated AT then inactivates factor Xa, thrombin, and other coagulation factors. Heparin can be used in vivo (by injection ... Anticoagulants, commonly known as blood thinners, are chemical substances that prevent or reduce coagulation of blood, ...
"Hepatocytes express blood coagulation factor XII (Hageman factor)". The Journal of Laboratory and Clinical Medicine. 115 (4): ... Multiple factor XII inhibitors have been developed and some of them are in clinical trials The gene for factor XII is located ... Coagulation factor XII, also known as Hageman factor, is a plasma protein. It is the zymogen form of factor XIIa, an enzyme (EC ... "Characterization of human blood coagulation factor XII cDNA. Prediction of the primary structure of factor XII and the tertiary ...
Warfarin is the preferred, and best studied anticoagulant, but direct factor Xa inhibitors may also be used. Many patients will ... Anti-coagulation is required for all patient's with Budd-Chiari syndrome, even if a cause of hypercoagulability is not found. ... The condition is caused by occlusion of the hepatic veins (usually due to a blood clot) that drain the liver. The symptoms are ... Factor V Leiden is responsible for 8% of cases. Other less common inherited disorders leading to the condition include factor ...
... activated blood-coagulation factor II, blood-coagulation factor IIa, factor IIa, E thrombin, beta-thrombin, gamma-thrombin) is ... Thrombin bound to thrombomodulin activates protein C, an inhibitor of the coagulation cascade. The activation of protein C is ... "The life cycle of coagulation factor VIII in view of its structure and function". Blood. 92 (11): 3983-96. doi:10.1182/blood. ... In the blood coagulation pathway, thrombin acts to convert factor XI to XIa, VIII to VIIIa, V to Va, fibrinogen to fibrin, and ...
A low molecular weight platelet inhibitor of factor XIa: purification, characterization, and possible role in blood coagulation ... The inhibition by PIXI of factor XIa-catalyzed activation of factor IX and its capacity to prevent factor XIa inactivation by ... alpha 1-protease inhibitor, combined with the specificity of PIXI for factor XIa among serine proteases found in blood, suggest ... Immunoblot analysis showed that PIXI is not the inhibitory domain of protease nexin II, a potent inhibitor of factor XIa also ...
TAP and antistasin were used to estimate factor Xa as a drug target. Blood coagulation is a complex process by which the blood ... and orally bioavailable inhibitor of blood coagulation factor Xa". J Med Chem. 50 (22): 5339-56. doi:10.1021/jm070245n. PMID ... and Orally Bioavailable Inhibitor of Blood Coagulation Factor Xa". Journal of Medicinal Chemistry. 50 (22): 5339-56. doi: ... and Orally Bioavailable Inhibitor of Blood Coagulation Factor Xa". Journal of Medicinal Chemistry. 50 (22): 5339-56. doi: ...
Categories: Blood Coagulation Factor Inhibitors Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, ...
... better known as disseminated intravascular coagulation (DIC), is characterized by abnormally increased activation of ... Plasma tissue factor and tissue factor pathway inhibitor levels in patients with disseminated intravascular coagulation. Am J ... Levi M, Scully M. How I treat disseminated intravascular coagulation. Blood. 2018 Feb 22. 131 (8):845-54. [QxMD MEDLINE Link]. ... TF binds to factor VII and converts factor VII to factor VIIa. The resultant dimeric TF-factor VIIa complex then activates ...
... and orally bioavailable inhibitor of blood coagulation factor Xa. ... The direct factor Xa inhibitor apixaban is safe, efficacious, ... Apixaban is an orally active, active site-targeting, highly potent and selective factor Xa (FXa) inhibitor (human/rabbit Ki = ... Apixaban is an oral, direct and highly selective factor Xa (FXa) inhibitor in late-stage clinical development for the ... We evaluated apixaban, a direct and highly selective factor Xa inhibitor, in combination with clinically relevant doses of ...
Blood Coagulation Factor Inhibitor Inhibitor, Blood Coagulation Factor Inhibitor, Coagulation Factor, Blood Inhibitors, Blood ... Blood Coagulation Factor Inhibitor. Inhibitor, Blood Coagulation Factor. Inhibitor, Coagulation Factor, Blood. Inhibitors, ... Blood Coagulation Factor Inhibitors - Preferred Concept UI. M0029342. Scope note. Substances, usually endogenous, that act as ... Blood Coagulation Factor Inhibitors Entry term(s). ... Blood Coagulation Factor. Inhibitors, Coagulation Factor, Blood ...
Have been told that you have inhibitors to blood coagulation factor VIII. ... Your body can form inhibitors to von Willebrand factor or factor VIII. An inhibitor is part of the bodys normal defense system ... to make sure you are carefully monitored with blood tests for the development of inhibitors to von Willebrand factor or factor ... If you form inhibitors, it may stop VONVENDI or factor VIII from working properly. Consult with your healthcare provider ...
have been told that you have inhibitors to von Willebrand factor. *have been told that you have inhibitors to blood coagulation ... Your doctor will perform blood tests to check your von Willebrand factor activity and the presence of any inhibitors. If high ... Blood Clots. Vonvendi may increase your risk of developing a blood clot, which could lead to pulmonary embolism (a clot in your ... Your first dose of Vonvendi for each bleeding episode may be given with a recombinant factor VIII (factor VIII not produced ...
... factor XII, high-molecular-weight kininogen (HK), and prekallikrein (PK). Factor XI is synthesized in the liver and ... The so-called contact factors include factor XI, ... Factor XI activation in a revised model of blood coagulation. ... A low molecular weight platelet inhibitor of factor XIa: purification, characterization, and possible role in blood coagulation ... Activation of human blood coagulation factor XI independent of factor XII. Factor XI is activated by thrombin and factor XIa in ...
UPDATE AVAILABLE ON-DEMANDThe report on the global blood plasma derivatives market highlights that the market is expected to ... These derivatives include albumin, factor VIII & IX, anti-inhibitor coagulation complex (AICC), immunoglobulins, including Rh ... Blood plasma is clear liquid component of blood in which red blood cells, white blood cells, and platelets are suspended. It ... The factors that drive the growth of the blood plasma derivatives market include increase in prevalence of life-threatening ...
It acts as a potent co-inhibitor of several activated coagulation factors, especially Factors Xa and IIa (thrombin). The ... Periodic complete blood counts including platelet count and hematocrit or hemoglobin, and stool tests for occult blood are ... Tinzaparin sodium induces release of tissue factor pathway inhibitor, which may contribute to the antithrombotic effect. ... Innohep (tinzaparin) is a blood thinner (anticoagulant) used together with warfarin (Coumadin) to treat a type of blood clot ...
Like all viruses, the EBOV largely relies on host cell factors and physiological processes for its entry, replication, and ... Recombinant nematode anticoagulant protein c2 and other inhibitors targeting blood coagulation factor VIIa/tissue factor. J ... 1) Convalescent blood serum. The WHO issued a consensus statement that the use of whole blood therapies and convalescent blood ... Treatment of Ebola virus infection with a recombinant inhibitor of factor VIIa/tissue factor: a study in rhesus monkeys. Lancet ...
Warfarin makes blood flow easily through the veins or arteries. Read below to know more about its dosage, use of side effects, ... coagulation disorders are qualitative or quantitative changes in blood cells or soluble coagulation factors and inhibitors. ... Introduction Acquired coagulation inhibitors are antibodies that neutralize the coagulation factors activity and fasten their ... Alloantibodies are inhibitors that occur in patients with acquired deficiencies of coagulation factors. In contrast, autoa... ...
This is one of the proteins in the body that helps the blood clot. ... This is one of the proteins in the body that helps the blood clot. ... The factor VIII assay is a blood test to measure the activity of factor VIII. ... The factor VIII assay is a blood test to measure the activity of factor VIII. ...
Anders O. and Nagel H.R., et al., Blood coagulation factors and proteinase inhibitors in cytostatic therapy of acute leukemia, ... In leukemia, the bone marrow makes abnormal white blood cells known as leukemia cells. They crowd out normal blood cells and ... Leukemia is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation of leukocytes. However, it ... Arbiser J.L. and Klauber N., et al., Curcumin is an in vivo inhibitor of angiogenesis, Mol Med, 4(6), 376-83 (1998) ...
... blood coagulation factors, pulmonary surfactant protein A (SP-A), metalloproteinase inhibitor DM64, and a serine protease ... The blood coagulation system consists of a strictly regulated proteolytic cascade of blood coagulation factors that convey ... epidermal growth factor (receptor); ER: endoplasmic reticulum; FX/FXa/FIIa: blood coagulation factors; GLIC: proton-gated ion ... Ultimately, a blood clot is formed to prevent blood loss from the injured blood vessel [105]. Several sPLA2s can affect this ...
The kinetic triplet (activation energy, kinetic function and pre-exponential factor) and the corresponding rate law were ... Bioassay-directed fractionation of a blood coagulation factor Xa inhibitor, betulinic acid from Lycopus lucidus ... The pre-exponential factor of step 1 is A1=3.86·1011s-1, the pre-exponential factor of step 2 is A2=5.60·1013 s-1. Calculation ... The order of factors observed for foam half-life at 220°C is A,D,C,B. The most important factor for foam half-life is still ...
... a factor-inhibitor assay is indicated. Although nearly all procoagulants have an inhibitor, the inhibitor to factor VIII is the ... revealing its importance as a functional inhibitor of the blood coagulation proteases. Thrombin, factor Xa, and factor IXa are ... Unlike other coagulation protease inhibitors, TFPI has inhibitory sites for factor Xa and for the factor VIIa/tissue factor (TF ... The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: ...
Vladimir Sulimov New Blood Coagulation Factor XIIa Inhibitors: Molecular Modeling, Synthesis, and Experimental Confirmation ... Blood coagulation factors bound to procoagulant platelets are concentrated in their cap structures to promote clotting Blood ... one as New Inhibitors of Factor Xa and Factor Xia Molecules 2020; 25,: 1889. ... a pyrimidinone moiety and characterization of their anticoagulant activity via inhibition of blood coagulation factors Xa and ...
... trying to develop new methods to more safely control blood clotting (Optimisation of coagulation factor XIIa inhibitors as ... Defining the targets of HDAC inhibitors in diffuse large B cell lymphoma). ...
... and Proteins Proteins Glycoproteins Protein S Biological Factors Blood Coagulation Factor Inhibitors Protein S, anabolen kopen ... Amino Acids, Peptides, and Proteins Proteins Blood Proteins Protein S Amino Acids, Peptides, ...
Mammalian Blood Coagulation Factors And Inhibitors 1993 and contact dynamics in America. ebook Arsenic and Old Mustard: ... The not hegemonic & of the Caribbean felt ia of their parts to address a Pdf Proteolytic Enzymes In Coagulation, Fibrinolysis, ...
Detecting and Evaluating Coagulation Inhibitors and Factor Deficiencies - 1 credit hour(s) ... Florida Board of Clinical Laboratory Science CE - General (Blood Banking / Immunohematology). *Introduction to the ABO Blood ... Warm Antibodies and Autoantibodies in Blood Banking - 1 credit hour(s). *Overview Of Major Antigens of the Rh Blood Group ... Describing a Red Blood Cell Population Using RBC Indices and Red Cell Distribution Width - 1 credit hour(s) ...
Library 3: Potential inhibitors of Human Coagulation Factor Xa. The prevention of blood coagulation is a major topic ... Compared to thrombin, factor Xa acts on an earlier level than thrombin. The mechanism of amplification in the blood coagulation ... Analysis of Activity for Factor Xa Inhibitors Based on Monte Carlo Simulations. J. Med. Chem. 2003, 46, 5691-5699. ... Reuveni, H. et al., Toward a PKB Inhibitor: Modification of a Selective PKA Inhibitor by Rational Design, Biochemistry, 2002, ...
... feeding off its salmon hosts skin and blood. Blood is rich in nutrients, among these iron and heme. These are essential ... Blood-feeding might therefore alter parasite gene expression. We infected Atlantic salmon with salmon louse copepodids and ... Lice of similar instar age sampled from body parts with differential access to blood, namely from gills versus lice from skin ... We found that lice started feeding on blood when becoming mobile preadults if sitting on the fish body; however, they may ...
Targeting anticoagulant protein S rebalances coagulation in hemophilia.Protein S in joints is a novel pathophysiological ... and the targeting of coagulation inhibitors such as tissue factor pathway inhibitor (TFPI) or antithrombin as a strategy to ... Hemophilia as a defect of the tissue factor pathway of blood coagulation: effect of factors VIII and IX on factor X activation ... Protein S enhances the tissue factor pathway inhibitor inhibition of factor Xa but not its inhibition of factor VIIa-tissue ...
The impact of antithrombin III activity AT-III and on prophylactic enoxaparin serum trough anti-factor Xa concentration anti-Xa ... blood coagulation factor inhibitors * blood cells * blood Subject Categories: *Medicine and Medical Research ... The impact of antithrombin III activity AT-III and on prophylactic enoxaparin serum trough anti-factor Xa concentration anti-Xa ...
... do not adversely affect blood clotting function, says a new study from Brazil. ... "Menopause is associated with elevated levels of coagulation factors such as factors VII and VIII in addition to fibrinogen. ... "Our results suggest that soy isoflavone had no adverse effect on coagulation inhibitors because the changes observed did not ... A range of biomarkers related to blood clotting, including factors VII and X, fibrinogen, were measured at the start and end of ...
Blood Coagulation Factor Inhibitors [D23.113] * Blood Coagulation Factors [D23.119] * Chemotactic Factors [D23.125] ...
  • Thrombin contributes to the activation of factors V, VIII, and XIII (fibrin-stabilizing factor) and has an activating effect on platelets. (medscape.com)
  • This mechanism includes generation of activated protein C and protein S and the activation of tissue-type plasminogen activator (tPA), with subsequent inhibition of activated factors V and VIII, plasminogen activator inhibitor-1 (PAI-1), and thrombin-activated fibrinolysis inhibitor (TAFI). (medscape.com)
  • Your first dose of VONVENDI for each bleeding episode may be administered with a recombinant factor VIII as instructed by your healthcare provider. (hemophiliafed.org)
  • Your healthcare provider will instruct you whether additional doses of VONVENDI with or without recombinant factor VIII are needed. (hemophiliafed.org)
  • Your body can make neutralizing antibodies which inhibit von Willebrand factor and/or factor VIII from working correctly. (rxwiki.com)
  • These derivatives include albumin, factor VIII & IX, anti-inhibitor coagulation complex (AICC), immunoglobulins, including Rh immune globulin, alpha 1-proteinase inhibitor concentrate, and anti-thrombin III concentrate. (pharmiweb.com)
  • The factor VIII assay is a blood test to measure the activity of factor VIII. (medlineplus.gov)
  • Although nearly all procoagulants have an inhibitor, the inhibitor to factor VIII is the most common. (medscape.com)
  • They are present in factor VIII inhibitors, which are IgG antibodies against factor VIII, occur in hemophilia A (alloantibodies). (medscape.com)
  • An inhibitor exists for nearly every procoagulant, with the inhibitor to factor VIII being the most common. (medscape.com)
  • Detection of factor VIII inhibitor is accomplished by mixing the test plasma with a known amount of factor VIII. (medscape.com)
  • Following a 2-hour incubation period at 37°C, a factor VIII assay is used to determine residual factor VIII activity. (medscape.com)
  • The presence or absence of a factor VIII inhibitor can be determined through comparison of the difference in factor VIII activity between the incubation mixture and a control mixture. (medscape.com)
  • Menopause is associated with elevated levels of coagulation factors such as factors VII and VIII in addition to fibrinogen. (nutraingredients.com)
  • The story of one woman's battle against acquired factor VIII inhibitor. (dwsdirectory.net)
  • Acquired hemophilia is a rare but potentially life-threatening bleeding disorder caused by the development of autoantibodies (inhibitors) directed against plasma coagulation factors, most frequently factor VIII (FVIII). (medscape.com)
  • and one, factor VIII deficiency due to her postpartum acquisition of a factor VIII inhibitor. (cdc.gov)
  • In nine cases, factor VIII concentrates have been the only blood product reportedly used in the 5 years before diagnosis of AIDS. (cdc.gov)
  • The factor V-deficient patient with Kaposi's sarcoma had not used factor VIII concentrate products but had used large volumes of plasma and factor IX concentrates. (cdc.gov)
  • In cooperation with numerous hemophilia treatment centers and physicians, CDC has studied over 200 recipients of factor VIII and 36 recipients of factor IX concentrates containing materials from U.S. donors. (cdc.gov)
  • Rates of AIDS virus antibody prevalence were 74% for factor VIII recipients and 39% for factor IX recipients (3,4). (cdc.gov)
  • In studies done at CDC, in cooperation with Cutter Laboratories, AIDS virus was added to factor VIII concentrate (virus titer 10((5))) and the factor was lyophilized and heated to 68 C (154.4 F). The residual virus titer was determined by an infectivity assay (6). (cdc.gov)
  • While many U.S. hemophilia-associated AIDS patients have received blood products other than factor concentrates in the 5 years preceding their AIDS diagnosis, the occurrence of nine cases with no known risk factor or exposure other than the use of factor VIII preparations implicates these products as potential vehicles of AIDS transmission. (cdc.gov)
  • Title : Reagent substitutions in the Centers for Disease Control and Prevention Nijmegen-Bethesda assay for factor VIII inhibitors Personal Author(s) : Miller, C. H.;Payne, A. B.;Driggers, J.;Ellingsen, D.;Boylan, B.;Bean, C. J. (cdc.gov)
  • Originally, rFVIIa was developed for the treatment of bleeding complications in patients with hemophilia with alloantibodies (inhibitors) against exogenous factor VIII or IX. (medscape.com)
  • We describe the uses of rFVIIa in conditions unrelated to hemophilia and the treatment of acquired inhibitors of factors VIII and IX. (medscape.com)
  • This increase in the thrombin burst occurs after direct rFVIIa activation of factors IX and X on the surface of activated platelets (even in the absence of factor VIII or IX). (medscape.com)
  • Heparin targets multiple factors in the blood coagulation cascade, one of them being FXa. (wikipedia.org)
  • These factors activate each other in a blood coagulation cascade that occurs through two separate pathways that interact, the intrinsic and extrinsic pathway. (wikipedia.org)
  • In addition to the conversion of fibrinogen to fibrin, thrombin has numerous other effects relative to the coagulation cascade. (medscape.com)
  • Warfarin blocks the function of vitamin K and disrupts the coagulation cascade to reduce the frequency and extent of thrombus formation. (icliniq.com)
  • The mechanism of amplification in the blood coagulation cascade causes a small amount of factor Xa to produce a large amount of thrombin. (inteligand.com)
  • Targeting the coagulation cascade, clinical trials of Factor XIa inhibitors have shown promising results in preventing blood clot formation without increasing the instances of spontaneous and/or pathological bleeding events. (bvsalud.org)
  • It is a highly specific factor Xa inhibitor , a component of the blood coagulation cascade and it is the first available active factor Xa inhibitor which is taken orally. (labiotech.eu)
  • Pradaxa® is a direct thrombin inhibitor which disrupts the coagulation cascade preventing the development of clots in the blood. (alixarx.com)
  • Sarode R, Kessler CM. Coagulation and fibrinolysis. (medlineplus.gov)
  • Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 2007 Sep 18 (6): 559-64. (cdc.gov)
  • Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis 2014 Jul 25 (5): 416-21. (cdc.gov)
  • The decrease in fibrinolysis might be due to an increase in thrombin-activatable fibrinolysis inhibitor and an increase in factor XIIIa. (medscape.com)
  • Immunoblot analysis showed that PIXI is not the inhibitory domain of protease nexin II, a potent inhibitor of factor XIa also secreted from platelets. (qxmd.com)
  • PIXI can prevent stable complex formation between alpha 1-protease inhibitor and factor XIa light chain as demonstrated by SDS-polyacrylamide gel electrophoresis. (qxmd.com)
  • The inhibition by PIXI of factor XIa-catalyzed activation of factor IX and its capacity to prevent factor XIa inactivation by alpha 1-protease inhibitor, combined with the specificity of PIXI for factor XIa among serine proteases found in blood, suggest a role for PIXI in the regulation of intrinsic coagulation. (qxmd.com)
  • Factor Xa is an activated serine protease that occupies a key role in the blood coagulation pathway by converting prothrombin to thrombin. (wikipedia.org)
  • Factor XI is synthesized in the liver and megakaryocytes and is an 80-kd zymogen precursor of a serine protease. (medscape.com)
  • Binding of factor XIa to activated platelets localizes it to the site of clot formation and protects it from plasma protease inhibitors. (medscape.com)
  • Among the many protease inhibitors in plasma, tissue factor pathway inhibitor (TFPI) and antithrombin are the ones that are most specifically involved in inhibition of coagulation factors. (medscape.com)
  • Another potentially important regulator of the coagulation system, the protein Z/protein Z-dependent protease inhibitor (ZPI) system, is also emerging. (medscape.com)
  • Unlike other coagulation protease inhibitors, TFPI has inhibitory sites for factor Xa and for the factor VIIa/tissue factor (TF) complex, and it cannot inhibit the factor VIIa/TF complex without being bound to factor Xa. (medscape.com)
  • Coagulation factors XIa and Xa are inhibited by ZPI, an Mr 72,000 serine protease inhibitor. (medscape.com)
  • Factor Xa is a trypsin-like serine protease that converts the prothrombin zymogen to its active form thrombin and initiates the final stage of the blood coagulation pathway. (inteligand.com)
  • Factor Xa was identified as a promising target for the development of new anticoagulants in the early 1980s. (wikipedia.org)
  • Concomitant use of other drugs that affect hemostasis, such as non-steroidal anti-inflammatory drugs (NSAIDs), platelet inhibitors, other anticoagulants. (rxlist.com)
  • Hence, the direct inhibition factor Xa is considered as more favorable regarding the safety/efficacy ratio compared to other anticoagulants. (inteligand.com)
  • Therefore, inhibition of factor Xa has appeared as an attractive target for the development of new anticoagulants. (inteligand.com)
  • This medication falls within the class of anticoagulants or blood thinners and decreases your body's ability to clot, helping prevent harmful clots from forming. (buy-pharma.md)
  • Functioning to reduce a patient's ability to produce blood clots, prescription rates for anticoagulants have been steadily rising year-over-year both in the United States and abroad. (bvsalud.org)
  • Effect of NOS inhibitors and anticoagulants on nitric oxide production in a tissue-factor induced rat DIC model. (kanazawa-u.ac.jp)
  • The aim of this Learning Zone is to give an overview of blood coagulation , anticoagulation , bleeding risk and the various methods for the management and treatment of bleeding in patients taking anticoagulants. (medthority.com)
  • The Oral Anticoagulants section goes on to provide information on the options available for oral anticoagulation, such as factor Xa and IIa inhibitors. (medthority.com)
  • and details of non-vitamin K oral anticoagulants, such as factor Xa inhibitors, rivaroxaban, apixaban, edoxaban, and the factor IIa inhibitor dabigatran are all included in this section. (medthority.com)
  • Blood coagulation is a complex process by which the blood forms clots. (wikipedia.org)
  • In addition to checking for neutralizing antibodies, your doctor will also check your von Willebrand factor levels to make sure they are not too high, which could increase your risk of blood clots. (rxwiki.com)
  • Innohep may interact with dextran, aspirin and other salicylates, and other medication used to prevent blood clots . (rxlist.com)
  • Warfarin is an FDA-approved (Food and Drug Administration) drug that reduces the formation of blood clots. (icliniq.com)
  • Warfarin is an anticoagulant sold under various brand names, used to treat and prevent the risk of future blood clots, especially if one has had one previously, such as in venous thrombosis and pulmonary embolism. (icliniq.com)
  • The drug prevents blood clots in people with irregular, mechanical heart valves or blood clotting disorders such as thrombophilia. (icliniq.com)
  • Heparin Gel is an anticoagulant (blood thinner) widely used across a range of medical conditions and procedures, helping prevent blood clots from forming within catheters (small plastic tubes used to draw medication or blood from veins over an extended period). (buy-pharma.md)
  • Heparin is an anticoagulant (blood thinner) given subcutaneously or intravenously by healthcare providers to manage blood clots. (buy-pharma.md)
  • VONVENDI is infused into your blood stream, where it acts like your body's natural von Willebrand factor (VWF), helping to form clots, and helping your own FVIII to work. (vonvendi.com)
  • A low molecular weight platelet inhibitor of factor XIa (PIXI) has been purified 250-fold from releasates of washed and stimulated human platelets. (qxmd.com)
  • At the site of injury, where there is an exposure of blood under the endothelium, the platelets gather and immediately form a plug. (wikipedia.org)
  • This results in intravascular fibrin deposition and decreased levels of hemostatic components, including platelets, fibrinogen, and other clotting factors. (medscape.com)
  • Blood plasma is clear liquid component of blood in which red blood cells, white blood cells, and platelets are suspended. (pharmiweb.com)
  • Washed RBCs are free of almost all traces of plasma, most white blood cells, and platelets. (msdmanuals.com)
  • for exchange transfusions, for patients who require cytomegalovirus-negative blood that is unavailable, and possibly for the prevention of human leukocyte antigen (HLA) alloimmunization to help prevent refractoriness to platelet transfusion (failure to achieve the target level of blood platelets after platelet transfusion). (msdmanuals.com)
  • Fresh frozen plasma (FFP) is an unconcentrated source of all clotting factors without platelets. (msdmanuals.com)
  • Born,G.V. and Cross,M.J. (1963): The Aggregation of Blood Platelets. (9dok.net)
  • In response to vascular injury, circulating platelets adhere, aggregate, and provide cell surface phospholipids for the assembly of blood clotting enzyme complexes, thrombin activation, and fibrin formation. (medscape.com)
  • The rFVIIa seems to work in a TF-independent manner directly on factors IX and X on the phospholipid surface of activated platelets. (medscape.com)
  • rFVIIa is able to activate factor X on phospholipid vesicles, activated platelets, or monocytes independent of TF, although the TF-independent generation of thrombin is much less efficient than the TF-dependent thrombin generation by rFVIIa. (medscape.com)
  • 1 It is caused by a deficiency or defective function of VWF, one of several types of proteins in the blood that are needed for proper blood clotting. (hemophiliafed.org)
  • 1 Â Due to this defective function or deficiency, blood is not able to clot effectively in people with VWD. (hemophiliafed.org)
  • Deficiency of factor XI is a congenital condition that is inherited in an autosomal-recessive fashion. (medscape.com)
  • A deficiency of antithrombin increases the risk of thrombosis, revealing its importance as a functional inhibitor of the blood coagulation proteases. (medscape.com)
  • In a mouse model, protein Z deficiency does not cause thrombosis, but it does significantly increase the thrombotic tendency of mice who simultaneously express the factor V Leiden genotype, a known thrombotic risk factor. (medscape.com)
  • This article reports the rare occurrence and investigation of a specific anti-factor XI inhibitor that arose after fresh-frozen plasma infusion into a patient with previously unrecognized Factor XI deficiency. (mcmaster.ca)
  • With the exception of one 31-year-old factor V-deficient individual with Kaposi's sarcoma (and without risk factors for AIDS other than his hemophilia), each patient had at least one opportunistic infection suggestive of an underlying cellular immune deficiency. (cdc.gov)
  • also known as Hageman factor deficiency. (lu.se)
  • A low molecular weight platelet inhibitor of factor XIa: purification, characterization, and possible role in blood coagulation. (qxmd.com)
  • The theoretical mechanism for the coagulation and hemostatic effects of rFVIIa are discussed. (medscape.com)
  • Tissue factor (TF), or thromboplastin, is the primary activating moiety for the extrinsic pathway of coagulation. (medscape.com)
  • Detailed exploration of pathophysiology involving inflammatory status and bleeding symptoms between lipopolysaccharide- and tissue factor-induced disseminated intravascular coagulation in rats. (kanazawa-u.ac.jp)
  • Previous studies have suggested that air pollutants alter blood coagulation through the induction of the tissue factor. (cxcrinhibitor.com)
  • 2003): Alternatively spliced human tissue factor: a circulating, soluble, thrombogenic protein. (9dok.net)
  • Bom,V.J. and Bertina,R.M. (1990): The contributions of Ca 2+ , phospholipids and tissue-factor apoprotein to the activation of human blood-coagulation factor X by activated factor VII. (9dok.net)
  • Polymorphisms of the tissue factor pathway inhibitor gene are associated with venous thromboembolism in the antiphospholipid syndrome and carriers of factor V Leiden. (cdc.gov)
  • Total tissue factor pathway inhibitor and venous thrombosis. (cdc.gov)
  • Genetic polymorphisms and plasma levels of tissue factor and tissue factor pathway inhibitor in venous thromboembolism. (cdc.gov)
  • Single nucleotide polymorphisms in an intergenic chromosome 2q region associated with tissue factor pathway inhibitor plasma levels and venous thromboembolism. (cdc.gov)
  • Association of single nucleotide polymorphisms of tissue factor and tissue factor pathway inhibitor with venous thromboembolism in patients with lung cancer]. (cdc.gov)
  • In conjunction with inflammation, changes in tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) have been associated with increased risk of cardiovascular disease. (cdc.gov)
  • At the site of injury, tissue factor (TF) and factor VIIa activate factors X and IX. (medscape.com)
  • It was shown to exert inhibitory effect on purified Factor XI and XIa both in the activated and nonactivated partial thromboplastin time assay. (mcmaster.ca)
  • In the treatment of identified pathology in patients, modern technologies for the treatment of blood diseases with coagulation factors and erythropoietin and the treatment of inhibitory forms of hemophilia are used. (odbtomsk.ru)
  • CAMBRIDGE, Massachusetts, January 31, 2022 - Takeda Pharmaceutical Company Limited ("Takeda") today announced that the U.S. Food & Drug Administration (FDA) approved VONVENDI ® [von Willebrand factor (Recombinant)] for routine prophylaxis to reduce the frequency of bleeding episodes in patients with severe Type 3 von Willebrand disease (VWD) receiving on-demand therapy. (hemophiliafed.org)
  • VONVENDI is the only recombinant von Willebrand factor (VWF) replacement therapy, and the first and only treatment to reduce the frequency of bleeding episodes for severe Type 3 VWD approved by the FDA for routine prophylactic use. (hemophiliafed.org)
  • Vonvendi is the first FDA approved recombinant von Willebrand factor. (rxwiki.com)
  • Vonvendi is used to replace von Willebrand factor that is missing in people with von Willebrand disease. (rxwiki.com)
  • Your doctor will perform blood tests to check your von Willebrand factor activity and the presence of any inhibitors. (rxwiki.com)
  • VONVENDI is the first and only recombinant von Willebrand factor (rVWF) treatment approved for on-demand and surgery for adults with all types of VWD (Type 1, Type 2, and Type 3). (vonvendi.com)
  • Have been told that you have inhibitors to von Willebrand factor (because VONVENDI may not work for you). (vonvendi.com)
  • Other anticoagulant substance classes like vitamin K antagonists or thrombin inhibitors are considered to have a higher bleeding risk than factor Xa inhibitors. (inteligand.com)
  • [ 1 ] Factor XI enhances generation of thrombin at the platelet surface. (medscape.com)
  • Disseminated Intravascular Coagulation (DIC) Disseminated intravascular coagulation (DIC) involves abnormal, excessive generation of thrombin and fibrin in the circulating blood. (msdmanuals.com)
  • Inhibition of factor Xa leads to antithrombotic effects by decreasing the amount of thrombin. (wikipedia.org)
  • The authors suggested that the risk of venous thrombosis and ischemic stroke may be significantly reduced by pharmacologic inhibition of factor XI, with no clear evidence demonstrating that this therapy would increase the risk for major bleeding. (medscape.com)
  • The presence of protein Z, a vitamin K-dependent plasma protein, increases its inhibition of factor Xa over 1000-fold. (medscape.com)
  • Antistasin is a polypeptide and a potent Xa inhibitor. (wikipedia.org)
  • In this context, PKB inhibitors have been demonstrated to be potent agents against cancer. (inteligand.com)
  • Ragni MV. Hemorrhagic disorders: coagulation factor deficiencies. (medlineplus.gov)
  • Since then, the number of U.S. patients with underlying coagulation disorders who develop AIDS has increased each year. (cdc.gov)
  • Rivaroxaban (Xarelto) was the first approved FXa inhibitor to become commercially available in Europe and Canada in 2008. (wikipedia.org)
  • Today there are four factor Xa inhibitors marketed: rivaroxaban, apixaban, edoxaban and betrixaban. (wikipedia.org)
  • Xarelto ( Rivaroxaban) is a blood thinner, which was originally developed by Bayer and is marketed by J&J in the US. (labiotech.eu)
  • Arterial antithrombotic and bleeding time effects of apixaban, a direct factor Xa inhibitor, in combination with antiplatelet therapy in rabbits. (sigmaaldrich.com)
  • Consumption coagulopathy, better known as disseminated intravascular coagulation (DIC), is not a diagnosis. (medscape.com)
  • COVID-19 associated coagulopathy and disseminated intravascular coagulation. (kanazawa-u.ac.jp)
  • The gene for factor XI is located on chromosome 4. (medscape.com)
  • A range of biomarkers related to blood clotting, including factors VII and X, fibrinogen, were measured at the start and end of study. (nutraingredients.com)
  • The inhibitor does not appear to be one of the platelet-specific, heparin-binding proteins, since it neither bound to nor was affected by heparin. (qxmd.com)
  • Potency is determined by means of a biological assay and interpreted by the first International Low Molecular Weight Heparin Standard as units of anti-factor Xa (anti-Xa) activity per milligram. (rxlist.com)
  • Unless it is complexed to TF in the presence of heparin or cell surface glycosaminoglycans, factor VIIa resists being inhibited by antithrombin. (medscape.com)
  • At an inhalation method of administration (inhalation) it is absorbed by alveolar macrophages, an endothelium of capillaries, big blood and absorbent vessels: these cells are the main place of deposition of heparin from which about it is gradually released, maintaining necessary concentration in blood plasma. (rxeli.com)
  • Participation in metabolism of a platelet factor of IV (anti-heparin factor) and also linking of heparin with the system of macrophages explain a fast biological inactivation and short duration of action. (rxeli.com)
  • The mechanism of effect of heparin is based first of all on its linking with antithrombin III - inhibitor of the activated blood-coagulation factors: thrombin, IXa, Xa, XIa, XIIa (the ability to inhibit thrombin and the activated factor of X is especially important). (rxeli.com)
  • Heparin is a glycosaminoglycan anticoagulant produced by various species, including hepatocytes, mast cells, and other hepatic and pulmonary cells, that works by inactivating thrombin and factor Xa. (buy-pharma.md)
  • Heparin is an effective inhibitor against blood coagulation by inactivating these coagulation components. (buy-pharma.md)
  • Heparin plays a significant role in blood plasma as a primary anticoagulant by prolonging activated partial thromboplastin time (aPTT) by inactivating thrombin. (buy-pharma.md)
  • Heparin works by inhibiting blood-clotting proteins found in your body. (buy-pharma.md)
  • Heparin works by blocking the activity of certain coagulation factors, particularly Factor Xa and IIa. (buy-pharma.md)
  • Furthermore, heparin prevents activation of fibrin stabilizing factors. (buy-pharma.md)
  • [ 10 ] which, though significant, are not as severe as those seen in hemophilia A or hemophilia B . This finding reflects the important role factor XI plays in hemostasis. (medscape.com)
  • The factors that drive the growth of the blood plasma derivatives market include increase in prevalence of life-threatening diseases such as immunodeficiency diseases and hemophilia, rise in awareness towards blood & plasma donation, upsurge in geriatric population, and growth in adoption of blood plasma derivatives products. (pharmiweb.com)
  • Eradication of the inhibitor with immunosuppression should be initiated as soon as the diagnosis of acquired hemophilia is established. (medscape.com)
  • [ 1 ] Because inhibitors to FVIII are the most frequently observed in clinical practice, this article focuses on the etiology and management of FVIII autoantibody inhibitors, or acquired hemophilia A. (medscape.com)
  • Three patients are known to have had risk factors for AIDS other than hemophilia. (cdc.gov)
  • These nine persons had no risk factors for AIDS other than hemophilia. (cdc.gov)
  • The possibility of blood or blood products being vehicles for AIDS transmission to hemophilia patients has been supported by the finding of risk of acquisition of AIDS for intravenous drug abusers (7) and, subsequently, by reports of transfusion-associated AIDS cases (8). (cdc.gov)
  • Recombinant factor VIIa (rFVIIa) has become available for treating people with hemophilia with inhibitors who experience bleeding or require surgery. (medscape.com)
  • [ 12 ] Recently, the effectiveness and safety of rFVIIa in patients with hemophilia with inhibitors has been reported in the hemophilia research society registry. (medscape.com)
  • At present, the only US Food and Drug Administration-approved use of rFVIIa is for the treatment of patients with hemophilia with inhibitors. (medscape.com)
  • It can deplete functional vitamin K reserves and thereby reduce the synthesis of active clotting factors by competitively inhibiting multi-unit vitamin K epoxide reductase complex. (icliniq.com)
  • In 2008 the first direct Xa inhibitor was approved for clinical use. (wikipedia.org)
  • The clinical picture in DIC is commonly one of bleeding with signs of shock out of proportion to the amount of blood loss. (medscape.com)
  • Additionally, medical students encountered X-ray stereotypes more than Inhibitors,research,lifescience,medical other modalities in clinical settings. (cxcrinhibitor.com)
  • This is one of the proteins in the body that helps the blood clot. (medlineplus.gov)
  • Amino Acids, Peptides, and Proteins Proteins Blood Proteins Protein S Amino Acids, Peptides, and Proteins Proteins Glycoproteins Protein S Biological Factors Blood Coagulation Factor Inhibitors Protein S, anabolen kopen achteraf betalen. (nourishmialmamedicalnutritiontherapy.com)
  • Communication with proteins of blood plasma - up to 95%, distribution volume very small - 0.06 l/kg (does not leave a vascular bed because of strong linking with proteins of blood plasma). (rxeli.com)
  • The fusion proteins bind VEGFs thereby inhibiting their activity and thus growth of blood vessels within the eye. (labiotech.eu)
  • The transfer of the major egg yolk proteins such as Very Low Density Lipoproteins (VLDL) containing essentially apovitellenin and apolipoprotein-B, but also vitellogenins and some other plasma proteins from the blood such as serum albumin to the interstitial fluid of the thecae is possible due to the presence of broad discontinuities in the capillary endothelium. (biomedcentral.com)
  • The coagulation of blood is maintained by cellular components and soluble plasma proteins. (medscape.com)
  • However, TFPI and antithrombin have a similar rate of reaction with factor Xa in plasma. (medscape.com)
  • The impact of antithrombin III activity AT-III and on prophylactic enoxaparin serum trough anti-factor Xa concentration anti-Xa has not been evaluated. (dtic.mil)
  • During the process, increased platelet aggregation and coagulation. (msdmanuals.com)
  • Prothrombin prolongs multiple coagulation tests, such as activated partial thromboplastin time (aPTT), prothrombin time and whole blood clotting time. (buy-pharma.md)
  • C polymorphism in intron 7 of the TFPI gene influences the risk of venous thromboembolism, independently of the factor V Leiden and prothrombin mutations. (cdc.gov)
  • This antibody inhibits the vascular endothelial growth factor A ( VEGF-A ) and thereby blocks angiogenesis , one of the hallmarks of cancer. (labiotech.eu)
  • The IgG fraction of the patient's plasma that contained anti-Factor XI antibody was isolated by chromatography on DEAE-Affigel and concentrated. (mcmaster.ca)
  • A reduction in coagulation time can increase the risk of cardiovascular diseases. (cxcrinhibitor.com)
  • A recently published study evaluated the thermostability of murine retroviruses inocculated into factor concentrates, using a cell transformation assay (5). (cdc.gov)
  • CNV and related manifestations (subretinal hemorrhage, detachment of the retinal pigment epithelium, and fibrovascular disciform scarring) are PI3K inhibitor the most common causes of severe vision loss resulting from AMD.5 Untreated, exudative AMD can lead to progressive and substantial loss of central vision and a reduction in quality of life. (cxcrinhibitor.com)
  • When considering noncardiac surgery, these factors and the need to weigh the risk of hemorrhage against that of thromboembolism must be analyzed on an individual patient basis. (medscape.com)
  • This has become the case for treatment of hemorrhage with recombinant factor VIIa (rFVIIa). (medscape.com)
  • It is an essential part of hemostasis and works by stopping blood loss from damaged blood vessels. (wikipedia.org)
  • [ 7 ] In a mouse model, factor XI appears to play a greater role in thrombosis than in hemostasis. (medscape.com)
  • Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand. (slideshare.net)
  • Hemostasis is a physiologic mechanism that maintains blood in a fluid state within the circulation. (medscape.com)
  • In mice, knockout of the gene for factor XI does not lead to death in utero. (medscape.com)
  • Blood-feeding might therefore alter parasite gene expression. (biomedcentral.com)
  • Lice of similar instar age sampled from body parts with differential access to blood, namely from gills versus lice from skin epidermis, were analysed for gene expression by RNA-sequencing in samples taken at day 10 for both experiments and at day 18 for one of the experiments. (biomedcentral.com)
  • Gill settlement results in an alteration in gene expression and a premature onset of blood-feeding likely causes the parasite to develop at a slower pace. (biomedcentral.com)
  • Lung inflammation and cardiovascular outcomes - whole blood gene expression studies in a lipopolysaccharide (LPS) pharyngeal aspiration mouse model. (cdc.gov)
  • Interestingly, whole blood showed similar gene expression induction of macrophage-inflammatory protein-2 (MIP-2) and tumor necrosis factor alpha (TNFá) following LPS by pharyngeal aspiration or IP injection. (cdc.gov)
  • Neither TF nor PAI-1 gene expression was elevated in blood following IP LPS although PAI-1 was strongly induced in the heart and lung. (cdc.gov)
  • In conclusion, lung inflammation results in activation of inflammatory and coagulation biomarkers associated with cardiovascular diseases and blood gene expression studies can identify biomarkers which predict cardiovascular outcomes in occupational-related respiratory exposures. (cdc.gov)
  • On the other hand, a study by Georgi et al indicated that in persons genetically disposed to lower concentrations of factor XI, the risk of venous thrombosis and ischemic stroke are reduced. (medscape.com)
  • Employing data related to genetic variants that alter factor XI levels, the investigators found that in these individuals, the odds ratios (ORs) for venous thrombosis and ischemic stroke were 0.1 and 0.47, respectively, with the OR for major bleeding being 0.7. (medscape.com)
  • Moreover, the results indicated that among patients with lower factor XI levels, the absolute risk reductions are greater in individuals at high risk for thrombosis, including those with atrial fibrillation or cancer. (medscape.com)
  • Innohep (tinzaparin) is a blood thinner ( anticoagulant ) used together with warfarin ( Coumadin ) to treat a type of blood clot called deep vein thrombosis , or DVT. (rxlist.com)
  • The prevention of blood coagulation is a major topic considering serious physiological reactions of undesired blood clotting that can lead to myocardial infarction, stroke, deep vein thrombosis and pulmonary embolism. (inteligand.com)
  • Remember Xarelto and Eliquis are Factor Xa inhibitors. (alixarx.com)
  • A study by Kyrle et al reported that in patients who had experienced an unprovoked venous thromboembolism (VTE), the 10-year probability of VTE recurrence was 31% in individuals below the 34th percentile for factor XIa, compared with 43% for those between the 34th and 67th percentiles, and 41% for patients in a higher percentile. (medscape.com)
  • An amount of PIXI which inhibited by 50% factor XIa cleavage of the chromogenic substrate S2366 (Pyr-Glu-Pro-Arg-pNA-2H2O) only slightly inhibited (5-9%) factor XIIa, plasma kallikrein, plasmin, and activated protein C and did not inhibit factor Xa, thrombin, tPA, or trypsin, suggesting specificity for factor XIa. (qxmd.com)
  • Plasma derivatives are products that are derived from blood plasma on fractionation, and are widely used to treat variety of diseases. (pharmiweb.com)
  • Rückerl et al.25 suggested that air pollutants can increase the occurrence of cardiovascular diseases by affecting coagulation state. (cxcrinhibitor.com)
  • This technology avoids the risk of spreading diseases through infected human blood. (vonvendi.com)
  • Even where hyper-homocysteinaemia is a well established risk factor, we do not know the exact mechanism whereby high homocysteine levels cause thromboembolic disease [4] and the issue has not been studied in Sudanese patients, where the prevalence of these diseases is assumed to be low. (who.int)
  • There are limited data, however, on fluctuations in homocysteine levels in these conditions, particularly malaria [5,6], and in protein-energy malnutrition (PEM) [7] to determine whether hyper-homocysteinaemia is also risk factor in these diseases. (who.int)
  • Div of Host Factors, Center for Infectious Diseases, CDC. (cdc.gov)
  • Recurrence referred to any recurrence is also risk factor in these diseases. (who.int)
  • Its diagnosis is based on finding a low plasma activity of the factor in coagulating assays. (lu.se)
  • Four drugs from the class of direct Xa inhibitors are marketed worldwide. (wikipedia.org)
  • Therefore, a new group of PKB inhibitors, 'Akstatins' are considered as potentially attractive drugs for the inhibition of PKB. (inteligand.com)
  • One emerging category of anticoagulant drugs are Factor XI/XIa (FXI) inhibitors. (bvsalud.org)
  • It can be activated in vitro by activated factor XII (XIIa). (medscape.com)
  • As a group, they also inhibit enzymes involved in processes other than blood coagulation, such as those from the complement system, fibrinolytic enzyme system, blood cells, and bacteria. (bvsalud.org)
  • Kinetic analyses of the effect of PIXI on factor XIa activity demonstrated mixed-type, noncompetitive inhibition of S2366 cleavage and of factor IX activation with Ki's of 7 x 10(-8) and 3.8 x 10(-9) M, respectively. (qxmd.com)
  • The mean tinzaparin sodium anti-factor Xa activity is approximately 100 IU per milligram. (rxlist.com)
  • [ 10 ] Protein Z/ZPI's physiologic activity in the coagulation system is unclear. (medscape.com)
  • Isoflavones from soy, despite having weak oestrogenic activity, do not adversely affect blood clotting function, says a new study from Brazil. (nutraingredients.com)
  • Increases a renal blood stream, increases brain vascular resistance, reduces activity of brain hyaluronidase, activates lipoproteinlipase and possesses hypolipidemic action. (rxeli.com)
  • Body mass, calcium nutriture, physical activity, growth and sex steroid hormones, and genetic factors are all thought to be important determinants of bone mass although the relative contribution of each remains controversial. (stanford.edu)
  • At 5.9% Growth Rate Blood Plasma Derivatives Market Expec. (pharmiweb.com)
  • The report on the global blood plasma derivatives market highlights that the market is expected to reach $23,613 million in 2016, and is projected to reach $44,333 million in 2023, registering a CAGR of 9.3% from 2017 to 2023. (pharmiweb.com)
  • The blood plasma derivatives report offers an in-depth analysis of the Covid-19 impact on various market segments and countries. (pharmiweb.com)
  • North America was the leading revenue contributor to the global blood plasma derivatives market in 2016, and is expected to dominate the market during the forecast period. (pharmiweb.com)
  • The albumin segment accounted for nearly one-sixth share of the global blood plasma derivatives market in 2016. (pharmiweb.com)
  • Longitudinal unbiased proteomic analysis of plasma and single-cell transcriptomics of peripheral blood cells conducted prior to and at multiple times after convalescent plasma transfusion identified the key biological processes associated with the transition from severe disease to disease-free state. (frontiersin.org)
  • Such leaky, abnormal blood vessels are characteristic for this disease. (labiotech.eu)
  • Parasite development and presence of host blood in their intestines were determined. (biomedcentral.com)
  • TF binds to factor VII and converts factor VII to factor VIIa. (medscape.com)
  • The resultant dimeric TF-factor VIIa complex then activates factors X and IX. (medscape.com)
  • Warfarin is a vitamin K antagonist that makes blood flow easily through the blood vessels. (icliniq.com)
  • Purple toes syndrome (blockage in the small blood vessels of the foot). (icliniq.com)
  • The choice is determined by the agents' availability and cost, and-for rpFVIII-baseline anti-porcine FVIII inhibitor titer and ability to monitor rpFVIII. (medscape.com)
  • of earlier education on radiology with regard to the basic science of radiology and the values, indications and limitations of imaging modalities and lack of appropriate guidelines.5 According to our close observations, other reasons could be that Inhibitors,research,lifescience,medical our medical students learn radiology concepts theoretically rather than practically in their radiology course. (cxcrinhibitor.com)
  • In our investigation, the majority of participants had an excellent knowledge level in terms of indications Inhibitors,research,lifescience,medical for X-ray modality. (cxcrinhibitor.com)
  • Directly targeting factor Xa is suggested to be an effective approach to anticoagulation. (wikipedia.org)
  • This trait is an asymptomatic anomaly of in vitro blood coagulation. (lu.se)
  • ABSTRACT This study investigated the role of hyperhomocysteinaemia as a risk factor in Sudanese adults suffering from cardiovascular disease or malaria and children with protein-energy malnutrition. (who.int)
  • This test is used to find the cause of too much bleeding (decreased blood clotting). (medlineplus.gov)
  • Thrombin catalyzes enzymatic reactions that result in the formation of fibrin, the important binding part for blood clotting. (inteligand.com)
  • In order to verify the role of isoflavones on blood clotting factors, the researchers recruited 47 postmenopausal women to receive either a daily isoflavone supplement (40 mg) or a casein placebo (40 mg) for six months. (nutraingredients.com)
  • Whole blood can provide improved oxygen-carrying capacity, volume expansion, and replacement of clotting factors and was previously recommended for rapid massive blood loss. (msdmanuals.com)
  • Vonvendi may increase your risk of developing a blood clot, which could lead to pulmonary embolism (a clot in your lungs), stroke, or heart attack. (rxwiki.com)
  • This condition sometimes occurs with a blood clot in lungs ( pulmonary embolism , or PE). (rxlist.com)
  • Endotoxin, tumor necrosis factor (TNF), interleukin-1 (IL-1), and other inflammatory mediators induce expression of TF in endothelial cells and monocytes, where only small amounts are normally expressed. (medscape.com)
  • Direct Xa inhibitors are just as efficacious as LMWH and warfarin but they are given orally and don't need as strict monitoring. (wikipedia.org)
  • In 1990 another naturally occurring Xa inhibitor was isolated, tick anticoagulant peptide (TAP) from extracts of the tick Ornithodoros moubata. (wikipedia.org)