Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process.Factor XIII: 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.Factor IX: 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).Factor X: 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.Factor Xa: 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.Factor VII: 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.Factor VIII: 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.Factor XIa: 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.Blood Coagulation Tests: Laboratory tests for evaluating the individual's clotting mechanism.Thromboplastin: 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.Factor VIIa: Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.Blood Coagulation Disorders: 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.Factor XI: 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.Factor IXa: 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.Coagulants: Agents that cause clotting.Factor V: 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.Prothrombin: 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.Disseminated Intravascular Coagulation: 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.Partial Thromboplastin Time: 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.Prothrombin Time: 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.Thrombin: An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.Factor XII: 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.Factor Va: Activated form of factor V. It is an essential cofactor for the activation of prothrombin catalyzed by factor Xa.Blood Coagulation Factor Inhibitors: 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.Protein C: 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.Factor VIIIa: 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.1-Carboxyglutamic Acid: 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.Hemophilia B: 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)Vitamin K: 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.Transglutaminases: 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.Hemophilia A: 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.Antithrombin III: 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.Arcidae: A family of ark shell mollusks, in the class BIVALVIA. They have soft bodies with platelike GILLS enclosed within two shells hinged together.Fibrinogen: 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.Thrombelastography: Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.Antithrombins: 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.Fibrin: A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.Anticoagulants: Agents that prevent clotting.Amino Acid Sequence: 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.Hemostasis: 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.Molecular Sequence Data: 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.Vitamin K Deficiency: 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)Benzamidines: Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Factor XII Deficiency: 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.Fibrinolysis: The natural enzymatic dissolution of FIBRIN.Factor XIIa: 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.Whole Blood Coagulation Time: The time required by whole blood to produce a visible clot.Kinetics: The rate dynamics in chemical or physical systems.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Blood Coagulation Disorders, Inherited: Hemorrhagic and thrombotic disorders that occur as a consequence of inherited abnormalities in blood coagulation.Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.Factor XI Deficiency: A hereditary deficiency of blood coagulation factor XI (also known as plasma thromboplastin antecedent or PTA or antihemophilic factor C) resulting in a systemic blood-clotting defect called hemophilia C or Rosenthal's syndrome, that may resemble classical hemophilia.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Factor XIII Deficiency: A deficiency of blood coagulation FACTOR XIII or fibrin stabilizing factor (FSF) that prevents blood clot formation and results in a clinical hemorrhagic diathesis.Coagulation Protein Disorders: Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.Thrombin Time: Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Protein S: The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Enzyme Precursors: Physiologically inactive substances that can be converted to active enzymes.Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Hydroxyethyl Starch Derivatives: Starches that have been chemically modified so that a percentage of OH groups are substituted with 2-hydroxyethyl ether groups.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Fibrin Fibrinogen Degradation Products: Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Factor XIIIa: Activated form of FACTOR XIII, a transglutaminase, which stabilizes the formation of the fibrin polymer (clot) culminating the blood coagulation cascade.Heparin: A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.Plasma Substitutes: Any liquid used to replace blood plasma, usually a saline solution, often with serum albumins, dextrans or other preparations. These substances do not enhance the oxygen- carrying capacity of blood, but merely replace the volume. They are also used to treat dehydration.Factor X Deficiency: Blood coagulation disorder usually inherited as an autosomal recessive trait, though it can be acquired. It is characterized by defective activity in both the intrinsic and extrinsic pathways, impaired thromboplastin time, and impaired prothrombin consumption.Cattle: Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.Hypoprothrombinemias: Absence or reduced levels of PROTHROMBIN in the blood.Kaolin: The most common mineral of a group of hydrated aluminum silicates, approximately H2Al2Si2O8-H2O. It is prepared for pharmaceutical and medicinal purposes by levigating with water to remove sand, etc. (From Merck Index, 11th ed) The name is derived from Kao-ling (Chinese: "high ridge"), the original site. (From Grant & Hackh's Chemical Dictionary, 5th ed)Factor V Deficiency: A deficiency of blood coagulation factor V (known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as Owren's disease or parahemophilia. It varies greatly in severity. Factor V deficiency is an autosomal recessive trait. (Dorland, 27th ed)Molecular Weight: The sum of the weight of all the atoms in a molecule.Factor VII Deficiency: An autosomal recessive characteristic or a coagulation disorder acquired in association with VITAMIN K DEFICIENCY. FACTOR VII is a Vitamin K dependent glycoprotein essential to the extrinsic pathway of coagulation.Prekallikrein: A plasma protein which is the precursor of kallikrein. Plasma that is deficient in prekallikrein has been found to be abnormal in thromboplastin formation, kinin generation, evolution of a permeability globulin, and plasmin formation. The absence of prekallikrein in plasma leads to Fletcher factor deficiency, a congenital disease.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.Hemorrhagic Disorders: Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Fibrinopeptide A: Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Hemostatics: Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an artificial clot or by providing a mechanical matrix that facilitates clotting when applied directly to the bleeding surface. These agents function more at the capillary level and are not effective at stemming arterial or venous bleeding under any significant intravascular pressure.Crystallography, X-Ray: The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.Plasma: The residual portion of BLOOD that is left after removal of BLOOD CELLS by CENTRIFUGATION without prior BLOOD COAGULATION.Hemorrhage: Bleeding or escape of blood from a vessel.Carbon-Carbon Ligases: Enzymes that catalyze the joining of two molecules by the formation of a carbon-carbon bond. These are the carboxylating enzymes and are mostly biotinyl-proteins. EC 6.4.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Platelet Activation: A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Reptilian Proteins: Proteins obtained from species of REPTILES.alpha-2-Antiplasmin: A member of the serpin superfamily found in plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin.Argon Plasma Coagulation: A method of tissue ablation and bleeding control that uses ARGON plasma (ionized argon gas) to deliver a current of thermocoagulating energy to the area of tissue to be coagulated.von Willebrand Factor: A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.Genetic Vectors: DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.Thrombophilia: A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Epidermal Growth Factor: A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.Macromolecular Substances: Compounds and molecular complexes that consist of very large numbers of atoms and are generally over 500 kDa in size. In biological systems macromolecular substances usually can be visualized using ELECTRON MICROSCOPY and are distinguished from ORGANELLES by the lack of a membrane structure.Kallikreins: Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 3.4.21.34), TISSUE KALLIKREIN (EC 3.4.21.35), and PROSTATE-SPECIFIC ANTIGEN (EC 3.4.21.77).Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Kininogens: Endogenous peptides present in most body fluids. Certain enzymes convert them to active KININS which are involved in inflammation, blood clotting, complement reactions, etc. Kininogens belong to the cystatin superfamily. They are cysteine proteinase inhibitors. HIGH-MOLECULAR-WEIGHT KININOGEN; (HMWK); is split by plasma kallikrein to produce BRADYKININ. LOW-MOLECULAR-WEIGHT KININOGEN; (LMWK); is split by tissue kallikrein to produce KALLIDIN.Crotalid Venoms: Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Receptor, PAR-1: A thrombin receptor subtype that couples to HETEROTRIMERIC GTP-BINDING PROTEINS resulting in the activation of a variety of signaling mechanisms including decreased intracellular CYCLIC AMP, increased TYPE C PHOSPHOLIPASES and increased PHOSPHOLIPASE A2.Platelet Count: The number of PLATELETS per unit volume in a sample of venous BLOOD.Afibrinogenemia: A deficiency or absence of FIBRINOGEN in the blood.Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Snake Venoms: Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.Receptors, Thrombin: A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.Phosphatidylserines: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.Antifibrinolytic Agents: Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.Thrombophlebitis: Inflammation of a vein associated with a blood clot (THROMBUS).Horseshoe Crabs: An arthropod subclass (Xiphosura) comprising the North American (Limulus) and Asiatic (Tachypleus) genera of horseshoe crabs.Plasminogen: Precursor of plasmin (FIBRINOLYSIN). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent.Hemodilution: Reduction of blood viscosity usually by the addition of cell free solutions. Used clinically (1) in states of impaired microcirculation, (2) for replacement of intraoperative blood loss without homologous blood transfusion, and (3) in cardiopulmonary bypass and hypothermia.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Viperidae: A family of snakes comprising three subfamilies: Azemiopinae (the mountain viper, the sole member of this subfamily), Viperinae (true vipers), and Crotalinae (pit vipers). They are widespread throughout the world, being found in the United States, Central and South America, Europe, Asia and Africa. Their venoms act on the blood (hemotoxic) as compared to the venom of elapids which act on the nervous system (neurotoxic). (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, pp333-36)Laser Coagulation: The use of green light-producing LASERS to stop bleeding. The green light is selectively absorbed by HEMOGLOBIN, thus triggering BLOOD COAGULATION.Surface Plasmon Resonance: A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding.Russell's Viper: A genus of snakes of the family VIPERIDAE. It is distributed in West Pakistan, most of India, Burma, Ceylon, Thailand, southeast China, Taiwan, and a few islands of Indonesia. It hisses loudly when disturbed and strikes with great force and speed. Very prolific, it gives birth to 20-60 young. This viper is the leading cause of snakebite in India and Burma. (Moore: Poisonous Snakes of the World, 1980, p127)Hirudins: Single-chain polypeptides of about 65 amino acids (7 kDa) from LEECHES that have a neutral hydrophobic N terminus, an acidic hydrophilic C terminus, and a compact, hydrophobic core region. Recombinant hirudins lack tyr-63 sulfation and are referred to as 'desulfato-hirudins'. They form a stable non-covalent complex with ALPHA-THROMBIN, thereby abolishing its ability to cleave FIBRINOGEN.Arthropod Proteins: Proteins synthesized by organisms belonging to the phylum ARTHROPODA. Included in this heading are proteins from the subdivisions ARACHNIDA; CRUSTACEA; and HORSESHOE CRABS. Note that a separate heading for INSECT PROTEINS is listed under this heading.Venous Thrombosis: The formation or presence of a blood clot (THROMBUS) within a vein.Invertebrate Hormones: Hormones produced by invertebrates, usually insects, mollusks, annelids, and helminths.Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Peptide Hydrolases: Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.Polygeline: A 3.5 per cent colloidal solution containing urea-cross-linked polymerized peptides. It has a molecular weight of approximately 35,000 and is prepared from gelatin and electrolytes. The polymeric solution is used as a plasma expander.Electrocoagulation: Procedures using an electrically heated wire or scalpel to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. It is different from ELECTROSURGERY which is used more for cutting tissue than destroying and in which the patient is part of the electric circuit.Viper Venoms: Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.Platelet Adhesiveness: The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.Thromboembolism: Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.Fibrinolysin: A product of the lysis of plasminogen (profibrinolysin) by PLASMINOGEN activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins.Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.Vitamin K Epoxide Reductases: OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.Plasma Kallikrein: A peptidohydrolytic enzyme that is formed from PREKALLIKREIN by FACTOR XIIA. It activates FACTOR XII; FACTOR VII; and PLASMINOGEN. It is selective for both ARGININE and to a lesser extent LYSINE bonds. EC 3.4.21.34.Snakes: Limbless REPTILES of the suborder Serpentes.Cadaverine: A foul-smelling diamine formed by bacterial decarboxylation of lysine.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Isoflurophate: A di-isopropyl-fluorophosphate which is an irreversible cholinesterase inhibitor used to investigate the NERVOUS SYSTEM.Point Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.Artocarpus: A plant genus of the family MORACEAE. Puag-haad extract, from A. lakoocha, contains STILBENES and related 4-substituted RESORCINOLS.Trimeresurus: A genus of snakes of the family VIPERIDAE. About 30 species are currently recognized, found in southeast Asia and adjacent island chains. The Okinawa habu frequently enters dwellings in search of rats and mice; the Chinese habu is often found in suburban and agricultural areas. They are quite irritable. (Moore: Poisonous Snakes of the World, 1980, p136)Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Sulfoglycosphingolipids: GLYCOSPHINGOLIPIDS with a sulfate group esterified to one of the sugar groups.Plasminogen Activator Inhibitor 1: A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.Activated Protein C Resistance: A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.Calcium Chloride: A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.Binding, Competitive: The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.Vitamin K Deficiency Bleeding: Hemorrhage caused by vitamin K deficiency.Protein C Deficiency: An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)Blood Loss, Surgical: Loss of blood during a surgical procedure.Blood Transfusion: The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Serpins: A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.Chromogenic Compounds: Colorless, endogenous or exogenous pigment precursors that may be transformed by biological mechanisms into colored compounds; used in biochemical assays and in diagnosis as indicators, especially in the form of enzyme substrates. Synonym: chromogens (not to be confused with pigment-synthesizing bacteria also called chromogens).Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Strongylida: An order of nematodes of the subclass SECERNENTEA. Characteristics include an H-shaped excretory system with two subventral glands.Ellagic Acid: A fused four ring compound occurring free or combined in galls. Isolated from the kino of Eucalyptus maculata Hook and E. Hemipholia F. Muell. Activates Factor XII of the blood clotting system which also causes kinin release; used in research and as a dye.Chromatography, Affinity: A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Cephapirin: Cephalosporin antibiotic, partly plasma-bound, that is effective against gram-negative and gram-positive organisms.CHO Cells: CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.Oligopeptides: Peptides composed of between two and twelve amino acids.Streptomycetaceae: A family of soil bacteria. It also includes some parasitic forms.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Mutagenesis, Site-Directed: Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.Disulfides: Chemical groups containing the covalent disulfide bonds -S-S-. The sulfur atoms can be bound to inorganic or organic moieties.Sequence Alignment: The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.Tosylarginine Methyl Ester: Arginine derivative which is a substrate for many proteolytic enzymes. As a substrate for the esterase from the first component of complement, it inhibits the action of C(l) on C(4).Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Receptors, Proteinase-Activated: A class of receptors that are activated by the action of PROTEINASES. The most notable examples are the THROMBIN RECEPTORS. The receptors contain cryptic ligands that are exposed upon the selective proteolysis of specific N-terminal cleavage sites.Endopeptidases: A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.Umbilical Veins: Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).Infant, Postmature: An infant born at or after 42 weeks of gestation.Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator.Viscoelastic Substances: Substances that display the physical properties of ELASTICITY and VISCOSITY. The dual-nature of these substances causes them to resist applied forces in a time-dependent manner.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Swine: Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).Lymphangiosarcoma: A malignant tumor originating from the endothelial cells of lymphatic vessels. Most lymphangiosarcomas arise in an arm secondary to radical mastectomy but they sometimes complicate idiopathic lymphedema. The lymphedema has usually been present for 6 to 10 years before malignant changes develop. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1866)Receptor, PAR-2: A G-protein-coupled, proteinase-activated receptor that is expressed in a variety of tissues including ENDOTHELIUM; LEUKOCYTES; and the GASTROINTESTINAL TRACT. The receptor is activated by TRYPSIN, which cleaves off the N-terminal peptide from the receptor. The new N-terminal peptide is a cryptic ligand for the receptor. The uncleaved receptor can also be activated by the N-terminal peptide present on the activated THROMBIN RECEPTOR and by small synthetic peptides that contain the unmasked N-terminal sequence.

Evidence suggesting the regulation of a coagulation factor levels in rabbits by a transferable plasma agent. (1/1153)

New Zealand white rabbits were given 30 ml of goat serum intravenously. This procedure resulted in an immediate decrease in platelet count, fibrinogen, and levels of coagulation factors II, V, VII, and X, due to consumption coagulopathy. These factors returned toward baseline levels approximately 12 hr after the injection. Plasma from rabbits who had received goat serum 48 hr previously (donor rabbits) was injected into recipient rabbits. This procedure resulted in a slight rise in the level of coagulation factor II (range, 20%-30%) and a significant rise in factors V (35%-75%), VII (35%-235%), and X (35%-75%) in the recipients. When plasma from control donor rabbits who had not received goat serum was injected into recipients, there was no change in these coagulation factors. It is postulated that the reduction in coagulation factor levels in donor rabbits induces a "coagulopoietin" for each factor or one "coagulopoietin" for all factors which stimulates increased synthesis and/or release of these factors in recipient rabbits.  (+info)

The induction of macrophage spreading: role of coagulation factors and the complement system. (2/1153)

Unstimulated mouse peritoneal macrophages, attached to either glass or plastic substrates, responded to factors generated in serum and plasma by spreading and increasing their apparent surface area up to eightfold. Two distinct and dissociable systems were involved. The first appears related to the distinct and dissociable systems were involved. The first appears related to the contact phase of blood coagulation. It is activated by glass and not plastic surfaces, depleted by kaolin adsorption, and inhibited by soybean trypsin inhibitor. In contrast, a separate complement-dependent system can be generated in kaolin-adsorbed plasma. Activation of the complement system can occur either by the alternate or classical pathways and generates a relatively small effector molecule which is dialyzable. These factors presumably influencing the surface membrane and underlying structures may explain the rapid spreading of activated macrophages observed after both infections and chemical peritoneal inflammatory agents.  (+info)

Reconstitution of the human endothelial cell protein C receptor with thrombomodulin in phosphatidylcholine vesicles enhances protein C activation. (3/1153)

Blocking protein C binding to the endothelial cell protein C receptor (EPCR) on the endothelium is known to reduce protein C activation rates. Now we isolate human EPCR and thrombomodulin (TM) and reconstitute them into phosphatidylcholine vesicles. The EPCR increases protein C activation rates in a concentration-dependent fashion that does not saturate at 14 EPCR molecules/TM. Without EPCR, the protein C concentration dependence fits a single class of sites (Km = 2.17 +/- 0.13 microM). With EPCR, two classes of sites are apparent (Km = 20 +/- 15 nM and Km = 3.2 +/- 1.7 microM). Increasing the EPCR concentration at a constant TM concentration increases the percentage of high affinity sites. Holding the TM:EPCR ratio constant while decreasing the density of these proteins results in a decrease in the EPCR enhancement of protein C activation, suggesting that there is little affinity of the EPCR for TM. Negatively charged phospholipids also enhance protein C activation. EPCR acceleration of protein C activation is blocked by anti-EPCR antibodies, but not by annexin V, whereas the reverse is true with negatively charged phospholipids. Human umbilical cord endothelium expresses approximately 7 times more EPCR than TM. Anti-EPCR antibody reduces protein C activation rates 7-fold over these cells, whereas annexin V is ineffective, indicating that EPCR rather than negatively charged phospholipid provide the surface for protein C activation. EPCR expression varies dramatically among vascular beds. The present results indicate that the EPCR concentration will determine the effectiveness of the protein C activation complex.  (+info)

Carbohydrate on human factor VIII/von Willebrand factor. Impairment of function by removal of specific galactose residues. (4/1153)

Human factor VIII/von Willebrand factor protein containing 120 +/- 12 nmol of sialic acid and 135 +/- 13 nmol of galactose/mg of protein was digested with neuraminidase. The affinity of native factor VIII/von Willebrand factor and its asialo form for the hepatic lectin that specifically binds asialoglycoproteins was assessed from in vitro binding experiments. Native factor VIII/von Willebrand factor exhibited negligible affinity while binding of the asialo derivative was comparable to that observed for asialo-alpha1-acid glycoprotein. Incubation of asialo-factor VIII/von Willebrand factor with Streptococcus pneumoniae beta-galactosidase removed only 62% of the galactose but abolished binding to the purified hepatic lectin. When the asialo derivative was incubated with purified beta-D-galactoside alpha2 leads to 6 sialyltransferase and CMP-[14C]NeuAc, only 61% of the galactose incorporated [14C]NeuAc. From the known specificites of these enzymes, it is concluded that galactose residues important in lectin binding are present in a terminal Gal/beta1 leads to 4GlcNAc sequence on asialo-factor VIII/von Willebrand factor. The relative ristocetin-induced platelet aggregating activity of native, asialo-, and agalacto-factor VIII/von Willebrand factor was 100:38:12, respectively, while procoagulant activity was 100:100:103.  (+info)

Unexpected crucial role of residue 225 in serine proteases. (5/1153)

Residue 225 in serine proteases of the chymotrypsin family is Pro or Tyr in more than 95% of nearly 300 available sequences. Proteases with Y225 (like some blood coagulation and complement factors) are almost exclusively found in vertebrates, whereas proteases with P225 (like degradative enzymes) are present from bacteria to human. Saturation mutagenesis of Y225 in thrombin shows that residue 225 affects ligand recognition up to 60,000-fold. With the exception of Tyr and Phe, all residues are associated with comparable or greatly reduced catalytic activity relative to Pro. The crystal structures of three mutants that differ widely in catalytic activity (Y225F, Y225P, and Y225I) show that although residue 225 makes no contact with substrate, it drastically influences the shape of the water channel around the primary specificity site. The activity profiles obtained for thrombin also suggest that the conversion of Pro to Tyr or Phe documented in the vertebrates occurred through Ser and was driven by a significant gain (up to 50-fold) in catalytic activity. In fact, Ser and Phe are documented in 4% of serine proteases, which together with Pro and Tyr account for almost the entire distribution of residues at position 225. The unexpected crucial role of residue 225 in serine proteases explains the evolutionary selection of residues at this position and shows that the structural determinants of protease activity and specificity are more complex than currently believed. These findings have broad implications in the rational design of enzymes with enhanced catalytic properties.  (+info)

Inflammation, sepsis, and coagulation. (6/1153)

The molecular links between inflammation and coagulation are unquestioned. Inflammation promotes coagulation by leading to intravascular tissue factor expression, eliciting the expression of leukocyte adhesion molecules on the intravascular cell surfaces, and down regulating the fibrinolytic and protein C anticoagulant pathways. Thrombin, in turn, can promote inflammatory responses. This creates a cycle that logically progresses to vascular injury as occurs in septic shock. Most complex systems are regulated by product inhibition. This inflammation-coagulation cycle seems to follow this same principle with the protein C pathway serving as the regulatory mechanism. The molecular basis by which the protein C pathway functions as an anticoagulant is relatively well established compared to the mechanisms involved in regulating inflammation. As one approach to identifying the mechanisms involved in regulating inflammation, we set out to identify novel receptors that could modulate the specificity of APC in a manner analogous to the mechanisms by which thrombomodulin modulates thrombin specificity. This approach led to the identification of an endothelial cell protein C receptor (EPCR). To understand the mechanism, we obtained a crystal structure of APC (lacking the Gla domain). The crystal structure reveals a deep groove in a location analogous to anion binding exosite 1 of thrombin, the location of interaction for thrombomodulin, platelet thrombin receptor and fibrinogen. Thrombomodulin blocks the activation of platelets and fibrinogen without blocking reactivity with chromogenic substrates or inhibitors. Similarly, in solution, EPCR blocks factor Va inactivation without modulating reactivity with protease inhibitors. Thus, these endothelial cell receptors for the protein C system share many properties in common including the ability to be modulated by inflammatory cytokines. Current studies seek to identify the substrate for the APC-EPCR complex as the next step in elucidating the mechanisms by which the protein C pathway modulates the response to injury and inflammation.  (+info)

Regulation and functions of the protein C anticoagulant pathway. (7/1153)

The protein C pathway plays a critical role in the negative regulation of the blood clotting process. We recently identified an endothelial cell receptor for protein C/activated protein C (APC). The receptor is localized almost exclusively on endothelial cells of large vessels and is present at only trace levels or indeed absent from capillaries in most tissues. Patients with sepsis or lupus erythematosus exhibit elevated levels of plasma EPCR which migrates on gels as a single band and is fully capable of binding protein C/APC. There is no correlation with thrombomodulin levels, probably due to different vascular localizations and/or cellular release mechanisms. To understand the mechanisms by which EPCR plasma levels are elevated, we examined EPCR mRNA expression in a rat endotoxin shock model. The EPCR mRNA gene exhibited an early immediate gene response to endotoxin with the mRNA levels increasing nearly 4 fold in the first 3-6 hrs, before returning toward baseline. Plasma levels of EPCR also rose about 4 fold with little change in tissue EPCR levels. Both processes were markedly attenuated by hirudin suggesting that thrombin was responsible for increases in mRNA and plasma EPCR levels. At the level of mRNA, the induction is mediated by a thrombin response element in the 5' flanking region of the gene. Direct thrombin infusion and cell culture experiments support this contention. On endothelium, thrombin is capable of releasing cell surface EPCR and this process is blocked by the metalloproteinase inhibitor orthophenanthroline. Taken together these studies indicate that elevation in soluble plasma EPCR reflects endothelial cell activation in the larger vessels and is likely to be an indication of local thrombin generation near these vessel surfaces.  (+info)

Inhibitory effect of sulfur-containing compounds in Scorodocarpus borneensis Becc. on the aggregation of rabbit platelets. (8/1153)

The inhibitory effects of three pure compounds isolated from wood garlic, 2,4,5-trithiahexane (I), 2,4,5,7-tetrathiaoctane (II), and 2,4,5,7-tetrathiaoctane 2,2-dioxide (III), on rabbit platelet aggregation induced by collagen, arachidonic acid, U46619, ADP (adenosine 5'-diphosphate), PAF (platelet aggregating factor), and thrombin were studied in vitro. The anti-aggregating activity of 2,4,5,7-tetrathiaoctane 4,4-dioxide (IV) was also measured with collagen and arachidonic acid. I, II, III, and IV inhibited the platelet aggregation induced by all tested agonists. I, II, and III exhibited a stronger inhibitory effect against the thrombin-induced aggregation of GFP (gel-filtered platelets) than against the aggregation induced by the other agonists. Notably, the IC50 value for III was 4 microM, which is approximately 2.5 times stronger than MATS (methyl allyl trisulfide), a major anti-platelet compound isolated from garlic. In inhibiting collagen-induced aggregation, II was as potent as MATS and aspirin, with a marked disaggregation effect on the secondary aggregation by arachidonic acid, at the rate of 47.05%/min at a concentration of 10(-4) M. I, II, and III also suppressed U46619-induced aggregation. These results suggest that sulfur-containing compounds in wood garlic not only inhibit arachidonic acid metabolism but also suppress aggregation in association with the function of the platelet plasma membrane.  (+info)

[107 Pages Report] Check for Discount on Global Coagulation Factor Concentrate Market Professional Survey Report 2017 report by QYResearch Group. This report studies Coagulation Factor Concentrate in Global market, especially...
There is uncertainty regarding the effectiveness and occurrence of thromboembolic events in patients treated with prothrombin complex concentrates (PCCs) for the management of major bleeding events (MBEs) on rivaroxaban or apixaban. We investigated the effectiveness of PCCs given for the management of MBEs in patients on rivaroxaban or apixaban. Between 1 January 2014 and 1 October 2016, we prospectively included patients on rivaroxaban or apixaban treated with PCCs for the management of MBEs. The effectiveness of PCCs was assessed by using the International Society of Thrombosis and Hemostasis Scientific and Standardization Subcommittee criteria for the assessment of the effectiveness of major bleeding management. The safety outcomes were thromboembolic events and all-cause mortality within 30 days after treatment with PCCs. A total of 84 patients received PCCs for the reversal of rivaroxaban or apixaban due to a MBE. PCCs were given at a median (interquartile range) dose of 2000 IU (1500-2000 ...
Mast cells (MCs) are immune sentinels, but whether they also function as antigen-presenting cells (APCs) remains elusive. Using mouse models of MC deficiency, we report on MC-dependent recruitment and activation of multiple T cell subsets to the skin and draining lymph nodes (DLNs) during dengue virus (DENV) infection. Newly recruited and locally proliferating γδ T cells were the first T cell subset to respond to MC-driven inflammation, and their production of IFN-γ was MC dependent. MC-γδ T cell conjugates were observed consistently in infected peripheral tissues, suggesting a new role for MCs as nonconventional APCs for γδ T cells. MC-dependent γδ T cell activation and proliferation during DENV infection required T cell receptor (TCR) signaling and the nonconventional antigen presentation molecule endothelial cell protein C receptor (EPCR) on MCs. γδ T cells, not previously implicated in DENV host defense, killed infected targeted DCs and contributed to the clearance of DENV in ...
Mast cells (MCs) are immune sentinels, but whether they also function as antigen-presenting cells (APCs) remains elusive. Using mouse models of MC deficiency, we report on MC-dependent recruitment and activation of multiple T cell subsets to the skin and draining lymph nodes (DLNs) during dengue virus (DENV) infection. Newly recruited and locally proliferating γδ T cells were the first T cell subset to respond to MC-driven inflammation, and their production of IFN-γ was MC dependent. MC-γδ T cell conjugates were observed consistently in infected peripheral tissues, suggesting a new role for MCs as nonconventional APCs for γδ T cells. MC-dependent γδ T cell activation and proliferation during DENV infection required T cell receptor (TCR) signaling and the nonconventional antigen presentation molecule endothelial cell protein C receptor (EPCR) on MCs. γδ T cells, not previously implicated in DENV host defense, killed infected targeted DCs and contributed to the clearance of DENV in ...
Mast cells (MCs) are immune sentinels, but whether they also function as antigen-presenting cells (APCs) remains elusive. Using mouse models of MC deficiency, we report on MC-dependent recruitment and activation of multiple T cell subsets to the skin and draining lymph nodes (DLNs) during dengue virus (DENV) infection. Newly recruited and locally proliferating γδ T cells were the first T cell subset to respond to MC-driven inflammation, and their production of IFN-γ was MC dependent. MC-γδ T cell conjugates were observed consistently in infected peripheral tissues, suggesting a new role for MCs as nonconventional APCs for γδ T cells. MC-dependent γδ T cell activation and proliferation during DENV infection required T cell receptor (TCR) signaling and the nonconventional antigen presentation molecule endothelial cell protein C receptor (EPCR) on MCs. γδ T cells, not previously implicated in DENV host defense, killed infected targeted DCs and contributed to the clearance of DENV in ...
Several proteins already known or implicated as metalloprotease-shed proteins were identified in this study using two different cell systems. These include amyloid A4 protein, IL-1R-2, IL-6R-1, l-selectin, M-CSFR, SorLA, AXLr, and endothelial cell protein C receptor (7, 8, 12, 13, 22-27). Thus, this proteomic technique was validated as a method that can be applied in studies of protein shedding. In addition, this study implicated a number of additional proteins as being shed by metalloproteases, including LDLr, SHPS-1, and Jagged 1. TACE was shown to be the responsible protease in the case of the LDLr and some of the previously identified shed proteins (e.g. AXLr and hybrid receptor SorLA) for which the sheddase had not been determined.. LDLr is known as a cell-surface receptor that binds to LDL, the major cholesterol-carrying lipoprotein in plasma, and transports LDL into cells by endocytosis (28). Other LDLr gene family proteins, including SorLA (see Fig. 4, a shed protein found here to be ...
Professional guide for Prothrombin Complex Concentrate (Human) [(Factors II, VII, IX, X), Protein C, and Protein S]. Includes: pharmacology, pharmacokinetics, contraindications, interactions, adverse reactions and more.
The Global Prothrombin Complex Concentrates Market is likely to gain traction due to the significant drop in demand for its counterpart fresh frozen plasma (FFP). PCC is available easily due to its lack of blood group specificity.
Proteinase-activated receptor 1 (PAR1) also known as Protease-activated receptor 1 or coagulation factor II (thrombin) receptor is a protein that in humans is encoded by the F2R gene. PAR1 is a G protein-coupled receptor involved in the regulation of thrombotic response. Proteolytic cleavage leads to the activation of the receptor. PAR-1 has multifaceted effects and plays a key role in mediating the interplay between coagulation and inflammation, which is important in the pathogenesis of inflammatory and fibrotic lung diseases. It is involved both in disruption and maintaining of endothelial barrier integrity, through interaction with either thrombin or activated protein C, respectively. Several selective antagonists for the PAR1 receptor have been developed, for use as anti-clotting agents for the treatment of heart disease. SCH-530,348 SCH530348 has been recently shown to attenuate the neutrophilic inflammatory response to Streptococcus pneumoniae by reducing levels of pro-inflamamtory ...
PAR-3 activates coagulation factor II thrombin receptor like 2 (F2RL2) in a dose-dependent manner (Figure). Available assay modes and other details are shown.
F2rl1 - F2rl1 (untagged) - Mouse coagulation factor II (thrombin) receptor-like 1 (cDNA clone MGC:29183 IMAGE:5006769), (10ug) available for purchase from OriGene - Your Gene Company.
EPCR signaling can decrease inflammation. APC binding to EPCR rescues baboons from E. coli sepsis.12 EPCR has also cardioprotective role in lipopolyscharide-induced endotoxemia in mice.14 In addition to the cell-surface EPCR, soluble EPCR lacking the transmembrane helix of native EPCR interacts with the integrin CD11b/CD18 (Mac-1) (αMβ2) (CR3) on leukocytes (Figure 1), suggesting that binding of soluble EPCR to Mac-1 might regulate leukocytes adhesion.15 Proteinase-3 (PR3), a serine protease with elastase-like properties stored in granules of neutrophils, binds both Mac-1 and soluble EPCR which may be implicated in APC mediated signaling and activation of PC on leukocytes, because soluble EPCR:PR3 complexes bind both APC and PC.15. Recent evidence indicates that EPCR is expressed on different cells beyond aortic endothelial cells. For example, EPCR is expressed on the surface of monocytes, CD56+ natural killer cells, neutrophils and eosinophils16-18, immature hematopoietic stem cells,19 brain ...
TY - JOUR. T1 - Genetics of the thrombomodulin-endothelial cell protein C receptor system and the risk of early-onset ischemic stroke. AU - Cole, John W.. AU - Xu, Huichun. AU - Ryan, Kathleen. AU - Jaworek, Thomas. AU - Dueker, Nicole. AU - McArdle, Patrick. AU - Gaynor, Brady. AU - Cheng, Yu Ching. AU - OConnell, Jeffrey. AU - Bevan, Steve. AU - Malik, Rainer. AU - Ahmed, Naveed Uddin. AU - Amouyel, Philippe. AU - Anjum, Sheraz. AU - Bis, Joshua C.. AU - Crosslin, David. AU - Danesh, John. AU - Engelter, Stefan T.. AU - Fornage, Myriam. AU - Frossard, Philippe. AU - Gieger, Christian. AU - Giese, Anne Katrin. AU - Grond-Ginsbach, Caspar. AU - Ho, Weang Kee. AU - Holliday, Elizabeth. AU - Hopewell, Jemma. AU - Hussain, M.. AU - Iqbal, W.. AU - Jabeen, S.. AU - Jannes, Jim. AU - Kamal, Ayeesha. AU - Kamatani, Yoichiro. AU - Kanse, Sandip. AU - Kloss, Manja. AU - Lathrop, Mark. AU - Leys, Didier. AU - Lindgren, Arne. AU - LongstrethJr, W. T.. AU - Mahmood, Khalid. AU - Meisinger, Christa. AU - ...
Background-Patients experiencing major bleeding while taking vitamin K antagonists (VKAs) require rapid VKA reversal. We performed a prospective clinical trial to compare non-activated four-factor prothrombin complex concentrate (4F-PCC) with plasma for urgent VKA reversal. Methods and Results-In this phase IIIb, multicenter, open-label, non-inferiority trial, non-surgical patients were randomized to 4F-PCC (containing coagulation factors II, VII, IX, X, and proteins C, S) or plasma. Primary analyses examined whether 4F-PCC was non-inferior to plasma for the co-primary endpoints of 24-hour hemostatic efficacy from start of infusion and INR correction (≤1.3) at 0.5 hours after end of infusion. The intent-to-treat-efficacy population comprised 202 patients (4F-PCC n=98; plasma n=104). Median (range) baseline INR was 3.90 (1.8-20.0) for the 4F-PCC group and 3.60 (1.9-38.9) for the plasma group. Effective hemostasis was achieved in 72.4% of patients receiving 4F-PCC versus 65.4% receiving plasma, ...
Background: Although endothelial cell protein C receptor (EPCR) gene Ser219Gly polymorphism has been associated with venous thromboembolism (VTE) susceptibility, no clear consensus has yet been reached. Objective and methods: A meta-analysis of 9,494 subjects from 13 individual studies was conducted to better elucidate the potential relationship between the EPCR gene Ser219Gly polymorphism and VTE. Pooled odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were evaluated by using fixed or random effect models.Results: The current meta-analysis suggested that there was a significant association between EPCR gene Ser219Gly polymorphism and VTE under allelic (OR: 1.42, 95% CI: 1.21-1.66, P=1.30×10-5), recessive (OR: 2.02, 95% CI: 1.44-2.85, P=5.35×10-5), homozygous (OR: 2.24, 95% CI: 1.59-3.16, P=3.66×10-6), and additive genetic models (OR: 1.63, 95% CI: 1.30-2.04, P=2.24×10-5). Conclusions: EPCR gene Ser219Gly polymorphism was associated with an elevated risk of VTE and the Gly
Expression of endothelial protein C receptor in cortical peritubular capillaries associates with a poor clinical response in lupus nephritis.
The management of bleeding patients on vitamin K antagonist (VKA) therapy is a common clinical challenge. Current American College of Chest Physician (ACCP) guidelines recommend the use of prothrombin complex concentrates (PCCs) for rapid reversal of VKA-induced coagulopathy.1. While efficacy and safety of PCC are well established for VKA reversal, a well-defined dosing strategy is still lacking.. Recently, we studied the effectiveness of a low fixed dose regimen of 1040 IU F IX PCC compared to variable dosing to counteract VKA associated emergency bleeding.2 This prospective study showed that low fixed PCC dose was non-inferior to variable dosing in terms of clinical outcome. In reaching the target INR, defined as INR less than 2, the fixed dose was non-inferior in patients with an initial INR below 7.5, but not in patients with a higher INR.. An important question from both a clinical and costing point of view is whether additional interventions were needed in the fixed dose cohort to reach ...
This page includes the following topics and synonyms: Prothrombin Complex Concentrate, Prothrombin Drug Combination, PCC, Beriplex, Octaplex, Kcentra, Cofact.
The protein encoded by this gene is a receptor for activated protein C, a serine protease activated by and involved in the blood coagulation pathway. The encoded protein is an N-glycosylated type I membrane protein that enhances the activation of protein C. Mutations in this gene have been associated with venous thromboembolism and myocardial infarction, as well as with late fetal loss during pregnancy. The encoded protein may also play a role in malarial infection and has been associated with cancer. [provided by RefSeq, Jul 2013 ...
Question about target INRs when treating coagulopathic patients with frozen plasma or prothrombin complex concentrate (PCC) Question: On page 36 of Bloody Easy 4: Blood Transfusions, Blood Alternatives and Transfusion Reactions. A Guide to Transfusion Medicine Fourth Edition (1), the threshold INR for plasma transfusion is greater than or equal to 1.8. On page 126, regarding the use of prothrombin complex concentrate (PCC) for emergency warfarin reversal, the threshold INR is greater than or equal to 1.5. Why is the INR threshold for plasma 1.8, and the threshold for PCCs 1.5? Shouldnt they be the same? Answer by Dr. Allison Collins, MD: Coagulation factors are at sufficient levels (30% of normal) for normal hemostasis at an INR of about 1.7 (2). The INR is a poor predictor of bleeding risk, particularly if only mildly elevated, and there is no good evidence for use of a target INR of 1.5 vs 1.8 for prevention or treatment of bleeding. INR reversal with plasma is not as effective as INR ...
Sales, means the sales volume of Human Prothrombin Complex Revenue, means the sales value of Human Prothrombin Complex This report studies sales (consumption) of Human Prothrombin Complex in United States market, focuses on the top players, with sales, price, revenue and market share for each player, covering Baxter CSL Bayer Grifols Octapharma Shanghai RAAS Hualan Bio
Results 45 patients were treated with PCC and included in the analysis. Mean patient age was 59.64 years, 42.2% were women and 57.77% men. The average dose was 1604 IU, the global survival after seven days was 73.33% and 35.55% had concomitant treatment with fibrinogen.. 11.11% of the patients had been treated with oral anticoagulants (OAT) prior to the emergency bleeding,. 48.89% had polytraumatic wounds,. 4.44% had thrombocytopenia secondary to hepatopathy,. 0% had haemophilia,. 75.55% had an active haemorrhage,. 68.89% underwent surgery, when the PCC was administered.. Quick time (s) (% // INR):. ...
Synonyms for Coagulation factors in Free Thesaurus. Antonyms for Coagulation factors. 2 synonyms for coagulation: clotting, curdling. What are synonyms for Coagulation factors?
[106 Pages Report] Check for Discount on Global Prothrombin Complex Market 2020 by Manufacturers, Regions, Type and Application, Forecast to 2025 report by Global Info Research. Market Overview The global Prothrombin Complex market size is expected...
When warfarin reversal must be accomplished rapidly, such as in cases of active bleeding or in preparation for an invasive procedure, multiple options exist, chief among them being fresh frozen plasma (FFP) and four factor prothrombin complex concentrate (4-PCC). Between those two options, the ACCP guidelines suggest (soft recommendation) 4-PCC over FFP. This was based on low level data (very small studies) showing more rapid INR reversal using the former. This study, which came out after publication of the ACCP guidelines, added further weight in favor of 4-PCC in patients deemed appropriate for rapid warfarin reversal in the emergency setting. Though considered low level in that it was a retrospective study, it was larger (around 150 patients in both groups) than prior studies. Despite mounting evidence in favor of 4-PCC some experts (e.g. the authors of this review) remain skeptical as to whether 4-PCC is superior, awaiting information from randomized controlled trials. One such trial has ...
Jerrold Levy, MD, of Duke University, discusses some of the late breaking clinical trial data and take-home points from ISTH 2015. The topics of greatest concern to clinicians in practice include: 1) There are evolving strategies for managing bleeding in patients taking direct oral anticoagulants, including the use of prothrombin complex concentrates, 2) the specific reversal strategies for Xa inhibitors and dabigatran are also evolving, 3) the approach to managing peri-procedural anticoagulation is changing due to the introduction of targeted NOAC reversal agents. , TV Network
A method for analyzing the protein site similarity was devised aiming at understanding selectivity of homologous proteins and guiding the design of new drugs. The method is based on calculating Cα distances between selected pocket residues and subsequent analysis by multivariate methods. Five closely related serine proteases, the coagulation factors II, VII, IX, X, and XI, were studied and their pocket similarity was illustrated by PCA clustering. OPLS-DA was then applied to identify the residues responsible for the variation. By combining these two multivariate methods, we could successfully cluster the different proteases according to class and identify the important residues responsible for the observed variation.
1st Edition Published on April 30, 1989 by CRC Press This book extensively reviews the purification and structure/function relationships of Factor VIII - von Wi
OBJECTIVE: The endothelial protein C-receptor (EPCR) is an endothelial transmembrane protein that binds protein C and activated protein C (APC) with equal affinity, thereby facilitating APC formation. APC has anticoagulant, antiapoptotic and antiinflammatory properties. Soluble EPCR, released by the endothelium, may bind activated neutrophils, thereby modulating cell adhesion. EPCR is therefore considered as a possible link between the anticoagulant properties of protein C and the inflammatory response of neutrophils. In the present study, we aimed to provide proof of concept for a direct binding of EPCR to the β2-integrin Mac-1 on monocytic cells under static and physiological flow conditions. MEASUREMENTS AND MAIN RESULTS: Under static conditions, human monocytes bind soluble EPCR in a concentration dependent manner, as demonstrated by flow cytometry. Binding can be inhibited by specific antibodies (anti-EPCR and anti-Mac-1). Specific binding was confirmed by a static adhesion assay, where a ...
ZeoVit Iodide Complex Concentrate, 50 ml. - At AquaCave, we offer Best Prices, 5% Back, and Free Shipping on ZeoVit Iodide Complex Concentrate, 50 ml.. - Buy ZeoVit Iodide Complex Concentrate, 50 ml. - Now Only $49.99 - ZeoVit Iodide Complex Concentrate, 50 ml.For an improved coloration corals need iodide in different forms as well as additional elements enabeling an optimal assimilation of the iodide. Contains organic and inorganic iodide as well as bromine, potassium and fluorine. Recommended in any tank system.Dosing: 1 drop per 100 L/25 gallons per day.- See more at: http://www.aquariumspecialty.com/zeovit-iodide-complex-concentrate-50ml#sthash.IWFZUPLE.dpufFor an improved coloration corals need iodide in different forms as well as additional elements enabeling an optimal assimilation of the iodide. Contains organic and inorganic iodide as well as bromine, potassium and fluorine. Recommended in any tank system.Dosing: 1 drop per 100 L/25 gallons per day.Enhances blue colors, especially in certain
2018 Elsevier Inc. All rights reserved. Transfusion medicine physicians and laboratory scientists are confronted daily with hemostasis and thrombosis-related concerns as they select and administer blood components, coagulation factor concentrates, anticoagulants, and agents to manage anticoagulant therapy. This chapter provides an introduction and overview of hemostasis. Primary hemostasis focuses on platelet function and interactions with the vasculature, endothelium, and the coagulation mechanism. Secondary hemostasis focuses on the coagulation cascade and is subdivided into the extrinsic, intrinsic, and common enzymatic pathways. Coagulation also includes control systems such as protein C, protein S, and antithrombin, and fibrinolysis. Depending on the defect, hemostasis disorders may be congenital or acquired, resulting in hemorrhage or thrombosis. The questions in this chapter will explore normal hemostasis, disorders of hemostasis, and the laboratory assays that predict, identify, and ...
For people with high responding inhibitors, utilizing factor is, in many cases, not possible because the inhibitor neutralizes even the largest possible dose of factor. In these cases treatment is based on the type of hemophilia and the nature of the bleed.. During a life or limb-threatening bleeding episode, physicians can remove antibodies from the body using a process called plasmapheresis, which lowers the level of antibodies to allow treatment with factor concentrate to treat the bleed. However, this is a temporary solution and within a few days the body will produce large amounts of new antibodies. For the person with a high responding inhibitor, most bleeding episodes are treated using bypassing products that include prothrombin complex concentrates (PCCs), activated prothrombin complex concentrates (APCCs) (i.e. Feiba VH, produced by Baxter). These bypassing products contain other factors that can stimulate the formation of a clot and stop bleeding. While these treatments are effective, ...
For people with high responding inhibitors, utilizing factor is, in many cases, not possible because the inhibitor neutralizes even the largest possible dose of factor. In these cases treatment is based on the type of hemophilia and the nature of the bleed.. During a life or limb-threatening bleeding episode, physicians can remove antibodies from the body using a process called plasmapheresis, which lowers the level of antibodies to allow treatment with factor concentrate to treat the bleed. However, this is a temporary solution and within a few days the body will produce large amounts of new antibodies. For the person with a high responding inhibitor, most bleeding episodes are treated using bypassing products that include prothrombin complex concentrates (PCCs), activated prothrombin complex concentrates (APCCs) (i.e. Feiba VH, produced by Baxter). These bypassing products contain other factors that can stimulate the formation of a clot and stop bleeding. While these treatments are effective, ...
To the best of our knowledge, this is the first study investigating TG-related parameters following PCC administration in acute trauma patients. PCC therapy resulted in significantly higher ETP than in patients who received fibrinogen concentrate only or no coagulation therapy at all and, importantly, this was sustained over the first 3 to 4 days following PCC administration. AT was significantly lower in the FC-PCC group from ER admission until 3 to 4 days later, reaching a nadir on day 2. Hemostasis relies on a delicate balance between pro- and anticoagulant factors, and between thrombin potential and thrombin inhibition potential. This balance may have been impaired in the FC-PCC group, during a period when fibrinogen levels were increased above the normal range; similar findings have been reported in previous studies [34, 35]. The overall picture is increased thrombin potential (day 1 to day 4), increased substrate for coagulation (that is, fibrinogen reaching a plateau on day 4) and ...
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Prostate cancer remains one of the most common forms of cancer affecting men today [ 1 ]. Patients with metastatic hormone-refractory prostate
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A prothrombin activity level of ~10% has been identified as the minimum level required for hemostasis per multiple national registries.27 However, to achieve and maintain hemostasis, FII troughs of 20% to 30% are recommended. The ideal method for replacement would be with a prothrombin concentrate. Unfortunately, prothrombin deficiency is one of the few RBDs without a dedicated factor concentrate for replacement.36 The mainstay of treatment for acute bleeding events or long-term prophylaxis remains prothrombin complex concentrates (PCC) or fresh frozen plasma (FFP).. FFP infusions at 15-20 ml/kg per dose can be used for acute bleeding and are expected to raise FII activity level by 25%.28 To maintain hemostasis in the post-surgical setting or in cases of severe bleeding, FFP at 3-10 ml/kg every 12-24 hours is advised to maintain safe and adequate correction.28,36,37 However the potential for volume overload with repeated FFP infusions could limit use in some patients with volume restrictions. ...
TY - JOUR. T1 - Structure of Ca+2 -free Gla diomain shed light on membrane binding of blood coagulation proteins. AU - Sunnerhagen, Maria. AU - Forsen, Sture. AU - Hoffren, Anna-Marja. AU - Drakenberg, Torbjörn. AU - Teleman, Olle. AU - Stenflo, Johan. N1 - Project code: B5SU00139. PY - 1995. Y1 - 1995. N2 - Reversible membrane binding of γ-carboxyglutamic acid (Gla)-containing coagulation factors requires Ca2+-binding to 10-12 Gla residues. Here we describe the solution structure of the Ca2+-free Gla-EGF domain pair of factor X which reveals a striking difference between the Ca2+-free and Ca2+-loaded forms. In the Ca2+-free form Gla residues are exposed to solvent and Phe 4, Leu 5 and Val 8 form a hydrophobic cluster in the interior of the domain. In the Ca2+-loaded form Gla residues ligate Ca22+ in the core of the domain pushing the side-chains of the three hydrophobic residues into the solvent. We propose that the Ca2+-induced exposure of hydrophobic side chains is crucial for membrane ...
Supplementary MaterialsS1 Methods: Detailed explanation of prekallikrein production and prothrombin/factor X lacking plasma assays. Aliquots of 10 L PD184352 ic50 had been taken and generated kallikrein enzymatic activity was determined using the specific chromogenic substrate S2302 (2 mM). The kinetics of p-nitroaniline formation were monitored at 405 nm and curves are representative data from at least three independent experiments. Inset shows the dose-response curve. The amounts of plasma derived kallikrein generated by LOBE was estimated using a calibration curve made with known concentrations of purified kallikrein and thus expressed as pmol of equivalent kallikrein/mL/min.(TIF) pntd.0007197.s004.tif (459K) GUID:?7403B6A2-C7C2-4032-B696-330A483F7AED S4 Fig: LOBE-induced kallikrein generation in factor X and prothrombin deficient PD184352 ic50 plasma. To further confirm LOBE-induced kallikrein activation specificity, the main procoagulant factors, FX and prothrombin (PThr), were depleted ...
|p||strong|Prothrombin|/strong| (coagulation factor II) (H2N-Tyr-Ile-His-Pro-OH) is produced in the liver and is post-translationally modified in a vitamin K-dependent reaction that converts ten glutamic acids on prothrombin into gamma-carboxyglutamic aci
Detailed drug Information for prothrombin complex human Intravenous. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
F2RL3 / PAR-4 antibody (coagulation factor II (thrombin) receptor-like 3) for IHC-P. Anti-F2RL3 / PAR-4 pAb (GTX71163) is tested in Human samples. 100% Ab-Assurance.
Treatment of high coagulation, hyperlipemia. High coagulation state may not be easy to understand, it refers to the patients blood coagulation factor is changed, thus in high blood coagulation state, especially when the plasma albumin is le
There is a large amount of experimental evidence that supports the concept of an association between blood coagulation and malignant disease. Since several chapters within this volume describe...
The development of Prothrombin Complex Concentrates (PCCs) has led to better outcomes in patients receiving emergency reversal of warfarin. However, most published data describes the use of PCCs in the setting of major bleeding or emergent major surgery, with little information on neuraxial blockade. We describe a case of rapid warfarin reversal using PCC and subsequent surgery under spinal anaesthesia in an 87-year-old lady, for whom general anaesthesia was deemed high risk. Her international normalised ratio (INR) on the morning of surgery was 1.8, precluding neuraxial blockade; however, it was felt that given, the need for imminent surgery, immediate reversal of the warfarin was indicated. We administered a single dose of 23 units/kg PCC and 5 mg vitamin K. Her INR 1 hour following PCC was 1.2, and spinal anesthetic was administered. The patient then underwent excision of melanoma deposits from her leg and groin dissection. There were no complications, the patient recovered
TY - JOUR. T1 - Endothelial protein C receptor-expressing hematopoietic stem cells reside in the perisinusoidal niche in fetal liver. AU - Iwasaki, Hiroko. AU - Arai, Fumio. AU - Kubota, Yoshiaki. AU - Dahl, Maria. AU - Suda, Toshio. PY - 2010/7/29. Y1 - 2010/7/29. N2 - Hematopoietic stem cells (HSCs) are maintained in specialized niches in adult bone marrow. However, niche and HSC maintenance mechanism in fetal liver (FL) still remains unclear. Here, we investigated the niche and the molecular mechanism of HSC maintenance in mouse FL using HSCs expressing endothelial protein C receptor (EPCR). The antiapoptotic effect of activated protein C (APC) on EPCR+ HSCs and the expression of protease-activated receptor 1 (Par-1) mRNA in these cells suggested the involvement of the cytoprotective APC/ EPCR/Par-1 pathway in HSC maintenance. Immunohistochemistry revealed that EPCR+ cells were localized adjacent to, or integrated in, the Lyve-1+ sinusoidal network, whereAPC and extracellular matrix (ECM) are ...
Factor VIII: 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.
Warfarin is a vitamin K antagonist, metabolized through the liver and can be reversed with vitamin K, prothrombin complex concentrates and frozen plasma.. LWMH inhibits factors Xa and IIa via accelerating the activity of ATIII. It is renally cleared and must be used with caution in patients with renal failure. Reversal can be obtained with protamine.. Rivaroxaban is an oral FXa inhibitor that is renally cleared and does not require coagulation monitoring. In cases of bleeding factor Xa levels can be used to monitor therapeutic levels. There are no approved antidotes for reversal and protocols for reversal are center dependent.. Dabigatran is an oral thrombin inhibitor that does not require coagulation monitoring. There is no reversible antidote and coagulation testing is typically not used to monitor PT/ PTT values. There are no antidotes for reversal but dialysis has been used with limited success.. Dentali F et al. Safety of prothrombin complex concentrates for rapid anticoagulation reversal ...
The 281st Critical Care Reviews Newsletter includes the latest critical care research and open access articles from this weeks medical literature. The highlight of this edition is the WOMAN randomised controlled trial, evaluating tranexamic acid in post partum haemorrhage. Also of interest are RCTs comparing coagulation factor concentrates with fresh frozen plasma for trauma-induced coagulopathy…
Stephan Moll, MD writes… A new drug for the urgent reversal of warfarin was approved by the FDA today, April 29th, 2013, (announcement by the FDA is here), called Kcentra. The drug is derived from the plasma of multiple healthy blood donors and contains the clotting factors that are low in warfarin-treated patients, i.e. factors II, VII, IX, and X. It is also referred to as a 4-factor concentrate, or non-activated Prothrombin Complex Concentrate (PCC). The drug prescribing information (package insert) is here.. Up until now only 3-factor concentrates (PCC) and fresh frozen plasma (FFP) were available in the U.S., in addition to vitamin K, to treat major bleeding in warfarin-treated patients or reverse warfarin in case major surgery was urgently needed. The new drug is a welcome addition to the armamentarium when having to treat warfarin-associated major bleeding. Where until now I used to give 3-factor PCCs, I will from now on give the 4-factor PCC, Kcentra.. Bleeding and the new oral ...
It was recently reported that early, i.e. in the first 48h of life, coagulation screening may identify infants at risk of severe IVH. Unfortunately, in the past screening for coagulation abnormalities and correction of haemostatic defects by prothrombin complex concentrate, cryoprecipitate or platelet concentrates) and fresh frozen plasma (FFP) had limited effects in preterm infants. This could have been due to the short duration of action, incomplete restoration of coagulation or the water and osmotic load associated with FFP administration. However recently, using a coagulopathy screening strategy (one blood sample within the first 2h after birth) and substitution with FFP decreased the risk of developing IVH in infants born at 23 to 26 weeks of gestation. Recombinant Factor VII (rFVII) provides a new therapeutic option to overcome FFP associated side effects. Small trials, including infants with pulmonary hemorrhage, showed the safety and effectiveness of rFVII in VLBW infants; however no ...
GPM.1.8.2.0003.15 Determination of blood coagulation factors activity Ministry of Health of the Russian Federation General Pharmacopoeia Monograph Determination
Blood coagulation functions as part of the innate immune system by preventing bacterial invasion and it is critical to stopping blood loss (hemostasis). Coagulation involves the external membrane surface of activated platelets and leukocytes. Using lipidomic, genetic, biochemical, and mathematical modeling approaches, we found that enzymatically oxidized phospholipids (eoxPLs) generated by the activity of leukocyte or platelet lipoxygenases (LOXs) were required for normal hemostasis and promoted coagulation factor activities in a Ca2+- and phosphatidylserine (PS)- dependent manner. In wild-type mice, hydroxyeicosatetraenoic acid-phospholipids (HETE-PLs) enhanced coagulation and restored normal hemostasis in clotting-deficient animals genetically lacking p12-LOX or 12/15-LOX activity. Murine platelets generated 22 eoxPL species, all of which were missing in the absence of p12-LOX. Humans with the thrombotic disorder antiphospholipid syndrome (APS) had statistically significantly increased ...
BACKGROUND: Acute myocardial infarction (AMI) is rare among young women. The search for unknown risk factors is warranted. Endothelial protein C receptor (EPCR) is largely present at the endothelial surface of large arteries. No studies about association of anti-EPCR autoantibodies (anti-EPCR) with AMI are available. METHODS: Plasma IgA, IgM and IgG anti-EPCR levels were measured by enzyme-linked immunosorbent assay in 165 women younger than 45 years who survived a first AMI and 165 healthy women, matched by age and geographical origin. RESULTS: Using the 90th percentile of IgA anti-EPCR in the control group, IgA anti-EPCR were independently associated with AMI after adjustment for cardiovascular risk factors (OR 5.1; 95% CI 1.7-15.6; P = 0.004). The risk apparently conferred by IgA anti-EPCR increased dose-dependently (P for trend =0.0002). IgM anti-EPCR were less consistently associated with AMI: a significant increase in the risk was found when women above the 90th percentile were compared ...
Als Äquivalent einer Habilitationsschrift werden drei Originalarbeiten zusammengefasst und eingereicht. Die aufgeführten Arbeiten beschreiben wie Gerinnungsproteasen via Protease aktivierbare Rezeptoren auf das Endothel wirken. Die Arbeiten zielen dahin, dass Gerinnungsfaktoren in Zukunft therapeutisch breiter und mit besserem Nutzen eingesetzt werden können. Quellenangabe der vorgestellten Publikationen: 1. Schuepbach RA, Feistritzer C, Brass LF, Riewald M. Activated protein C-cleaved protease activated receptor-1 is retained on the endothelial cell surface even in the presence of thrombin. Blood. 2008 Mar 1;111(5):2667-73. 2. Schuepbach RA*, Feistritzer C*, Fernandez JA, Griffin JH and Riewald M. Protection of Vascular Barrier Integrity by Activated Protein C Dependent on Protease-Activated Receptor-1. Thromb Haemost. 2009 Apr;101(4):724-33 3. Schuepbach RA and Riewald M. Clotting Factor Xa Cleaves PAR1 and Mediates Signaling Dependent on Binding to the Endothelial Protein C Receptor. J ...
Individuals with chronically elevated glucose, most patients with type-2 diabetes, have increased inflammation (hs-CRP levels) and accelerated atherosclerosis, associated with acute vascular events. Up to date, it is not known whether hs-CRP or elevated glucose alter the expression and pre-mRNA splicing of tissue factor (TF), the primary initiator of blood coagulation. We have tested the hypothesis that hs-CRP and hyperglycemia singly or combined may increase tissue factor isoform expression. First, we determined changes in tissue factor isoform expression in whole blood and procoagulant activity (PCA) in human monocytic cells obtained from healthy volunteers (controls, n=20) and insulin-treated patients with type-2 diabetes (n=60). TF m-RNA was quantified for the full-length and soluble isoform by real-time PCR. To assess the impact of hs-CRP on TF, the patients were divided into two groups according to their hs-CRP (hs-CRP,0.3 mg/dl or ,0.3 mg/dl). Secondarily, PMN cells were isolated and ...
Langhammer, B., Sunnerhagen, K. S., Stanghelle, J. K., Sällström, S., Becker, F., & Fugl-Meyer, K. (2017). Life satisfaction in persons with severe stroke-A longitudinal report from the Sunnaas International Network (SIN) stroke study. European Stroke Journal, 2396987317695140.. Lindström, L., Skjærven, R., Bergman, E., Lundgren, M., Klungsøyr, K., Cnattingius, S., & Wikström, A. K. (2017). Chronic Hypertension in Women after Perinatal Exposure to Preeclampsia, Being Born Small for Gestational Age or Preterm. Paediatric and Perinatal Epidemiology.. Schultz, N. H., Tran, H. T. T., Bjørnsen, S., Henriksson, C. E., Sandset, P. M., & Holme, P. A. (2017). The reversal effect of prothrombin complex concentrate (PCC), activated PCC and recombinant activated factor VII against anticoagulation of Xa inhibitor. Thrombosis Journal, 15(1), 6.. Sulo, E., Nygård, O., Vollset, S. E., Igland, J., Ebbing, M., Østbye, T., Jørgensen, T., Sulo, G., & Tell, G. S. (2017). Time Trends and Educational ...
Thrombin is a serine protease that in humans is encoded by the F2 gene. Prothrombin (coagulation factor II) is proteolytically cleaved to form thrombin in the coagulation
Supplementary MaterialsElectronic Supporting Information. VEGF165 in both ALC and CALCR SPR measurements, with slight exceptions. Of the investigated HBPs, a peptide based on the heparin-binding domain of human platelet factor 4 showed greatest binding affinities toward all of the SPs, consistent with its stronger binding to heparin. The affinity between SPa and PF4ZIP was indicated via SPR (KD = 5.27 M) and confirmed via ITC (KD = 8.09 M). The binding by SPa of both VEGF and HBPs suggests its use as a binding partner to multiple species, and the use of these interactions in assembly of materials. Given that the peptide sequences can be varied to control binding affinity and selectivity, opportunities are also suggested for the production of a wider array of matrices with purchase Amyloid b-Peptide (1-42) human selective binding and release properties useful for biomaterials applications. according to the reported protocol [68,70,71], purchase Amyloid b-Peptide (1-42) human and purified via ...
Blood vessel contraction, platelet activation and formation, and activation of coagulation factors, and their use in diagnosing coagulation defects and monitoring anticoagulant therapy. This course has a fee that is non-refundable once the term begins.
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This study aimed to sequence and characterize two pro-coagulant genes, coagulation factor II (f2) and fibrinogen gamma chain (fgg), from the liver of the African lungfish Protopterus annectens, and to determine their hepatic mRNA expression levels during three phases of aestivation. The protein abundances of F2 and Fgg in the liver and plasma were determined by immunoblotting. Results indicated that F2 and Fgg of P. annectens were phylogenetically closer to those of amphibians than those of teleosts. Three days of aestivation resulted in an up-regulation in the hepatic fgg mRNA expression level, while 6 days of aestivation led to a significant increase (3-fold) in the protein abundance of Fgg in the plasma. Hence, there could be an increase in the blood clotting ability in P. annectens during the induction phase of aestivation. By contrast, the blood clotting ability in P. annectens might be reduced in response to decreased blood flow and increased possibility of thrombosis during the ...
KING OF PRUSSIA, Pa. and MONTREAL, Feb. 16, 2011 /PRNewswire/ -- As a means of aiding the World Federation of Hemophilias (WFH) progress in improving the diagnosis and treatment of hemophilia in developing countries through its Global Alliance for Progress (GAP) program, CSL Behring has committed to donating more factor VIII concentrate (FVIII) to WFH. The donated product will be used in South America, Thailand, the Philippines, parts of eastern Europe, parts of the Middle East, and in Tunisia. The donation, the total market value of which is approximately $500,000, will be made using coagulation factor concentrate with a minimum shelf-life of one year.. CSL Behring has pledged to support the WFH with separate financial contributions totaling nearly $1 million over a period of three years. This most recent donation is part of that commitment.. "As a long-standing contributor to GAP, CSL Behring is pleased to once again be in a position to assist hemophilia patients who have a critical need for ...
Acquired von Willebrand syndrome (avWS) has gained more attention during the last years. An International Registry has been compared with the literature. It could be shown that the data collected from 123 publications compared well with the data from the registry, albeit with differences in the number of patients suffering from lymphoproliferative diseases and cardiovascular disorders, that were more prominent in the registry and the group of miscellaneous conditions underrepresented in the registry. Our data are clearly different for the lymphoproliferative diseases with only four patients in 2 years. These patients usually suffer from severe bleeding complications together with low to very low factor VIII/von Willebrand factor (FVIII/vWF) concentrations and thus will not go undiagnosed. In contrast to this, patients with cardiovascular disorders usually bleed only during surgical procedures or catheter procedures. At that time they have increased vWF parameters. Because of this and because the ...
Factor IX Complex is a sterile, lyophilized concentrate composed of a number of Vitamin K-dependent clotting factors found in functioning human plasma. Also known as prothrombin complex concentrate, products containing this complex often include Factor IX (antihemophilic factor B), Factor II (prothrombin), Factor X (Stuart-Prower Factor), and low levels of Factor VII (proconvertin) derived from human plasma. Many commercially available products also contain low levels of other antithrombotic proteins. For example, Kcentra (FDA) also contains the antithrombotic proteins C and S, while Bebulin VH (FDA) contains heparin. Coagulation factors are purified from pooled human plasma and subsequently sterilized and treated. Although Factor IX Complex products contain many different coagulation components, Factor IX is the lead component for potency and efficacy, particularly when used for the treatment of bleeding associated with Hemophilia B (Factor IX deficiency). As the product Kcentra, Factor IX ...
Looking for Coagulation factor XIa? Find out information about Coagulation factor XIa. A procoagulant present in normal blood but deficient in hemophiliacs. Also known as plasma thromboplastin antecedent Explanation of Coagulation factor XIa
Activated protein C (aPC), in a complex with protein S, inactivates procoagulant factors Va and VIIIa by proteolytic cleavage at specific arginine residues.7,10,11 This serves to control coagulation and limit the extent of thrombus formation. The functionality of the aPC inhibitory system in a given individual can be assessed through an in vitro clotting assay. Addition of aPC to a patients plasma serves to extend the activated partial thromboplastin time (aPTT) for individuals who are sensitive to aPC. Individuals are considered to be aPC resistant when addition of aPC fails to extend the time to clot formation in this assay. More than 95% of cases of aPC resistance are caused by a specific polymorphism in the factor V gene that is referred to as factor V Leiden.8 This single point mutation results in a substitution of glutamine for arginine at amino acid number 506 of factor V. Arginine number 506 is an aPC cleavage site of normal factor V, making factor V Leiden resistant to inactivation by ...
Supplementary MaterialsS1 Methods: Detailed explanation of prekallikrein production and prothrombin/factor X lacking plasma assays. Aliquots of 10 L PD184352 ic50 had been taken and generated kallikrein enzymatic activity was determined using the specific chromogenic substrate S2302 (2 mM). The kinetics of p-nitroaniline formation were monitored at 405 nm and curves are representative data from at least three independent experiments. Inset shows the dose-response curve. The amounts of plasma derived kallikrein generated by LOBE was estimated using a calibration curve made with known concentrations of purified kallikrein and thus expressed as pmol of equivalent kallikrein/mL/min.(TIF) pntd.0007197.s004.tif (459K) GUID:?7403B6A2-C7C2-4032-B696-330A483F7AED S4 Fig: LOBE-induced kallikrein generation in factor X and prothrombin deficient PD184352 ic50 plasma. To further confirm LOBE-induced kallikrein activation specificity, the main procoagulant factors, FX and prothrombin (PThr), were depleted ...
Oxidized cholesterol compounds or oxysterols are thought to be potent membrane-destabilizing agents. Anionic phospholipids, chiefly phosphatidylserine, have a procoagulant potential due to their ability to favour the membrane assembly of the characteristic clotting enzyme complexes including the tissue factor-dependent initiating complex. However, in resting cells, phosphatidylserine is sequestered in the inner leaflet of the plasma membrane. When THP-1 monocytic cells were cultured in the presence of 7β-hydroxycholesterol (7β-OH) or 25-hydroxycholesterol (25-OH), prothrombinase, which reflects anionic phospholipid exposure and tissue factor (TF) procoagulant activities, increased in a time- and dose-dependent manner. 7β-OH appeared 1.5- to 2-fold more potent than 25-OH. Interestingly, no effect of cholesterol itself could be detected on procoagulant activities. Nevertheless, no difference in TF activity could be detected between oxysterol-treated and control cells after disruption. TF ...
London, April 27 (IANS) A patient suffering from fatty liver disease is prone to an increased risk of heart disease as well as the mortality rates associated with it, a new study has found. Non-alcoholic fatty liver disease (NAFLD) is an increasingly common condition in patients with obesity, type 2 diabetes and arterial hypertension - where high blood pressure in the arteries is persistently elevated.. The findings showed that NAFLD is an independent risk factor for atherosclerosis - the build-up of fats, cholesterol and other substances in and on the artery walls - which may lead to the advent of cardiovascular disease (CVD) - heart diseases - related deaths.. "Evidence indicates that the fatty and inflamed liver expresses several pro-inflammatory and procoagulant factors, as well as genes involved in accelerated atherogenesis," said led researcher Raluca Pais from Pierre and Marie Curie University in Paris, France.. "This raises the possibility that the link between NAFLD and cardiovascular ...
For proper functioning, coagulation Factor II (Thrombin), Factor VII, Factor IX, and Factor X, Protein C, and Protein S must undergo gamma-carboxylation of their glutamate residues. The enzyme that performs this reaction requires the presence of Vitamin K as a cofactor. During this enzymatic modification, Vitamin K is oxidized and must be regenerated. The enzyme which regenerates Vitamin K is competitively antagonized by warfarin, resulting in accumulation of oxidized Vitamin K and ultimately an inability to properly modify Factors II, VII, XI, X as well as Protein C/S. The end result is reduced hepatic synthesis of these coagulation factors and their gradual decline within the plasma ...
PURPOSE OF REVIEW: This review describes the most recent progress in xeno lung transplantation (XLTx) to date. It describes the potential mechanisms of early xeno lung graft loss, as well as the latest therapeutic strategies to overcome them. RECENT FINDINGS: Using ex-vivo perfusion models of porcine lungs with human blood, the use of genetically modified pig lungs along with novel pharmaceutical approaches has recently been studied. Strategies that have demonstrated improved lung survival include the knockout of known xenoantigens (GalTKO and N-glycolylneuraminic acid-KO), genes that regulate complement activation (hCD46 and hCD55), as well as the inflammation/coagulation cascade (human leukocyte antigen-E, human thrombomodulin, human endothelial protein C receptor, hCD47, hCD39, hCD73 and heme oxygenase-1 ...
Other approaches to treating patients with FVIII inhibitors include the following: Porcine FVIII, which has low cross-reactivity with human FVIII antibody Activated prothrombin complex concentrate (... more
Supplementary MaterialsDocument S1. and T?cell responsiveness to BTNL3-BTNL8-expressing cells. Conversely, CDR3 and CDR3 loops mediated LES TCR binding to endothelial protein C receptor, a clonally restricted autoantigen, with IEGF minimal CDR1, CDR2, or HV4 contributions. Therefore, the TCR can use two discrete binding modalities: a non-clonotypic, superantigen-like connection mediating subset-specific rules by BTNL/BTN molecules and CDR3-dependent, antibody-like relationships mediating adaptive T?cell biology. How these findings might broadly apply to T? cell rules is also examined. to microbial phosphoantigens (P-Ags) (Morita et?al., 2007), the V9V2 subset provides an early line of defense against particular microbial infections likely, such as for example those regarding eubacterial and mycobacterial types that make the extremely potent P-Ag (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMBPP). Conversely, adaptive paradigms seem most in a position to explain conspicuous clonal effector ...
Abcams Von Willebrand Factor ELISA Kit (ab108918) suitable for Cell culture supernatant, Serum, Plasma in human. Reliably quantify 2.5 mU/ml of Von Willebrand…
... such as factor V, factor VIII and factor X play a role in blood clotting. Lab tests can measure clotting factors to help diagnose the cause of excessive bleeding (bleeding disorder).
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Coagulation Factor Increased & Sloping Shoulders Symptom Checker: Possible causes include Birth & Puerperium & Microangiopathy. Check the full list of possible causes and conditions now! Talk to our Chatbot to narrow down your search.
Global Blood Coagulation Testing Market Information by instruments (prothrombin time, APTT, thrombo test) by methods (Global test, Local test) by End Users (Hospitals, clinics, Research Institutes) - Forecast to 2027
Make sure your doctor knows if you have had a stroke, heart attack, deep vein thrombosis (DVT), or any other heart or blood clot problem in the last 3 months. This medicine may increase your risk of blood clots. Tell your doctor right away if you have a sudden or severe headache, problems with vision or speech, chest pain, trouble breathing or swallowing, swelling or tenderness in your leg, or numbness or weakness ...
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PROTHROMBINEX-VF is a freeze-dried preparation of proteins called human prothrombin complex. PROTHROMBINEX-VF contains concentrated factor IX, factor II, factor X and low level of factor VII.
pep:known chromosome:VEGA66:1:164151838:164220277:1 gene:OTTMUSG00000034808 transcript:OTTMUST00000088478 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:F5 description:coagulation factor V ...
Increased Production and Expression of Tissue Thromboplastin-Like Procoagulant Activity In Vitro by Allogeneically Stimulated Human Leukocytes: Intravascular co
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Это страница команды биофизиков, биохимиков, математиков и врачей, которая исследует тромбоциты - самые маленькие, но крайне загадочные клетки нашего организма. Мы изучаем фундаментальные особенности их жизни и смерти - внутриклеточную сигнализацию, метаболизм, запрограммированную клеточную смерть, механизмы адгезии, взаимодействие со свертыванием крови и иммунитетом, роли в тромбозе и гемостазе, - а затем применяем это знание для практических целей: разработки новых и изучения уже существующих лекарств, создания и усовершенствования методов
After hemodilution both groups showed statistically significant increased clotting times (CT), clot formation times (CFT), and decreased maximum clot firmnesses (MCF). After fibrinogen and PCC administration, CT and CFT decreased whereas MCF increased statistically significantly. Median blood loss after liver injury was significantly smaller in the animals treated with clotting factor concentrates versus the placebo group: 240.0 ml (50.0-830.0) vs 1.800 ml (1.500-2.500) (P , 0.0001). All animals, treated with fibrinogen and PCC survived, whereas 80% of the placebo group died after liver laceration (P , 0.0001). ...
Coumadin is a Brand name for an anticoagulant (or blood thinner) drug that contains warfarin as an active ingredient. Warfarin prevents the formation of blood clots as well as their migration by inhibiting vitamin K-dependent coagulation factors. Coumadin is indicated for: treatment and prophylaxis of venous thrombosis and pulmonary embolism as its extension, treatment and prophylaxis of thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement, reduction of recurrent myocardial infarction and thromboembolic events (such as stroke or systemic embolization) after myocardial infarction and therefore the reduction the risk of death.. Coumadin has no effects on an established thrombus, and cant reverse ischemic tissue damage. The main targets of anticoagulant therapy are to prevent further extension of the formed blood clot and to prevent the risk of secondary thromboembolic complications that may result in serious and possibly fatal outcomes. Despite its ...
Regulatory subunit of the blood coagulation factor X- and IX-activating enzyme. The enzyme activates coagulation factor X (F10) by cleaving the Arg-Ile bond and is also able to activate coagulation factor IX (F9) and protein S (PROS1) by specific cleavage of Arg-Ile and Arg-Val bonds. May serve as an exosite by which the enzyme recognizes and binds to the Gla domain of factor X (F10) and factor IX (F9) in a calcium-dependent manner.
A deficiency in blood coagulation factor VIII (fVIII) is responsible for the inherited bleeding disorder hemophilia A, which affects approximately 1 in 5000 males. The development of inhibitory antibodies is a significant issue faced by hemophilia A patients receiving therapeutic infusions of fVIII. The C-terminal C2 domain of fVIII has been shown to be highly immunogenic and the site of binding for numerous antibodies of both the classical and non-classical classifications. A detailed understanding of the structural components involved in C2-antibody binding interactions is vital for the development of improved therapeutics for hemophilia patients. Here we present the structure of the classical antibody 3E6 bound to human C2 at 2.6 Å resolution. Previous studies have suggested that pairs of classical and non-classical antibodies may exhibit binding cooperativity. Comparison of the C2:3E6 structure with a previously determined ternary structure of C2 bound simultaneously to both 3E6 and the non
A Pipeline Assessment, Market Survey and Corporate Benchmark Analysis" provides a description, evaluation and assessment of the recombinant coagulation factor R&D pipelines as of October 2011. The authors analyze and assess the target pipeline for each of the coagulation factors for haemophilia and work out the target profiles of development projects. A market research study was conducted to challenge industrys target profiles and evaluate the sensitivity for pricing.. The report is built upon primary and secondary search for information and use of a proprietary database and news portal. A market survey was conducted among haematologists from haemophilia care centers. In house analysts with experience in biopharmaceutical R&D and business development authored the report and analysed and assessed the findings.. Global sales of the five major recombinant products of coagulation factors VIII, IX and VIIa in 2010 were US$ 6.2 bln (with $ conversion rate October 19, 2010). The first Marketing ...
A Pipeline Assessment, Market Survey and Corporate Benchmark Analysis" provides a description, evaluation and assessment of the recombinant coagulation factor R&D pipelines as of October 2011. The authors analyze and assess the target pipeline for each of the coagulation factors for haemophilia and work out the target profiles of development projects. A market research study was conducted to challenge industrys target profiles and evaluate the sensitivity for pricing.. The report is built upon primary and secondary search for information and use of a proprietary database and news portal. A market survey was conducted among haematologists from haemophilia care centers. In house analysts with experience in biopharmaceutical R&D and business development authored the report and analysed and assessed the findings.. Global sales of the five major recombinant products of coagulation factors VIII, IX and VIIa in 2010 were US$ 6.2 bln (with $ conversion rate October 19, 2010). The first Marketing ...
Protein-membrane interactions are a critical component of the coagulation cascade. For many coagulation factors, these interactions are mediated via γ-carboxyglutamate rich regions, or GLA domains, in a Ca2+-dependent manner. Nearly all studies of GLA domain-containing coagulation factors, and coagulation in general, have utilized supraphyisologic Ca2+ concentrations in order to fully occupy the 7 GLA domain metal binding sites (and thus maximize activity). Recent work has indicated that under physiologic conditions, 2-3 of the GLA domain metal binding sites are actually occupied by Mg2+; furthermore, the concentration of Ca2+ required to maximize coagulation factor activity is reduced to near-physiologic levels in the presence of physiologic concentrations of Mg2+. Together, these results suggest an important role for Mg2+ in coagulation. To investigate the role of Mg2+ further, I first demonstrated that tissue factor is required for the Mg2+-dependent rate enhancements and that tissue factor ...
This monoclonal antibody recognizes different epitopes on the von Willebrand factor protein, and allows the analysis of functions related to different domains.
endoplasmic reticulum sites of Gla protein synthesis. In the case of the blood coagulation proteins, the sole site of synthesis is the liver. Each carboxylated protein has a C-terminal propeptide sequence that binds the carboxylase enzyme, and directs a coordinated series of carboxylations of the recipient gluta-myl residues, before the propeptide is removed and the fully carboxylated protein is then secreted into the extracellular space for transport into the plasma.. Vitamin K acts as the essential recycling cofactor (or cosubstrate) for all protein carboxylation, Gla-forming reactions (Figure 3). In its dihydro or quinol form, the vitamin reacts with molecular oxygen, thereby creating a highly reactive, high-energy carba-nion at the Glu site for insertion of carbon dioxide, creating a new Gla residue. This vitamin K quinol oxidation step provides the essential energy for the endothermic carboxylation step. The other product of the reaction is the epoxide of vitamin K, comprising a ...
The development of factor VIII inhibitors occurs in approximately 30 to 40% of patients with severe Haemophilia A. The main negative clinical and cost consequence is the ineffectiveness of replacement therapy in patients with high-titer antibodies, who have a shorter life and greater morbidity than those who do not develop inhibitors. It is known from immunology that a regular and frequent exposure to the antigen of FVIII can induce tolerance of the immune system of the patient with inhibitors. This effect, called immune tolerance induction (ITI) is usually achieved after a prolonged exposure of the patient to FVIII, and is a common way of managing the condition of patients with inhibitors as well as the treatment of bleeding episodes with large amounts of hemostatic agents. In vitro and retrospective clinical studies suggest that FVIII/VWF complex concentrates may have less immunogenicity with respect to those plasma-derived concentrates purified with monoclonal antibodies (MABs), and ...
CSL Behring announced that the FDA has accepted for standard review its Biologics License Application (BLA) for a human 4-factor prothrombin complex concentrate (PCC) for the urgent reversal of vitamin K-antagonist therapy (eg, warfarin) in patients with acute major bleeding.
Blood coagulation factors[edit]. *Coagulation factor VIIIα. *Coagulation factor IXα ... Blood products of human origin and plasma substitutes[edit]. Blood and blood components[edit]. ... 11 Blood products of human origin and plasma substitutes *11.1 Blood and blood components ... Anti-vascular endothelial growth factor (VEGF)[edit]. *Bevacizumabα. Medicines for reproductive health and perinatal care[edit] ...
Gailani D, Broze GJ (Aug 1991). "Factor XI activation in a revised model of blood coagulation". Science. 253 (5022): 909-12. ... In contrast to HMWK, LMWK is not involved in blood coagulation. Kininogen-1 is a constituent of the blood coagulation system as ... HMWK is essential for blood coagulation and assembly of the kallikrein-kinin system. Also, bradykinin, a peptide causing ... Williams-Fitzgerald-Flaujeac factor or the HMWK-kallikrein factor is a protein that in humans is encoded by the KNG1 gene. ...
These are important in protein-protein interactions with blood coagulation factors. The name Kringle comes from the ... Patthy L (1985). "Evolution of the proteases of blood coagulation and fibrinolysis by assembly from modules". Cell. 41 (3): 657 ... and coagulation factor XII". J. Mol. Evol. 26 (4): 358-369. doi:10.1007/BF02101155. PMID 3131537. ... "Amino acid sequence of the heavy chain of human alpha-factor XIIa (activated Hageman factor)". J. Biol. Chem. 260 (9): 5328- ...
Type II domains have also been found in a range of proteins including blood coagulation factor XII; bovine seminal plasma ... Structural similarity of the protease precursor to blood coagulation factor XII". J. Biol. Chem. 268 (14): 10024-10028. PMID ... Fibronectins are involved in a number of important functions e.g., wound healing; cell adhesion; blood coagulation; cell ... Kornfeld S (1992). "Structure and function of the mannose 6-phosphate/insulinlike growth factor II receptors". Annu. Rev. ...
... of the blood coagulation-factor activity of FFP. Given the fact that there is typically an overabundance of coagulation factors ... Much of the donor blood supply is obtained at "remote" blood donation events, such as blood drives at colleges, community ... However, the (male) donor blood can be separated into packed red blood cells and plasma within 24 hours (and usually less). ... It differs from fresh-frozen plasma (FFP) in that it is frozen within 24 hours of blood collection, whereas FFP is frozen ...
Dutta-Roy, A.; Ray, T.; Sinha, A. (1986). "Prostacyclin stimulation of the activation of blood coagulation factor X by ... Impact of Maternal Nutrition Early Nutrition and Lifestyle Factors: Effects on First Trimester Placenta Human Blood Platelet ... growth factor secretion and expression of several adhesive factors. In addition, hyperactive platelets are involved in the well ... Dutta-Roy, A. K.; Sinha, A. K. (1987). "Purification and properties of prostaglandin E1/prostacyclin receptor of human blood ...
Takahashi N, Takahashi Y, Putnam FW (1986). "Primary structure of blood coagulation factor XIIIa (fibrinoligase, ... Other names in common use include: factor XIIIa, fibrin stabilizing factor, fibrinoligase, glutaminylpeptide gamma- ... This enzyme participates in complement and coagulation cascades and Huntington's disease. It employs one cofactor, calcium. ...
... stasis of blood, vessel wall injury, and altered blood coagulation.[9][10] Some risk factors predispose for venous thrombosis ... Disturbed blood flow[edit]. Further information: Blood flow. Causes of disturbed blood flow include stagnation of blood flow ... The main mechanism is exposure of tissue factor to the blood coagulation system.[22] Inflammatory and other stimuli (such as ... and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the ...
Examples are blood clots (coagulation factor XIII), as well as skin and hair. The catalytic reaction is generally viewed as ... The exact biochemical activity of transglutaminases was discovered in blood coagulation protein factor XIII in 1968. Eight ... Deficiency of factor XIII (a rare genetic condition) predisposes to hemorrhage; concentrated enzyme can be used to correct the ... doi:10.1016/0003-9861(59)90413-8. Pisano JJ, Finlayson JS, Peyton MP (1968). "[Cross-link in fibrin polymerized by factor 13: ...
... activated blood-coagulation factor II, blood-coagulation factor IIa, factor IIa, E thrombin, beta-thrombin, gamma-thrombin) is ... In the blood coagulation pathway, thrombin acts to convert factor XI to XIa, VIII to VIIIa, V to Va, fibrinogen to fibrin, and ... "The life cycle of coagulation factor VIII in view of its structure and function". Blood. 92 (11): 3983-96. PMID 9834200. Plow ... Prothrombin (coagulation factor II) is proteolytically cleaved to form thrombin in the clotting process. Thrombin in turn acts ...
TAP and antistasin were used to estimate factor Xa as a drug target. Blood coagulation is a complex process by which the blood ... Heparin targets multiple factors in the blood coagulation cascade, one of them being FXa. At first, it had many side effects ... Factor Xa is an activated serine protease that occupies a key role in the blood coagulation pathway by converting prothrombin ... These factors activate each other in a blood coagulation cascade that occurs through two separate pathways that interact, 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). Standalone Kunitz domains are used as a framework for the development of new ... a factor Xa inhibitor from the tick Ornithodoros moubata". FEBS Lett. 352 (2): 251-7. doi:10.1016/0014-5793(94)00941-4. PMID ... tissue factor pathway inhibitor precursor; and Kunitz STI protease inhibitor contained in legume seeds. Kunitz domains are ...
"Lonomia obliqua Caterpillar Spicules Trigger Human Blood Coagulation via Activation of Factor X and Prothrombin". Thrombosis ... This anti-clotting agent would attach to another protein to the body's cells and cause them to leak as blood is unable to clot ... If blood products are required, they must be given cautiously to avoid fueling the constant consumptive coagulapathy. An ... Lonomia obliqua has a toxic venom that causes disseminated intravascular coagulation and a consumptive coagulopathy, which can ...
... the blood coagulation factors II (prothrombin), VII, IX, and X, the anticoagulant proteins C and S, and the factor X-targeting ... involved in coagulation Factor VII (F7) - involved in coagulation Factor IX (F9) - involved in coagulation Factor X (F10) - ... "Identification of the phospholipid binding site in the vitamin K-dependent blood coagulation protein factor IX". J. Biol. Chem ... Coagulation factor, Gla region InterPro: IPR002383 Only major, known functions are listed in this list; knowledge about these ...
... blood coagulation factors V (Fa V) and VIII (Fa VIII); yeast Fet3p (FET3) required for ferrous iron uptake; yeast hypothetical ... Mann KG, Jenny RJ, Krishnaswamy S (1988). "Cofactor proteins in the assembly and expression of blood clotting enzyme complexes ...
... a factor determining the spatial dynamics of blood coagulation". Physics-Uspekhi. 45: 619-636. doi:10.3367/UFNr.0172.200206c. ... autowaves and bifurcation memory in the blood coagulation system); A.Yu. Loskutov (general autowave theory as well as dynamic ... "Intricate regimes of propagation of an excitation and self-organization in the blood clotting model". Physics-Uspekhi. 50: 79- ...
... a factor determining the spatial dynamics of blood coagulation". Phys. Usp. (journal). 45 (6): 619-636. doi:10.1070/ ... Subsequently, similar phenomena were also found in biological systems - in the system of blood coagulation and in one of the ... "Intricate regimes of propagation of an excitation and self-organization in the blood clotting model". Phys. Usp. (journal). 50 ...
This treatment results in activation of the extrinsic pathway of blood coagulation. ... Recombinant factor VIIa (rFVIIa) is a form of blood factor VII that has been manufactured via recombinant technology. The most ... rFVIIa, which is an activated form of factor VII, bypasses factors VIII and IX and causes coagulation without the need for ... It can't be given without inhibitor.[citation needed] It is important for some patients to shift to proper blood factors ...
... may be caused by reduced levels or absence of blood-clotting proteins, known as clotting factors or coagulation ... Factor V deficiency Prolonged Prolonged Unaffected Unaffected Factor X deficiency as seen in amyloid purpura Prolonged ... In replacement therapy, the reduced or absent clotting factors are replaced with proteins derived from human blood or created ... Disseminated intravascular coagulation Prolonged Prolonged Prolonged Decreased Von Willebrand disease Unaffected Prolonged or ...
... is major protein domain of many blood coagulation factors. Blood coagulation factors V and VIII contain a C-terminal, twice ... Davie EW, Kane WH (1986). "Cloning of a cDNA coding for human factor V, a blood coagulation factor homologous to factor VIII ... Davie EW, Kane WH (1988). "Blood coagulation factors V and VIII: structural and functional similarities and their relationship ... In coagulation factors V and VIII the repeated domains compose part of a larger functional domain which promotes binding to ...
... is a complex of a dozen blood coagulation factors that functions in catalyzing prothrombin into thrombin ... Prothrombin activator is released in the body by a cascade of chemical reactions in response to damage in a blood vessel. ...
Leytus SP, Foster DC, Kurachi K, Davie EW (1986). „Gene for human factor X: a blood coagulation factor whose gene organization ... Blood coagulation factors in human embryonic-fetal development: preferential expression of the FVII/tissue factor pathway". ... 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: ...
Coagulation factor XIII is the last zymogen to become activated in the blood coagulation cascade. Plasma factor XIII is a ... Coagulation factor XIII B chain is a protein that in humans is encoded by the F13B gene. This gene encodes coagulation factor ... 1993). "Two genetic defects in a patient with complete deficiency of the b-subunit for coagulation factor XIII". Blood. 82 (1 ... Muszbek L, Adány R, Mikkola H (1997). "Novel aspects of blood coagulation factor XIII. I. Structure, distribution, activation, ...
... discovery of the Hageman factor in blood clotting, a major discovery in blood coagulation research; first description of how ... Research History: Development of the modern technique for human blood transfusion using a cannula to connect blood vessels; ... 1969 - William Insull, MD describes the role of cholesterol in blood vessel disease. 1975 - Discovery that human renin, an ... George Washington Crile (1887 MD alumnus) - Performed first blood transfusion. Established Lakeside Hospital of what is now ...
Factor Xa (FXa) is an essential blood coagulation factor that is responsible for the initiation of the coagulation cascade. FXa ... This leads to a decrease in blood clot formation in a dose dependent manner. Reducing blood clot formation will decrease blood ... Darexaban (YM150) is a direct inhibitor of factor Xa created by Astellas Pharma. It is an experimental drug that acts as an ... Atrial fibrillation is an abnormal heart rhythm that causes a reduction in the cardiac output and blood flow to the brain. It ...
High levels of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) are also associated with worsened acne.[42] Both ... ductus arteriosus blood vessel.[47][150] Prolonged use of salicylic acid over significant areas of the skin or under occlusive ... These gene candidates include certain variations in tumor necrosis factor-alpha (TNF-alpha), IL-1 alpha, and CYP1A1 genes, ... Risk factors for the development of acne, other than genetics, have not been conclusively identified. Possible secondary ...
Activated Factor XIII catalyzes the formation of covalent crosslinking between peptide chains through ε-(γ- ... A highly sensitive label-free assay for the determination of blood coagulation Factor XIII activity is demonstrated through the ... A highly sensitive label-free assay for the determination of blood coagulation Factor XIII activity is demonstrated through the ... Controlled assembly of peptide-functionalized gold nanoparticles for label-free detection of blood coagulation Factor XIII ...
Key words: Adenovirus vector, human blood coagulation factor VIII, mammary gland, milk, goat, recombinant protein. ... here could be a low cost and further increase expression efficacy for the recombinant human blood coagulation factor and other ... at the different physiological stage were infected with the recombinant adenovirus containing a human blood coagulation factor ... High-level expression of recombinant human blood coagulation factor in milk of farm animals at a large scale provides a ...
Patients with congenital factor X deficiency can present at any age. Generally, patients with mo... more ... Factor X deficiency has no known racial or ethnic predilection. Males and females are equally affected. ... Blood coagulation factor X deficiency causes partial embryonic lethality and fatal neonatal bleeding in mice. Thromb Haemost. ... Utility of factor X concentrate for the treatment of acquired factor X deficiency in systemic light-chain amyloidosis. Blood. ...
SEARCH RESULTS for: Blood Coagulation Factor [Drug Class] (630 results) *Share : JavaScript needed for Sharing tools. Bookmark ... ALPHANINE SD (coagulation factor ix (human)) kit. NDC Code(s): 63323-185-10, 68516-1002-2, 68516-3601-2, 68516-3602-2, view ...
Coagulation Factor IX Human. Coagulation factor X. target. DB13152. Coagulation Factor IX Human. Coagulation factor XI. target ... Coagulation factor VII human. Coagulation factor X. target. DB13150. Coagulation factor VII human. Coagulation factor IX. ... Coagulation Factor IX Human. Coagulation factor VII. target. DB13152. Coagulation Factor IX Human. Coagulation factor VIII. ... Coagulation Factor IX (Recombinant). Coagulation factor X. target. DB00100. Coagulation Factor IX (Recombinant). Coagulation ...
... with modulatory effects or modulated by the coagulation cascade have been reported to affect the pathophysiology of the central ... being able to interfere with synaptic homeostasis other than coagulation itself. These specific functions modulate neuronal ... Blood coagulation factors and other proteins, with modulatory effects or modulated by the coagulation cascade have been ... "Neuro-Coagulopathy: Blood Coagulation Factors in Central Nervous System Diseases." Int. J. Mol. Sci. 18, no. 10: 2128. ...
Assessment of Plasma Coagulation on Liver Tissue in a Large Animal Model In Vivo, Surface Engineering of Pancreatic Islets ... Video articles in JoVE about blood coagulation factors include An In Vitro Model of a Parallel-Plate Perfusion System to Study ... Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process. . ... Assessment of Plasma Coagulation on Liver Tissue in a Large Animal Model In Vivo. Tim R. Glowka1, Pascal Paschenda2, Michael ...
Factor VII glycoforms. Jun. 7, 2005. 6884616. DNA-construct for the tissue-specific expression of a blood coagulation factor. ... Process for the pasteurization of plasma or concentrates of blood coagulation factors II, VII, IX and X. Feb. 12, 2002. ... Name: Drug, bio-affecting and body treating compositions > Fibrinopeptides, blood-coagulation factors or derivatives. ... Description: Subject matter wherein the peptide composition is related to fibrinopeptides, blood-coagulation factors or ...
Global Blood Coagulation Testing Market Information by instruments (prothrombin time, APTT, thrombo test) by methods (Global ... Pune, Maharashtra -- (SBWIRE) -- 01/25/2017 -- Market Synopsis of Blood Coagulation Testing Market:. Blood Coagulation Testing ... Global Blood Coagulation Testing Market Growth Opportunities, Key Driven Factors, Market Scenario Forecast to 2027. Global ... To provide insights about factors affecting the market growth. - To Analyze the Global Blood Coagulation Testing Market based ...
The synthesis of a series of novel macrocyclic compounds designed to target blood coagulation Factor XIa is described. The ... Design and synthesis of macrocyclic indoles targeting blood coagulation cascade Factor XIa. Hanessian, Stephen ... Several compounds displayed modest activity and good selectivity for Factor XIa. Within the series, a promising lead structure ...
2016)‎. Collaborative study on the 2nd International Standard for Blood Coagulation Factor XI, Plasma (‎15/180)‎: assignment of ... Collaborative study on the 1st international standard for blood coagulation factor XII, plasma: assignment of functional (‎FXII ... Collaborative study on the 2nd International Standard for Blood Coagulation Factor XI, Plasma (‎15/180)‎: assignment of ... Collaborative study for value assignment of the 4th [‎fourth]‎ international standard for factors II, VII, IX, X, plasma / by ...
Miller, J., Dalm, D., Koyfman, A. Y., Grushin, K., Stoilova-McPhie, S. Helical Organization of Blood Coagulation Factor VIII on ... 3-Dimensional structure of membrane-bound coagulation factor VIII: modeling of the factor VIII heterodimer within a 3- ... Parmenter, C. D., Stoilova-McPhie, S. Binding of recombinant human coagulation factor VIII to lipid nanotubes. FEBS letters. ... Parmenter, C. D., Cane, M. C., Zhang, R., Stoilova-McPhie, S. Cryo-electron microscopy of coagulation Factor VIII bound to ...
Coagulation Factors 2009: Target Pipeline and Corporate Benchmark Analysis. The "Coagulation Factors 2009: Target Pipeline and ... Coagulation Factors 2009: Target Pipeline and Corporate Benchmark Analysis. Publisher: La Merie Publishing ×. La Merie ... The market size of recombinant and plasma-derived coagulation factor products exceeded US$ 7.5 bln in 2008, the majority (US$ ... The authors analyze and assess the target pipeline for each of the coagulation factors used for systemic and topical ...
Blood coagulation and fibrinolysis of the newborn viewed äs perinatal factors. II. Fibrinolytic studies in the respiratory ...
The method prevents complex formation between tissue factor and factor VII/VIIa and thus inhibits coagulation of blood in ... Anti-tissue factor monoclonal antibodies produced by hybridoma cell lines TFS-5G9 or TF9-6B4 may be used in the claimed methods ... of a therapeutically effective amount of a monoclonal antibody which inhibits the ability of tissue factor to bind to factor ... This invention provides a method of inhibiting coagulation in extracorporeal circulation in a subject, comprising ...
New VCell model of blood coagulation factors 2016 -06-09 Hysteresis-like binding of coagulation factors x/xa to procoagulant ...
Blood Coagulation & Fibrinolysis" on DeepDyve, the largest online rental service for scholarly research with thousands of ... "In silico thrombin and factor Xa generation profiles in adult patients after Fontan operation, ... Abnormalities in blood coagulation, fibrinolysis, and platelet activation in adult patients after the Fontan procedure ... Add Journal to My Library Blood Coagulation & Fibrinolysis , Volume 29 (2) - Mar 1, 2018 ...
Calculation of costs was based on the price for blood products and coagulation factor concentrates in 2009: 1 U PRBC, 85 euros ... Overall costs for allogeneic blood products and coagulation factor concentrates per patient decreased by 6.5%, corresponding to ... Coagulation Factor Concentrates Combined with Point-of-Care Coagulation Testing Is Associated with Decreased Allogeneic Blood ... Coagulation Factor Concentrates Combined with Point-of-Care Coagulation Testing Is Associated with Decreased Allogeneic Blood ...
Expression and characterization of a codon-optimized blood coagulation factor VIII. J Thromb Haemost 2017; 15: 709-20, which ... Coagulation Factor VIII; LRP1 protein, human; von Willebrand Factor, Lentivirus; Hemophilia A ... Expression and characterization of a codonoptimized blood coagulation factor VIII Journal of Thrombosis and Haemostasis, 15 (4 ... Background: Production of recombinant factor VIII (FVIII) is challenging due to its low expression. It was previously shown ...
Impact of G406S and G420R mutants associated with Blood Coagulation Factor Xa: Molecular simulation approach, Shabana kouser ... Factor X is activated into Xa by Factor IX and Factor VII with its cofactor and tissue Factors. Factor X is the starting Factor ... Factor Xa is the activated form of coagulation Factor thrombokinase, also known as a stuartprower Factor. The chromosomal ... Factor Xa is a serine protease which activates thrombin and plays a significant role in blood coagulation pathway. Mutations in ...
3 Coagulation Factor Markets. 3.1 Recombinant Factor VIIIa Market 3.2 Recombinant Factor IXa Market 3.3 Recombinant Factor VIIa ... 5.1 Factor VIII 5.2 Factor IX 5.3 Factor VII 5.4 Alternative Procoagulants & Adjuncts 5.5 Factor XIII 5.6 von Willebrand Factor ... Coagulation Factors 3.7 Plasma-Derived Coagulation Factors. 4 Pipeline Changes since September 2010 4.1 Alnylam Pharmaceuticals ... Table 47 Pharmstandards Coagulation Factor Pipeline Table 48 Pfizers Coagulation Factor Pipeline Table 49 Pfizers Strategic ...
... initiates blood coagulation by promoting FXa generation (extrinsic-Xa). Subsequent generation of intrinsic FXa … ... Proteolysis of blood coagulation factor VIII by the factor VIIa-tissue factor complex: generation of an inactive factor VIII ... Proteolysis of blood coagulation factor VIII by the factor VIIa-tissue factor complex: generation of an inactive factor VIII ... Selective factor VIII activation by the tissue factor-factor VIIa-factor Xa complex. Blood. 2017;130:1661-70. PubMed ...
Furthermore, Asp(476) and Asp(479) play a role in modulating calcium-dependent conformational changes that cause factor XIIIa ... Blood coagulation factor XIIIa is a calcium-dependent enzyme that covalently ligates fibrin molecules during blood coagulation ... Blood coagulation factor XIIIa is a calcium-dependent enzyme that covalently ligates fibrin molecules during blood coagulation ... Factor XIII: a coagulation factor with multiple plasmatic and cellular functions.. László Muszbek, Zsuzsanna Bereczky, Zsuzsa ...
ABO blood group was determined by indirect technique. FVIII:C and Fbg were measured by clotting assays. VWF antigen (VWF:Ag), ... Conclusions ABO blood group, age, and gender showed different effects on plasma levels of FVIII:C, Fbg, VWF:Ag, VWF:CBA, VWF: ... and von Willebrand factor (VWF). Age and gender have been shown to influence FVIII, VWF, fibrinogen (Fbg), and ADAMTS13 (A ... Background ABO blood group is a hereditary factor of plasma levels of coagulation factor VIII (FVIII) ...
  • Factor V Leiden is the most common hereditary hypercoagulability (prone to clotting) disorder amongst ethnic Europeans. (wikipedia.org)
  • The rapid availability of results helps to discriminate surgical bleeding from a true haemostasis disorder and improves the therapy with blood products, factor concentrates, anticoagulants and protamine, hemostyptic and antifibrinolytic drugs. (wikipedia.org)
  • It is the fourth most common coagulation disorder after von Willebrand's disease and haemophilia A and B. In the United States, it is thought to affect 1 in 100,000 of the adult population, making it 10% as common as haemophilia A. In terms of the signs/symptoms of haemophilia C, unlike individuals with Haemophilia A and B, people affected by it are not ones to bleed spontaneously. (wikipedia.org)
  • We investigated FVIII/FVIIa/TF/FXa relationships in early coagulation mechanisms. (springermedizin.de)
  • Overall, these data suggest that FVIII-associated intrinsic-Xa, governed by both FVIIa/TF-induced and FXa-induced FVIII activation mediated by FVIII-TF interactions, together with FVIIa-dependent extrinsic-Xa mechanisms, may be central to the initiation phase of coagulation. (springermedizin.de)
  • Mutations in FVIII result in mild to severe Haemophilia type A, a life-threatening blood condition affecting one in 5000 of the male population (Wacey et al. (grantome.com)
  • Blood Adv (2017) 1 (15): 1080-1087. (ashpublications.org)
  • Blood (2017) 130 (23): 2463-2468. (ashpublications.org)
  • Published in 2017, a retrospective observational study in four major adult tertiary-care hospitals concluded that implementation of a unique, jurisdiction-wide PBM program was associated with improved patient outcomes, reduced blood product utilization, and product-related cost savings. (wikipedia.org)
  • The major factors contributing to the market growth is essentially determined by the expanding increase in population of cardiovascular diseases, increase in prevalence of death due to diabetic population, rise in geriatric population and rising awareness of diabetes. (sbwire.com)
  • Prevalence of hypertension and associated cardiovascular risk factors in an urban slum in Nairobi, Kenya: a population-based survey. (ac.ir)
  • Elderly patients or those with chronic medical conditions may have less tolerance to blood loss, less ability to compensate, and may take medications such as betablockers that can potentially blunt the cardiovascular response. (wikipedia.org)
  • 14 - 18 However, these studies vary widely with respect to the scope of POC measurements performed, availability and use of coagulation factor concentrates, and by consideration of either the intraoperative or postoperative period. (asahq.org)
  • There are two commercially available Factor X concentrates: "Factor X P Behring" manufactured by CSL Behring, and high purity Factor X "Coagadex" produced by Bio Products Laboratory and approved for use in the United States by the FDA in October 2015 and in the EU on 16th March 2016 after earlier acceptance by CHMP and COMP. (wikipedia.org)
  • In light of ongoing expiration of substance patents, about 40 new recombinant coagulation factor projects are in the pipeline indicating a changing marketplace over the next decade. (pipelinereview.com)
  • Ongoing patent expirations and failed life cycle management efforts leave the established companies vulnerable regarding the future growth perspective of their recombinant coagulation factor business, but at the same time opens the door to potential new market entrants. (pipelinereview.com)
  • The heavy chain contains two fibronectin-type domains, two epidermal growth factor (EGF)-like domains, a kringle domain and a proline-rich domain, whereas the light chain contains only a catalytic domain. (nih.gov)
  • The EGF-like domain includes 6 cysteine residues which in the epidermal growth factor have been shown to form 3 disulfide bonds. (wikipedia.org)
  • All members of this family share five highly conserved structural domains: an extracellular N-terminal ligand-binding domain with cysteine-rich repeats (also called ligand-binding repeats), an epidermal growth factor (EGF), an O-linked glycosylation sugar domain, a single transmembrane sequence, and a cytoplasmic domain which contains an NPxY sequence. (wikipedia.org)
  • The light chain contains an N-terminal γ-carboxyglutamic acid domain (Gla domain) and two epidermal growth factor-like domains (EGF1 and EGF2). (wikipedia.org)