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.Antithrombin III Deficiency: An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis.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.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.Antithrombin Proteins: An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.Thrombin: An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.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 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.Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Heparin Cofactor II: A sulfated plasma protein with a MW of approximately 66kDa that resembles ANTITHROMBIN III. The protein is an inhibitor of thrombin in plasma and is activated by dermatan sulfate or heparin. It is a member of the serpin superfamily.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.Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.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.Blood Coagulation Tests: Laboratory tests for evaluating the individual's clotting mechanism.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.Anticoagulants: Agents that prevent clotting.Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process.Thrombophlebitis: Inflammation of a vein associated with a blood clot (THROMBUS).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.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.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 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.Thrombophilia: A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.Protein S Deficiency: An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)ThiohydantoinsHirudins: 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.p-Dimethylaminoazobenzene: A reagent used mainly to induce experimental liver cancer. According to the Fourth Annual Report on Carcinogens (NTP 85-002, p. 89) published in 1985, this compound "may reasonably be anticipated to be a carcinogen." (Merck, 11th ed)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.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.Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.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.Kinetics: The rate dynamics in chemical or physical systems.Heparin Lyase: An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC 4.2.2.7.alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.Immunoelectrophoresis, Two-Dimensional: Immunoelectrophoresis in which a second electrophoretic transport is performed on the initially separated antigen fragments into an antibody-containing medium in a direction perpendicular to the first electrophoresis.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).Pentosan Sulfuric Polyester: A sulfated pentosyl polysaccharide with heparin-like properties.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.Dermatan Sulfate: A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed)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.Heparin Antagonists: Coagulant substances inhibiting the anticoagulant action of heparin.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.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)Oligosaccharides: Carbohydrates consisting of between two (DISACCHARIDES) and ten MONOSACCHARIDES connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form.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.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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Complement C1 Inactivator Proteins: Serum proteins that inhibit, antagonize, or inactivate COMPLEMENT C1 or its subunits.alpha-Macroglobulins: Glycoproteins with a molecular weight of approximately 620,000 to 680,000. Precipitation by electrophoresis is in the alpha region. They include alpha 1-macroglobulins and alpha 2-macroglobulins. These proteins exhibit trypsin-, chymotrypsin-, thrombin-, and plasmin-binding activity and function as hormonal transporters.Heparitin Sulfate: A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.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.Fibrinolysis: The natural enzymatic dissolution of FIBRIN.Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).Cetacea: An order of wholly aquatic MAMMALS occurring in all the OCEANS and adjoining seas of the world, as well as in certain river systems. They feed generally on FISHES, cephalopods, and crustaceans. Most are gregarious and most have a relatively long period of parental care and maturation. Included are DOLPHINS; PORPOISES; and WHALES. (From Walker's Mammals of the World, 5th ed, pp969-70)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.Fibrinopeptide B: Two small peptide chains removed from the N-terminal segment of the beta chains of fibrinogen by the action of thrombin. Each peptide chain contains 20 amino acid residues. The removal of fibrinopeptides B is not required for coagulation.Protease Nexins: Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.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.Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or N-acetylgalactosamine.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 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 VIIa: Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.Heparinoids: Heparin derivatives. The term has also been used more loosely to include naturally occurring and synthetic highly-sulphated polysaccharides of similar structure. Heparinoid preparations have been used for a wide range of applications including as anticoagulants and anti-inflammatories and they have been claimed to have hypolipidemic properties. (From Martindale, The Extra Pharmacopoeia, 30th, p232)Phlebitis: Inflammation of a vein, often a vein in the leg. Phlebitis associated with a blood clot is called (THROMBOPHLEBITIS).Benzamidines: Amidines substituted with a benzene group. Benzamidine and its derivatives are known as peptidase inhibitors.Umbelliferones: 7-Hydroxycoumarins. Substances present in many plants, especially umbelliferae. Umbelliferones are used in sunscreen preparations and may be mutagenic. Their derivatives are used in liver therapy, as reagents, plant growth factors, sunscreens, insecticides, parasiticides, choleretics, spasmolytics, etc.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.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.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.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).Fibrin: A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.Pipecolic AcidsActivated 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.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).Molecular Weight: The sum of the weight of all the atoms in a molecule.Thromboembolism: Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.Dansyl Compounds: Compounds that contain a 1-dimethylaminonaphthalene-5-sulfonyl group.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.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.PolysaccharidesThromboplastin: 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.Pregnadienes: Pregnane derivatives containing two double bonds anywhere within the ring structures.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.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.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Eosine I Bluish: A red fluorescein dye used as a histologic stain. It may be cytotoxic, mutagenic, and inhibit certain mitochondrial functions.Fluoresceins: A family of spiro(isobenzofuran-1(3H),9'-(9H)xanthen)-3-one derivatives. These are used as dyes, as indicators for various metals, and as fluorescent labels in immunoassays.Fluorescein: A phthalic indicator dye that appears yellow-green in normal tear film and bright green in a more alkaline medium such as the aqueous humor.Respiratory Distress Syndrome, Adult: A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Prognosis: A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.Goats: Any of numerous agile, hollow-horned RUMINANTS of the genus Capra, in the family Bovidae, closely related to the SHEEP.Anterior Cruciate Ligament: A strong ligament of the knee that originates from the posteromedial portion of the lateral condyle of the femur, passes anteriorly and inferiorly between the condyles, and attaches to the depression in front of the intercondylar eminence of the tibia.Extracorporeal Circulation: Diversion of blood flow through a circuit located outside the body but continuous with the bodily circulation.Heparan Sulfate Proteoglycans: Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)Heart Defects, Congenital: Developmental abnormalities involving structures of the heart. These defects are present at birth but may be discovered later in life.Cardiopulmonary Bypass: Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs.Cellular Phone: Analog or digital communications device in which the user has a wireless connection from a telephone to a nearby transmitter. It is termed cellular because the service area is divided into multiple "cells." As the user moves from one cell area to another, the call is transferred to the local transmitter.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.Aorta: The main trunk of the systemic arteries.

Sperm chemotaxis. (1/874)

Communication between spermatozoa and egg before contact by chemotaxis appears to be prevalent throughout the animal kingdom. In non-mammalian species, sperm chemotaxis to factors secreted from the egg is well documented. In mammals, sperm chemotaxis to follicular factors in vitro has been established in humans and mice. The attractants of female origin in non-mammalian species are heat-stable peptides or proteins of various sizes, or other small molecules, depending on the species. Species specificity of the attractants in non-mammalian species may vary from high species specificity, through specificity to families with no specificity within a family, to absence of specificity. The mammalian sperm attractants have not been identified but they appear to be heat-stable peptides. The claim that progesterone is the attractant for human spermatozoa has failed to be substantiated, neither have claims for other mammalian sperm attractants been verified. The molecular mechanism of sperm chemotaxis is not known. Models involving modulation of the intracellular Ca2+ concentration have been proposed for both mammalian and non-mammalian sperm chemotaxis. The physiological role of sperm chemotaxis in non-mammalian species appears to differ from that in mammals. In non-mammalian species, sperm chemotaxis strives to bring as many spermatozoa as possible to the egg. However, in mammals, the role appears to be recruitment of a selective population of capacitated ('ripe') spermatozoa to fertilize the egg.  (+info)

Age-related changes in blood coagulation and fibrinolysis in mice fed on a high-cholesterol diet. (2/874)

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

Single and combined prothrombotic factors in patients with idiopathic venous thromboembolism: prevalence and risk assessment. (3/874)

The inherited thrombophilias--deficiencies of protein C, protein S, and antithrombin III--and the prothrombotic polymorphisms factor V G1691A and factor II G20210A predispose patients toward venous thromboembolism (VTE). The aim of this study was to determine the prevalence of single and combined prothrombotic factors in patients with idiopathic VTE and to estimate the associated risks. The study group consisted of 162 patients referred for work-up of thrombophilia after documented VTE. The controls were 336 consecutively admitted patients. In all subjects factor V G1691A, factor II G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T were analyzed by specific polymerase chain reactions and restriction enzymes. Activities of antithrombin III and protein C, free protein S antigen, and lupus anticoagulant were determined in a subset of 109 patients who were not receiving oral anticoagulants. The prevalences of heterozygotes and homozygotes for factor V G1691A and factor II G20210A among patients and controls were 40.1% versus 3.9% and 18.5% versus 5.4%, respectively (P=0.0001). The prevalence of homozygotes for MTHFR C677T in patients was 22.8% and in controls, 14.3% (P=0.025). Heterozygous and homozygous factor V G1691A, factor II G20210A, and homozygous MTHFR C677T were found to be independent risk factors for VTE, with odds ratios of 16.3, 3.6, and 2.1, respectively. Two or more polymorphisms were detected in 27 of 162 patients (16.7%) and in 3 of 336 controls (0.9%). Logistic regression analysis disclosed odds ratios of 58.6 (confidence interval [CI], 22.1 to 155.2) for joint occurrence of factor V and factor II polymorphisms, of 35.0 (CI, 14.5 to 84.7) for factor V and MTHFR polymorphisms, and of 7.7 (CI, 3.0 to 19.6) for factor II and MTHFR polymorphisms. Among 109 patients in whom a complete thrombophilic work-up was performed, 74% had at least 1 underlying defect. These data indicate that in most patients referred for evaluation of thrombophilia due to idiopathic VTE, 1 or more underlying genetic predispositions were discernible. The presence of >1 of the prothrombotic polymorphisms was associated with a substantial risk of VTE.  (+info)

Oxidation of methionine residues in antithrombin. Effects on biological activity and heparin binding. (4/874)

Commercially available human plasma-derived preparations of the serine protease inhibitor antithrombin (AT) were shown to contain low levels of oxidation, and we sought to determine whether oxidation might be a means of regulating the protein's inhibitory activity. A recombinant form of AT, with similarly low levels of oxidation as purified, was treated with hydrogen peroxide in order to study the effect of oxidation, specifically methionine oxidation, on the biochemical properties of this protein. AT contains two adjacent methionine residues near the reactive site loop cleaved by thrombin (Met314 and Met315) and two exposed methionines that border on the heparin binding region of AT (Met17 and Met20). In forced oxidations with hydrogen peroxide, the methionines at 314 and 315 were found to be the most susceptible to oxidation, but their oxidation did not affect either thrombin-inhibitory activity or heparin binding. Methionines at positions 17 and 20 were significantly oxidized only at higher concentrations of peroxide, at which point heparin affinity was decreased. However at saturating heparin concentrations, activity was only marginally decreased for these highly oxidized samples of AT. Structural studies indicate that highly oxidized AT is less able to undergo the complete conformational change induced by heparin, most probably due to oxidation of Met17. Since this does not occur in less oxidized, and presumably more physiologically relevant, forms of AT such as those found in plasma preparations, oxidation does not appear to be a means of controlling AT activity.  (+info)

Dose response of intravenous heparin on markers of thrombosis during primary total hip replacement. (5/874)

BACKGROUND: Thrombogenesis in total hip replacement (THR) begins during surgery on the femur. This study assesses the effect of two doses of unfractionated intravenous heparin administered before femoral preparation during THR on circulating markers of thrombosis. METHODS: Seventy-five patients undergoing hybrid primary THR were randomly assigned to receive blinded intravenous injection of either saline or 10 or 20 U/kg of unfractionated heparin after insertion of the acetabular component. Central venous blood samples were assayed for prothrombin F1+2 (F1+2), thrombin-antithrombin complexes (TAT), fibrinopeptide A (FPA), and D-dimer. RESULTS: No changes in the markers of thrombosis were noted after insertion of the acetabular component. During surgery on the femur, significant increases in all markers were noted in the saline group (P < 0.0001). Heparin did not affect D-dimer or TAT. Twenty units per kilogram of heparin significantly reduced the increase of F1+2 after relocation of the hip joint (P < 0.001). Administration of both 10 and 20 U/kg significantly reduced the increase in FPA during implantation of the femoral component (P < 0.0001). A fourfold increase in FPA was noted in 6 of 25 patients receiving 10 U/kg of heparin but in none receiving 20 U/kg (P = 0.03). Intraoperative heparin did not affect intra- or postoperative blood loss, postoperative hematocrit, or surgeon's subjective assessments of bleeding. No bleeding complications were noted. CONCLUSIONS: This study demonstrates that 20 U/kg of heparin administered before surgery on the femur suppresses fibrin formation during primary THR. This finding provides the pathophysiologic basis for the clinical use of intraoperative heparin during THR.  (+info)

Effect of thrombin inhibition in vascular dementia and silent cerebrovascular disease. An MR spectroscopy study. (6/874)

BACKGROUND AND PURPOSE: Silent cerebrovascular disease (CVD) has been proposed as a predisposing condition for clinically overt stroke and vascular dementia. Recently, we found increased thrombin generation in silent CVD patients. Here, we report the effect of thrombin inhibition using a potent selective thrombin inhibitor on the cerebral metabolism and function in peripheral arterial occlusive disease (PAOD) patients with or without silent CVD. METHODS: We examined 17 mild chronic PAOD patients, including 2 cases of vascular dementia. We divided the patients into 2 groups: 1 was the advanced CVD group with multiple lacunar infarction and/or advanced periventricular hyperintensity detected by brain MRI (n=12), and the other was the no CVD group that had none of these abnormalities (n=5). We assessed the cerebral biochemical compounds in the deep white matter area and cerebellar hemisphere (8 cm3) by proton MR spectroscopy before and after infusion of argatroban (10 mg/d IV) over 2 hours for 7 days. RESULTS: The ratio of N-acetylasparate (NAA) to total creatine (Cre) in the deep white matter area was significantly lower in the advanced CVD group than in the no CVD group, whereas there were no significant differences in this ratio in the cerebellar hemisphere between the 2 groups. In the former group, this decreased NAA/Cre ratio significantly increased after argatroban therapy, whereas there was no change in the latter group. The 2 patients with vascular dementia showed clinical improvement with marked increases in the NAA/Cre ratio and mini-mental score. CONCLUSIONS: These results suggest that increased thrombin generation may have some pathophysiological roles in developing vascular dementia and its chronic predisposing conditions. Thrombin inhibition may break this vicious cycle and lead to clinical improvement.  (+info)

Comparison of the antithrombotic effect of PEG-hirudin and heparin in a human ex vivo model of arterial thrombosis. (7/874)

Polyethylene glycol (PEG)-hirudin is a derivative of hirudin with a long plasma half-life. We have compared the efficacy of PEG-hirudin with unfractionated heparin (UH) in preventing arterial thrombosis. Arterial thrombus formation was induced ex vivo in 12 healthy human volunteers by exposing a tissue factor-coated coverslip positioned in a parallel-plate perfusion chamber to flowing nonanticoagulated human blood drawn directly from an antecubital vein at an arterial wall shear rate of 2600 s-1 for 3.5 minutes. PEG-hirudin, UH, or saline (as control) were administered ex vivo through a heparin-coated mixing device positioned proximal to the perfusion chamber. Platelet and fibrin deposition was quantified by immunoenzymatic measure of the P-selectin and D-dimer content of dissolved plasmin-digested thrombi, respectively. UH was administered to a plasma concentration of 0.35 IU/mL. This concentration prolonged the activated partial thromboplastin time from 32+/-1 seconds to 79+/-4 seconds (P<0.01). UH did not significantly prevent platelet deposition. However, fibrin deposition was reduced by 39% (P<0.05). PEG-hirudin in plasma concentrations of 0.5, 2.5, and 5 microg/mL prolonged the activated partial thromboplastin time to 48+/-2, 87+/-4, and 118+/-4 seconds, respectively. In contrast to UH, PEG-hirudin prevented both platelet and fibrin deposition in a dose-dependent manner with a >80% reduction at 5 microg/mL (P<0.01). Furthermore, the plasma level of PEG-hirudin required to significantly prevent fibrin deposition (0.5 microg/mL) corresponded to a much shorter prolongation of activated partial thromboplastin time (48+/-2 seconds) than that needed for UH (79+/-4 seconds). Thus, our results are compatible with the view that thrombin is greatly involved in recruitment of platelets in evolving thrombi, and that PEG-hirudin is an effective agent for preventing arterial thrombosis in a human ex vivo experimental model.  (+info)

Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction. (8/874)

OBJECTIVES: The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND: Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS: Blood samples were obtained from 64 patients (mean age 67 +/- 11 years; 49 male) with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS: The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during the follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86; 95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94; 95% CI 0.90-0.99), FPA (hazard ratio 1.54; 95% CI 1.13-2.10), F1+2 (hazard ratio 2.03; 95% CI 1.17-3.53) and TAT (hazard ratio 1.88; 95% CI 1.27-2.79) as significant factors associated with cardiac mortality. In multivariate analyses, only FPA level (hazard ratio 1.84; 95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93; 95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS: Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction.  (+info)

*Antithrombin III deficiency

... (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary ... Information on antithrombin from UIUC Non-profit advocacy group for patients and families with antithrombin deficiency. ... ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a major natural pathway of ... Antithrombin Editor: Robert J Kurman, Blaustein's Pathology of the Female Genital Tract, Fifth Edition, 2002, Ch. 23, Diseases ...

*List of OMIM disorder codes

PITX3 Antithrombin III deficiency; 613118; AT3 Antley-Bixler syndrome; 207410; FGFR2 Antley-Bixler syndrome-like with ... GNPTAB Mucolipidosis III alpha/beta; 252600; GNPTAB Mucolipidosis III gamma; 252605; GNPTAG Mucolipidosis IV; 252650; MCOLN1 ... SDHAF1 Mitochondrial complex III deficiency; 124000; BCS1L Mitochondrial complex III deficiency; 124000; UQCRB Mitochondrial ... type III; 130020; COL3A1 Ehlers-Danlos syndrome, type IV; 130050; COL3A1 Ehlers-Danlos syndrome, type VI; 225400; PLOD Ehlers- ...

*Margaret Oakley Dayhoff

... antithrombin-III, alpha-antitrypsin, and ovalbumin; epidermal growth factor and the light chain of coagulation factor X; and ... Dayhoff also served on the editorial boards of three journals: DNA, Journal of Molecular Evolution and Computers in Biology and ... apolipoproteins A-I, A-II, C-I and C-III. Based on this work, Dayhoff and her coworkers developed a set of substitution ...

*Nephrotic syndrome

... particularly those caused by a decrease in blood antithrombin III levels due to leakage. Antithrombin III counteracts the ... is a greater predisposition for the formation of blood clots that is caused by a decrease in the levels of antithrombin III in ... Treatment is with oral anticoagulants (not heparin as heparin acts via anti-thrombin 3 which is lost in the proteinuria so it ... antithrombin or the immunoglobulins to pass through the cell membrane and appear in urine. Albumin is the main protein in the ...

*Antithrombin

... is also termed Antithrombin III (AT III). The designations Antithrombin I through to Antithrombin IV originate in ... Antithrombin III (AT III) refers to a substance in plasma that inactivates thrombin. Antithrombin IV (AT IV) refers to an ... AT III is generally referred to solely as "Antithrombin" and it is Antithrombin III that is discussed in this article. ... Native antithrombin can be converted to latent antithrombin (L-antithrombin) by heating alone or heating in the presence of ...

*Heparinoid

Some examples of heparin binding proteins include antithrombin III. It is thought that much protein interaction with heparin is ... 3 (5984): 614-6. doi:10.1136/bmj.3.5984.614. JSTOR 20406780. PMC 1674425 . PMID 51664. Rutjes AW, Jüni P, da Costa BR, Trelle S ... 157 (3): 180-91. doi:10.7326/0003-4819-157-3-201208070-00473. PMID 22868835. Template:Nieforth, Karl A., and Zbigniew J. ... Pharmacopeia Heparin Stage Two Monograph Revisions Open Microphone Web Meeting March 3, 2009 Powerpoint Presentation. Morris, ...

*Reptilase time

Unlike thrombin, reptilase is resistant to inhibition by antithrombin III. Thus, the reptilase time is not prolonged in blood ...

*Serpin

Petitou M, van Boeckel CA (June 2004). "A synthetic antithrombin III binding pentasaccharide is now a drug! What comes next?". ... Hunt LT, Dayhoff MO (July 1980). "A surprising new protein superfamily containing ovalbumin, antithrombin-III, and alpha 1- ... All typically have three β-sheets (named A, B and C) and eight or nine α-helices (named hA-hI). The most significant regions to ... "Antithrombin-S195A factor Xa-heparin structure reveals the allosteric mechanism of antithrombin activation". The EMBO Journal. ...

*Anti-thrombin antibodies

... antithrombin III), which can be distinguished from autoimmune anti-thrombin. Anti-thrombin antibodies can react with both types ... Autoimmune anti-thrombin was also found to inhibit the binding of antithrombin III to thrombin. Such activities are more often ... "Antigenic changes produced by complex formation between thrombin and antithrombin-III". J. Immunol. 127 (1): 239-44. PMID ... "Monoclonal antibodies directed against human alpha-thrombin and the thrombin-antithrombin III complex". Thromb. Res. 36 (5): ...

*Anticoagulant

It works by activating antithrombin III, which blocks thrombin from clotting blood. Heparin can be used in vivo (by injection ... The antithrombin protein itself is used as a protein therapeutic that can be purified from human plasma or produced ... "Thrombate III label" (PDF). Archived from the original (PDF) on 2012-11-15. Research, Center for Biologics Evaluation and. " ... Fondaparinux is a synthetic sugar composed of the five sugars (pentasaccharide) in heparin that bind to antithrombin. It is a ...

*Hypercoagulability in pregnancy

However, the other major anticoagulants, protein C and antithrombin III, remain constant. Fibrinolysis is impaired by an ... and antithrombin III deficiency. Hypercoagulability in pregnancy, particularly due to inheritable thrombophilia, can lead to ... Both anti-IIa and anti-Xa activity may return up to three hours after protamine reversal, possibly due to release of additional ... Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal ...

*Acute fatty liver of pregnancy

Castro MA, Goodwin TM, Shaw KJ, Ouzounian JG, McGehee WG (1996). "Disseminated intravascular coagulation and antithrombin III ... Deficiency of LCHAD (3-hydroxyacyl-CoA dehydrogenase) leads to an accumulation of medium and long chain fatty acids. When this ... 20 (3): 420-422. doi:10.1023/A:1005310903004. PMID 9266371. Wanders RJ, Vreken P, den Boer ME, Wijburg FA, van Gennip AH, IJlst ... It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the mother, caused by long-chain 3- ...

*Prothrombinase

After the antithrombin III binds to Factor Xa, the Fondaparinux is released and can activate another antithrombin. Another drug ... Fondaparinux binds to antithrombin III and activates the molecule for Factor Xa inhibition. In fact, Fondaparinux imparts an ... Idraparinux also binds antithrombin III, however with a 30-fold increase in affinity as compared to Fondaparinux. Idraparinux ... Factor Xa is inhibited by the antithrombin III/heparin system, which also acts to inhibit thrombin. Deficiencies of either ...

*Warfarin necrosis

Kiehl R, Hellstern P, Wenzel E (January 1987). "Hereditary antithrombin III (AT III) deficiency and atypical localization of a ... and antithrombin III deficiency. Although the above theory is the most commonly accepted theory, others believe that it is a ... Warfarin necrosis usually occurs three to five days after drug therapy is begun, and a high initial dose increases the risk of ... which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in ...

*HS3ST1

"Enzymatic modification of heparan sulfate on a biochip promotes its interaction with antithrombin III". Biochem. Biophys. Res. ... Heparan sulfate glucosamine 3-O-sulfotransferase 1 is an enzyme that in humans is encoded by the HS3ST1 gene. Heparan sulfate ... The D-glucosaminyl 3-O-sulfotransferase reaction: target and inhibitor saccharides". J. Biol. Chem. 270 (19): 11267-75. doi: ... "Entrez Gene: HS3ST1 heparan sulfate (glucosamine) 3-O-sulfotransferase 1". Razi N, Lindahl U (1995). "Biosynthesis of heparin/ ...

*Heparin cofactor II

Pizzo SV (1989). "Serpin receptor 1: a hepatic receptor that mediates the clearance of antithrombin III-proteinase complexes". ... heparin cofactor activities in a family with hereditary antithrombin III deficiency: evidence for a second heparin cofactor in ... This protein shares homology with antithrombin and other members of the alpha 1-antitrypsin superfamily. Mutations in this gene ... "minor antithrombin"). The product encoded by this gene is a serine proteinase inhibitor which rapidly inhibits thrombin in the ...

*Histidine-rich glycoprotein

Koide T, Odani S, Ono T (November 1985). "Human histidine-rich glycoprotein: simultaneous purification with antithrombin III ... 31 (3): 239-46. doi:10.1203/00006450-199203000-00009. PMID 1561009. van den Berg EA, le Clercq E, Kluft C, Koide T, van der Zee ... 34 (3): 307-12. doi:10.1007/s12016-007-8058-6. PMID 18219588. Hennis BC, van Boheemen PA, Wakabayashi S, Koide T, Hoffmann JJ, ... 412 (3): 559-62. doi:10.1016/S0014-5793(97)00827-2. PMID 9276466. Shigekiyo T, Yoshida H, Matsumoto K, Azuma H, Wakabayashi S, ...

*Reference ranges for blood tests

MedlinePlus Encyclopedia 003652 Antithrombin III at eMedicine Antithrombin CO000300 in Coagulation Test Handbook at ... 80 (3): 752-8. PMID 15321818. Reusch J, Ackermann H, Badenhoop K (May 2009). "Cyclic changes of vitamin D and PTH are primarily ... 18 (3): 228-37. doi:10.1016/j.ghir.2007.09.005. PMID 17997337. Taken from the assay method giving the lowest and highest ... 25 (3): 274-5. doi:10.1097/00043426-200303000-00019. PMID 12621252. Derived from mass values using molar mass of 44324.5 g/mol ...

*Purpura fulminans

... acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates". Intensive Care Med. 16 (2): 121 ... resulting in decreased synthesis of the regulatory proteins antithrombin, protein C and protein S, with increased synthesis of ... 16 (3): 233-237. doi:10.1080/088800199277281. PMID 10326221. Levin M, Eley BS, Louis J, Cohen H, Young L, Heyderman RS (1995 ... 42 (3): 572-581. doi:10.1016/j.yjmcc.2006.11.018. PMC 1983066 . PMID 17276456. Goldenberg NA, Manco-Johnson MJ (2008). "Protein ...

*Fondaparinux

Unlike direct factor Xa inhibitors, it mediates its effects indirectly through antithrombin III, but unlike heparin, it is ... Binding of heparin/HS to ATIII has been shown to increase the anti-coagulant activity of antithrombin III 1000 fold. In ... this monomeric sequence is thought to form the high-affinity binding site for the anti-coagulant factor antithrombin III (ATIII ... Heart J. 29 (3): 324-31. doi:10.1093/eurheartj/ehm616. PMID 18245119. Arixtra home page Alchemia home page. ...

*Inverted repeat

The antithrombin III gene's coding region is an example of an imperfect inverted repeat as shown in the figure on the right. ... The three main repeats which are largely found in particular DNA constructs include the closely precise homopurine- ... Specifically, the missense mutation would lead to a defective gene and a deficiency in antithrombin which could result in the ... Sets 1 and 2 are the stem of stem-loop A and are part of the loop for stem-loop B. Similarly, sets 3 and 4 are the stem for ...

*Sulodexide

... sulodexide potentiates the antiprotease activities of both antithrombin III and heparin cofactor II simultaneously. Clinically ... 46 (3): 797-806. doi:10.1038/ki.1994.335. PMID 7527876. Škrha J, Perušičová J, Pont'uch P, Okša A, et al. (1997). "Treatment ... 24 (3-4): 214-26. doi:10.1111/j.1527-3466.2006.00214.x. PMID 17214598. Harenberg J (1998). "Review of pharmacodynamics, ...

*Johannes Hoffmann (vascular surgeon)

Inthorn D, Hoffmann JN, Hartl WH, Mühlbayer D, Jochum M (1997): Antithrombin III supplementation in severe sepsis: beneficial ... Inthorn D, Hoffmann JN, Hartl WH, Mühlbayer D, Jochum M (1998): Effect of antithrombin III supplementation on inflammatory ... Antithrombin effects on endotoxin-induced microcirculatory disorders are mediated mainly by its interaction with microvascular ... Gierer P, Laue F, Hoffmann JN, Rotter R, Mittlmeier T, Gradl G, Vollmar B. Antithrombin reduces inflammation and ...

*Vertebrobasilar insufficiency

Screening for protein C, protein S, or antithrombin III deficiency is sometimes recommended but these are more usually ... 3] Savitz SI, Caplan LR (2005). "Vertebrobasilar disease". N. Engl. J. Med. 352 (25): 2618-26. doi:10.1056/NEJMra041544. PMID ...

*Fibrin scaffold

YKKIIKKL are from antithrombin III, modified antithrombin III, neural cell adhesion molecule and platelet factor 4, ... Complete re-epithelialization on the ocular surface with no symptom is achieved in 3 weeks. Results show that fibrin glue ... Acidic and basic fibroblast growth factor, neurotrophin 3, transforming growth factor beta 1, transforming growth factor beta 2 ...

*Susan K. Gilmour

In her examination of thrombin's effects on cancer growth, Gilmour has demonstrated that the antithrombin drug dabigatran ... 77 (3): 345-60. doi:10.1002/(SICI)1097-4644(20000601)77:3. 3.0.CO;2-P. PMID 10760944. Gilmour, SK; Avdalovic, N; Madara, T; ... 224 (3): 249-56. doi:10.1016/j.taap.2006.11.023. PMC 2098876 . PMID 17234230. Gilmour, SK; Birchler, M; Smith, MK; Rayca, K; ... 3 (1): e27360. doi:10.4161/onci.27360. PMC 3976981 . PMID 24711956. Evageliou, NF; Haber, M; Vu, A; Laetsch, TW; Murray, J; ...
Abcams Antithrombin III ELISA Kit suitable for Cell culture supernatant, Saliva, Milk, Urine, Serum, Plasma, Cell culture media, Cerebral Spinal Fluid in…
ATryn® (also known as ATIII) is a recombinant form of human antithrombin. This product demonstrates the high potential for the use of transgenic technology in the production of biotherapeutics. Antithrombin is a plasma protein with anti-coagulative and anti-inflammatory properties that, like many other proteins currently derived from human blood supply, has been difficult to manufacture using conventional recombinant protein production methods.. ...
TY - JOUR. T1 - A triangular iron(III) complex potentially relevant to iron(III)-binding sites in ferreascidin. AU - Bill, Eckhard. AU - Krebs, Carsten. AU - Winter, Manuela. AU - Gerdan, Michael. AU - Trautwein, Alfred X.. AU - Flörke, Ulrich. AU - Haupt, Hans Jürgen. AU - Chaudhuri, Phalguni. PY - 1997/1/1. Y1 - 1997/1/1. N2 - An asymmetric triangular Fe111 complex has been synthesized by an unusual Fe11-promoted activation of salicylaldoxime. Formation of tile ligand 2(bis(salicylideneamino)methyl)phenol in situ is believed to occur through the reductive deoximation of salicylaldoxime by ferrous ions. The trinuclear ferric complex has been characterized on the basis of elemental analysis. IR, variable-temperature magnetic susceptibility, and EPR and Mossbauer spectroscopies. The molecular structure established by X-ray diffraction consists of a trinuclear structure with a [Fe3(μ3-O)(μ2-OPh]61 core. Two iron ions are in a distorted octahedral environment having FEN2O4 coordination spheres, ...
Abstract. Human antithrombin III (ATIII) is a plasma inhibitor of several serine proteases of the blood coagulation system. Previous investigations have report
This study is the first to evaluate the long-term prognostic significance of hemostatic factor measurements in patients with angina pectoris and known coronary angiographic status. The clinical follow-up spanned 9.5 years, and complete follow-up information was available for 93% of the 225 patients initially recruited to the study. Although the number of patients investigated was comparatively small, the 58 patients with cardiac events, who represented more than a quarter of the original patient sample, allowed meaningful conclusions on risk relationships with hemostatic and angiographic baseline variables. Some earlier cross-sectional studies have indicated lower antithrombin III antigen or activity in patients with CAD compared with individuals without,32 33 34 35 while others have reported higher rather than lower values.36 37 In contrast, more recent investigations in large populations or patient cohorts failed to demonstrate an association of antithrombin III with the prevalence or extent ...
The primary objective of the study is to explore the efficacy and safety of ATryn® (antithrombin alfa) for the treatment of disseminated intravascular coagulation (DIC) associated with severe sepsis, when administered by continuous intravenous (IV) infusion over five days ...
antithrombin III Glasgow: abnormal antithrombin with increased heparin affinity & reduced ability to inactivate thrombin; associated with familial thrombosis; tryptic peptides Ala(371)-Arg(393) & Ser(394)-Arg(399) present in reduced amounts; Asp(187) replaced by Lys
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The results for both activity and antigen tests are given as percentages. Different labs use slightly different normal ranges, but in general, 80% to 120% is considered normal for adults. Newborns usually have about half as much antithrombin as adults. Thrombin levels in infants rise to adult levels by about 6 months of age. People with genetically inherited antithrombin deficiency typically have test results between 40% and 60%. In both type 1 and type 2 AT deficiency, the antithrombin activity test shows a low result because you dont have as much working antithrombin as you should have. When the AT activity test shows that levels are low, the antithrombin antigen test can then be used to find out whether the deficiency is type 1 or type 2. If the follow-up ...
Gentaur molecular products has all kinds of products like :search , Molecular Innovations \ Human antithrombin \ HATIII-I for more molecular products just contact us
TY - JOUR. T1 - Antithrombin III milano 2. T2 - A single base substitution in the thrombin binding domain detected with PCR and direct genomic sequencing. AU - Olds, R. J.. AU - Lane, D.. AU - Caso, R.. AU - Tripodi, A.. AU - Mannucci, P. M.. AU - Thein, S. L.. PY - 1989/12/25. Y1 - 1989/12/25. UR - http://www.scopus.com/inward/record.url?scp=0024844519&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0024844519&partnerID=8YFLogxK. U2 - 10.1093/nar/17.24.10511. DO - 10.1093/nar/17.24.10511. M3 - Article. C2 - 2602168. AN - SCOPUS:0024844519. VL - 17. SP - 10511. JO - Nucleic Acids Research. JF - Nucleic Acids Research. SN - 0305-1048. IS - 24. ER - ...
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Antithrombin III for critically ill patients Edited (no change to conclusions) answers are found in the Cochrane Abstracts powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
Buy our Antithrombin III 293T transfected lysate (positive control). ab94043 has been validated in western blot. Abcam now offers a 12-month guarantee.
OBJECTIVE: To evaluate the efficacy and safety of fondaparinux compared with nadroparin for prevention of venous thromboembolism after arthroplasty. PATIENTS AND METHODS: One hundred fifteen patients were randomized into 2 treatment groups. Patients were given fondaparinux in Group I and nadroparin in Group II. Measurements were performed on Days 1, 5, and 21. The wound area was assessed with a subjective visual analog scale. RESULTS: The blood counts, clinical biochemical tests, and coagulation tests (ie, thrombin time, partial thromboplastin time, activated partial thromboplastin time, fibrinogen, prothrombin time-International Normalized Ratio, and antithrombin III activity) did not show statistically significant differences between Group I and Group II ...
Antithrombin-III exerts antiinflammatory effects via ligation of heparan sulfate proteoglycans. Here we show in vitro that recombinant human antithrombin-III attenuates CD11b/CD18 expression of activated neutrophils and monocytes in whole blood ex vivo. As leukocyte integrin expression is triggered by extracorporeal circulation, this observation may be of relevance for pharmacological treatment during cardiopulmonary bypass ...
Evidence of decreased activation of the coagulation and fibrinolytic systems represented by a difference in the mean of the ATIII (functional assay) of the control and ATIII groups at T1, T2, T3, T5, T6 and T7 (Baseline, 30 min after study drug, 30 min on CPB, Arrival in ICU, POD 2, and POD 4). Data reported as % Functional Activity, which is calculated as the ability of Antithrombin (AT) to suppress FIIa or FXa in the presence of heparin compared to normograms, and expressed as a percentage ...
... is a protein in the blood that helps regulate blood clot formation. Antithrombin testing is used to investigate the cause of recurrent blood clot formation (such as DVT) and to identify an antithrombin deficiency.
METHODS AND RESULTS Fifty-five patients were treated with urokinase-preactivated prourokinase (n = 35) or tissue-type plasminogen activator (n = 20) for acute myocardial infarction and underwent coronary angiography at 90 minutes and at 24-36 hours into thrombolysis, and fibrinogen (Ratnoff-Menzie), D-dimer (ELISA) and thrombin-antithrombin III complex levels (ELISA) were measured. Primary patency was achieved in 39 patients (70.9%), 13 of whom (33.3%) suffered early reocclusion. Nonsignificant decreases in fibrinogen levels were observed while D-dimer levels increased +3,008 +/- 4,047 micrograms/l (p less than 0.01), differences not being significant in respect to the thrombolytic agents or to the clinical course. In contrast, while thrombin-antithrombin III complex levels decreased -4.4 +/- 13.0 micrograms/l in patients with persistent patency, they increased +7.5 +/- 13.6 micrograms/l in case of nonsuccessful thrombolysis (p less than 0.02) and +11.9 +/- 23.8 micrograms/l in case of early ...
Antithrombin III (AT III) supplementation has proven to be effective in the treatment of disseminated intravascular coagulation. According to the study by the Kumamoto University School of Medicine , administration of AT III is also useful for prevention of organ failure in animals challenged with endotoxin or bacteria and it increases the survival rate of such animals. Since inhibition of coagulation abnormalities failed to prevent organ failure in animals given bacteria, AT III may exert a therapeutic effect independent of its anticoagulant effect. This therapeutic mechanism of AT III has been explored using an animal model of septicemia. AT III prevented pulmonary vascular injury by inhibiting leukocyte activation in rats given endotoxin. This effect is mediated by the promotion of endothelial release of prostacyclin which inhibits leukocyte activation. Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect. ...
Fondaparinux (trade name Arixtra) is an anticoagulant medication chemically related to low molecular weight heparins. It is marketed by GlaxoSmithKline. A generic version developed by Alchemia is marketed within the US by Dr. Reddys Laboratories. Fondaparinux is a synthetic pentasaccharide factor Xa inhibitor. Apart from the O-methyl group at the reducing end of the molecule, the identity and sequence of the five monomeric sugar units contained in fondaparinux is identical to a sequence of five monomeric sugar units that can be isolated after either chemical or enzymatic cleavage of the polymeric glycosaminoglycans heparin and heparin sulfate (HS). Within heparin and heparin sulfate this monomeric sequence is thought to form the high-affinity binding site for the anti-coagulant factor antithrombin III (ATIII). Binding of heparin/HS to ATIII has been shown to increase the anti-coagulant activity of antithrombin III 1000 fold. In contrast to heparin, fondaparinux does not inhibit thrombin. ...
Fondaparinux (Arixtra) is a synthetic pentasaccharide anticoagulant. Apart from the O-methyl group at the reducing end of the molecule, the identity and sequence of the five monomeric sugar units contained in fondaparinux is identical to a sequence of five monomeric sugar units that can be isolated after either chemical or enzymatic cleavage of the polymeric glycosaminoglycan heparin and heparan sulfate (HS). This monomeric sequence in heparin and HS is thought to form the high affinity binding site for the natural anti-coagulant factor, antithrombin III (ATIII). Binding of heparin/HS to ATIII has been shown to increase the anti-coagulant activity of antithrombin III 1000-fold. Fondaparinux potentiates the neutralizing action of ATIII on activated Factor X 300-fold. Fondaparinux may be used: to prevent venous thromboembolism in patients who have undergone orthopedic surgery of the lower limbs (e.g. hip fracture, hip replacement and knee surgery); to prevent VTE in patients undergoing abdominal ...
Preferred Name: Tinzaparin Sodium Definition: The sodium salt of a low molecular weight heparin (LMWH), obtained by controlled enzymatic depolymerization of heparin from porcine intestinal mucosa, with antithrombotic properties. Tinzaparin is a potent inhibitor of several activated coagulation factors, especially Factors Xa and IIa (thrombin); its primary activity is mediated through the plasma protease inhibitor antithrombin. In addition, this agent may inhibit angiogenesis through: 1) competitive binding of the heparin-binding sites on endothelial cells for the proangiogenic cytokines vascular endothelial growth factor (VEGF) and beta-fibroblast growth factor (beta-FGF) and 2) increasing the release of tissue factor pathway inhibitor (TFPI), a negative regulator of angiogenesis. NCI-GLOSS Definition: A drug that is used with another drug, warfarin, to treat blood clots that form deep in the veins and to prevent new blood clots from forming. It is a type of anticoagulant. Display Name: ...
Doppler ultrasonography of the affected extremity with compression should be performed at diagnosis and then used in follow-up to determine resolution of an acute thrombus. Venography or MR angiograph... more
Shop Antithrombin ELISA Kit, Recombinant Protein and Antithrombin Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Opens the Highlight Feature Bar and highlights feature annotations from the FEATURES table of the record. The Highlight Feature Bar can be used to navigate to and highlight other features and provides links to display the highlighted region separately. Links in the FEATURES table will also highlight the corresponding region of the sequence. More... ...
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a plasma protease inhibitor and a member of the serpin superfamily. This protein inhibits thrombin as well as other activated serine proteases of the coagulation system, and it regulates the blood coagulation cascade. The protein includes two functional domains: the heparin binding-domain at the N-terminus of the mature protein, and the reactive site domain at the C-terminus. The inhibitory activity is enhanced by the presence of heparin. More than 120 mutations have been identified for this gene, many of which are known to cause antithrombin-III deficiency. [provided by RefSeq, Jul 2009 ...
Draw blood in a light-blue top (sodium citrate) tube. Spin down and send 1 mL citrated plasma frozen in plastic vial.   Note: Separate specimens must be submitted when multiple tests are ordered.
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A long standing problem in anti-cancer drug development has been the limited value of preclinical mouse tumor models to reliably predict subsequent clinical activity. All too often highly encouraging preclinical results in mice are followed by complete failure in clinical trials, especially at the randomized phase III level. There are many possible reasons that have been postulated for this preclinical/clinical discrepancy. One which we have been studying for the past decade is the failure to use mouse models which duplicate the challenging circumstance of treating advanced (established) visceral metastatic disease after primary tumors have been surgically resected. Instead, preclinical treatment of established primary tumors or low volume (micro)metastatic disease, often confined to the lungs, have been the historical preclinical model norms. To address this problem we have developed several models of postsurgical advanced metastatic disease involving human tumor xenografts grown in SCID mice, ...
Iam not able to watch the video.Its not buffering at all. Any one has any ideas about this? Thanks. Posted on 2009-10-21 19:13:28 by Dr. Santhosh Reddy Mannem.. ...
目前胃癌的细胞毒药物治疗已进入一个平台期。随着分子生物学研究的深入开展,胃癌的诊断及治疗进入了分子水平。大量的基础和临床研究正在探索胃癌的分子靶点包括:人表皮生长因子受体2、人表皮生长因子受体1、哺乳动物雷帕霉素靶蛋白、血管内皮生长因子、血管内皮生长因子2、纤维母细胞生长因子受体2、肝细胞生长因子受体以及聚腺苷酸二磷酸核糖转移酶等。目前,仅有人表皮生长因子受体2的靶向药物曲妥珠单抗及血管内皮生长因子受体2靶向药物ramucirumab被III期临床研究证实在晚期胃癌中有显著疗效,针对上述靶点的其他药物需进一步研究和开发。
Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). Inheritance is usually autosomal dominant, though a few recessive cases have been noted. The disorder was first described by Egeberg in 1965. The patients are treated with anticoagulants or, more rarely, with antithrombin concentrate. In kidney failure, especially nephrotic syndrome, antithrombin is lost in the urine, leading to a higher activity of Factor II and Factor X and in increased tendency to thrombosis. Heparin enhances ATIII activity and neutralizes "activated serine protease coagulation factors." Patients with ATIII deficiency requiring anticoagulant therapy with heparin will need higher doses of heparin. ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a ...
This should be performed in all patients with antithrombin III deficiency, especially if they have evidence of arterial thrombus. Arterial thrombosis due to antithrombin III deficiency is uncommon. Ve... more
Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. The results for both activity and antigen tests are given as percentages. Different labs use slightly different normal ranges, but in general, 80% to 120% is considered normal for adults. Newborns usually have about half as much antithrombin as adults. Thrombin levels in infants rise to adult levels by about 6 months of age.. People with genetically inherited antithrombin deficiency typically have test results between 40% and 60%.. In both type 1 and type 2 AT deficiency, the antithrombin activity test shows a low result because you dont have as much working antithrombin as you should have. When the AT activity test shows that levels are low, the antithrombin antigen test can then be used to find out whether the deficiency is type 1 or type 2.. If the follow-up ...
A method for the differential determination of plasma antithrombins, antithrombin III and alpha2 macroglobulin, is described. The method is based on the selective inactivation of plasma alpha2 macroglobulin by treatment with 0-1 M methylamine for 10 minutes at 37 degrees C and on the observation that antithrombin III and alpha2 macroglobulin inhibited in defibrinated plasma low concentrations of thrombin without mutual interference and according to pseudo-first order reaction. In healthy subjects antithrombin III was shown to account for about 70% of the total antithrombin activity. But in patients with liver cirrhosis, where low levels of total antithrombin activity were observed, the relative contribution of antithrombin III was found to be noticeably lower.. ...
Warfarin exerts its anticoagulant effect by interfering with the synthesis of the vitamin K dependent clotting factors (VII, IX, X, and thrombin). Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. Top of page Abstract. It also inhibits. Warfarin exerts its anticoagulant effect by interfering with the synthesis of the vitamin K dependent clotting factors (VII, IX, X, and thrombin). It also inhibits. Tensive experimental evidence shows that platelets support tumour metastasis. http://pvessaynjun.edu-essay.com Antithrombin III (ATIII) is a nonvitamin K dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa. E activation of platelets and the coagulation system have a. Antithrombin III (ATIII) is ...
Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.. Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria. This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is called tissue plasminogen activator (tPA). This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme plasmin.[3] There are also some anticoagulants that come ...
Base dose on pretreatment functional antithrombin activity and body weight. Initiate before delivery (peri-partum use) or about 24 hrs before surgery (surgical patients). If pregnant and undergoing surgery other than C-section, use peri-partum dose regimen. Give loading dose as 15 mins IV infusion, then maintenance dose by continuous IV infusion. Monitor antithrombin activity once or twice daily and adjust to maintain antithrombin activity between 80% and 120% of normal. May give another bolus dose if antithrombin activity is ,80% immediately post-procedure (use most recent antithrombin activity data to calculate dose). Thereafter, restart maintenance dose at the same rate of infusion as before the bolus. See literature.. ...
The anticlotting activities on some steps of the coagulation cascade of mollusc and mammalian heparins were studied. AT III-high affinity heparin is a more potent inhibitor than unfractionated heparin and mollusc heparin in the intrinsic and extrinsic pathways of thrombin and factor Xa generation. Mollusan heparin has about the same activity as the AT III high affinity-heparin on the inhibition of factor Xa and thrombin in the presence of antithrombin III and four times more inhibitory activity than unfractionated heparin on the heparin cofactor II mediated inhibition of thrombin ...
肝素經由它的硫化五糖序列與酵素抑制劑抗凝血酶(英语:antithrombin)III結合,使其構形改變而活化[35]。 活化的抗凝血酶III接著抑制凝血酶與凝血因子Xa(英语:factor Xa)以及其他蛋白酶,抑制的效果可因為肝素的加入而上升一千倍[36]。硫化五糖序列如下: GlcNAc/NS(6S)-GlcA-GlcNS(3S,6S)-IdoA(2S)-GlcNS(6S) 抗凝血酶III與肝素結合後導致的構形改變,造成它可抑制凝血因子Xa。至於凝血酶與抗凝血酶III之間的作用,除了酵素以外,還需要同時與肝素結合形成三元複合體(英语:ternary complex)才能達到抑制的效果;這部分肝素的高陰電性擔任了重要的角色[12]。因此,至少要具有十八個糖的肝素才能與凝血酶及抗凝血酶III產生有效的作用;但是與凝血因子Xa的作用只需要硫化五糖序列就可以了[37]。 ...
NPC313Hu01, AT3; ATIII; SERPINC1; Anti-Thrombin Antibodies; Serpin Peptidase Inhibitor Clade C Member 1; Coding Sequence Signal Peptide Antithrombin Part 1 | Products for research use only!
An ultra-thin hybrid film of amphiphilic iridium(III) complexes and synthetic saponite was manipulated by means of the modified Langmuir-Blodgett method. In the film deposited onto a quartz substrate, the external mixed molecular layer of amphiphilic iridium(III) complexes was reinforced by the inner layer of exfoliated synthetic saponite. As components of the molecular layer, two iridium(III) complexes were used: [Ir(dfppy)2(dc9bpy)]+ (dfppyH = 2-(4′,6′-difluorophenyl) pyridine; dc9bpy = 4,4′-dinonyl-2,2′-bipyridine) (denoted as DFPPY) and [Ir(piq)2(dc9bpy)]+ (piqH = 1-phenyisoquinoline)) denoted as PIQ). The emission spectra from the films changed from blue to red maxima with the decrease of a ratio of DFPPY/PIQ due to the energy transfer from excited DFPPY to PIQ. The intensity of red decreased with the increase of oxygen pressure through the quenching of excited iridium(III) complexes, promising a possibility as an oxygen-sensing film.
Binds to endothelial cell surfaces and plasma proteins and its activity depends on antithrombin. Heparin binds to antithrombin, causes a conformational change in the inhibitor, exposing its active site for more rapid interaction with proteases. Heparin acts as a co factor for the antithrombin-proteases reaction Antithrombin inhibits proteases espec thrombin 2a, 9a, 10a by forming stable complexes with them and the presence of heparin accelerates this reaction 1000x. The binding of AT Ill and unfractionated heparin t degradation of both factor Xa and thrombin. Pass: Binds to AT III. ...
Heparin was first studied in ACS in 1988 and has been a mainstay for acute ischemic heart disease therapy since then. Heparins represent a heterogeneous group of negatively charged, heavily sulfated glycosaminoglycans. Heparins have a heterogeneous effect on the coagulation cascade, although most of the effect is mediated through binding with antithrombin, causing a conformational change leading to inactivation of multiple enzymes in the coagulation cascade. While factors IXa, XIa, and XIIa are targets as well, thrombin (factor IIa) and factor Xa are the most clinically relevant. As mentioned, thrombin inhibition leads to inhibition of fibrin formation and factors needed for its cross-linking and stabilization. Heparins also have an impact on arterial and venous thrombosis by increasing vessel wall permeability and binding to von Willebrand factor, leading to some inhibition in platelet activation. Unfractionated heparin (UFH) represents a heterogeneous compound with some important limitations: ...
Antithrombin, a plasma serpin, is relatively inactive as an inhibitor of the coagulation proteases until it binds to the heparan side chains that line the microvasculature. The binding specifically occurs to a core pentasaccharide present both in the heparans and in their therapeutic derivative heparin. The accompanying conformational change of antithrombin is revealed in a 2.9-A structure of a dimer of latent and active antithrombins, each in complex with the high-affinity pentasaccharide. Inhibitory activation results from a shift in the main sheet of the molecule from a partially six-stranded to a five-stranded form, with extrusion of the reactive center loop to give a more exposed orientation. There is a tilting and elongation of helix D with the formation of a 2-turn helix P between the C and D helices. Concomitant conformational changes at the heparin binding site explain both the initial tight binding of antithrombin to the heparans and the subsequent release of the antithrombin-protease ...
An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance. . ...
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Since its discovery in 1917, heparin has been a fascinating, and in a way elusive, molecule. Heparin is a glycosoaminoglycan (GAG) formed by repeated sulphated oligosaccharide units. Natural preparations of heparin (usually obtained from bovine lung or porcine intestinal mucosa) can vary in the length of the polymeric unit and therefore have different molecular weights. As such, the biological actions of this GAG can vary quantitatively between different batches of the molecule. The initial activity ascribed to heparin was its capacity to prolong the process of blood clotting, an effect due to its potentiating interaction with the natural inhibitor of thrombin, antithrombin III. These properties have led to widespread use of heparin as an anticoagulant although scant attention has been paid to other biological activities of this GAG.. This situation has changed in recent years. In fact is has long been recognised that heparin has a wide range of biological effects in addition to its well ...
To the Editor:. The contribution by Troldborg, et al1 is a valuable addition to our understanding of disease, addressing half the question. Serine proteases do not function in isolation, but are also part of an enzyme-inhibitor interaction2. Noting higher enzyme concentrations in their cross-sectional study of patients with systemic lupus erythematosus1, direct correlation with nephritis and titers of anti-dsDNA, and inverse correlation with complement C3, the authors have demonstrated that serine protease levels appear to be markers of disease activity. It may also be worthwhile to assess whether their results reflect disease activity or alteration by the medications used in its treatment, as has been demonstrated for the major serine protease inhibitors, α-1-antitrypsin, α-2-macroglobulin, and antithrombin III2,3,4,5,6. Their implication of a pathophysiologic involvement is an interesting speculation, especially if a moderating component is considered.. Serine protease inhibitor levels are ...
From the hemocyte granules of the horseshoe crabs Limulus and Tachypleus. Factor C is activated by Gram-negative bacterial lipopolysaccharides and chymotrypsin. Inhibited by antithrombin III. In peptidase family S1 (trypsin family ...
A Prospective, Randomized, Investigator-Blind, Controlled, Clinical Study of Phase III on the Efficacy and Tolerability of hMG-IBSA (IBSA) Vs Menopure (Ferring) Administered s.c. [subcutaneously] in Women Undergoing COH [controlled ovarian hyperstimulation] in an ART Programme (IVF) [in vitro fertilisation ...
Navarro-Fernandez, J.; Perez-Sanchez, H.; Martinez-Martinez, I.; Meliciani, I.; Guerrero, J.A.; Vicente, V.; Corral, J.; Wenzel, W ...
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24.Comparison of Relative Concentrations of Antithrombin and Plasminogen between Five Species of Heterotherm Vertebrates. WANG Yun1, HAN Xu-dong1, LI Xin1, LIU Xiao-bao2, LU Wei-xing1, GAO Ming1, HUO Shu-ying1, LI Shuang-a. [Abstract] [Download] ...
It is not possible to provide analytics on the exact number of times a template has been used. It is possible though to look at activity reports before and after the implementation of Ardens, which will hopefully show a positive correlation.. Example reports can include:. ...
製藥大廠Cytokinetics最近宣布,公司開發的用於治療肌萎縮性脊髓側索硬化症(ALS)新藥tirasemtiv,在臨床 III 期研究中未能達到目標而宣告失敗。受這一結果影響,公司宣布將暫停該藥物的研發,公司股價應聲下跌 33%。 Cytoki...
Looking for online definition of antithrombin III deficiency in the Medical Dictionary? antithrombin III deficiency explanation free. What is antithrombin III deficiency? Meaning of antithrombin III deficiency medical term. What does antithrombin III deficiency mean?
The thrombosis in IBD is generally considered to result from the presence of a hypercoagulable state. Other contributing factors include bedrest, toxemia, and surgical procedures. Hemostatic abnormalities include thrombocytosis, elevated fibrinogen, factors V and VII, vitamin K, and decreased protein C and S, factor XIII, and antithrombin III levels (172,181,182). Sixty-three percent of CD and 25% of UC patients demonstrate free protein S deficiency. Protein C deficiency also occurs. Protein C activity may return to normal on disease remission or following subtotal colectomy (183). Other abnormalities include the presence of fibrin microclots. Platelets circulate in an activated state in IBD, and the increased platelet activation and aggregation found in this disorder may contribute to the risk of systemic thromboembolism and mucosal inflammation secondary to ischemia. Circulating immune complexes contribute to the development of vasculitis (184), which then predisposes to thrombosis. ...
TY - JOUR. T1 - Antithrombin during extracorporeal membrane oxygenation in adults. T2 - National survey and retrospective analysis. AU - Iapichino, Giacomo E.. AU - Protti, Alessandro. AU - Andreis, Davide T.. AU - Panigada, Mauro. AU - Artoni, Andrea. AU - Novembrino, Cristina. AU - Pesenti, Antonio. AU - Gattinoni, Luciano. PY - 2019/3/1. Y1 - 2019/3/1. N2 - The impact of antithrombin replacement during extracorporeal membrane oxygenation (ECMO) in adults remains unclear. This work comprises a survey, showing that antithrombin is routinely supplemented in many Italian ECMO-Centers, and a retrospective analysis on 66 adults treated with veno-venous ECMO and unfractionated heparin at our Institution. Twenty-four to 72 h after the beginning of ECMO, antithrombin activity was ≤70% in 47/66 subjects and activated partial thromboplastin time (aPTT) ratio was ,1.5 in 20/66 subjects. Activated partial thromboplastin time ratio ,1.5 was associated not with lower antithrombin activity (61 ± 17 vs. 63 ...
The complexation of Cm(iii) with human serum transferrin was investigated in a pH range from 3.5 to 11.0 using time-resolved laser fluorescence spectroscopy (TRLFS). At pH [greater-than-or-equal] 7.4 Cm(iii) is incorporated at the Fe(iii) binding site of transferrin whereas at lower pH a partially bound Cm(iii) transferrin species is formed. At physiological temperature (310 K) at pH 7.4{,} about 70% of the partially bound and 30% of the incorporated Cm(iii) transferrin species are present in solution. The Cm(iii) results obtained by TRLFS are in very good agreement with Am(iii) EXAFS results{,} confirming the incorporation of Am(iii) at the Fe(iii) binding site at pH 8.5 ...
During attempted cannulation of the right internal jugular vein, you puncture the carotid artery in a patient who is to be heparinized intraoperatively.. 1. What is your management?. 2. Would you proceed with the case?. 3. How does heparin anticoagulate?. Heparin binds to antithrombin III and the activated forms of factors II, X, XI, XII, and XIII, having an anticoagulant effect of about ninety minutes. It may produce qualitative or quantitative platelet abnormalities.. 4. The patient is resistant to heparinization. What is the defect?. Antithrombin III deficiency. 5. What is the treatment? Fresh frozen plasma.. 5. What tests measure the intrinsic and common pathways? For the intrinsic pathway, phospholipid is added to the patients plasma, and the time taken for clot formation is taken. Decreased fibrinogen and dysfibrinogenemias prolong both intrinsic and extrinsic pathways. The partial thromboplastin time, or PTT, measures all factors of the intrinsic and common paths, except factor XIII. A ...
TY - JOUR. T1 - Issues in antithrombin therapy for UA/NSTEMI. AU - Alpert, Joseph S. AU - Budaj, A. J.. AU - Gurfinkel, E. P.. AU - Henry, T. D.. PY - 2001. Y1 - 2001. N2 - In September 2000, participants at the 4th Annual Experts Meeting of the International Cardiology Forum convened to discuss guidelines for the management of unstable angina/non-ST-elevation MI, recently published by North American and European task forces. Discussion of new recommendations for antithrombin therapy focused on the role of low-molecular-weight heparin (LMWH). Although most participants found the new guidelines largely consistent with existing data, and sufficiently adaptable to most clinical settings, there was concern that neither task force specified LMWH as the antithrombin of choice for the medical management of these patients. The new guidelines continue to endorse the use of unfractionated heparin, particularly for high-risk patients, despite the evidence for the efficacy of LMWH in this setting. This is ...
The present invention provides compositions and methods for the treatment of cardiovascular diseases. More particularly, the present invention relates to modifying thrombus formation by administering an agent which, inter alia, is capable of (1) inactivating fluid-phase thrombin and thrombin which is bound either to fibrin in a clot or to some other surface by catalyzing antithrombin; and (2) inhibiting thrombin generation by catalyzing factor Xa inactivation by antithrombin III (ATIII). The compositions and methods of the present invention are particularly usefull for preventing thrombosis in the circuit of cardiac bypass apparatus and in patients undergoing renal dialysis, and for treating patients suffering from or at risk of suffering from thrombus-related cardiovascular conditions, such as unstable angina, acute myocardial infarction (heart attack), cerebrovascular accidents (stroke), pulmonary embolism, deep vein thrombosis, arterial thrombosis, etc.
Plant annexins show distinct differences in comparison with their animal orthologues. In particular, the endonexin sequence, which is responsible for coordination of calcium ions in type II binding sites, is only partially conserved in plant annexins. The crystal structure of calcium-bound cotton annexin Gh1 was solved at 2.5Šresolution and shows three metal ions coordinated in the first and fourth repeat in types II and III binding sites. Although the protein has no detectable affinity for calcium in solution, in the presence of phospholipid vesicles, we determined a stoichiometry of four calcium ions per protein molecule using isothermal titration calorimetry. Further analysis of the crystal structure showed that binding of a fourth calcium ion is structurally possible in the DE loop of the first repeat. Data from this study are in agreement with the canonical membrane binding of annexins, which is facilitated by the convex surface associating with the phospholipid bilayer by a calcium ...
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WebMD describes how warfarin compares to new blood thinners that are prescribed to prevent blood clots and stroke.It is responsible for continuously pumping oxygen and nutrient-rich blood throughout your body to sustain.. It can be in the form of sodium citrate or acid-citrate-dextrose.Lifescript offers answers to your common health and medical questions.Drugs such as rivaroxaban, apixaban and edoxaban work by inhibiting factor Xa directly (unlike the heparins and fondaparinux, which work via antithrombin activation).Fondaparinux is a synthetic sugar composed of the five sugars (pentasaccharide) in heparin that bind to antithrombin ...
Chromogenic anti-IIa method for measuring homogeneously heparin in purified systems, using a kinetics/competitive method. Offers a wide measurement range from 0 to 6 IU/mL and is appropriatefor testing heparins for their antithrombin activity.
Eclipse also sets the stage for Zetsubou No Shima, the highly-anticipated, all-new entry in the Call of Duty: Black Ops III Zombies storyline that spans the four DLC Map Packs for Black Ops III this year. The Origins characters continue on their mission to stop the zombie apocalypse not only in this universe but in all universes. Our heroes find themselves stranded on a remote Pacific island which is home to the Division 9 facility: a secret biological research lab whose experiments with Element 115 and its effects on human, animal, and plant biology has created horrors beyond belief. Zetsubou No Shima features a foliage rich island map including new terrifying zombie enemies, a variety of innovative transport mechanics, more devastating traps and classic Zombies side quests.. The Call of Duty: Black Ops III Eclipse DLC Map Pack is available at a discounted rate via the Call of Duty: Black Ops III DLC Season Pass, which features four DLC Map Packs planned for the year.. ...
MANILA, Feb. 14 -- In an effort to make every Filipino healthy and free from illness, President Benigno S. Aquino III on Valentine s Day inaugurated the
TY - JOUR. T1 - Bioequivalence of two intravenous formulations of antithrombin III. T2 - A two-way crossover study in healthy Korean subjects. AU - Kim, Kyoung Ah. AU - Lim, Yoon Young. AU - Kim, Sun Ho. AU - Park, Ji-Young. PY - 2013/11/1. Y1 - 2013/11/1. N2 - Background Treatment with antithrombin (AT)-III is indicated for patients with sepsis or hereditary AT deficiency. Objective The purpose of this study was to compare the pharmacokinetic and pharmacodynamic characteristics of 2 AT-III formulations in healthy Korean volunteers to satisfy the regulatory requirements for bioequivalence for marketing purposes. Methods A single-center, single-dose, open-label, randomized, 2-period, 2-sequence crossover study was conducted in healthy Korean volunteers. Blood samples for the drug analysis were collected for up to 216 hours after drug administration. Participants received either the test or reference formulation of AT-III 100 U/kg IV for 20 minutes in the first period and the alternative ...
Abstract: 53 patients with lung tuberculosis were divided in 3 groups in accordance with severety of disease. Leukocyte elastase, cationic proteins in neutrophils, activities of a 1-proteinase and a 2-macroglobulin were determined in patients plasma. Thromboelastographic, coagulating, fibrinolytic indices, and antithrombin III activity were also determined in 28 patients of all 3 groups. Results demonstrated the high level of leukocyte elastase (6-fold more than normal) in plasma of patients with acute tuberculosis process. This group of patients demonstrated activation of intravascular coagulation proceeded on the background of significant decrease (up to 60%) of AT III activity. Conclusion: Acuity and severety of tuberculosis process in lung may be characterized by high activity of leukocyte elastase. Degranulating activity of neutrophils and releasing of elastase are the reason of AT III deficiency and increasing of intravascular coagulating activity in tuberculosis ...
Novel conjugates of glycosaminoglycans, particularly heparin and dermatan sulfate, and amine containing species and therapeutic uses thereof are described. In particular, mild methods of conjugating heparins to proteins, such as antithrombin III and heparin cofactor II, which provide covalent conjugates which retain maximal biological activity are described. Uses of these conjugates to prevent thrombogenesis, in particular in lung airways, such as found in infant and adult respiratory distress syndrome are also described.
TY - JOUR. T1 - Cerebral thrombosis associated with active Crohns disease.. AU - Calderón, R.. AU - Cruz-Correa, M. R.. AU - Torres, E. A.. PY - 1998. Y1 - 1998. N2 - An increased incidence of cerebral thromboembolic events has been reported in young patients with inflammatory bowel disease (IBD). It has been suggested that a hypercoagulable state is associated with clinical activity of the disease, with elevation of factors V, VIII, fibrinogen and platelets and a lowering of anti-thrombin III. We present the case of a 35 y/o male with refractory Crohns disease who complained of headaches, blurred vision and tonic-clonic seizures. The studies demonstrated an ischemic stroke of the left cerebral hemisphere, without vascular abnormalities. Elevation of factor VIII, platelets, and antithrombin III were found. The symptoms were relieved with medical treatment and the patient has continued in good health after resection of the diseased terminal ileum.. AB - An increased incidence of cerebral ...
Ardeparin, marketed under the US trade name Normiflo, is a low molecular weight heparin (LMWH) anticoagulant used for the prevention of postoperative venous thrombosis. Ardeparin is derived via peroxide degradation of heparin extracted from porcine intestinal mucosa. Its molecular weight ranges from 2000 to 15,000 with an average molecular weight of 5500 to 6500. Normiflo was withdrawn from the US market in March 2000.
Thrombin-antithrombin III complex (TAT) concentration was measured in 27 control and 155 intensive care patients to (a) establish normal reference ranges, (b) measure thrombin generation in critically ill patients, and (c) determine the characteristics of the TAT assay for the diagnosis of disseminated intravascular coagulation (DIC) in children. The normal reference range was 1-4.3 micrograms/l (median 2.3 micrograms/l), and 89.7% of patients had raised TAT concentrations. Median TAT concentrations in the presence of DIC (27 micrograms/l) were significantly higher than in its absence (8 micrograms/l). Sensitivity, specificity, and positive and negative predictive values of the assay were 97.3%, 28.3%, 76.3%, and 81.3%, respectively, at a cut off of 4 micrograms/l. Excess thrombin production occurs in the majority of critically ill children. The TAT assay is potentially useful in the diagnosis of DIC in children.. ...
How can this seemingly disparate evidence be integrated with what was known before? Older data, upon which the guidelines were based, had established that thrombophilia testing was predictive of the relative risk for initial VTE. The situation is completely different for patients who have already had a spontaneous VTE. Why? It has long been known that patients with spontaneous VTE are hypercoagulable, (untreated recurrence rates of 2% to 5% per year) no matter the result of thrombophilia testing. In part this is because comprehensive laboratory testing of clinically thrombophilic patients will yield negative results---no "laboratory lesion"--- in about 30%-40% of cases. The thinking is that those patients have a thrombophilic state that hasnt been discovered yet. To keep it in perspective, remember that the concept of hereditary thrombophilia has been around since the discovery, in 1963, of antithrombin deficiency (Egeberg O: Inherited antithrombin deficiency causing thrombophilia. Thrombosis ...
Two drugs that are direct inhibitors of thrombin but that do not involve antithrombin III or vitamin K in their mechanism of action have been approved to
Fraser, J. F., Kimble R. M., Rowell, J., Choo, K., Kempf, M. M. and Muller, M. J. (2002). Smoke inhalation results in depletion of protein C and antithrombin III in an ovine model. In: Annual Scientific Congress Joint Meeting with the Royal College of Surgeons of Edinburgh Adelaide 11-15 May 2002 Abstracts in Australian and New Zealand Journal of Surgery. Annual Scientific Congress Joint Meeting with the Royal College of Surgeons of Edinburgh, Adelaide, (A68-A69). 11-15 May 2002. doi:10.1046/j.1445-2197.72.s1.13.x ...
Targeted gene delivery using non-viral vectors is a highly touted scheme to reduce the potential for toxic or immunological side effects by reducing dose. In previous reports, TAT polyplexes with DNA have shown relatively poor gene delivery. The transfection efficiency has been enhanced by condensing TAT/DNA complexes to a small particle size using calcium. To explore the targetability of these condensed TAT complexes, LABL peptide targeting intercellular cell-adhesion molecule-1 (ICAM-1) was conjugated to TAT peptide using a polyethylene glycol (PEG) spacer. PEGylation reduced the transfection efficiency of TAT, but TAT complexes targeting ICAM-1 expressing cells regained much of the lost transfection efficiency. Targeted block peptides properly formulated with calcium offer promise for gene delivery to ICAM-1 expressing cells at sites of injury or inflammation. ...
The invention relates to iron(III) complex compounds and pharmaceutical compositions comprising them for the use as medicaments, in particular for the treatment and/or prophylaxis of iron deficiency
Age of Wonders III is the long anticipated sequel to the award-winning strategy series. Delivering a unique mix of Empire Building, Role Playing and Warfare, Age of Wonders III offers the ultimate in turn-based fantasy strategy for veterans of the series and new players alike!
Age of Wonders III is the long anticipated sequel to the award-winning strategy series. Delivering a unique mix of Empire Building, Role Playing and Warfare, Age of Wonders III offers the ultimate in turn-based fantasy strategy for veterans of the series and new players alike!
How is Retinoic Acid Induced Heparin Binding Protein abbreviated? RI-HB stands for Retinoic Acid Induced Heparin Binding Protein. RI-HB is defined as Retinoic Acid Induced Heparin Binding Protein rarely.
Thrombin Receptor山羊多克隆抗体(ab87647)可与人样本反应并经WB实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
Im a mild Tiger-Mom who happens to be from the Caribbean so my kids have to deal with high expectations. Sorry, its in my blood. Actually, Im not sorry at all. I expect them to aim for high grades, work hard at activities that they choose and never live with a sense of entitlement. I have a hard time lowering my expectations…except when it comes to myself. (More on that in another post). I grew up in this type of environment, so its all I know. My bio-daughter is used to it as well. She is the classic overachiever and seems to thrive when she is challenged. My stepdaughter is also brilliant, insanely athletic and very creative but being pushed doesnt motivate her. It actually stifles her. She needs more nurturing. I realized when she came to live with us, I had taken on the role of "Governess". For those of you who dont know what this means, think back to The Sound of Music and the oldest daughter, Liesl repeatedly saying "I dont need a governess!" A governess is an educated woman who ...
Elated by the better-than-expected 7.8-percent GDP growth, President Benigno Aquino III on Friday pushed for an accelerated phase of industrialization to turn the country into a
ECHA състави списък на веществата, които е вероятно да отговарят на критериите по приложение III към регламента REACH. Целта е да се подпомогнат регистрантите при определяне дали са приложими намалени изисквания за информация, или е необходимо да предоставят пълния набор информация по приложение VII.. Списъкът е изготвен въз основа на експериментални данни от публично достъпни бази данни и на резултати, получени от (Q)SAR модели. Показателите за опасни токсикологични и екотоксикологични свойства, както и информацията за употреби и друга налична свързана ...
BACKGROUND AND OBJECTIVES: The G20210A polymorphism in the prothrombin gene is a common cause of inherited thrombophilia. Scarce information is available about the circumstances of the heralding thrombotic manifestation at different ages. The aim of this study was to determine the risk of spontaneous or secondary venous thromboembolism (VTE) among younger and older carriers of the G20210A prothrombin polymorphism. DESIGN AND METHODS: We performed a case-control study, investigating 650 patients with a first objectively documented deep venous thrombosis of the legs or pulmonary embolism and 703 individuals with no history of vascular disease. In all of them we carried out laboratory screening for antithrombin III, protein C and protein S deficiencies, and for the presence of the factor V Leiden and the G20210A prothrombin polymorphisms. RESULTS. After adjustment for other inherited causes of thrombophilia (deficiency of antithrombin III, protein C or S, factor V Leiden) the overall risk for VTE ...
TY - JOUR. T1 - Optically active β-ketoiminato manganese(III) complexes as efficient catalysts in enantioselective aerobic epoxidation of unfunctionalized olefins. AU - Nagata, Takushi. AU - Imagawa, Kiyomi. AU - Yamada, Tohru. AU - Mukaiyama, Teruaki. PY - 1994/6/1. Y1 - 1994/6/1. N2 - A novel manganese(III) complex having an optically active N, N′-ethylenebis-β-ketoimine ligand was prepared and characterized crystallographically. The manganese(III) complexes behave as effective catalysts in enantioselective epoxidation of unfunctionalized olefins by combined use of molecular oxygen, an oxidant, and pivalaldehyde, a reductant. Dihydronaphthalene derivatives were converted into the corresponding optically active epoxides with good to high enantioselectivities.. AB - A novel manganese(III) complex having an optically active N, N′-ethylenebis-β-ketoimine ligand was prepared and characterized crystallographically. The manganese(III) complexes behave as effective catalysts in enantioselective ...
Fibrin split product D-dimer (DD) is most probably involved in the development of vascular disorders. At 1.5 μM concentration DD inhibited the incorporation of D-[1-3H]glucosamine hydrochloride and [2-14C]acetate · Na into pericellular heparan sulphate (HS) of rabbit coronary endothelial cells without affecting other groups of glycosaminoglycans (GAGs). At the same time, DD reduced HS ability to bind antithrombin (AT) and suppressed NO production. The effect of DD on pericellular GAGs was similar to that of Nw-methyl-L-arginine, the competitive inhibitor of endothelial NO synthase (eNOS). L-Ascorbic acid, eNOS activator, increased the level of endogenous NO in the DD-treated cells, and restored HS accumulation and antithrombin binding. It is suggested that DD influence on endothelial HS may be mediated by NO production. Another effect of DD, namely, stimulation of plasminogen activator inhibitor-1 (PAI-1) secretion did not depend on the NO level. The decreased HS content, reduced anticoagulant ...
Hypertension is an important risk factor of atherothrombosis development. An additional cardiovascular risk of thromboembolic complications in hypertensive patients may be partly due to an imbalance between prothrombotic and fibrinolytic factors in the blood circulation. Its cause is mainly due to increased shear stress and renin-angiotensin-aldosterone (RAA) system pathological activation, especially angiotensin-converting enzyme (ACE) and angiotensin II (ANG II). A prothrombotic state in arterial hypertension and left ventricular hypertrophy increase the risk of ischemic stroke eightfold and heart infarction fourfold. The fibrinolytic system is one of the defense mechanisms for the prevention of intravascular thrombosis. Important components are protein anticoagulants (antithrombin III, protein C and S, heparin cofactor II) and short-acting, endothelial platelet inhibitors - nitric oxide (NO) and prostacyclin [3]. Hemostatic risk factors in arterial hypertension are: plasminogen activator ...
Physician assistants and nurse practitioners use Clinical Advisor for updated medical guidance to diagnose and treat common medical conditions in daily practice.
Changes in the fibrinolytic system may lead to coagulation disorders in acute trauma patients. This study examined fibrin degradation by measuring D-dimer crosslinked fibrin degradation products (indicates hypercoagulability), plasminogen activators (fibrinolysis), and antithrombin III in 42 adult t...
INTENDED USE: BIOPHEN H-CoII kit is a chromogenic assay for measuring Heparin Cofactor II activity in human plasma or in purified systems, using a chromogenic method, manual or automated, based on the inhibition of a constant but in excess amount of thrombin. TEST PRINCIPLE: Heparin Cofactor II is an anticoagulant protein which inhibits specifically thrombin. This inhibition is highly enhanced by glycoaminoglycans such as Dermatan Sulfate (1). By contrast with Heparin, Dermatan Sulfate activates specifically Heparin Cofactor II (7). The BIOPHEN H-CoII assay is a chromogenic method based on the inhibition of a constant and in excess amount of thrombin, by the tested Heparin Cofactor II in presence of dermatan sulfate, and measurement of residual thrombin by its amidolytic activity on a thrombin specific chromogenic substrate (SIIa-01). pNA is then released from the substrate. The amount of pNA released is directly related to the residual thrombin activity. There is an inverse relationship
OBJECTIVE: To investigate the effects of short term atorvastatin treatment on forearm vasodilatory response to reactive hyperaemia (RH%) and on components of the thrombosis-fibrinolysis system (antithrombin III, proteins and S, factors V and VII, von Willebrand factor, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1)) in patients with heart failure. PATIENTS AND METHODS: 35 patients with heart failure were enrolled in this study; 17 patients received atorvastatin 10 mg/day and 18 patients received no statin for four weeks. Forearm blood flow (FBF) was measured by venous occlusion strain gauge plethysmography. RH% and forearm vasodilatory response to nitrate were defined as the percentage change of FBF from rest to the maximum flow during reactive hyperaemia and after nitrate administration, respectively. Plasma concentrations of antithrombin III, protein C, protein S, factor V, factor VII, von Willebrand factor, tPA, and PAI-1 were determined before and after treatment.
Activated Clotting Time (ACT) (1), Activated Protein C Resistance, Activated PTT (APTT), Alpha 2-Antiplasmin, Antithrombin III, Bleeding Time, D-Dimer, Factor II, Factor V, Factor V Leiden, Factor VII, Factor VIII, Factor IX, Factor Ixa, Factor X (Stuart Factor), Factor Xa, Factor XI, Factor XII, Factor XIII, Fibrin Degradation Products, Fibrinogen, Fletcher Factor/Pre-Kallikrein Factor Activation, Heparin/Anti-Factor Xa, Heparin-Induced Thrombocytopenia, Plasmin, Plasminogen, Plasminogen Activator Inhib., Platelet Function/Aggregation, Protein C, Protein S, Prothrombin Mutation, Prothrombin Time (PT), Reptilase Time, Thrombin Time, Von Willebrands Factor Fav/Ag, and others ...
Although widely used for its anti-estrogen properties tamoxifen has estrogen like effects on a number of tissues including bone and liver. Previous studies suggest a preservation of lumbar spine density in postmenopausal women but the effect on the hip had not been addressed. To determine whether tamoxifen prevents bone loss in the early postmenopausal period bone mineral density at the lumbar spine and femoral neck was measured using dual energy X-ray absorptiometry at presentation and 6 monthly thereafter for 1 year in a prospective controlled study. Also indices of bone turnover, serum osteocalcin and urinary hydroxyproline excretion, were assessed. Fifteen early postmenopausal women with Stage I or II breast cancer treated with tamoxifen and 21 normal postmenopausal women were studied. Sex hormone binding globulin and antithrombin III levels in serum were also measured as indices of the hepatic estrogenic activity. Tamoxifen (20 mg daily) prevented bone loss at the femoral neck and lumbar spine.
Treatments include medications (anti inflammatory medicine, anticoagulants), increased ambulation, compression stockings and focusing on causative factors (antibiotics for infections). Other treatment modalities may include varicose vein stripping, insertion of a filter in the main vein in the abdomen (vena cava) and clot removal or bypass Medications used in treatment include Heparin, Reteplase (Retavase), Penicillin G, Clindamycin (Cleocin), Metronidazole (Flagyl), Amphotericin B (AmBisome). The edema associated with thrombophlebitis should subside upon treatment of the condition. If not, gentle decongestive therapy may be necessary. Medications used in treatment might include IV heparin, warfarin, oxymetholone, antithrombin III, Stanozolol, ethylestrenol. Medications will be based on underling or complication medical conditions, type and severity of thrombophlebitis, whether aseptic or septic. Taking an analgesic, such as aspirin or another nonsteroidal anti-inflammatory drug (NSAIDs) usually ...

Antithrombin III deficiency - WikipediaAntithrombin III deficiency - Wikipedia

Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary ... Information on antithrombin from UIUC Non-profit advocacy group for patients and families with antithrombin deficiency. ... ATIII binds to thrombin and then forms the thrombin-anti thrombin complex or TAT complex. This is a major natural pathway of ... Antithrombin Editor: Robert J Kurman, Blausteins Pathology of the Female Genital Tract, Fifth Edition, 2002, Ch. 23, Diseases ...
more infohttps://en.wikipedia.org/wiki/Antithrombin_III_deficiency

What are the sexual predilections of antithrombin III (ATIII) deficiency?What are the sexual predilections of antithrombin III (ATIII) deficiency?

No sex-related difference is noted in terms of the prevalence of congenital antithrombin III deficiency. Women of childbearing ... Antithrombin III Deficiency Q&A What are the sexual predilections of antithrombin III (ATIII) deficiency?. Updated: Feb 10, ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ... Women who are antithrombin III-deficient heterozygotes are at an increased risk of thrombosis when taking OCs, which have also ...
more infohttps://www.medscape.com/answers/954688-119851/2056380-overview

What is the role of echocardiography in the workup of antithrombin III (ATIII) deficiency?What is the role of echocardiography in the workup of antithrombin III (ATIII) deficiency?

Arterial thrombosis due to antithrombin III deficiency is uncommon. Ve... more ... This should be performed in all patients with antithrombin III deficiency, especially if they have evidence of arterial ... Antithrombin III Deficiency Q&A What is the role of echocardiography in the workup of antithrombin III (ATIII) deficiency?. ... Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J. 2014 Apr-Jun. 40 (2):141 ...
more infohttps://www.medscape.com/answers/954688-119865/1267714-overview

Analysis of the N-glycans of recombinant human Factor IX purified from transgenic pig milk<...Analysis of the N-glycans of recombinant human Factor IX purified from transgenic pig milk<...

While tg-FIX contains only complex structures, antithrombin III (goat), C1 inhibitor (rabbit), and lactoferrin (cow) have both ... While tg-FIX contains only complex structures, antithrombin III (goat), C1 inhibitor (rabbit), and lactoferrin (cow) have both ... While tg-FIX contains only complex structures, antithrombin III (goat), C1 inhibitor (rabbit), and lactoferrin (cow) have both ... While tg-FIX contains only complex structures, antithrombin III (goat), C1 inhibitor (rabbit), and lactoferrin (cow) have both ...
more infohttps://nebraska.pure.elsevier.com/en/publications/analysis-of-the-n-glycans-of-recombinant-human-factor-ix-purified

Factor V Leiden Mutation and PT 20210 Mutation: The TestFactor V Leiden Mutation and PT 20210 Mutation: The Test

Related tests: Antithrombin; Protein C and Protein S; Homocysteine; MTHFR Mutation; Factor V R2 A4070G Mutation ... which is associated with 2.5 to 3 fold greater risk of developing a venous thromboembolism (VTE) in Caucasians; there is not ...
more infohttps://labtestsonline.org/understanding/analytes/factor-v-and-pt20210/tab/test

Antithrombin III and Atherosclerosis | SpringerLinkAntithrombin III and Atherosclerosis | SpringerLink

U. Hedner, I.M. Nilsson, Antithrombin III in clinical material. Thrombos. Res. 3:631-641 (1973).CrossRefGoogle Scholar ... J.R. OBrien, Antithrombin III and heparin clotting times in thrombosis and atherosclerosis. Thromb. Piathes. Haemorrh. 32:116- ... O.R. Odegard, M.K. Fagerhol, M. Lie, Heparin cofactor activity and antithrombin III concentration in plasma related to age and ... R.H. Yue, M.M. Gertler, T. Staar, R. Koutrouby, Alteration of plasma antithrombin III levels in ischemic heart disease. ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4684-8616-2_6

Antithrombin III activity in baboons | SpringerLinkAntithrombin III activity in baboons | SpringerLink

The results indicate that antithrombin III-heparin cofactor activity is significantly lower... ... The antithrombin III-heparin cofactor activity of 65 baboons and 130 healthy human subjects was measured. ... Antithrombin III deficiency in a Dutch family.J. Clin. Path., 26: 532-538.PubMedGoogle Scholar ... Antithrombin III, antifactor Xa and Heparin.Brit. J. Haemat., 19: 283-305.PubMedGoogle Scholar ...
more infohttps://link.springer.com/article/10.1007/BF02382805

antithrombin-III precursor [Bos taurus] - Protein - NCBIantithrombin-III precursor [Bos taurus] - Protein - NCBI

LSBio Antithrombin-III Elisa Kits [LifeSpan BioSciences, Inc.] LSBio Antithrombin-III Elisa Kits. LifeSpan BioSciences, Inc. ... LSBio Antithrombin-III Proteins [LifeSpan BioSciences, Inc.] LSBio Antithrombin-III Proteins. LifeSpan BioSciences, Inc. ... LSBio Antithrombin-III Antibodies [LifeSpan BioSciences, Inc.] LSBio Antithrombin-III Antibodies. LifeSpan BioSciences, Inc. ... antithrombin-III precursor [Bos taurus] antithrombin-III precursor [Bos taurus]. gi,77736341,ref,NP_001029870.1, ...
more infohttps://www.ncbi.nlm.nih.gov/protein/77736341

Congenital antithrombin III deficiency: MedlinePlus Medical EncyclopediaCongenital antithrombin III deficiency: MedlinePlus Medical Encyclopedia

Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. ... The abnormal gene leads to a low level of the antithrombin III protein. This low level of antithrombin III can cause abnormal ... Antithrombin III is a protein in the blood that blocks abnormal blood clots from forming. It helps the body keep a healthy ... Congenital antithrombin III deficiency is an inherited disease. It occurs when a person receives one abnormal copy of the ...
more infohttps://medlineplus.gov/ency/article/000558.htm

Antithrombin III blood test: MedlinePlus Medical EncyclopediaAntithrombin III blood test: MedlinePlus Medical Encyclopedia

AT III) is a protein that helps control blood clotting. A blood test can determine the amount of AT III present in your body. ... Functional antithrombin III; Clotting disorder - AT III; DVT - AT III; Deep vein thrombosis - AT III ... Antithrombin III (AT III) is a protein that helps control blood clotting. A blood test can determine the amount of AT III ... Antithrombin III (AT-III) test - diagnostic. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ...
more infohttps://medlineplus.gov/ency/article/003661.htm

Species: Antithrombin-III (IPR015555) | InterPro | EMBL-EBISpecies: Antithrombin-III (IPR015555) | InterPro | EMBL-EBI

Species: Antithrombin-III (IPR015555). Key Species. Key species. Number of proteins. FASTA. Protein IDs. ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR015555/taxonomy

Antithrombin III Deficiency: Practice Essentials, Pathophysiology, EpidemiologyAntithrombin III Deficiency: Practice Essentials, Pathophysiology, Epidemiology

Antithrombin III activity is markedly potentiated by heparin, the principle mechanism by which both heparin and low molecular ... Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa. ... encoded search term (Antithrombin III Deficiency) and Antithrombin III Deficiency What to Read Next on Medscape. Related ... In these patients, replacement of antithrombin III using antithrombin III concentrates or fresh frozen plasma is recommended. ...
more infohttps://emedicine.medscape.com/article/954688-overview

Anti-Antithrombin III antibody (ab124259) | AbcamAnti-Antithrombin III antibody (ab124259) | Abcam

Sheep polyclonal Antithrombin III antibody validated for IHC, ID, DID, Ie and tested in Human. Immunogen corresponding to full ... Type III: alteration of the heparin-binding domain. Plasma AT-III antigen levels are normal in type II and III. Type IV: ... Defects in SERPINC1 are the cause of antithrombin III deficiency (AT3D) [MIM:613118]. AT3D is an important risk factor for ... ab124259, at 5µg/ml, staining Antithrombin III in formalin-fixed, paraffin-embedded Human intestine vessels tissue. ...
more infohttps://www.abcam.com/antithrombin-iii-antibody-ab124259.html

Antithrombin III 293T transfected lysate (ab94043)Antithrombin III 293T transfected lysate (ab94043)

Buy our Antithrombin III 293T transfected lysate (positive control). ab94043 has been validated in western blot. Abcam now ... All lanes : Anti-Antithrombin III antibody (ab66234) at 1/500 dilution. Lane 1 : Antithrombin III overexpression 293T lysate ( ... Type III: alteration of the heparin-binding domain. Plasma AT-III antigen levels are normal in type II and III. Type IV: ... 293T cell transfected lysate in which Human Antithrombin III has been transiently over-expressed using a pCMV-Antithrombin III ...
more infohttp://www.abcam.com/antithrombin-iii-overexpression-293t-lysate-whole-cell-ab94043.html

Antithrombin III | Medical Tests | UCSF Medical CenterAntithrombin III | Medical Tests | UCSF Medical Center

Antithrombin III. Definition. Antithrombin III (AT III) is a protein that helps control blood clotting. A blood test can ... Functional antithrombin III; Clotting disorder - AT III; DVT - AT III; Deep vein thrombosis - AT III ... Antithrombin III (AT-III) test - diagnostic. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ... This can occur when there is not enough AT III in your blood, or when there is enough AT III in your blood, but the AT III does ...
more infohttps://www.ucsfhealth.org/tests/003661.html

Antithrombin III deficiency - wikidocAntithrombin III deficiency - wikidoc

Differentiating Antithrombin III deficiency from other Diseases. Epidemiology and Demographics. Risk Factors. Screening. ... primary: Antithrombin III deficiency - Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden ... Synonyms and Keywords: Antithrombin 3 deficiency Overview. Historical Perspective. Pathophysiology. Causes. ... WHO-III/malignant (Acute monocytic leukemia, Malignant histiocytosis, Erdheim-Chester disease). Other. Chronic granulomatous ...
more infohttp://www.wikidoc.org/index.php/Antithrombin_III_deficiency

Universitätsklinikum Halle(Saale): Antithrombin IIIUniversitätsklinikum Halle(Saale): Antithrombin III

Erwachsene. m/w: 80 - 120 % Quelle: Packungsbeilage STA-Stachchrom ATIII. Kinder. 1 Tag: 58-90 %. 3 Tage: 60-89 %. 1-12 Monate: 72-134 %. 1-5 Jahre: 101-131 %. 6-10 Jahre: 95-134 %. 11-16 Jahre: 96-126 %. Quelle: Referenzbereiche bei Kindern, Fa. Stago Ref. 26184 ...
more infohttps://www.medizin.uni-halle.de/index.php?id=4899&L=1%2527&BF=

RCSB PDB 









- 1DZG: N135Q-S380C-ANTITHROMBIN-III Macromolecule Annotations PageRCSB PDB - 1DZG: N135Q-S380C-ANTITHROMBIN-III Macromolecule Annotations Page

The Conformational Activation of Antithrombin. A 2. 85-A Structure of a Fluorescein Derivative Reveals an Electrostatic Link ... Antithrombin; Chain I, domain 2 Antithrombin, subunit I, domain 2 L1. 1dzgL01. Mainly Beta Roll Alpha-1-antitrypsin; domain 1 ... Antithrombin Human (Homo sapiens) [TaxId: 9606] L. d1dzgl_. Multi-domain proteins (alpha and beta) Serpins Serpins Serpins ...
more infohttp://www.rcsb.org/pdb/explore/derivedData.do?structureId=1DZG

Serpin C1/Antithrombin-III: Novus BiologicalsSerpin C1/Antithrombin-III: Novus Biologicals

Browse our Serpin C1/Antithrombin-III all backed by our Guarantee+. ... Serpin C1/Antithrombin-III available through Novus Biologicals. ...
more infohttps://www.novusbio.com/gene-name/serpinc1

antithrombin III Glasgow
     Summary Report | CureHunterantithrombin III Glasgow Summary Report | CureHunter

... abnormal antithrombin with increased heparin affinity & reduced ability to inactivate thrombin; associated with familial ... antithrombin III Glasgow. Subscribe to New Research on antithrombin III Glasgow abnormal antithrombin with increased heparin ... 08/01/1987 - "Antithrombin III Glasgow: a variant with increased heparin affinity and reduced ability to inactivate thrombin, ... AT III Glasgow; Glasgow antithrombin III; antithrombin Glasgow III. Networked: 1 relevant articles (0 outcomes, 0 trials/ ...
more infohttp://www.curehunter.com/public/keywordSummaryC054089-antithrombin-III-Glasgow.do

anti-Antithrombin III antibody  | GeneTexanti-Antithrombin III antibody | GeneTex

... antithrombin), member 1) for ELISA. Anti-Antithrombin III pAb (GTX30705) is tested in Human samples. 100% Ab-Assurance. ... Antithrombin III antibody (serpin peptidase inhibitor, clade C ( ... many of which are known to cause antithrombin-III deficiency. [ ... serpin peptidase inhibitor, clade C (antithrombin), member 1. Background. The protein encoded by this gene is a plasma protease ...
more infohttp://www.genetex.com/Antithrombin-III-antibody-GTX30705.html

antithrombin III ELISA Kits from MyBioSource.com | Biocompare.comantithrombin III ELISA Kits from MyBioSource.com | Biocompare.com

Compare antithrombin III ELISA Kits from MyBioSource.com from leading suppliers on Biocompare. View specifications, prices, ... antithrombin III ELISA Kits from MyBioSource.com. The ELISA (enzyme-linked immunosorbent assay) is a well-established antibody- ... Your search returned 79 antithrombin III ELISA ELISA Kit across 1 supplier. ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-338694/ELISA_Kit/ELISA_antithrombin_III?vids=104355

Antithrombin III | BioVendorAntithrombin III | BioVendor

You are here: Home Products by Molecule of Interest Antithrombin III Antithrombin III. Antithrombin III is a plasma protein ... Antithrombin III is a heparin-binding glycoprotein that acts as the major inhibitor of thrombin. Also it interferes with ... In addition, a number of recent studies have shown that antithrombin III has antiinflammatory properties, which are independent ...
more infohttps://www.biovendor.com/antithrombin-iii

RCSB PDB 









- 1DZH: P14-FLUORESCEIN-N135Q-S380C-ANTITHROMBIN-III Methods Report PageRCSB PDB - 1DZH: P14-FLUORESCEIN-N135Q-S380C-ANTITHROMBIN-III Methods Report Page

The Conformational Activation of Antithrombin. A 2. 85-A Structure of a Fluorescein Derivative Reveals an Electrostatic Link ... 5MG/ML 1:1 MIX OF INHIBITORY: LATENT ANTITHROMBIN-III, 10.5% PEG 4000, 65 MM NACACODYLATE, PH 6.5. ...
more infohttp://www.rcsb.org/pdb/explore/materialsAndMethods.do?structureId=1DZH

Antithrombin III injection - AHealthyMe - Blue Cross Blue Shield of MassachusettsAntithrombin III injection - AHealthyMe - Blue Cross Blue Shield of Massachusetts

Antithrombin III injection. What is this medicine?. ANTITHROMBIN III (AN te throm bin) is a natural protein. It is used to ... an unusual or allergic reaction to antithrombin III, goat or goat milk proteins, other medicines, foods, dyes, or preservatives ... treat patients with low levels of antithrombin III. People with this condition may have an increased risk for developing blood ...
more infohttp://www.ahealthyme.com/Library/DiseasesConditions/Adult/Cardiovascular/121,1274
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