Chemicals and Drugs
AntithrombinsAntithrombin ProteinsHeparin
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.
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.
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.

Anticoagulant heparan sulfate precursor structures in F9 embryonal carcinoma cells. (1/701)

To understand the mechanisms that control anticoagulant heparan sulfate (HSact) biosynthesis, we previously showed that HSact production in the F9 system is determined by the abundance of 3-O-sulfotransferase-1 as well as the size of the HSact precursor pool. In this study, HSact precursor structures have been studied by characterizing [6-3H]GlcN metabolically labeled F9 HS tagged with 3-O-sulfates in vitro by 3'-phosphoadenosine 5'-phospho-35S and purified 3-O-sulfotransferase-1. This later in vitro labeling allows the regions of HS destined to become the antithrombin (AT)-binding sites to be tagged for subsequent structural studies. It was shown that six 3-O-sulfation sites exist per HSact precursor chain. At least five out of six 3-O-sulfate-tagged oligosaccharides in HSact precursors bind AT, whereas none of 3-O-sulfate-tagged oligosaccharides from HSinact precursors bind AT. When treated with low pH nitrous or heparitinase, 3-O-sulfate-tagged HSact and HSinact precursors exhibit clearly different structural features. 3-O-Sulfate-tagged HSact hexasaccharides were AT affinity purified and sequenced by chemical and enzymatic degradations. The 3-O-sulfate-tagged HSact hexasaccharides exhibited the following structures, DeltaUA-[6-3H]GlcNAc6S-GlcUA-[6-3H]GlcNS3(35)S+/-6S-++ +IdceA2S-[6-3H]Glc NS6S. The underlined 6- and 3-O-sulfates constitute the most critical groups for AT binding in view of the fact that the precursor hexasaccharides possess all the elements for AT binding except for the 3-O-sulfate moiety. The presence of five potential AT-binding precursor hexasaccharides in all HSact precursor chains demonstrates for the first time the processive assembly of specific sequence in HS. The difference in structures around potential 3-O-sulfate acceptor sites in HSact and HSinact precursors suggests that these precursors might be generated by different concerted assembly mechanisms in the same cell. This study permits us to understand better the nature of the HS biosynthetic pathway that leads to the generation of specific saccharide sequences.  (+info)

Exosites 1 and 2 are essential for protection of fibrin-bound thrombin from heparin-catalyzed inhibition by antithrombin and heparin cofactor II. (2/701)

Assembly of ternary thrombin-heparin-fibrin complexes, formed when fibrin binds to exosite 1 on thrombin and fibrin-bound heparin binds to exosite 2, produces a 58- and 247-fold reduction in the heparin-catalyzed rate of thrombin inhibition by antithrombin and heparin cofactor II, respectively. The greater reduction for heparin cofactor II reflects its requirement for access to exosite 1 during the inhibitory process. Protection from inhibition by antithrombin and heparin cofactor II requires ligation of both exosites 1 and 2 because minimal protection is seen when exosite 1 variants (gamma-thrombin and thrombin Quick 1) or an exosite 2 variant (Arg93 --> Ala, Arg97 --> Ala, and Arg101 --> Ala thrombin) is substituted for thrombin. Likewise, the rate of thrombin inhibition by the heparin-independent inhibitor, alpha1-antitrypsin Met358 --> Arg, is decreased less than 2-fold in the presence of soluble fibrin and heparin. In contrast, thrombin is protected from inhibition by a covalent antithrombin-heparin complex, suggesting that access of heparin to exosite 2 of thrombin is hampered when ternary complex formation occurs. These results reveal the importance of exosites 1 and 2 of thrombin in assembly of the ternary complex and the subsequent protection of thrombin from inhibition by heparin-catalyzed inhibitors.  (+info)

Thrombophilia as a multigenic disease. (3/701)

BACKGROUND AND OBJECTIVE: Venous thrombosis is a common disease annually affecting 1 in 1000 individuals. The multifactorial nature of the disease is illustrated by the frequent identification of one or more predisposing genetic and/or environmental risk factors in thrombosis patients. Most of the genetic defects known today affect the function of the natural anticoagulant pathways and in particular the protein C system. This presentation focuses on the importance of the genetic factors in the pathogenesis of inherited thrombophilia with particular emphasis on those defects which affect the protein C system. INFORMATION SOURCES: Published results in articles covered by the Medline database have been integrated with our original studies in the field of thrombophilia. STATE OF THE ART AND PERSPECTIVES: The risk of venous thrombosis is increased when the hemostatic balance between pro- and anti-coagulant forces is shifted in favor of coagulation. When this is caused by an inherited defect, the resulting hypercoagulable state is a lifelong risk factor for thrombosis. Resistance to activated protein C (APC resistance) is the most common inherited hypercoagulable state found to be associated with venous thrombosis. It is caused by a single point mutation in the factor V (FV) gene, which predicts the substitution of Arg506 with a Gln. Arg506 is one of three APC-cleavage sites and the mutation results in the loss of this APC-cleavage site. The mutation is only found in Caucasians but the prevalence of the mutant FV allele (FV:Q506) varies between countries. It is found to be highly prevalent (up to 15%) in Scandinavian populations, in areas with high incidence of thrombosis. FV:Q506 is associated with a 5-10-fold increased risk of thrombosis and is found in 20-60% of Caucasian patients with thrombosis. The second most common inherited risk factor for thrombosis is a point mutation (G20210A) in the 3' untranslated region of the prothrombin gene. This mutation is present in approximately 2% of healthy individuals and in 6-7% of thrombosis patients, suggesting it to be a mild risk factor of thrombosis. Other less common genetic risk factors for thrombosis are the deficiencies of natural anticoagulant proteins such as antithrombin, protein C or protein S. Such defects are present in less than 1% of healthy individuals and together they account for 5-10% of genetic defects found in patients with venous thrombosis. Owing to the high prevalence of inherited APC resistance (FV:Q506) and of the G20210A mutation in the prothrombin gene, combinations of genetic defects are relatively common in the general population. As each genetic defect is an independent risk factor for thrombosis, individuals with multiple defects have a highly increased risk of thrombosis. As a consequence, multiple defects are often found in patients with thrombosis.  (+info)

Acceleration of Ca2+ ionophore-induced arachidonic acid liberation by thrombin without the proteolytic action toward the receptor in human platelets. (4/701)

We investigated the regulation of arachidonic acid liberation catalyzed by group-IV cytosolic phospholipase A2 (cPLA2) in human platelets upon stimulation with thrombin through interaction with protease-activated receptor-1 (PAR-1) or glycoprotein Ib. Leupeptin, a protease inhibitor, completely inhibited thrombin-induced arachidonic acid liberation and Ca2+ mobilization, with inhibition of its protease activity. However, preincubation with thrombin in the presence of leupeptin potentiated Ca2+ ionophore-induced arachidonic acid liberation. The preincubation did not affect the intracellular Ca2+ level or cPLA2 activity in response to ionomycin. Human leukocyte elastase, which cleaves glycoprotein Ib, did not inhibit the enhancement of arachidonic acid liberation by thrombin in the presence of leupeptin. However, the effect of thrombin with leupeptin was abolished by a peptide corresponding to residues 54-65 of hirudin (hirudin peptide), which impairs the binding of thrombin to PAR-1. Furthermore, Phe-Pro-Arg chloromethyl ketone (PPACK)-thrombin, which binds to platelets but has no protease activity, also enhanced Ca2+ ionophore-induced arachidonic acid liberation. In contrast, trypsin with leupeptin did not mimic the effect of thrombin with leupeptin, and furthermore trypsin-induced arachidonic acid liberation was insensitive to hirudin peptide. On the basis of the present results, we suggest that thrombin may accelerate cPLA2-catalyzed arachidonic acid liberation through non-proteolytic action toward PAR-1 but not toward glycoprotein Ib in co-operation with the proteolytic action leading to Ca2+ mobilization.  (+info)

Antithrombin activity during the period of percutaneous coronary revascularization: relation to heparin use, thrombotic complications and restenosis. (5/701)

OBJECTIVES: This study evaluated changes in antithrombin (AT) activity around the time of percutaneous transluminal coronary revascularization (PTCR) with unfractionated heparin anticoagulation and the effects these changes had on major thrombotic complications of PTCR. BACKGROUND: Heparin is used during PTCR to prevent thrombosis. However, heparin, a cofactor for AT, causes AT activity to fall. AT activity <70% is associated with thrombosis. There is a prothrombotic state after heparin discontinuation that has not been well explained. METHODS: Antithrombin activity was sampled at the start and end of PTCR and the next two mornings in 250 consecutive patients. We recorded occurrence of major thrombotic events, defined as 1) major thrombotic complications of PTCR; 2) major in-lab thrombus formation; or 3) subacute occlusion. Discriminant analysis was employed to evaluate the relationship of AT activity to these events. Change in AT activity and its relationship to heparin was evaluated. Evidence of restenosis at six months was obtained. RESULTS: There were 14 major thrombotic events. Antithrombin activity <70% was strongly (p = 0.006) associated with these events. The AT activity fell significantly through the morning after PTCR when 21% of patients had AT activity <70%; AT activity did not normalize until >20 h after heparin discontinuation. Pre-PTCR use of heparin led to lower AT activity in proportion to duration of heparin use. There was no relationship between AT activity and restenosis. CONCLUSIONS: Low AT activity may contribute to major thrombotic complications of PTCR. The way heparin is used before and after PTCR is important to development of low AT activity.  (+info)

Risk of venous thromboembolism and clinical manifestations in carriers of antithrombin, protein C, protein S deficiency, or activated protein C resistance: a multicenter collaborative family study. (6/701)

Deficiencies of antithrombin (AT), protein C (PC) or protein S (PS), and activated protein C resistance (APCR) are very well-established coagulation defects predisposing to venous thromboembolism (VTE). We performed a retrospective cohort family study to assess the risk for VTE in individuals with AT, PC, or PS deficiency, or APCR. Five hundred thirteen relatives from 9 Italian centers were selected from 233 families in which the proband had had at least 1 episode of VTE. We calculated the incidence of VTE in the whole cohort and in the subgroups after stratification by age, sex, and defect. The overall incidence of VTE (per 100 patient-years) in the group of relatives was 0.52. It was 1.07 for AT, 0.54 for PC, 0.50 for PS, 0.30 for APCR, and 0.67 in the group with a double defect. The incidence was associated with age, but not with sex. The mean age at onset was between 30 and 40 years for all the coagulation defects. Women had the peak of incidence in the age range of 21 to 40 years, earlier than men. The lifetime risk for VTE was 4.4 for AT versus APCR, 2.6 for AT versus PS, 2.2 for AT versus PC, 1.9 for PC versus APCR, and 1.6 for PS versus APCR. AT deficiency seems to have a higher risk for VTE than the other genetic defects. There is a relation between age and occurrence of thrombosis for both men and women. The latter had the peak of incidence earlier than the former.  (+info)

Structure of heparin-derived tetrasaccharide complexed to the plasma protein antithrombin derived from NOEs, J-couplings and chemical shifts. (7/701)

A complex of the synthetic tetrasaccharide AGA*IM [GlcN, 6-SO3-alpha(1-4)-GlcA-beta(1-4)-GlcN,3, 6-SO3-alpha(1-4)-IdoA-alphaOMe] and the plasma protein antithrombin has been studied by NMR spectroscopy. 1H and 13C chemical shifts, three-bond proton-proton (3JH-H) and one-bond proton-carbon coupling constants (1JC-H) as well as transferred NOEs and rotating frame Overhauser effects (ROEs) were monitored as a function of the protein : ligand molar ratio and temperature. Considerable changes were observed at both 20 : 1 and 10 : 1 ratios (AGA*IM : antithrombin) in 1H as well as 13C chemical shifts. The largest changes in 1H chemical shifts, and the linewidths, were found for proton resonances (A1, A2, A6, A6', A1*, A2*, A3*, A4*) in GlcN, 6-SO3 and GlcN,3,6-SO3 units, indicating that both glucosamine residues are strongly involved in the binding process. The changes in the linewidths in the IdoA residue were considerably smaller than those in other residues, suggesting that the IdoA unit experienced different internal dynamics during the binding process. This observation was supported by measurements of 3JH-H and 1JC-H. The magnitude of the three-bond proton-proton couplings (3JH1-H2 = 2.51 Hz and 3JH4-H5 = 2.23 Hz) indicate that in the free state an equilibrium exists between 1C4 and 2S0 conformers in the ratio of approximately 75 : 25. The chair form appears the more favourable in the presence of antithrombin, as inferred from the magnitude of the coupling constants. In addition, two-dimensional NOESY and ROESY experiments in the free ligand, as well as transferred NOESY and ROESY spectra of the complex, were measured and interpreted using full relaxation and conformational exchange matrix analysis. The theoretical NOEs were computed using the geometry of the tetrasaccharide found in a Monte Carlo conformational search, and the three-dimensional structures of AGA*IM in both free and bound forms were derived. All monitored NMR variables, 1H and 13C chemical shifts, 1JC-H couplings and transferred NOEs, indicated that the changes in conformation at the glycosidic linkage GlcN, 6-SO3-alpha(1-4)-GlcA were induced by the presence of antithrombin and suggested that the receptor selected a conformer different from that in the free state. Such changes are compatible with the two-step model [Desai, U.R., Petitou, M., Bjork, I. & Olson, S. (1998) J. Biol. Chem. 273, 7478-7487] for the interaction of heparin-derived oligosaccharides with antithrombin, but with a minor extension: in the first step a low-affinity recognition complex between ligand and receptor is formed, accompanied by a conformational change in the tetrasaccharide, possibly creating a complementary three-dimensional structure to fit the protein-binding site. During the second step, as observed in a structurally similar pentasaccharide [Skinner, R., Abrahams, J.-P., Whisstock, J.C., Lesk, A.M., Carrell, R.W. & Wardell, M.R. (1997) J. Mol. Biol. 266, 601-609; Jin, L., Abrahams, J.-P., Skinner, R., Petitou, M., Pike, R. N. & Carrell, R.W. (1997) Proc. Natl Acad. Sci. USA 94, 14683-14688], conformational changes in the binding site of the protein result in a latent conformation.  (+info)

Effect of thrombin inhibition in vascular dementia and silent cerebrovascular disease. An MR spectroscopy study. (8/701)

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)

A method for the differential determination of plasma antithrombins. | Journal of Clinical PathologyA method for the differential determination of plasma antithrombins. | Journal of Clinical Pathology
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.. ...
http://jcp.bmj.com/content/29/1/63
Issues in antithrombin therapy for UA/NSTEMI<...
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 - 2001/8/27. Y1 - 2001/8/27. 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 ...
https://arizona.pure.elsevier.com/en/publications/issues-in-antithrombin-therapy-for-uanstemi
Surface modification with an antithrombin-heparin complex for anticoagulation: Studies on a model surface with gold as substrate
Surface modification with an antithrombin-heparin complex for anticoagulation: Studies on a model surface with gold as substrate Academic Article ...
https://experts.mcmaster.ca/display/publication85195
Antithrombin Therapies | Interventional Cardiology, 2e | AccessCardiology | McGraw-Hill MedicalAntithrombin Therapies | Interventional Cardiology, 2e | AccessCardiology | McGraw-Hill Medical
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: ...
http://accesscardiology.mhmedical.com/content.aspx?bookid=1986§ionid=161618682
1azx - Proteopedia, life in 3D1azx - Proteopedia, life in 3D
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 ...
http://proteopedia.org/wiki/index.php/1azx
ATRYN - Renal and Urology NewsATRYN - Renal and Urology News
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.. ...
https://www.renalandurologynews.com/drug/atryn/
An Improved Potent Direct Thrombin Inhibitor Shows Efficacy With Low Bleeding Risk
Live from AHA 2017 Dr. Datta from VERSEON Pharmaceuticals discusses a new Direct Thrombin Inhibitor in Phase 1 Clinical Development., TV Network
http://www.thrombosis.tv/ThrombosisTVNetwork/TabId/2032/VideoId/1962/An-Improved-Potent-Direct-Thrombin-Inhibitor-Shows-Efficacy-With-Low-Bleeding-Risk.aspx
Thrombosis as a conformational disease | HaematologicaThrombosis as a conformational disease | Haematologica
Conformational diseases are a newly recognized group of heterogeneous disorders resulting from the conformational instability of individual proteins. Such instability allows the formation of intermolecular linkages between b-sheets, to give protein aggregation and inclusion body formation. The serpin family of serine protease inhibitors provides the best-studied examples of the structural changes involved. Notably, mutations of a-1-antitrypsin result in its intracellular polymerization and accumulation in the liver leading eventually to cirrhosis. Here we consider how other conformational changes in another serpin, antithrombin, can cause its inactivation with consequent thrombosis. Thirteen different missense mutations in antithrombin are associated with either oligomer formation or with conversion of the active molecule into an inactive latent form. Each of these variant antithrombins is associated with an increased risk of thrombosis that typically occurs in an unexpectedly severe and sudden ...
http://www.haematologica.org/content/90/2/238
DeCS Ingl s+escopo
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. . ...
http://trigramas.bireme.br/cgi-bin/mx/[email protected]?collection=DeCSxi&lang=i&minsim=0.30&maxrel=10&text=Prothrombinase
Have you powered up your lab with INNOVANCE reagents?Have you powered up your lab with INNOVANCE reagents?
By partnering with Siemens Healthcare Diagnostics, you can experience the assurance of an integrated hemostasis solution that can help improve both clinical and operational performance throughout your entire laboratory. Our INNOVANCE® line will help you gain efficiencies, increase operational workflow and throughput, and better manage your resources.. INNOVANCE DTI Assay. Our INNOVANCE DTI Assay* is an automated chromogenic testing solution for the quantitative determination of direct thrombin inhibitors in citrated human plasma. It delivers the high specificity and stability needed to confidently test for the direct oral anticoagulant dabigatran.. INNOVANCE Heparin Assay ...
https://www.siemens-healthineers.com/de/hemostasis/have-you-powered-up-your-lab-with-innovance
Direct thrombin inhibitors | definition of direct thrombin inhibitors by Medical dictionaryDirect thrombin inhibitors | definition of direct thrombin inhibitors by Medical dictionary
Looking for online definition of direct thrombin inhibitors in the Medical Dictionary? direct thrombin inhibitors explanation free. What is direct thrombin inhibitors? Meaning of direct thrombin inhibitors medical term. What does direct thrombin inhibitors mean?
https://medical-dictionary.thefreedictionary.com/direct+thrombin+inhibitors
Direct thrombin inhibitors after orthopedic surgery | The Hospital LeaderDirect thrombin inhibitors after orthopedic surgery | The Hospital Leader
In this Cochrane meta-analysis, researchers analyzed the overall efficacy and safety of direct thrombin inhibitors, compared to warfarin or LMWH, in preventing VTE after orthopedic surgeries (hip and knee arthroplasty). In14 studies involving over 20,000 participants, they found no difference in efficacy between direct thrombin inhibitors, warfarin, or LMWH, but did find higher mortality and bleeding in the thrombin group compared to LMWH (but no difference between the thrombin group and warfarin) (abstract). The timing of the thrombin inhibitors also matters, as pre-operative dosing results in fewer VTEs but likely higher bleeding. Dabigatran is the oral direct thrombin inhibitor that is currently approved in Canada and throughout Europe, but US FDA approval is pending.. ...
http://thehospitalleader.org/direct-thrombin-inhibitors-after-orthopedic-surgery/
Evaluation of anticoagulant effects of direct thrombin inhibitors, dabigatran and argatroban, based on the Lineweaver-Burk plot...Evaluation of anticoagulant effects of direct thrombin inhibitors, dabigatran and argatroban, based on the Lineweaver-Burk plot...
Direct thrombin inhibitors (DTIs) represented by dabigatran were expected to be available for therapeutic use without the need for routine monitoring, in contrast to warfarin. However, clinical concerns regarding impacts of plasma dabigatran concentrations on the rate of major bleeding have been raised.1 Clinical and basic aspects of DTIs aid in studying how best to address concerns regarding bleeding risk in therapeutic use. Based on enzymatic examinations with a synthetic substrate, S-2238, it has been well recognised that dabigatran and another DTI argatroban reversibly and competitively inhibit thrombin reaction.2 ,3 However, it still remains unclear whether the type of inhibition by DTIs of thrombin reaction with S-2238 can be applied to the anticoagulant effects.. The Clauss assay is classical but most popular even now for quantification of plasma fibrinogen concentrations.4 This is based on the quantitative relationship between fibrinogen concentrations and time for fibrin clot formation ...
http://jcp.bmj.com/content/69/4/370
ISAR-REACT 3 Pits Bivalirudin vs. Unfractionated Hepa... ( Will direct thrombin inhibitor excel...)ISAR-REACT 3 Pits Bivalirudin vs. Unfractionated Hepa... ( Will direct thrombin inhibitor excel...)
... Will direct thrombin inhibitor excel with high-dose clopidogrel on bo...CHICAGO March 29 /- A large randomized trial will shedl...The Intracoronary Stenting and Antithrombotic Regimen: Rapid EarlyAct...Bivalirudin has outperformed unfractionated heparin in some previouss...,ISAR-REACT,3,Pits,Bivalirudin,vs.,Unfractionated,Heparin,in,PCI,medicine,advanced medical technology,medical laboratory technology,medical device technology,latest medical technology,Health
http://www.bio-medicine.org/medicine-technology-1/ISAR-REACT-3-Pits-Bivalirudin-vs--Unfractionated-Heparin-in-PCI-1618-1/
Dabigatran Etexilate MesylateDabigatran Etexilate Mesylate
DIRECT THROMBIN INHIBITORS : USES: Direct thrombin inhibitors (DTIs) are used as anticoagulants. Argatroban, bivalirudin, desirudin, and lepirudin are used parenterally and are indicated for adjuvant anticoagulation for percutaneous cardiac interventions or as a substitution for heparin/low-molecular-weight heparins in cases of heparin-induced thrombocytopenia. Dabigatran etexilate is an oral medication approved for treatment of venous thromboembolism and stroke prophylaxis in atrial fibrillation. PHARMACOLOGY: These agents directly inhibit thrombin, leading to inhibition of clot formation and stabilization. TOXICOLOGY: The toxic effects are extensions of the pharmacologic effects and primarily include bleeding complications. EPIDEMIOLOGY: Outpatient overdose has not yet been reported. Inpatient medication errors may occur in 1% to 2% of patients receiving DTIs. The incidence of overdose is likely to increase as new DTIs are approved for in-hospital parenteral use and oral anticoagulation ...
https://www.medpagetoday.com/drugs/Dabigatran-Etexilate-Mesylate/929742
New Assays For Measuring Direct Thrombin Inhibitors in Plasma | Quadratech DiagnosticsNew Assays For Measuring Direct Thrombin Inhibitors in Plasma | Quadratech Diagnostics
Direct Thrombin Inhibitors (DTIs) have increasing and promising curative, preventive or prophylactic applications in severe clinical situations. Laboratory methods are required for adjustment of drug efficacy and for avoiding overdosage. Specialized calibrated clotting and chromogenic assays for quantitating various DTIs have been developed and compared for their efficacy. Results show excellent performance with Hirudin and analogues, but were not found to be suitable for the Argatroban® usual therapeutic range.
https://www.quadratech.co.uk/news/new-assays-for-measuring-direct-thrombin-inhibitors-in-plasma/
Effect of Nonspecific Binding to Plasma Proteins on the Antithrombin Activities of Unfractionated Heparin, Low-Molecular-Weight...
Effect of Nonspecific Binding to Plasma Proteins on the Antithrombin Activities of Unfractionated Heparin, Low-Molecular-Weight Heparin, and Dermatan Sulfate Academic Article ...
https://experts.mcmaster.ca/display/publication763468
Argatroban - DrugBankArgatroban - DrugBank
Argatroban is a direct, selective thrombin inhibitor. The American College of Cardiologists (ACC) recommend using bivalirudin or argatroban in patients who have had, or at risk for, heparin induced thrombocytopenia (HIT) and are undergoing percutaneous coronary intervention. Argatroban is a non-heparin anticoagulant shown to both normalize platelet count in patients with HIT and prevent the formation of thrombi. Parental anticoagulants must be stopped and a baseline activated partial thromboplastin time must be obtained prior to administering argatroban.
https://www.drugbank.ca/drugs/DB00278
Comparison of the Antithrombotic Effectiveness of the Direct Thrombin Inhibitor, Dabigatran Etexilate, and Two Factor Xa...Comparison of the Antithrombotic Effectiveness of the Direct Thrombin Inhibitor, Dabigatran Etexilate, and Two Factor Xa...
Abstract. Inhibition of two key serine proteases in the coagulation cascade, thrombin (IIa) and factor Xa, are currently being exploited for direct, oral antit
https://ashpublications.org/blood/article/110/11/3154/75457/Comparison-of-the-Antithrombotic-Effectiveness-of
ASSA14-12-15 Efficacy and safety of direct thrombin inhibitor of bivalirudin during percutaneous coronary intervention therapy...ASSA14-12-15 Efficacy and safety of direct thrombin inhibitor of bivalirudin during percutaneous coronary intervention therapy...
Methods 488 patients were enrolled which comfirmed AMI by coronary angiography from July, 2012 to February, 2013, in which 10 patients were induced to come out Heparin-Induced Thrombocytopenia, 6 females, aged 48-79 years. The incidence of HIT patients was 2.0%. All patients were applied to bivalirudin (0.25 g, intravenous injection) during PCI. We summarised the characteristics of the patients, record incidence of in-hospital minor bleeding, major bleeding, platelet reduction and incidence of major adverse cardiac events (MACE) during hospitalisation and 1 month after discharge.. ...
https://heart.bmj.com/content/101/Suppl_1/A39.3
Recombinant Human Antithrombin - XVIVO | Scientific AnimationRecombinant Human Antithrombin - XVIVO | Scientific Animation
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.. ...
http://www.xvivo.net/animation/recombinant-human-antithrombin/
Direct Thrombin Inhibitor Anticoagulants - PharmacologyDirect Thrombin Inhibitor Anticoagulants - Pharmacology
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
https://www.alpfmedical.info/pharmacology/direct-thrombin-inhibitor-anticoagulants.html
Gentaur Molecular :Molecular Innovations \ Human antithrombin \ HATIII-IGentaur Molecular :Molecular Innovations \ Human antithrombin \ HATIII-I
Gentaur molecular products has all kinds of products like :search , Molecular Innovations \ Human antithrombin \ HATIII-I for more molecular products just contact us
http://www.antibody-antibodies.com/product_det.php?id=244482&supplier=search&name=Human%20antithrombin
Antithrombin DeficiencyAntithrombin Deficiency
Psychiatry healthcare professionals gain a thorough knowledge base of psychiatric disorder information to offer the best patient care. Get our FREE app now.
http://www.psychiatryadvisor.com/labmed/antithrombin-deficiency/article/614360/
Direct Thrombin Inhibitors - StrokeSciencesDirect Thrombin Inhibitors - StrokeSciences
Abstract Thrombolysis is the current standard of care for ischemic stroke. In order to better understand its underlying mechanisms, a closer look at the basic... ...
https://strokesciences.com/category/direct-thrombin-inhibitors/
bivalirudinbivalirudin
Bivalirudin is an anticoagulant (thrombin inhibitor) that helps prevent the formation of blood clots. Bivalirudin is used to prevent blood clots in people with severe chest pain or other conditions who are undergoing a procedure called angioplasty (to open blocked arteries). Bivalirudin may also be used for purposes not...
https://www.johnstonhealth.org/fitness-health/library/document-viewer/?id=d04744a1
Bivalirudin - Jolly Healthcare
Use of bivalirudin 250 mg injection is contraindicated in patients with active major bleeding and hypersensitivity. Patients should be carefully monitored after primary PCI for signs/symptoms consistent with myocardial ischemia. An increased risk of the thrombus formation, including fatal outcomes, may occur with the use of bivalirudin 250 mg injection in gamma brachytherapy. This medication should be used with caution in patients with disease states associated with an increased risk of bleeding. The infusion dose of bivasave may require to be decreased, and status of anticoagulant should be monitored in patients with renal impairment. Use of bivalirudin injection and aspirin during pregnancy needs to be avoided. Caution must be exercised when this medication is administered to a nursing woman.. ...
https://jollyhealthcare.org/product/bivalirudin/
Thrombin Inhibitors | Thrombin inhibitors are one type of anticoagulant medication | Page 3
Differentiated osteoclasts were generated and then cultured for 48 h in serum-free medium supplemented with 20 ng/ml M-CSF and 2 ng/ml RANKL. Conditioned medium was harvested, centrifuged. to remove cells and debris, and 600 μl/well was added to 24-well plates. Serum-free medium and medium containing 10% FBS, were supplemented with M-CSF and RANKL, and used as negative and positive controls, respectively. Wortmannin order Prior to the chemotaxis assay, γδ T cells were activated for 12 h with 100 U/ml rhIL-2. γδ T cells were then re-suspended in serum-free medium at 106 cells/ml and 80 μl of cell suspension was added into Transwell inserts (8 μm pore size). γδ T cells were incubated for 4 h at 37 °C to allow migration through the http://www.selleckchem.com/products/Staurosporine.html Transwell membrane. Cells that had migrated into the bottom chamber were harvested and quantified using flow cytometric analysis on an LSRII flow cytometer (BD Biosciences) by counting an equivalent volume ...
http://thrombininhibitors.com/page/3
Thrombin Inhibitors | Thrombin inhibitors are one type of anticoagulant medication
The highest DNA binding by 3-NBA in ES cells was observed at 10 μM after 24 h with 863 ± 74 adducts per 108 nucleotides (Fig. 3C). Interestingly, and in contrast to BaP, adduct levels for 3-NBA in MEFs were only 1.5-fold higher. (1266 ± 188 adduct per 108 nucleotides) under the same experimental conditions (Fig. 3D). DNA binding LDK378 in vivo was highest in MEFs at 10 μM after 48 h with 2478 ± 455 adducts per 108 nucleotides. Previously, in primary HUFs previously treated with 10 μM 3-NBA for 48 h, adduct levels were 680 ± 147 adducts per 108 nucleotides (Kucab et al., 2012). As 3-NBA is predominantly activated by NQO1 (Arlt et al., 2005), the expression of Nqo1 was studied in ES cells and MEFs by RT-PCR and revealed that Nqo1 mRNA expression increased in both cell types up to ∼60-fold; the induction was higher in MEFs than in ES cells ( Fig. 6C and D). This is in line with a previous study showing that Nqo1 protein levels were inducible in primary and immortal HUFs upon treatment with ...
http://thrombininhibitors.com
Buy cheap Pradaxa online without prescription | Visa & MasterCard acceptedBuy cheap Pradaxa online without prescription | Visa & MasterCard accepted
The generic name of Pradaxa is Dabigatran which is an anticoagulant medication orally administered to the patient, it belongs to the class of direct thrombin inhibitor.
http://www.uafp.org/product/pradaxa.html
Aniara BIOPHEN Heparin Anti-IIa (kinetics)Aniara BIOPHEN Heparin Anti-IIa (kinetics)
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.
http://www.aniara.com/mm5/merchant.mvc?Screen=PROD&Category_Code=MEASUREMENTOFHEPARIN&Product_Code=A221020&Sort_By=disp_order&Store_Code=ANIA&RelatedOffset=10&Offset=10
antithrombin-III precursor [Bos taurus] - Protein - NCBIantithrombin-III precursor [Bos taurus] - Protein - NCBI
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... ...
https://www.ncbi.nlm.nih.gov/protein/77736341
ARGATROBAN (injection) | FDA Warnings & Precations | Healthgrades.comARGATROBAN (injection) | FDA Warnings & Precations | Healthgrades.com
The FDA requires all potential medication risks for ARGATROBAN (injection) be disclosed to consumers, no matter how rare. Here are the warnings and precautions for Argatroban.
https://www.healthgrades.com/drugs/argatroban/warnings
What Is Heparin sodium? | eBioChem
Heparin sodium is a sulphated glycosaminoglycans prepared from the intestinal mucosa of healthy pigs. it has the characteristic property of delaying the clotting of freshly shed blood through its action on antithrombin iii which inhibits the ...
http://blog.ebiochem.com/2013/02/18/what-is-heparin-sodium/
Bivalirudin (Angiomax) | Daviss Drug GuideBivalirudin (Angiomax) | Daviss Drug Guide
Find information on Bivalirudin (Angiomax) in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, mechanism of action, half life, administration, and more. Davis Drug Guide PDF.
https://im.unboundmedicine.com/medicine/view/Davis-Drug-Guide/51104/all/bivalirudin
Bivalirudin (Angiomax) | Daviss Drug GuideBivalirudin (Angiomax) | Daviss Drug Guide
Find information on Bivalirudin (Angiomax) in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, mechanism of action, half life, administration, and more. Davis Drug Guide PDF.
https://www.unboundmedicine.com/washingtonmanual/view/Davis-Drug-Guide/51104/all/bivalirudin?refer=true
Argatroban | Daviss Drug GuideArgatroban | Daviss Drug Guide
Find information on Argatroban in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, mechanism of action, half life, administration, and more. Davis Drug Guide PDF.
https://anesth.unboundmedicine.com/anesthesia/view/Davis-Drug-Guide/51070/all/argatroban
Argatroban | Daviss Drug GuideArgatroban | Daviss Drug Guide
Find information on Argatroban in Daviss Drug Guide including dosage, side effects, interactions, nursing implications, mechanism of action, half life, administration, and more. Davis Drug Guide PDF.
https://www.unboundmedicine.com/washingtonmanual/view/Davis-Drug-Guide/51070/6/argatroban
Dr. Sunil Rao presents Pharmacology and Mechanisms of Anti-Thrombin TherapyDr. Sunil Rao presents Pharmacology and Mechanisms of Anti-Thrombin Therapy
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.. ...
http://tv.clinicaltrialresults.org/play.php?submission_id=694
Atrophy of Spared Gray Matter Tissue Predicts Poorer Motor Recovery and Rehabilitation Response in Chronic Stroke | StrokeAtrophy of Spared Gray Matter Tissue Predicts Poorer Motor Recovery and Rehabilitation Response in Chronic Stroke | Stroke
Background and Purpose-Although the motor deficit after stroke is clearly due to the structural brain damage that has been sustained, this relationship is attenuated from the acute to chronic phases. We investigated the possibility that motor impairment and response to constraint-induced movement therapy in patients with chronic stroke may relate more strongly to the structural integrity of brain structures remote from the lesion than to measures of overt tissue damage.. ...
http://stroke.ahajournals.org/content/early/2011/11/17/STROKEAHA.111.633255
Dabigatran etexilate a novel oral direct thrombin inhibitor for preventing thromboembolic events after knee replacement...
Background: Dabigatran etexilate is one of the few direct thrombin inhibitors with anti-coagulant activities and the following distinctive features: taken orally, no need to closely monitor for complications, and no need for regular dose adjustments. Relying on the above mentioned valuable advantages, dabigatran etexilate can be considered as a premier choice ...
http://tumj.tums.ac.ir/browse.php?a_id=178&slc_lang=en
Antithrombin deficiency | Providence OregonAntithrombin deficiency | Providence Oregon
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 ...
https://oregon.providence.org/health-library/a/antithrombin-deficiency/
Discovery and development of direct thrombin inhibitors - WikipediaDiscovery and development of direct thrombin inhibitors - Wikipedia
Direct thrombin inhibitors (DTIs) are a class of anticoagulant drugs that can be used to prevent and treat embolisms and blood clots caused by various diseases. They inhibit thrombin, a serine protease which affects the coagulation cascade in many ways. DTIs have undergone rapid development since the 90s. With technological advances in genetic engineering the production of recombinant hirudin was made possible which opened the door to this new group of drugs. Before the use of DTIs the therapy and prophylaxis for anticoagulation had stayed the same for over 50 years with the use of heparin derivatives and warfarin which have some well known disadvantages. DTIs are still under development, but the research focus has shifted towards factor Xa inhibitors, or even dual thrombin and fXa inhibitors that have a broader mechanism of action by both inhibiting factor IIa (thrombin) and Xa. A recent review of patents and literature on thrombin inhibitors has demonstrated that the development of allosteric ...
https://en.wikipedia.org/wiki/Discovery_and_development_of_direct_thrombin_inhibitors
Antithrombin Deficiency: Practice Essentials, Background, PathophysiologyAntithrombin Deficiency: Practice Essentials, Background, Pathophysiology
Antithrombin III (henceforth referred to as antithrombin or AT) is a 58-kDa molecule belonging to the serine protease inhibitor (serpin) superfamily that plays a central role in anticoagulation and in regulating appropriate wound healing in mammalian circulation systems. Antithrombin deficiency, which may be congenital or acquired, results in...
https://emedicine.medscape.com/article/198573-overview
Heparin cofactor II - WikipediaHeparin cofactor II - Wikipedia
Heparin cofactor II (HCII), a protein encoded by the SERPIND1 gene, is a coagulation factor that inhibits IIa, and is a cofactor for heparin and dermatan sulfate (minor antithrombin). The product encoded by this gene is a serine proteinase inhibitor which rapidly inhibits thrombin in the presence of dermatan sulfate or heparin. The gene contains five exons and four introns. This protein shares homology with antithrombin and other members of the alpha 1-antitrypsin superfamily. Mutations in this gene are associated with heparin cofactor II deficiency. Heparin Cofactor II deficiency can lead to increased thrombin generation and a hypercoagulable state. GRCh38: Ensembl release 89: ENSG00000099937 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000022766 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Entrez Gene: SERPIND1 serpin peptidase inhibitor, clade D (heparin cofactor), member 1. Griffith MJ, Carraway T, White GC, Dombrose FA (1983). Serpin receptor 1: ...
https://en.wikipedia.org/wiki/Heparin_cofactor_II
The effect of Dabigatran on select specialty coagulation assays<...
TY - JOUR. T1 - The effect of Dabigatran on select specialty coagulation assays. AU - Adcock, Dorothy M.. AU - Gosselin, Robert. AU - Kitchen, Steve. AU - Dwyre, Denis M. PY - 2013/1. Y1 - 2013/1. N2 - Dabigatran etexilate is a new oral anticoagulant that functions as a direct thrombin inhibitor. An inhibitor of thrombin has the potential to interfere with essentially all clot-based coagulation assays and select chromogenic assays, whereas the drug would not be expected to interfere in antigen-based assays. The purpose of this study was to evaluate the effect of dabigatran on various specialized coagulation assays using normal plasma specimens with varying concentrations of dabigatran (the active form of dabigatran etexilate). We have demonstrated that samples containing therapeutic levels of dabigatran may lead to underestimation of intrinsic factor activities with abnormal activated partial thromboplastin time (aPTT) mixing study results and a false-positive factor VIII Bethesda titer; ...
https://ucdavis.pure.elsevier.com/en/publications/the-effect-of-dabigatran-on-select-specialty-coagulation-assays
Localization of anticoagulantly active heparan sulfate proteoglycans in vascular endothelium: antithrombin binding on cultured...Localization of anticoagulantly active heparan sulfate proteoglycans in vascular endothelium: antithrombin binding on cultured...
We have studied the interaction of 125I-antithrombin (125I-AT) with microvascular endothelial cells (RFPEC) to localize the cellular site of anticoagulantly active heparan sulfate proteoglycans (HSPG). The radiolabeled protease inhibitor bound specifically to the above HSPG with a Kd of approximately 50 nM. Confluent monolayer RFPEC cultures exhibited a linear increase in the amount of AT bound per cell for up to 16 d, whereas suspension RFPEC cultures possessed a constant number of protease inhibitor binding sites per cell for up to 5 d. These results suggest that monolayer RFPEC cultures secrete anticoagulantly active HSPG, which then accumulate in the extracellular matrix. This hypothesis was confirmed by quantitative light and EM level autoradiography which demonstrated that the AT binding sites are predominantly located in the extracellular matrix with only small quantities of protease inhibitor complexed to the cell surface. We have also pinpointed the in vivo position of anticoagulantly ...
https://rupress.org/jcb/article/111/3/1293/59610/Localization-of-anticoagulantly-active-heparan
Antithrombin (Activity and Antigen) - Health Encyclopedia - University of Rochester Medical CenterAntithrombin (Activity and Antigen) - Health Encyclopedia - University of Rochester Medical Center
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 ...
https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=antithrombin_activity_antigen
Antithrombin (Activity and Antigen) - AHealthyMe - Blue Cross Blue Shield of Massachusetts
The antithrombin activity and antigen tests are used to help find out what may be causing abnormal blood clots in your body.
https://www.ahealthyme.com/RelatedItems/167,antithrombin_activity_antigen
heparin Archives - ED ECMOheparin Archives - ED ECMO
Do you give heparin to your ECMO patients? Well, lets rethink this. This episode is All Things Anticoagulation! Zack talks with Troy Seelhammer, an intensivist from Mayo Clinic Rochester. He manages ECMO patients in his daily practice there. He has become a master of the subject of anticoagulation. He will talk about heparin, bilvalirudin, or maybe no anticoagulation. We talk about how TEG can affect our management. We talk about PCC and Protamine when bleeding just wont stop. He talks about the when to be aggressive and when to cut back. Below is a wonderful synopsis of Troys thoughts on anticoagulation on pump.. Goal Heparin levels are far from perfect but some suggestions. APTT 1.5 to 2.5 times normal. ACT level - 180-220 seconds. Antithrombin Levels - next generation. Seelhammer doc on Bivalirudin - Bivalirudin & TEG During ECMO. ...
https://edecmo.org/tag/heparin/
Glial cells maintain synapses by inhibiting an activity-dependent retrograde protease signalGlial cells maintain synapses by inhibiting an activity-dependent retrograde protease signal
Glial cells regulate multiple aspects of synaptogenesis. In the absence of Schwann cells, a peripheral glial cell, motor neurons initially innervate muscle but then degenerate. Here, using a genetic approach, we show that neural activity-regulated negative factors produced by muscle drive neurodegeneration in Schwann cell-deficient mice. We find that thrombin, the hepatic serine protease central to the hemostatic coagulation cascade, is one such negative factor. Trancriptomic analysis shows that expression of the antithrombins serpin C1 and D1 is significantly reduced in Schwann cell-deficient mice. In the absence of peripheral neuromuscular activity, neurodegeneration is completely blocked, and expression of prothrombin in muscle is markedly reduced. In the absence of muscle-derived prothrombin, neurodegeneration is also markedly reduced. Together, these results suggest that Schwann cells regulate NMJs by opposing the effects of activity-regulated, muscle-derived negative factors and provide ...
https://scholarworks.unr.edu/handle/11714/6422
Fibrin D-dimer impairs the accumulation and anticoagulant properties of heparan sulphate and stimulates secretion of...
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 ...
http://psjd.icm.edu.pl/psjd/element/bwmeta1.element.bwnjournal-article-abpv50i1p279kz?q=bwmeta1.element.bwnjournal-number-abp-2003-50-1
Native Antithrombin (AT) | NPC313Hu01 | Homo sapiens (Human) CLOUD-CLONE CORP.(CCC)Native Antithrombin (AT) | NPC313Hu01 | Homo sapiens (Human) CLOUD-CLONE CORP.(CCC)
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!
http://cloud-clone.com/products/NPC313Hu01.html
Attenuation of leukocyte beta 2-integrin expression by antithrombin-III. - ScienceOpenAttenuation of leukocyte beta 2-integrin expression by antithrombin-III. - ScienceOpen
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 ...
https://www.scienceopen.com/document?vid=533cd1f3-40f7-4c3e-9176-470b4c600401
Intraluminal Prostheses Having Polymeric Material with Selectively Modified Crystallinity and Methods of Making Same -...Intraluminal Prostheses Having Polymeric Material with Selectively Modified Crystallinity and Methods of Making Same -...
0038] Pharmacological agents suitable for inclusion in prosthesis materials and/or coatings, according to embodiments of the present invention include, but are not limited to, drugs and other biologically active materials, and may be intended to perform a variety of functions, including, but not limited to: anti-cancer treatment (e.g., Resan), anti-clotting or anti-platelet formation, the prevention of smooth muscle cell growth and migration on a vessel wall, and cell cycle inhibitors. Pharmacological agentsmay include antineoplastics, antimitotics, antiinflammatories, antiplatelets, anticoagulants, antifibrins, antithrombins, antiproliferatives, antibiotics, antioxidants, immunosuppressives, and antiallergic substances as well as combinations thereof. Examples of such antineoplastics and/or antimitotics include paclitaxel (e.g., TAXOL® by Bristol-Myers Squibb Co., Stamford, Conn.), docetaxel (e.g., TAXOTERE® from Aventis S. A., Frankfurt, Germany) methotrexate, azathioprine, vincristine, ...
http://www.patentsencyclopedia.com/app/20110169198
AntithrombinAntithrombin
Antithrombin 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.
https://labtestsonline.org/tests/antithrombin
Notes from Dr. RW: December 2005Notes from Dr. RW: December 2005
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 ...
http://doctorrw.blogspot.com/2005/12/
Heparin cofactor II deficiency
Heparin cofactor II (HCII) is a serine proteinase inhibitor in human plasma that rapidly inhibits thrombin in the presence of dermatan sulfate or heparin. To understand the molecular mechanism for HCII deficiency in a patient with reduced circulating HCII antigen, we studied a Japanese .... ...
http://diseaseinfosearch.org/Heparin+cofactor+II+deficiency/8506
Thrombin (Inhibitors Agonists Modulators Antagonists)-MedChemExpress.comThrombin (Inhibitors Agonists Modulators Antagonists)-MedChemExpress.com
Thrombin is a serine protease that in humans is encoded by the F2 gene. Thrombin is an intriguing coagulation protease demonstrating an array of effects on endothelial cells, vascular smooth muscle cells (VSMC), monocytes, and platelets, all of which are involved in the pathophysiology of atherosclerosis. There is mounting evidence that thrombin acts as a powerful modulator of many processes like regulation of vascular tone, permeability, migration and proliferation of VSMC, recruitment of monocytes into the atherosclerotic lesions, induction of diverse pro-inflammatory markers, and all of these are related to the progression of cardiovascular disease. Recent studies in transgenic mice models indicate that the deletion of the natural thrombin inhibitor heparin cofactor II promotes an accelerated atherogenic state. The combined evidence points to thrombin as a pivotal contributor to vascular pathophysiology. Considering the clinical development of selective anticoagulants including direct ...
https://www.medchemexpress.com/Targets/Thrombin.html
Familial Overexpression of β Antithrombin Caused by an Asn135Thr Substitution | Blood | American Society of HematologyFamilial Overexpression of β Antithrombin Caused by an Asn135Thr Substitution | Blood | American Society of Hematology
Abstract. We have investigated the basis of antithrombin deficiency in an asymptomatic individual (and family) with borderline levels (≈70% antigen and activit
https://ashpublications.org/blood/article/93/12/4242/260893/Familial-Overexpression-of-Antithrombin-Caused-by
Changing outcomes and treatment strategies for wire induced coronary perforations in the era of bivalirudin useChanging outcomes and treatment strategies for wire induced coronary perforations in the era of bivalirudin use
Cardiac tamponade and major adverse cardiac events from WPs were less frequent with bivalirudin use compared to heparin use. This beneficial effect of bivalirudin may be explained on the basis of its short half-life and reversible thrombin inhibition property. Therefore, bivalirudin may offer a safe …
https://pubmed.ncbi.nlm.nih.gov/19496119/?dopt=Abstract
FDA releases safety data on dabigatran bleeding risks relative to warfarin | European Federation of Internal Medicine
Current recommendations and labeling regarding the use of dabigatran will not change, based on the results of a large observational cohort study comparing the risks of the direct thrombin inhibitor...
http://efim.org/news/internal-medicine-news-cardiology/fda-releases-safety-data-dabigatran-bleeding-risks-relative
Sodium in the structure of Thrombin Inhibition By Pyridin Derivatives (pdb 3qtv)
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Sodium atom in PDB 3qtv: Thrombin Inhibition By Pyridin Derivatives
http://sodium.atomistry.com/pdb3qtv.html
Sodium in the structure of Thrombin Inhibition By Pyridin Derivatives (pdb 3qx5)
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Sodium atom in PDB 3qx5: Thrombin Inhibition By Pyridin Derivatives
http://sodium.atomistry.com/pdb3qx5.html
Thrombin Inhibitor act as anticoagulants by inhibiting the enzyme thrombin
Thrombin Inhibitor-Direct thrombin inhibitors are a class of medication that act as anticoagulants by directly inhibiting the enzyme thrombin
http://www.medimarkinfo.co.in/medicines/thrombin-inhibitor-direct.html
Even so,in accordance to electrophoretic information, secreted antithrombin from silenced cells displays similar sizeto that of...
The plasma antithrombin stages, determined as anti-FXa action, experienced a typical distribution in the GAIT study, with a medium worth of 109.05% of the
http://urat1inhibitor.com/2016/01/10/even-soin-accordance-to-electrophoretic-information-secreted-antithrombin-from-silenced-cells-displays-similar-sizeto-that-of-control-cellsdetermine-3a/
Heparin-Binding Domains in Vascular Biology | Arteriosclerosis, Thrombosis, and Vascular BiologyHeparin-Binding Domains in Vascular Biology | Arteriosclerosis, Thrombosis, and Vascular Biology
Heparin functions as an anticoagulant primarily through activation of AT-mediated inhibition of blood coagulation factors such as thrombin and factor Xa. Several steps are involved in the interaction of heparin with AT and serine proteases. First, a low-affinity interaction between GAG and AT takes place, mediated by a well-defined unique pentasaccharide sequence within heparin (Figure 1B). This binding generates a conformational change in the structure of AT, which enables additional interactions between AT and heparin, resulting in stronger binding. The conformational change also expels a protease reactive loop in AT.54,55 A ternary complex is formed, after which the AT interaction reverts to low-affinity binding, resulting in the release of heparin from the covalent AT-protease complex.. The structure of the heparin-binding site in AT was mapped initially through the chemical modification of specific residues, resulting in decreased heparin affinity and by studying natural recombinant ...
http://atvb.ahajournals.org/content/24/9/1549
CVS Drugs 31 to 40 - ACEMprimary.com
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. ...
http://acemprimary.com/pharmacology/cardiovascular/cvs-pharm-31-to-40/
The heart of the matter: WHERE ARE WE WITH THE -XABANS, -GATRANS? IN ACS?The heart of the matter: WHERE ARE WE WITH THE -XABANS, -GATRANS? IN ACS?
The first decade of the 21st century had seen the proliferation of a whole host of new anti-coagulants, which were touted as an alternative to the famous rat poison, warfarin. These new groups, some of whose names I have difficulty pronouncing, I often call the -xatans, and the - gatrans. They include dabigatran, apixaban, rivaroxaban, etc., etc. They are all either factor Xa inhibitors or direct thrombin inhibitors. They are expensive ( obviously more expensive than warfarin, which is dirt cheap ). After all these years of trials, what is their role. I suppose, their role in preventing DVT is established. Dabigatrans role in stroke prevention is also FDA approved, but I must say that my own reading tells me that the 110mg dose does carry with it an increase risk of bleebing, which is of great concern for us ...
http://hmatter.blogspot.com/2012/09/where-are-we-with-xabans-gatrans-in-acs.html
Search Articles | University of Toronto Libraries
New Technologies, Diagnostic Tools and Drugs Effects of the oral, direct thrombin inhibitor dabigatran on five common coagulation assays Tomas L. Lindahl 1 ...
https://query.library.utoronto.ca/index.php/search/q?kw=SubjectTerms:New%20Technologies,%20Diagnostic%20Tools%20and%20Drugs
Antithrombin elisa and antibodyAntithrombin elisa and antibody
Shop Antithrombin ELISA Kit, Recombinant Protein and Antithrombin Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
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JoVE Author Search: Baglin TP
Anticoagulants, Risk, Bioavailability, Direct Thrombin Inhibitors, Enzymes, Factor Xa, Glycosaminoglycans, Half-life, Heparin, Hirudin, Inhibition, Injection, Lmwh, Osteoporosis, Patients, Pharmacology, Plasma, Plasma Proteins, Proteins, Subcutaneous Injection
http://labindex.jove.com/author/Baglin-TP
Technoclot DTI Kit 2 x 20 T. - DialineTechnoclot DTI Kit 2 x 20 T. - Dialine
Dilute thrombin-based method for quantitative determination direct thrombin inhibitors in human citrated plasma.. Recomended for: Hospital, Private laboratory, Life Science. CE. Art.Nr.(SKU): 36-5100025CH. ...
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Characterisation of a Novel Mutant form of Antithrombin III (Antithrcmbin Dublin) | Clinical Science | Portland PressCharacterisation of a Novel Mutant form of Antithrombin III (Antithrcmbin Dublin) | Clinical Science | Portland Press
M. Daly, A. OMeara, F. Hallinan; Characterisation of a Novel Mutant form of Antithrombin III (Antithrcmbin Dublin). Clin Sci (Lond) 1 January 1986; 71 (s15): 84P. doi: https://doi.org/10.1042/cs071084P. Download citation file:. ...
https://portlandpress.com/clinsci/article-abstract/71/s15/84P/105780/Characterisation-of-a-Novel-Mutant-form-of?redirectedFrom=fulltext
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 offers a 12-month guarantee.
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Bivalirudin Ill-Suited for Speedy Stenting? - Nick A. Gallegoss BlogBivalirudin Ill-Suited for Speedy Stenting? - Nick A. Gallegoss Blog
(MedPage Today) -- More stent thrombosis seen with fast-acting drug in brief procedures via Bivalirudin Ill-Suited for Speedy Stenting? by from Blogger http://ift.tt/2lyXYpqvia https://www.youtube.com/channel/UC6RqJb8h-y4xS4g-vzofotQ/videos
https://nickagallegos.wordpress.com/2017/03/02/bivalirudin-ill-suited-for-speedy-stenting/
An Open-Label, Dose-Finding, Pharmacokinetic, Safety and Efficacy Study of Bivalirudin in Children Between 6 Months and 18...An Open-Label, Dose-Finding, Pharmacokinetic, Safety and Efficacy Study of Bivalirudin in Children Between 6 Months and 18...
This study is investigating the efficacy of bivalirudin in children and adolescents with deep vein thrombosis. The primary endpoint is thrombosis event rate
http://adisinsight.springer.com/trials/700040175?error=cookies_not_supported&code=db845499-8fcb-4c52-beb3-eed8a38e0e13
Angiomax (Bivalirudin) Side effects, Images, Uses, Dosage, Overdose at RxListAngiomax (Bivalirudin) Side effects, Images, Uses, Dosage, Overdose at RxList
What is Angiomax (Bivalirudin)? Learn about drug imprint, side effects, uses (treating), dosage, interaction, overdose, and warnings.
https://www.rxlist.com/angiomax-drug/patient-images-side-effects.htm
GB1997001575 THROMBIN INHIBITORSGB1997001575 THROMBIN INHIBITORS
This patent search tool allows you not only to search the PCT database of about 2 million International Applications but also the worldwide patent collections. This search facility features: flexible search syntax; automatic word stemming and relevance ranking; as well as graphical results.
https://patentscope.wipo.int/search/en/detail.jsf?docId=WO1998000443
Dabigatran
Dabigatran is a blood thinner used to prevent blood clots and strokes. This eMedTV article offers an in-depth look at this prescription drug, including details on possible side effects, how it works, dosing tips, and what to discuss with your doctor.
http://heart-disease.emedtv.com/m/dabigatran/dabigatran.html
ChemIDplus - 1015167-40-4 - CSZFDMHIDSUHPI-KWONYSJQSA-N - Dabigatran 1-acylglucuronide - Similar structures search, synonyms,...ChemIDplus - 1015167-40-4 - CSZFDMHIDSUHPI-KWONYSJQSA-N - Dabigatran 1-acylglucuronide - Similar structures search, synonyms,...
1015167-40-4 - CSZFDMHIDSUHPI-KWONYSJQSA-N - Dabigatran 1-acylglucuronide - Similar structures search, synonyms, formulas, resource links, and other chemical information.
https://chem.nlm.nih.gov/chemidplus/rn/1015167-40-4
RCSB PDB - 1MU6: Crystal Structure of Thrombin in Complex with L-378,622 Methods Report PageRCSB PDB - 1MU6: Crystal Structure of Thrombin in Complex with L-378,622 Methods Report Page
1MU6: Metabolism-directed optimization of 3-aminopyrazinone acetamide thrombin inhibitors. Development of an orally bioavailable series containing P1 and P3 pyridines.
http://www.rcsb.org/pdb/explore/materialsAndMethods.do?structureId=1MU6
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AntithrombinAntithrombin
... is also termed antithrombin III (AT III). The designations antithrombin I through to antithrombin IV originate in ... Native antithrombin can be converted to latent antithrombin (L-antithrombin) by heating alone or heating in the presence of ... Type I antithrombin deficiency is characterized by a decrease in both antithrombin activity and antithrombin concentration in ... Type II antithrombin deficiency is characterized by normal antithrombin levels but reduced antithrombin activity in the blood ...
https://en.wikipedia.org/wiki/Antithrombin
Antithrombin III deficiencyAntithrombin III deficiency
Antithrombin Găman AM, Găman GD (2014). "Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature". ... Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. This deficiency may be ... The prevalence of antithrombin deficiency is estimated at ~0.02 to 0.2% of the general population, and 1-5% of patients with ... Testing for antithrombin activity can confirm deficiency if the levels are less than 70%. Deficiency can result from genetic ...
https://en.wikipedia.org/wiki/Antithrombin_III_deficiency
Anti-thrombin antibodiesAnti-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 ... Inhibitory anti-thrombin antibodies can be divided into 2 groups, those that inhibit coagulation activity and those the inhibit ... Anti-thrombin antibodies are autoantibodies directed against thrombin that may constitute a fraction of lupus anticoagulant and ...
https://en.wikipedia.org/wiki/Anti-thrombin_antibodies
Thrombin-antithrombin complexThrombin-antithrombin complex
... (TAT) is a protein complex of thrombin and antithrombin. It is a marker of net activation of ... Since thrombin is rapidly bound by antithrombin, TAT is a useful measure for thrombin level in the blood. Thrombin can pass the ... "Analysis of thrombin-antithrombin complex contents in plasma and hematoma fluid of hypertensive intracerebral hemorrhage ...
https://en.wikipedia.org/wiki/Thrombin–antithrombin_complex
Anti-thrombin aptamersAnti-thrombin aptamers
... are G-quadruplex-bearing oligonucleotides, which recognizes the exosites of human thrombin. The first ... anti-thrombin aptamer, TBA, was generated through via SELEX (Systematic Evolution of Ligands by Exponential Enrichment) ...
https://en.wikipedia.org/wiki/Anti-thrombin_aptamers
List of OMIM disorder codesList of OMIM disorder codes
PITX3 Antithrombin III deficiency; 613118; AT3 Antley-Bixler syndrome; 207410; FGFR2 Antley-Bixler syndrome-like with ... antithrombin\' Pittsburgh; 613490; SERPINA1 Hemosiderosis, systemic, due to aceruloplasminemia; 604290; CP Hennekam ...
https://en.wikipedia.org/wiki/List_of_OMIM_disorder_codes
Alpha-1 antitrypsinAlpha-1 antitrypsin
An extremely rare form of Pi, termed PiPittsburgh, functions as an antithrombin (a related serpin), due to a mutation ( ... Owen MC, Brennan SO, Lewis JH, Carrell RW (September 1983). "Mutation of antitrypsin to antithrombin. alpha 1-antitrypsin ...
https://en.wikipedia.org/wiki/Alpha-1_antitrypsin
ThrombophiliaThrombophilia
Antithrombin deficiency is present in 0.2% of the general population and 0.5-7.5% of people with venous thrombosis. Protein C ... Even small perturbances of proteins, such as the reduction of antithrombin to only 70-80% of the normal level, can increase the ... The process is inhibited by TFPI (which inactivates the first step catalyzed by factor VIIa/tissue factor), antithrombin (which ... The first major form of thrombophilia to be identified by medical science, antithrombin deficiency, was identified in 1965, ...
https://en.wikipedia.org/wiki/Thrombophilia
SerpinSerpin
Austin RC, Rachubinski RA, Ofosu FA, Blajchman MA (May 1991). "Antithrombin-III-Hamilton, Ala 382 to Thr: an antithrombin-III ... "Antithrombin-S195A factor Xa-heparin structure reveals the allosteric mechanism of antithrombin activation". The EMBO Journal. ... In the dimer (of antithrombin), the RCL and part of the A-sheet incorporates into the A-sheet of another serpin molecule. The ... Similarly, antithrombin can also spontaneously convert to the latent state, as an additional modulation mechanism to its ...
https://en.wikipedia.org/wiki/Serpin
Factor IXFactor IX
... is inhibited by antithrombin. Factor IX expression increases with age in humans and mice. In mouse models, mutations ...
https://en.wikipedia.org/wiki/Factor_IX
Margaret Oakley DayhoffMargaret Oakley Dayhoff
... antithrombin-III, alpha-antitrypsin, and ovalbumin; epidermal growth factor and the light chain of coagulation factor X; and ...
https://en.wikipedia.org/wiki/Margaret_Oakley_Dayhoff
heparan sulfate)-glucosamine 3-sulfotransferase 1heparan sulfate)-glucosamine 3-sulfotransferase 1
O-sulfation of the antithrombin-binding region". J. Biol. Chem. 263 (30): 15474-84. PMID 3139669. Shworak NW, Fritze LM, Liu J ...
https://en.wikipedia.org/wiki/(heparan_sulfate)-glucosamine_3-sulfotransferase_1
GlycosaminoglycanGlycosaminoglycan
Jin L, Abrahams JP, Skinner R, Petitou M, Pike RN, Carrell RW (1997). "The anticoagulant activation of antithrombin by heparin ...
https://en.wikipedia.org/wiki/Glycosaminoglycan
Nephrotic syndromeNephrotic syndrome
... particularly those caused by a decrease in blood antithrombin III levels due to leakage. Antithrombin III counteracts the ... 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 ... is a greater predisposition for the formation of blood clots that are caused by a decrease in the levels of antithrombin III in ...
https://en.wikipedia.org/wiki/Nephrotic_syndrome
HeparinoidHeparinoid
Some examples of heparin binding proteins include antithrombin III. It is thought that much protein interaction with heparin is ...
https://en.wikipedia.org/wiki/Heparinoid
ATrynATryn
GTC states that one genetically modified goat can produce the same amount of antithrombin in a year as 90,000 blood donations. ... Microinjection was used to insert human antithrombin genes into the cell nucleus of their embryos. ATryn is the first medicine ... ATryn is the brand name of the anticoagulant antithrombin manufactured by the Massachusetts-based U.S. company rEVO Biologics ( ... Jones, Phillip B. C. (April 2006). "European Regulators Curdle Plans for Goat Milk Human Antithrombin". Archived from the ...
https://en.wikipedia.org/wiki/ATryn
BiopharmaceuticalBiopharmaceutical
"European Regulators Curdle Plans for Goat Milk Human Antithrombin" (PDF). Retrieved 2006-06-23. "Go-ahead for 'pharmed' goat ...
https://en.wikipedia.org/wiki/Biopharmaceutical
Reptilase timeReptilase time
Unlike thrombin, reptilase is resistant to inhibition by antithrombin III. Thus, the reptilase time is not prolonged in blood ...
https://en.wikipedia.org/wiki/Reptilase_time
Acute-phase proteinAcute-phase protein
Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin. The decrease of such ...
https://en.wikipedia.org/wiki/Acute-phase_protein
ThrombinThrombin
In human adults, the normal blood level of antithrombin activity has been measured to be around 1.1 units/mL. Newborn levels of ... Heparin increases the affinity of antithrombin to thrombin (as well as factor Xa). The direct thrombin inhibitors, a newer ... Thrombin is also inactivated by antithrombin, a serine protease inhibitor. The molecular weight of prothrombin is approximately ...
https://en.wikipedia.org/wiki/Thrombin
FondaparinuxFondaparinux
... binds antithrombin and accelerates its inhibition of factor Xa. Apart from the O-methyl group at the reducing end ... Unlike direct factor Xa inhibitors, it mediates its effects indirectly through antithrombin III, but unlike heparin, it is ... Binding of heparin or HS to AT has been shown to increase the anti-coagulant activity of antithrombin 1000 fold. In contrast to ... sulfate this monomeric sequence is thought to form the high-affinity binding site for the anti-coagulant factor antithrombin ( ...
https://en.wikipedia.org/wiki/Fondaparinux
FibrinogenFibrinogen
This activity, sometimes referred to as antithrombin I, limits clotting. Fibrin also mediates blood platelet and endothelial ...
https://en.wikipedia.org/wiki/Fibrinogen
HirudinHirudin
The principal inhibitor of thrombin in normal blood circulation is antithrombin. Similar to antithrombin, the anticoagulant ... Unlike antithrombin, hirudin binds to and inhibits only the activated thrombin, with a specific activity on fibrinogen. ...
https://en.wikipedia.org/wiki/Hirudin
BatroxobinBatroxobin
In contrast, batroxobin isn't inhibited by antithrombin and heparin cofactor II. Batroxobin also has a high Kd value for ... There are also clotting inhibitors like antithrombin and heparin cofactor II, which prevent clotting when it isn't necessary. ...
https://en.wikipedia.org/wiki/Batroxobin
Developmental HaemostasisDevelopmental Haemostasis
Antithrombin: the levels of antithrombin increase with age. Antithrombin levels in newborns are less than 50% of the levels in ... Antithrombin is an anticoagulant protein and is important in preventing blood clotting. In animal studies, Antithrombin in ... There is an increase in the concentration of a specific isoform of Antithrombin, Latent Antithrombin with age. This form of ... There is also an increased activity of another form of Antithrombin, Beta Antithrombin in newborns compared to older children ...
https://en.wikipedia.org/wiki/Developmental_Haemostasis
HeparinHeparin
Chuang YJ, Swanson R, Raja SM, Olson ST (May 2001). "Heparin enhances the specificity of antithrombin for thrombin and factor ... Since heparins depend on the activity of antithrombin, they are considered anticoagulants. Specifically it is also used in the ... Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation ... It also rapidly binds to endothelial cells, which precludes the binding to antithrombin that results in anticoagulant action. ...
https://en.wikipedia.org/wiki/Heparin
AnticoagulantAnticoagulant
The antithrombin protein itself is used as a protein therapeutic that can be purified from human plasma or produced ... Fondaparinux is a synthetic sugar composed of the five sugars (pentasaccharide) in heparin that bind to antithrombin. It is a ... "Antithrombin (Recombinant) US Package Insert ATryn for Injection February 3, 2009" (PDF). Food and Drug Administration. ... UFH binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation. The ...
https://en.wikipedia.org/wiki/Anticoagulant
Hypercoagulability in pregnancyHypercoagulability 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 ...
https://en.wikipedia.org/wiki/Hypercoagulability_in_pregnancy
Acute fatty liver of pregnancyAcute fatty liver of pregnancy
Castro MA, Goodwin TM, Shaw KJ, Ouzounian JG, McGehee WG (1996). "Disseminated intravascular coagulation and antithrombin III ...
https://en.wikipedia.org/wiki/Acute_fatty_liver_of_pregnancy
ProthrombinaseProthrombinase
After the antithrombin III binds to Factor Xa, the Fondaparinux is released and can activate another antithrombin. Another drug ... "Role of the antithrombin-binding pentasaccharide in heparin acceleration of antithrombin-proteinase reactions. Resolution of ... 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 ...
https://en.wikipedia.org/wiki/Prothrombinase
Hereditary antithrombin deficiency: MedlinePlus GeneticsHereditary antithrombin deficiency: MedlinePlus Genetics
Hereditary antithrombin deficiency is a disorder of blood clotting. Explore symptoms, inheritance, genetics of this condition. ... This gene provides instructions for producing a protein called antithrombin (previously known as antithrombin III). This ... Hereditary antithrombin deficiency is a disorder of blood clotting. People with this condition are at higher than average risk ... Hereditary antithrombin deficiency is estimated to occur in about 1 in 2,000 to 3,000 individuals. Of people who have ...
https://medlineplus.gov/genetics/condition/hereditary-antithrombin-deficiency
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 ...
https://medlineplus.gov/ency/article/000558.htm
SCOPe 2.07: Protein: AntithrombinSCOPe 2.07: Protein: Antithrombin
Timeline for Protein Antithrombin from e.1.1.1: Serpins: *Protein Antithrombin from e.1.1.1: Serpins first appeared (with ... Protein Antithrombin from e.1.1.1: Serpins appears in SCOPe 2.06. *Protein Antithrombin from e.1.1.1: Serpins appears in the ... Lineage for Protein: Antithrombin. *Root: SCOPe 2.07 *. Class e: Multi-domain proteins (alpha and beta) [56572] (71 folds). ... More info for Protein Antithrombin from e.1.1.1: Serpins. ...
http://scop.berkeley.edu/sunid=56584&ver=2.07
Webpages tagged with «antithrombin» - Institute of Clinical MedicineWebpages tagged with «antithrombin» - Institute of Clinical Medicine
Javier Corral will present a guest lecture on "What nature tells us about antithrombin". ...
https://www.med.uio.no/klinmed/english/?vrtx=tags&tag=antithrombin
Siemens Healthineers INNOVANCE Antithrombin Kit:Blood, Hematology and Coagulation | Fisher ScientificSiemens Healthineers INNOVANCE Antithrombin Kit:Blood, Hematology and Coagulation | Fisher Scientific
Chromogenic assay for the automated quantitation of functionally active antithrombin in human citrated plasma. Shop Siemens ... The INNOVANCE™ Antithrombin assay is an automated, ready-to-use, chromogenic assay that exhibits excellent precision and ... This quantitative assay for the determination of functional antithrombin utilizes human anti-Xa substrate and avoids ... Chromogenic assay for the automated quantitation of functionally active antithrombin in human citrated plasma. ...
https://www.fishersci.com/shop/products/innovance-antithrombin-kit-2/p-7235900
Thrombate III (antithrombin III) dosing, indications, interactions, adverse effects, and moreThrombate III (antithrombin III) dosing, indications, interactions, adverse effects, and more
... antithrombin III), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & lactation ... antithrombin alfa. Serious - Use Alternative (1)antithrombin alfa and antithrombin III both increase anticoagulation. Avoid or ... antithrombin alfa. antithrombin alfa and antithrombin III both increase anticoagulation. Avoid or Use Alternate Drug. ... encoded search term (antithrombin III (Thrombate III)) and antithrombin III (Thrombate III) What to Read Next on Medscape ...
http://reference.medscape.com/drug/342868
Rhesus thrombin-antithrombin complex (TAT) ELISA Kit | CSB-EQ027237RH | CusabioRhesus thrombin-antithrombin complex (TAT) ELISA Kit | CSB-EQ027237RH | Cusabio
Rhesus thrombin-antithrombin complex (TAT) ELISA Kit from Cusabio. Cat#: CSB-EQ027237RH. US, UK & Europe Distribution. Online ... Rhesus thrombin-antithrombin complex (TAT) ELISA Kit , CSB-EQ027237RH Cusabio Elisa Rhesus thrombin-antithrombin complex (TAT) ... Rat thrombin-antithrombin complex, TAT ELISA Kit , CSB-E08432r , CusabioRat thrombin-antithrombin complex, TAT ELISA Kit is ... Pig thrombin-antithrombin complex, TAT ELISA Kit , CSB-E13995p , CusabioPig thrombin-antithrombin complex, TAT ELISA Kit is ...
https://joplink.net/rhesus-thrombin-antithrombin-complex-tat-elisa-kit-csb-eq027237rh/
Table of Content - Antithrombin Market | Fortune Business InsightsTable of Content - Antithrombin Market | Fortune Business Insights
4.4 Technological Advancements in Anti-Thrombin Market. 5. Global Anti-Thrombin Market Analysis, Insights and Forecast, 2015- ... Antithrombin Market Size, Share and Industry Analysis By Application (Therapeutics, Research, Diagnostics & Others), Source ( ... 6. North America Anti-Thrombin Market Analysis, Insights and Forecast, 2015-2026 ... 8. Asia Pacific Anti-Thrombin Market Analysis, Insights and Forecast, 2015-2026 ...
https://www.fortunebusinessinsights.com/industry-reports/toc/antithrombin-market-100470
Antithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic valve | Revista Española de CardiologíaAntithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic valve | Revista Española de Cardiología
Hereditary deficiency of antithrombin (AT), previously called AT III, is a hereditary thrombophilia of low prevalence (0.02%- ... January 2021 Antithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic... ... Antithrombin deficiency as a cause of aortic valve thrombosis in a bicuspid aortic valve ... Thrombosis of an aortic porcine xenobioprosthesis associated with familial antithrombin III deficiency. ...
https://www.revespcardiol.org/en-antithrombin-deficiency-as-cause-aortic-articulo-S1885585720303066
Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine...Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine...
Cobas Meyer, M., Vangerow, B., Ahrens, J. et al. Effects of Antithrombin III on body cavity effusions, fluid balance, colloid ... Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine ... Effects of Antithrombin III on body cavity effusions, fluid balance, colloid osmotic pressure and hemodynamics in porcine ... It has been suggested that Antithrombin III (AT III) might have an anti-inflammatory effect in addition to its well known anti- ...
https://ccforum.biomedcentral.com/articles/10.1186/cc744
Antithrombin / Protein C deficiency in pregnancy | UKOSS | NPEU
Antithrombin Deficiency:. Any pregnant woman with known antithrombin deficiency and found to have an antithrombin level below ... UKOSS Antithrombin/Protein C deficiency data collection form. References. *^ Knight M, Nair M, Tuffnell D, Shakespeare J, ... Re-exploration after Caesarean Section Antithrombin / Protein C deficiency in pregnancy Fontan and Pregnancy COVID-19 ... Inherited thrombophilias, including antithrombin and protein C deficiency, are important risk factors for venous ...
https://www.npeu.ox.ac.uk/ukoss/completed-surveillance/ant
Abstract of Multiple Arterial Thrombosis in Anti Thrombin IIIAbstract of Multiple Arterial Thrombosis in Anti Thrombin III
Antithrombin III (AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. AT III deficiency ... Abstract: Antithrombin III (AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. AT III ... Dhruvin Shah, Hetal Pandya, Siraj Vadhvaniya, "Multiple Arterial Thrombosis in Anti Thrombin III Deficiency", International ...
https://www.ijsr.net/get_abstract.php?paper_id=ART2016597
Living ~ Not Just Surviving | My Life With Antithrombin III Deficiency | Page 2Living ~ Not Just Surviving | My Life With Antithrombin III Deficiency | Page 2
This entry was posted on June 11, 2014, in Survivor and tagged American Heart Association, Antithrombin Deficiency, blood, ... This entry was posted on April 18, 2014, in Survivor and tagged American Heart Association, Antithrombin Deficiency, blood, ... This entry was posted on March 30, 2014, in Survivor, Travel and tagged American Heart Association, Antithrombin Deficiency, ... This entry was posted on March 30, 2014, in Survivor, Travel and tagged American Heart Association, Antithrombin Deficiency, ...
https://livingnotjustsurviving.wordpress.com/page/2/
Adjuvant tamoxifen in primary breast cancer: influence on plasma lipids and antithrombin III levels.Adjuvant tamoxifen in primary breast cancer: influence on plasma lipids and antithrombin III levels.
... G. Bertelli;P. Pronzato;D ... Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 ... Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 ... The possible estrogenic effects of tamoxifen on plasma lipids and antithrombin III levels were investigated in 91 breast cancer ...
https://iris.unimore.it/handle/11380/738328
Antithrombin Deficiency Guidelines: Guidelines SummaryAntithrombin Deficiency Guidelines: Guidelines Summary
Antithrombin deficiency, which may be congenital or acquired, results in... ... henceforth referred to as antithrombin or AT) is a 58-kDa molecule belonging to the serine protease inhibitor (serpin) ... Molecular bases of antithrombin deficiency: twenty-two novel mutations in the antithrombin gene. Hum Mutat. 2006 Jun. 27(6):600 ... Role of antithrombin concentrate in treatment of hereditary antithrombin deficiency. An update. Thromb Haemost. 2009 May. 101(5 ...
https://emedicine.staging.medscape.com/article/198573-guidelines
IMSEAR at SEARO: Antithrombin III activity in cerebrovascular accidents.
Antithrombin III activity in cerebrovascular accidents.. Authors: Singh, V P. Singh, M K. Kumar, V. Sinha, M K. Dwivedi, R C. ... CONCLUSION: Decrease of antithrombin III in occlusive and increase in haemorrhagic stroke indicates that these changes have at ... Singh VP, Singh MK, Kumar V, Sinha MK, Dwivedi RC, Rai M, Dube B. Antithrombin III activity in cerebrovascular accidents. ... METHOD: Biological activity of antithrombin III was done by the method as described by Innerfield et al (1976). Immunological ...
https://imsear.searo.who.int/handle/123456789/94231
Hereditary and Acquired Hypercoagulability Workup: Laboratory StudiesHereditary and Acquired Hypercoagulability Workup: Laboratory Studies
Which antithrombin for whom? Identifying the patient population that benefits most from novel antithrombin agents. Curr Cardiol ... Antithrombin and prothrombin abnormalities. Available studies for antithrombin deficiency include both functional and antigenic ... Testing for antithrombin functional activity should not be done while the patient is on unfractionated heparin or low molecular ... Antithrombin, protein S, and protein C levels may be decreased during acute thromboembolism; therefore, both protein assays and ...
https://www.medscape.com/answers/211039-77451/which-studies-are-performed-in-the-diagnosis-of-a-protein-c-deficiency-in-hereditary-and-acquired-hypercoagulability
Antithrombin 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. ... Laboratory studies that can be performed in the workup for antithrombin III deficiency include the following:. * Antithrombin ... Acquired antithrombin III deficiency is a deficiency of antithrombin primarily due to consumption or decreased production. It ...
https://www.staging.medscape.com/answers/954688-119844/what-is-the-pathophysiology-of-antithrombin-iii-atiii-deficiency
Ecat | Antithrombin activityEcat | Antithrombin activity
Reagent: Liquid. Method: Chromogenic. Assay principle: Anti Xa. Interferences: No interference of heparin , 2 U/ml, heparin cofactor II , 400 mg/L, hirudin , 5 mg/L, therapeutic doses of oral direct factor Xa inhibitors may cause erroneously ...
http://www.ecat.nl/ecat-education/assays/antithrombin-activity/
Polyurethane modified with an antithrombin-heparin complex via polyethylene oxide linker/spacers: Influence of PEO molecular...
Polyurethane modified with an antithrombin-heparin complex via polyethylene oxide linker/spacers: Influence of PEO molecular ...
https://experts.mcmaster.ca/display/publication412128
Antithrombin-III | Drug Guide - MedSchoolAntithrombin-III | Drug Guide - MedSchool
Treatment and prophylaxis of thrombosis in patients with hereditary antithrombin-III deficiency. ...
https://medschool.co/drug-guide/antithrombin-iii
MeSH | Antithrombin III Deficiency (D020152)MeSH | Antithrombin III Deficiency (D020152)
Diseases [C] » Hemic and Lymphatic Diseases [C15] » Hematologic Diseases » Thrombophilia » Antithrombin III Deficiency ... Diseases [C] » Hemic and Lymphatic Diseases [C15] » Hematologic Diseases » Blood Protein Disorders » Antithrombin III ... An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis. MeSH ...
https://www.cdek.liu.edu/mesh/D020152/
Antithrombin (AT) | Lab Tests | 5MinuteConsultAntithrombin (AT) | Lab Tests | 5MinuteConsult
AT, also known as antithrombin III, is a natural inhibitor of thrombin and of other clotting factors essential in the ...
https://5minuteconsult.com/collectioncontent/2-152202/lab-tests/antithrombin-at
Instructions for Classifying Multiple Causes of Death, 2021 - AppendixInstructions for Classifying Multiple Causes of Death, 2021 - Appendix
AT atherosclerosis; atherosclerotic; atrial tachycardia; antithrombin. ATC all-terrain cycle. ATN acute tubular necrosis ...
https://www.cdc.gov/nchs/nvss/manuals/2b-appendix-2021.htm
Antithrombin (Activity and Antigen) | Northwestern MedicineAntithrombin (Activity and Antigen) | Northwestern Medicine
The antithrombin activity and antigen tests are used to help find out what may be causing abnormal blood clots in your body. ...
https://encyclopedia.nm.org/YourFamily/Women/167,antithrombin_activity_antigen
ANTITHROMBIN III ANTIGEN - Warde Medical LaboratoryANTITHROMBIN III ANTIGEN - Warde Medical Laboratory
We can help you find the right test or let you know if we have a fulfillment partner.. ...
https://wardelab.com/test/antithrombin-iii-antigen/
Polyclonal Antibody to Antithrombin (AT) - danabioPolyclonal Antibody to Antithrombin (AT) - danabio
Polyclonal Antibody to Antithrombin (AT). PAC313Ra01 * $38000 $380.00 Unit price/ per ...
https://danabiosci.com/products/polyclonal-antibody-to-antithrombin-at-pac313ra01
Antithrombin (AT) Deficiency Profile | Evexia DiagnosticsAntithrombin (AT) Deficiency Profile | Evexia Diagnostics
Antithrombin (AT) Deficiency Profile laboratory test. Providing comprehensive, state-of-the-art, clinical laboratory services ... Antithrombin (AT), often referred to as antithrombin III, is a glycoprotein produced in the liver.7-9 AT is a serine protease ...
https://www.evexiadiagnostics.com/test-menu/antithrombin-at-deficiency-profile/
Mouse Apolipoprotein M (APOM) ELISA kit | CSB-EL001947MO | CusabioMouse Apolipoprotein M (APOM) ELISA kit | CSB-EL001947MO | Cusabio
Rat thrombin-antithrombin complex, TAT ELISA Kit , CSB-E08432r , CusabioRat thrombin-antithrombin complex, TAT ELISA Kit is ...
https://joplink.net/mouse-apolipoprotein-m-apom-elisa-kit-csb-el001947mo/
AT and the coagulation cascadeAT and the coagulation cascade
Learn more about how antithrombin impact the coagulation cascade. ... Antithrombin (AT) activity inhibits many clotting factors in ... Role of antithrombin concentrate in hereditary antithrombin deficiency: an update. Thromb Haemost. 2009;101(5):806-812. 20. Di ... THROMBATE III® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and ... Antithrombin participates in a feedback loop in which blood can clot rapidly when needed but does not clot all of the time25 ...
https://www.thrombate.com/sk/at-coagulation-cascade
Acquired antithrombin deficiencyThrombate IIIDiagnosed with antithrombin III deficiThrombophiliaHereditaryThrombin-antithrombin complexCongenitalThrombosisEffects of antithrombinInhibitorATIIISerpinAssaysCoagulation cascadeDeficiency in pregnancyInhibits thrombinProteinsProtein C deficienThromboticProthrombinHeterozygousAnagrelideGenePlatelet aggregationInhibitorsInhibitionFibrinPregnancyDosageLaboratoryAlfaChromogenicAnti-inflammatoryAntibodyAnticoagulationPatientsActivityTherapeuticsAbnormalBloodIncreased riskSeverity
Acquired antithrombin deficiency1
  • Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis and treatment options. (medlineplus.gov)
Thrombate III1
  • THROMBATE III ® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and prevention of thromboembolism and for prevention of perioperative and peripartum thromboembolism. (thrombate.com)
Diagnosed with antithrombin III defici1
  • Once a person is diagnosed with antithrombin III deficiency, all close family members should be screened for this disorder. (medlineplus.gov)
Thrombophilia3
  • Hereditary deficiency of antithrombin (AT), previously called AT III, is a hereditary thrombophilia of low prevalence (0.02%-0.2%) that was first described in 1965 and has autosomal dominant inheritance and variable penetrance. (revespcardiol.org)
  • Among the most important risk factors for venous thromboembolism in pregnancy is the presence of thrombophilia such as antithrombin deficiency. (ox.ac.uk)
  • Egeberg O. Inherited antithrombin deficiency causing thrombophilia. (medscape.com)
Hereditary15
  • Hereditary antithrombin deficiency is a disorder of blood clotting. (medlineplus.gov)
  • In hereditary antithrombin deficiency, abnormal blood clots usually form only in veins, although they may rarely occur in arteries. (medlineplus.gov)
  • About half of people with hereditary antithrombin deficiency will develop at least one abnormal blood clot during their lifetime. (medlineplus.gov)
  • Other factors can increase the risk of abnormal blood clots in people with hereditary antithrombin deficiency. (medlineplus.gov)
  • The combination of hereditary antithrombin deficiency and other inherited disorders of blood clotting can also influence risk. (medlineplus.gov)
  • Women with hereditary antithrombin deficiency are at increased risk of developing an abnormal blood clot during pregnancy or soon after delivery. (medlineplus.gov)
  • Hereditary antithrombin deficiency is estimated to occur in about 1 in 2,000 to 3,000 individuals. (medlineplus.gov)
  • Of people who have experienced an abnormal blood clot, about 1 in 20 to 200 have hereditary antithrombin deficiency. (medlineplus.gov)
  • Hereditary antithrombin deficiency is caused by mutations in the SERPINC1 gene. (medlineplus.gov)
  • Most of the mutations that cause hereditary antithrombin deficiency change single protein building blocks (amino acids) in antithrombin, which disrupts its ability to control blood clotting. (medlineplus.gov)
  • Brouwer JL, Lijfering WM, Ten Kate MK, Kluin-Nelemans HC, Veeger NJ, van der Meer J. High long-term absolute risk of recurrent venous thromboembolism in patients with hereditary deficiencies of protein S, protein C or antithrombin. (medlineplus.gov)
  • Bauer KA, Issues in the Diagnosis and Management of Hereditary Antithrombin Deficiency. (ox.ac.uk)
  • Treatment and prophylaxis of thrombosis in patients with hereditary antithrombin-III deficiency. (medschool.co)
  • Prevention and treatment of venous thromboembolism in pregnancy and patients with hereditary antithrombin deficiency. (thrombate.com)
  • 10. Pabinger I, Schneider B. Thrombotic risk in hereditary antithrombin III protein C, or protein S deficiency. (thrombate.com)
Thrombin-antithrombin complex1
  • Rhesus thrombin-antithrombin complex (TAT) ELISA Kit is Available at Gentaur Genprice with the fastest delivery. (joplink.net)
Congenital5
  • Congenital antithrombin III deficiency is a genetic disorder that causes the blood to clot more than normal. (medlineplus.gov)
  • Congenital antithrombin III deficiency is an inherited disease. (medlineplus.gov)
  • Congenital antithrombin III deficiency is an autosomal dominant disorder in which an individual inherits one copy of the SERPINC1 (also called AT3 ) gene on chromosome 1q25.1, which encodes antithrombin III. (medscape.com)
  • Severe congenital antithrombin III deficiency, in which the individual inherits two defective genes, is a rare autosomal recessive condition associated with increased thrombogenesis, typically noted in the neonatal period or early infancy. (medscape.com)
  • Once a patient with congenital antithrombin III deficiency has developed thrombosis, anticoagulation is more strongly indicated. (medscape.com)
Thrombosis2
  • An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis. (liu.edu)
  • Clinical outcomes of antithrombin III-based therapy for patients with portal vein thrombosis: A retrospective, multicenter study. (bvsalud.org)
Effects of antithrombin7
  • amobarbital decreases effects of antithrombin III by increasing metabolism. (medscape.com)
  • azithromycin increases effects of antithrombin III by decreasing metabolism. (medscape.com)
  • bazedoxifene/conjugated estrogens decreases effects of antithrombin III by pharmacodynamic antagonism. (medscape.com)
  • cefamandole increases effects of antithrombin III by pharmacodynamic synergism. (medscape.com)
  • cefazolin increases effects of antithrombin III by pharmacodynamic synergism. (medscape.com)
  • clarithromycin increases effects of antithrombin III by decreasing metabolism. (medscape.com)
  • Inhibitory effects of antithrombin III against leukocyte rolling and infiltration during endotoxin-induced uveitis in rats. (medscape.com)
Inhibitor3
  • Antithrombin: the principal inhibitor of thrombin. (medscape.com)
  • AT, also known as antithrombin III, is a natural inhibitor of thrombin and of other clotting factors essential in the coagulation cascade. (5minuteconsult.com)
  • 2 ] Since both venous and arterial thrombotic complications are commonly observed in patients with coronavirus disease 2019 (COVID-19) and appear to have a significant impact on patient prognosis,[ 4 ] we performed a literature search to identify all clinical studies that measured antithrombin in COVID-19 patients and correlated the values of this endogenous inhibitor with disease severity. (thieme-connect.com)
ATIII4
  • Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by neutralizing the enzymatic activity of thrombin (factors IIa, IXa, Xa). (medscape.com)
  • Affinity's Antithrombin - ATIII Paired Antibody Set consists of matched capture and detecting antibodies that have been titrated and optimized for use in sandwich style ELISA assays. (affinitybiologicals.com)
  • This Antithrombin - ATIII Paired Antibody Set is intended to facilitate the end user in establishing an "in-house" immunoassay for research purposes only and must not be used for diagnostic applications. (affinitybiologicals.com)
  • This recombinant protein (r-Antidote, PRT064445) is catalytically inactive and lacks the membrane-binding γ-carboxyglutamic acid domain of native fXa but retains the ability of native fXa to bind direct fXa inhibitors as well as low molecular weight heparin-activated antithrombin III (ATIII). (nih.gov)
Serpin2
  • Cell-surface heparan sulfate proteoglycan-mediated regulation of human neutrophil migration by the serpin antithrombin III. (medscape.com)
  • Antithrombin, a 432-aminoacid serpin produced by the liver, is now recognized as one of the most powerful endogenous anticoagulants, which functions by competitively inhibiting the activity of thrombin and activated factor X (FXa). (thieme-connect.com)
Assays1
  • A typical lab can meet 91% of its Hemostasis testing needs with HemosIL liquid, ready-to-use assays, including PT, APTT, D-Dimer and Antithrombin. (werfen.com)
Coagulation cascade1
  • How does antithrombin impact the coagulation cascade? (thrombate.com)
Deficiency in pregnancy3
  • [2] There is a lack of straightforward guidance or a strong evidence base for management of antithrombin deficiency in pregnancy and it is currently unknown how this cohort of women is managed in the UK. (ox.ac.uk)
  • What is the prevalence of antithrombin/protein C deficiency in pregnancy in the UK? (ox.ac.uk)
  • This is a recorded version of our webinar on addressing the management challenges of antithrombin deficiency in pregnancy, presented by Dr. Andra H. James and Dr. Barbara Konkle that took place on June 27, 2017. (fwgbd.org)
Inhibits thrombin1
  • Antithrombin III (AT III) inhibits thrombin and activated clotting factors like factor Xa, IXa and VIIa. (ijsr.net)
Proteins2
  • Antithrombin blocks the activity of proteins that promote blood clotting, especially a protein called thrombin. (medlineplus.gov)
  • Individuals with this condition do not have enough functional antithrombin to inactivate clotting proteins, which results in the increased risk of developing abnormal blood clots. (medlineplus.gov)
Protein C deficien4
  • Inherited thrombophilias, including antithrombin and protein C deficiency, are important risk factors for venous thromboembolism (VTE). (ox.ac.uk)
  • This study will help us estimate the current prevalence of antithrombin III and heterozygous protein C deficiency among pregnant women in the UK and describe treatment methods and outcomes with a view to developing guidance to identify women at risk, improve management and reduce VTE risk in this group. (ox.ac.uk)
  • To use the UK Obstetric Surveillance System (UKOSS) to determine the prevalence of antithrombin/protein c deficiency in pregnant women in the UK and examine the management of the condition as well maternal and neonatal outcomes. (ox.ac.uk)
  • How are pregnant women with antithrombin/protein C deficiency managed in the UK? (ox.ac.uk)
Thrombotic3
  • It has been suggested that Antithrombin III (AT III) might have an anti-inflammatory effect in addition to its well known anti-thrombotic properties. (biomedcentral.com)
  • 1 ] [ 2 ] Both inherited and acquired antithrombin deficiencies are associated with a magnified thrombotic risk, especially venous thromboembolism. (thieme-connect.com)
  • The study suggests that thrombocytosis, increased platelet aggregation and decreased natural coagulation inhibitors [‎protein C and antithrombin III]‎ in splenectomized thalassaemic children may be significant in thrombotic complications in such patients. (who.int)
Prothrombin2
  • Additional tests include chromogen (amidolytic) based assay - the formation of chromogenic colour is proportional to the amount of Activated protein-C - APC (hence Protein-C) in the plasma sample specimen (test results can be interfered with by hemolysis, lipemia, icterus etc), partially activated Protein-C test, antithrombin, lupus anticoagulant, antiphospholipid antibodies, factor V Leiden test, prothrombin test etc. (rtdiagnostics.net)
  • Subjects with detection of FV Leiden or Prothrombin G20210A mutation, protein C or S deficiency, antithrombin deficiency, or antiphospholipid antibody syndrome at Screening. (who.int)
Heterozygous1
  • Most affected neonates, however, have heterozygous antithrombin III deficiency rather than the homozygous state. (medscape.com)
Anagrelide1
Gene3
  • This gene provides instructions for producing a protein called antithrombin (previously known as antithrombin III). (medlineplus.gov)
  • It occurs when a person receives one abnormal copy of the antithrombin III gene from a parent with the disease. (medlineplus.gov)
  • The abnormal gene leads to a low level of the antithrombin III protein. (medlineplus.gov)
Platelet aggregation2
  • viscosity, reduced red cell deformability, The main objectives of this study were abnormal red cell adhesive properties, en- to assess platelet aggregation patterns and dothelial intimal proliferation, bone marrow levels of PC, PS and AT III in SCA patients or fat embolism and a chronic hypercoagula- in the steady state and in vaso-occlusive ble state [6]. (who.int)
  • The patients' levels of protein C, antithrombin III and in vitro platelet aggregation in response to collagen were compared with those of 20 controls. (who.int)
Inhibitors3
  • This quantitative assay for the determination of functional antithrombin utilizes human anti-Xa substrate and avoids interference with heparin cofactor II and direct thrombin inhibitors, such as hirudin. (fishersci.com)
  • Inteferences: Therapeutic doses of hirudin or other direct thrombin inhibitors will cause erroneously increased antithrombin III activity. (ecat.nl)
  • 5 mg/L, therapeutic doses of oral direct factor Xa inhibitors may cause erroneously increased antithrombin activity. (ecat.nl)
Inhibition4
  • Rosenberg JS, McKenna PW, Rosenberg RD. Inhibition of human factor IXa by human antithrombin. (medscape.com)
  • Stead N, Kaplan AP, Rosenberg RD. Inhibition of activated factor XII by antithrombin-heparin cofactor. (medscape.com)
  • Mechanism of antithrombin III inhibition of factor VIIa/tissue factor activity on cell surfaces. (medscape.com)
  • Enhances the inhibition rate of clotting proteases by antithrombin III. (bcas.ca)
Fibrin1
  • Of these, Antithrombin I (see FIBRIN ) and ANTITHROMBIN III appear to be of major importance. (bvsalud.org)
Pregnancy1
  • This Webinar will bring together two leading experts in the area of Antithrombin (AT) deficiency and its obstetric and hematologic management who will disseminate the consensus of our previously held meeting, on the correct diagnosis and the optimal treatment and management of women with AT deficiency during pregnancy and in the postpartum period. (fwgbd.org)
Dosage1
  • This section also provides the overall information and data analysis of the global Antithrombin Market with respect to the leading market segments based on major application segment, source segment, and dosage form segment. (euprwire.com)
Laboratory3
  • Any pregnant woman with known antithrombin deficiency and found to have an antithrombin level below the lower limit of normal for their local reference laboratory. (ox.ac.uk)
  • 7. Kottke-Marchant K, Duncan A. Antithrombin deficiency: issues in laboratory diagnosis. (thrombate.com)
  • Describe the laboratory assessment of antithrombin deficiency. (fwgbd.org)
Alfa5
  • antithrombin alfa and antithrombin III both increase anticoagulation. (medscape.com)
  • omega 3 carboxylic acids, antithrombin alfa. (medscape.com)
  • Introducción: El ensayo clínico PROWESS ha demostrado que el tratamiento con drotrecogina alfa (activada) en pacientes con sepsis grave se asocia a una reducción del riesgo absoluto de muerte en comparación con el tratamiento estándar. (scielo.org)
  • El objetivo del estudio fue evaluar el coste-efectividad de drotrecogina alfa (activada), frente a tratamiento estándar, en el tratamiento de la sepsis grave en España. (scielo.org)
  • Pacientes y métodos: Se elaboró un modelo de análisis de decisión en el que se compararon los costes hasta el alta hospitalaria y la eficacia a largo plazo de drotrecogina alfa (activada) frente a tratamiento estándar de pacientes con sepsis grave en España, desde la perspectiva del financiador de los servicios sanitarios. (scielo.org)
Chromogenic2
  • Chromogenic assay for the automated quantitation of functionally active antithrombin in human citrated plasma. (fishersci.com)
  • The INNOVANCE™ Antithrombin assay is an automated, ready-to-use, chromogenic assay that exhibits excellent precision and reliability. (fishersci.com)
Anti-inflammatory1
  • Okajima K, Uchiba M. The anti-inflammatory properties of antithrombin III: new therapeutic implications. (medscape.com)
Antibody1
  • Antithrombin III antibody (biotin) was purified by affinity chromatography. (thrombrin.com)
Anticoagulation2
  • antithrombin III and bemiparin both increase anticoagulation. (medscape.com)
  • Antithrombin III activity is markedly potentiated by heparin, the principal mechanism by which both heparin and low-molecular-weight heparin result in anticoagulation. (medscape.com)
Patients10
  • The possible estrogenic effects of tamoxifen on plasma lipids and antithrombin III levels were investigated in 91 breast cancer patients. (unimore.it)
  • Mean values of total, HDL and LDL cholesterol, triglycerides, glucose, uric acid, and antithrombin III were evaluated in 55 patients on adjuvant tamoxifen for at least 3 months and compared with those found in 36 patients on no therapy. (unimore.it)
  • Total cholesterol, LDL cholesterol, and antithrombin III levels were significantly lower in treated patients (p less than 0.05). (unimore.it)
  • RESULTS: The biological and immunological activity of antithrombin III was measured in 98 patient of occlusive and 56 patients of haemorrhagic strokes. (who.int)
  • Common conditions that result in acquired antithrombin III deficiency include disseminated intravascular coagulation (DIC) , microangiopathic hemolytic anemias due to endothelial damage (ie, hemolytic-uremic syndrome ), veno-occlusive disease (VOD) (in patients undergoing bone marrow transplantation ), sepsis, liver disease, and nephrotic syndrome. (medscape.com)
  • In these patients, replacement of antithrombin III using antithrombin III concentrates or fresh frozen plasma is recommended. (medscape.com)
  • The study involved 58 VTE patients under age 45 years, 45 of whom had at least one inherited risk factor, including 14 with antithrombin III deficiency. (medscape.com)
  • This study aimed to evaluate the outcome in patients with PVT who received antithrombin III-based therapy . (bvsalud.org)
  • 3 ] Importantly, reduced antithrombin levels are also observed in patients with intravascular consumption coagulopathies, including those caused by bacteria, viruses, and other microorganisms. (thieme-connect.com)
  • A pooled analysis was finally performed, calculating the weighted mean difference (WMD) along with its 95% confidence interval (95% CI), of antithrombin values in COVID-19 patients with or without severe illness. (thieme-connect.com)
Activity4
  • IMSEAR at SEARO: Antithrombin III activity in cerebrovascular accidents. (who.int)
  • METHOD: Biological activity of antithrombin III was done by the method as described by Innerfield et al (1976). (who.int)
  • In antithrombin III deficiency, however, the activity of LMWH is not as reliable as in an otherwise healthy person. (medscape.com)
  • I. 100 U/mg) activity and low resistance Ⅱ a or antithrombin (28 i. (qjbchina.com)
Therapeutics1
  • Based on the application type, the antithrombin market has been segmented into: therapeutics, research and diagnostics. (euprwire.com)
Abnormal2
  • Antithrombin III is a protein in the blood that blocks abnormal blood clots from forming. (medlineplus.gov)
  • This low level of antithrombin III can cause abnormal blood clots (thrombi) that can block blood flow and damage organs. (medlineplus.gov)
Blood2
  • The health care provider can also order a blood test to check if you have a low level of antithrombin III. (medlineplus.gov)
  • Extract normalizes prostate function and contributes to the antithrombotic action of the blood serum due to the increased production of antithrombin. (hotpolkadot.com)
Increased risk1
  • Pregnant women are already at increased risk of VTE due to their hypercoagulable state so those with antithrombin deficiency are therefore at very high risk of VTE. (ox.ac.uk)
Severity1
  • Our initial electronic search generated a total number of 60 documents, of which 54 were excluded because they were review articles ( n = 24), did not report antithrombin data ( n = 12), were editorial material ( n = 9) or case reports ( n = 5), did not stratify antithrombin values according to disease severity ( n = 3), or had an insufficient sample size ( n = 1). (thieme-connect.com)
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