Activated Protein C Resistance: A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.Factor V: Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.Protein C Deficiency: An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)Thrombophilia: A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.Protein S Deficiency: An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)Protein S: The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.Factor V Deficiency: A deficiency of blood coagulation factor V (known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as Owren's disease or parahemophilia. It varies greatly in severity. Factor V deficiency is an autosomal recessive trait. (Dorland, 27th ed)Lupus Coagulation Inhibitor: An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.Partial Thromboplastin Time: The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.Blood Coagulation Tests: Laboratory tests for evaluating the individual's clotting mechanism.Abortion, Habitual: Three or more consecutive spontaneous abortions.Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.Coagulation Protein Disorders: Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.Antibodies, Anticardiolipin: Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.Retinal Vein Occlusion: Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Protein C Inhibitor: A member of the serpin family of proteins that is found in plasma and urine. It is dependent on heparin and is able to inhibit activated PROTEIN C; THROMBIN; KALLIKREIN; and other SERINE ENDOPEPTIDASES.Venous Thrombosis: The formation or presence of a blood clot (THROMBUS) within a vein.Thromboembolism: Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Homozygote: An individual in which both alleles at a given locus are identical.Point Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.Drug Resistance, Microbial: The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Drug Resistance, Bacterial: The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Drug Resistance, Neoplasm: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process.Pulmonary Surfactant-Associated Protein C: A pulmonary surfactant associated protein that plays a role in alveolar stability by lowering the surface tension at the air-liquid interface. It is a membrane-bound protein that constitutes 1-2% of the pulmonary surfactant mass. Pulmonary surfactant-associated protein C is one of the most hydrophobic peptides yet isolated and contains an alpha-helical domain with a central poly-valine segment that binds to phospholipid bilayers.Drug Resistance, Multiple: Simultaneous resistance to several structurally and functionally distinct drugs.Disease Resistance: The capacity of an organism to defend itself against pathological processes or the agents of those processes. This most often involves innate immunity whereby the organism responds to pathogens in a generic way. The term disease resistance is used most frequently when referring to plants.

Synergistic effects of prothrombotic polymorphisms and atherogenic factors on the risk of myocardial infarction in young males. (1/111)

Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C --> T, factor V (F V) nt 1691G --> A (F V Leiden), and factor II (F II) nt 20210 G --> A on the risk of myocardial infarction. In the present study, we analyzed the effect of these prothrombotic polymorphisms, as well as apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and hypercholesterolemia, on the risk of myocardial infarction in young males. We conducted a case-control study of 112 young males with first acute myocardial infarction (AMI) before the age of 52 and 187 healthy controls of similar age. The prevalences of heterozygotes for F V G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among cases and controls, respectively). In contrast, the prevalence of MTHFR 677T homozygosity and the allele frequency of Apo E4 were significantly higher among patients (24.1% v 10.7% and 9.4% v 5.3% among cases and controls, respectively). Concomitant presence of hypertension, hypercholesterolemia, or diabetes and one or more of the four examined polymorphisms increased the risk by almost ninefold (odds ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5) and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed simultaneously by a logistic model, the combination of prothrombotic and Apo E4 polymorphisms with current smoking increased the risk 25-fold (OR = 24.7; 95% CI, 7.17 to 84.9). The presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of AMI, as was recently found in a similar cohort of women.  (+info)

Thrombophilia as a multigenic disease. (2/111)

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)

Factor V Leiden and antibodies against phospholipids and protein S in a young woman with recurrent thromboses and abortion. (3/111)

We describe the case of a 39-year-old woman who suffered two iliofemoral venous thromboses, a cerebral ischemic infarct and recurrent fetal loss. Initial studies showed high levels of antiphospholipid antibodies (APAs) and a moderate thrombocytopenia. After her second miscarriage, laboratory diagnosis revealed that the woman was heterozygous for the factor V Leiden mutation and had a functional protein S deficiency as well as anti-protein S and anti-beta 2-glycoprotein I antibodies. The impairment of the protein C pathway at various points could well explain the recurrent thromboses in the patient and supports the role of a disturbed protein C system in the pathophysiology of thrombosis in patients with APAs.  (+info)

Simultaneous detection of FV Q506 and prothrombin 20210 A variation by allele-specific PCR. (4/111)

BACKGROUND AND OBJECTIVE: Factor V Leiden is the most important risk factor for hereditary thromboembolism, whereas the mutation in the 3'-untranslated region of the prothrombin gene seems to be only a mild risk factor for thrombotic events. On the other hand the factor V mutation (Arg 506) is frequently coinherited with the prothrombin 3'-untranslated region G20210A variant and there is increasing evidence that the co-segregated prothrombin variant is an additional risk factor for venous thromboembolism, contributing to thrombotic manifestations. A rapid, simple and cost-effective screening method is, therefore, required for the detection of both factor V Leiden and the prothrombin variant A20210G. DESIGN AND METHODS: Eighty-eight patients were enrolled in this study. Forty-four had a previously identified factor V and/or prothrombin mutation, the remaining 44 patients served as negative controls. A multiplex allele specific oligonucleotide PCR was established for the simultaneous detection of the two genetic risk factors for thrombophilia. To test the specificity of the simultaneous ASO PCR approach, the mutated and physiological factor V and prothrombin amplification products were sequenced. RESULTS: The factor V Leiden mutation and the prothrombin variant were correctly identified in all of 44 patients with known mutations. Furthermore the test was able to detect the mutated factor V and the II variant alone, as well as in the cosegregated pattern. Five patients with a homozygous pattern of factor V Leiden or prothrombin variant were also correctly identified. The sensitivity of the test is therefore 100%. In none of the 44 control cases were false positive results seen. INTERPRETATION AND CONCLUSIONS: The ASO PCR test is a rapid, simple and cost-effective screening test for thrombophilia.  (+info)

Coagulation factors II, V, VII, and X, prothrombin gene 20210G-->A transition, and factor V Leiden in coronary artery disease: high factor V clotting activity is an independent risk factor for myocardial infarction. (5/111)

Increased levels of hemostatic factors and genetic mutations of proteins involved in coagulation may play a role in the pathogenesis of coronary artery disease. We investigated clotting activity of factors II (FII:C), V (FV:C), VII (FVII:C), and X (FX:C), the prothrombin gene 20210G-->A transition, and the factor V Leiden mutation in 200 survivors of myocardial infarction and in 100 healthy controls. FV:C (P<0.0001) and FVII:C (P<0.0001) were found to be independent risk factors for myocardial infarction. High FV:C or high FVII:C combined with smoking or arterial hypertension increased the relative risk for myocardial infarction up to 50-fold. One of 177 patients (0.6%) and 4 of 89 controls (4.5%) had the prothrombin 20210 AG genotype. Eleven of 177 patients (6.2%) and 6 of 89 controls (6.7%) were heterozygous for the factor V Leiden mutation. No homozygous carrier for these mutations was found. Neither the prothrombin gene 20210G-->A transition (odds ratio [OR], 0.1; 95% confidence interval [CI], 0.01 to 1.1) nor the factor V Leiden mutation (OR, 1.0; 95% CI, 0.4 to 2.8) were associated with an increased relative risk for myocardial infarction. In conclusion, our data indicate that neither the prothrombin gene 20210G-->A transition nor the factor V Leiden mutation are risk factors for myocardial infarction. High FVII:C was confirmed to be an independent risk factor for myocardial infarction. Moreover, we describe for the first time that high FV:C is an independent risk factor for myocardial infarction.  (+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. (6/111)

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)

Activated protein C resistance: effect of platelet activation, platelet-derived microparticles, and atherogenic lipoproteins. (7/111)

Plasma and platelet factor Va represent different substrates for activated protein C (APC). In this study, we have measured platelet-dependent APC resistance and the effect of aspirin and a platelet glycoprotein IIbIIIa antagonist (GR144053F) on this phenomenon. In platelet rich plasma (PRP), progressive APC resistance was observed with increasing platelet activation. APC sensitivity ratios of 1.8, 1.7, and 1.4 were observed after platelet activation with thrombin receptor activating peptide (TRAP), collagen, and A23187, respectively. Ultracentrifugation at 77,000g for 1 hour abolished APC resistance indicating that the phenotype is associated exclusively with the platelet membrane. APC resistance was not observed in the presence of phosphatidylcholine-phosphatidylserine (PCPS) vesicles or purified human plasma lipoproteins. APC resistance was observed in the presence of platelet-derived microparticles, but to a lesser degree than that in the presence of activated platelets. The platelet-dependent APC resistance phenotype was also observed when endogenous APC was generated by Protac (American Diagnostica, Inc, Greenwich, CT). In vitro inhibition of platelet activation with aspirin had no effect, but the fibrinogen receptor antagonist, GR144053F, inhibited platelet-dependent APC resistance. These results indicate that platelet activation results in an APC-resistant phenotype comparable to that observed in the plasma of patients with factor V gene mutations affecting critical APC cleavage sites. This suggests that platelet activation at the site of endothelial damage downregulates a critical natural anticoagulant mechanism. The antithrombotic effect of aspirin may be due to an indirect effect on platelet-dependent APC resistance with reduced platelet retention within a developing thrombus. The more potent antithrombotic effect of glycoprotein IIbIIIa antagonists may in addition be the result of reduced platelet factor Va expression and modulation of the platelet-dependent APC resistance phenotype.  (+info)

A possible role for activated protein C resistance in patients with first and second trimester pregnancy failure. (8/111)

Thrombophilia was recently suggested as a possible factor in recurrent pregnancy losses. We studied prospectively 125 patients (mean age 31.4 +/- 5.6 years) with one or more first or second trimester pregnancy losses for the prevalence of activated protein C resistance (APCR). Proteins C and S antigens, antithrombin III, anticardiolipin, and lupus anti-coagulant were also evaluated. Patients with uterine malformations, hormonal abnormalities, chromosomal translocations and infectious causes were excluded. A control group of 125 women with no past fetal loss were matched with the study group. Whenever the APC-sensitivity ratio (APC-SR) was +info)

*Factor V Leiden

Prothrombin G20210A De Stefano V, Leone G (1995). "Resistance to activated protein C due to mutated factor V as a novel cause ... May 1994). "Mutation in blood coagulation factor V associated with resistance to activated protein C". Nature. 369 (6475): 64-7 ... Russell viper venom-based and activated partial thromboplastin time-based screening assays for resistance to activated protein ... activated Protein C). The gene that codes the protein is referred to as F5. Mutation of this gene-a single nucleotide ...

*Venous thrombosis

Low free protein S Activated protein C resistance High factor VIII levels Hyperhomocysteinemia High fibrinogen levels High ... Antithrombin deficiency Protein C deficiency Protein S deficiency (type I) Factor V Leiden Prothrombin G20210A ... Hypoxia also causes reactive oxygen species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-κB), ... Specifically, the two pathways of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by ...

*Protein C

Activated protein C resistance occurs when APC is unable to perform its functions. This disease has similar symptoms to protein ... "Product Information: Human Activated Protein C - Bovine Activated Protein C - Mouse Activated Protein C". Haematologic ... The protein C zymogen is activated when it binds to thrombin, another protein heavily involved in coagulation, and protein C's ... Walker FJ (June 1980). "Regulation of activated protein C by a new protein. A possible function for bovine protein S". The ...

*Activated protein C resistance

Activated protein C (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. Activated protein C resistance is the ... Activated protein C resistance (APCR) is a hemostatic disorder characterized by a poor anticoagulant response to activated ... Sheppard DR (2000). "Activated protein C resistance: the most common risk factor for venous thromboembolism". J Am Board Fam ... Dahlbäck B (2003). "The discovery of activated protein C resistance". J. Thromb. Haemost. 1 (1): 3-9. doi:10.1046/j.1538- ...

*Acroangiodermatitis

"Mali acroangiodermatitis in homozygous activated protein C resistance". Arch Dermatol. 141 (3): 396-7. doi:10.1001/archderm. ...

*Prothrombinase

Rosendorff A, Dorfman DM (June 2007). "Activated protein C resistance and factor V Leiden: a review". Arch. Pathol. Lab. Med. ... Factor Va is inactivated following cleavage by activated protein C. Activated protein C cleaves Factor Va in both its light and ... if Factor V is cleaved by activated protein C instead of thrombin, it can serve as a cofactor for activated protein C. Once ... Contributions of protein-protein and protein-membrane interactions toward complex formation". J. Biol. Chem. 265 (7): 3708-18. ...

*Warfarin necrosis

There have also been cases in patients with other deficiency, including protein S deficiency, activated protein C resistance ( ... Makris M, Bardhan G, Preston FE (March 1996). "Warfarin induced skin necrosis associated with activated protein C resistance". ... Protein C is an innate anticoagulant, and as warfarin further decreases protein C levels, it can lead to massive thrombosis ... common treatments in this setting include fresh frozen plasma or pure activated protein C. Since the clot-promoting effects of ...

*Sticky platelet syndrome

ISBN 0-521-87082-8. Chaturvedi S, Dzieczkowski JS (1999). "Protein S deficiency, activated protein C resistance and sticky ... it has been described as a coagulation disorder that can present in conjunction with protein S deficiency and Factor V Leiden. ...

*APCR

... may refer to: Armour-piercing, composite rigid - a type of armor piercing projectile Activated protein C resistance - a ...

*Factor V

... make it resistant to cleavage by activated protein C ("APC resistance"). It therefore remains active and increases the rate of ... after which the protein no longer assists in activating protein C. The protein is now divided to a heavy chain, consisting of ... "Mutation in blood coagulation factor V associated with resistance to activated protein C". Nature. 369 (6475): 64-7. doi: ... "Binding of protein S to factor Va associated with inhibition of prothrombinase that is independent of activated protein C". The ...

*Moyamoya disease

... activated protein C resistance, or head trauma can develop moyamoya malformations. It is more common in women than in men, ... There are also several protein biomarkers that have been linked to the moyamoya disease diagnosis. Although the sample size of ... The pathogenesis of moyamoya disease is unknown, although the gene ring finger protein 213 (RNF213) has been implicated. Once ... and proteins as well as cellular changes that occur in cases of moyamoya. Similar to moyamoya disease, there are conditions ...

*Gene-for-gene relationship

When it detects interference with the guardee protein, it activates resistance. Several experiments support this hypothesis, e. ... This makes Pto the guardee protein, which is protected by the NBS-LRR protein Prf. However, Pto is a resistance gene alone, ... LRRs are involved in protein-protein interactions, and the greatest variation amongst resistance genes occurs in the LRR domain ... The protein products encoded by this class of resistance gene are located within the plant cell cytoplasm. The PRR class of R ...

*List of MeSH codes (C16)

... activated protein c resistance MeSH C16.320.099.056 --- afibrinogenemia MeSH C16.320.099.075 --- antithrombin iii deficiency ... protein c deficiency MeSH C16.320.099.820 --- thrombasthenia MeSH C16.320.099.900 --- von willebrand disease MeSH C16.320. ...

*List of diseases (A)

... resistance Atelectasis Actinic keratosis Actinomycetales causes anal infection Actinomycosis Activated protein C resistance ...

*List of MeSH codes (C15)

... coagulation protein disorders MeSH C15.378.100.141.036 --- activated protein c resistance MeSH C15.378.100.141.072 --- ... activated protein c resistance MeSH C15.378.100.425.056 --- afibrinogenemia MeSH C15.378.100.425.075 --- antithrombin iii ... activated protein c resistance MeSH C15.378.925.075 --- antithrombin iii deficiency MeSH C15.378.925.220 --- disseminated ... protein c deficiency MeSH C15.378.147.890 --- protein s deficiency MeSH C15.378.190.196 --- anemia, aplastic MeSH C15.378. ...

*Major vault protein

"Human T-cell lymphotropic virus type I Tax activates lung resistance-related protein expression in leukemic clones established ... "Adult T-cell leukemia cells over-express the multidrug-resistance-protein (MRP) and lung-resistance-protein (LRP) genes". ... The relationship between expression of lung resistance-related protein gene or multidrug resistance-associated protein gene and ... Major vault protein is a protein that in humans is encoded by the MVP gene. 78 copies of the protein assemble into the large ...

*TRIB2

"TRIB2 confers resistance to anti-cancer therapy by activating the serine/threonine protein kinase AKT". Nature Communications. ... 2004). "Human tribbles, a protein family controlling mitogen-activated protein kinase cascades". J. Biol. Chem. 279 (41): 42703 ... 2006). "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. ... Tribbles homolog 2 is an atypical protein kinase that is encoded in human by the TRIB2 gene. TRIB2 is a pseudokinase member of ...

*Ceramide-activated protein phosphatase

... involvement in insulin resistance via Akt, serine/arginine-rich protein 40, and ... Ceramide-activated protein phosphatases (CAPPs) are a group of enzymes that are activated by the lipid second messenger ... Long chain ceramides activate protein phosphatase-1 and protein phosphatase-2A. Activation is stereospecific and regulated by ... Wolff, R., Dobrowsky, R., Bielawska, A., Obeid, L., & Hannun, Y. (1994). Role of ceramide-activated protein phosphatase in ...

*Michael Stuart Brown

"Sterol resistance in CHO cells traced to point mutation in SREBP cleavage-activating protein". Cell. 87 (3): 415-26. doi: ... Nov 1984). "The human LDL receptor: a cysteine-rich protein with multiple Alu sequences in its mRNA". Cell. 39 (1): 27-38. doi: ... Reiss Y, Goldstein JL, Seabra MC, Casey PJ, Brown MS (Jul 1990). "Inhibition of purified p21ras farnesyl:protein transferase by ... Oct 1993). "SREBP-1, a basic-helix-loop-helix-leucine zipper protein that controls transcription of the low density lipoprotein ...

*Pathogenesis-related protein

They are induced as part of systemic acquired resistance. Infections activate genes that produce PR proteins. Some of these ... Many proteins found in wine are grape pathogen-related proteins. Those include thaumatin-like proteins and chitinases. ... Salicylic acid plays a role in the resistance to pathogens by inducing the production of pathogenesis-related proteins. ... Pathogenesis-related (PR) proteins are proteins produced in plants in the event of a pathogen attack. ...

*Antineoplastic resistance

IL-6 activates the CCAAT enhancer-binding protein transcription factors which activate MDR1 gene expression (see Alteration of ... Antineoplastic resistance, often used interchangeably with chemotherapy resistance, is the multiple drug resistance of ... MDR1 is activated through NF-κB, a protein complex which acts as a transcription factor. In the rat, an NF-κB binding site is ... MDR proteins are known to be drug-resistance genes, and are highly expressed in various cancers. Inhibition of the MDR genes ...

*PAK1

"Hepatitis B virus X protein confers resistance of hepatoma cells to anoikis by up-regulating and activating p21-activated ... PAK proteins, a family of serine/threonine p21-activated kinases, include PAK1, PAK2, PAK3 and PAK4. These proteins serve as ... Shin YJ, Kim YB, Kim JH (September 2013). "Protein kinase CK2 phosphorylates and activates p21-activated kinase 1". Molecular ... ARG-binding protein 2γ, hepatitis B virus X protein, STE20-related kinase adaptor protein α, RhoI, Klotho, N-acetylglucosaminyl ...

*Protein inhibitor of activated STAT

In cell culture, overexpression of PIAS3 demonstrated an increased resistance of HeLa cells to ionizing radiation. This ... Protein inhibitor of activated STAT (PIAS), also known as E3 SUMO-protein ligase PIAS, is a protein that regulates ... PIAS proteins act as transcriptional co-regulators with at least 60 different proteins in order to either activate or repress ... PIAS protein entry at the Protein Information Resource (PIR) PIAS Proteins at the US National Library of Medicine Medical ...

*CEBPB

Genes coding for transporter proteins that confer multidrug resistance to the cells have also been found to be activated by ... CCAAT/enhancer-binding protein beta is a protein that in humans is encoded by the CEBPB gene. The protein encoded by this ... It can also form heterodimers with the related proteins CEBP-alpha, CEBP-delta, and CEBP-gamma. The encoded protein is ... "The human multidrug resistance protein 2 gene: functional characterization of the 5'-flanking region and expression in hepatic ...

*Plant disease resistance

When this phosphorylation is reduced, EIN2 protein is cleaved and a portion of the protein moves to the nucleus to activate ... A plant line with acceptable resistance against one pathogen may lack resistance against others. Breeding for resistance ... proteins with nucleotide-binding and leucine-rich repeat domains, also known as NLR proteins or STAND proteins, among other ... Responses activated by PTI and ETI receptors include ion channel gating, oxidative burst, cellular redox changes, or protein ...

*Interferon

Type I IFNs further activate p38 mitogen-activated protein kinase (MAP kinase) to induce gene transcription. Antiviral and ... and thus protein) mutation. The H5N1 influenza virus, also known as bird flu, has resistance to interferon and other anti-viral ... For instance, both type I and type II IFNs activate a member of the CRK family of adaptor proteins called CRKL, a nuclear ... PI3K activates P70-S6 Kinase 1, an enzyme that increases protein synthesis and cell proliferation; phosphorylates of ribosomal ...
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Although PHT induced substantial increases in nAPCsr and decreases in TFPI, these changes were not related to the increased risks of ischemic stroke observed in the WHI trials. The mechanisms underlying the increased stroke risks on PHT remain elusive, although hemostatic mechanisms remain the most likely culprits with increases in d-dimer implicated in prior analyses of a subset of WHI data.3 Without knowledge of a mechanism, it is difficult to design strategies to prevent this complication of oral PHT. Transdermal estradiol does not appear to share the prothrombotic potential of oral estrogens with respect to venous thrombosis or stroke, but randomized trial evidence is lacking.23,24. The relationships of nAPCsr and TFPI to ischemic stroke risk are complex. Contrary to our hypothesis that reduced anticoagulant function would increase risk of ischemic stroke, in this study, baseline free TFPI levels were higher in cases compared with control subjects, whereas no significant differences were ...
See Coagulation Studies in Special Instructions.. Specimen Type: Platelet-poor plasma. Collection Container/Tube: Light-blue top (citrate). Submission Container/Tube: Polypropylene vial. Specimen Volume: 1 mL. Collection Instructions:. 1. Spin down, remove plasma. 2. Spin plasma again; remove plasma aliquot without disturbing bottom 0.5 mL. 3. Freeze specimen aliquot immediately at or below -40° C, if possible but no longer than 4 hours after collection. Additional Information:. 1. Double-centrifuged specimen is critical for accurate results as platelet contamination may cause spurious results.. 2. If priority specimen, mark request form, give reason, and request a call-back.. 3. Each coagulation assay requested should have its own vial.. ...
See Coagulation Studies in Special Instructions.. Specimen Type: Platelet-poor plasma. Collection Container/Tube: Light-blue top (citrate). Submission Container/Tube: Polypropylene vial. Specimen Volume: 1 mL. Collection Instructions:. 1. Spin down, remove plasma. 2. Spin plasma again; remove plasma aliquot without disturbing bottom 0.5 mL. 3. Freeze specimen aliquot immediately at or below -40° C, if possible but no longer than 4 hours after collection. Additional Information:. 1. Double-centrifuged specimen is critical for accurate results as platelet contamination may cause spurious results.. 2. If priority specimen, mark request form, give reason, and request a call-back.. 3. Each coagulation assay requested should have its own vial.. ...
Free, official coding info for 2018 ICD-10-CM D68.51 - includes detailed coding rules & notes, synonyms, ICD-9-CM conversion, index & annotation crosswalks, DRG grouping and more.
Objectives: To analyze the economic impact of testing for activated protein C resistance (APC-R) due to factor V Leiden (FVL) mutation with APC-R with ...
In article ,31EBA253.C83 at resulb.ulb.ac.be,, Stephane Corteel ,scorteel at resulb.ulb.ac.be, wrote: , A few weeks ago, we were informed that my wife (28 years old) is affected by a , genetic disease called APCR. , , The only information we have about this disease are : , , - it is a genetic disease apparently due to the mutation of gene , , - it has been recently discovered (2 or 3 years ago) , , - it is related to blood coagulation , , - The effects are increased if the patient eats food containing a high , concentration in vitamin K , , - Due to this disease, my wife has alrealy made 2 pulmonary embolisms , in 1 year. , , Can someon provide us with more information about this problem, references , in scientific litterature, known treatments, aso... , , Thank you for all your answers. , Stephane Corteel, scorteel at resulb.ulb.ac.be I think you are referring to activated Protein C resistance, which is caused by a mutation in the gene encoding for the factor V molecule. This molecule greatly ...
ReportsnReports.com adds report 2014 Strategies for the UK Coagulation Testing Market to its store. This comprehensive report contains 409 pages, 35 tables, and is designed to help current suppliers and potential market entrants identify and evaluate business opportunities emerging in the UK coagulation testing market during the next five years.. The report explores business and technological trends in the UK coagulation testing market; provides estimates of the test volume, as well as sales and market shares of leading competitors; compares features of major analyzers; profiles leading market players; and identifies specific product and business opportunities facing instrument and consumable suppliers during the next five years.. Coagulation Tests. Activated Clotting Time (ACT) (1), Activated Protein C Resistance, Activated PTT (APTT), Alpha 2-Antiplasmin, Antithrombin III, Bleeding Time, D-Dimer, Factor II, Factor V, Factor V Leiden, Factor VII, Factor VIII, Factor IX, Factor Ixa, Factor X ...
Complete report $6,100. DataPack (test volumes, sales forecasts, supplier shares) $3,950.. Summary. This comprehensive report contains 405 pages, 35 tables, and is designed to help current suppliers and potential market entrants identify and evaluate business opportunities emerging in the French coagulation testing market during the next five years. The report explores business and technological trends in the French coagulation testing market; provides estimates of the test volume, as well as sales and market shares of leading competitors; compares features of major analyzers; profiles leading market players; and identifies specific product and business opportunities facing instrument and consumable suppliers during the next five years.. Coagulation Tests. Activated Clotting Time (ACT) (1), Activated Protein C Resistance ...
ReportsnReports.com adds report 2014 Strategies for the Italian Hemostasis Diagnostic Testing Market to its store. This comprehensive report contains 402 pages, 35 tables, and is designed to help current suppliers and potential market entrants identify and evaluate business opportunities emerging in the Italian coagulation testing market during the next five years.. Complete report is available at http://www.reportsnreports.com/reports/274215-2014-strategies-for-the-italian-hemostasis-diagnostic-testing-market.html. The report explores business and technological trends in the Italian coagulation testing market; provides estimates of the test volume, as well as sales and market shares of leading competitors; compares features of major analyzers; profiles leading market players; and identifies specific product and business opportunities facing instrument and consumable suppliers during the next five years.. Coagulation Tests. Activated Clotting Time (ACT) (1), Activated Protein C Resistance, ...
Complete report $6,100. DataPack (test volumes, sales forecasts, supplier shares) $3,950.. Summary. This comprehensive report contains 400 pages, 37 tables, and is designed to help current suppliers and potential market entrants identify and evaluate business opportunities emerging in the Spanish coagulation testing market during the next five years. The report explores business and technological trends in the Spanish coagulation testing market; provides estimates of the test volume, as well as sales and market shares of leading competitors; compares features of major analyzers; profiles leading market players; and identifies specific product and business opportunities facing instrument and consumable suppliers during the next five years.. Coagulation Tests. Activated Clotting Time (ACT) (1), Activated Protein C Resistance ...
Yetino, M., Ozeke, O., Deveci, B., Timur Selcuk, M. and Aras, D. (2006) Multichamber intracardiac thrombi associated with activated protein C resistance in a patient with dilated cardiomyopathy. The International Journal of Cardiovascular Imaging, 22, 59-61.
Describes how Factor V Leiden mutation and PT 20210 mutation tests are used, when Factor V Leiden mutation and PT 20210 mutation tests are ordered, and what the results of Factor V Leiden mutation and PT 20210 mutation tests might mean
Describes how Factor V Leiden mutation and PT 20210 mutation tests are used, when Factor V Leiden mutation and PT 20210 mutation tests are ordered, and what the results of Factor V Leiden mutation and PT 20210 mutation tests might mean
Activated protein C (aPC), in a complex with protein S, inactivates procoagulant factors Va and VIIIa by proteolytic cleavage at specific arginine residues.7,10,11 This serves to control coagulation and limit the extent of thrombus formation. The functionality of the aPC inhibitory system in a given individual can be assessed through an in vitro clotting assay. Addition of aPC to a patients plasma serves to extend the activated partial thromboplastin time (aPTT) for individuals who are sensitive to aPC. Individuals are considered to be aPC resistant when addition of aPC fails to extend the time to clot formation in this assay. More than 95% of cases of aPC resistance are caused by a specific polymorphism in the factor V gene that is referred to as factor V Leiden.8 This single point mutation results in a substitution of glutamine for arginine at amino acid number 506 of factor V. Arginine number 506 is an aPC cleavage site of normal factor V, making factor V Leiden resistant to inactivation by ...
Factor V Leiden is a common inherited genetic disorder in which your blood has an increased tendency to form clots (thrombophilia), usually in your veins.. Although blood clots can form at any age, for most people the increased risk of clotting doesnt begin until adulthood. Most people with factor V Leiden never develop abnormal clots. However, some people with factor V Leiden develop clots that lead to long-term health problems or are life-threatening.. Both men and women can have factor V Leiden, but women may have an increased tendency to develop blood clots during pregnancy or when taking the hormone estrogen.. If you have factor V Leiden, medications can lessen your risk of developing blood clots and help you avoid potentially serious complications.. Its possible to have factor V Leiden without ever developing signs or symptoms. However, the first indication that you have the disorder may be the development of a blood clot (thrombosis).. Some clots do no damage and disappear on their own. ...
Factor V Leiden, also known as Activated Protein C Resistance, is a hereditary blood disorder that causes hypercoagulability and an increased risk of thrombosis.
Factor V Leiden concern . I have Factor V Leiden mutation. When I was diagnosed in 2003 at the age of 19, I was told that all I needed to do was take a baby asprin everyday. But the more I research and read on this disorder, the more I wonder if I should be doing more. Im al... ... Conditions and Diseases - Blood Disorders
English-language studies were identified using MEDLINE (1993 to April 1997) with the search terms factor V, mutation, protein C, resistance, thromboembolism, prevalence, diagnosis, screening, therapy, and prevention. Bibliographies of relevant papers were also reviewed ...
... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative laboratory research and development. ARUP offers an extensive test menu of highly complex and unique medical tests in clinical and anatomic pathology. Owned by the University of Utah, ARUP Laboratories client,medicine,medical supply,medical supplies,medical product
Most patients with factor V Leiden never develop symptoms, according to Mayo Clinic. However, blood clots that develop as a result of the disorder range from being harmless and disappearing without...
My new addiction is House, M.D, he is my DVT kindred spirit and knows what its like to experience the pain and muscle death that goes with it. The stabbing pains that I get seem to be coming back with greater intensity and frequency. I dont if thats because of my increased mobility or whether its because the muscle is dying or if its because the clot is moving around or if its because of some increased swelling but on the other hand it could be something completely different ...
So far this week I havent really done any proper rehab. Ive had one day so far that I actually set aside some time to focus on rehab. Yesterday was a very lazy day, we spent the day tidying and I managed to get in some squats (15), push ups (15), and crunches, but that was it, no walking, nothing ...
Looking for online definition of factor V Leiden mutation in the Medical Dictionary? factor V Leiden mutation explanation free. What is factor V Leiden mutation? Meaning of factor V Leiden mutation medical term. What does factor V Leiden mutation mean?
What is factor V Leiden? The most common genetic risk factor for venous thrombosis is factor V Leiden, present in 5 percent of the general population. Factor V is one of the normal blood clotting factors. Factor V Leiden is a changed or "mutated" form of factor V that is inactivated 10 times slower than the normal factor V. This causes it to persist longer in the circulation, resulting in a hypercoagulable state. In other words, the blood continues clotting, resulting in possible obstruction.. One copy of the factor V Leiden gene increases the risk for venous thrombosis 4 to 8 times, while two copies of the gene increase the risk 80-fold.. Other coexisting coagulation defects can occur with factor V Leiden, and in general, the risk for thrombosis increases in patients with more than one genetic defect.. The factor V Leiden mutation is involved in 20 to 40 percent of venous thrombosis cases and is suspected in individuals who have a medical history of venous thrombosis or in families with a high ...
Grant Support: By the Zorg Onderzoek Nederland (grant 28-2783).. Requests for Single Reprints: Saskia Middeldorp, MD, Department of Vascular Medicine, Academic Medical Center F4-277, Box 22700, 1100 DE Amsterdam, the Netherlands.. Current Author Addresses: Drs. Middeldorp, Koopman, and Büller: Department of Vascular Medicine, Academic Medical Center F4-277, Box 22700, 1100 DE Amsterdam, the Netherlands.. Drs. Meinardi and van der Meer: Department of Hematology, Division of Hemostasis, Thrombosis and Rheology, University Hospital Groningen, Hanzeplein 1, 9713 GZ Groningen, the Netherlands.. Drs. van Pampus and Hamulyák: Department of Hematology, Academic Hospital Maastricht, P. Debyelaan 25, 6229 HX Maastricht, the Netherlands.. Dr. Prins: Department of Clinical Epidemiology and Medical Technology Assessment, Academic Hospital Maastricht, P. Debyelaan 25, 6229 HX Maastricht, the Netherlands.. Author Contributions: Conception and design: S. Middeldorp, M.M.W. Koopman, K. Hamulyák, J. van der ...
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It is now accepted that thrombophilia is a multigenic disorder. Indeed, VT episodes rarely occur in individuals with a single genetic defect but frequently in individuals with 2 or more genetic defects. The aim of this study was to evaluate the role of genetic polymorphisms located in the PAI-1 gene in the risk of VT in heterozygous FV Leiden carriers.. Because the asymptomatic subjects referred to our thrombophilic center belonged mostly to families with a history of VT, we decided to also select a group of individuals (group 3) in whom the FV Leiden mutation was discovered through systematic screening for the FV Leiden mutation on the occasion of a health checkup examination at 3 different health centers. This procedure avoids selection bias due to the inclusion of asymptomatic individuals from thrombophilic families.. The 20210 A allele of the prothrombin gene was observed in 7% of patients with VT compared with 4% of asymptomatic individuals, this difference being not significant. This ...
The mutation G1691A (R506Q) in the human factor V gene is associated with the resistance to activated protein C (APC) that represents a major risk of development of venous thrombosis. A population...
Dr. Blinski has provided a very extensive and helpful education for all on this issue. Factor V Leiden is one of the many differences in the...
What is a thrombophilia, definition of thrombophilia, meaning of thrombophilia, thrombophilia anagrams, words beginning with thrombophilia.
The assay utilizes the Invader Plus® chemistry manufactured by Hologic for the detection of the FVL(F5) c.1601G,A, R506Q mutation in genomic DNA (NM_000130.4 transcript isoform). Invader and allele-specific probes match the mutant and the wild-type alleles and have overlapping 5-ends that are cleaved upon perfect hybridization to the amplified DNA. The cleaved 5-end of the primary probes transiently hybridize with a corresponding fluorescence resonance energy transfer (FRET) cassettes triggering the cleavage of the fluorophore from the cassette by the cleavase enzyme and allowing signal release and detection.. ...
You should reduce your risk of forming clots by working on the risk factors that can be changed. You should not smoke, should exercise regularly & watch your weight. You should never take hormone supplements (birth control or hormone replacement therapies) that contain estrogen. If you are traveling or otherwise sitting for long periods of time, you should periodically take breaks to move around as much as possible. You should notify your doctor if you ever have surgery so you can be treated prophylactically with blood thinners. It is important to always stay well hydrated ...
동물실험에서 페마렐은 뇌와 뼈에서 에스트로겐 수용체에 대한 자극효과를 보였다[3][4]. 이 약물은 홍조 감소[5], 뼈밀도 개선[6] 등의 효과를 보이는 것으로 보고되었으며, 분리된 유방암 세포주[7]나 시궁쥐의 자궁세포주[4][8]에 대해서 안전한 것으로 알려져있다. 페마렐은 조골세포의 활동을 증진시키는 방법으로 뼈 밀도를 증가시키는 것으로 보이며[9], 이 때문에 폐경기 골다공증 증세에 대한 약으로 사용 가능성이 있다. 에스트로겐 수용체를 자극하지만, 페마렐은 혈중 호르몬 수치에 변화를 주지 않는 것으로 보인다[5] 최근의 연구에 따르면 페마렐은 정상인 여성이나 혈전성향증(thrombophilia)을 가진 여성 모두에서 혈전 형성에 영향을 미치지 않는 것으로 나타났다[10].. ...
article{c33ca7f8-9858-4cde-a6a7-3f927ab55a53, abstract = {Resistance to activated protein C (APC) is a major cause of familial thrombophilia, and can be corrected by an anticoagulant activity expressed by purified factor V. We investigated linkage between APC resistance and the factor V gene in a large kindred with familial thrombophilia. Restriction fragment length polymorphisms in exon 13 of the factor V gene were informative in 14 family members. The 100% linkage between factor V gene polymorphism and APC resistance strongly suggested a factor V gene mutation as a cause of APC resistance. A point mutation changing Arg506 in the APC cleavage site to a Gln was found in APC resistant individuals. These results suggest factor V gene mutation to be the most common genetic cause of thrombophilia.}, author = {Zöller, Bengt and Dahlbäck, Björn}, issn = {1474-547X}, keyword = {gentic linkage,factor V,point mutation,protein S deficiency,venous thromboembolism}, language = {eng}, number = {8912}, ...
Deficiency of the naturally occurring anticoagulant proteins, such as antithrombin, protein C and protein S, and activated protein C resistance due to the factor V Leiden gene mutation is associated with inherited thrombophilia. So far, no direct comparison of the thrombotic risk associated with these genetic defects is available. In this study, we wish to compare the lifetime probability of developing thrombosis, the type of thrombotic symptoms, and the role of circumstantial triggering factors in 723 first- and second-degree relatives of 150 index patients with different thrombophilic defects. We found higher risks for thrombosis for subjects with antithrombin (risk ratio 8.1, 95% confidence interval [CI], 3.4 to 19.6), protein C (7.3, 95% CI, 2.9 to 18.4) or protein S deficiency (8.5, 95% CI, 3.5 to 20.8), and factor V Leiden (2.2, 95% CI, 1.1 to 4.7) than for individuals with normal coagulation. The risk of thrombosis for subjects with factor V Leiden was lower than that for those with all ...
Congenital anomaly of the inferior vena cava and factor V Leiden mutation predisposing to deep vein thrombosis Brooke M Lamparello,1,* Cameron R Erickson,2,* Arun Kulthia,3 Vasudev Virparia,3 Zeyar Thet3 1St Georges University, Grenada, West Indies; 2Northeast Ohio Medical University, Rootstown, OH, USA; 3Department of Medicine, Coney Island Hospital, Brooklyn, NY, USA *These authors contributed equally to this work Abstract: A previously healthy 21-year-old man presented with back pain, bilateral extremity pain, and right lower extremity weakness, paresthesias, and swelling. Sonographic examination revealed diffuse deep vein thrombosis (DVT) in the femoral and popliteal venous system. CT imaging revealed hypoplasia of the hepatic inferior vena cava (IVC) segment with formation of multiple varices and collateral veins around the kidneys. Hematologic workup also discovered a factor V Leiden mutation, further predisposing the patient to DVT. The rare, often overlooked occurrence of attenuated IVC,
Thrombophilias are commonly associated with increased risk for VTE in both pregnant and nonpregnant patients.5 6 7 8 9 10 11 12 However, the evidence of the association of thrombophilia with both ischemic arterial and venous cerebrovascular events, such as cerebrovascular accident (CVA), transient ischemic attack (TIA) and CVT is inconsistent. Several studies reported that patients with the prothrombin gene variant (G20210A) and factor V Leiden mutation are at higher risk for developing CVT.10 12 14 In contrast, Biousse et al11 found the prothrombin gene mutation (G20210A) in only 2 of 35 patients with CVT, and both had some other risk factors for thrombosis. Moreover, in several studies, the prothrombin gene mutation, the factor V Leiden mutation, and deficiencies of antithrombin III, protein S, or protein C were not associated with acute cerebral ischemic events, such as stroke and TIA.6 13 14 15 17 18 19 Finally, 2 recent studies reported that inherited thrombophilias are rarely associated ...
Background. If a thrombophilia (clotting disorder) has been identified in a patient with blood clots (venous thromboembolism = VTE), the question arises whether other family members should be tested for the same thrombophilia.. My Clinical Approach. My approach in clinical practice to thrombophilia testing in family members is summarized in table 1: Family Member Testing. If the patient has a "strong" inherited thrombophilia (i.e. homozygous factor V Leiden, homozygous prothrombin 20210 mutation, double heterozygous factor V Leiden plus prothrombin 20210 mutation, deficiency of protein C, S or antithrombin) then I consider and discuss testing of other family members. However, if the patient only has heterozygous factor V Leiden or heterozygous prothrombin 20210 mutation, I do not recommend testing of family members, as the finding of one of these "mild" thrombophilias typically has no impact on management of family members also affected by one of those "mild" thrombophilias.. Finding of a ...
The team found that 51 patients had mesenteric venous thrombosis, and 6 were diagnosed at autopsy. The highest incidence of 11 per 100, 000 person-years was in the age category 70 to 79 years. The research team noted that activated protein C resistance was present in 13 of 29 patients tested. D-dimer at admission was raised in all 5 patients tested. Multidetector row computed tomography in the portal venous phase was diagnostic in all 20 patients investigated, of whom 19 were managed conservatively. The researchers found that the median length of resected bowel in 12 patients who had surgery was 0.6 m. The overall 30-day mortality rate was 20%.. The team observed that intestinal infarction, treatment on a non-surgical ward, and computed tomography not done were associated with increased mortality. Cancer was independently associated with long-term mortality.. Portal venous phase computed tomography appeared sensitive in diagnosing mesenteric venous thrombosis. Dr Acosta s team concluded, As ...
The prothrombin G20210A mutation is the second most common inherited thrombophilia after the factor V Leiden mutation. Challenging clinical issues include the decisions regarding when to test for the mutation and how to manage individuals with the mu
Care should also be exercised in patients with Factor V (five) Leiden. This is a variation in a gene that affects the clotting process, increasing coagulation. Factor V Leiden is the most common inherited blood disorder in the United States. It is present in 4 to 6 percent of Caucasians; 2 percent of Hispanic Americans; a little over 1 percent of African Americans and Native Americans and about 0.5 of one percent of Asian Americans. Treatment is typically unwarranted unless there is evidence of a blood clot, in which case warfarin or other anticoagulants are prescribed. Depending on the situation, anticoagulants may be recommended to help afford advance protection against the development of blood clots. For example, women with a Factor V Leiden mutation may be advised to take anticoagulants during pregnancy and in the postpartum period.. ...
Kendall Ann has blessed our lives in so many ways. She is truly a gift from God and has proven herself to be a fighter from the beginning. She was born with many neurological and optical abnormalities, which we now know is due to a stroke in utero...probably due to her Factor V Leiden mutation and two copies of the MTHFR gene (1-14-09). Oh, and NOW she has Type 1 Diabetes (8-19-09) And NOW (12-16-10) she has problems with her Mitochondria ... and NOW (2-11-13) a neurogenic bladder resulting in a vesicostomy. Of course there is a possibility of a Mitochondrial Disorder, and a possibility CDLK5 caused all the problems and Mito secondary...but we will never know, because weve decided no more testing! When she was born she came right home...no NICU stay...and we had no idea anything was wrong! She has undergone numerous hospital stays and a number of surgeries, but through it all, she has maintained a smile that wins the hearts of everyone who meets her. Please join us in our journey of life with a ...
Kendall Ann has blessed our lives in so many ways. She is truly a gift from God and has proven herself to be a fighter from the beginning. She was born with many neurological and optical abnormalities, which we now know is due to a stroke in utero...probably due to her Factor V Leiden mutation and two copies of the MTHFR gene (1-14-09). Oh, and NOW she has Type 1 Diabetes (8-19-09) And NOW (12-16-10) she has problems with her Mitochondria ... and NOW (2-11-13) a neurogenic bladder resulting in a vesicostomy. Of course there is a possibility of a Mitochondrial Disorder, and a possibility CDLK5 caused all the problems and Mito secondary...but we will never know, because weve decided no more testing! When she was born she came right home...no NICU stay...and we had no idea anything was wrong! She has undergone numerous hospital stays and a number of surgeries, but through it all, she has maintained a smile that wins the hearts of everyone who meets her. Please join us in our journey of life with a ...
As a new feature of CNNhealth.com, our team of expert doctors will answer readers questions. Heres a question for Dr. Gupta. Asked by Sharon, Montgomery, Texas I just heard that this month is Deep Vein Thrombosis Awareness month, and that Heidi Collins has had DVT.
A quick reference on Thrombophilias in Pregnancy, covering the clinical presentation, investigative approach, and key principles of management
This woman had a stroke at the age of 29 she is now 34. Prior to the stroke she was fit and healthy. Her stroke was due to a clot in the left-hand side of her brain and was caused by hereditary clotting disorders Factor V Leiden and MTHFR, it was found her parents each had one of the clotting disorders. Other members of the family have had tests since her stroke. She was taking the contraceptive pill at the time of her stroke but had to stop taking it because she is at high risk of having another stroke. ...
Thrombophilia is a pathology of the blood system, characteristic of which is the formation of blood clots. The ailment is dangerous, since it can provoke the
The relation between factor V mutation and risk for venous thromboembolism was confirmed in a prospective study of 14 916 men with no history of cardiovascular disease or cancer followed for a mean of 8.6 years. 11.6% of men with venous thromboembolism had the mutation compared with 6.0% of those with no thromboembolism (relative risk [RR] 2.7, 95% CI 1.3 to 5.6, P = 0.008). Risks were higher for patients with idiopathic events (RR 3.5, CI 1.5 to 8.4, P = 0.004) and for men , 60 years of age (adjusted RR 4.0, CI 1.6 to 9.7, P = 0.003). A prospective study showed that men with both factor V mutation and moderate hyperhomocystinemia had an increased risk for any form of venous thromboembolism (RR 9.7, P = 0.009) and for idiopathic venous thromboembolism (RR 21.8, P , 0.001) compared with men who had neither abnormality. In a case-control study comparing 155 premenopausal women who had deep venous thrombosis unrelated to a malignant condition with 169 women who had no history of thrombosis, the ...
Marc Rodger and colleagues report the results of their systematic review and meta-analysis of prospective cohort studies that estimated the association of maternal factor V Leiden and prothrombin gene mutation carrier status and placenta-mediated pregnancy complications.
O Factor V é um factor de coagulação (proacelerina ou protromboquinase). Na realidade não se trata de uma enzima, mas sim de um co-factor enzimático. Existem algumas variantes deste factor, como o factor V Leiden. Nicolaes GA, Dahlback B (2002). «Factor V: Factor V and thrombotic disease: description of a janus-faced protein». ATVB. 22 (4): 530-538. PMID 11950687 Segers K, Dahlback B, Nicolaes GA (2007). «Coagulation factor V and thrombophilia: background and mechanisms.». Thrombosis Haemost. 98 (3): 530-542. PMID 17849041 !CS1 manut: Nomes múltiplos: lista de autores (link) Hooper WC, De Staercke C (2006). «The relationship between FV Leiden and pulmonary embolism». Respir. Res. 3. 8 páginas. PMC 64819. PMID 11806843. doi:10.1186/rr180 Schrijver I, Houissa-Kastally R, Jones CD; et al. (2002). «Novel factor V C2-domain mutation (R2074H) in two families with factor V deficiency and bleeding». Thromb. Haemost. 87 (2): 294-9. PMID 11858490 !CS1 manut: Uso explícito de et al. (link) ...
Cerebrovascular accidents in patients with sickle cell anemia are among the most devastating complications of the disease. It has recently been demonstrated that some patients have a hypercoagulable state on the basis of the presence of an abnormal f
Patient Presentation A 6-month-old female came to clinic for her health maintenance visit. She was growing well physically. Her mother had several questions regarding her normal development which were easily answered. The mother was most concerned because the family history was now positive for her sister (patients maternal aunt) having a recent deep venous thrombosis…
Show your commitment to the APCR by renewing your annual membership today! The APCR is here to support your profession and promote excellence in clinical research.. ...
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I am 5 months pregnant and my doctor called me today to tell me that my protein c is elevated and I need to see a specialist. I tried to google it but I cant understand a word those sights have to sa...
Sigma-Aldrich offers Sigma-P5818, Protein C, Activated, Fragment 390-404 human for your research needs. Find product specific information including CAS, MSDS, protocols and references.
The antiphospholipid syndrome (APS) is characterised by the presence of antiphospholipid antibodies (aPA) associated with thrombosis (arterial and venous) and pregnancy morbidity. This thesis has aimed to investigate the frequency of protein C pathway defects in patients with aPA and to study clinical correlates examine the mechanisms of antiphospholipid interference in the protein C pathway and to assess activated protein C (APC) resistance in patients with aPA in terms of thrombin generation. Although have I have discovered a high degree of heterogeneity in the phenotype of patients with APS, I have demonstrated APC resistance and increased thrombin generation in the majority of patients with APS. While in some cases, APC resistance is clearly immunoglobulin mediated, it is a multifactorial phenomenon with many confounding variables. My data suggest that immunoglobulin dependent APC resistance may occur through P2 glycoprotein-I dependent and independent mechanisms. In a detailed study of ...
Factor V Leiden (rs6025) is a variant (mutated form) of human factor V (one of several substances that helps blood clot), which causes an increase in blood clotting (hypercoagulability). With this mutation, the anticoagulant protein secreted (which normally inhibits the pro-clotting activity of factor V) is not able to bind normally to Factor V, leading to a hypercoagulable state, i.e., an increased tendency for the patient to form abnormal and potentially harmful blood clots. Factor V Leiden is the most common hereditary hypercoagulability (prone to clotting) disorder amongst ethnic Europeans. It is named after the Dutch city Leiden, where it was first identified in 1994 by Prof R. Bertina et al. Abnormal, recurrent venous thromboses. In the normal person, factor V functions as a cofactor to allow factor Xa to activate prothrombin, resulting in the enzyme thrombin. Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a ...
A total of 53 patients with central retinal vein occlusion (CRVO) were distributed to Group 1: Central retinal vein occlusion treated with ranibizumab (43 patients) and Group 2: central retinal vein occlusion treated with aflibercept (10 patients). The diagnosis evaluation of the CRVO begins with an anamnesis review and a complete ophthalmologic examination. Cooperation with a practitioner is required in order to assure the best compensation of risk factors to adjust therapy; the factors being: hypertension, diabetes mellitus, hyperlipidemia; and in the group of patients under 50 was also performed examination of hypercoagulable state, particularly factor V Leiden and activated Protein C resistance. The ophthalmologic examination during the treatment period included the best corrected visual acuity, slit-lamp examination and fundoscopy, colour fundus photography, central retinal thickness (CRT) was measured with optical coherence tomography and fluorescein angiography. We were able to use the ...
In a 12-member, 3-generation kindred with conjoint inheritance of G1691A factor V Leiden (FVL) and G20210A prothrombin gene (PTG) mutations, identified through a proband with amaurosis fugax and his father with nonarteritic ischemic optic neuropathy
Rahimi Z, Felehgari V, Rahimi M, Mozafari H, Yari K, Vaisi-Raygani A, Rezaei M, Malek-Khosravi S, Khazaie H. The frequency of factor V Leiden mutation, ACE gene polymorphism, serum ACE activity and response to ACE inhibitor and angiotensin II receptor antagonist drugs in Iranians type II diabetic patients with microalbuminuria, Molecular Biology Reports, 2010; [Epub ahead of print]. Rezaie L, Khazaie H, Soleimani A, Schwebel DC. Is self-immolation a distinct method for suicide? A comparison of Iranian patients attempting suicide by self-immolation and by poisoning, Burns, 2010; [Epub ahead of print]. Tahmasian M, Khazaie H, Sepehry AA, Russo, MB. Ambulatory Monitoring of Sleep Disorders [Review article], Journal of Pakistan Medical Association (JPMA), 2010; 60(6) 480-487. Ahmadi A, Mohammadi R, Schwebel DC, Khazaie H, Yeganeh N, Almasi A. Demographic risk factors of self-immolation: A case-control study, Burns, 2009; 35, 580-586. Khazaie H, Rezaei L, Tahmasian M, Schwebel DC. Insomnia Treatment ...
Throughout this stage im you will also start to note that your breasts changing into extra tender and sore and some ladies report that they observed an increase in the dimension of their breasts at the moment. On inherited thrombophilias in pregnancy other hand, you in all probability dont need to skimp out on a being pregnant test - its a thing the place youll wish to inherited thrombophilias in pregnancy in its results. Her urine being yellow is probably because she is dehydrated and needs to drink more water. Imagine going about your everyday business and having someone say you should inherjted hung upside down with your ovaries set on fire. It is going to turn out to be tougher to thrombopbilias a comfy sleeping position throughout the closing weeks of being pregnant, so ladies could also be extremely drained, Burch said. Its possible youll no symptoms of pregnancy at 3 weeks have enough iron resulting from menstrual bleeding and a poor food regimen. Nevertheless, if it adjustments in ...
Science & Technology, Life Sciences & Biomedicine, Immunology, Surgery, Transplantation, IMMUNOLOGY, SURGERY, TRANSPLANTATION, ACTIVATED PROTEIN-C, COAGULATION-FACTOR-V, CORONARY-ARTERY-DISEASE, VENOUS THROMBOSIS, MYOCARDIAL-INFARCTION, INHIBITOR-1 PAI-1, FIBRINOGEN LEVELS, RESISTANCE, PLASMA, THROMBOPHILIA ...
John Pauls nosebleeds continue to be a problem. Hes seen our PCP (you rock yet again, Dr. LaSalle) a couple of times about this. She has recommended, and we have done, all the standard efforts to reduce his bloody nose frequency. They did become less frequent for awhile, then returned with a vengence in mid-January. Dr. LaSalle had recommened that if the frequency spead up again that we get a CBC (Complete Blood Count) to see if that gave us any clues. This, of course, was something I did not want to do. A blood draw is naturally terrifing for a 7 year-old. I also had an irrational fear that it would show he had leukemia (even though my leakemia is not hereditary. But doctors had told me that the chances of either of my children inheriting Factor V Leiden from me was slim to none, and that both getting was almost statistically improbable, and they both did). But after a four inch clot came out one morning, I threw in the towel and told myself to get a grip on my fears and do what needed to be ...
We thank Dr. Berse and colleagues for their correspondence about our paper.1,2 We are pleased they agreed with our conclusion: Thrombophilia testing has limited
Jacob Feala is the author of this article in the Journal of Visualized Experiments: Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
There are 4 fourteen-letter words containing A, B, 2H and M: ARITHMOPHOBIAS MOUTHBREATHERS RHOMBENCEPHALA & THROMBOPHILIAS. Every word on this site can be used while playing scrabble. Create other lists, that start with or end with letters of your choice.
Causes. The 2 main causes of arterial thromboembolism are certainly arteriosclerosis and atrial fibriallation. Only uncommonly do arterial clots occur in persons less than 40 or 50 years of age who do not have arteriosclerosis or atrial fibrillation. Under these circumstances, a number of uncommon conditions, including thrombophilias, should be considered and investigated (see table 1: Causes and work-up).. Thrombophilias. Thrombophilias do not play much of a role in arterial thrombosis. Heterozygous factor V Leiden and heterozygous prothrombin 20210 mutation by themselves do not (factor V Leiden) or only minimally (prothrombin 20210 mutation) increase the risk for arterial thromboembolism (ref 1). Whether the risk is increased in the individual with homozygous factor V Leiden, homozygous prothrombin 20210 mutation, and double heterozygous individual (who has both factor V Leiden and the prothrombin 20210 mutation) is not known. Protein C deficiency and protein S deficiency appear to put a ...
Inherited resistance to activated protein C (APC) was recently recognized as a novel cause underlying venous thrombophilia. In most cases APC-resistance is due to a single point mutation in the factor V gene leading to a replacement of Arg506 with Gln (factor V Leiden). Amino acid substitution occurs at one of the APC cleavage sites of factor Va, rendering it resistant to APC inactivation. Plasma anticoagulant response to exogenous APC as a simple diagnostic assay of APC- resistance shows good sensitivity and specificity as compared to gene analysis, yet standardization of the results needs to be improved. The APC-resistance trait is present in 2%-6% of the general population and was found to be associated with venous thrombophilia in about 20% of patients with unexplained thrombosis. Clinical features are substantially similar to other congenital plasma abnormalities predisposing to thrombosis (antithrombin III, protein C, protein S deficiencies); yet the overall clinical penetrance of the ...
SUMMARY Thrombophilia refers to laboratory abnormalities that increase the risk of venous thromboembolism (VTE). Over the last several decades numerous factors have been identified. The most prevalent examples of hereditary forms of thrombophilia include the factor V Leiden and prothrombin G20210A mutations; deficiencies of the natural anticoagulants antithrombin, protein C, and protein S; persistently elevated levels of coagulation factor VIII; and mild hyperhomocysteinemia. Taken together, some form of hereditary thrombophilia can be identified in more than 50 percent of patients with VTE who are without obvious reasons for VTE, such as trauma or prolonged stasis. Moreover, hereditary thrombophilia has been associated with arterial cardiovascular disease and obstetric complications such as (recurrent) pregnancy loss and preeclampsia. The high yield of thrombophilia testing has led to widespread testing for these abnormalities in patients. Nevertheless, thrombophilia testing remains a topic of ...
One of the main objectives of this study was to establish the lifetime risk for VTE in subjects with 1 of the 4 main coagulation defects related to inherited thrombophilia (AT, PC, PS, and APCR) and to compare the clinical features of the different defects. Particular attention was taken to include only families with documented inherited defects and to avoid selection bias, by considering only relatives. Of the 1143 subjects of whom we received data, 746, from 233 kindreds, fulfilled the inclusion criteria. The 513 relatives were included in the study.. The lifetime risk for VTE in the AT group was 4-fold greater than in the APCR group, 3-fold than in the PS group, and 2-fold than in the PC group. It was 2-fold greater in PC than in APCR, whereas no difference was found between the PS and APCR groups. The probability that a subject with APCR will be free of thrombosis at the age of 45 is 0.88, compared with 0.59 for AT, 0.74 for PC, and 0.79 for PS. This finding is in agreement with the study of ...
Factor V Leiden is an autosomal dominant condition which exhibits incomplete dominance and results in a Factor V variant which cannot be as easily degraded by aPC. The gene that codes the protein is referred to as F5. Mutation of this gene-a single nucleotide polymorphism (SNP) is located in exon 10.[6] As a missense substitution it changes a proteins amino acid from arginine to glutamine. Depending on the chosen start the position of the nucleotide variant is either at position 1691 or 1746.[7] It also affects the amino acid position for the variant which is either 506 or 534. Together with the general lack of nomenclature standard it means that the SNP can be referred to in several ways such as G1691A, c.1601G,A, 1691G,A, c.1746G,A, p.Arg534Gln, Arg506Gln, R506Q or rs6025! Since this amino acid is normally the cleavage site for aPC, the mutation prevents efficient inactivation of factor V. When factor V remains active, it facilitates overproduction of thrombin leading to excess fibrin ...
Looking for online definition of protein C in the Medical Dictionary? protein C explanation free. What is protein C? Meaning of protein C medical term. What does protein C mean?
In broad terms patients who have a propensity to thrombosis do so because they have a disorder of the blood (e.g. a coagulation defect or a cellular abnormality such as polycythaemia) or a defect of the vessel wall. Where enhanced coagulation is the primary cause the disorder is referred to as thrombophilia.1 In this article we review the causes, diagnosis and management of thrombophilia. ...
View our interactive tool, designed to share best practices on how to perform and interpret thrombophilia tests that aid in better patient management.
Information provided on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing or treating a health problem or disorder, or prescribing any medication. The Preeclampsia Foundation presents all data as is, without any warranty of any kind, express or implied, and is not liable for its accuracy, for mistakes or omissions of any kind, nor for any loss or damage caused by a users reliance on information obtained on the site. Professional opinions on this condition vary greatly. The Preeclampsia Foundation endorses no one course of treatment or "cure ...
Thrombosis is a blood clot in a blood vessel. Thrombophilia increases the risk of clots. Seattle Childrens doctors are experts at diagnosing and treating clots.
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Absolute risk of pregnancy-associated venous thromboembolism (VTE) varied depending on the type of thrombophilia among women with a family history of VTE, a systematic review and meta-analysis found.. While all thrombophilias increased the risk of pregnancy-associated VTE, those with the highest absolute risk were antithrombin deficiency, protein C deficiency, protein S deficiency and homozygous factor V Leiden, reported F. Nanne Croles, MD, of Erasmus University Medical Centre in the Netherlands, and colleagues.. But absolute risks of pregnancy-associated VTE were much lower for women with heterozygous factor V Leiden, heterozygous prothrombin G20210A mutations, or compound heterozygous factor V Leiden and prothrombin G20210A mutations, the authors wrote in The BMJ.. They noted that the 2012 American College of Chest Physicians (ACCP) guidelines about absolute risk estimates of pregnancy-associated VTE in women with inherited thrombophilia "are based on a limited number of cohort studies" and ...
1. Inada K, Shirai N, Hayashi M, Matsumoto K, Hirose M. Postoperative deep venous thrombosis in Japan. Incidence and prophylaxis. Am J Surg 1983;45:775-9. 2. Dhillon KS, Askander A, Doraisamy S. Postoperative deep venous thrombosis in Asian patients is not a rarity. J Bone Joint Surg 1996;78B:427-30. 3. Fujita S, Hirota S, Oda T, Kato Y, Yasunori T, Fuji T. Deep venous thrombosis after total hip or total knee arthroplasty in patients in Japan. Clin Orthop Res 2000;375:168-74. 4. Garrow JS, Webster J. Quetelets index (W/H2) as a measure of fatness. Int J Obesity 1985;9:147-53. 5. Guyton JL. Arthroplasty of ankle and knee. In: Canale TL. Campbells Operative Orthopedics. 9th edition. Missouri: Mosby Year book 1998;pp 232-95. 6. Herrmann FH, Koesling M, Schosder W, Altman R, Jimenez BR, Lopaciuk S, et al. Prevalence of factor V Leiden mutation in various populations. Genet Epidemiol 1997;14:403-11. 7. Rees DC, Cox M, Clegg JB. World distribution of factor V Leiden. Lancet 1995;346:1133-4. 8. Ho ...
Livedo vasculitis is a chronic, recurrent painful ulcerations on the ankles and feet. This chronic disease is characterized by healed white, atrophic scars named atrophie blanche. The histopathological exam on the lesion site reveals fibrin deposition within the vessel walls. It has been reported to be related to factor V Leiden mutation (heterozygous) (22.2%), prothrombin G20210A gene mutation (8.3%), PAI promotor 4G/4G genotype and methylenetetrahydrofolate reductase (MTHFR) C677T mutation in about total 30% livedo vasculitis patients. This study is trying to find the correlation between Taiwanese patients and these four genes ...
Thrombophilia (sometimes hypercoagulability or a prothrombotic state) is an abnormality of blood coagulation that increases the risk of thrombosis (blood clots in blood vessels). Such abnormalities can be identified in 50% of people who have an episode of thrombosis (such as deep vein thrombosis in the leg) that was not provoked by other causes. A significant proportion of the population has a detectable abnormality, but most of these only develop thrombosis in the presence of an additional risk factor. There is no specific treatment for most thrombophilias, but recurrent episodes of thrombosis may be an indication for long-term preventative anticoagulation. The first major form of thrombophilia, antithrombin deficiency, was identified in 1965, while the most common abnormalities (including factor V Leiden) were described in the 1990s. The most common conditions associated with thrombophilia are deep vein thrombosis (DVT) and pulmonary embolism (PE), which are referred to collectively as venous ...
Looking for Prothrombin g20210a mutation? Find out information about Prothrombin g20210a mutation. see blood clotting blood clotting, process by which the blood coagulates to form solid masses, or clots. In minor injuries, small oval bodies called... Explanation of Prothrombin g20210a mutation
Many people believe you can, so let us give you some advice you may wish to try if you want increase those chances of a baby boy. They cause sleepiness, so they are usually taken before bed. Hi everyone. Now is also a good time to evaluate supplements and medications you take regularly. A Exdrcises infection can remain symptomless for many years. Nutrition is an important how many kegel exercises per day during pregnancy of everybodys life.. The ligaments then pull on nerve fibers and sensitive structures which cause pain. The very next day there was light bleeding and we consulted doctor. Its easy to add into a daily smoothie and because its a food, you dont need to worry about getting precise durimg. Birth control without any hormones is the safest method of birth control for anyone who best products for stretch marks pregnancy a history of blood clot, DVT, pulmonary embolism, Factor V Leiden, or any clotting conditions or thrombophilias.. More… ...
The above factors can all be measured in the laboratory with specific genetic tests, coagulation or antibody-based tests. Other acquired causes (regarded as risk factors) include malignancy, OCP, HRT, immobilisation, obesity, smoking, pregnancy and major surgery. Consideration should be given to screening patients with a DVT, especially in travellers at possible risk. Referral to a haematologist if thrombophilia is proved or suspected is advisable. Of particular interest is factor V Leiden, which occurs in about 5% of Caucasians, and the risk of venous thrombosis is increased three to seven times in heterozygotes and 80 times in homozygotes.2 ...
Background: The incidence of thrombotic complications in patients with malignancy is higher than in the general population. There is little data about..
LEIDEN, The Netherlands -- Sprains, bruises, and other minor leg injuries triple the risk of venous thrombosis within three months, investigators here found.
Research published this week in PLoS Medicine finds that pregnant women with an inherited condition that makes them more likely to form blood clots only face a small increase in the risk that they might have a miscarriage or stillbirth. The findings also show that there is no significant association between this condition, known as inherited thrombophilia, and placenta-related problems in pregnancy, suggesting that the prescription of drugs to women with thrombophilia to prevent these problems would be premature.. Marc Rodger, of the University of Ottawa in Canada, and colleagues conducted a systematic review of studies investigating placenta-related problems in pregnancy and women with thrombophilia. More than one in twenty pregnancies have complications that are linked to the placenta, These complications include pregnancy loss, pre-eclampsia (high blood pressure), pregnancies that result in the baby not growing properly in the womb, and problems occurring when the placenta becomes separated ...
The pathogenesis of arterial and venous thrombosis in Behçets disease is not completely understood. It is generally accepted that vasculitis, a hallmark of Behçets disease, partially explains the initiation of thrombosis in small as well as large blood vessels.13 Attempts to identify additional prothrombotic factors have so far been conflicting. For example, in Turkey, where the prevalence of Behçets disease is probably the highest in the world, factor V Leiden was associated with the occurrence of thrombosis in several but not all studies,6,14 and recent studies from Italy and Spain also did not reveal such an association.15,16 In the present study none of the common prothrombotic polymorphisms nor homocysteine concentration was significantly associated with thrombosis. Increased factor VIII level, recently shown to be a risk factor for idiopathic venous thrombosis,17 was the only prothrombotic variable which appeared to be associated with the occurrence of thrombosis.. We are aware of ...
Impact-R, a test for platelet function, has potential use as adjunctive diagnostic test to identify protein C or S deficiency. What is protein C or S
Thank you for your interest in spreading the word about Haematologica.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
Ive been using Affimer® technology in my research for the past year and the data generated has been remarkable. My interest lies in understanding the mechanisms for blood clot formation and breakdown with the long-term aim of reducing heart attacks and strokes in high risk patients. A number of Affimer candidates have shown significant effects on the clotting process, which will help to develop novel therapeutic targets aiming to reduce thrombosis risk ...
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...
Oral contraceptives such as the pill put women at a very high risk for blood clots, DVT, and pulmonary embolism. After a blood clot or diagnosis with a clotting condition women need a safe contraceptive. There are high risk hormone based contraceptives, lower risk hormonal contraceptives, and risk free contraceptives that will not cause clots.

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

Also known as: Activated Protein C Resistance; APC Resistance; Factor V R506Q; PT G20210A; Factor II 20210; Factor II Mutation ... evaluation for the presence of a Factor V Leiden mutation can begin with a test for activated protein C (APC) resistance, ... About 90% of the time, APC resistance is due to a Factor V Leiden mutation. If resistance is present, then a test for the ... Related tests: Antithrombin; Protein C and Protein S; Homocysteine; MTHFR Mutation; Factor V R2 A4070G Mutation ...
more infohttps://labtestsonline.org/understanding/analytes/factor-v-and-pt20210/tab/test

Factor V Leiden | B-health blogFactor V Leiden | B-health blog

This is known as an activated protein C (APC) resistance assay. If your blood is resistant to activated protein C, its likely ... Activated protein C resistance test. Your blood sample may be tested to determine whether your blood is resistant to activated ... youre likely to have only the genetic test because blood-thinning drugs interfere with the activated protein C resistance test ... One of the clotting proteins is factor V. People with factor V Leiden have a genetic mutation that results in factor V protein ...
more infohttp://bhealthblog.com/factor-v-leiden/

Role of Hypersensitivity to Female Sex Hormones in Women With Unexplained Recurrent Pregnancy Loss - Full Text View -...Role of Hypersensitivity to Female Sex Hormones in Women With Unexplained Recurrent Pregnancy Loss - Full Text View -...

Hereditary thrombophilias (Factor V Leiden, Activated protein C resistance, MTHFR (C677T), Factor II mutation (G20201A)) ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01175759

Comorbidity in patients with branch retinal vein occlusion: case-control study | The BMJComorbidity in patients with branch retinal vein occlusion: case-control study | The BMJ

Blood viscosity, coagulation, and activated protein C resistance in central retinal vein occlusion: a population controlled ... 11 12 13 deficiency in the protein C pathway,14 high α2 globulin concentrations,4 higher activated factor VII concentrations,15 ... 11 12 13 deficiency in the protein C pathway,14 high α2 globulin concentrations,4 higher activated factor VII concentrations,15 ... Is activated factor VII associated with retinal vein occlusion? Br J Ophthalmol2001;85:1174-8. ...
more infohttp://www.bmj.com/content/345/bmj.e7885.long

Factor V Leiden Mutation and PT 20210 MutationFactor V Leiden Mutation and PT 20210 Mutation

2001 January 10, Modified). Coagulation Test Descriptions, Factor V Leiden (Activated Protein C Resistance Pcr Assay) and ... During hemostasis, factor V is normally inactivated by a protein called activated protein C (APC) to prevent the blood clot ... evaluation for the presence of a Factor V Leiden mutation can begin with a test for activated protein C (APC) resistance, ... About 90% of the time, APC resistance is due to a Factor V Leiden mutation. If resistance is present, then a test for the ...
more infohttps://labtestsonline.org/tests/factor-v-leiden-mutation-and-pt-20210-mutation

EURETINA Official | Official EURETINA Website | European Society of Retina SpecialistsEURETINA Official | Official EURETINA Website | European Society of Retina Specialists

... particularly factor V Leiden and activated Protein C resistance. The ophthalmologic examination during the treatment period ...
more infohttp://www.euretina.org/barcelona2017/programme/posters-details.asp?id=14211

Protein S deficiency | HaematologicaProtein S deficiency | Haematologica

1995) Variable interference of activated protein C resistance in the measurement of protein S activity by commercial assays. ... 1980) Regulation of activated protein C by a new protein. A possible function for bovine protein S. J Biol Chem 255:5521-4. ... 1994) Factor V and protein S as synergistic cofactors to activated protein C in degradation of factor VIIIa. J Biol Chem 269: ... 1997) Protein S alters the active site location of activated protein C above the membrane surface. A fluorescence resonance ...
more infohttp://www.haematologica.org/content/93/4/498

Activated Protein C ResistanceActivated Protein C Resistance

... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative ... The Quest ACTester Activated Clotting Time System. 7. Total Protein. 8. Total Protein Reagent. 9. Total Protein Reagent Set. 10 ... Bipolar Hand Activated Forceps. 3. Bipolar Foot Activated Forceps. 4. European Bipolar Foot Activated Forceps. 5. Titanium Foot ... Proteomelab™ XL-A/XL-I Protein Characterization System. 11. Proteomelab™ PA 800 Protein Characterization System. ...
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117762: Activated Protein C Resistance (APCR) | LabCorp117762: Activated Protein C Resistance (APCR) | LabCorp

Activated protein C resistance assay detects thrombotic risk factors other than factor V Leiden. Am J Clin Pathol. 2003 Jan; ... Activated Protein C Resistance. 13590-5. 117763. Act.Prt.C Resist.. ratio. 13590-5. ... 8. Van Cott EM, Soderberg BL, Laposata M. Activated protein C resistance, the factor V Leiden mutation, and a laboratory ... Screening test for the factor V Leiden gene mutation and other causes of activated protein C resistance ...
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Activated Protein C Resistance
      - APC Resistance
     Summary Report | CureHunterActivated Protein C Resistance - APC Resistance Summary Report | CureHunter

... is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance. ... A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor ... Activated Protein C Resistance (APC Resistance). Subscribe to New Research on Activated Protein C Resistance ... related to Activated Protein C Resistance: 1. factor V LeidenIBA 02/01/1997 - "Thus the activated protein C resistance assay is ...
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Activated protein C resistance in Behcets diseaseActivated protein C resistance in Behcet's disease

The aim of this study is to evaluate the prevalence of activated protein C resistance (APC-R) in Egyptian patients with ... The APC resistance ratio mean in the group of patients with vascular involvement was 2.6 ± 0.8 which was less than the group ...
more infohttps://mospace.umsystem.edu/xmlui/handle/10355/38977

Activated protein C resistance - WikipediaActivated protein C resistance - Wikipedia

Activated protein C (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. Activated protein C resistance is the ... Activated protein C resistance (APCR) is a hemostatic disorder characterized by a poor anticoagulant response to activated ... Sheppard DR (2000). "Activated protein C resistance: the most common risk factor for venous thromboembolism". J Am Board Fam ... Dahlbäck B (2003). "The discovery of activated protein C resistance". J. Thromb. Haemost. 1 (1): 3-9. doi:10.1046/j.1538- ...
more infohttps://en.wikipedia.org/wiki/Activated_protein_C_resistance

Activated protein C resistance | definition of activated protein C resistance by Medical dictionaryActivated protein C resistance | definition of activated protein C resistance by Medical dictionary

What is activated protein C resistance? Meaning of activated protein C resistance medical term. What does activated protein C ... Looking for online definition of activated protein C resistance in the Medical Dictionary? activated protein C resistance ... Activated protein C resistance is caused by a failure of protein C to cleave Factor Va and/or Factor VIIIa.. activated protein ... activated protein C resistance. Also found in: Acronyms, Wikipedia. Activated Protein C Resistance. An inherited (autosomal ...
more infohttps://medical-dictionary.thefreedictionary.com/activated+protein+C+resistance

Activated Protein C ResistanceActivated Protein C Resistance

Explore clotting assays for quantitative determination of activated protein C resistance activity and its calibrators and ... Antithrombin Protein C: Activity and Antigen Protein S: Activity and Antigen Activated Protein C Resistance Protein Z Lupus ... Activated Protein C Resistance. Clotting assay for quantitative determination of Activated Protein C Resistance activity and ... Heparins and their Analogues Direct Anti-Xa Inhibitors Direct Thrombin Inhibitors Activated Protein C resistance Protein S D- ...
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Activated Protein C Resistance [22] - Quest Diagnostics Nichols Institute of ValenciaActivated Protein C Resistance [22] - Quest Diagnostics Nichols Institute of Valencia

The CPT codes provided are based on AMA guidelines and are for informational purposes only. CPT coding is the sole responsibility of the billing party. Please direct any questions regarding coding to the payer being billed ...
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Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanoma.  - PubMed - NCBISystems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanoma. - PubMed - NCBI

Establishing mitogen activated protein kinase inhibitor-resistant melanoma models. a A mitogen activated protein kinase BRAF ... Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanoma.. Zecena H1, Tveit D1, ... a Establishing cellular models of mitogen activated protein kinase inhibitor resistance using SK-MEL-28 malignant melanoma cell ... Transcription factor motif analysis of mitogen activated protein kinase inhibitor resistance in cellular models of malignant ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Zecena+H%5Bau%5D&dispmax=50

Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Coronary Heart Disease Due To Combined Estrogen...Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Coronary Heart Disease Due To Combined Estrogen...

Activated Protein C Resistance/blood. *Activated Protein C Resistance/complications*. *Activated Protein C Resistance/diagnosis ... activated protein C resistance; coronary disease; estrogens; hemostatics; progestins; tissue factor pathway inhibitor activity ... Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Coronary Heart Disease Due To Combined Estrogen ... Tissue factor pathway inhibitor, activated protein C resistance, and risk of coronary heart disease due to combined estrogen ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/26681757

Activated Protein C Resistance Test | Medichecks.comActivated Protein C Resistance Test | Medichecks.com

Activated Protein C resistance means that when your body forms clots, those clots are more dur... ... Activated Protein C is a natural anticoagulant in the blood. ... Activated Protein C resistance means that when your body forms ... If you need it, a PDF copy of your Activated Protein C Resistance Test results can be downloaded for your doctor. ... track your orders and view your Activated Protein C Resistance Test results. ...
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Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Ischemic Stroke due to Postmenopausal Hormone...Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Ischemic Stroke due to Postmenopausal Hormone...

... levels or activated protein C resistance (normalized activated protein C resistance ratio [nAPCsr]) modify the increased risk ... The endogenous thrombin potential-based activated protein C resistance test (ETP-based APC resistance test) was performed at ... Activated protein C resistance and acute ischemic stroke: relation to stroke causation and age. J Neurol. 2001;248:701-704. ... Adjusted Ischemic Stroke Risk per SD Higher Baseline Tissue Factor Pathway Inhibitor and Activated Protein C Resistance (N=455 ...
more infohttp://stroke.ahajournals.org/content/43/4/952

Gentaur Molecular :BlueGen \ Rat anti-activated protein C resistance,APCR ELISA Kit \ E02A0843Gentaur Molecular :BlueGen \ Rat anti-activated protein C resistance,APCR ELISA Kit \ E02A0843

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Activated Protein C Resistance -
Seattle Childrens HospitalActivated Protein C Resistance - Seattle Children's Hospital

Test Code APCR Activated Protein C Resistance Important Note. This assay can be used during heparin or oral anticoagulant ... Activated Protein C Cofactor. APC Cofactor Ration. APC Cofactor Screen. APC Resistance. ...
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Placental thrombosis and second trimester miscarriage in association with activated protein C resistance.  - UCL DiscoveryPlacental thrombosis and second trimester miscarriage in association with activated protein C resistance. - UCL Discovery

Placental thrombosis and second trimester miscarriage in association with activated protein C resistance. Br J Obstet Gynaecol ... Placental thrombosis and second trimester miscarriage in association with activated protein C resistance. ... Placental thrombosis and second trimester miscarriage in association with activated protein C resistance.. ...
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Activated Protein C Resistance Blood Levels Test- HealthtopquestionsActivated Protein C Resistance Blood Levels Test- Healthtopquestions

Activated protein C resistance blood test is used to determine whether you have an inherited gene mutation that increases your ... A high activated protein C resistance blood test value may indicate activated protein C resistance disorder in which clotting ... Homeactivated protein c resistance blood levels testActivated Protein C Resistance Blood Levels Test ... Activated protein C resistance blood test is used to determine whether you have an inherited gene mutation that increases your ...
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PRIME PubMed | Opposite functions of a rice mitogen-activated protein kinase during the process of resistance against...PRIME PubMed | Opposite functions of a rice mitogen-activated protein kinase during the process of resistance against...

PubMed journal article Opposite functions of a rice mitogen-activated protein kinase during the process of resistance against ... Opposite functions of a rice mitogen-activated protein kinase during the process of resistance against Xanthomonas oryzae.. ... "Opposite Functions of a Rice Mitogen-activated Protein Kinase During the Process of Resistance Against Xanthomonas Oryzae." The ... Opposite functions of a rice mitogen-activated protein kinase during the process of resistance against Xanthomonas oryzae. ...
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Activated Protein C Resistance V (APCRV), Plasma -
United Clinical Laboratories Test CatalogActivated Protein C Resistance V (APCRV), Plasma - United Clinical Laboratories Test Catalog

Test Code APCRV Activated Protein C Resistance V (APCRV), Plasma Additional Codes. MLAB: Y8W ... Epic: LAB2265 Activated Protein C Resistance. MA Cerner: Activated Protein C Resistance V. ... for the presence or absence of coagulation abnormalities or conditions that may affect interpretation of the APC resistance ...
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  • Tissue Factor Pathway Inhibitor, Activated Protein C Resistance, and Risk of Coronary Heart Disease Due To Combined Estrogen Plus Progestin Therapy. (nih.gov)
  • To examine whether tissue factor pathway inhibitor or acquired activated protein C (APC) resistance influences the increased risk of coronary heart disease (CHD) due to estrogen plus progestin therapy. (nih.gov)
  • Compared with placebo, estrogen plus progestin decreased tissue factor pathway inhibitor activity and increased APC resistance but these changes did not seem to modify or mediate the effect of estrogen plus progestin on CHD risk. (nih.gov)
  • Tissue factor pathway inhibitor activity and APC resistance are related to CHD risk in women, but may not explain the increased CHD risk due to estrogen plus progestin therapy. (nih.gov)
  • Background and Purpose- To test whether changes in plasma tissue factor pathway inhibitor (TFPI) levels or activated protein C resistance (normalized activated protein C resistance ratio [nAPCsr]) modify the increased risk of ischemic stroke due to postmenopausal hormone therapy. (ahajournals.org)
  • 6 - 9 Reduction in tissue factor pathway inhibitor (TFPI) and protein S are thought to be important mechanisms underlying the activation of coagulation and acquired protein C resistance associated with oral contraceptives, and both have been implicated in venous thromboembolism. (ahajournals.org)
  • The underlying mechanism of treatment resistance and pathway rewiring was uncovered to be based on non-genomic adaptation and validated in two distinct melanoma models, SK-MEL-28 and A375. (nih.gov)
  • Nuclear localization of OsMPK6 was essential for local resistance, suggesting that modulating the expression of defense-responsive genes through transcription regulators may be the primary mechanism of OsMPK6-mediated local resistance. (unboundmedicine.com)
  • After multivariable covariate adjustment, both baseline tissue factor pathway activity (P=0.01) and APC resistance (P=0.004) were associated positively with CHD risk. (nih.gov)
  • Baseline tissue factor pathway activity and APC resistance singly or jointly did not significantly modify the effect of estrogen plus progestin on CHD risk. (nih.gov)
  • In addition, by using PVX-induced gene silencing, we demonstrated that the suppression of all three known components in the NtMEK2-SIPK/WIPK pathway attenuated N gene-mediated TMV resistance. (berkeley.edu)
  • Together with previous reports that SIPK and WIPK are activated by TMV in a gene-for-gene-dependent manner, we conclude that NtMEK2-SIPK/WIPK pathway plays a positive role in N gene-mediated resistance, possibly through regulating HR cell death. (berkeley.edu)
  • To establish the mean levels of PCA ratio (measure of protein C resistance) of among our pregnant women since maternal mortality rate of the country is on the increase despite efforts to reduce this trend. (jbcrs.org)
  • Summary Our research shows that Cas can be needed for apoptosis that is normally activated by proteasome inhibition, and by other loss of life stimuli potentially. (elevateblogconference.com)
  • A high activated protein C resistance blood test value may indicate activated protein C resistance disorder in which clotting factors are resistant to deactivation by activated protein C. (healthtopquestions.com)
  • PXR is a potential biomarker for predicting outcome and activates MRP3 transcription by directly binding to its promoter resulting in an increased L-OHP efflux capacity, and resistance to L-OHP or platinum drugs in CRC. (biomedcentral.com)
  • Activation of OsMPK6 resulted in the formation of lesion mimics and local resistance to Xoo, accompanied by the accumulation of salicylic acid (SA) and jasmonic acid (JA), and the induced expression of SA- and JA-signaling genes. (unboundmedicine.com)
  • 7 Abnormal results can also be seen in pregnancy, especially during the third trimester, due to decreased levels of protein S and increased levels of factors V and VIII. (labcorp.com)
  • Acquired resistance to protein C in pregnancy has been established as one of the factors associated with thromboembolic phenomenon, an important cause of maternal mortality and morbidity. (jbcrs.org)
  • If you need it, a PDF copy of your Activated Protein C Resistance Test results can be downloaded for your doctor. (medichecks.com)
  • Once you have placed your order you will receive login details to mymedichecks.com where you can manage your account, track your orders and view your Activated Protein C Resistance Test results. (medichecks.com)
  • These mutants were also defective in interacting with SIPK and WIPK, suggesting protein-protein interaction is required for the functional integrity of this MAPK cascade. (berkeley.edu)
  • We report the first prospective study of the associations of acquired APC resistance and of TFPI levels with stroke, and we examine whether PHT-induced changes in these factors are associated with stroke risk in the WHI trials. (ahajournals.org)
  • 10 Cross-sectional studies suggest that low levels of TFPI or increased APC resistance may play a role in childhood ischemic stroke, but their roles in adult strokes are unclear. (ahajournals.org)
  • To eliminate Agrobacterium that is known to activate a number of defense responses in transient transformation experiments, we generated permanent transgenic plants. (berkeley.edu)