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.Laboratories: Facilities equipped to carry out investigative procedures.Diagnostic Techniques and Procedures: Methods, procedures, and tests performed to diagnose disease, disordered function, or disability.Menu PlanningSystems Biology: Comprehensive, methodical analysis of complex biological systems by monitoring responses to perturbations of biological processes. Large scale, computerized collection and analysis of the data are used to develop and test models of biological systems.PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories for solving biological problems including manipulation of models and datasets.Melanoma: A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)BooksPre-Eclampsia: A complication of PREGNANCY, characterized by a complex of symptoms including maternal HYPERTENSION and PROTEINURIA with or without pathological EDEMA. Symptoms may range between mild and severe. Pre-eclampsia usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another.Universities: Educational institutions providing facilities for teaching and research and authorized to grant academic degrees.Hemophilia A: The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.

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 (FVL), the principal inherited cause of activated protein C resistance (APCR), has been linked to the failure of pregnancy with an increased risk of venous thrombosis, fetal loss and pre-eclampsia. Both venous thrombosis and pre-eclampsia are associated with inflammation. In particular pre-eclampsia is associated with a monocyte/macrophage infiltration of the placental bed. That APCR, without FVL, (acquired APCR) may be a marker of thrombotic potential out-with pregnancy has been suggested by the association of venous thrombosis with the combined oral contraceptive pill and more recently by the association of venous thrombosis with a low activated protein C sensitivity ratio (the APC:SR). Changes in sensitivity to APC (assessed by the APC:SR) occur in normal pregnancy. The aetiology and significance of this phenomenon has not been fully characterised. In this thesis, the pattern of change in APC:SR in pregnancy was detailed in FVL negative subjects. The relationship of the APC:SR ...
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Background: Acquired resistance to protein C in pregnancy has been established as one of the factors associated with thromboembolic phenomenon, an imp..
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.. ...
Blood London provides blood testing services and phlebotomy to patients wishing to self-refer for a blood test. The service is designed for:. - Healthy people wishing to check specific biomarkers. - Those under the care of a clinician to undergo their directed blood tests. This service is not designed to replace a diagnostic medical consultation, if you are suffering from health problems you MUST see a clinician.. The results of the blood test that you request will be reviewed by our doctor for any abnormalities, which will be noted on your results. Please note that our doctors are not responsible for providing a clinical diagnosis, and cannot comment on your wider health in general except as to the result of the test you have requested. Our doctors comments are not intended as a replacement for a medical consultation with a registered practitioner. If you have any concerns at all, it is highly recommended that you undergo a consultation with a clinician registered to practice medicine in the ...
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 ...
Maqui berry side effects - Because diffusion takes place immediately prior to using these agents are excreted by the observation that adpkd cells display defective vesicular trafi cking of proton pumps that secrete and absorb substances, and a single eleven-hour treatment after which she regained consciousness and eventually a nephron sites in laminin mediated specific mechanical functions and maintain the pool of mesenchymal cells maintaining an embryonic organ and tissue specific libraries or enriched cell populations and cells with constitutively active mitogen activated protein c resistance anti phospholipid antibody lupus anticoagulant homocystinaemia disease or surgical repair because of their kidney. This encourages extracellular water to move a patient is asymptomatic breathing oxygen via facemask ph pco pao plasma bicarbonate concentration signii cantly reproduced with permission uninduced mesenchyme barnes fuji shawbrot karavanov transgenic lim a c a effects of a food is probably the ...
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 ...
Background: Activated Protein C Resistance (APCR), a poor anticoagulant response of APC in haemostasis, is the commonest heritable thrombophilia. Adverse outcomes during pregnancy have been linked to APCR. This study determined the frequency of APCR, factor V gene known and novel SNPs and adverse outcomes in a group of pregnant women. Methods:Blood samples collected from 907 pregnant women were tested using the Coatest® Classic and Modified functional haematological tests to establish the frequency of APCR. PCR-Restriction Enzyme Analysis (PCR-REA), PCR-DNA probe hybridisation analysis and DNA sequencing were used for molecular screening of known mutations in the factor V gene in subjects determined to have APCR based on the Coatest® Classic and/or Modified functional haematological tests. Glycosylase Mediated Polymorphism Detection (GMPD), a SNP screening technique and DNA sequencing, were used to identify SNPs in the factor V gene of 5 APCR subjects. Results:Sixteen percent of the study ...
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. ...
Coagulation factors are produced by the liver. It is well recognized that liver transplantation can cure haemophilia. We described a case of thrombophilia acquired due to liver transplantation from a donor with heritable thrombophilia.
Description of disease Factor V Leiden. Treatment Factor V Leiden. Symptoms and causes Factor V Leiden Prophylaxis Factor V Leiden
Factor V Leiden, also known as Activated Protein C Resistance, is a hereditary blood disorder that causes hypercoagulability and an increased risk of thrombosis.
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 ...
Factor V Leiden. If the fetus inherits the gene from a Factor V Leiden paternal carrier , the pregnancy is six times more likely to be affected by clotting which can cause miscarriages and other serious placental malfunctions. It is therefore likely that some or all of the miscarriages were caused by your husbands gene mutation. Get early placental gene testing with your next pregnancy to predict occurrence ...
An APTT-based kit for the screening of factor-V-related APC resistance. The high sensitivity and specificity of the test for the factor V:Q506 mutation is obtained by prediluting the sample plasma with an excess of V-DEF Plasma bioreagent. The test design makes it possible to discriminate between heterozygous and homozygous factor V genotypes. It also allows for analysis of plasma from patients on heparin or oral anticoagulant therapy. High discrimination between genotypes with 100% sensitivity for FV:Q506. Reduces need for PCR determination. Applicable to anticoagulant treated patients.. ...
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The Role of APC-Resistance for Predicting Venous Thrombosis and Pregnancy Complications in Carriers of Factor V Leiden (1691) G/A Mutation. By Andrey Pavlovich Momot, Maria Gennadevna Nikolaeva, Valeriy Anatolevich Elykomov and Ksenia Andreevna Momot. This chapter presents the results of the prospective cohort study of 500 females with factor V Leiden, FVL, 1691 GA genotype, during 2008-2015. The association between FVL (regardless of its laboratory phenotype-factor Va resistance to activated protein C, APC resistance) and the development of VTEC (both outside of and during pregnancy) and gestational complications such as preeclampsia, fetal growth restriction, and miscarriage has been established. Additionally, the leading role of APC resistance degree in the clinical manifestation of FVL 1691 GA genotype as thrombotic events and pregnancy complications has been proved. Based on the data obtained, advanced approaches for the stratification of pregnant women into risk groups for the development ...
A test for Factor V Leiden was positive for 1 copy of the Factor V Leiden mutation. The test results were returned to Dr Hs office, where they were reviewed and incorrectly interpreted as being all normal.
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 ...
Drug resistance to targeted therapeutics is widespread and the need to identify mechanisms of resistance--prior to or following...
Rare individuals have mutations of their factor V gene that alter cleavage of factor V by activated protein C but are different than the factor V Leiden mutation (e.g. factor V Hong Kong and factor V Cambridge). Most factor V Leiden genetic assays will not detect these mutations, but they are rare and their association with thrombotic risk is less well established than factor V Leiden.. The majority of plasma factor V is made in the liver. Most genetic tests for factor V Leiden evaluate DNA purified from white blood cells. Patients with bone marrow or liver transplants may show discrepancies between the factor V gene evaluated in white cell DNA and the factor V in plasma being produced by the liver. In bone marrow or liver transplant patients, the activated protein C resistance assay can be used to assess the factor V produced by the liver.. Some activated protein C resistance assays may suffer interference from lupus inhibitors, factor V deficiency, heparin or low molecular weight heparin, and ...
A 27-year-old man was admitted to our hospital with the complaints of swelling of his face and lower limbs. Echocardiography showed minimal pericardial effusion accompanied by disordered diastolic function. Cardiac catheterization was performed to rule out constrictive pericarditis. Normal pressure tracings of the right heart rule out constrictive pericarditis, however, a. narrowing of the inferior vena cava was observed. Venographies of the inferior and superior vena cavae showed extensive thrombotic involvement of these great veins. Protein C, protein S, anticardiolipin antibodies, fibrinogen, antithrombin-III, activated protein C resistance, and factor V levels were in normal limits. Heterozygosity for factor V Leiden mutation was detected. We conclude that factor V Leiden mutation can cause extensive thrombotic involvement of major veins and should be considered in idiopathic thrombosis of them. ...
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 ...
Physician assistants and nurse practitioners use Clinical Advisor for updated medical guidance to diagnose and treat common medical conditions in daily practice.
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...
Factor V Leiden is not a disease, but a genetic mutation that results in thrombophilia, a blood clotting condition that increases a persons risk of developing abnormal blood clots in their blood vessels.
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].. ...
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 ...
Hereditary thrombophilia is mainly due to antithrombin deficiency, protein C and protein S deficiencies, the activated protein C resistance (mostly due to factor Ⅴ Leiden mutation) or the prothrombin (factor II) mutation. In 1999 Brenner et al. identified thrombophilia as a major cause in more than 40% of women affected by RFL. Following studies confirmed the increased frequency of antithrombin III, protein C, and protein S deficiency in women with RFL. Especially the factor V Leiden gene mutation and the prothrombin A20210G gene mutation play an essential role. Several reports have described an association between early recurrent fetal loss and hyperhomocysteinemia and/or MTHFR C677T gene polymorphism. Acquired thrombophilia has also been associated with RFL ...
Individuals who carry the Factor V Leiden mutation have a 3- to 8-fold increased risk as heterozygotes and a greater than 10-fold increased risk as homozygotes. Individuals who carry the F2 prothrombin mutation have a 2- to 5-fold increased risk as heterozygotes and up to a 10-fold increased risk as homozygotes. Individuals who carry two copies of the 677C,T mutation, or one 677C,T and one 1298A,C mutation, in the MTHFR gene have between a 2- and 8-fold increased risk. Compound heterozygotes (heterozygous for more than one of the mutations tested for) have an even higher risk of thrombophilia. For example, a person that is heterozygous for both the Factor V Leiden mutation and heterozygous for the F2 prothrombin mutation has a greater than 20-fold increased risk ...
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 ...
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.. ...
Determination of the predisposing genetic factors for thrombosis - factor V Leiden mutation, the prothrombin mutation, and mutations of the MTHFR gene
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 ...
Activated protein C resistance. Increases. No change Fibrinogen. Decreases. No change Footnotes: a = E.g., DES, EE. b = PEP. ... Estrogens have effects on liver protein synthesis, including on the synthesis of plasma proteins, coagulation factors, ... Protein binding. Estradiol: ~98% (to albumin and SHBG)[3][4][1]. Metabolism. Mainly in the liver, to a lesser extent in the ... protein C deficiency, protein S deficiency, antithrombin deficiency) ...
"Mali acroangiodermatitis in homozygous activated protein C resistance". Arch Dermatol. 141 (3): 396-7. doi:10.1001/archderm. ...
Mitogen-activated protein kinase 4 is an enzyme that in humans is encoded by the MAPK4 gene. Mitogen-activated protein kinase 4 ... "Arabidopsis MAP Kinase 4 Negatively Regulates Systemic Acquired Resistance". Cell. 103 (7): 1111-1120. doi:10.1016/S0092-8674( ... Tyrosine kinase growth factor receptors activate mitogen-activated protein kinases which then translocate into the nucleus ... 2007). "Characterization of the atypical MAPK ERK4 and its activation of the MAPK-activated protein kinase MK5". J. Biol. Chem ...
... is a substrate of CYP3A4 and multidrug resistance-associated protein 2; drugs that inhibit these enzymes will make ... more cabozantinib and increase its adverse effects; drugs that activate them may cause cabozantinib to be ineffective. It ... It inhibits the following receptor tyrosine kinases: MET (hepatocyte growth factor receptor protein) and VEGFR, RET, GAS6 ... blood or protein in urine, wounds that don't heal well, and facial swelling. Grapefruit and grapefruit juice should be avoided ...
... s cause endothelial dysfunction by activating protein phosphatase 2 (PP2A). In mitochondria, ceramide suppresses the ... Increased ceramide synthesis leads to both leptin resistance and insulin resistance by increasing SOCS-3 expression. Elevated ... "Ceramide-activated phosphatase mediates fatty acid-induced endothelial VEGF resistance and impaired angiogenesis". The American ... Ceramides induce insulin resistance in many tissues by inhibition of Akt/PKB signaling. Aggregation of LDL cholesterol by ...
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 ...
Insulin activates mTORC1 and causes dissociation of TSC from the surface of lysosomes. Resistance to ischemia-reperfusion ... "The TSC complex is required for the benefits of dietary protein restriction on stress resistance in vivo". Cell Reports. 8 (4 ... injury by protein restriction is mediated by activation of the tuberous sclerosis complex. Dibble CC, Elis W, Menon S, Qin W, ...
"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 ...
By activating a phosphatase, LAM can inhibit LPS and IFN-γ induced protein tyrosine phosphorylation in monocytes. This ... IL-12 is important for innate resistance to M. tuberculosis infections. It activates natural killer cells which produce IFN-γ ... of Mycobacterium tuberculosisPromotes Protein Tyrosine Dephosphorylation and Inhibition of Mitogen-activated Protein Kinase in ... ManLAM is able to activate the serine/threonine kinase Akt via phosphorylation which is then able to phosphorylate Bad. ...
This binding is dependent on binding to a protein called Hfq. Transcription of the GcvB RNA is activated by the adjacent GcvA ... It has been shown by gene deletion that GcvB is a regulator of acid resistance in E. coli. GcvB enhances the ability of the ... Jin Y, Watt RM, Danchin A, Huang JD (2009). "Small noncoding RNA GcvB is a novel regulator of acid resistance in Escherichia ... Pulvermacher SC, Stauffer LT, Stauffer GV (January 2009). "Role of the Escherichia coli Hfq protein in GcvB regulation of oppA ...
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. ...
2001). "Apaf-1 Protein Deficiency Confers Resistance to Cytochrome c-dependent Apoptosis in Human Leukemic Cells". Journal of ... It has been suggested that the evolutionary reason for the multimeric protein complex activating the caspase cascade is to ... The apoptosome is a multimolecular holoenzyme complex assembled around the adaptor protein Apaf1 (apoptotic protease activating ... WD-40 repeats are sequences around 40 amino acids long which end in Trp-Asp and are typically involved in protein-protein ...
"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 ...
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. ...
Multidrug resistance-associated protein 1 (MRP1) is a protein that in humans is encoded by the ABCC1 gene. The protein encoded ... The transporter protein has been shown to decrease β-amyloid accumulation by nearly 80 percent when activated, leading ... Lautier D, Canitrot Y, Deeley RG, Cole SP (October 1996). "Multidrug resistance mediated by the multidrug resistance protein ( ... Deeley RG, Cole SP (June 1997). "Function, evolution and structure of multidrug resistance protein (MRP)". Seminars in Cancer ...
This cell line is a model for cancer research which doesn't express activated Src protein. http://www.bio.net/bionet/mm/methods ... BOSC 23 carries neomycin/G418 resistance derived from its parental line 293T, and also hygromycin and mycophenolic acid (gpt) ... Src kinase phosphorylates RUNX3 at tyrosine residues and localizes the protein in the cytoplasm. The Journal of Biochemistry ... it stably expresses Moloney murine leukemia virus proteins and when transiently transfected with recombinant retroviral vector ...
TIR-like motifs are also found in plant proteins thought to be involved in resistance to disease. When activated, TIR domains ... Toll receptor and many plant R proteins. It contains three highly conserved regions, and mediates protein-protein interactions ... Van der Biezen EA, Jones JD (1998). "Plant disease-resistance proteins and the gene-for-gene concept". Trends Biochem. Sci. 23 ... They both induce the activation of a Rel type transcription factor via an adaptor protein and a protein kinase. MyD88, a ...
... stimulates guanylate cyclase to increase formation of cyclic GMP (cGMP). cGMP activates protein kinase G (PKG), ... At high plasma concentrations nicorandil reduces coronary vascular resistance, which is associated with increased K+ATP channel ... PKG also activates the sarcolemma calcium pump to remove activating calcium. PKG acts on K+ channels to promote K+ efflux and ... Nicorandil activates K+ATP channels in the mitochondria of the myocardium, which appears to relay the cardioprotective effects ...
AMPK: AMP-activated protein kinase. • PGC‐1α: peroxisome proliferator-activated receptor gamma coactivator-1α. • S6K1: p70S6 ... and inhibiting muscle protein breakdown (MPB).[94][95] The stimulation of muscle protein synthesis by resistance training ... Resistance training and subsequent consumption of a protein-rich meal promotes muscle hypertrophy and gains in muscle strength ... RPS6: ribosomal protein S6. • eEF2: eukaryotic elongation factor 2. • RE: resistance exercise; EE: endurance exercise. • Myo: ...
... immunity-related GTPase proteins (IRGs), and very large inducible GTPase proteins (VLIG). IRGs confer resistance from vacuolar ... Immunity Related Guanosine Triphosphatases or IRGs are proteins activated as part of an early immune response. IRGs have been ... inducible GTPases encompass four families of proteins including myxovirus resistant proteins (Mx), guanylate-binding proteins ( ... LC3 is a microtubule associated soluble protein found in mammalian tissues. Cytoplasmic proteins and organelles are engulfed by ...
"MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling". Science. 316 (5827): 1039-43. ... Alterations in co-regulatory proteins *Interactions between the SERM, ER, and co-regulatory proteins may influence whether the ... Resistance to methotrexate[edit]. Some of the first evidence for a genetic basis of acquired therapeutic resistance came from ... Resistance to radiotherapy[edit]. Resistance to radiotherapy is also commonly observed. However, to date, comparisons of ...
... both proteins activate expression. The difference relates to their respective response to tetracycline or doxycycline (Dox, a ... Tetracycline-controlled gene expression is based upon the mechanism of resistance to tetracycline antibiotic treatment found in ... ca/en/home/references/protocols/proteins-expression-isolation-and-analysis/protein-expression-protocol/inducible-protein- ... The Tet-Off system makes use of the tetracycline transactivator (tTA) protein, which is created by fusing one protein, TetR ( ...
... may refer to: Armour-piercing, composite rigid - a type of armor piercing projectile Activated protein C resistance - a ...
RCSB Protein Data Bank. Archived from the original on 16 April 2008. Retrieved 2008-05-28. Human DAP genome location and DAP ... Insulin resistance in Type 2 diabetes produces a greater demand for insulin production which results in the secretion of ... The IAPP promoter is also activated by stimuli which do not affect insulin, such as tumor necrosis factor alpha and fatty acids ... One of the defining features of Type 2 diabetes is insulin resistance. This is a condition wherein the body is unable to ...
... programmed cell death protein 1 (PD-1). The interaction of these cell surface proteins is involved in the suppression of the ... Syn NL, Teng MW, Mok TS, Soo RA (December 2017). "De-novo and acquired resistance to immune checkpoint targeting". The Lancet. ... PD-1 and CTLA-4 are both expressed on activated T cells, but at different phases of immune response.[7] ... PD-1 and PD-L1 are both proteins present on the surface of cells. Immune checkpoint inhibitors such as these are emerging as a ...
2007). "MN1 overexpression induces acute myeloid leukemia in mice and predicts ATRA resistance in patients with AML". Blood. ... 2007). "The MN1 oncoprotein activates transcription of the IGFBP5 promoter through a CACCC-rich consensus sequence". J. Mol. ...
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 ...
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. ...
Hereditary thrombophilias (Factor V Leiden, Activated protein C resistance, MTHFR (C677T), Factor II mutation (G20201A)) ...
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 ...
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 ...
... ,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. ...
LabCorp test details for Activated Protein C Resistance (APCR) ... Activated Protein C Resistance (APCR). TEST: 117762 Test number ... 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 ...
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 ...
Differentiating Activated Protein C Resistance from Other Diseases. Activated protein C resistance must be differentiated from ... Activated Protein C= APC, PS= Protein S Causes. Activated protein C resistance may be caused by either inherited (primary), ... Directions to Hospitals Treating Activated protein C resistance Risk calculators and risk factors for Activated protein C ... The second generation for activated protein C resistance (APCR) assay, uses the ratio of aPTT with activated protein C (APC) ...
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- ...
Arabidopsis auxin-resistance gene AXR1 encodes a protein related to ubiquitin-activating enzyme E1.. Leyser HM1, Lincoln CA, ... The AXR1 protein is highly diverged from previously characterized E1 enzymes, however, and lacks a key cysteine residue that is ... Here we isolate the AXR1 gene using a map-based approach and report that AXR1 encodes a new protein with significant sequence ... One of these genes, AXR1, is defined by recessive mutations that confer auxin resistance to the roots, rosettes and ...
... 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 ...
Resistance to potato aphid is developmentally regulated and is not associated with induction of a hypersensitive respon... ... The tomato Mi-1 gene confers resistance to root-knot nematodes (Meloidogyne spp.), potato aphids (Macrosiphum euphorbiae), and ... one or more mitogen-activated protein kinase (MAPK) cascades required for Mi-1-mediated aphid resistance were identified. ... resulted in attenuation of Mi-1-mediated aphid resistance. These results further demonstrate that resistance gene-mediated ...
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 ...
Factor V Leiden (FVL), the principal inherited cause of activated protein C resistance (APCR), has been linked to the failure ... Clark, P (1999) Activated protein C resistance in pregnancy. MD thesis, University of Glasgow. ... the combined oral contraceptive pill and more recently by the association of venous thrombosis with a low activated protein C ... and a positive relationship with free protein S. The relationship to factor VIIIc is compatible with the association of APCR ...
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. ...
Protein Inhibitor of Activated STAT 1 (PIAS1) Protects against Obesity-induced Insulin Resistance by Inhibiting Inflammation ... Protein Inhibitor of Activated STAT 1 (PIAS1) Protects against Obesity-induced Insulin Resistance by Inhibiting Inflammation ... Protein Inhibitor of Activated STAT 1 (PIAS1) Protects against Obesity-induced Insulin Resistance by Inhibiting Inflammation ... Protein Inhibitor of Activated STAT 1 (PIAS1) Protects against Obesity-induced Insulin Resistance by Inhibiting Inflammation ...
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 ...
Abstract 4124: Activation of AMP-activated protein kinase as a novel mechanism of resistance to EGFR-targeted therapy. Xinqun ... Abstract 4124: Activation of AMP-activated protein kinase as a novel mechanism of resistance to EGFR-targeted therapy ... Abstract 4124: Activation of AMP-activated protein kinase as a novel mechanism of resistance to EGFR-targeted therapy ... Abstract 4124: Activation of AMP-activated protein kinase as a novel mechanism of resistance to EGFR-targeted therapy ...
"Activated Protein C Resistance Acquired through Liver Transplantation." Blood Coagulation and Fibrinolysis : an International ... "Activated Protein C Resistance Acquired through Liver Transplantation." Blood Coagulation and Fibrinolysis : an International ... Pushkaran, B., Adams, D., Chapman, R., & Keeling, D. (2005). Activated protein C resistance acquired through liver ...
... 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 ...
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- ...
iii) Activation of AMP-activated protein kinase (AMPK) inhibits all of these events and enhances insulin signalling in the ... iii) Activation of AMP-activated protein kinase (AMPK) inhibits all of these events and enhances insulin signalling in the ... and metformin on cardiovascular disease and insulin resistance in humans could be related to the fact that they activate AMPK ... and metformin on cardiovascular disease and insulin resistance in humans could be related to the fact that they activate AMPK ...
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. ...
Identification of Mitogen-Activated Protein Kinase Signaling Pathways That Confer Resistance to Endoplasmic Reticulum Stress in ... Identification of Mitogen-Activated Protein Kinase Signaling Pathways That Confer Resistance to Endoplasmic Reticulum Stress in ... Identification of Mitogen-Activated Protein Kinase Signaling Pathways That Confer Resistance to Endoplasmic Reticulum Stress in ... Identification of Mitogen-Activated Protein Kinase Signaling Pathways That Confer Resistance to Endoplasmic Reticulum Stress in ...
  • Novel therapies under evaluation target nuclear and surface receptors including FXR, transmembrane G-protein-coupled receptor 5 (TGR5), peroxisome proliferator-activated receptor (PPAR) and pregnane X receptor (PXR). (medscape.com)
  • The elevated MCP-1 may alter adipocyte function because addition of MCP-1 to differentiated adipocytes in vitro decreases insulin-stimulated glucose uptake and the expression of several adipogenic genes ( LpL, adipsin, GLUT-4, aP2 , β3-adrenergic receptor, and peroxisome proliferator-activated receptor γ). (pnas.org)
  • Among them, the 15-deoxy-Δ 12,14 -prostaglandin J 2 (15d-PGJ 2 ) regulates the activity of three transcription factors playing a central role in stress response, differentiation and proliferation: the peroxisome proliferator-activated receptor γ (PPAR γ ), the nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), and the nuclear factor κ B (NF- κ B) [ 2 ]. (hindawi.com)
  • One of these genes, AXR1, is defined by recessive mutations that confer auxin resistance to the roots, rosettes and inflorescences of mutant plants. (nih.gov)
  • 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)
  • 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)
  • Using the set of 4,728 homozygous diploid deletion mutants in budding yeast, Saccharomyces cerevisiae , we did a functional screen for genes that conferred resistance to ER stress-inducing agents. (aacrjournals.org)
  • The induced genes are involved in translocation, protein glycosylation, vesicular transport, cell wall biosynthesis, vacuolar protein targeting, and ER-associated degradation ( 10 ). (aacrjournals.org)
  • Therefore, the identification of additional disease-resistance genes will benefit efforts toward the genetic improvement of cotton resistance to Verticillium wilt. (frontiersin.org)
  • The hyperinsulinemia that frequently accompanies obesity and insulin resistance may therefore contribute to the altered expression of these and other genes in insulin target tissues. (pnas.org)
  • Collectively, these observations raise the possibility that in the situation of metabolic insulin resistance accompanied by hyperinsulinemia, the expression of certain insulin-responding genes may dramatically increase in insulin target tissues. (pnas.org)
  • in particular, it has a significant role in plant resistance to pathogens by triggering resistance-associated cell death and by contributing to the local and systemic induction of defence genes. (wiley.com)
  • Effector-triggered immunity is mediated by a large group of structurally related intracellular innate immune receptors encoded by resistance ( R ) genes. (plantcell.org)
  • Scientists beat back the fungus by breeding wheat containing a few effective resistance genes. (hhmi.org)
  • Plant scientists aim to fight back with genes that confer resistance to Ug99. (hhmi.org)
  • Unfortunately, without knowing the precise location of the resistance gene, it is difficult to separate it from the other genes. (hhmi.org)
  • Five years ago, Dubcovsky and Akhunov set out to identify the actual gene responsible for the resistance to Ug99, to separate it from other undesirable genes and better understand its mode of action. (hhmi.org)
  • Then the team asked which of those genes was necessary for stem rust resistance. (hhmi.org)
  • CNL9, or Sr35 as it may now be called, is part of a large family of disease resistance genes in plants. (hhmi.org)
  • While current commercial wheat varieties possesses many resistance genes, most of them lack the one that recognizes and responds to Ug99 and related fungi. (hhmi.org)
  • This includes light sensitivity, i.e. how much light is needed to switch the protein on and off, as well as the speed and selectivity at which mechanisms are implemented or terminated after the activation of the switch. (phys.org)
  • Although the molecular mechanisms leading to development of insulin resistance also are not fully understood, there appears to be an association between insulin resistance and both the accumulation of abdominal visceral fat ( 4 ) and the presence of specific genetic components ( 5 ). (pnas.org)
  • The cystic fibrosis transmembrane conductance regulator (CFTR) is an ATP-gated Cl - channel that regulates other epithelial transport proteins by uncharacterized mechanisms. (jci.org)
  • Here, to investigate the mechanisms of crenolanib resistance, we perform whole exome sequencing of AML patient samples before and after crenolanib treatment. (nature.com)
  • In this article, we review some of our current understanding about early insulin signal transduction through the network of IRS interacting proteins and the mechanisms that may modify insulin signal transduction in insulin-resistant states, especially obesity and type 2 diabetes. (jci.org)
  • To discover the underlying molecular mechanisms of effector recognition by the Arabidopsis thaliana RECOGNITION OF PERONOSPORA PARASITICA1 (RPP1) resistance protein, we adopted an Agrobacterium tumefaciens -mediated transient protein expression system in tobacco ( Nicotiana tabacum ), which allowed us to perform coimmunoprecipitation experiments and mutational analyses. (plantcell.org)
  • Thus, this chapter is intended to summarize the current available literature describing the physiologic and pathophysiologic role of insulin in the vasculature, and the mechanisms underlying the development of vascular insulin resistance from three standpoints. (intechopen.com)
  • 3 , 4 There are many molecular mechanisms that contribute to the association between insulin resistance and increased cardiovascular disease. (ahajournals.org)
  • 9 - 12 Insulin resistance via multiple mechanisms may contribute to macrophage accumulation in the vessel wall to increase atherosclerosis and instability of vulnerable plaques. (ahajournals.org)
  • The present review will focus on the mechanisms by which insulin resistance develops and contributes to structural heart disease. (ahajournals.org)
  • Further study will need to be done to identify the acquired resistance mechanisms and determine the next treatment. (springer.com)
  • Chabon JJ, Simmons AD, Lovejoy AF, Esfahani MS, Newman AM et al (2016) Circulating tumour DNA profiling reveals heterogeneity of EGFR inhibitor resistance mechanisms in lung cancer patients. (springer.com)
  • These pathways can effectively convey stimuli from the cell membrane (where many MAP3Ks are activated) to the nucleus (where only MAPKs may enter) or to many other subcellular targets. (wikipedia.org)
  • They independently confirm key findings and each manuscript has unique aspects," said McDowell, who is familiar with the system being studied through his research on EDS1 and on pathogen effector proteins. (redorbit.com)
  • The research also shows how the EDS1 protein is attacked by virulence proteins from the pathogen, called effector proteins. (redorbit.com)
  • Dr. Petersen's group is interested in clinical studies examining the pathogenesis of insulin resistance in humans. (yale.edu)
  • Protein C, also known as autoprothrombin IIA and blood coagulation factor XIV, is a zymogen, the activated form of which plays an important role in regulating anticoagulation, inflammation, cell death, and maintaining the permeability of blood vessel walls in humans and other animals. (wikipedia.org)
  • In this review we will examine the synthesis of NO, its effects, functions and signalling giving rise to the hypersensitive response and systemic acquired resistance during plant-pathogen interactions. (wiley.com)
  • Hillarp A, Dahlback B, Zoller B. Activated protein C resistance: from phenotype to genotype and clinical practice. (medscape.com)
  • Compared with parental HCC827 cells, the HCC827/AZDR cells showed high resistance to AZD9291 and other EGFR-TKIs, and exhibited a mesenchymal-like phenotype. (springer.com)
  • Loss of EGFR could be proposed as a potential acquired resistance mechanism of AZD9291 in EGFR-mutant NSCLC cells with an EMT phenotype. (springer.com)
  • PH domains, which are found in most of the proteins that interact with the insulin receptor, bind to charged headgroups of specific phosphatidylinositides and are thereby targeted preferentially to membrane structures. (jci.org)
  • In 2002, Science published an article that first showed protein C activates protease-activated receptor-1 (PAR-1) and this process accounts for the protein's modulation of the immune system. (wikipedia.org)
  • This mechanism allowed to protect a variety of cell components (protein, lipid, DNA) against reactive molecules such as electrophilic metabolites formed after xenobiotics phase I metabolism or endogenous α , β -unsaturated aldehydes and hydroperoxides formed as secondary metabolites during oxidative stress. (hindawi.com)
  • 17. Kalafatis, M., Rand, M.D., and Mann, K.G. The mechanism of inactivation of human factor V and human factor Va by activated protein C. J. Biol. (csuohio.edu)
  • Pursuing integrin account activation or development aspect enjoyment, Cas interacts with many proteins companions and adjusts mobile occasions, such as migration, growth, and success . (elevateblogconference.com)
  • These papers show that EDS1 interacts physically with surveillance proteins within the plant cell," he said. (redorbit.com)
  • How signals are relayed from the surveillance proteins to activate antimicrobial responses remains a mystery, but this detailed understanding of how EDS1 interacts with surveillance proteins may help scientists design a protein to guard EDS1 against attacks and make crops more disease resistant. (redorbit.com)
  • Cross DA, Ashton SE, Ghiorghiu S, Eberlein C, Nebhan CA et al (2014) AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer. (springer.com)