Activated Protein C Resistance
Protein C
Factor V
Protein C Deficiency
Thrombophilia
Protein S Deficiency
Protein S
Factor V Deficiency
Lupus Coagulation Inhibitor
Partial Thromboplastin Time
Drug Resistance
Coagulation Protein Disorders
Antibodies, Anticardiolipin
Retinal Vein Occlusion
Prothrombin
Blood Coagulation
Protein C Inhibitor
Thromboembolism
Mutation
Point Mutation
Mitomycin
Drug Resistance, Microbial
Drug Resistance, Bacterial
Phenotype
Thrombomodulin
Case-Control Studies
Risk Factors
Drug Resistance, Neoplasm
Pregnancy
Blood Coagulation Factors
Pulmonary Surfactant-Associated Protein C
Drug Resistance, Multiple
Disease Resistance
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)Activated Protein C (APC) resistance is a condition in which the body's natural anticoagulant system is impaired, leading to an increased risk of thrombosis or blood clot formation. APC is an enzyme that plays a crucial role in regulating blood coagulation by inactivating clotting factors Va and VIIIa.
APC resistance is most commonly caused by a genetic mutation in the Factor V gene, known as Factor V Leiden. This mutation results in the production of a variant form of Factor V called Factor V Leiden, which is resistant to APC-mediated inactivation. As a result, the body's ability to regulate blood clotting is impaired, leading to an increased risk of thrombosis.
APC resistance can be measured by performing a functional assay that compares the activity of APC in normal plasma versus plasma from a patient with suspected APC resistance. The assay measures the rate of inactivation of Factor Va by APC, and a reduced rate of inactivation indicates APC resistance.
It is important to note that not all individuals with APC resistance will develop thrombosis, and other factors such as age, obesity, pregnancy, oral contraceptive use, and smoking can increase the risk of thrombosis in individuals with APC resistance.
Protein C is a vitamin K-dependent protease that functions as an important regulator of coagulation and inflammation. It is a plasma protein produced in the liver that, when activated, degrades clotting factors Va and VIIIa to limit thrombus formation and prevent excessive blood clotting. Protein C also has anti-inflammatory properties by inhibiting the release of pro-inflammatory cytokines and reducing endothelial cell activation. Inherited or acquired deficiencies in Protein C can lead to an increased risk of thrombosis, a condition characterized by abnormal blood clot formation within blood vessels.
Factor V, also known as proaccelerin or labile factor, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor V acts as a cofactor for the activation of Factor X to Factor Xa, which is a critical step in the coagulation cascade.
When blood vessels are damaged, the coagulation cascade is initiated to prevent excessive bleeding. During this process, Factor V is activated by thrombin, another protein involved in coagulation, and then forms a complex with activated Factor X and calcium ions on the surface of platelets or other cells. This complex converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.
Deficiency or dysfunction of Factor V can lead to bleeding disorders such as hemophilia B or factor V deficiency, while mutations in the gene encoding Factor V can increase the risk of thrombosis, as seen in the Factor V Leiden mutation.
Protein C deficiency is a genetic disorder that affects the body's ability to control blood clotting. Protein C is a protein in the blood that helps regulate the formation of blood clots. When blood clots form too easily or do not dissolve properly, they can block blood vessels and lead to serious medical conditions such as deep vein thrombosis (DVT) or pulmonary embolism (PE).
People with protein C deficiency have lower than normal levels of this protein in their blood, which can increase their risk of developing abnormal blood clots. The condition is usually inherited and present from birth, but it may not cause any symptoms until later in life, such as during pregnancy, after surgery, or due to other factors that increase the risk of blood clots.
Protein C deficiency can be classified into two types: type I and type II. Type I deficiency is characterized by lower than normal levels of both functional and immunoreactive protein C in the blood. Type II deficiency is characterized by normal or near-normal levels of immunoreactive protein C, but reduced functional activity.
Protein C deficiency can be diagnosed through blood tests that measure the level and function of protein C in the blood. Treatment may include anticoagulant medications to prevent blood clots from forming or dissolve existing ones. Regular monitoring of protein C levels and careful management of risk factors for blood clots are also important parts of managing this condition.
Thrombophilia is a medical condition characterized by an increased tendency to form blood clots (thrombi) due to various genetic or acquired abnormalities in the coagulation system. These abnormalities can lead to a hypercoagulable state, which can cause thrombosis in both veins and arteries. Commonly identified thrombophilias include factor V Leiden mutation, prothrombin G20210A mutation, antithrombin deficiency, protein C deficiency, and protein S deficiency.
Acquired thrombophilias can be caused by various factors such as antiphospholipid antibody syndrome (APS), malignancies, pregnancy, oral contraceptive use, hormone replacement therapy, and certain medical conditions like inflammatory bowel disease or nephrotic syndrome.
It is essential to diagnose thrombophilia accurately, as it may influence the management of venous thromboembolism (VTE) events and guide decisions regarding prophylactic anticoagulation in high-risk situations.
Protein S deficiency is a genetic disorder that affects the body's ability to coagulate blood properly. Protein S is a naturally occurring protein in the blood that helps regulate the clotting process by deactivating clotting factors when they are no longer needed. When Protein S levels are too low, it can lead to an increased risk of abnormal blood clots forming within blood vessels, a condition known as thrombophilia.
There are three types of Protein S deficiency: Type I (quantitative deficiency), Type II (qualitative deficiency), and Type III (dysfunctional protein). These types refer to the amount or function of Protein S in the blood. In Type I, there is a decrease in both free and total Protein S levels. In Type II, there is a decrease in functional Protein S despite normal total Protein S levels. In Type III, there is a decrease in free Protein S with normal total Protein S levels.
Protein S deficiency can be inherited or acquired. Inherited forms of the disorder are caused by genetic mutations and are usually present from birth. Acquired forms of Protein S deficiency can develop later in life due to certain medical conditions, such as liver disease, vitamin K deficiency, or the use of certain medications that affect blood clotting.
Symptoms of Protein S deficiency may include recurrent blood clots, usually in the legs (deep vein thrombosis) or lungs (pulmonary embolism), skin discoloration, pain, and swelling in the affected area. In severe cases, it can lead to complications such as chronic leg ulcers, pulmonary hypertension, or damage to the heart or lungs.
Diagnosis of Protein S deficiency typically involves blood tests to measure Protein S levels and function. Treatment may include anticoagulant medications to prevent blood clots from forming or growing larger. Lifestyle modifications such as regular exercise, maintaining a healthy weight, and avoiding smoking can also help reduce the risk of blood clots in people with Protein S deficiency.
Protein S is a vitamin K-dependent protein found in the blood that functions as a natural anticoagulant. It plays a crucial role in regulating the body's clotting system by inhibiting the activation of coagulation factors, thereby preventing excessive blood clotting. Protein S also acts as a cofactor for activated protein C, which is another important anticoagulant protein.
Protein S exists in two forms: free and bound to a protein called C4b-binding protein (C4BP). Only the free form of Protein S has biological activity in inhibiting coagulation. Inherited or acquired deficiencies in Protein S can lead to an increased risk of thrombosis, or abnormal blood clot formation, which can cause various medical conditions such as deep vein thrombosis (DVT) and pulmonary embolism (PE). Regular monitoring of Protein S levels is essential for patients with a history of thrombotic events or those who have a family history of thrombophilia.
Factor V deficiency is a rare bleeding disorder that is caused by a mutation in the gene that produces coagulation factor V, a protein involved in the clotting process. This condition can lead to excessive bleeding following injury or surgery, and may also cause menorrhagia (heavy menstrual periods) in women.
Factor V deficiency is inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) in order to develop the condition. People who inherit only one copy of the mutated gene are carriers and may have a milder form of the disorder or no symptoms at all.
Treatment for factor V deficiency typically involves replacement therapy with fresh frozen plasma or clotting factor concentrates, which can help to reduce bleeding episodes and prevent complications. In some cases, medications such as desmopressin or antifibrinolytics may also be used to manage the condition.
I'm sorry for any confusion, but "Lupus Coagulation Inhibitor" is not a recognized medical term or concept in hematology or immunology.
Systemic Lupus Erythematosus (SLE), often referred to simply as lupus, is an autoimmune disease where the body's immune system mistakenly attacks healthy tissue. However, this does not result in a specific coagulation inhibitor.
If you're asking about lupus anticoagulants, these are antibodies that can interfere with clotting tests but paradoxically increase the risk of blood clots in vivo. They are sometimes seen in patients with SLE and other autoimmune diseases.
Please provide more context if you meant something else, so I can give a more accurate response.
Partial Thromboplastin Time (PTT) is a medical laboratory test that measures the time it takes for blood to clot. It's more specifically a measure of the intrinsic and common pathways of the coagulation cascade, which are the series of chemical reactions that lead to the formation of a clot.
The test involves adding a partial thromboplastin reagent (an activator of the intrinsic pathway) and calcium to plasma, and then measuring the time it takes for a fibrin clot to form. This is compared to a control sample, and the ratio of the two times is calculated.
The PTT test is often used to help diagnose bleeding disorders or abnormal blood clotting, such as hemophilia or disseminated intravascular coagulation (DIC). It can also be used to monitor the effectiveness of anticoagulant therapy, such as heparin. Prolonged PTT results may indicate a bleeding disorder or an increased risk of bleeding, while shortened PTT results may indicate a hypercoagulable state and an increased risk of thrombosis.
Blood coagulation tests, also known as coagulation studies or clotting tests, are a series of medical tests used to evaluate the blood's ability to clot. These tests measure the functioning of various clotting factors and regulatory proteins involved in the coagulation cascade, which is a complex process that leads to the formation of a blood clot to prevent excessive bleeding.
The most commonly performed coagulation tests include:
1. Prothrombin Time (PT): Measures the time it takes for a sample of plasma to clot after the addition of calcium and tissue factor, which activates the extrinsic pathway of coagulation. The PT is reported in seconds and can be converted to an International Normalized Ratio (INR) to monitor anticoagulant therapy.
2. Activated Partial Thromboplastin Time (aPTT): Measures the time it takes for a sample of plasma to clot after the addition of calcium, phospholipid, and a contact activator, which activates the intrinsic pathway of coagulation. The aPTT is reported in seconds and is used to monitor heparin therapy.
3. Thrombin Time (TT): Measures the time it takes for a sample of plasma to clot after the addition of thrombin, which directly converts fibrinogen to fibrin. The TT is reported in seconds and can be used to detect the presence of fibrin degradation products or abnormalities in fibrinogen function.
4. Fibrinogen Level: Measures the amount of fibrinogen, a protein involved in clot formation, present in the blood. The level is reported in grams per liter (g/L) and can be used to assess bleeding risk or the effectiveness of fibrinogen replacement therapy.
5. D-dimer Level: Measures the amount of D-dimer, a protein fragment produced during the breakdown of a blood clot, present in the blood. The level is reported in micrograms per milliliter (µg/mL) and can be used to diagnose or exclude venous thromboembolism (VTE), such as deep vein thrombosis (DVT) or pulmonary embolism (PE).
These tests are important for the diagnosis, management, and monitoring of various bleeding and clotting disorders. They can help identify the underlying cause of abnormal bleeding or clotting, guide appropriate treatment decisions, and monitor the effectiveness of therapy. It is essential to interpret these test results in conjunction with a patient's clinical presentation and medical history.
The medical definition of "Habitual Abortion" refers to a woman who has three or more consecutive pregnancies that end in spontaneous miscarriages before 20 weeks of gestation. The cause of habitual abortions can be difficult to determine and may involve genetic, anatomical, hormonal, or immune system factors. Treatment is often aimed at addressing any underlying issues that may be contributing to the recurrent miscarriages. It's important to note that the terminology has changed over time and the term "recurrent pregnancy loss" is now more commonly used in place of "habitual abortion".
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
Coagulation protein disorders are a group of medical conditions that affect the body's ability to form blood clots properly. These disorders can be caused by genetic defects or acquired factors, such as liver disease or vitamin K deficiency.
The coagulation system is a complex process that involves various proteins called clotting factors. When there is an injury to a blood vessel, these clotting factors work together in a specific order to form a clot and prevent excessive bleeding. In coagulation protein disorders, one or more of these clotting factors are missing or not functioning properly, leading to abnormal bleeding or clotting.
There are several types of coagulation protein disorders, including:
1. Hemophilia: This is a genetic disorder that affects the clotting factor VIII or IX. People with hemophilia may experience prolonged bleeding after injuries, surgery, or dental work.
2. Von Willebrand disease: This is another genetic disorder that affects the von Willebrand factor, a protein that helps platelets stick together and form a clot. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
3. Factor XI deficiency: This is a rare genetic disorder that affects the clotting factor XI. People with this condition may experience prolonged bleeding after surgery or trauma.
4. Factor VII deficiency: This is a rare genetic disorder that affects the clotting factor VII. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
5. Acquired coagulation protein disorders: These are conditions that develop due to other medical factors, such as liver disease, vitamin K deficiency, or the use of certain medications. These disorders can affect one or more clotting factors and may cause abnormal bleeding or clotting.
Treatment for coagulation protein disorders depends on the specific condition and severity of symptoms. In some cases, replacement therapy with the missing clotting factor may be necessary to prevent excessive bleeding. Other treatments may include medications to control bleeding, such as desmopressin or antifibrinolytic agents, and lifestyle changes to reduce the risk of injury and bleeding.
Anticardiolipin antibodies are a type of autoantibody that targets and binds to cardiolipin, a phospholipid component found in the inner mitochondrial membrane of cells. These antibodies are clinically significant because they have been associated with a variety of autoimmune disorders, including antiphospholipid syndrome (APS).
APS is a condition characterized by recurrent blood clots, pregnancy losses, and thrombocytopenia (low platelet count). Anticardiolipin antibodies are one of the three main types of autoantibodies found in APS, along with lupus anticoagulant and anti-β2 glycoprotein I antibodies.
The presence of high levels of anticardiolipin antibodies in the blood can lead to abnormal blood clotting, which can cause serious complications such as deep vein thrombosis, pulmonary embolism, and stroke. Anticardiolipin antibodies can also contribute to pregnancy losses by causing placental insufficiency or abnormal blood clotting in the placenta.
Anticardiolipin antibodies are typically detected through a blood test that measures their levels in the serum. A positive result is usually confirmed with a second test performed at least 12 weeks later to establish persistence. Treatment for anticardiolipin antibody-related disorders typically involves anticoagulation therapy to prevent blood clots and other complications.
Retinal vein occlusion (RVO) is a medical condition that occurs when one of the retinal veins, which drains blood from the retina, becomes blocked by a blood clot or atherosclerotic plaque. This blockage can cause hemorrhages, fluid accumulation, and damage to the retinal tissue, leading to vision loss.
There are two types of RVO: branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). BRVO affects a smaller branch retinal vein, while CRVO affects the main retinal vein. CRVO is generally associated with more severe vision loss than BRVO.
Risk factors for RVO include hypertension, diabetes, high cholesterol levels, smoking, and glaucoma. Age is also a significant risk factor, as RVO becomes more common with increasing age. Treatment options for RVO may include controlling underlying medical conditions, laser therapy, intravitreal injections of anti-VEGF agents or steroids, and surgery in some cases.
Prothrombin is a protein present in blood plasma, and it's also known as coagulation factor II. It plays a crucial role in the coagulation cascade, which is a complex series of reactions that leads to the formation of a blood clot.
When an injury occurs, the coagulation cascade is initiated to prevent excessive blood loss. Prothrombin is converted into its active form, thrombin, by another factor called factor Xa in the presence of calcium ions, phospholipids, and factor Va. Thrombin then catalyzes the conversion of fibrinogen into fibrin, forming a stable clot.
Prothrombin levels can be measured through a blood test, which is often used to diagnose or monitor conditions related to bleeding or coagulation disorders, such as liver disease or vitamin K deficiency.
Blood coagulation, also known as blood clotting, is a complex process that occurs in the body to prevent excessive bleeding when a blood vessel is damaged. This process involves several different proteins and chemical reactions that ultimately lead to the formation of a clot.
The coagulation cascade is initiated when blood comes into contact with tissue factor, which is exposed after damage to the blood vessel wall. This triggers a series of enzymatic reactions that activate clotting factors, leading to the formation of a fibrin clot. Fibrin is a protein that forms a mesh-like structure that traps platelets and red blood cells to form a stable clot.
Once the bleeding has stopped, the coagulation process is regulated and inhibited to prevent excessive clotting. The fibrinolytic system degrades the clot over time, allowing for the restoration of normal blood flow.
Abnormalities in the blood coagulation process can lead to bleeding disorders or thrombotic disorders such as deep vein thrombosis and pulmonary embolism.
Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.
Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.
Protein C inhibitor is a natural anticoagulant protein found in the blood. It plays a crucial role in regulating the coagulation system by controlling the activity of activated protein C, which is a key enzyme that helps to break down clots and prevent excessive bleeding. Protein C inhibitor works by binding to and inhibiting the activity of activated protein C, thereby ensuring that the coagulation process is balanced and that clots are formed only when necessary.
Inherited or acquired deficiencies in protein C inhibitor can lead to an increased risk of thrombosis or abnormal blood clotting, which can cause serious health complications such as deep vein thrombosis (DVT), pulmonary embolism (PE), and disseminated intravascular coagulation (DIC). Therefore, protein C inhibitor is an essential component of the coagulation system and its activity is tightly regulated to maintain normal hemostasis.
Venous thrombosis is a medical condition characterized by the formation of a blood clot (thrombus) in the deep veins, often in the legs (deep vein thrombosis or DVT), but it can also occur in other parts of the body such as the arms, pelvis, or lungs (pulmonary embolism).
The formation of a venous thrombus can be caused by various factors, including injury to the blood vessel wall, changes in blood flow, and alterations in the composition of the blood. These factors can lead to the activation of clotting factors and platelets, which can result in the formation of a clot that blocks the vein.
Symptoms of venous thrombosis may include swelling, pain, warmth, and redness in the affected area. In some cases, the clot can dislodge and travel to other parts of the body, causing potentially life-threatening complications such as pulmonary embolism.
Risk factors for venous thrombosis include advanced age, obesity, smoking, pregnancy, use of hormonal contraceptives or hormone replacement therapy, cancer, recent surgery or trauma, prolonged immobility, and a history of previous venous thromboembolism. Treatment typically involves the use of anticoagulant medications to prevent further clotting and dissolve existing clots.
Thromboembolism is a medical condition that refers to the obstruction of a blood vessel by a thrombus (blood clot) that has formed elsewhere in the body and then been transported by the bloodstream to a narrower vessel, where it becomes lodged. This process can occur in various parts of the body, leading to different types of thromboembolisms:
1. Deep Vein Thrombosis (DVT): A thrombus forms in the deep veins, usually in the legs or pelvis, and then breaks off and travels to the lungs, causing a pulmonary embolism.
2. Pulmonary Embolism (PE): A thrombus formed elsewhere, often in the deep veins of the legs, dislodges and travels to the lungs, blocking one or more pulmonary arteries. This can lead to shortness of breath, chest pain, and potentially life-threatening complications if not treated promptly.
3. Cerebral Embolism: A thrombus formed in another part of the body, such as the heart or carotid artery, dislodges and travels to the brain, causing a stroke or transient ischemic attack (TIA).
4. Arterial Thromboembolism: A thrombus forms in an artery and breaks off, traveling to another part of the body and blocking blood flow to an organ or tissue, leading to potential damage or loss of function. Examples include mesenteric ischemia (intestinal damage due to blocked blood flow) and retinal artery occlusion (vision loss due to blocked blood flow in the eye).
Prevention, early detection, and appropriate treatment are crucial for managing thromboembolism and reducing the risk of severe complications.
A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.
A homozygote is an individual who has inherited the same allele (version of a gene) from both parents and therefore possesses two identical copies of that allele at a specific genetic locus. This can result in either having two dominant alleles (homozygous dominant) or two recessive alleles (homozygous recessive). In contrast, a heterozygote has inherited different alleles from each parent for a particular gene.
The term "homozygote" is used in genetics to describe the genetic makeup of an individual at a specific locus on their chromosomes. Homozygosity can play a significant role in determining an individual's phenotype (observable traits), as having two identical alleles can strengthen the expression of certain characteristics compared to having just one dominant and one recessive allele.
A point mutation is a type of genetic mutation where a single nucleotide base (A, T, C, or G) in DNA is altered, deleted, or substituted with another nucleotide. Point mutations can have various effects on the organism, depending on the location of the mutation and whether it affects the function of any genes. Some point mutations may not have any noticeable effect, while others might lead to changes in the amino acids that make up proteins, potentially causing diseases or altering traits. Point mutations can occur spontaneously due to errors during DNA replication or be inherited from parents.
Mitomycin is an antineoplastic antibiotic derived from Streptomyces caespitosus. It is primarily used in cancer chemotherapy, particularly in the treatment of various carcinomas including gastrointestinal tract malignancies and breast cancer. Mitomycin works by forming cross-links in DNA, thereby inhibiting its replication and transcription, which ultimately leads to cell death.
In addition to its systemic use, mitomycin is also used topically in ophthalmology for the treatment of certain eye conditions such as glaucoma and various ocular surface disorders. The topical application of mitomycin can help reduce scarring and fibrosis by inhibiting the proliferation of fibroblasts.
It's important to note that mitomycin has a narrow therapeutic index, meaning there is only a small range between an effective dose and a toxic one. Therefore, its use should be closely monitored to minimize side effects, which can include myelosuppression, mucositis, alopecia, and potential secondary malignancies.
Microbial drug resistance is a significant medical issue that refers to the ability of microorganisms (such as bacteria, viruses, fungi, or parasites) to withstand or survive exposure to drugs or medications designed to kill them or limit their growth. This phenomenon has become a major global health concern, particularly in the context of bacterial infections, where it is also known as antibiotic resistance.
Drug resistance arises due to genetic changes in microorganisms that enable them to modify or bypass the effects of antimicrobial agents. These genetic alterations can be caused by mutations or the acquisition of resistance genes through horizontal gene transfer. The resistant microbes then replicate and multiply, forming populations that are increasingly difficult to eradicate with conventional treatments.
The consequences of drug-resistant infections include increased morbidity, mortality, healthcare costs, and the potential for widespread outbreaks. Factors contributing to the emergence and spread of microbial drug resistance include the overuse or misuse of antimicrobials, poor infection control practices, and inadequate surveillance systems.
To address this challenge, it is crucial to promote prudent antibiotic use, strengthen infection prevention and control measures, develop new antimicrobial agents, and invest in research to better understand the mechanisms underlying drug resistance.
Bacterial drug resistance is a type of antimicrobial resistance that occurs when bacteria evolve the ability to survive and reproduce in the presence of drugs (such as antibiotics) that would normally kill them or inhibit their growth. This can happen due to various mechanisms, including genetic mutations or the acquisition of resistance genes from other bacteria.
As a result, bacterial infections may become more difficult to treat, requiring higher doses of medication, alternative drugs, or longer treatment courses. In some cases, drug-resistant infections can lead to serious health complications, increased healthcare costs, and higher mortality rates.
Examples of bacterial drug resistance include methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococci (VRE), and multidrug-resistant tuberculosis (MDR-TB). Preventing the spread of bacterial drug resistance is crucial for maintaining effective treatments for infectious diseases.
A phenotype is the physical or biochemical expression of an organism's genes, or the observable traits and characteristics resulting from the interaction of its genetic constitution (genotype) with environmental factors. These characteristics can include appearance, development, behavior, and resistance to disease, among others. Phenotypes can vary widely, even among individuals with identical genotypes, due to differences in environmental influences, gene expression, and genetic interactions.
Thrombomodulin is a protein that is found on the surface of endothelial cells, which line the interior surface of blood vessels. It plays an important role in the regulation of blood coagulation (clotting) and the activation of natural anticoagulant pathways. Thrombomodulin binds to thrombin, a protein involved in blood clotting, and changes its function from promoting coagulation to inhibiting it. This interaction also activates protein C, an important anticoagulant protein, which helps to prevent the excessive formation of blood clots. Thrombomodulin also has anti-inflammatory properties and is involved in the maintenance of the integrity of the endothelial cell lining.
A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.
Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.
Medical Definition:
"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.
Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.
Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.
Pregnancy is a physiological state or condition where a fertilized egg (zygote) successfully implants and grows in the uterus of a woman, leading to the development of an embryo and finally a fetus. This process typically spans approximately 40 weeks, divided into three trimesters, and culminates in childbirth. Throughout this period, numerous hormonal and physical changes occur to support the growing offspring, including uterine enlargement, breast development, and various maternal adaptations to ensure the fetus's optimal growth and well-being.
Blood coagulation factors, also known as clotting factors, are a group of proteins that play a crucial role in the blood coagulation process. They are essential for maintaining hemostasis, which is the body's ability to stop bleeding after injury.
There are 13 known blood coagulation factors, and they are designated by Roman numerals I through XIII. These factors are produced in the liver and are normally present in an inactive form in the blood. When there is an injury to a blood vessel, the coagulation process is initiated, leading to the activation of these factors in a specific order.
The coagulation cascade involves two pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is activated when there is damage to the blood vessel itself, while the extrinsic pathway is activated by tissue factor released from damaged tissues. Both pathways converge at the common pathway, leading to the formation of a fibrin clot.
Blood coagulation factors work together in a complex series of reactions that involve activation, binding, and proteolysis. When one factor is activated, it activates the next factor in the cascade, and so on. This process continues until a stable fibrin clot is formed.
Deficiencies or abnormalities in blood coagulation factors can lead to bleeding disorders such as hemophilia or thrombosis. Hemophilia is a genetic disorder that affects one or more of the coagulation factors, leading to excessive bleeding and difficulty forming clots. Thrombosis, on the other hand, occurs when there is an abnormal formation of blood clots in the blood vessels, which can lead to serious complications such as stroke or pulmonary embolism.
Pulmonary surfactant-associated protein C (SP-C) is a small hydrophobic protein that is a component of pulmonary surfactant. Surfactant is a complex mixture of lipids and proteins that reduces surface tension in the alveoli of the lungs, preventing collapse during expiration and facilitating lung expansion during inspiration. SP-C plays a crucial role in maintaining the structural integrity and stability of the surfactant film at the air-liquid interface of the alveoli.
Deficiency or dysfunction of SP-C has been associated with several pulmonary diseases, including respiratory distress syndrome (RDS) in premature infants, interstitial lung diseases (ILDs), and pulmonary fibrosis. Mutations in the gene encoding SP-C (SFTPC) can lead to abnormal protein processing and accumulation, resulting in lung injury and inflammation, ultimately contributing to the development of these conditions.
"Multiple drug resistance" (MDR) is a term used in medicine to describe the condition where a patient's infection becomes resistant to multiple antimicrobial drugs. This means that the bacteria, virus, fungus or parasite that is causing the infection has developed the ability to survive and multiply despite being exposed to medications that were originally designed to kill or inhibit its growth.
In particular, MDR occurs when an organism becomes resistant to at least one drug in three or more antimicrobial categories. This can happen due to genetic changes in the microorganism that allow it to survive in the presence of these drugs. The development of MDR is a significant concern for public health because it limits treatment options and can make infections harder, if not impossible, to treat.
MDR can develop through several mechanisms, including mutations in the genes that encode drug targets or enzymes involved in drug metabolism, as well as the acquisition of genetic elements such as plasmids and transposons that carry resistance genes. The overuse and misuse of antimicrobial drugs are major drivers of MDR, as they create selective pressure for the emergence and spread of resistant strains.
MDR infections can occur in various settings, including hospitals, long-term care facilities, and communities. They can affect people of all ages and backgrounds, although certain populations may be at higher risk, such as those with weakened immune systems or chronic medical conditions. Preventing the spread of MDR requires a multifaceted approach that includes surveillance, infection control, antimicrobial stewardship, and research into new therapies and diagnostics.
Disease resistance, in a medical context, refers to the inherent or acquired ability of an organism to withstand or limit infection by a pathogen, such as bacteria, viruses, fungi, or parasites. This resistance can be due to various factors including the presence of physical barriers (e.g., intact skin), chemical barriers (e.g., stomach acid), and immune responses that recognize and eliminate the pathogen.
Inherited disease resistance is often determined by genetics, where certain genetic variations can make an individual more or less susceptible to a particular infection. For example, some people are naturally resistant to certain diseases due to genetic factors that prevent the pathogen from infecting their cells or replicating within them.
Acquired disease resistance can occur through exposure to a pathogen, which triggers an immune response that confers immunity or resistance to future infections by the same pathogen. This is the basis of vaccination, where a weakened or dead form of a pathogen is introduced into the body to stimulate an immune response without causing disease.
Overall, disease resistance is an important factor in maintaining health and preventing the spread of infectious diseases.
Activated protein C resistance
Activated protein C resistance test
Factor V Leiden
SREBP cleavage-activating protein
Protein C
Acroangiodermatitis
MAPK4
Protein inhibitor of activated STAT
Pathogenesis-related protein
Prothrombinase
Björn Dahlbäck
Protein kinase R
Ceramide
Thrombophilia
Calibrated automated thrombogram
Transforming protein RhoA
Cabozantinib
Antineoplastic resistance
Ethylene signaling pathway
Tuberous sclerosis complex tumor suppressors
Warfarin necrosis
De novo synthesis
Ceramide-activated protein phosphatase
Mixed-phenotype acute leukemia
Tetracycline-controlled transcriptional activation
Lipoarabinomannan
Michael Stuart Brown
GNA12
Acanthosis nigricans
Mechanosensitive channels
Activated protein C resistance - Wikipedia
Activated Protein C Resistance (Factor V Leiden) Assay: Reference Range, Interpretation, Collection and Panels
The prevalence of poor anticoagulant response to activated protein C (APC resistance) among patients suffering from stroke or...
Rat Activated protein C resistance ELISA kit, AMS.E02A0843 | AMSBIO
ACTIVATED PROTEIN C RESISTANCE UNIVERSITY | Biochemistry
activated protein C resistance ratio assay | Taber's Medical Dictionary
Protein arginine methyltransferase 1 may be involved in pregnane x receptor-activated overexpression of multidrug resistance 1...
Activated Protein C Resistance (Factor V Leiden) Assay: Reference Range, Interpretation, Collection and Panels
Activated Protein C Resistance (Factor V Leiden) Assay: Reference Range, Interpretation, Collection and Panels
Factor V Resistance to Activated Protein C (APC) - Hematology and Oncology - MSD Manual Professional Edition
Frontiers | Identification of broadly-conserved parasitic nematode proteins that activate immunity
Salicylic acid in the machinery of hypersensitive cell death and disease resistance | SpringerLink
Neurologic Disease and Pregnancy: Overview, General Considerations, New-Onset Neurologic Complications
Increased Prevalence of Activated Protein C Resistance During Pregnancy may Implicate Venous Thrombo Embolic Disorders as a...
Increased resistance to activated protein C after short-term oral hormone replacement therapy in healthy post-menopausal women<...
Factor V Leiden thrombophilia: MedlinePlus Genetics
Neurologic Disease and Pregnancy: Overview, General Considerations, New-Onset Neurologic Complications
Clostridium septicum α-toxin activates the NLRP3 inflammasome by engaging GPI-anchored proteins - French National ANTIBIOTIC...
Hemlibra (Emicizumab-Kxwh Injection, for Subcutaneous Use): Uses, Dosage, Side Effects, Interactions, Warning
Michael Kalafatis | Cleveland State University
PDF) The Time Course for Elevated Muscle Protein Synthesis Following Heavy Resistance Exercise
Investigating the Enteroenteric Recirculation of Apixaban, a Factor Xa Inhibitor: Administration of Activated Charcoal to Bile...
Hypercoagulable Disorders
Adenine Inhibits the Growth of Colon Cancer Cells via AMP-Activated Protein Kinase Mediated Autophagy
The Emerging Portrait of Glial Cell Line-derived Neurotrophic Factor Family Receptor Alpha (GFRα) in Cancers
Retinal vein occlusion - Symptoms, diagnosis and treatment | BMJ Best Practice US
Specimen Collection Guides and Resources - Meadville Medical Center
Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance | Nature
Classifications for Combined Hormonal Contraceptives | CDC
Mitogen-activa5
- NF-E2- related factor-2(Nrf-2), as well as mitogen-activated protein kinase (MAPK), is regulated by SFN. (nih.gov)
- This study is to investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in tert -butyl hydroperoxide ( t BHP)-induced apoptosis of human trabecular meshwork (iHTM) cells. (molvis.org)
- One treatment targets the mitogen-activated protein kinase cancer pathway that sustains the growth of many types of cancer. (uclahealth.org)
- The anti-inflammatory effects of SHE treatment involved blocking of the mitogen-activated protein kinase and signal transducer and activator of transcription 1 signaling pathways. (researchgate.net)
- Genes within the Mitogen Activated Protein Kinase (MAPK) pathway are frequently mutated driver oncogenes in cancer. (ladydavis.ca)
Kinase9
- Rapid and transient activation of myelin basic protein kinase in tobacco leaves treated with hairpin from Erwinia amylovora . (springer.com)
- The data showed that adenine activated AMP-activated protein kinase (AMPK) signaling contributing to autophagic cell death through mTOR in both colon cancer cell lines. (hindawi.com)
- Involvement of AMP-activated protein kinase (AMPK) in anticancer property of adenine was also investigated. (hindawi.com)
- Glutamate excitation induced a rapid alteration in the AMP:ATP ratio that was associated with the activation of the AMP-activated protein kinase (AMPK). (jneurosci.org)
- Notably, inhibition of the CaMKK (calmodulin-dependent protein kinase kinase) had little affect on GLUT translocation, whereas the inhibition or knockdown of AMPK (compound C, siRNA) activity prevented GLUT3 translocation to the cell surface after glutamate excitation. (jneurosci.org)
- This gene encodes a member of the protein kinase C (PKC) family of serine/threonine protein kinases. (nih.gov)
- This protein kinase is calcium-independent and phospholipid-dependent. (nih.gov)
- This kinase is found to be necessary for BCL-ABL-mediated resistance to drug-induced apoptosis and therefore protects leukemia cells against drug-induced apoptosis. (nih.gov)
- A: The most unexpected and promising finding is that activation of AMP-activated protein kinase (AMPK), major bioenergetic sensor and metabolic regulator, effectively reversed the maladaptive phenotype of lung fibroblasts. (uab.edu)
Misfolded proteins in the endoplasmic reticulum1
- MAPK8 (JNK1) is activated by the presence of misfolded proteins in the endoplasmic reticulum. (thermofisher.com)
AMPK1
- AMPK pathways inhibit biosynthetic pathways with energy consumption, such as protein, fatty acid and glycogen synthesis. (springer.com)
Anti-apoptotic proteins4
- Anti-apoptotic proteins such as BCL-2 counteract BAX-mediated cell death. (nature.com)
- Although an interaction site that confers survival functionality has been defined for anti-apoptotic proteins, an activation site has not been identified for BAX, rendering its explicit trigger mechanism unknown. (nature.com)
- Here we demonstrate by NMR analysis that BIM SAHB binds BAX at an interaction site that is distinct from the canonical binding groove characterized for anti-apoptotic proteins. (nature.com)
- In conclusion, it appears that apoptotic signaling contributes to training-induced hypertrophy in skeletal muscle of young animals, by down regulation of pro- and up regulation of anti-apoptotic proteins. (cdc.gov)
Apoptosis3
- However, one pitfall observed throughout the years in in vitro and in in a multitude of human trials in vivo , is the resistance of cancer cell lines to hTRAIL-induced apoptosis. (csuohio.edu)
- Akt pathways have effects on apoptosis, protein synthesis, metabolism and cell cycle. (springer.com)
- We also provided new mechanistic insights to myofibroblast maladaptive reprogramming associated with defective autophagy and ECM turnover, as well as mitochondrial dysfunction linked to myofibroblast resistance to apoptosis. (uab.edu)
Assay9
- The APCR assay uses snake venoms to activate factor V and prothrombin, thus triggering the lower portion of the clotting pathway and eliminating interference by factor VIII and by lupus anticoagulants (in the absence of phospholipid complexes). (medscape.com)
- Although the APCR assay is no longer based directly on the activated partial thromboplastin time (aPTT), it is expressed as a ratio of aPTT with APC:aPTT without APC. (medscape.com)
- A poor anticoagulant response to activated protein C (APC) in an activated partial thromboplastin time (aPTT) assay (APC resistance) was recently reported to be a cause of familial thrombophilia. (nih.gov)
- 0.0001) between the results of this functional protein S assay and APC resistance (represented by the ratio (Rs value) of clotting time with and without addition of activated protein C) was observed. (nih.gov)
- Assessment of protein S activity with a second protein S clotting assay using factor Va as substrate confirmed only 47% of the decreased levels of the thromboplastin-based protein S clotting assay. (nih.gov)
- Nursing Central , nursing.unboundmedicine.com/nursingcentral/view/Tabers-Dictionary/775507/all/activated_protein_C_resistance_ratio_assay. (unboundmedicine.com)
- The activated protein C resistance assay is a screening test for the presence of factor V Leiden. (msdmanuals.com)
- Antinuclear antithrombin, protein C, protein S or pres- antibodies were investigated with standard- ence of antiphospholipid antibodies, are ized enzyme-linked immunosorbent assay common in patients with retinal vein occlu- sions and may contribute to the etiology of (ELISA). (who.int)
- Thrombosis may also result if factor V is normal but there is deficiency of Protein C or Protein S or there is abnormal Protein C. The APCR assay is not completely specific for factor V Leiden as it may be positive in any condition that affects the activity of APC. (ndtv.com)
MAPK1
- It belongs to the MAPK superfamily of stress-activated protein kinases. (thermofisher.com)
Insulin resistance7
- Thus, cytohesin inhibition results in hepatic insulin resistance. (nature.com)
- Because insulin resistance is among the earliest pathological changes in type 2 diabetes, our results show the potential of chemical biology for dissecting the molecular pathogenesis of this disease. (nature.com)
- Impaired cytohesin function results in hepatic insulin resistance. (nature.com)
- Polycystic ovary syndrome (PCOS) is a heterogeneous familial disorder characterized by insulin resistance and an increased risk of type 2 diabetes mellitus (T2DM), a disorder with epidemic public health significance. (pitt.edu)
- Generalized linear modeling was utilized to test for association of genotype with subclinical measures of CHD, including insulin resistance (HOMA-IR) and C-reactive protein (CRP). (pitt.edu)
- In conclusion, the significant risk of T2DM attributed to women by PCOS was not explained by genetic SNPs analyzed here, however, a significant association of G972R and G972RxPCOS interaction with CRP concentrations was found, further supporting the growing body of evidence of associations between insulin resistance and systemic inflammation. (pitt.edu)
- It is also a crucial mediator of insulin resistance and obesity. (thermofisher.com)
Thrombin6
- APC resistance is the inability of protein C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. (wikipedia.org)
- There are two types of APC resistance tests with different properties: the activated partial thromboplastin (aPTT)-based test and the endogenous thrombin potential (ETP)-based test. (wikipedia.org)
- Activated protein C (APC) is the enzymatically active form of protein C after proteolytic cleavage by thrombomodulin-bound thrombin. (medscape.com)
- Normalized activated protein C sensitivity ratios (nAPCsr) were determined by quantifying the effect of activated protein C on the endogenous thrombin potential. (amsterdamumc.org)
- The heparin-antithrombin complex then inactivates thrombin, activated factor X (fXa), and other activated clotting factors. (acponline.org)
- Protein C inhibits thrombin generation by changing into its active form, activated protein C (APC). (ndtv.com)
Recombinant Proteins1
- A cocktail of five recombinant proteins optimized for conserved GI nematode targets was used immunize pigs and test for active antibody responses in both the serum and intestinal ileal fluid of immunized pigs. (frontiersin.org)
APTT1
- This patient's clinical presentation is consistent with heparin resistance, which occurs when the activated partial thromboplastin time (aPTT) does not increase into the therapeutic range despite increasing doses of heparin or when unusually high doses of heparin are required to achieve a therapeutic aPTT. (acponline.org)
Gene13
- Protein arginine methyltransferase 1 may be involved in pregnane x receptor-activated overexpression of multidrug resistance 1 gene during acquired multidrug. (oncotarget.com)
- Pregnane x receptor (PXR) - activated overexpression of the multidrug resistance 1 (MDR1) gene is an important way for tumor cells to acquire drug resistance. (oncotarget.com)
- PRMT1 may be an important co-activator of PXR in activating MDR1 gene during acquired resistance, and PRMT1 inhibitor combined with chemotherapy drugs may be a new strategy for overcoming tumor MDR. (oncotarget.com)
- The F5 gene provides instructions for making a protein called coagulation factor V. This protein plays a critical role in the coagulation system, which is a series of chemical reactions that forms blood clots in response to injury. (medlineplus.gov)
- The culprit in the colon cancer treatment examined in the Nature paper is the KRAS gene, which is responsible for producing a protein to regulate cell division. (sciencedaily.com)
- When activated, the gene helps cancer cells develop resistance to targeted-therapy drugs, effectively making the treatment useless. (sciencedaily.com)
- To better understand what role the KRAS gene plays in drug resistance, a team of researchers led by Bert Vogelstein, the Clayton Professor of Oncology and Pathology at the Johns Hopkins Kimmel Cancer Center, launched a study that began by testing patients to determine if the KRAS gene was activated in their tumors. (sciencedaily.com)
- Patients without an activated KRAS gene underwent a normal round of targeted therapy treatment, and the initial results -- as expected -- were successful. (sciencedaily.com)
- Tests performed after the treatment broke down, however, showed a surprising result: The KRAS gene had been activated. (sciencedaily.com)
- In particular, acquisition of macrophage tropism for a serotype 2 FCoV has previously been mapped to the spike gene ( 16 ), further suggesting that key mutations within spike protein may be important for the biotype switch. (cdc.gov)
- This gene product is a bZIP protein, which was also identified as a cellular transcription factor that binds to an enhancer in the promoter of the T cell leukemia virus type 1 promoter. (cancerindex.org)
- It has been found that upon accumulation of unfolded proteins in the endoplasmic reticulum (ER), the mRNA of this gene is processed to an active form by an unconventional splicing mechanism that is mediated by the endonuclease inositol-requiring enzyme 1 (IRE1). (cancerindex.org)
- What does this gene/protein do? (cancerindex.org)
Pathways5
- Both pathways involve a number of plasma proteins as listed in Table 1. (apcresistance.com)
- The experimental approaches involve integrating apixaban elimination pathways with pharmacokinetic profiles obtained from bile duct-cannulated (BDC) rats and dogs receiving i.v. doses together with oral administration of activated charcoal (AC). (aspetjournals.org)
- NF-κB pathways can be mainly activated by two pathways. (springer.com)
- Here, we investigated the signaling pathways activated in response to the energetic stress created by transient glutamate excitation in cerebellar granule neurons. (jneurosci.org)
- JNK pathways are activated by stress and inflammatory signals. (thermofisher.com)
Prothrombin3
- Several proteins, including factors II (prothrombin), VII, IX and X, protein C and protein S, are subjected to vitamin K-dependent g-carboxylation of glutamic acid residues during their synthesis in the liver. (apcresistance.com)
- 100 U/kg/24 hours of activated prothrombin complex concentrate was administered for 24 hours or more to patients receiving HEMLIBRA prophylaxis . (rxlist.com)
- For instance, factor V Leiden mutation (resistance to activated protein C [APC]) and the prothrombin G20210A mutation (increased prothrombin activity) are more prevalent in white populations. (medscape.com)
Deficiency4
- However, people with homozygous factor V Leiden, and people with heterozygous factor V Leiden who have an additional thrombophilic condition (e.g., antithrombin deficiency, protein C deficiency, or protein S deficiency), should be considered for lifelong oral anticoagulation therapy. (wikipedia.org)
- Pupura fulminas is the result of severe (homozygous) Protein C or Protein S deficiency causing massive thromboembolic complications (a form disseminated intravascular coagulation) in newborns shortly after birth. (labtestsonline.org.uk)
- Diagnose antithrombin deficiency as a cause of heparin resistance. (acponline.org)
- There may also be coexistent Protein C deficiency along with factor V Leiden. (ndtv.com)
Factor V Leiden2
- The most common cause of hereditary APC resistance is factor V Leiden mutation. (wikipedia.org)
- If an individual has the factor V Leiden mutation, there is a change in the structure of factor V and APC/Protein S can no longer inactivate it. (ndtv.com)
Drug Resistance4
- A Harvard researcher studying the evolution of drug resistance in cancer says that, in a few decades, "many, many cancers could be manageable. (sciencedaily.com)
- Analyzing the clinical results, Allen and Bozic were able to mathematically describe the exponential growth of the cancer and determine whether the mutation that led to drug resistance was pre-existing, or whether it occurred after treatment began. (sciencedaily.com)
- In 1995 he participated in a study, also published in Nature, that focused on the rapid evolution of drug resistance in HIV. (sciencedaily.com)
- Nevertheless, BC might acquire drug resistance and sometimes relapse. (wjgnet.com)
Kinases2
- Mitogen-activated protein kinases (MAPKs) comprise a large family of proteins activated by a wide range of proinflammatory cytokines and environmental stress. (molvis.org)
- MAPKs are Serine-threonine protein kinases that are activated in response to a variety of extracellular stimuli, and mediate signal transduction from the cell surface to the nucleus. (thermofisher.com)
Genes3
- Interferons (IFNs) are secreted cytokines with the ability to activate expression of IFN stimulated genes that increase resistance of cells to virus infections. (lu.se)
- These loci include genes encoding phage shock proteins, tellurite resistance related proteins, signal peptide peptidase, and proteins that synthesize and modify teichoic acids. (cornell.edu)
- My work has made substantial progress on defining the resistance mechanisms associated with these genes. (cornell.edu)
Ratio3
- The normal reference value for the activated protein C resistance (APCR) ratio is greater than 2.1. (medscape.com)
- 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)
- His reports says: APCR ratio (Activated protein C resistance) is 0.95 L and a normal person should have anywhere between 1.67- 3.75. (ndtv.com)
Immunity3
- Screening the array with sera and ileal fluid samples from immunized pigs suggested cross-reactivity among homologous proteins and a general activation of immunity. (frontiersin.org)
- Proteins that activated immunity are potential antigens for immunization and the multi-omics phylum-spanning prioritization database that was created is a valuable resource for identifying target proteins in a wide array of different parasitic nematodes. (frontiersin.org)
- The IRE1 endoplasmic reticulum stress sensor activates natural killer cell immunity in part by regulating c-Myc. (cancerindex.org)
Anticoagulant2
- People with APC resistance and initial DVT are treated with a standard anticoagulant regimen, for instance intravenous heparin therapy followed by oral anticoagulation. (wikipedia.org)
- The condition APC resistance is a resistance to the anticoagulant function of APC, which promotes clotting of blood in the blood vessels (thrombosis). (ndtv.com)
Expression8
- Hydrogen peroxide does not function downstream of salicylic acid in the induction of PR protein expression. (springer.com)
- A mutation in Arabidopsis that leads to constitutive expression of systemic acquired resistance. (springer.com)
- Levels of phosphorylation and protein expression were determined using western blotting. (hindawi.com)
- It may increase expression of viral proteins by acting as the DNA binding partner of a viral transactivator. (cancerindex.org)
- Scope includes mutations and abnormal protein expression. (cancerindex.org)
- Ma DD , 2007 , 'Expression of Neurofilament Proteins in Adult Bone Marrow Mesenchymal Stem Cells and Embryonic Stem Cells and Their Clinical Potential' , in Davenport LP (ed. (edu.au)
- Unexpectedly, 8-oxoguanine DNA glycosylase1 (Ogg1) knockout mice show enhanced stimuli-driven IFN expression that confers increased resistance to viral and bacterial infections and allergen challenges. (lu.se)
- Here, we tested the hypothesis that the DNA repair protein OGG1 recognizes 8-oxoguanine (8-oxoGua) in promoters modulating IFN expression. (lu.se)
Mutation1
- The most common cause of APC resistance (APCR) is a genetic mutation referred to as factor V Leiden. (ndtv.com)
Receptor3
- When GFLs bind with GFRα, they form complexes and associate with the RET receptor, subsequently activating downstream signaling. (medsci.org)
- Genetic variants analyzed for association with PCOS and subclinical coronary heart disease (CHD) risk measures were the peroxisome proliferator-activated receptor-gamma (PPAR-gamma) single nucleotide polymorphism (SNP) P12A, insulin receptor substrate-1 (IRS-1) SNP G972R, one novel SNP of lipoprotein lipase (LPL), and three novel SNPs from acetyl-CoA carboxylase-beta (ACC-beta). (pitt.edu)
- Because FCoV spike protein plays critical roles in receptor binding (S1) and fusion (S2), we focused on structural changes in this protein and potential role in altered cellular tropism. (cdc.gov)
Amino acid1
- This unique amino acid modification allows the proteins to bind calcium ions necessary for phospholipid binding and thereby to participate efficiently in multimolecular complexes in the coagulation cascade. (apcresistance.com)
Platelets5
- Within seconds of injury the damaged vessel contracts and circulating, disc-shaped cell components called thrombocytes or platelets are activated and start to adhere to the site of injury. (apcresistance.com)
- The activated platelets then aggregate to form a loose plug that reduces or temporarily stops the bleeding. (apcresistance.com)
- The activated platelets also release a large number of molecules that accelerate platelet plug formation and begin the process of wound healing. (apcresistance.com)
- This major biochemical process takes place at the surface of negatively charged phospholipid membranes provided by activated platelets and damaged cells. (apcresistance.com)
- The blood clotting system of the body comprises multiple plasma proteins that interact with platelets (a type of blood cells) to promote physiological coagulation. (ndtv.com)
Mutations1
- Mutations of factor V make it resistant to its normal cleavage and inactivation by activated protein C, and they also predispose to venous thrombosis. (msdmanuals.com)
Plasma3
- 19 Tissue factor forms a complex with factor VII, which becomes activated and then activates factors IX and X. The intrinsic pathway is initiated by the exposure of 'contact' factors in plasma (i.e. factor XII, HMW kininogen and prekallikrein) to a negatively charged surface, such as connective tissue in vivo or glass in a test tube. (apcresistance.com)
- Activated protein C is added to a 5-fold dilution of patient plasma, and the coagulation time is measured. (msdmanuals.com)
- It is life-threatening causing tissue death (necrosis) and bleeding under the skin and other organs, without treatment with Protein C concentrate or fresh frozen plasma. (labtestsonline.org.uk)
Venous3
- An estimated 64 percent of patients with venous thromboembolism may have APC resistance. (wikipedia.org)
- As hormone replacement therapy is associated with an early excess risk of venous thrombosis, we investigated the effect of different oral hormone replacement therapies on resistance to activated protein C, and on levels of factor VIII antigen (FVIII:Ag) and factor XI antigen (FXI:Ag). (amsterdamumc.org)
- Antiphospholipid antibodies are acquired autoantibodies against phospholipids and phospholipid-binding proteins, such as cardiolipin and β 2 -glycoprotein I. In vitro, they can prolong clotting tests, but in vivo, they increase the risk of venous and arterial thrombosis. (acponline.org)
Regulatory2
- In normal haemostasis once the body has activated the clotting process, there are regulatory feedback mechanisms , which limit and control the clotting process (natural anticoagulants), prevent the complete blocking of the vessel by excessive clot formation and by removal of the fibrin clot once the injury has healed (fibrinolysis). (labtestsonline.org.uk)
- G proteins are an important class of regulatory switches in all living systems. (nature.com)
Apoptotic7
- BAX is a pro-apoptotic protein of the BCL-2 family that is stationed in the cytosol until activated by a diversity of stress stimuli to induce cell death. (nature.com)
- Huang, D. C. & Strasser, A. BH3-only proteins-essential initiators of apoptotic cell death. (nature.com)
- Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. (nature.com)
- Resistance training-induced apoptotic signaling in rat skeletal muscle. (cdc.gov)
- Therefore, this s tudy investigated the effect of resistance training with stretch-shortening contractions on apoptotic markers in young rat skeletal muscle. (cdc.gov)
- The anit-apoptotic Bcl2 protein level was significantly (p=0.033) increased by 28.7%, while the proapoptotic Bax protein content remained unchanged in experimental compared to control muslces after the training period. (cdc.gov)
- Additionally, the level of pro-apoptotic AIF protein, which is thought to play a role in caspase independent signaling, was significantly decreased (p=0.046) by 51.7% in experimental as compared to control muscles. (cdc.gov)
Tumors1
- Here, we demonstrate that the endoplasmic reticulum stress sensor inositol-requiring enzyme 1 (IRE1α) and its substrate transcription factor X-box-binding protein 1 (XBP1) drive NK cell responses against viral infection and tumors in vivo. (cancerindex.org)
Coagulation factors2
- 17-18 The current scheme as seen in figure 4, involves a series of proteolytic reactions, in which inactive coagulation factors in a precursor or zymogen form are activated by one or more cleavages. (apcresistance.com)
- During the cascade process, the body sequentially activates coagulation factors , which are proteins that create a net of fibrin threads, which weave them through the platelet plug making a stable firm fibrin blood clot, whilst still allowing blood to flow through the damage vessel. (labtestsonline.org.uk)
Cells5
- We are a global provider of human and animal biospecimens: including frozen & FFPE tissue, DNA, RNA, total proteins, blood products and primary cells. (amsbio.com)
- Those results suggest that PRMT1 may be involved in PXR-activated overexpression of MDR1 in resistant breast cancer cells, and AMI-1 may suppress MDR1 by disrupting the interaction between PRMT1 and PXR. (oncotarget.com)
- This suggested that overexpression of Nrf-2 resulted in enhanced resistance of cancer cells to chemotherapeutic agents. (nih.gov)
- IRE1α-XBP1 were essential for expansion of activated mouse and human NK cells and are situated downstream of the mammalian target of rapamycin signaling pathway. (cancerindex.org)
- By understanding the genomic instability mechanisms behind early seeds of resistance, we hope to develop new therapies that can stop cancer cells from becoming resistant and reduce the need for additional treatments to control the cancer. (uclahealth.org)
Cellular2
- Adenine forms several biological compounds involved in a variety of cellular physiological processes such as adenosine triphosphate (ATP) in cellular respiration and deoxyribonucleic acid (DNA) in protein synthesis. (hindawi.com)
- The coronavirus spike protein is a class I fusion protein, which typically requires activation by cellular proteases. (cdc.gov)
Heterozygous2
- Asymptomatic individuals with APC resistance (e.g., heterozygous factor V Leiden) are not normally treated unless additional risk factors for thrombosis are also present. (wikipedia.org)
- In patients with homozygous or heterozygous factor V Leiden resistance , the prolongation of the clotting time is significantly reduced because their factor V is resistant to cleavage by activated protein C. (msdmanuals.com)
Regulation1
- It is regulated so that clots don't form too easily or too quickly and this regulation of factor V is done by APC and another substance called Protein S. Activated protein C combines with Protein S to inactivate factor V so that clotting stops. (ndtv.com)
BIOCHEMISTRY2
- My laboratory has a great deal of expertise in the biochemistry of coagulation and especially in the biochemistry of proteins composing prothrombinase. (csuohio.edu)
- Thèse de Doctorat de l'Université Paris VI en Biochimie ( Ph.D. University of Paris in Biochemistry) 1989. (csuohio.edu)
Form complexes1
- Several of the activated coagulation proteases form complexes with their specific cofactors on the phospholipid surface, amplifying their activation of subsequent zymogens. (apcresistance.com)
Overexpression1
- In the present study, we aimed to investigate whether protein arginine methyl transferase 1(PRMT1) is involved in PXR - activated overexpression of MDR1 during acquired multidrug resistant. (oncotarget.com)
Spontaneous1
- Spontaneous central vein thrombosis in a patient with activated protein C resistance and dengue infection: An association or causation? (medscape.com)
Degradation1
- This results in resistance to degradation of the activated factor V, thus promoting clotting. (ndtv.com)
Accumulation1
- both events are implicated in accumulation of activated myofibroblasts during persistent fibrosis. (uab.edu)
Mechanisms4
- If the clotting process activates inappropriately, or feedback mechanisms fail to work effectively to limit formation or removal of fibrin clot, then there can be inappropriate and/or excessive blood clot formation. (labtestsonline.org.uk)
- The second project focuses on ECF factor-mediated lantibiotic resistance mechanisms in B. subtilis. (cornell.edu)
- This trial is actively enrolling and includes a number of correlative endpoints, which will allow the identification molecular mechanisms of therapeutic resistance. (ladydavis.ca)
- We use highly robust pre-clinical in vitro and in vivo mouse models of NRAS and nonV600 BRAF mutated cancers to investigate the molecular mechanisms of therapeutic response and resistance. (ladydavis.ca)
APCR3
- Activated protein C resistance (APCR) is a hypercoagulability (an increased tendency of the blood to clot) characterized by a lack of a response to activated protein C (APC), which normally helps prevent blood from clotting excessively. (wikipedia.org)
- APC resistance (APCR) is a hypercoagulability disorder in which factor V cannot be inactivated by APC. (medscape.com)
- In other words, factor V Leiden is characterised by APC resistance but not all APCR is caused by factor V Leiden. (ndtv.com)
Transcription1
- Activated transcription factors in conjunction with chromatin remodelers induce epigenetic changes that reprogram IFN responses. (lu.se)
Tumor2
- Importantly, increasing numbers of novel reports suggest that the GFRα-mediated signaling pathway acts as an oncogenic promoter related to tumor proliferation, invasion, and metastasis as well as treatment resistance. (medsci.org)
- The role of BCSCs in cancer formation, growth, invasiveness, therapy resistance and tumor recurrence is becoming increasingly clear. (wjgnet.com)
Patients3
- Nine out of 14 patients (64%) with poor APC response showed protein S activities below the normal range. (nih.gov)
- However, after initial responses, about 20%-40% of patients experience a relapse as the cancer develops resistance to the therapies. (uclahealth.org)
- Two patients with antiphospholipid antibodies associated with resistance to activated protein C had unfavourable outcomes. (who.int)
Degrades1
- APC (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. (wikipedia.org)
MRNA1
- The mRNA and protein levels of MDR1 were detected by real-time PCR and western blotting analysis. (oncotarget.com)