Fibrin Fibrinogen Degradation Products
Fibrin
Fibrinogen
Disseminated Intravascular Coagulation
Plasminogen
Fibrinolysin
Phlebitis
Blood Coagulation
Urokinase-Type Plasminogen Activator
Fibrin Tissue Adhesive
Disease Notification
Public Health
Population Surveillance
Trichomonas
Communicable Diseases
Fibrinolytic activation markers predict myocardial infarction in the elderly. The Cardiovascular Health Study. (1/870)
Coagulation factor levels predict arterial thrombosis in epidemiological studies, but studies of older persons are needed. We studied 3 plasma antigenic markers of fibrinolysis, viz, plasminogen activator inhibitor-1 (PAI-1), fibrin fragment D-dimer, and plasmin-antiplasmin complex (PAP) for the prediction of arterial thrombosis in healthy elderly persons over age 65. The study was a nested case-control study in the Cardiovascular Health Study cohort of 5201 men and women >/=65 years of age who were enrolled from 1989 to 1990. Cases were 146 participants without baseline clinical vascular disease who developed myocardial infarction, angina, or coronary death during a follow-up of 2.4 years. Controls remained free of cardiovascular events and were matched 1:1 to cases with respect to sex, duration of follow-up, and baseline subclinical vascular disease status. With increasing quartile of D-dimer and PAP levels but not of PAI-1, there was an independent increased risk of myocardial infarction or coronary death, but not of angina. The relative risk for D-dimer above versus below the median value (>/=120 microg/L) was 2.5 (95% confidence interval, 1.1 to 5.9) and for PAP above the median (>/=5.25 nmol/L), 3.1 (1.3 to 7.7). Risks were independent of C-reactive protein and fibrinogen concentrations. There were no differences in risk by sex or presence of baseline subclinical disease. D-dimer and PAP, but not PAI-1, predicted future myocardial infarction in men and women over age 65. Relationships were independent of other risk factors, including inflammation markers. Results indicate a major role for these markers in identifying a high risk of arterial disease in this age group. (+info)Purification and characterization of a serine protease with fibrinolytic activity from Tenodera sinensis (praying mantis). (2/870)
Mantis egg fibrolase (MEF) was purified from the egg cases of Tenodera sinensis using ammonium sulfate fractionation, gel filtration on Bio-Gel P-60 and affinity chromatography on DEAE Affi-Gel blue gel. The protease was assessed homogeneous by SDS-polyacrylamide gel electrophoresis and has a molecular mass of 31500 Da. An isoelectric point of 6.1 was determined by isoelectric focusing. Amino acid sequencing of the N-terminal region established a primary structure composed of Ala-Asp-Val-Val-Gln-Gly-Asp-Ala-Pro-Ser. MEF readily digested the Aalpha- and Bbeta-chains of fibrinogen and more slowly the gamma-chain. The nonspecific action of the enzyme results in extensive hydrolysis of fibrinogen and fibrin releasing a variety of fibrinopeptide. The enzyme is inactivated by Cu2+ and Zn2+ and inhibited by PMSF and chymostatin, yet elastinal, aprotinin, TLCK, TPCK, EDTA, EGTA, cysteine, beta-mercaptoethanol, iodoacetate, E64, benzamidine and soybean trypsin inhibitor do not affect activity. Antiplasmin was not sensitive to MEF but antithrombin III inhibited the enzymatic activity of MEF. Among chromogenic protease substrates, the most sensitive to MEF hydrolysis was benzoyl-Phe-Val-Arg-p-nitroanilide with maximal activity at pH 7.0 and 30 degrees C. MEF preferentially cleaved the oxidized B-chain of insulin between Leu15 and Tyr16. D-Dimer concentrations increased on incubation of cross-linked fibrin with MEF, indicating the enzyme has a strong fibrinolytic activity. (+info)A novel high molecular weight fibrinogenase from the venom of Bitis arietans. (3/870)
A fibrinogenase (Ba100) with an apparent molecular mass of 100 kDa under non-reducing conditions and a pI of 5.4 was purified from the venom of the African puff adder (Bitis arietans) by fibrinogen affinity chromatography. Under reducing conditions the protease dissociates into subunits of 21 kDa and 16 kDa. N-Terminal amino acid sequencing showed these two chains to have 66.7% homology and homology to C-type lectins. The fibrinogenase activity of Ba100 cleaves the Aalpha and Bbeta chain of fibrinogen rendering the molecule unable to polymerise into fibrin clots. Ba100 inhibited platelet aggregation in platelet rich plasma, and clot formation in whole blood, in a concentration dependent manner. (+info)Fragment E derived from both fibrin and fibrinogen stimulates interleukin-6 production in rat peritoneal macrophages. (4/870)
Fibrin derived from fibrinogen after thrombin cleavage plays an essential role in forming blood clots. Fibrin as well as fibrinogen is also involved in the induction of platelet aggregation, leukocyte cell adhesion and phagocytosis. An additional biological role of fibrin and fibrinogen is presented in this study. One of the proteolytic peptides of fibrin/fibrinogen, fragment E, and not fragment D, was able to stimulate rat peritoneal macrophages to express interleukin-6 (IL-6). The stimulation of fibrin/fibrinogen fragment E on macrophages appeared to work in a dose- and time-dependent manner. Adherent fibrin fragment E was able to stimulate IL-6 expression as well as IL-6 protein production. The effect of fibrin fragment E was inhibited by the addition of an excess amount of GPRP tetrapeptide, but not by GHRP, which are the amino acids derived from the amino terminus of fibrin alpha and beta chains, respectively. These results suggest that fibrin as well as fibrinogen function as a stimulator to macrophages, and leukocyte integrin p150,95 (CD11c/ CD18), not Mac-I (CD11b/CD18), is involved in mediating fibrin stimulatory activity in macrophages. (+info)Usefulness of D-dimer, blood gas, and respiratory rate measurements for excluding pulmonary embolism. (5/870)
BACKGROUND: A study was undertaken to assess the usefulness of the SimpliRED D-dimer test, arterial oxygen tension, and respiratory rate measurement for excluding pulmonary embolism (PE) and venous thromboembolism (VTE). METHODS: Lung scans were performed in 517 consecutive medical inpatients with suspected acute PE over a one year period. Predetermined end points for objectively diagnosed PE in order of precedence were (1) a post mortem diagnosis, (2) a positive pulmonary angiogram, (3) a high probability ventilation perfusion lung scan when the pretest probability was also high, and (4) the unanimous opinion of an adjudication committee. Deep vein thrombosis (DVT) was diagnosed by standard ultrasound and venography. RESULTS: A total of 40 cases of PE and 37 cases of DVT were objectively diagnosed. The predictive value of a negative SimpliRED test for excluding objectively diagnosed PE was 0.99 (error rate 2/249), that of PaO2 of > or = 80 mm Hg (10.7 kPa) was 0.97 (error rate 5/160), and that of a respiratory rate of < or = 20/min was 0.95 (error rate 14/308). The best combination of findings for excluding PE was a negative SimpliRED test and PaO2 > or = 80 mm Hg, which gave a predictive value of 1.0 (error rate 0/93). The predictive value of a negative SimpliRED test for excluding VTE was 0.98 (error rate 5/249). CONCLUSIONS: All three of these observations are helpful in excluding PE. When any two parameters were normal, PE was very unlikely. In patients with a negative SimpliRED test and PaO2 of > or = 80 mm Hg a lung scan is usually unnecessary. Application of this approach for triage in the preliminary assessment of suspected PE could lead to a reduced rate of false positive diagnoses and considerable resource savings. (+info)Tissue factor pathway inhibitor expression in human crescentic glomerulonephritis. (6/870)
BACKGROUND: Tissue factor (TF) pathway inhibitor (TFPI), the major endogenous inhibitor of extrinsic coagulation pathway activation, protects renal function in experimental crescentic glomerulonephritis (GN). Its glomerular expression and relationship to TF expression and fibrin deposition in human crescentic GN have not been reported. METHODS: Glomerular TFPI, TF, and fibrin-related antigen (FRA) expression were correlated in renal biopsies from 11 patients with crescentic GN. Biopsies from 11 patients with thin basement membrane disease and two normal kidneys were used as controls. RESULTS: TFPI was undetectable in control glomeruli but was detectable in interstitial microvessels. In crescentic biopsies, TFPI was detected in cellular crescents and was more prominent in fibrous/fibrocellular crescents, indicating a correlation with the chronicity of crescentic lesions. TFPI appeared to be associated with macrophages but not endothelial or epithelial cells. TFPI was generally undetectable in regions of the glomerular tuft with minimal damage. In contrast, TF and FRA were strongly expressed in regions of minimal injury, as well as in more advanced proliferative and necrotizing lesions. Despite prominent TF expression, FRA was less prominent in fibrous/fibrocellular crescents in which TFPI expression was maximal. CONCLUSIONS: These data suggest that TFPI is strongly expressed in the later stages of crescent formation and is inversely correlated with the presence of FRA in human crescentic GN. This late induction of TFPI may inhibit TF activity and favor reduced fibrin deposition in the chronic stages of crescent formation. (+info)Dose response of intravenous heparin on markers of thrombosis during primary total hip replacement. (7/870)
BACKGROUND: Thrombogenesis in total hip replacement (THR) begins during surgery on the femur. This study assesses the effect of two doses of unfractionated intravenous heparin administered before femoral preparation during THR on circulating markers of thrombosis. METHODS: Seventy-five patients undergoing hybrid primary THR were randomly assigned to receive blinded intravenous injection of either saline or 10 or 20 U/kg of unfractionated heparin after insertion of the acetabular component. Central venous blood samples were assayed for prothrombin F1+2 (F1+2), thrombin-antithrombin complexes (TAT), fibrinopeptide A (FPA), and D-dimer. RESULTS: No changes in the markers of thrombosis were noted after insertion of the acetabular component. During surgery on the femur, significant increases in all markers were noted in the saline group (P < 0.0001). Heparin did not affect D-dimer or TAT. Twenty units per kilogram of heparin significantly reduced the increase of F1+2 after relocation of the hip joint (P < 0.001). Administration of both 10 and 20 U/kg significantly reduced the increase in FPA during implantation of the femoral component (P < 0.0001). A fourfold increase in FPA was noted in 6 of 25 patients receiving 10 U/kg of heparin but in none receiving 20 U/kg (P = 0.03). Intraoperative heparin did not affect intra- or postoperative blood loss, postoperative hematocrit, or surgeon's subjective assessments of bleeding. No bleeding complications were noted. CONCLUSIONS: This study demonstrates that 20 U/kg of heparin administered before surgery on the femur suppresses fibrin formation during primary THR. This finding provides the pathophysiologic basis for the clinical use of intraoperative heparin during THR. (+info)Effects of Ro 31-8220 on smooth muscle cell proliferation induced by fibrinogen degradation products. (8/870)
AIM: To study the mitogenic activity of fibrin fibrinogen degradation products (FFDP) and the effect of a new selectively potent protein kinase C (PKC) inhibitor Ro 31-8220 (Ro). METHODS: Rat aortic smooth muscle cells (SMC) proliferation in culture was measured by crystal violet staining assay. RESULTS: FFDP stimulated the proliferation of SMC during the experimental period of 72 h, Ro 0.01-1 mumol.L-1 inhibited FFDP-induced cell proliferation in a concentration-dependent manner. CONCLUSION: Ro exerted inhibitory effect on cell proliferation induced by FFDP. (+info)Fibrin(ogen) degradation products (FDPs) are a group of proteins that result from the breakdown of fibrinogen and fibrin, which are key components of blood clots. This process occurs during the normal physiological process of fibrinolysis, where clots are dissolved to maintain blood flow.
FDPs can be measured in the blood as a marker for the activation of the coagulation and fibrinolytic systems. Elevated levels of FDPs may indicate the presence of a disorder that causes abnormal clotting or bleeding, such as disseminated intravascular coagulation (DIC), deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of cancer.
It is important to note that FDPs are not specific to any particular disorder and their measurement should be interpreted in conjunction with other clinical and laboratory findings.
Fibrin is defined as a protein that is formed from fibrinogen during the clotting of blood. It plays an essential role in the formation of blood clots, also known as a clotting or coagulation cascade. When an injury occurs and bleeding starts, fibrin threads form a net-like structure that entraps platelets and red blood cells to create a stable clot, preventing further loss of blood.
The process of forming fibrin from fibrinogen is initiated by thrombin, another protein involved in the coagulation cascade. Thrombin cleaves fibrinogen into fibrin monomers, which then polymerize to form long strands of fibrin. These strands cross-link with each other through a process catalyzed by factor XIIIa, forming a stable clot that protects the wound and promotes healing.
It is important to note that abnormalities in fibrin formation or breakdown can lead to bleeding disorders or thrombotic conditions, respectively. Proper regulation of fibrin production and degradation is crucial for maintaining healthy hemostasis and preventing excessive clotting or bleeding.
Fibrinogen is a soluble protein present in plasma, synthesized by the liver. It plays an essential role in blood coagulation. When an injury occurs, fibrinogen gets converted into insoluble fibrin by the action of thrombin, forming a fibrin clot that helps to stop bleeding from the injured site. Therefore, fibrinogen is crucial for hemostasis, which is the process of stopping bleeding and starting the healing process after an injury.
Fibrinolysis is the natural process in the body that leads to the dissolution of blood clots. It is a vital part of hemostasis, the process that regulates bleeding and wound healing. Fibrinolysis occurs when plasminogen activators convert plasminogen to plasmin, an enzyme that breaks down fibrin, the insoluble protein mesh that forms the structure of a blood clot. This process helps to prevent excessive clotting and maintains the fluidity of the blood. In medical settings, fibrinolysis can also refer to the therapeutic use of drugs that stimulate this process to dissolve unwanted or harmful blood clots, such as those that cause deep vein thrombosis or pulmonary embolism.
Disseminated Intravascular Coagulation (DIC) is a complex medical condition characterized by the abnormal activation of the coagulation cascade, leading to the formation of blood clots in small blood vessels throughout the body. This process can result in the consumption of clotting factors and platelets, which can then lead to bleeding complications. DIC can be caused by a variety of underlying conditions, including sepsis, trauma, cancer, and obstetric emergencies.
The term "disseminated" refers to the widespread nature of the clotting activation, while "intravascular" indicates that the clotting is occurring within the blood vessels. The condition can manifest as both bleeding and clotting complications, which can make it challenging to diagnose and manage.
The diagnosis of DIC typically involves laboratory tests that evaluate coagulation factors, platelet count, fibrin degradation products, and other markers of coagulation activation. Treatment is focused on addressing the underlying cause of the condition while also managing any bleeding or clotting complications that may arise.
Plasminogen is a glycoprotein that is present in human plasma, and it is the inactive precursor of the enzyme plasmin. Plasmin is a serine protease that plays a crucial role in the dissolution of blood clots by degrading fibrin, one of the major components of a blood clot.
Plasminogen can be activated to form plasmin through the action of various activators, such as tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Once activated, plasmin can break down fibrin and other proteins, helping to prevent excessive clotting and promoting the normal turnover of extracellular matrix components.
Abnormalities in plasminogen activation have been implicated in various diseases, including thrombosis, fibrosis, and cancer. Therefore, understanding the regulation and function of plasminogen is important for developing therapies to treat these conditions.
Fibrinolysin is defined as a proteolytic enzyme that dissolves or breaks down fibrin, a protein involved in the clotting of blood. This enzyme is produced by certain cells, such as endothelial cells that line the interior surface of blood vessels, and is an important component of the body's natural mechanism for preventing excessive blood clotting and maintaining blood flow.
Fibrinolysin works by cleaving specific bonds in the fibrin molecule, converting it into soluble degradation products that can be safely removed from the body. This process is known as fibrinolysis, and it helps to maintain the balance between clotting and bleeding in the body.
In medical contexts, fibrinolysin may be used as a therapeutic agent to dissolve blood clots that have formed in the blood vessels, such as those that can occur in deep vein thrombosis or pulmonary embolism. It is often administered in combination with other medications that help to enhance its activity and specificity for fibrin.
Phlebitis is a medical term that refers to the inflammation of a vein, usually occurring in the legs. The inflammation can be caused by blood clots (thrombophlebitis) or other conditions that cause irritation and swelling in the vein's lining. Symptoms may include redness, warmth, pain, and swelling in the affected area. In some cases, phlebitis may lead to serious complications such as deep vein thrombosis (DVT) or pulmonary embolism (PE), so it is essential to seek medical attention if you suspect you have this condition.
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.
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.
Urokinase-type plasminogen activator (uPA) is a serine protease enzyme that plays a crucial role in the degradation of the extracellular matrix and cell migration. It catalyzes the conversion of plasminogen to plasmin, which then breaks down various proteins in the extracellular matrix, leading to tissue remodeling and repair.
uPA is synthesized as a single-chain molecule, pro-uPA, which is activated by cleavage into two chains, forming the mature and active enzyme. uPA binds to its specific receptor, uPAR, on the cell surface, where it exerts its proteolytic activity.
Abnormal regulation of uPA and uPAR has been implicated in various pathological conditions, including cancer, where they contribute to tumor invasion and metastasis. Therefore, uPA is a potential target for therapeutic intervention in cancer and other diseases associated with excessive extracellular matrix degradation.
A fibrin tissue adhesive is a type of surgical glue that is used to approximate and secure together cut or wounded tissues in the body during surgical procedures. It is made from fibrin, a protein involved in blood clotting, and is often combined with other substances like thrombin and calcium chloride to promote clot formation and enhance adhesion.
Fibrin tissue adhesives work by mimicking the body's natural clotting process. When applied to the wound site, the fibrinogen component of the adhesive is converted into fibrin by the thrombin component, creating a stable fibrin clot that holds the edges of the wound together. This helps to promote healing and reduce the risk of complications such as bleeding or infection.
Fibrin tissue adhesives are commonly used in various surgical procedures, including dermatologic, ophthalmic, orthopedic, and neurologic surgeries. They offer several advantages over traditional suturing methods, such as reduced operation time, less trauma to the tissues, and improved cosmetic outcomes. However, they may not be suitable for all types of wounds or surgical sites, and their use should be determined by a qualified healthcare professional based on individual patient needs and circumstances.
Disease notification is the process by which health care professionals, laboratories, or other relevant individuals or organizations inform public health authorities about cases of specific diseases or conditions that are reportable (also known as notifiable) within a particular jurisdiction. Reportable diseases are those that have been designated by law or regulation as posing a significant risk to public health and for which timely reporting is necessary to enable effective surveillance, control measures, and prevention strategies.
The specific diseases and conditions that must be reported, as well as the procedures for reporting, vary by jurisdiction. Common reportable diseases include infectious diseases such as tuberculosis, measles, and sexually transmitted infections (STIs), as well as non-infectious conditions like cancer and lead poisoning.
The purpose of disease notification is to provide public health officials with accurate and up-to-date information about the occurrence and spread of diseases in a population. This information can help inform policy decisions, guide resource allocation, and support the development and implementation of evidence-based interventions to protect and promote the health of communities.
Public Health Administration refers to the leadership, management, and coordination of public health services and initiatives at the local, state, or national level. It involves overseeing and managing the development, implementation, and evaluation of policies, programs, and services aimed at improving the health and well-being of populations. This may include addressing issues such as infectious disease control, chronic disease prevention, environmental health, emergency preparedness and response, and health promotion and education.
Public Health Administration requires a strong understanding of public health principles, leadership and management skills, and the ability to work collaboratively with a variety of stakeholders, including community members, healthcare providers, policymakers, and other organizations. The ultimate goal of Public Health Administration is to ensure that public health resources are used effectively and efficiently to improve the health outcomes of populations and reduce health disparities.
Public health is defined by the World Health Organization (WHO) as "the art and science of preventing disease, prolonging life and promoting human health through organized efforts of society." It focuses on improving the health and well-being of entire communities, populations, and societies, rather than individual patients. This is achieved through various strategies, including education, prevention, surveillance of diseases, and promotion of healthy behaviors and environments. Public health also addresses broader determinants of health, such as access to healthcare, housing, food, and income, which have a significant impact on the overall health of populations.
Population surveillance in a public health and medical context refers to the ongoing, systematic collection, analysis, interpretation, and dissemination of health-related data for a defined population over time. It aims to monitor the health status, identify emerging health threats or trends, and evaluate the impact of interventions within that population. This information is used to inform public health policy, prioritize healthcare resources, and guide disease prevention and control efforts. Population surveillance can involve various data sources, such as vital records, disease registries, surveys, and electronic health records.
Trichomonas is a genus of protozoan parasites that are commonly found in the human body, particularly in the urogenital tract. The most well-known species is Trichomonas vaginalis, which is responsible for the sexually transmitted infection known as trichomoniasis. This infection can cause various symptoms in both men and women, including vaginitis, urethritis, and pelvic inflammatory disease.
T. vaginalis is a pear-shaped flagellate protozoan that measures around 10 to 20 micrometers in length. It has four flagella at the anterior end and an undulating membrane along one side of its body, which helps it move through its environment. The parasite can attach itself to host cells using a specialized structure called an adhesion zone.
Trichomonas species are typically transmitted through sexual contact, although they can also be spread through the sharing of contaminated towels or clothing. Infection with T. vaginalis can increase the risk of acquiring other sexually transmitted infections, such as HIV and human papillomavirus (HPV).
Diagnosis of trichomoniasis typically involves the detection of T. vaginalis in a sample of vaginal or urethral discharge. Treatment usually involves the administration of antibiotics, such as metronidazole or tinidazole, which are effective at killing the parasite and curing the infection.
Communicable diseases, also known as infectious diseases, are illnesses that can be transmitted from one person to another through various modes of transmission. These modes include:
1. Direct contact: This occurs when an individual comes into physical contact with an infected person, such as touching or shaking hands, or having sexual contact.
2. Indirect contact: This happens when an individual comes into contact with contaminated objects or surfaces, like doorknobs, towels, or utensils.
3. Airborne transmission: Infectious agents can be spread through the air when an infected person coughs, sneezes, talks, or sings, releasing droplets containing the pathogen into the environment. These droplets can then be inhaled by nearby individuals.
4. Droplet transmission: Similar to airborne transmission, but involving larger respiratory droplets that don't remain suspended in the air for long periods and typically travel shorter distances (usually less than 6 feet).
5. Vector-borne transmission: This occurs when an infected animal or insect, such as a mosquito or tick, transmits the disease to a human through a bite or other means.
Examples of communicable diseases include COVID-19, influenza, tuberculosis, measles, hepatitis B, and malaria. Preventive measures for communicable diseases often involve public health initiatives like vaccination programs, hygiene promotion, and vector control strategies.
I'm sorry for any confusion, but "State Government" is not a medical term. It refers to the level of government in the United States that is responsible for governing each of the individual states. This includes executives (such as governors), legislative bodies (like state senates and houses of representatives), and courts.
If you have any questions related to medicine or healthcare, I'd be happy to try and help answer those for you!
Fibrin degradation product
Thrombin time
Fibrinolysis
Kasabach-Merritt syndrome
Disseminated intravascular coagulation
Hyperfibrinolysis
Bothrops neuwiedi
Hementin
Fibrinogenolysis
Primary fibrinogenolysis
Purpura fulminans
Hemolytic-uremic syndrome
D-dimer
Coagulation screen
Coagulation
Coagulation testing
Thromboelastometry
Ancrod
Fibrinogen beta chain
Fibrinogen alpha chain
Transglutaminase
Batroxobin
Discovery and development of direct thrombin inhibitors
Deep vein thrombosis
Sulfatide
Transurethral resection of the prostate syndrome
Thrombus
Exoenzyme
Rheumatoid arthritis
Biochemical cascade
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Disseminated intravascul3
- Fibrin and fibrinogen degradation product (FDP) testing is commonly used to diagnose disseminated intravascular coagulation (DIC). (medscape.com)
- Fibrinogen degradation product (FDP) testing is commonly used to aid in the diagnosis of disseminated intravascular coagulation (DIC). (medscape.com)
- Platelets less than or equal to 100,000/mm 3 (less than or equal to 100 x 10 6 /L) or disseminated intravascular coagulation defined by prolonged clotting times, low fibrinogen level, and the presence of fibrin degradation products. (cdc.gov)
Plasmin7
- Plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases. (biovendor.com)
- Plasmin converts fibrinogen initially into X component, which is cleaved into component Y and component D. Component Y is cleaved into component D and component E. Component D is also called D-dimers. (medscape.com)
- Once clots have formed, plasminogen is activated by tissue plasminogen activator into plasmin, which breaks down the fibrin meshwork of the clot. (vin.com)
- Plasmin activity is also reduced by thrombin-activatable fibrinolysis inhibitor (TAFI), which modifies fibrin to make a less potent cofactor for the tPA-mediated plasminogen activation. (wikidoc.org)
- When plasmin breaks down fibrin, a number of soluble parts are produced. (wikidoc.org)
- Plasmin , in addition to lysing fibrin clots, also cleaves the complement system component C3, and fibrin degradation products have some vascular permeability inducing effects. (wikidoc.org)
- The molecular weights, mass distribution, chain composition, and structure of soluble fibrin degradation products released from a fibrin clot perfused with plasmin. (wikidoc.org)
Soluble3
- Fibrin Degradation Products (FDP) that occur are very heterogeneous and include products derived from fibrin, soluble complexes, degradation products from fibrinogen, and from nonstabilized fibrin. (biovendor.com)
- During plasma coagulation, soluble fibrin is generated by the influence of thrombin on fibrinogen. (horiba.com)
- The soluble fibrin is cross-linked to the vessel walls by factor Xllla. (horiba.com)
Fibrinolysis10
- Fibrinolysis is the enzymatic breakdown of fibrin in blood clots. (biovendor.com)
- Under normal conditions, the fibrinolytic process is localized on the fibrin clots because alpha2-antiplasmin and the plasminogen activator inhibitors prevent fibrinolysis from spreading. (biovendor.com)
- Increased FDPs are seen in primary fibrinolysis as well as during fibrin clot breakdown. (biovendor.com)
- D-Dimers is degradation products of fibrin, biomarker for activation of plasma coagulation and/or fibrinolysis. (horiba.com)
- 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)
- Pharmacokinetic studies showed that at 30,000 U/kg, streptokinase caused systemic fibrinolysis in the Fischer rat, as demonstrated by the thrombin time and fibrin plate lysis assay. (ox.ac.uk)
- Analysis of fibrin degradation products in the streptokinase-treated group suggested that this effect might be secondary to fibrinolysis. (ox.ac.uk)
- The products of fibrinolysis that are released as microthromboses are broken down during DIC may be detected as circulating fibrin degradation products (FDP) or (more specifically) d-dimers. (vin.com)
- Because DIC is a consumptive process with regards to coagulation factors, most of the bedside diagnostics are focused on the demonstration of consumption of platelets and coagulation factors, or on the discovery of elevated products of fibrinolysis and clot breakdown (e.g. (vin.com)
- Fibrinolysis is the process where a fibrin clot , the product of coagulation , is broken down. (wikidoc.org)
Ogen1
- Plasminogen contains secondary structure motifs known as kringles, which bind specifically to lysine and arginine residues on fibrin(ogen). (wikidoc.org)
Thrombin3
- FDPs compete with thrombin, and so slow down the conversion of fibrinogen to fibrin (and thus slows down clot formation). (wikidoc.org)
- Two small peptide chains removed from the N-terminal segment of the beta chains of fibrinogen by the action of thrombin. (bvsalud.org)
- This test method involves measuring the rate of fibrinogen to fibrin conversion in diluted sample under the influence of excess thrombin. (cdc.gov)
Cross-linked fibrin3
- 1000 μg/L and AT ˂0.85 kIU/L. We observed an elevated fraction of incompletely degraded D-dimer fragments in COVID-19+ patients with low PAP, indicating impaired fibrinolytic breakdown of cross-linked fibrin. (lu.se)
- 0.001) for patients with PAP <1000 μg/L and D-dimer >0.5 mg/L and 15.5 (CI95 2.8-87, p = 0.002) for patients with PAP <1000 μg/L and AT ˂0.85 kIU/L. We observed an elevated fraction of incompletely degraded D-dimer fragments in COVID-19+ patients with low PAP, indicating impaired fibrinolytic breakdown of cross-linked fibrin. (lu.se)
- When splitting this cross-linked fibrin, characteristic products called D-dimers are released. (horiba.com)
FDPs3
- These broken fibrin fragments are called fibrin degradation products (FDPs). (medscape.com)
- Fibrin degradation products (FDPs), also known as fibrin split products, are components of the blood produced by clot degeneration. (wikipedia.org)
- Because most veterinarians in private first-opinion practices rely on traditional coagulation assessments (prothrombin time [PT] and activated partial thromboplastin time [aPTT]), and fibrinogen, with occasional measurement of antithrombin (AT), protein C (PC), D-dimers, and fibrin degradation products (FDPs), it is important to acknowledge the complexities that these may not reflect. (msdvetmanual.com)
Formation2
- 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)
- Factor V Leiden mutation enhances fibrin formation and dissolution in vivo in a human endotoxemia model. (cdc.gov)
Platelet7
- Fibrin was originally thought to be essential for platelet aggregation, based on in vitro studies using anticoagulated blood. (biovendor.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)
- One aspect of the metastatic process involves entrapment of tumor cells within the microcirculation of organs in a "fibrin-platelet mesh. (ox.ac.uk)
- Key features of this disorder include a lack of bleeding risk, only mildly low platelet counts, elevated plasma fibrinogen levels, and detection of both severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and complement components in regions of thrombotic microangiopathy (TMA). (nature.com)
- The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). (lookformedical.com)
- A protective effect against DIC was noted in the rats treated with 10 or 100μg/kg/h of ONO-3307 in the following parameters: fibrinogen and fibrin degradation products, platelet count, fibrinogen level, prothrombin time, partial thromboplastin time and the number of renal glomeruli with fibrin thrombi. (go.jp)
- Fibrinogen is an essential blood-clotting factor and is involved in a range of other functions, including platelet aggregation and smooth muscle proliferation. (cdc.gov)
Plasminogen2
- Hyperfibrinolysis by degradation of plasminogen activator inhibitor? (biomedcentral.com)
- Although plasminogen cannot cleave fibrin, it still has an affinity for it, and is incorporated into the clot when it is formed. (wikidoc.org)
Fragments1
- When the clot and fibrin net dissolve, fragments of protein are released into the body. (wikipedia.org)
Substances1
- It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. (lookformedical.com)
Hemorrhage1
- Fibrin deposition is also associated with infection, where it protects against IFNG-mediated hemorrhage. (biovendor.com)
Plasma3
- In COVID-19+ patients, we found pronounced increases in plasma levels of von Willebrand factor (vWF) and fibrinogen. (lu.se)
- On the STA-Compact, the fibrinogen concentration in plasma is determined quantitatively by the Clauss clotting method. (cdc.gov)
- Since under these conditions the fibrinogen content is rate limiting, the clotting time can be used as a measure of the concentration of the fibrinogen and in fact, the clotting time is inversely proportional to the level of fibrinogen in the plasma. (cdc.gov)
Insoluble2
- Fibrinogen alpha (FGA), fibrinogen beta (FGB), and fibrinogen gamma (FGG) polymerize to form an insoluble fibrin matrix. (biovendor.com)
- The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot. (lookformedical.com)
Clots2
- Fibrin has a major function in hemostasis as one of the primary components of blood clots. (biovendor.com)
- These fibrin threads form a mesh to clump platelets because they are cross-linked to form blood clots. (medscape.com)
Deep vein throm1
- Fibrin split products are used to rule out venous thromboembolism (including deep vein thrombosis and pulmonary embolism). (medscape.com)
Mesh1
- as it is slowly activated, it breaks down the fibrin mesh. (wikidoc.org)
Renal2
- This reagent should be used in conjunction with a panel of antibodies to aid in the identification of fibrinogen in target tissue (e.g., in the diagnosis of renal or dermal pathologies). (roche.com)
- 5 Immunofluorescent detection of fibrinogen in human renal tissue has been previously documented. (roche.com)
Enhances1
- Fibrin enhances expression of SELP in activated platelets via an ITGB3-dependent pathway. (biovendor.com)
Antigen1
- The enzymatic activation of the chromogen results in a visible reaction product at the antigen site. (roche.com)
Tissue4
- FITC anti-Fibrinogen is intended for laboratory use to qualitatively stain sections of frozen tissue on a Ventana automated slide stainer. (roche.com)
- Language": "en", "Country": "XG", "Code": "Intended Use" }, { "Name": "Background Information", "Value": "Fluorescent antibodies have been used to detect specific antigens in cells or tissue for over 40 years. (roche.com)
- Language": "en", "Country": "XG", "Code": "Background Information" }, { "Name": "Principle", "Value": "FITC anti-Fibrinogen may be used as the primary antibody for immunohistochemical staining of frozen tissue sections. (roche.com)
- Tissue factor pathway inhibitor relates to fibrin degradation in patients with acute deep venous thrombosis. (cdc.gov)
Reagent1
- Language": "en", "Country": "XG", "Code": "Storage Conditions (Product)" }, { "Name": "Content", "Value": "FITC anti-Fibrinogen contains sufficient reagent for 50 tests. (roche.com)
Levels3
- On admission, both patients had levels of fibrinogen lower than 35 mg/dL, D-dimer higher than 10,000 ng/mL. (bvsalud.org)
- A growing body of evidence has identified fibrinogen as an important risk factor for cardiovascular disease, the major cause of death in the U.S. The objective of including this measure is to provide data on laboratory, clinical, and socio- demographic correlates of fibrinogen levels. (cdc.gov)
- Of particular importance in NHANES, the data will be used to study the relationship between fibrinogen levels and clinically measured lower extremity arterial blood flow as assessed by the Ankle-Brachial Index in the Lower Extremity Disease component. (cdc.gov)
Flow1
- Flow chart of fibrin split products. (medscape.com)
Laboratory1
- We are an international group of biotechnology companies focusing on the development, production and distribution of IVD products and technologies for laboratory automation. (biovendor.com)
Polyclonal Antibody3
- contains a goat polyclonal antibody directed against human fibrinogen approximately 1.4 µg/mL. (roche.com)
- Ventana ® Medical Systems' (Ventana) FITC anti-Fibrinogen Primary Antibody is a goat derived polyclonal antibody labeled with fluorescein and specifically directed against human fibrinogen. (roche.com)
- FITC anti-Fibrinogen contains a goat polyclonal antibody raised against purified human fibrinogen. (roche.com)
Factor4
- False-positives results on fibrinogen degradation product (FDP) testing may be caused by rheumatoid factor. (medscape.com)
- Recurrent miscarriage may be a feature of some congenital factor (eg, factor XIII) and fibrinogen deficiencies. (medscape.com)
- Within a single strand, the fibrin monomers are covalently linked through the actions of coagulation factor XIII . (wikidoc.org)
- A fibrinogen and the factor XIII A subunit (FXIII-A) Val34Leu polymorphism in cancer-associated venous thrombosis. (cdc.gov)
Blood3
- Blood is normally in a fluid state (anticoagulated) within the body to enable flowing through a vessel network of arteries, capillaries and veins, delivering oxygen and nutrients to the organs of the body and removing carbon dioxide and waste products. (labtestsonline.org.uk)
- Intravenous immunoglobulins, a product made from human blood, has been used with some success in a few cases of IMHA. (petplace.com)
- 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. (lookformedical.com)
Form1
- Fibrin monomers, when polymerized, form protofibrils . (wikidoc.org)
Human1
- 6 FITC anti-Fibrinogen binds specifically with human fibrinogen and its degradation products. (roche.com)
Split2
- Fibrinogen split products. (medscape.com)
- The necrotic epithelium becomes embedded in exuding fibrin and fibrinogen degradation products fibrin split products are present, they may show up in bed. (elastizell.com)
Threads2
- Fibrin threads are produced during the coagulation process. (medscape.com)
- Clotting, also called coagulation, at the wound site produces a mass of fibrin threads called a net that remains in place until the cut is healed. (wikipedia.org)
Wound1
- In addition, fibrin functions during the early stages of wound repair to stabilize the lesion and guide cell migration during re-epithelialization. (biovendor.com)