Complement Pathway, Alternative
Complement C3-C5 Convertases
Complement Factor B
Complement C3 Convertase, Alternative Pathway
Complement System Proteins
Complement Pathway, Classical
Proprotein Convertase 2
Proprotein Convertase 1
Complement Activating Enzymes
Complement Inactivator Proteins
Complement Factor H
Complement Factor D
Proprotein Convertase 5
Complement Membrane Attack Complex
Complement C3b Inactivator Proteins
Receptors, Complement 3b
Complement C3 Nephritic Factor
Complement Factor I
Complement C3-C5 Convertases, Alternative Pathway
Complement Inactivating Agents
Complement Hemolytic Activity Assay
Complement C5 Convertase, Alternative Pathway
Receptors, Complement 3d
Receptor, Anaphylatoxin C5a
Complement C4b-Binding Protein
Molecular Sequence Data
Complement C1 Inactivator Proteins
Complement C3 Convertase, Classical Pathway
Neuroendocrine Secretory Protein 7B2
Amino Acid Sequence
Complement C5 Convertase, Classical Pathway
Complement Fixation Tests
Complement Pathway, Mannose-Binding Lectin
Complement C1 Inhibitor Protein
Complement C3-C5 Convertases, Classical Pathway
Blood Bactericidal Activity
Protein Structure, Tertiary
Protein Processing, Post-Translational
Mannose-Binding Protein-Associated Serine Proteases
Lupus Erythematosus, Systemic
Sequence Homology, Amino Acid
Electrophoresis, Polyacrylamide Gel
Enzyme-Linked Immunosorbent Assay
Aspartic Acid Endopeptidases
Surface Plasmon Resonance
Disease Models, Animal
Gene Expression Regulation
Polymerase Chain Reaction
Dose-Response Relationship, Immunologic
Genetic Complementation Test
Complement C5a, des-Arginine
Reverse Transcriptase Polymerase Chain Reaction
NF-kappa B p52 Subunit
Recombinant Fusion Proteins
Animal Testing Alternatives
Dose-Response Relationship, Drug
Major Histocompatibility Complex
Structural and functional analysis of a C3b-specific antibody that selectively inhibits the alternative pathway of complement. (1/1)(+info)
There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.
The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.
Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.
The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).
The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.
There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.
The main complications of GNM include:
1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.
It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
The symptoms of HUS include:
* Abdominal pain
* Shortness of breath
* Pale or yellowish skin
* Easy bruising or bleeding
If you suspect that someone has HUS, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order blood tests to diagnose the condition. Treatment for HUS typically involves addressing the underlying cause of the condition, such as stopping certain medications or treating an infection. In some cases, hospitalization may be necessary to manage complications such as kidney failure.
Preventative measures to reduce the risk of developing HUS include:
* Practicing good hygiene, especially during outbreaks of diarrheal illnesses
* Avoiding certain medications that are known to increase the risk of HUS
* Maintaining a healthy diet and staying hydrated
* Managing any underlying medical conditions such as high blood pressure or diabetes.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Nephritis is often diagnosed through a combination of physical examination, medical history, and laboratory tests such as urinalysis and blood tests. Treatment for nephritis depends on the underlying cause, but may include antibiotics, corticosteroids, and immunosuppressive medications. In severe cases, dialysis may be necessary to remove waste products from the blood.
Some common types of nephritis include:
1. Acute pyelonephritis: This is a type of bacterial infection that affects the kidneys and can cause sudden and severe symptoms.
2. Chronic pyelonephritis: This is a type of inflammation that occurs over a longer period of time, often as a result of recurrent infections or other underlying conditions.
3. Lupus nephritis: This is a type of inflammation that occurs in people with systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple organs.
4. IgA nephropathy: This is a type of inflammation that occurs when an antibody called immunoglobulin A (IgA) deposits in the kidneys and causes damage.
5. Mesangial proliferative glomerulonephritis: This is a type of inflammation that affects the mesangium, a layer of tissue in the kidney that helps to filter waste products from the blood.
6. Minimal change disease: This is a type of nephrotic syndrome (a group of symptoms that include proteinuria, or excess protein in the urine) that is caused by inflammation and changes in the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
7. Membranous nephropathy: This is a type of inflammation that occurs when there is an abnormal buildup of antibodies called immunoglobulin G (IgG) in the glomeruli, leading to damage to the kidneys.
8. Focal segmental glomerulosclerosis: This is a type of inflammation that affects one or more segments of the glomeruli, leading to scarring and loss of function.
9. Post-infectious glomerulonephritis: This is a type of inflammation that occurs after an infection, such as streptococcal infections, and can cause damage to the kidneys.
10. Acute tubular necrosis (ATN): This is a type of inflammation that occurs when there is a sudden loss of blood flow to the kidneys, causing damage to the tubules, which are tiny tubes in the kidneys that help to filter waste products from the blood.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are two main types of MD:
1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.
The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:
* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision
MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.
There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:
* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.
It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.
Arteriolosclerosis is often associated with conditions such as hypertension, diabetes, and atherosclerosis, which is the buildup of plaque in the arteries. It can also be caused by other factors such as smoking, high cholesterol levels, and inflammation.
The symptoms of arteriolosclerosis can vary depending on the location and severity of the condition, but may include:
* Decreased blood flow to organs or tissues
* Shortness of breath
* Dizziness or lightheadedness
* Pain in the affected limbs or organs
Arteriolosclerosis is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, angiography, or blood tests. Treatment for the condition may include lifestyle changes such as exercise and dietary modifications, medications to control risk factors such as hypertension and high cholesterol, and in some cases, surgical intervention to open or bypass blocked arterioles.
In summary, arteriolosclerosis is a condition where the arterioles become narrowed or obstructed, leading to decreased blood flow to organs and tissues and potentially causing a range of health problems. It is often associated with other conditions such as hypertension and atherosclerosis, and can be diagnosed through a combination of physical examination, medical history, and diagnostic tests. Treatment may include lifestyle changes and medications to control risk factors, as well as surgical intervention in some cases.
People with agammaglobulinemia are more susceptible to infections, particularly those caused by encapsulated bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae type b. They may also experience recurrent sinopulmonary infections, ear infections, and gastrointestinal infections. The disorder can be managed with intravenous immunoglobulin (IVIG) therapy, which provides antibodies to help prevent infections. In severe cases, a bone marrow transplant may be necessary.
Agammaglobulinemia is an autosomal recessive disorder, meaning that a person must inherit two mutated copies of the BTK gene (one from each parent) to develop the condition. It is relatively rare, affecting approximately one in 1 million people worldwide. The disorder can be diagnosed through genetic testing and a complete blood count (CBC) that shows low levels of immunoglobulins.
Treatment for ag
There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:
* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.
Lupus Nephritis can cause a range of symptoms, including:
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Joint pain
Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.
The most common form of this disease is Meningococcal Group B (MenB). Symptoms often develop within hours or days after exposure, but can be nonspecific, such as fever, headache, and muscle aches.
Early signs that are more specific and suggestive of the diagnosis include neck stiffness, confusion, seizures, and rash. Diagnosis is by culture or PCR of a sterile site. Treatment consists of antibiotics that cover Neisseria meningitidis, which should be initiated promptly after recognition of the signs and symptoms.
Prevention with vaccines is recommended for infants at 2 months of age; boosters are given at 4 months, 6 months, and 12 to 15 months of age.
There are three main forms of ACH:
1. Classic congenital adrenal hyperplasia (CAH): This is the most common form of ACH, accounting for about 90% of cases. It is caused by mutations in the CYP21 gene, which codes for an enzyme that converts cholesterol into cortisol and aldosterone.
2. Non-classic CAH (NCAH): This form of ACH is less common than classic CAH and is caused by mutations in other genes involved in cortisol and aldosterone production.
3. Mineralocorticoid excess (MOE) or glucocorticoid deficiency (GD): These are rare forms of ACH that are characterized by excessive production of mineralocorticoids (such as aldosterone) or a deficiency of glucocorticoids (such as cortisol).
The symptoms of ACH can vary depending on the specific form of the disorder and the age at which it is diagnosed. In classic CAH, symptoms typically appear in infancy and may include:
* Premature puberty (in girls) or delayed puberty (in boys)
* Abnormal growth patterns
* Distended abdomen
* Weight gain or obesity
* Easy bruising or bleeding
In NCAH and MOE/GD, symptoms may be less severe or may not appear until later in childhood or adulthood. They may include:
* High blood pressure
* Low blood sugar (hypoglycemia)
* Weight gain or obesity
* Mood changes
If left untreated, ACH can lead to serious complications, including:
* Adrenal gland insufficiency
* Heart problems
* Bone health problems
* Increased risk of infections
* Mental health issues (such as depression or anxiety)
Treatment for ACH typically involves hormone replacement therapy to restore the balance of hormones in the body. This may involve taking medications such as cortisol, aldosterone, or other hormones to replace those that are deficient or imbalanced. In some cases, surgery may be necessary to remove an adrenal tumor or to correct physical abnormalities.
With proper treatment, many individuals with ACH can lead healthy, active lives. However, it is important for individuals with ACH to work closely with their healthcare providers to manage their condition and prevent complications. This may involve regular check-ups, hormone level monitoring, and lifestyle changes such as a healthy diet and regular exercise.
Symptoms of meningococcal meningitis typically develop within 3-7 days after exposure and may include fever, headache, stiff neck, confusion, nausea and vomiting, sensitivity to light, and seizures. In severe cases, the infection can lead to shock, organ failure, and death within hours of the onset of symptoms.
Diagnosis is typically made by a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment typically involves antibiotics, intravenous fluids, and supportive care to manage fever, pain, and other symptoms. In severe cases, hospitalization in an intensive care unit may be necessary.
Prevention of meningococcal meningitis includes the use of vaccines, good hygiene practices (such as frequent handwashing), and avoidance of close contact with people who are sick. A vaccine is available for children and teens, and some colleges and universities require students to be vaccinated before moving into dorms.
Early diagnosis and treatment are crucial in preventing long-term complications and reducing the risk of death from meningococcal meningitis. If you suspect that you or someone else may have meningococcal meningitis, it is important to seek medical attention immediately.
Lipodystrophy can be caused by genetic mutations, hormonal imbalances, or certain medications. It can also be associated with other medical conditions such as metabolic disorders, endocrine problems, and neurological diseases.
The symptoms of lipodystrophy can vary depending on the type and severity of the condition. Common symptoms include:
1. Muscle wasting and weakness
2. Fat redistribution to certain areas of the body (such as the face, neck, and torso)
3. Metabolic problems such as insulin resistance and high blood sugar
4. Hormonal imbalances
5. Abnormal body shape and proportions
6. Poor wound healing
7. Easy bruising and bleeding
8. Increased risk of infections
9. Joint pain and stiffness
10. Mood changes such as depression, anxiety, and irritability
Treatment for lipodystrophy depends on the underlying cause of the condition. Medications, lifestyle modifications, and surgery may be used to manage symptoms and improve quality of life. In some cases, lipodystrophy can be a sign of an underlying medical condition that needs to be treated.
Lipodystrophy can have a significant impact on an individual's quality of life, affecting their physical appearance, self-esteem, and ability to perform daily activities. It is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, individuals with lipodystrophy can improve their symptoms and overall health.
These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.
Some common experimental arthritis models include:
1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.
Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.
The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.
Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.
Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.
Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
Complement membrane attack complex
Alternative complement pathway
Classical complement pathway
List of EC numbers (EC 3)
M. Amin Arnaout
Complement factor B
Outline of immunology
Complement component 4
List of MeSH codes (D12.776.124)
Functional Hemolytic Test for Complement Alternative Pathway Convertase Activity - PubMed
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DeCS 2017 - December 21, 2017 version
CFB - Early...
- A serine protease that cleaves multiple COMPLEMENT C5 into COMPLEMENT C5A (anaphylatoxin) and COMPLEMENT C5B in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY . (nih.gov)
- The membrane attack complex is initiated when the complement protein C5 convertase cleaves C5 into C5a and C5b. (promisekit.org)
- The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. (lookformedical.com)
- This complex is a C3/C5 convertase that cleaves both complement components C3 and C5. (expasy.org)
- Each generates a C3 convertase, a serine protease that cleaves the central complement protein C3, and generates the major cleavage fragment C3b. (eaglebio.com)
- 37. Interaction of C3b(2)--IgG complexes with complement proteins properdin, factor B and factor H: implications for amplification. (nih.gov)
- The soluble membrane attack complex (sMAC, a.k.a., sC5b-9 or TCC) is generated on activation of complement and contains the complement proteins C5b, C6, C7, C8, C9 together with the regulatory proteins clusterin and/or vitronectin. (promisekit.org)
- The interaction of the proteins C3, factor B, and factor D results in the formation of the alternative C3- and C5-convertases, i.e. (hycultbiotech.com)
- The FH-related (FHR) proteins share common ligands with FH, due to their homology with this complement regulator, but they lack the domains that mediate the complement inhibitory activity of FH. (frontiersin.org)
- Based on these results, we generated proteins one-fourth the size of CR1 but with enhanced decay accelerating activity for the C3 convertases. (wustl.edu)
- Factor H and other complement proteins regulate the amplification of C3 activation [ 8 ]. (chikd.org)
- It is the complex of ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) with an additional COMPLEMENT C3B , or C3bBb3b. (nih.gov)
- It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. (lookformedical.com)
- The assembly of C3 convertase (C3bBb) requires the combination of factor B and C3b (C3.H2O), and factor D-mediated cleavage of the binding factor B leads to the release of Ba (MW 33 kD). (creative-biolabs.com)
- Properdin can bind C3b and activate the alternative complement pathway and also stabilizes the C3bBb alternative pathway C3 convertase enzyme, thereby directing the deposition of C3 fragments to the cell surface and driving the amplification loop ( 17 - 19 ). (frontiersin.org)
- Bb, a serine protease, then combines with complement factor 3b to generate the C3 or C5 convertase. (nih.gov)
- The active subunit Bb is a serine protease which associates with C3b to form the alternative pathway C3 convertase. (nih.gov)
- Factor D, a 24 kD serine protease of the alternative complement pathway, is synthesized as a precursor single-chain molecule. (hycultbiotech.com)
- C3b is an opsonin itself, and C3 convertase facilitates the activation of the terminal pathway and the formation of the membrane attack complex C5b-9. (medscape.com)
- The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- 26. Regulation of the amplification C3 convertase of human complement by an inhibitory protein isolated from human erythrocyte membrane. (nih.gov)
- Unlike endogenous C3b/Bb, CVF/Bb is a stable complex which is completely resistant to the actions of complement inhibitory factors H (CFH) and I (CFI) . (expasy.org)
- Also, please note that, what is in black are the activation pathways, what is in red are the inhibitory elements in the complexity of the system. (hstalks.com)
Reduced complement activation1
- We observed reduced complement activation when FXI activation was inhibited in a baboon model of lethal systemic inflammation, suggesting cross-talk between FXI and the complement cascade. (bvsalud.org)
- 23. Analysis of the interaction between properdin and factor B, components of the alternative-pathway C3 convertase of complement. (nih.gov)
- 30. C3 and C5-cleaving properdin enzymes formed on zymosan incubated with human serum: the decay and the regeneration of the enzymes. (nih.gov)
- 31. The Role of Properdin in C5 Convertase Activity and C5b-9 Formation in the Complement Alternative Pathway. (nih.gov)
- 39. The role of properdin in the assembly of the alternative pathway C3 convertases of complement. (nih.gov)
- C3 convertase is stabilized by the binding of properdin. (creative-biolabs.com)
- These multicomponent enzymes assemble on the surface of alternative pathway of complement activators and are stabilized by properdin (P). The participation of the alternative pathway of complement has been implicated in the pathogenesis of a wide variety of human diseases. (hycultbiotech.com)
- HG-4, a monoclonal antibody that targets MASP-2, a key enzyme in the lectin pathway, inhibited lectin pathway functional activity in vitro, with an IC50 of circa 10nM. (bvsalud.org)
- The monoclonal antibody M20/6 recognizes human complement factor B/Ba. (creative-biolabs.com)
- C3G complement blockade with eculizumab, a monoclonal antibody targeted against complement C5, inhibits activation of the alternative complement pathway. (chikd.org)
- Recently, plasma exchange/plasma infusion and provision of eculizumab, a monoclonal antibody against C5, can be used in cases of nephritic syndrome and/or decreased renal function in patients with C3GN. (chikd.org)
- Complement factor H (CFH) is the major inhibitor of the alternative pathway of the complement system and is structurally related to beta2-glycoprotein I, which itself is known to bind to ligands, including coagulation factor XI (FXI). (bvsalud.org)
- Our study provides, to our knowledge, a novel molecular link between the contact pathway of coagulation and the complement system. (bvsalud.org)
- 27. C5 convertase of the alternative complement pathway: covalent linkage between two C3b molecules within the trimolecular complex enzyme. (nih.gov)
- Factor D is the rate-linking C3 convertase enzyme of the alternative pathway. (hycultbiotech.com)
- The human complement factor D ELISA is a ready-to-use solid-phase enzyme-linked immunosorbent assay based on the sandwich principle with a working time of 3½ hours. (hycultbiotech.com)
- use DICARBOXYLIC ACIDS 1970-1979 MH - 3-Phosphoshikimate 1-Carboxyvinyltransferase UI - D051229 MN - D8.811.913.225.735 MS - An enzyme of the shikimate pathway of AROMATIC AMINO ACID biosynthesis, it generates 5-enolpyruvylshikimate 3-phosphate and ORTHOPHOSPHATE from PHOSPHOENOLPYRUVATE and SHIKIMATE-3-PHOSPHATE. (nih.gov)
- 21. C3 nephritic factor (C3NeF): stabilization of fluid phase and cell-bound alternative pathway convertase. (nih.gov)
- Small amounts of C3b are constantly being formed in the circulation, which are inactivated by factors H and I. The binding of C3b to a foreign antigen decreases its affinity for factor H and allows for the formation of increasing amounts of the alternate pathway convertase. (medscape.com)
- Impairment of the complement regulatory protein Factor H (FH) is implicated in the physiopathological mechanisms of different diseases like atypical hemolytic and uremic syndrome and C3 glomerulopathies. (bvsalud.org)
- Factor B which is part of the alternate pathway of the complement system is cleaved by factor D into 2 fragments: Ba and Bb. (nih.gov)
- This gene encodes complement factor B, a component of the alternative pathway of complement activation. (nih.gov)
- Upon activation of the alternative pathway, it is cleaved by complement factor D yielding the noncatalytic chain Ba and the catalytic subunit Bb. (nih.gov)
- It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. (lookformedical.com)
- It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001). (lookformedical.com)
- Complement factor B is a single-chain molecule of 764 amino acids (with a molecular weight of 90 kD), including a leader peptide of 25 amino acids. (creative-biolabs.com)
- Factor B provides the catalytic subunit of the C3/C5 convertase that replaces the complement pathway. (creative-biolabs.com)
- In addition to complement activation, factor B fragments also participate in other immune functions. (creative-biolabs.com)
- Furthermore, factor D plays a role in fatty tissue distinct from its role as a complement protein. (hycultbiotech.com)
- The human complement factor D ELISA kit is to be used for the in vitro quantitative determination of human complement factor D in serum, plasma and urine samples. (hycultbiotech.com)
- Samples and standards are incubated in microtiter wells coated with antibodies recognizing human complement factor D. Biotinylated tracer antibody will bind to the captured human complement factor D. Streptavidin-peroxidase conjugate will bind to the biotinylated tracer antibody. (hycultbiotech.com)
- A standard curve is obtained by plotting the absorbance (linear) versus the corresponding concentrations of the human complement factor D standards (log). (hycultbiotech.com)
- The human complement factor D concentration of samples, which are run concurrently with the standards, can be determined from the standard curve. (hycultbiotech.com)
- Factor H (FH), a major soluble complement inhibitor, binds to dead cells and inhibits excessive complement activation on their surface, preventing lysis, and the release of intracellular material, including DNA. (frontiersin.org)
- Notably, these pentraxins may also recruit soluble complement regulators, such as factor H (FH) and C4b-binding protein (C4BP), which in turn limit excessive complement activation on the surface ( 11 - 14 ). (frontiersin.org)
- Decay-accelerating factor (DAF, CD55) is a glycophosphatidyl inositol-anchored glycoprotein that regulates the activity of C3 and C5 convertases. (ox.ac.uk)
- The common coding variant Y402H in the complement factor H ( CFH ) gene was the first identified. (medscape.com)
- [ 21 ] Such rare variants have been described in the complement factor H ( CFH ), complement factor I ( CFI ), complement factor 9 ( C9 ), and complement factor 3 ( C3) genes. (medscape.com)
- 29. Role of the C3b-binding site on C4b-binding protein in regulating classical pathway C5 convertase. (nih.gov)
- Another complement protein, C6, binds to C5b. (promisekit.org)
- In mammals , complement component C3 is the most important protein of the complement system as it is activated by all three pathways (classical, lectin, and alternative pathways), and its various activation products are crucial for mediating, directly or indirectly, virtually all biological functions of complement. (expasy.org)
- The purified refolded recombinant protein was active against both classical and alternative pathway assays of complement activation and had similar biological activity to soluble human DAF expressed in Pichia pastoris. (ox.ac.uk)
- Crystals of the E. coli-derived protein were obtained and diffracted to 2.2 Å, thus permitting the first detailed X-ray crystallography studies on a functionally active human complement regulator protein with direct therapeutic potential. (ox.ac.uk)
- To that end, truncated derivatives of CR1 whose extracellular part is composed of 30 tandem repeating modules, termed complement control protein repeats (CCPs), were generated. (wustl.edu)
- Homo sapiens] C5AR1 engage in crosstalk with TLR2 and Porphyromonas gingivalis, a major oral and systemic pathogen with complement C5 convertase-like activity, synergizes with C5a (fragment of complement protein C5) to increase cyclic adenosine monophosphate (cAMP) concentrations, resulting in suppression of macrophage immune function and enhanced pathogen survival. (innatedb.com)
- multiple cross-links are organic in often all normal surfaces where they suffer acylated first pathways been on their G-protein download data mining and predictive analysis intelligence gathering and. (evakoch.com)
- The classic and alternate pathway convertases cause C3 activation, forming C3a and C3b. (medscape.com)
Cleavage of complement2
- Here, we tested whether inhibition of the lectin pathway of complement could reduce the pathology and improve the outcomes in a murine model of LPS-induced lung injury that closely mimics ARDS in human. (bvsalud.org)
- This binding initiates deposition of the complement activation products C3b, C4b and C5b-9 on LPS via the lectin pathway. (bvsalud.org)
- Administration of HG4 (5mg/kg) in mice led to almost complete inhibition of the lectin pathway activation for 48hrs, and 50% inhibition at 60hrs post administration. (bvsalud.org)
- Inhibition of the lectin pathway in mice prior to LPS-induced lung injury improved all pathological markers tested. (bvsalud.org)
- Toxoplasma activated both the lectin (LP) and alternative (AP) pathways, and the deposition of C3b was both strain and lectin-dependent. (nih.gov)
- Dying cells also expose ligands that bind initiator molecules of the various complement pathways, so that complement activation and opsonin deposition on the dead cell surface may enhance phagocytotic clearance ( 1 , 8 ). (frontiersin.org)
- Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES. (lookformedical.com)
- The complement system is a key humoral component of innate immunity, and in addition to its many other functions, it is involved in the clearance of waste material, such as immune complexes and apoptotic and necrotic cells ( 1 , 2 ). (frontiersin.org)
- The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways and ultimately generate the cytolytic MAC (C5b-9). (eaglebio.com)
- It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A. (lookformedical.com)
Mediated the decay1
- Site 1 (CCPs 1-3) alone mediated the decay acceleration of the classical and alternative pathway C3 convertases. (wustl.edu)
- 40. Inhibition of human complement by a C3-binding peptide isolated from a phage-displayed random peptide library. (nih.gov)
- In addition to understanding the mechanism of complement inhibition by DAF through structural studies, there is also an interest in the possible therapeutic potential of the molecule. (ox.ac.uk)
- The classic pathway is activated by the interaction of C1 with an antigen-antibody complex. (medscape.com)
- This interaction results in the formation of C4b2a, which is the classic pathway C3b convertase. (medscape.com)
- First of all, complement can be activated through different mechanisms which are referred to as the classic pathway, the alternative pathway based on bacterial life of polysaccharide, and the alternative pathway based on spontaneous hydrolysis of C3. (hstalks.com)
- So, these three pathways, one, two and three, they all converge on one component called C5, that is hydrolyzed by what is called the C5 convertase, of which there are two types, one produced by the alternative pathways and the other produced by the classic pathway. (hstalks.com)
- But when an antigen-antibody reaction takes place here then C1q is recruited, the classic pathway starts. (hstalks.com)
- This provides a positive amplification loop for the classical and alternative complement pathways. (creative-biolabs.com)
- 22. Covalent association of C3b with C4b within C5 convertase of the classical complement pathway. (nih.gov)
- In vitro, LPS binds to murine and human collectin 11, human MBL and murine MBL-A, but not to C1q, the recognition subcomponent of the classical pathway. (bvsalud.org)
- All three pathways of the complement system (classical, lectin and alternative pathways) initiate the formation of MAC. (promisekit.org)
- A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. (lookformedical.com)
- This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY. (lookformedical.com)
- Interactions of the FHRs with pentraxins resulted in enhanced activation of both the classical and the alternative complement pathways on dead cells when exposed to human serum. (frontiersin.org)
- The initiator molecules of the classical (C1q) and lectin pathways (e.g. (frontiersin.org)
- Clinical presentations are similar for the three types of MPGN, but they manifest somewhat different mechanisms of complement activation and predisposition to recur in kidney transplants. (medscape.com)
- Complement activation in ARDS initiates a robust inflammatory reaction that can cause progressive endothelial injury in the lung. (bvsalud.org)
- The Bb fragment may be regarded as a better indicator of the complement activation pathway than Ba, because impaired renal filtration does directly affect Ba levels. (creative-biolabs.com)
- Because their roles in complement regulation is controversial and incompletely understood, we studied the interaction of FHR-1 and FHR-5 with DNA and dead cells and investigated whether they influence the regulatory role of FH and the complement activation on DNA and dead cells. (frontiersin.org)
- Both FHRs caused increased complement activation on DNA. (frontiersin.org)
- [ 3 ] The existence of multiple, complement-related AMD risk alleles has lent further support to this theory and has shed light on the role of uncontrolled alternative complement pathway activation in this disease. (medscape.com)
- There are three pathways of complement activation. (eaglebio.com)
- As a result the activation of the complement system is blocked. (eaglebio.com)
- And this can work at about thousand times faster than the spontaneous complement activation. (hstalks.com)
- But the spontaneous complement activation means that all the time, the complement must be regulated in order, as I said before, to avoid mischief. (hstalks.com)
- In affected patients, the alternative pathway produces C3 convertase, which amplifies C3 activation, resulting in the creation of C3b particles, and finally, the formation of C5 convertase to assemble MAC C5b-9. (chikd.org)
- The larger fragment C3b binds with C3 convertase to form C5 convertase. (lookformedical.com)
- The alternative pathway of complement represents an important humoral component of natural defense against microbial attack. (hycultbiotech.com)
- The complement system is an evolutionarily ancient key component of innate immunity required for the detection and removal of invading pathogens. (nih.gov)
- The complement system plays important roles in both innate and adaptive immune response and can produce an inflammatory and protective reaction to challenges from pathogens before an adaptive response can occur. (eaglebio.com)
- The leukocyte-specific complement receptor 3 (CR3, αMß2, CD11b/CD18) and complement receptor 4 (CR4, αXß2, CD11c/CD18) belong to the family of ß2-integrins. (bvsalud.org)
- Decay accelerating activity of complement receptor type 1 (CD35). (wustl.edu)
- Dive into the research topics of 'Decay accelerating activity of complement receptor type 1 (CD35). (wustl.edu)
- The polyadenylation site of this gene is 421 bp from the 5' end of the gene for complement component 2. (nih.gov)
- The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. (lookformedical.com)
- The biochemical basis of these, what are being called pathways but also being called cascades, is in general and that there are enzymatic reactions. (hstalks.com)
- 34. Formation of high-affinity C5 convertases of the alternative pathway of complement. (nih.gov)
- 33. The interaction of glycoprotein C of herpes simplex virus types 1 and 2 with the alternative complement pathway. (nih.gov)
- 36. The low C5 convertase activity of the C4A6 allotype of human complement component C4. (nih.gov)
- These results suggest that FXIa generation enhances the activity of the complement system and thus may potentiate the immune response. (bvsalud.org)
- Therefore, CVF continuously activates complement, resulting in the depletion of complement activity. (expasy.org)
- In contrast, for the C5 convertase, site 1 had only 0.5% of the decay accelerating activity, while site 2 had no detectable activity. (wustl.edu)
- Efficient C5 decay accelerating activity was detected in recombinants that carried both site 1 and site 2. (wustl.edu)
- The results indicate that, for the C5 convertases, decay accelerating activity is mediated primarily by site 1. (wustl.edu)
- The normal complement system consists of the classic and alternative pathways. (medscape.com)
- It is unknown whether FXI or its activated form, activated FXI (FXIa), directly interacts with the complement system. (bvsalud.org)
- In particular, work on the impact of complement on T cell responses led to the surprising discoveries that the complement system also functions within cells and is involved in regulating basic cellular processes, predominantly those of metabolic nature. (nih.gov)
- Rare genetic variants in the complement system have also been found to play an important role in AMD. (medscape.com)
- I will not discuss in detail the complement system which is illustrated here in this pathway. (hstalks.com)
- 2-5 The complement system recognizes features of microbial surfaces andmarks them for destruction by coating them with C3b. (qinqianshan.com)
- 32. Interaction of beta1H globulin with cell-bound C3b: quantitative analysis of binding and influence of alternative pathway components on binding. (nih.gov)
- The alternative pathway utilizes C3 and factors B and D to form the alternative pathway convertase C3b,Bb. (medscape.com)
- Several genes not involved in the complement cascade have also been implicated. (medscape.com)
- Regulating complement is an important step in the establishment of infection by microbial pathogens. (nih.gov)
- Both C3GN and idiopathic MPGN are caused by alternative complement pathway activations [ 3 ]. (chikd.org)
- Recently, new therapies have been suggested to target complement pathways, owing to an improvement in the understanding of the pathogenesis of C3G. (chikd.org)
- The first one is dedicated to explore the FH capacity to dissociate the alternative pathway C3 convertase, whereas the second one is designed to explore the capacity of FH to bind cell surfaces and to protect them from complement attack. (bvsalud.org)
- In venom , complement C3 homolog is a structural and functional analog of complement component C3b, the activated form of C3. (expasy.org)
- I will start with other hemolytic anaemias and then I will continue with Paroxysmal Nocturnal Hemoglubinuria or PNH, a disease on which I've worked on for many years, and in which the role of complement is particularly prominent and also important because it has been the target of a new form of therapy. (hstalks.com)
- C3GN also includes disease entities associated with complement mutation, which is causally associated with the underlying renal pathology, such as familial DDD with C3 mutation and familial C3GN with mutations in the CFHR genes. (chikd.org)
- The only other point I'd like to particularly bring to your attention is this, the alternative pathway shown here called spontaneous C3 hydrolysis means that at a low rate, the complement is activated all the time. (hstalks.com)