Sodium-Potassium-Exchanging ATPase
Adenosine Triphosphatases
Calcium-Transporting ATPases
Proton-Translocating ATPases
Adenosine Triphosphate
Sarcoplasmic Reticulum
Calcium
Vacuolar Proton-Translocating ATPases
Ouabain
Sarcoplasmic Reticulum Calcium-Transporting ATPases
Rabbits
Cell Membrane
Magnesium
Thapsigargin
Molecular Sequence Data
Amino Acid Sequence
Adenosine Diphosphate
CA1 Region, Hippocampal
Vanadates
Hydrogen-Ion Concentration
Potassium
CA3 Region, Hippocampal
Sodium
Binding Sites
Dicyclohexylcarbodiimide
Sodium-Calcium Exchanger
Protein Binding
Myosins
Calmodulin
Plasma Membrane Calcium-Transporting ATPases
Enzyme Inhibitors
Calcium-Binding Proteins
Protein Conformation
Enzyme Activation
Ion Transport
Calcium Channel Blockers
Phosphorylation
Fura-2
Caffeine
Fluorescent Dyes
Mutation
Biological Transport
Cytosol
Myocardium
Vanadium
Vacuoles
Biological Transport, Active
Oligomycins
Calcium Channels, L-Type
Intracellular Membranes
Protein Structure, Tertiary
Cation Transport Proteins
4-Nitrophenylphosphatase
Patch-Clamp Techniques
Cattle
Inositol 1,4,5-Trisphosphate
Saccharomyces cerevisiae
Macromolecular Substances
Ryanodine Receptor Calcium Release Channel
Rats, Sprague-Dawley
Microsomes
Chelating Agents
Dose-Response Relationship, Drug
Base Sequence
Electrophoresis, Polyacrylamide Gel
Protein Subunits
Inositol 1,4,5-Trisphosphate Receptors
Mitochondria
Actomyosin
Rats, Wistar
Swine
Cations, Divalent
Membrane Proteins
Models, Molecular
Escherichia coli
Adenylyl Imidodiphosphate
Proteolipids
Models, Biological
Ryanodine
Proton Pumps
Electrophysiology
Rubidium
Potassium Chloride
Myosin Subfragments
Osmolar Concentration
Isoenzymes
Ion Pumps
Carrier Proteins
Actins
Mitochondrial Proton-Translocating ATPases
Macrolides
Ionomycin
Lanthanum
Gills
Sequence Homology, Amino Acid
Mutagenesis, Site-Directed
Calcium Signaling
Aurovertins
Protons
Ionophores
DNA Helicases
Ruthenium Red
Cloning, Molecular
Calcium Radioisotopes
Nucleotides
Myocytes, Cardiac
Peptide Fragments
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Cytoplasm
Muscle, Skeletal
Cells, Cultured
Dogs
Temperature
Microscopy, Electron
Strontium
Fluorescein-5-isothiocyanate
CA2 Region, Hippocampal
Ion Channel Gating
Saccharomyces cerevisiae Proteins
Muscle, Smooth
Signal Transduction
Trypsin
Indoles
Myofibrils
Guinea Pigs
Kidney
Catalysis
Calcimycin
Valinomycin
Nifedipine
Hippocampus
Trifluoperazine
Blotting, Western
Manganese
Structure-Activity Relationship
Substrate Specificity
RNA, Messenger
Xanthenes
Membrane Potentials
Neurons
Barium
Troponin
Calcium Channel Agonists
Aequorin
4-Chloro-7-nitrobenzofurazan
Microscopy, Confocal
Recombinant Fusion Proteins
Cations
Potassium Channels
Ion Channels
Submitochondrial Particles
Erythrocyte Membrane
Erythrosine
Rutamycin
Calmodulin-Binding Proteins
Detergents
Potassium Channels, Calcium-Activated
Exocytosis
Action Potentials
Molecular Chaperones
Carbachol
Protein Structure, Secondary
Parietal Cells, Gastric
Cardiac Glycosides
Fluoresceins
Bacterial Proton-Translocating ATPases
Carbonyl Cyanide m-Chlorophenyl Hydrazone
Cyclic AMP
Troponin C
Muscle Fibers, Skeletal
HSP70 Heat-Shock Proteins
The main symptoms of Menkes syndrome are:
1. Steel-gray or kinky hair, which starts to appear within the first few months of life.
2. Failure to thrive, poor muscle tone, and low birth weight.
3. Developmental delays and intellectual disability.
4. Seizures and poor coordination.
5. Poor immune function and recurrent infections.
6. Gradual loss of vision and hearing.
7. Osteoporosis and fragile bones.
8. Increased risk of liver disease, including cirrhosis and portal hypertension.
The diagnosis of Menkes syndrome is based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment is focused on managing the symptoms and preventing complications, and may include copper supplements, anticonvulsants, and other medications.
The prognosis for Menkes syndrome is poor, with most individuals dying in childhood or adolescence due to complications such as liver disease, infections, or seizures. However, some individuals may live into their 20s or 30s with appropriate management and care.
Darier disease is a rare genetic disorder that affects the skin and mucous membranes, characterized by thickened, crusted, or scaly skin plaques and blisters on the palms of the hands and soles of the feet. It is caused by mutations in the gene encoding the enzyme keratin 5 (KRT5), which leads to abnormal production of keratin proteins that are essential for maintaining the skin's integrity. The disease is named after Dr. Jean Darier, a French dermatologist who first described it in the early 20th century.
Etymology: Named after Jean Darier, a French dermatologist who first described the condition in the early 20th century.
Symptoms of Darier disease typically appear in the first few months of life and may include:
* Thickened, crusted, or scaly skin plaques on the palms of the hands and soles of the feet
* Blisters that may burst and crust over
* Cracks in the skin that can become infected
* Redness and swelling around the affected areas
* Skin fold dermatitis (inflammation of the skin folds, such as those found in the armpits or groin)
Darier disease is a rare condition, affecting approximately 1 in 50,000 to 1 in 100,000 individuals worldwide. It can be challenging to diagnose, as it can resemble other skin conditions such as eczema or psoriasis. A diagnosis of Darier disease is typically made based on a combination of clinical features and genetic testing.
Treatment for Darier disease may include topical medications, such as corticosteroids or retinoids, to reduce inflammation and promote skin healing. In severe cases, systemic medications such as antibiotics or immunosuppressants may be prescribed. Phototherapy, which involves exposure to specific wavelengths of light, can also be helpful in managing the condition.
In addition to these treatments, individuals with Darier disease may need to take precautions to protect their skin from irritation and infection. This may include avoiding harsh soaps or detergents, wearing loose-fitting clothing, and staying hydrated to maintain skin moisture.
Overall, while Darier disease can be a challenging condition to manage, with appropriate treatment and self-care, individuals with this condition can lead fulfilling lives. It is important for individuals with Darier disease to work closely with their healthcare provider to develop a personalized treatment plan that meets their individual needs.
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.
The symptoms of BFP typically appear in early adulthood and can include:
* Blisters and sores on the skin and mucous membranes
* Pain and discomfort
* Scarring and disfigurement
* Difficulty swallowing (in severe cases)
BFP is diagnosed through a combination of clinical evaluation, family history, and genetic testing. Treatment for the condition typically involves managing the symptoms and preventing complications. This may include:
* Topical medications to reduce inflammation and promote healing
* Oral medications to suppress the immune system and prevent further blistering
* Physical therapy to improve mobility and reduce pain
While there is no cure for BFP, early diagnosis and appropriate treatment can help to manage the symptoms and improve quality of life. The condition is typically inherited in an autosomal dominant pattern, which means that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations rather than inheritance.
There are several types of RTA, including:
1. Type 1 RTA: This is caused by a defect in the genes that code for the proteins involved in acid secretion in the renal tubules.
2. Type 2 RTA: This is caused by damage to the renal tubules, such as from exposure to certain drugs or toxins.
3. Type 4 RTA: This is caused by a deficiency of the hormone aldosterone, which helps regulate electrolyte levels in the body.
Symptoms of RTA can include:
* Nausea and vomiting
* Abdominal pain
* Fatigue
* Weakness
* Dehydration
* Increased heart rate
* Decreased urine production
RTA can be diagnosed through blood tests that measure the pH levels in the body, as well as tests that assess kidney function and electrolyte levels. Treatment for RTA typically involves correcting any underlying causes, such as stopping certain medications or addressing electrolyte imbalances. In some cases, medications may be prescribed to help regulate acid levels in the body.
Prevention of RTA includes maintaining proper hydration, avoiding exposure to harmful substances, and managing any underlying medical conditions that may increase the risk of developing RTA. Early detection and treatment can help prevent complications and improve outcomes for individuals with RTA.
The hepatolenticular tract is a complex system of nerve fibers that connect the liver and other organs in the body, allowing for the exchange of information and coordination of bodily functions. HLD occurs when these nerve fibers are damaged or destroyed, leading to problems with brain function and communication.
The symptoms of HLD can vary depending on the severity of the damage and the specific areas of the brain affected. Common symptoms include difficulty with memory and cognitive function, poor coordination and balance, and changes in behavior and personality. In severe cases, HLD can lead to coma or even death.
There is currently no cure for HLD, but there are several treatments available that can help manage the symptoms and slow the progression of the disease. These may include medications to reduce inflammation and oxidative stress, as well as physical therapy and rehabilitation to improve cognitive and motor function. In some cases, liver transplantation may be necessary to treat underlying liver disease.
Overall, hepatobilayer degeneration is a serious condition that can have significant effects on brain function and quality of life. If you suspect that you or someone you know may be experiencing symptoms of HLD, it is important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.
Medical Term: Cardiomegaly
Definition: An abnormal enlargement of the heart.
Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.
Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.
Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.
Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.
Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.
There are two main types of heart failure:
1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.
Symptoms of heart failure may include:
* Shortness of breath
* Fatigue
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness
Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).
It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
Causes of Potassium Deficiency:
There are several factors that can contribute to potassium deficiency, including:
1. Poor diet: A diet that is low in potassium-rich foods, such as fruits, vegetables, and whole grains, can lead to a deficiency.
2. Diarrhea and vomiting: These gastrointestinal issues can cause the body to lose excessive amounts of potassium, leading to a deficiency.
3. Certain medications: Diuretics, laxatives, and certain antibiotics can cause potassium loss in the urine or stool.
4. Kidney problems: Kidney disease or dysfunction can impair the body's ability to retain potassium, leading to a deficiency.
5. Hormonal imbalances: Certain hormonal imbalances, such as excessive production of aldosterone, can cause potassium loss and deficiency.
Symptoms of Potassium Deficiency:
The symptoms of potassium deficiency can vary in severity and may include:
1. Muscle weakness and cramping
2. Fatigue and lethargy
3. Heart palpitations and arrhythmias
4. Abnormal heart rhythms
5. Constipation
6. Nausea and vomiting
7. Headaches
8. Muscle twitching and spasms
9. Inability to regulate blood pressure
10. Decreased reflexes and response to stimuli
Diagnosis of Potassium Deficiency:
Potassium deficiency is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Blood tests: Measurement of potassium levels in the blood can confirm a deficiency.
2. Urine tests: Measurement of potassium excretion in the urine can help identify excessive potassium loss.
3. Electrocardiogram (ECG): An ECG can detect abnormal heart rhythms and signs of potassium deficiency.
4. Physical examination: Signs such as muscle weakness, cramping, and twitching can indicate potassium deficiency.
Treatment of Potassium Deficiency:
The treatment of potassium deficiency typically involves correcting the underlying cause and supplementing with potassium salts. The goal is to restore normal potassium levels and prevent complications such as cardiac arrhythmias and muscle weakness. Treatment may include:
1. Dietary changes: Increasing potassium-rich foods such as bananas, avocados, and leafy greens can help restore normal potassium levels.
2. Potassium supplements: Oral or intravenous supplements can be used to replenish potassium stores.
3. Addressing underlying causes: Identifying and treating conditions such as diabetes, kidney disease, or excessive vomiting can help resolve the potassium deficiency.
4. Monitoring: Regular blood tests and electrocardiograms are necessary to monitor potassium levels and ensure that the treatment is effective.
In conclusion, potassium deficiency can have serious consequences if left untreated. It is important to be aware of the causes, symptoms, and treatment options for this condition. If you suspect you or someone you know may have a potassium deficiency, consult with a healthcare professional for proper diagnosis and treatment.
There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:
1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.
It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.
The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.
Symptoms of malignant hyperthermia can include:
* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure
If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.
Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
The normal range for potassium levels in the blood varies depending on age, gender, and other factors, but generally it is between 3.5 and 5.5 mEq/L (milliequivalents per liter).
Hypokalemia can be caused by a variety of factors such as diarrhea, vomiting, certain medications (diuretics, laxatives), kidney disease or malfunctioning of the parathyroid glands.
The most common cause of hyperthyroidism is an autoimmune disorder called Graves' disease, which causes the thyroid gland to produce too much thyroxine (T4) and triiodothyronine (T3). Other causes include inflammation of the thyroid gland (thyroiditis), thyroid nodules, and certain medications.
Symptoms of hyperthyroidism can vary depending on the severity of the condition, but may include:
* Rapid weight loss
* Nervousness or irritability
* Increased heart rate
* Heat intolerance
* Changes in menstrual cycle
* Fatigue
* Muscle weakness
* tremors
If left untreated, hyperthyroidism can lead to more serious complications such as heart problems, bone loss, and eye problems. Treatment options for hyperthyroidism include medications to reduce hormone production, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.
In pregnant women, untreated hyperthyroidism can increase the risk of miscarriage, preterm labor, and intellectual disability in the baby. Treatment options for pregnant women with hyperthyroidism are similar to those for non-pregnant adults, but may need to be adjusted to avoid harm to the developing fetus.
It is important for individuals suspected of having hyperthyroidism to seek medical attention as soon as possible to receive proper diagnosis and treatment. Early treatment can help prevent complications and improve quality of life.
There are several possible causes of dilated cardiomyopathy, including:
1. Coronary artery disease: This is the most common cause of dilated cardiomyopathy, and it occurs when the coronary arteries become narrowed or blocked, leading to a decrease in blood flow to the heart muscle.
2. High blood pressure: Prolonged high blood pressure can cause the heart muscle to become weakened and enlarged.
3. Heart valve disease: Dysfunctional heart valves can lead to an increased workload on the heart, which can cause dilated cardiomyopathy.
4. Congenital heart defects: Some congenital heart defects can lead to an enlarged heart and dilated cardiomyopathy.
5. Alcohol abuse: Chronic alcohol abuse can damage the heart muscle and lead to dilated cardiomyopathy.
6. Viral infections: Some viral infections, such as myocarditis, can cause inflammation of the heart muscle and lead to dilated cardiomyopathy.
7. Genetic disorders: Certain genetic disorders, such as hypertrophic cardiomyopathy, can cause dilated cardiomyopathy.
8. Obesity: Obesity is a risk factor for developing dilated cardiomyopathy, particularly in younger people.
9. Diabetes: Diabetes can increase the risk of developing dilated cardiomyopathy, especially if left untreated or poorly controlled.
10. Age: Dilated cardiomyopathy is more common in older adults, with the majority of cases occurring in people over the age of 65.
It's important to note that many people with these risk factors will not develop dilated cardiomyopathy, and some people without any known risk factors can still develop the condition. If you suspect you or someone you know may have dilated cardiomyopathy, it's important to consult a healthcare professional for proper diagnosis and treatment.
Measurement:
Cardiac output is typically measured using invasive or non-invasive methods. Invasive methods involve inserting a catheter into the heart to directly measure cardiac output. Non-invasive methods include echocardiography, MRI, and CT scans. These tests can provide an estimate of cardiac output based on the volume of blood being pumped out of the heart and the rate at which it is being pumped.
Causes:
There are several factors that can contribute to low cardiac output. These include:
1. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs, leading to fatigue and shortness of breath.
2. Anemia: A low red blood cell count can reduce the amount of oxygen being delivered to the body's tissues, leading to fatigue and weakness.
3. Medication side effects: Certain medications, such as beta blockers, can slow down the heart rate and reduce cardiac output.
4. Sepsis: A severe infection can lead to inflammation throughout the body, which can affect the heart's ability to pump blood effectively.
5. Myocardial infarction (heart attack): This occurs when the heart muscle is damaged due to a lack of oxygen, leading to reduced cardiac output.
Symptoms:
Low cardiac output can cause a range of symptoms, including:
1. Fatigue and weakness
2. Dizziness and lightheadedness
3. Shortness of breath
4. Pale skin
5. Decreased urine output
6. Confusion and disorientation
Treatment:
The treatment of low cardiac output depends on the underlying cause. Treatment may include:
1. Medications to increase heart rate and contractility
2. Diuretics to reduce fluid buildup in the body
3. Oxygen therapy to increase oxygenation of tissues
4. Mechanical support devices, such as intra-aortic balloon pumps or ventricular assist devices
5. Surgery to repair or replace damaged heart tissue
6. Lifestyle changes, such as a healthy diet and regular exercise, to improve cardiovascular health.
Prevention:
Preventing low cardiac output involves managing any underlying medical conditions, taking medications as directed, and making lifestyle changes to improve cardiovascular health. This may include:
1. Monitoring and controlling blood pressure
2. Managing diabetes and other chronic conditions
3. Avoiding substances that can damage the heart, such as tobacco and excessive alcohol
4. Exercising regularly
5. Eating a healthy diet that is low in saturated fats and cholesterol
6. Maintaining a healthy weight.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.
Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:
1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.
Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.
Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.
ATP2B2
List of MeSH codes (D08)
Michael Fehlings
Digoxin immune fab
Sodium-hydrogen exchange regulatory cofactor 2
Virophage
Iberiotoxin
Discovery and development of proton pump inhibitors
Tumor necrosis factor receptor 1
Macrolide
Magnesium deficiency
List of examples of convergent evolution
Posaconazole
Omeprazole
Heat shock protein 90kDa alpha (cytosolic), member A1
Neuroprotection
P-type ATPase
Friedreich's ataxia
S100A11
Hashimoto's encephalopathy
Copper toxicity
Esomeprazole
Pumiliotoxin 251D
Muscle contraction
CHD3
Methylene blue
Nicotinic acid adenine dinucleotide phosphate
Nucleoid
Human tooth development
Adeno-associated virus
Cells | Free Full-Text | Melatonin in Medicinal and Food Plants: Occurrence, Bioavailability, and Health Potential for Humans
Publication Detail
Mouse/Rat CD39L1/ENTPD2 Antibody AF5797: R&D Systems
Pesquisa | Portal Regional da BVS
Biomarkers Search
Neuroprotective effects of α-Lipoic acid alone and in combination with ferulic acid in diabetic neuropathy induced rats | E...
Green Tea Extract | Herbal Magic Dietary Supplement
N-Ethylmaleimide - CAS 128-53-0 - Calbiochem | 34115
Physiology, Glycosuria - StatPearls - NCBI Bookshelf
Peter W Schuck | National Institute of Biomedical Imaging and Bioengineering
MH - Aberrant Motor Behavior in Dementia
Effects of benzo(a)pyrene exposure on the ATPase activity and calcium concentration
in the hippocampus of neonatal rats
...
Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy
The effect of extracts of the roots of the stinging nettle (Urtica dioica) on the interaction of SHBG with its receptor on...
The use of ER targeted aequorin to study store-operated Ca²z inflow in a liver cell line - Rare & Special e-Zone
Sodium chloride decreases cadmium accumulation and changes the response of metabolites to cadmium stress in the halophyte...
Study of some Indian medicinal plants by application of INAA and AAS techniques
Isolation of Waddlia malaysiensis, A Novel Intracellular Bacterium, from Fruit Bat (Eonycteris spelaea) - Volume 11, Number 2...
Comparative Analysis of Spontaneous and Stimulus-Evoked Calcium Transients in Proliferating and Differentiating Human Midbrain...
P2X2 receptor subunit interfaces are missense variant hotspots where mutations tend to increase apparent ATP affinity | bioRxiv
Metabolic Acidosis: Practice Essentials, Background, Etiology
OCT4 cooperates with distinct ATP-dependent chromatin remodelers in naïve and primed pluripotent states in human | Nature...
NLM/TIRC-81/2
Ecto-ATPase - New dimension in therapeutic targeting of BCL-2 family
THE TOXIC METAL CONNECTION by B. Windham - Fluoridation Australia
Endoplasmic reticulum4
- Apoaequorin was targeted to the cytosol, nucleus, and endoplasmic reticulum of HeLa cells in order to determine the effect of Ca(2+) release from the ER on protein degradation. (nih.gov)
- Also inhibits sarco/endoplasmic reticulum Ca 2+ -ATPase (IC 50 = 5 - 50 μ M). (tocris.com)
- One of the main physiological roles of SOCs is to maintain an adequate Ca 2+ concentration in the endoplasmic reticulum (ER). (edu.hk)
- The bacteria interfere with BiP-assisted folding of newly-made Na-K-ATPase subunits in the endoplasmic reticulum, accelerating their ubiquitylation and proteasomal degradation and decreasing efficiency of the assembly of native enzyme. (takebackamericabook.com)
Adenosine triphosphatase3
- Calcium-adenosine triphosphatase (Ca(++)-ATPase) and sodium, potassium, magnesium-adenosine triphosphatase (Na+, K+, Mg(++)-ATPase) activities were significantly increased after 4 or 2 hours incubation with 20 microM Triol, respectively. (nih.gov)
- Almost all enzymes involved in phosphorus reactions (eg, adenosine triphosphatase [ATPase]) require magnesium for activation. (medscape.com)
- The activity of calcium adenosine triphosphatase (Ca 2+ -ATPase), sodium-potassium adenosine triphosphatase (Na + -K + -ATPase) and calcium-magnesium adenosine triphosphatase (Ca 2+ -Mg 2+ -ATPase) in the hippocampus were detected by commercial kits. (ijomeh.eu)
Enzymes1
- To test this hypothesis, endothelial monolayers were treated with 20 microM Triol and the activities of selected membrane enzymes were measured at 0, 2, 4, 6, 12 and 24 hours. (nih.gov)
Glutathione4
- On the last day of the treatment, the animals´ brains were extracted to measure the levels of oxidative stress markers [H2O2, Ca2+,Mg2+-ATPase, glutathione and lipid peroxidation (TBARS)], dopamine and 5-HIAA in the cortex, striatum and cerebellum/medulla oblongata by validated methods. (bvsalud.org)
- Their brains were extracted to measure H2O2, Ca+2, Mg+2 ATPase, glutathione (GSH), lipid peroxidation (Tbars) and Dopamine. (bvsalud.org)
- The animals were sacrificed and their brains were obtained and used to measure lipoperoxidation (TBARS), H2O2, Na+, K+ ATPase, glutathione (GSH), serotonin metabolite (5-HIAA) and dopamine. (bvsalud.org)
- Biochemical parameters of blood glucose, nitric oxide, level of lipid peroxidase, reduced glutathione, and membrane-bound ATPases activities were also studied. (e-namtila.com)
SERCA1
- SERCA ATPase blocker. (tocris.com)
Calcium3
- 2. Intracellular Ca(2+)-Mg(2+)-ATPase regulates calcium influx and acrosomal exocytosis in bull and ram spermatozoa. (nih.gov)
- We provide evidence for the existence of intracellular calcium stores that respond to muscarinic activation of the cells, having sensitivity for ryanodine and thapsigargin possibly reflecting IP 3 receptor activity and the presence of ryanodine receptors and calcium ATPase pumps. (hindawi.com)
- Removal of calcium was dependent on plasma membrane calcium pump activity and Na + -Ca 2+ exchange [ 25 - 27 ]. (hindawi.com)
Neonatal4
- 1-Mekail, A., Raof, A. Study the activity of Na+-K+-ATPase and Ca+2-Mg+2- ATPase in Neonatal and adult rats intoxicated with Diazinon,Carbaryl, And Lambdacyhalothrin. (uod.ac)
- Eighty neonatal Sprague Dawley (SD) rats were randomly divided into 5 groups (untreated control group, vehicle group, 0.02 mg/kg, 0.2 mg/kg and 2 mg/kg B(a)P-exposed group). (ijomeh.eu)
- Benzo(a)pyrene exposure caused the significant decrease in the ATPase activity in the hippocampus and caused Ca 2+ overload in the synaptic, besides, the ROS concentration increased significantly which may further induce neurobehavioral impairment of the neonatal rats. (ijomeh.eu)
- Our findings suggest that postnatal B(a)P exposure may cause the neurobehavioral impairments in the neonatal rats, which were mediated by the decreased ATPase activity and elevated Ca 2+ concentration. (ijomeh.eu)
Lipid1
- Hemoglobin degradation, lipid peroxidation, and inhibition of Na /K( )-ATPase in rat erythrocytes exposed to acrylonitrile. (nih.gov)
Rats3
- 2-Abdal TA et al.Effects of aloe vera extracted on liver and kidney function changes induced by hydrogen peroxide in rats.Int J Res Med Sci. (uod.ac)
- Diabetic neuropathy in rats was induced by administering a freshly prepared single dose of streptozotocin (60 mg/kg, i.p). (e-namtila.com)
- After development of neuropathy the rats were treated with α-lipoic acid (25 mg/kg/day, p.o), ferulic acid (10 mg/kg/day, p.o) and standard drug Pregabalin (30 mg/kg/day i.p). (e-namtila.com)
MicroM2
- However, release of Ca(2+) from the ER, initiated by the addition of inhibitors of the ER Ca(2+)/Mg(2+) ATPase such as 2 microM thapsigargin or 1 microM ionomycin, initiated rapid loss of apoaequorin in the ER, but had no detectable effect on apoaequorin turnover in the cytosol nor the nucleus. (nih.gov)
- Compared with all concentrations tested 40 microM Triol increased Ca(++)-ATPase activity most markedly, with a significant increase already after a 2-hour exposure. (nih.gov)
Inhibits1
- Sulfhydryl alkylating reagent that inhibits H + -ATPase and suppresses the short circuit current (IC₅₀ = 22 µM) in pancreatic duct cells. (emdmillipore.com)
Concentration3
- Normal plasma magnesium concentration is 1.7-2.1 mg/dL (0.7-0.9 mmol, or 1.4-1.8 mEq/L). (medscape.com)
- Fura-2 pentakis(acetoxymethyl) (Fura-2/AM) probe and reactive oxygen species (ROS) reagent kit were used for measuring the concentration of Ca 2+ and ROS in the hippocampus synapse, respectively. (ijomeh.eu)
- It is clear, however, that the activation of SOCs is triggered by a decrease in the concentration of Ca 2+ in the ER. (edu.hk)
Thapsigargin1
- 4. Thapsigargin-sensitive Ca(2+)-ATPases account for Ca2+ uptake to inositol 1,4,5-trisphosphate-sensitive and caffeine-sensitive Ca2+ stores in adrenal chromaffin cells. (nih.gov)
Transient2
- Transient increases in aequorin-generated luminescence induced by Ca 2+ addition were also imaged in single H4-IIE cells using a Photon Imaging Microscope. (edu.hk)
- Transient receptor potential melastatin member 4 (TRPM4), a Ca 2+ -activated nonselective cation channel, has been found to mediate cell membrane depolarization in immune response, insulin secretion, cardiovascular diseases, and cancer. (biomedcentral.com)
Decrease1
- An effect of around the Na-K-ATPase has been suggested in the past, in two studies with data demonstrating that broth culture filtrate from cytotoxin-producing strains of prospects to a decrease in K+-dependent Prasugrel Hydrochloride phosphatase activity (55, 58). (takebackamericabook.com)
Potent2
- Also a potent inhibitor of both Mg 2+ and Ca 2+ /Mg 2+ -stimulated DNA fragmentation in rat liver nuclei. (emdmillipore.com)
- Paxilline is a potent blocker of high-conductance Ca 2+ -activated K + (BK Ca , K Ca 1.1) channels. (tocris.com)
Protein2
Intracellular3
- 7. An inositol 1,4,5-trisphosphate receptor-gated intracellular Ca(2+) store is involved in regulating sperm hyperactivated motility. (nih.gov)
- Hypomagnesemia-serum levels of magnesium levels below the usual reference range of 1.5 to 2.5 mg/dL-can result from decreased intake, redistribution of magnesium from the extracellular to the intracellular space, or increased renal or gastrointestinal loss. (medscape.com)
- One of the central pathophysiological mechanisms leading to axonal and cellular injury is intracellular Na + /Ca 2+ overload to which neurons and oligodendrocytes demonstrate a selective vulnerability [ 5 ]. (biomedcentral.com)
20001
- 2000 Proceedings of the Second International Workshop on Ecto-ATPases and Related Ectonucleotidases:18. (rndsystems.com)
Molecular1
- Kumaran Ramamurthi received his Ph.D. in Molecular Biology from the University of California, Los Angeles (UCLA), where he studied the secretion of bacterial virulence proteins. (nih.gov)
Endothelial2
- Stimulates arachidonic acid release through activation of PLA 2 in endothelial cells. (emdmillipore.com)
- Zyrianova T, Lopez B, Liao A, Gu C, Wong L, Ottolia M, Olcese R, Schwingshackl A. BK Channels Regulate LPS-induced CCL-2 Release from Human Pulmonary Endothelial Cells. . (ucla.edu)
Activity2
- However, these studies did not directly measure Na-K-ATPase large quantity or activity, so the aim of the present study was to determine whether indeed targets the Na-K-ATPase in gastric epithelial cells. (takebackamericabook.com)
- Reformulation of an extant ATPase active site to mimic ancestral GTPase activity reveals a nucleotide base requirement for function. (nih.gov)
Membrane3
- Store-Operated Ca 2+ Channels (SOCs) are present in the plasma membrane of liver cells, all other "non-excitable" cells and many "excitable" animal cells. (edu.hk)
- The Na-K-ATPase is an essential membrane transport enzyme expressed in the vast majority of animal cells. (takebackamericabook.com)
- The results demonstrate that this attachment of to gastric cells impairs chaperone-assisted maturation of the Na-K-ATPase in the ER, leading to the defective assembly of /-heterodimers, accelerates ER-associated degradation of unassembled subunits, and decreases levels of mature Na-K-ATPase molecules in the plasma membrane. (takebackamericabook.com)
Degradation1
- Thus, katanin levels are stringently controlled upon the species catalyze ATP-dependent microtubule severing in transition from meiosis to mitosis via two parallel proteo- vitro, and fidgetin causes microtubule disassembly when lytic degradation pathways, the CUL-3 and MBK-2 path- overexpressed in vivo [7 ]. (nih.gov)
Streptozotocin1
- DM was induced by streptozotocin (40 mg/kg, i.p. (biomedcentral.com)
Enzyme1
- CD39L1 is a Ca 2+ - and Mg 2+ -dependent enzyme that activates platelets by preferentially converting ATP to ADP (2). (rndsystems.com)
Vascular2
- It is considered to be a therapeutic target for thromboregulation and the treatment of vascular inflammation (2, 4). (rndsystems.com)
- Binds to the α -subunit of BK Ca (K i = 1.9 nM for block of currents in α -subunit-expressing oocytes) and enhances binding of charybdotoxin to BK Ca channels in vascular smooth muscle. (tocris.com)
Roles1
- Geering K. Functional roles of Na,K-ATPase subunits. (takebackamericabook.com)
Dose1
- Cln1 −/− mice received an oral dose (100 mg/kg/day) of CBD for six months and were evaluated for changes in pathological markers of disease and seizures. (nature.com)
Neuronal1
- The hallmark of demyelinating disease is the formation of the sclerotic plaque, which represents the end of a pathological process involving inflammation, oligodendrocyte depletion, astrocytosis, and neuronal and axon degeneration [ 2 ]. (biomedcentral.com)
Antioxidants3
- One group received the combination of antioxidants, i.e.,α-lipoic acid (12mg/kg, p.o) and ferulic acid (05 mg/kg/day, p.o) respectively, for two weeks. (e-namtila.com)
- Several studies have reported the preventive role of antioxidants in the progression of neuropathic pain [2]. (e-namtila.com)
- 1,2,3,4 Antioxidants are required to help quench these toxins and reduce damage to surrounding environments. (herbalmagic.ca)
Life Sci1
- Cell Mol Life Sci 80 (2): 54. (genetargeting.com)
Doses2
- group 4, insulin + three doses of sildenafil every 24 hours (50 U kg-1 + 50 mg kg-1). (bvsalud.org)
- Doses up to 240 mg daily have been administered. (nih.gov)
Activation1
- The aim of my project was to use aequorin, a Ca 2+ -sensitive photoprotein, specifically targeted to the ER (ERAEQ) to further investigate the role of ER Ca 2+ and the part played by (Ca 2+ + Mg 2+ ) ATPases (SERCAs) in the activation of SOCs. (edu.hk)
Describes1
- A 2-dimensional ratchet model describes assembly initiation of a specialized bacterial cell surface. (nih.gov)
Release1
- 20 mg, light yellow to yellow color, oval shaped, biconvex, delayed-release tablets imprinted "A6" with black ink on one side and plain on the other side. (nih.gov)
Presence2
- 20 min) was completely inhibited in the presence of 1 mM Ca(2+), and this effect was independent of the ER retention signal KDEL at the C-terminus. (nih.gov)
- and 5 ) The degree of ER-refilling that occurs in the presence of the cytoplasmic Ca 2+ chelator DBB-AM, suggests that Ca 2+ entering the cell via SOCs passes into the ER by a more direct route through the subplasmalemmal space, rather than through the deeper cytoplasmic space. (edu.hk)
Injury1
- The Na-K-ATPase comprises a catalytic -subunit and a structural could represent a potential source of gastric injury. (takebackamericabook.com)
Role2
Occurs1
- In contrast with other ions, magnesium is treated differently in two major respects: (1) bone, the principal reservoir of magnesium, does not readily exchange magnesium with circulating magnesium in the extracellular fluid space and (2) only limited hormonal modulation of urinary magnesium excretion occurs. (medscape.com)
Receipt1
- Simply email [email protected] within seven (7) days of receipt of your order to obtain a Return Merchandise Authorization (RMA#). (herbalmagic.ca)