umarjan11/Medical-qna huggingface dataset:
Question: How to prevent Parasites - Lymphatic Filariasis ?

Answer: The best way to prevent lymphatic filariasis is to avoid mosquito bites. The mosquitoes that carry the microscopic worms usually bite between the hours of dusk and dawn. If you live in an area with lymphatic filariasis:
   
    - at night 
     
      - sleep in an air-conditioned room or
      - sleep under a mosquito net
     
    - between dusk and dawn 
     
      - wear long sleeves and trousers and
      - use mosquito repellent on exposed skin.
     
   
   
Another approach to prevention includes giving entire communities medicine that kills the microscopic worms -- and controlling mosquitoes. Annual mass treatment reduces the level of microfilariae in the blood and thus, diminishes transmission of infection. This is the basis of the global campaign to eliminate lymphatic filariasis.
   
Experts consider that lymphatic filariasis, a neglected tropical disease (NTD), can be eradicated and a global campaign to eliminate lymphatic filariasis as a public health problem is under way. The elimination strategy is based on annual treatment of whole communities with combinations of drugs that kill the microfilariae. As a result of the generous contributions of these drugs by the companies that make them, tens of millions of people are being treated each year. Since these drugs also reduce levels of infection with intestinal worms, benefits of treatment extend beyond lymphatic filariasis. Successful campaigns to eliminate lymphatic filariasis have taken place in China and other countries.
   
More on: Insect Bite Prevention
Question: What are the genetic changes related to Bart-Pumphrey syndrome ?

Answer: Bart-Pumphrey syndrome is caused by mutations in the GJB2 gene. This gene provides instructions for making a protein called gap junction beta 2, more commonly known as connexin 26. Connexin 26 is a member of the connexin protein family. Connexin proteins form channels called gap junctions that permit the transport of nutrients, charged atoms (ions), and signaling molecules between neighboring cells that are in contact with each other. Gap junctions made with connexin 26 transport potassium ions and certain small molecules.  Connexin 26 is found in cells throughout the body, including the inner ear and the skin. In the inner ear, channels made from connexin 26 are found in a snail-shaped structure called the cochlea. These channels may help to maintain the proper level of potassium ions required for the conversion of sound waves to electrical nerve impulses. This conversion is essential for normal hearing. In addition, connexin 26 may be involved in the maturation of certain cells in the cochlea. Connexin 26 also plays a role in the growth, maturation, and stability of the outermost layer of skin (the epidermis).  The GJB2 gene mutations that cause Bart-Pumphrey syndrome change single protein building blocks (amino acids) in the connexin 26 protein. The altered protein probably disrupts the function of normal connexin 26 in cells, and may interfere with the function of other connexin proteins. This disruption could affect skin growth and also impair hearing by disturbing the conversion of sound waves to nerve impulses.
Question: What is (are) renal tubular dysgenesis ?

Answer: Renal tubular dysgenesis is a severe kidney disorder characterized by abnormal development of the kidneys before birth. In particular, kidney structures called proximal tubules are absent or underdeveloped. These structures help to reabsorb needed nutrients, water, and other materials into the blood and excrete everything else into the urine. Without functional proximal tubules, the kidneys cannot produce urine (a condition called anuria).  Fetal urine is the major component of the fluid that surrounds the fetus (amniotic fluid), and anuria leads to decreased amniotic fluid levels (oligohydramnios). Amniotic fluid helps cushion and protect the fetus and plays a role in the development of many organs, including the lungs. Oligohydramnios causes a set of abnormalities called the Potter sequence, which includes distinctive facial features such as a flattened nose and large, low-set ears; excess skin; inward- and upward-turning feet (clubfeet); and underdeveloped lungs.  Renal tubular dysgenesis also causes severe low blood pressure (hypotension). In addition, bone development in the skull is abnormal in some affected individuals, causing a large space between the bones of the skull (fontanels).  As a result of the serious health problems caused by renal tubular dysgenesis, affected individuals usually die before birth, are stillborn, or die soon after birth from respiratory failure. Rarely, with treatment, affected individuals survive into childhood. Their blood pressure usually normalizes, but they quickly develop chronic kidney disease, which is characterized by reduced kidney function that worsens over time.
Question: What is (are) Kidney Failure: Eat Right to Feel Right on Hemodialysis ?

Answer: Before you were on dialysis, your doctor may have told you to follow a low-protein diet. Being on dialysis changes this. Most people on dialysis are encouraged to eat as much high-quality protein as they can. Protein helps you keep muscle and repair tissue. The better nourished you are, the healthier you will be. You will also have greater resistance to infection and recover from surgery more quickly.
                
Your body breaks protein down into a waste product called urea. If urea builds up in your blood, it's a sign you have become very sick. Eating mostly high-quality proteins is important because they produce less waste than others. High-quality proteins come from meat, fish, poultry, and eggs (especially egg whites).
                

                
Talk With a Dietitian   Meat, fish, and chicken are good sources of protein. Talk with a dietitian about the meats you eat.   I will eat ______ servings of meat each day. A regular serving size is 3 ounces. This is about the size of the palm of your hand or a deck of cards.   Try to choose lean (low-fat) meats that are also low in phosphorus. If you are a vegetarian, ask about other ways to get your protein.   Low-fat milk is a good source of protein. But milk is high in phosphorus and potassium. And milk adds to your fluid intake. Talk with a dietitian to see if milk fits into your food plan.   I (will) (will not) drink milk. I will drink ______ cup(s) of milk a day.
Question: What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

Answer: Most peoplewith or without CKDcan get the daily protein they need by eating two 3-ounce servings of meat or meat substitute. A 3-ounce serving of meat is about the size of a deck of cards or the palm of a persons hand.
                
A renal dietitian can help people learn about the amount and sources of protein in their diet. Animal protein in egg whites, cheese, chicken, fish, and red meats contain more of the essential nutrients a body needs. With careful meal planning, a well-balanced vegetarian diet can also provide these nutrients. A renal dietitian can help people with advanced CKD make small adjustments in their eating habits that can result in significant protein reduction. For example, people can lower their protein intake by making sandwiches using thinner slices of meat and adding lettuce, cucumber slices, apple slices, and other garnishes. The following table lists some higher-protein foods and suggestions for lower-protein alternatives that are better choices for people with CKD trying to limit their protein intake.
                
Higher- and Lower-protein Foods
                
Based on about a 3 oz. portion        Higher-Protein Foods    Lower-protein Alternatives        Ground beef Halibut Shrimp Salmon Tuna Chicken breast Roasted chicken     Chili con carne Beef stew Egg substitutes Tofu Imitation crab meat
                
When kidney function declines to the point where dialysis becomes necessary, patients should include more protein in their diet because dialysis removes large amounts of protein from the blood.
Question: What is (are) Goodpasture Syndrome ?

Answer: Goodpasture syndrome is a pulmonary-renal syndrome, which is a group of acute illnesses involving the kidneys and lungs. Goodpasture syndrome includes all of the following conditions:
                
- glomerulonephritisinflammation of the glomeruli, which are tiny clusters of looping blood vessels in the kidneys that help filter wastes and extra water from the blood  - the presence of anti-glomerular basement membrane (GBM) antibodies; the GBM is part of the glomeruli and is composed of collagen and other proteins  - bleeding in the lungs
                
In Goodpasture syndrome, immune cells produce antibodies against a specific region of collagen. The antibodies attack the collagen in the lungs and kidneys.
                
Ernest Goodpasture first described the syndrome during the influenza pandemic of 1919 when he reported on a patient who died from bleeding in the lungs and kidney failure. Diagnostic tools to confirm Goodpasture syndrome were not available at that time, so it is not known whether the patient had true Goodpasture syndrome or vasculitis. Vasculitis is an autoimmune conditiona disorder in which the bodys immune system attacks the bodys own cells and organsthat involves inflammation in the blood vessels and can cause similar lung and kidney problems.
                
Goodpasture syndrome is sometimes called anti-GBM disease. However, anti-GBM disease is only one cause of pulmonary-renal syndromes, including Goodpasture syndrome.
                
Goodpasture syndrome is fatal unless quickly diagnosed and treated.
Question: How to diagnose Heart Attack ?

Answer: Several tests are used to diagnose a heart attack. - An electrocardiogram, also called an EKG, measures the rate and regularity of your heartbeat.  - Blood tests identify and measure markers in the blood that can show how much damage was done to your heart. These tests are often repeated at specific time periods to check for changes.  - A nuclear heart scan uses radioactive tracers to show damage to heart chambers and major blood vessels.  - Cardiac catheterization involves passing a thin flexible tube through an artery in your groin or arm to look at your coronary arteries. It allows your doctor to examine the blood flow in your heart's chambers.  - Cardiac angiography is usually performed along with cardiac catheterization, using a dye injected through the cardiac catheter. The dye allows the doctor to see where there may be blockages in the coronary arteries. An electrocardiogram, also called an EKG, measures the rate and regularity of your heartbeat. Blood tests identify and measure markers in the blood that can show how much damage was done to your heart. These tests are often repeated at specific time periods to check for changes. A nuclear heart scan uses radioactive tracers to show damage to heart chambers and major blood vessels. Cardiac catheterization involves passing a thin flexible tube through an artery in your groin or arm to look at your coronary arteries. It allows your doctor to examine the blood flow in your heart's chambers. Cardiac angiography is usually performed along with cardiac catheterization, using a dye injected through the cardiac catheter. The dye allows the doctor to see where there may be blockages in the coronary arteries.
Question: what research (or clinical trials) is being done for Thymoma and Thymic Carcinoma ?

Answer: New types of treatment are being tested in clinical trials.
                    This summary section describes treatments that are being studied in clinical trials. It may not mention every new treatment being studied. Information about clinical trials is available from the NCI website.
                
                
                    Patients may want to think about taking part in a clinical trial.
                    For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment.   Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment.   Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.
                
                
                    Patients can enter clinical trials before, during, or after starting their cancer treatment.
                    Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment.   Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
Question: What are the symptoms of Hirschsprung disease type d brachydactyly ?

Answer: What are the signs and symptoms of Hirschsprung disease type d brachydactyly? The Human Phenotype Ontology provides the following list of signs and symptoms for Hirschsprung disease type d brachydactyly. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Aganglionic megacolon 90% Aplastic/hypoplastic toenail 90% Abnormality of the hallux 50% Anonychia 50% Brachydactyly syndrome 50% Short toe 50% Short thumb - Type D brachydactyly - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of Hemochromatosis type 4 ?

Answer: What are the signs and symptoms of Hemochromatosis type 4? The Human Phenotype Ontology provides the following list of signs and symptoms for Hemochromatosis type 4. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of iron homeostasis 90% Arthralgia 90% Generalized hyperpigmentation 90% Joint swelling 90% Limitation of joint mobility 90% Abdominal pain 50% Hepatic steatosis 50% Cirrhosis 7.5% Congenital hepatic fibrosis 7.5% The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of Medium-chain 3-ketoacyl-coa thiolase deficiency ?

Answer: What are the signs and symptoms of Medium-chain 3-ketoacyl-coa thiolase deficiency? The Human Phenotype Ontology provides the following list of signs and symptoms for Medium-chain 3-ketoacyl-coa thiolase deficiency. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Decreased liver function - Dehydration - Metabolic acidosis - Myoglobinuria - Neonatal death - Rhabdomyolysis - Vomiting - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of Hamanishi Ueba Tsuji syndrome ?

Answer: What are the signs and symptoms of Hamanishi Ueba Tsuji syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Hamanishi Ueba Tsuji syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Camptodactyly of finger 90% Decreased nerve conduction velocity 90% Impaired pain sensation 90% Skeletal muscle atrophy 90% Hypohidrosis 50% Abnormality of the musculature - Autosomal recessive inheritance - Polyneuropathy - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What is (are) Wilson Disease ?

Answer: Wilson disease (WD) is a rare inherited disorder of copper metabolism in which excessive amounts of copper accumulate in the body. The buildup of copper leads to damage in the liver, brain, and eyes. Although copper accumulation begins at birth, symptoms of the disorder only appear later in life. The most characteristic sign of WD is the Kayser-Fleisher ring  a rusty brown ring around the cornea of the eye that can best be viewed using an ophthalmologists slit lamp. The primary consequence for most individuals with WD is liver disease, appearing in late childhood or early adolescence as acute hepatitis, liver failure, or progressive chronic liver disease in the form of chronic active hepatitis or cirrhosis of the liver. In others, the first symptoms are neurological, occur later in adulthood, and commonly include slurred speech (dysarthria), difficulty swallowing (dysphagia), and drooling. Other symptoms may include tremor of the head, arms, or legs; impaired muscle tone, and sustained muscle contractions that produce abnormal postures, twisting, and repetitive movements (dystonia); and slowness of movements (bradykinesia). Individuals may also experience clumsiness (ataxia) and loss of fine motor skills. One-third of individuals with WD will also experience psychiatric symptoms such as an abrupt personality change, bizarre and inappropriate behavior, depression accompanied by suicidal thoughts, neurosis, or psychosis. WD is diagnosed with tests that measure the amount of copper in the blood, urine, and liver.
Question: What are the genetic changes related to pilomatricoma ?

Answer: Mutations in the CTNNB1 gene are found in almost all cases of isolated pilomatricoma. These mutations are somatic, which means they are acquired during a person's lifetime and are present only in tumor cells. Somatic mutations are not inherited.  The CTNNB1 gene provides instructions for making a protein called beta-catenin. This protein plays an important role in sticking cells together (cell adhesion) and in communication between cells. It is also involved in cell signaling as part of the WNT signaling pathway. This pathway promotes the growth and division (proliferation) of cells and helps determine the specialized functions a cell will have (differentiation). WNT signaling is involved in many aspects of development before birth, as well as the maintenance and repair of adult tissues.  Among its many activities, beta-catenin appears to be necessary for the normal function of hair follicles. This protein is active in cells that make up a part of the hair follicle known as the matrix. These cells divide and mature to form the different components of the hair follicle and the hair shaft. As matrix cells divide, the hair shaft is pushed upward and extends beyond the skin.  Mutations in the CTNNB1 gene lead to a version of beta-catenin that is always turned on (constitutively active). The overactive protein triggers matrix cells to divide too quickly and in an uncontrolled way, leading to the formation of a pilomatricoma.  Most pilomatrix carcinomas, the malignant version of pilomatricoma, also have somatic mutations in the CTNNB1 gene. It is unclear why some pilomatricomas are cancerous but most others are not.