umarjan11/Medical-qna huggingface dataset:
Question: How to diagnose Adult Acute Myeloid Leukemia ?

Answer: Tests that examine the blood and bone marrow are used to detect (find) and diagnose adult AML. The following tests and procedures may be used:         -   Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patients health habits and past illnesses and treatments will also be taken.     -   Complete blood count (CBC): A procedure in which a sample of blood is drawn and checked for the following:                - The number of red blood cells, white blood cells, and platelets.      - The amount of hemoglobin (the protein that carries oxygen) in the red blood cells.      - The portion of the sample made up of red blood cells.             -   Peripheral blood smear : A procedure in which a sample of blood is checked for blast cells, the number and kinds of white blood cells, the number of platelets, and changes in the shape of blood cells.     -   Bone marrow aspiration and biopsy : The removal of bone marrow, blood, and a small piece of bone by inserting a hollow needle into the hipbone or breastbone. A pathologist views the bone marrow, blood, and bone under a microscope to look for signs of cancer.     -   Cytogenetic analysis : A laboratory test in which the cells in a sample of blood or bone marrow are viewed under a microscope to look for certain changes in the chromosomes. Other tests, such as fluorescence in situ hybridization (FISH), may also be done to look for certain changes in the chromosomes.    -   Immunophenotyping : A process used to identify cells, based on the types of antigens or markers on the surface of the cell. This process is used to diagnose the subtype of AML by comparing the cancer cells to normal cells of the immune system. For example, a cytochemistry study may test the cells in a sample of tissue using chemicals (dyes) to look for certain changes in the sample. A chemical may cause a color change in one type of leukemia cell but not in another type of leukemia cell.    -   Reverse transcriptionpolymerase chain reaction test (RTPCR): A laboratory test in which cells in a sample of tissue are studied using chemicals to look for certain changes in the structure or function of genes. This test is used to diagnose certain types of AML including acute promyelocytic leukemia (APL).
Question: what research (or clinical trials) is being done for Childhood Liver Cancer ?

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.     Targeted therapy     Targeted therapy is a type of treatment that uses drugs or other substances to attack specific cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do. Targeted therapy is being studied for the treatment of undifferentiated embryonal sarcoma of the liver and liver cancer that has come back.
                
                
                    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.
                
                
                    Treatment Options in Clinical Trials
                    Check the list of NCI-supported cancer clinical trials that are now accepting patients with childhood liver cancer. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your child's doctor about clinical trials that may be right for your child. General information about clinical trials is available from the NCI website.
Question: What causes Iron-Deficiency Anemia ?

Answer: Not having enough iron in your body causes iron-deficiency anemia. Lack of iron usually is due to blood loss, poor diet, or an inability to absorb enough iron from food.
                
Blood Loss
                
When you lose blood, you lose iron. If you don't have enough iron stored in your body to make up for the lost iron, you'll develop iron-deficiency anemia.
                
In women, long or heavy menstrual periods or bleeding fibroids in the uterus may cause low iron levels. Blood loss that occurs during childbirth is another cause of low iron levels in women.
                
Internal bleeding (bleeding inside the body) also may lead to iron-deficiency anemia. This type of blood loss isn't always obvious, and it may occur slowly. Some causes of internal bleeding are:
                
A bleeding ulcer, colon polyp, or colon cancer
                
Regular use of aspirin or other pain medicines, such as nonsteroidal anti-inflammatory drugs (for example, ibuprofen and naproxen)
                
Urinary tract bleeding
                
Blood loss from severe injuries, surgery, or frequent blood drawings also can cause iron-deficiency anemia.
                
Poor Diet
                
The best sources of iron are meat, poultry, fish, and iron-fortified foods (foods that have iron added). If you don't eat these foods regularly, or if you don't take an iron supplement, you're more likely to develop iron-deficiency anemia.
                
Vegetarian diets can provide enough iron if you eat the right foods. For example, good nonmeat sources of iron include iron-fortified breads and cereals, beans, tofu, dried fruits, and spinach and other dark green leafy vegetables.
                
During some stages of life, such as pregnancy and childhood, it may be hard to get enough iron in your diet. This is because your need for iron increases during these times of growth and development.
                
Inability To Absorb Enough Iron
                
Even if you have enough iron in your diet, your body may not be able to absorb it. This can happen if you have intestinal surgery (such as gastric bypass) or a disease of the intestine (such as Crohn's disease or celiac disease).
                
Prescription medicines that reduce acid in the stomach also can interfere with iron absorption.
Question: What is (are) spastic paraplegia type 15 ?

Answer: Spastic paraplegia type 15 is part of a group of genetic disorders known as hereditary spastic paraplegias. These disorders are characterized by progressive muscle stiffness (spasticity) and the development of paralysis of the lower limbs (paraplegia). Spastic paraplegia type 15 is classified as a complex hereditary spastic paraplegia because it involves all four limbs as well as additional features, including abnormalities of the brain. In addition to the muscles and brain, spastic paraplegia type 15 affects the peripheral nervous system, which consists of nerves connecting the brain and spinal cord to muscles and sensory cells that detect sensations such as touch, pain, heat, and sound.  Spastic paraplegia type 15 usually becomes apparent in childhood or adolescence with the development of weak muscle tone (hypotonia), difficulty walking, or intellectual disability. In almost all affected individuals, the tissue connecting the left and right halves of the brain (corpus callosum) is abnormally thin and becomes thinner over time. Additionally, there is often a loss (atrophy) of nerve cells in several parts of the brain, including the cerebral cortex, which controls thinking and emotions, and the cerebellum, which coordinates movement.  People with this form of spastic paraplegia can have numbness, tingling, or pain in the arms and legs (sensory neuropathy); impairment of the nerves used for muscle movement (motor neuropathy); exaggerated reflexes (hyperreflexia) of the lower limbs; muscle wasting (amyotrophy); or reduced bladder control. Rarely, spastic paraplegia type 15 is associated with a group of movement abnormalities called parkinsonism, which includes tremors, rigidity, and unusually slow movement (bradykinesia). People with spastic paraplegia type 15 may have an eye condition called pigmentary maculopathy that often impairs vision. This condition results from the breakdown (degeneration) of tissue at the back of the eye called the macula, which is responsible for sharp central vision.  Most people with spastic paraplegia type 15 experience a decline in intellectual ability and an increase in muscle weakness and nerve abnormalities over time. As the condition progresses, many people require walking aids or wheelchair assistance in adulthood.
Question: What is (are) Paget's Disease of Bone ?

Answer: Enlarged and Misshapen Bones Paget's disease of bone causes affected bones to become enlarged and misshapen. Our bones are living tissue, and our bodies are constantly breaking down old bone and replacing it with new bone. In Paget's disease, however, old bone is broken down and replaced at a faster rate than normal. The new bone is larger and weaker than normal bone. Paget's disease can occur in any bone in the body, but it is most common in the pelvis, spine, skull, and leg bones. It may occur in just one bone or in several bones, but it does not affect the entire skeleton or spread from affected bones to normal bones. Common symptoms include pain, misshapen bones, and a greater chance of broken bones. Complications Paget's disease can also lead to complications, such as arthritis, headaches, hearing loss, or nervous system problems, depending on which bones are affected. If not treated, Paget's disease can reduce a person's ability to perform activities of daily living, thereby reducing quality of life. Although it is the second most common bone disease after osteoporosis, Paget's disease is still uncommon. According to Bone Health and Osteoporosis: A Report of the Surgeon General, an estimated 1 million people in the U.S. have Paget's disease, or about 1.3 people per 100 men and women age 45-74. The disease is more common in older people and those of Northern European heritage. Men are more likely than women to have the disease. Cause is Unknown Paget's disease is named after the British surgeon, Sir James Paget, who first identified the disease in 1877. Researchers are not sure what causes it. Heredity may be a factor in some cases. Research suggests that a close relative of someone with Paget's disease is seven times more likely to develop the disease than someone without an affected relative. However, most people with Paget's disease do not have any relatives with the disease. Researchers think the disease also may be caused by other factors, such as a slow-acting virus. A Treatable Disease The good news is that Paget's disease of bone is treatable, especially if it is diagnosed early. In recent years, the Food and Drug Administration has approved several medications that can stop or slow the disease's progression. In some cases, surgery can help patients manage the symptoms and complications of the disease.
Question: What are the symptoms of Lymphedema-distichiasis syndrome ?

Answer: What are the signs and symptoms of Lymphedema-distichiasis syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Lymphedema-distichiasis 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) Corneal erosion 90% Distichiasis 90% Photophobia 90% Cataract 50% Muscle weakness 50% Ptosis 50% Abnormality of the pulmonary vasculature 7.5% Arrhythmia 7.5% Benign neoplasm of the central nervous system 7.5% Diabetes mellitus 7.5% Glomerulopathy 7.5% Patent ductus arteriosus 7.5% Proteinuria 7.5% Recurrent urinary tract infections 7.5% Renal duplication 7.5% Sarcoma 7.5% Skin ulcer 7.5% Webbed neck 7.5% Cleft palate 4% Cleft upper lip 4% Abnormality of the musculature - Autosomal dominant inheritance - Conjunctivitis - Corneal ulceration - Lymphedema - Predominantly lower limb lymphedema - Recurrent corneal erosions - Tetralogy of Fallot - Varicose veins - Ventricular septal defect - 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 Spondylometaphyseal dysplasia type A4 ?

Answer: What are the signs and symptoms of Spondylometaphyseal dysplasia type A4? The Human Phenotype Ontology provides the following list of signs and symptoms for Spondylometaphyseal dysplasia type A4. 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 the hip bone 90% Micromelia 90% Platyspondyly 90% Short stature 90% Brachydactyly syndrome 50% Enlarged thorax 7.5% Limitation of joint mobility 7.5% Autosomal recessive inheritance - Broad ischia - Costochondral joint sclerosis - Coxa valga - Disproportionate short-limb short stature - Dolichocephaly - Enlargement of the costochondral junction - Flat acetabular roof - Hypoplasia of the capital femoral epiphysis - Irregular capital femoral epiphysis - Irregular patellae - Metaphyseal irregularity - Metaphyseal sclerosis - Metaphyseal widening - Narrow greater sacrosciatic notches - Osteoporotic metatarsal - Osteoporotic tarsals - Ovoid vertebral bodies - Pectus carinatum - Sclerotic humeral metaphysis - Severe short stature - Spondylometaphyseal dysplasia - 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 Polycythemia vera ?

Answer: What are the signs and symptoms of Polycythemia vera? The Human Phenotype Ontology provides the following list of signs and symptoms for Polycythemia vera. 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) Abdominal pain 90% Acute leukemia 90% Bruising susceptibility 90% Coronary artery disease 90% Epistaxis 90% Gastrointestinal hemorrhage 90% Gingival bleeding 90% Hepatomegaly 90% Migraine 90% Myelodysplasia 90% Splenomegaly 90% Tinnitus 90% Vertigo 90% Weight loss 90% Arthralgia 50% Respiratory insufficiency 50% Arterial thrombosis 7.5% Cerebral ischemia 7.5% Portal hypertension 7.5% Pruritus 7.5% Thrombophlebitis 7.5% Autosomal dominant inheritance - Budd-Chiari syndrome - Cerebral hemorrhage - Increased hematocrit - Increased hemoglobin - Increased megakaryocyte count - Increased red blood cell mass - Leukocytosis - Somatic mutation - Sporadic - Thrombocytopenia - Thrombocytosis - Thromboembolism - 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 treatments for Asbestos-Related Lung Diseases ?

Answer: No treatments can reverse the effects of asbestos on your lungs. However, treatments may help relieve symptoms and prevent or delay complications. If you have lung cancer, treatments may help slow the progress of the disease.
                
Treatments for Pleural Plaque, Pleural Effusion, and Asbestosis
                
If you have pleural plaque, pleural effusion, or asbestosis and you smoke, your doctor will advise you to quit smoking. People who have these conditions can lower their risk for lung cancer if they quit smoking.
                
Talk with your doctor about programs and products that can help you quit smoking. Also, try to avoid secondhand smoke.
                
If you have trouble quitting smoking on your own, consider joining a support group. Many hospitals, workplaces, and community groups offer classes to help people quit smoking.
                
For more information about how to quit smoking, go to the Diseases and Conditions Index Smoking and Your Heart article and the National Heart, Lung, and Blood Institutes Your Guide to a Healthy Heart. Although these resources focus on heart health, they include general information about how to quit smoking.
                
If you have trouble breathing or shortness of breath and a very low blood oxygen level, your doctor may recommend oxygen therapy. For this treatment, you're given oxygen through nasal prongs or a mask. Oxygen therapy may be done at home or in a hospital or other health facility.
                
If excess fluid around the lungs (pleural effusion) is making it hard for you to breathe, thoracentesis (THOR-ah-sen-TE-sis) may help. For this procedure, your doctor will insert a thin needle or plastic tube into the space between your lungs and chest wall. He or she will then draw out the excess fluid.
                
Treatments for Lung Cancer and Mesothelioma
                
If you have lung cancer or mesothelioma, your treatment may include surgery, chemotherapy, radiation therapy, and/or targeted therapy. (Targeted therapy uses medicines or other substances to find and attack specific lung cancer cells without harming normal cells.)
                
Your doctor may prescribe medicines to prevent fluid buildup, ease pain, or relieve other complications of your disease.
                
If you have lung cancer or mesothelioma, talk with your doctor about whether you should get flu and pneumonia vaccines. These vaccines can help lower your risk for lung infections.
Question: What are the genetic changes related to cytochrome c oxidase deficiency ?

Answer: Cytochrome c oxidase deficiency is caused by mutations in one of at least 14 genes. In humans, most genes are found in DNA in the cell's nucleus (nuclear DNA). However, some genes are found in DNA in specialized structures in the cell called mitochondria. This type of DNA is known as mitochondrial DNA (mtDNA). Most cases of cytochrome c oxidase deficiency are caused by mutations in genes found within nuclear DNA; however, in some rare instances, mutations in genes located within mtDNA cause this condition.  The genes associated with cytochrome c oxidase deficiency are involved in energy production in mitochondria through a process called oxidative phosphorylation. The gene mutations that cause cytochrome c oxidase deficiency affect an enzyme complex called cytochrome c oxidase, which is responsible for one of the final steps in oxidative phosphorylation. Cytochrome c oxidase is made up of two large enzyme complexes called holoenzymes, which are each composed of multiple protein subunits. Three of these subunits are produced from mitochondrial genes; the rest are produced from nuclear genes. Many other proteins, all produced from nuclear genes, are involved in assembling these subunits into holoenzymes.  Most mutations that cause cytochrome c oxidase alter proteins that assemble the holoenzymes. As a result, the holoenzymes are either partially assembled or not assembled at all. Without complete holoenzymes, cytochrome c oxidase cannot form. Mutations in the three mitochondrial genes and a few nuclear genes that provide instructions for making the holoenzyme subunits can also cause cytochrome c oxidase deficiency. Altered subunit proteins reduce the function of the holoenzymes, resulting in a nonfunctional version of cytochrome c oxidase. A lack of functional cytochrome c oxidase disrupts the last step of oxidative phosphorylation, causing a decrease in energy production.  Researchers believe that impaired oxidative phosphorylation can lead to cell death by reducing the amount of energy available in the cell. Certain tissues that require large amounts of energy, such as the brain, muscles, and heart, seem especially sensitive to decreases in cellular energy. Cell death in other sensitive tissues may also contribute to the features of cytochrome c oxidase deficiency.