umarjan11/Medical-qna huggingface dataset:
Question: What causes What I need to know about Erectile Dysfunction ?

Answer: Erectile dysfunction often has more than one cause. Many diseases can damage nerves, arteries, and muscles. Some can lead to ED, such as
                
- high blood pressure  - diabetes, when your blood glucose, also called blood sugar, is too high  - clogged arteries  - heart and blood vessel disease  - chronic kidney disease  - multiple sclerosis, a disease that attacks the nerves  - treatments for prostate cancer, including radiation, surgery to remove the prostate, and hormone treatments  - injury to the penis, spinal cord, prostate, bladder, or pelvis  - surgery for bladder cancer  - Peyronies disease, in which scar tissue, called a plaque, forms in the penis
                
Unhealthy lifestyle choices, such as smoking, drinking too much alcohol, using illegal drugs, being overweight, and not exercising, can lead to ED.
                
Mental health problems such as the following can also cause or worsen ED:
                
- depression  - fear of sexual failure  - guilt  - low self-esteem  - stress  - worry
                
Even when ED has a physical cause, mental health problems can make ED worse. For example, a physical problem may slow your sexual arousal, which may make you more nervous and worsen your ED.
                
In addition, ED can be a side effect of many common medicines. A small number of ED cases result from low testosterone, a male hormone.
Question: What to do for Insulin Resistance and Prediabetes ?

Answer: - Insulin is a hormone that helps cells throughout the body absorb glucose and use it for energy. Insulin resistance is a condition in which the body produces insulin but does not use it effectively.  - Insulin resistance increases the risk of developing type 2 diabetes and prediabetes.  - The major contributors to insulin resistance are excess weight, especially around the waist, and physical inactivity.  - Prediabetes is a condition in which blood glucose or A1C levelswhich reflect average blood glucose levelsare higher than normal but not high enough for a diagnosis of diabetes.  - The Diabetes Prevention Program (DPP) study and its follow-up study, the Diabetes Prevention Program Outcomes Study (DPPOS), confirmed that people with prediabetes can often prevent or delay diabetes if they lose a modest amount of weight by cutting fat and calorie intake and increasing physical activity.  - By losing weight and being more physically active, people can reverse insulin resistance and prediabetes, thus preventing or delaying type 2 diabetes.  - People with insulin resistance and prediabetes can decrease their risk for diabetes by eating a healthy diet and reaching and maintaining a healthy weight, increasing physical activity, not smoking, and taking medication.  - The DPP showed the diabetes medication metformin to be most effective in preventing or delaying the development of type 2 diabetes in younger and heavier people with prediabetes and women who have had gestational diabetes.
Question: what research (or clinical trials) is being done for Ovarian Low Malignant Potential Tumors ?

Answer: New types of treatment are being tested in clinical trials.
                    Information about clinical trials is available from the NCI Web site.
                
                
                    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 medical research process. Clinical trials are done to find out if new treatments are safe and effective or better than the standard treatment.   Many of today's standard treatments for disease 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 diseases 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 treatment.
                    Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose disease has not gotten better. There are also clinical trials that test new ways to stop a disease from recurring (coming back) or reduce the side effects of 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 clinical trials database.
Question: What is (are) Gout ?

Answer: Gout is a common, painful form of arthritis. It causes swollen, red, hot and stiff joints.    Gout happens when uric acid builds up in your body. Uric acid comes from the breakdown of substances called purines. Purines are in your body's tissues and in foods, such as liver, dried beans and peas, and anchovies. Normally, uric acid dissolves in the blood. It passes through the kidneys and out of the body in urine. But sometimes uric acid can build up and form needle-like crystals. When they form in your joints, it is very painful. The crystals can also cause kidney stones.    Often, gout first attacks your big toe. It can also attack ankles, heels, knees, wrists, fingers, and elbows. At first, gout attacks usually get better in days. Eventually, attacks last longer and happen more often.    You are more likely to get gout if you       - Are a man    - Have family member with gout    - Are overweight    - Drink alcohol    - Eat too many foods rich in purines       Gout can be hard to diagnose. Your doctor may take a sample of fluid from an inflamed joint to look for crystals. You can treat gout with medicines.    Pseudogout has similar symptoms and is sometimes confused with gout. However, it is caused by calcium phosphate, not uric acid.    NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
Question: What are the symptoms of Short stature syndrome, Brussels type ?

Answer: What are the signs and symptoms of Short stature syndrome, Brussels type? The Human Phenotype Ontology provides the following list of signs and symptoms for Short stature syndrome, Brussels type. 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 metabolism/homeostasis - Delayed epiphyseal ossification - Horseshoe kidney - Microretrognathia - Narrow chest - Relative macrocephaly - Short stature - Triangular face - 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 Hemophilia B ?

Answer: What are the signs and symptoms of Hemophilia B? The Human Phenotype Ontology provides the following list of signs and symptoms for Hemophilia B. 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) Abnormal bleeding - Degenerative joint disease - Gastrointestinal hemorrhage - Joint hemorrhage - Persistent bleeding after trauma - Prolonged partial thromboplastin time - Prolonged whole-blood clotting time - Reduced factor IX activity - X-linked recessive inheritance - 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 Griscelli syndrome type 3 ?

Answer: What are the signs and symptoms of Griscelli syndrome type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Griscelli syndrome type 3. 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) Generalized hypopigmentation 90% Ocular albinism 7.5% Autosomal recessive inheritance - Heterogeneous - Large clumps of pigment irregularly distributed along hair shaft - Silver-gray hair - White eyelashes - 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 Rhizomelic chondrodysplasia punctata type 3 ?

Answer: What are the signs and symptoms of Rhizomelic chondrodysplasia punctata type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Rhizomelic chondrodysplasia punctata type 3. 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 - Epiphyseal stippling - Failure to thrive - Rhizomelia - Short femur - Short humerus - 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 Maturity-onset diabetes of the young, type 3 ?

Answer: What are the signs and symptoms of Maturity-onset diabetes of the young, type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Maturity-onset diabetes of the young, type 3. 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 dominant inheritance - Hyperglycemia - Infantile onset - Maturity-onset diabetes of the young - Type II diabetes mellitus - 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) X-linked sideroblastic anemia ?

Answer: X-linked sideroblastic anemia is an inherited disorder that prevents developing red blood cells (erythroblasts) from making enough hemoglobin. People with X-linked sideroblastic anemia have mature red blood cells that are smaller than normal (microcytic) and appear pale (hypochromic) because of the shortage of hemoglobin. This disorder also leads to an abnormal accumulation of iron in red blood cells. The iron-loaded erythroblasts, which are present in bone marrow, are called ring sideroblasts. These abnormal cells give the condition its name. The signs and symptoms of X-linked sideroblastic anemia result from a combination of reduced hemoglobin and an overload of iron. They range from mild to severe and most often appear in young adulthood. Common features include fatigue, dizziness, a rapid heartbeat, pale skin, and an enlarged liver and spleen (hepatosplenomegaly). Over time, severe medical problems such as heart disease and liver damage (cirrhosis) can result from the buildup of excess iron in these organs. X-linked sideroblastic anemia is caused by mutation in the ALAS2 gene. In rare cases, mutations are found in both the HFE gene and the ALAS2 gene, resulting in a more severe form of X-linked sideroblastic anemia. X-linked sideroblastic anemia is inherited in an X-linked recessive pattern.
Question: What is (are) Charcot-Marie-Tooth disease type 4 ?

Answer: Charcot-Marie-Tooth type 4 (CMT4) is a congenital neurologic hereditary disease, part of a group of peripheral neuropathies known as Charcot-Marie-Tooth disease (CMT). It is classified in CMT4A, CMT4B1, CMT4B2, CMT4C, CMT4D, CMT4E, CMT4F, CMT4H and CMT4J. Each sub-type is very rare and may affect a particular ethnic group. In general, people with CMT4 develop symptoms of leg weakness in childhood and by adolescence they may not be able to walk. Other signs and symptoms include distal muscle tissue loss (muscle atrophy) associated with sensory loss and, an abnormally high arched foot (pes cavus). Sub-types may have slightly different clinical features between them. Several genes have been identified as causing CMT4, including GDAP1 (CMT4A), MTMR13 (CMT4B1), MTMR2 (CMT4B2), SH3TC2 (CMT4C), NDG1(CMT4D), EGR2 (CMT4E), PRX (CMT4F), FDG4 (CMT4H), and FIG4 (CMT4J). CMT4 is distinguished from other forms of CMT by its autosomal recessive inheritance. Treatment is symptomatic and includes physical therapy, corrective surgery (when needed) and pain medication.
Question: What is (are) Vasculitis Syndromes of the Central and Peripheral Nervous Systems ?

Answer: Vasculitis is an inflammation of blood vessels, which includes the veins, arteries, and capillaries. Inflammation occurs with infection or is thought to be due to a faulty immune system response. It also can be caused by other immune system disease, an allergic reaction to medicines or toxins, and by certain blood cancers. Vasculitic disorders can cause problems in any organ system, including the central (CNS) and peripheral (PNS) nervous systems. Vasculitis disorders, or syndromes, of the CNS and PNS are characterized by the presence of inflammatory cells in and around blood vessels, and secondary narrowing or blockage of the blood vessels that nourish the brain, spinal cord, or peripheral nerves.
                
A vasculitic syndrome may begin suddenly or develop over time. Symptoms include headaches, especially a headache that doesnt go away; fever, rapid weight loss; confusion or forgetfulness leading to dementia; swelling of the brain, pain while chewing or swallowing; paralysis or numbness, usually in the arms or legs; and visual disturbances, such as double vision, blurred vision, or blindness
                
Some of the better understood vasculitis syndromes are temporal arteritis (also called giant cell arteritis or cranial arteritis--a chronic inflammatory disorder of large blood vessels) and Takayasus disease, which affects larger aortas and may cause stoke.
Question: What is (are) Isaacs' Syndrome ?

Answer: Issacs' syndrome (also known as neuromyotonia, Isaacs-Mertens syndrome, continuous muscle fiber activity syndrome, and quantal squander syndrome) is a rare neuromuscular disorder caused by hyperexcitability and continuous firing of the peripheral nerve axons that activate muscle fibers. Symptoms, which include progressive muscle stiffness, continuously contracting or twitching muscles (myokymia), cramping, increased sweating, and delayed muscle relaxation, occur even during sleep or when individuals are under general anesthesia. Many people also develop weakened reflexes and muscle pain, but numbness is relatively uncommon. In most people with Issacs' syndrome, stiffness is most prominent in limb and trunk muscles, although symptoms can be limited to cranial muscles. Speech and breathing may be affected if pharyngeal or laryngeal muscles are involved. Onset is between ages 15 and 60, with most individuals experiencing symptoms before age 40. There are hereditary and acquired (occurring from unknown causes) forms of the disorder. The acquired form occasionally develops in association with peripheral neuropathies or after radiation treatment, but more often is caused by an autoimmune condition. Autoimmune-mediated Issacs' syndrome is typically caused by antibodies that bind to potassium channels on the motor nerve. Issacs' syndrome is only one of several neurological conditions that can be caused by potassium channel antibodies.
Question: What is (are) T-cell immunodeficiency, congenital alopecia, and nail dystrophy ?

Answer: T-cell immunodeficiency, congenital alopecia, and nail dystrophy is a type of severe combined immunodeficiency (SCID), which is a group of disorders characterized by an almost total lack of immune protection from foreign invaders such as bacteria and viruses. People with this form of SCID are missing functional immune cells called T cells, which normally recognize and attack foreign invaders to prevent infection. Without functional T cells, affected individuals develop repeated and persistent infections starting early in life. The infections result in slow growth and can be life-threatening; without effective treatment, most affected individuals live only into infancy or early childhood.  T-cell immunodeficiency, congenital alopecia, and nail dystrophy also affects growth of the hair and nails. Congenital alopecia refers to an absence of hair that is apparent from birth. Affected individuals have no scalp hair, eyebrows, or eyelashes. Nail dystrophy is a general term that describes malformed fingernails and toenails; in this condition, the nails are often ridged, pitted, or abnormally curved.  Researchers have described abnormalities of the brain and spinal cord (central nervous system) in at least two cases of this condition. However, it is not yet known whether central nervous system abnormalities are a common feature of T-cell immunodeficiency, congenital alopecia, and nail dystrophy.
Question: What are the genetic changes related to progressive external ophthalmoplegia ?

Answer: Progressive external ophthalmoplegia is a condition caused by defects in mitochondria, which are structures within cells that use oxygen to convert the energy from food into a form cells can use. This process is called oxidative phosphorylation. Although most DNA is packaged in chromosomes within the nucleus (nuclear DNA), mitochondria also have a small amount of their own DNA, called mitochondrial DNA or mtDNA.  Progressive external ophthalmoplegia can result from mutations in several different genes. In some cases, mutations in the MT-TL1 gene, which is located in mtDNA, cause progressive external ophthalmoplegia. In other cases, mutations in nuclear DNA are responsible for the condition, particularly mutations in the POLG, SLC25A4, and C10orf2 genes. These genes are critical for mtDNA maintenance. Although the mechanism is unclear, mutations in any of these three genes lead to large deletions of mtDNA, ranging from 2,000 to 10,000 DNA building blocks (nucleotides).  Researchers have not determined how deletions of mtDNA lead to the specific signs and symptoms of progressive external ophthalmoplegia, although the features of the condition are probably related to impaired oxidative phosphorylation. It has been suggested that eye muscles are commonly affected by mitochondrial defects because they are especially dependent on oxidative phosphorylation for energy.