umarjan11/Medical-qna huggingface dataset:
Question: What are the symptoms of Multiple self healing squamous epithelioma ?

Answer: What are the signs and symptoms of Multiple self healing squamous epithelioma? The Human Phenotype Ontology provides the following list of signs and symptoms for Multiple self healing squamous epithelioma. 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 skin - Autosomal dominant inheritance - Neoplasm - Onset - 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: Who is at risk for Parasites - Zoonotic Hookworm? ?

Answer: Dog and cat hookworms are found throughout the world, especially in warmer climates. In the United States, zoonotic hookworms are found everywhere but more commonly along the East Coast than the West Coast. Worldwide, zoonotic hookworms are found in tropical and subtropical regions where the parasite is better able to survive because of environmental conditions. However, there is one type of dog and cat hookworm that is more commonly found in cooler climates.
    
The global burden of zoonotic hookworm in dogs and cats is not known; also, the amount of disease in people caused by these parasites is also unknown. Cutaneous larva migrans (CLM) is most often reported by returning travelers to tropical regions who have had soil and/or sand exposures in places where dogs and cats are likely to have hookworms. However, CLM is likely causing significant problems for the people who live in less developed parts of the world, even though the disease is not reported regularly. In less developed areas of the world, dogs and cats are often free-ranging and have high rates of infection with hookworm which leads to widespread contamination of sand and soil. In a survey of a rural population in Brazil, the prevalence of CLM during the rainy season was 14.9% among children less than 5 years old and 0.7% among adults aged 20 years and older.
Question: How to prevent Bronchopulmonary Dysplasia ?

Answer: Taking steps to ensure a healthy pregnancy might prevent your infant from being born before his or her lungs have fully developed. These steps include:
                
Seeing your doctor regularly during your pregnancy
                
Following a healthy diet
                
Not smoking and avoiding tobacco smoke, alcohol, and illegal drugs
                
Controlling any ongoing medical conditions you have
                
Preventing infection
                
If your doctor thinks that you're going to give birth too early, he or she may give you injections of a corticosteroid medicine.
                
The medicine can speed up surfactant production in your baby. Surfactant is a liquid that coats the inside of the lungs. It helps keep them open so your infant can breathe in air once he or she is born.
                
Usually, within about 24 hours of your taking this medicine, the baby's lungs start making enough surfactant. This will reduce the infant's risk of respiratory distress syndrome (RDS), which can lead to bronchopulmonary dysplasia (BPD).
                
Corticosteroids also can help your baby's lungs, brain, and kidneys develop more quickly while he or she is in the womb.
                
If your baby does develop RDS, it will probably be fairly mild. If the RDS isn't mild, BPD will likely develop.
Question: Who is at risk for Sudden Cardiac Arrest? ?

Answer: The risk of sudden cardiac arrest (SCA) increases:
                
With age
                
If you are a man. Men are more likely than women to have SCA.
                
Some studies show that blacksparticularly those with underlying conditions such as diabetes, high blood pressure, heart failure, and chronic kidney disease or certain cardiac findings on tests such as an electrocardiogramhave a higher risk forSCA.
                
Major Risk Factor
                
The major risk factor for SCA is coronary heart disease. Most people who have SCA have some degree of coronary heart disease; however, many people may not know that they have coronary heart disease until SCA occurs. Usually their coronary heart disease is silentthat is, it has no signs or symptoms. Because of this, doctors and nurses have not detected it.
                
Many people who have SCA also have silent, or undiagnosed, heart attacks before sudden cardiac arrest happens. These people have no clear signs of heart attack, and they dont even realize that theyve had one. Read more about coronary heart disease risk factors.
                
Other Risk Factors
                
Other risk factors for SCA include:
                
A personal history of arrhythmias
                
A personal or family history of SCA or inherited disorders that make you prone toarrhythmias
                
Drug or alcohol abuse
                
Heart attack
                
Heart failure
Question: What are the treatments for Migraine ?

Answer: There is no absolute cure for migraine since its pathophysiology has yet to be fully understood. There are two ways to approach the treatment of migraine headache with drugs: prevent the attacks, or relieve the symptoms during the attacks. Prevention involves the use of medications and behavioral changes. Drugs originally developed for epilepsy, depression, or high blood pressure to prevent future attacks have been shown to be extremely effective in treating migraine. Botulinum toxin A has been shown to be effective in prevention of chronic migraine. Behaviorally, stress management strategies, such as exercise, relaxation techniques, biofeedback mechanisms, and other therapies designed to limit daily discomfort, may reduce the number and severity of migraine attacks. Making a log of personal triggers of migraine can also provide useful information for trigger-avoiding lifestyle changes, including dietary considerations, eating regularly scheduled meals with adequate hydration, stopping certain medications, and establishing a consistent sleep schedule. Hormone therapy may help some women whose migraines seem to be linked to their menstrual cycle. A weight loss program is recommended for obese individuals with migraine.
                
Relief of symptoms, or acute treatments, during attacks consists of sumatriptan, ergotamine drugs, and analgesics such as ibuprofen and aspirin. The sooner these treatments are administered, the more effective they are.
Question: What are the genetic changes related to arrhythmogenic right ventricular cardiomyopathy ?

Answer: ARVC can result from mutations in at least eight genes. Many of these genes are involved in the function of desmosomes, which are structures that attach heart muscle cells to one another. Desmosomes provide strength to the myocardium and play a role in signaling between neighboring cells.  Mutations in the genes responsible for ARVC often impair the normal function of desmosomes. Without normal desmosomes, cells of the myocardium detach from one another and die, particularly when the heart muscle is placed under stress (such as during vigorous exercise). These changes primarily affect the myocardium surrounding the right ventricle, one of the two lower chambers of the heart. The damaged myocardium is gradually replaced by fat and scar tissue. As this abnormal tissue builds up, the walls of the right ventricle become stretched out, preventing the heart from pumping blood effectively. These changes also disrupt the electrical signals that control the heartbeat, which can lead to arrhythmia.  Gene mutations have been found in 30 to 40 percent of people with ARVC. Mutations in a gene called PKP2 are most common. In people without an identified mutation, the cause of the disorder is unknown. Researchers are looking for additional genetic factors, particularly those involved in the function of desmosomes, that may play a role in causing ARVC.
Question: What are the genetic changes related to spastic paraplegia type 15 ?

Answer: Mutations in the ZFYVE26 gene cause spastic paraplegia type 15. This gene provides instructions for making a protein called spastizin. This protein is important in a process called autophagy, in which worn-out cell parts and unneeded proteins are recycled within cells. Specifically, spastizin is involved in the formation and maturation of sacs called autophagosomes (or autophagic vacuoles) that transport unneeded materials to be broken down. Spastizin also plays a role in the process by which dividing cells separate from one another (cytokinesis).  Many ZFYVE26 gene mutations that cause spastic paraplegia type 15 result in a shortened spastizin protein that is quickly broken down. As a result, functional autophagosomes are not produced, autophagy cannot occur, and recycling of materials within cells is decreased. An inability to break down unneeded materials, and the subsequent accumulation of these materials in cells, leads to cell dysfunction and often cell death. The loss of cells in the brain and other parts of the body is responsible for many of the features of spastic paraplegia type 15.  It is unclear whether a lack of spastizin protein interferes with normal cytokinesis and whether impaired cell division contributes to the signs and symptoms of spastic paraplegia type 15.
Question: What are the genetic changes related to choroideremia ?

Answer: Mutations in the CHM gene cause choroideremia. The CHM gene provides instructions for producing the Rab escort protein-1 (REP-1). As an escort protein, REP-1 attaches to molecules called Rab proteins within the cell and directs them to the membranes of various cell compartments (organelles). Rab proteins are involved in the movement of proteins and organelles within cells (intracellular trafficking). Mutations in the CHM gene lead to an absence of REP-1 protein or the production of a REP-1 protein that cannot carry out its protein escort function. This lack of functional REP-1 prevents Rab proteins from reaching and attaching (binding) to the organelle membranes. Without the aid of Rab proteins in intracellular trafficking, cells die prematurely.  The REP-1 protein is active (expressed) throughout the body, as is a similar protein, REP-2. Research suggests that when REP-1 is absent or nonfunctional, REP-2 can perform the protein escort duties of REP-1 in many of the body's tissues. Very little REP-2 protein is present in the retina, however, so it cannot compensate for the loss of REP-1 in this tissue. Loss of REP-1 function and subsequent misplacement of Rab proteins within the cells of the retina causes the progressive vision loss characteristic of choroideremia.
Question: What are the genetic changes related to Sandhoff disease ?

Answer: Mutations in the HEXB gene cause Sandhoff disease. The HEXB gene provides instructions for making a protein that is part of two critical enzymes in the nervous system, beta-hexosaminidase A and beta-hexosaminidase B. These enzymes are located in lysosomes, which are structures in cells that break down toxic substances and act as recycling centers. Within lysosomes, these enzymes break down fatty substances, complex sugars, and molecules that are linked to sugars. In particular, beta-hexosaminidase A helps break down a fatty substance called GM2 ganglioside.  Mutations in the HEXB gene disrupt the activity of beta-hexosaminidase A and beta-hexosaminidase B, which prevents these enzymes from breaking down GM2 ganglioside and other molecules. As a result, these compounds can accumulate to toxic levels, particularly in neurons of the brain and spinal cord. A buildup of GM2 ganglioside leads to the progressive destruction of these neurons, which causes many of the signs and symptoms of Sandhoff disease.  Because Sandhoff disease impairs the function of lysosomal enzymes and involves the buildup of GM2 ganglioside, this condition is sometimes referred to as a lysosomal storage disorder or a GM2-gangliosidosis.
Question: What is (are) PRICKLE1-related progressive myoclonus epilepsy with ataxia ?

Answer: PRICKLE1-related progressive myoclonus epilepsy with ataxia is a rare inherited condition characterized by recurrent seizures (epilepsy) and problems with movement. The signs and symptoms of this disorder usually begin between the ages of 5 and 10.  Problems with balance and coordination (ataxia) are usually the first symptoms of PRICKLE1-related progressive myoclonus epilepsy with ataxia. Affected children often have trouble walking. Their gait is unbalanced and wide-based, and they may fall frequently. Later, children with this condition develop episodes of involuntary muscle jerking or twitching (myoclonus), which cause additional problems with movement. Myoclonus can also affect muscles in the face, leading to difficulty swallowing and slurred speech (dysarthria).  Beginning later in childhood, some affected individuals develop tonic-clonic or grand mal seizures. These seizures involve a loss of consciousness, muscle rigidity, and convulsions. They often occur at night (nocturnally) while the person is sleeping.  PRICKLE1-related progressive myoclonus epilepsy with ataxia does not seem to affect intellectual ability. Although a few affected individuals have died in childhood, many have lived into adulthood.
Question: Do you have information about Ebola

Answer: Summary : Ebola hemorrhagic fever is caused by a virus. It is a severe and often fatal disease. It can affect humans and other primates. Researchers believe that the virus first spreads from an infected animal to a human. It can then spread from human to human through direct contact with a patient's blood or secretions.    Symptoms of Ebola may appear anywhere from 2 to 21 days after exposure to the virus. Symptoms usually include       - Fever    - Headache    - Joint and muscle aches    - Weakness    - Diarrhea    - Vomiting    - Stomach pain    - Lack of appetite       Other symptoms including rash, red eyes, and internal and external bleeding, may also occur.    The early symptoms of Ebola are similar to other, more common, diseases. This makes it difficult to diagnose Ebola in someone who has been infected for only a few days. However, if a person has the early symptoms of Ebola and there is reason to suspect Ebola, the patient should be isolated. It is also important to notify public health professionals. Lab tests can confirm whether the patient has Ebola.    There is no cure for Ebola. Treatment involves supportive care such as fluids, oxygen, and treatment of complications. Some people who get Ebola are able to recover, but many do not.    Centers for Disease Control and Prevention
Question: What are the treatments for Factor XIII deficiency ?

Answer: How might factor XIII be treated? The amount of Factor XIII necessary for a normal response to trauma is only about 10 percent of that in the normal plasma. People with Factor XIII deficiency are generally given small infusions of fresh or frozen blood plasma (cryoprecipitates), or Factor XIII concentrates every three or four weeks. This has proven to be a highly successful preventive treatment for the disorder. Patients typically have a normal response to trauma while on these transfusions. When patients with Factor XIII deficiency have a high incidence of bleeding inside the head (intracranial), preventive treatment is necessary. In February 2011, the US Food and Drug Administration approved Corifact, a product manufactured by CSL Behring of Marburg, Germany, to prevent bleeding in people with congenital Factor XIII deficiency. Corifact is made from the pooled plasma of healthy donors. It can be used for individuals with absent or decreased levels of FXIII.  People receiving Corifact may develop antibodies against Factor XIII that may make the product ineffective. It potentially can cause adverse events from abnormal clotting if doses higher than the labeled dose are given to patients. Cryoprecipitate should not be used to treat patients with factor XIII deficiency except in life- and limb-threatening emergencies when Factor XIII concentrate is not immediately available.
Question: What are the symptoms of Dysautonomia like disorder ?

Answer: What are the signs and symptoms of Dysautonomia like disorder? The Human Phenotype Ontology provides the following list of signs and symptoms for Dysautonomia like disorder. 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 - Dysautonomia - Intellectual disability - Peripheral neuropathy - 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 Optic atrophy 5 ?

Answer: What are the signs and symptoms of Optic atrophy 5? The Human Phenotype Ontology provides the following list of signs and symptoms for Optic atrophy 5. 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 - Central scotoma - Optic atrophy - Slow decrease in visual acuity - Tritanomaly - 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 Faciomandibular myoclonus, nocturnal ?

Answer: What are the signs and symptoms of Faciomandibular myoclonus, nocturnal? The Human Phenotype Ontology provides the following list of signs and symptoms for Faciomandibular myoclonus, nocturnal. 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) Bruxism - Myoclonus - 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 Sertoli cell-only syndrome ?

Answer: What are the signs and symptoms of Sertoli cell-only syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Sertoli cell-only 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) Abnormality of metabolism/homeostasis - Abnormality of the thorax - Gynecomastia - Obesity - 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.