umarjan11/Medical-qna huggingface dataset:
Question: What is the outlook for Spinal Cord Injury ?

Answer: Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day.
                
Surgery to relieve compression of the spinal tissue by surrounding bones broken or dislocated by the injury is often necessary, through timing of such surgery may vary widely. A recent prospective multicenter trial called STASCIS is exploring whether performing decompression surgery early (less than 24 hours following injury) can improve outcomes for patients with bone fragments or other tissues pressing on the spinal cord.
Question: What are the genetic changes related to MyD88 deficiency ?

Answer: MyD88 deficiency is caused by mutations in the MYD88 gene, which provides instructions for making a protein that plays an important role in stimulating the immune system to respond to bacterial infection. The MyD88 protein is part of a signaling pathway that is involved in early recognition of pathogens and the initiation of inflammation to fight infection. This signaling pathway is part of the innate immune response.  Mutations in the MYD88 gene lead to the production of a nonfunctional protein or no protein at all. The loss of functional MyD88 protein prevents the immune system from triggering inflammation in response to pathogens that would normally help fight the infections. Because the early immune response is insufficient, bacterial infections occur often and become severe and invasive.  Researchers suggest that as the immune system matures, other systems compensate for the loss of MyD88 protein, accounting for the improvement in the condition that occurs by adolescence.
Question: What are the genetic changes related to ataxia with vitamin E deficiency ?

Answer: Mutations in the TTPA gene cause ataxia with vitamin E deficiency. The TTPA gene provides instructions for making the -tocopherol transfer protein (TTP), which is found in the liver and brain. This protein controls distribution of vitamin E obtained from the diet (also called -tocopherol) to cells and tissues throughout the body. Vitamin E helps cells prevent damage that might be done by free radicals.  TTPA gene mutations impair the activity of the TTP protein, resulting in an inability to retain and use dietary vitamin E. As a result, vitamin E levels in the blood are greatly reduced and free radicals accumulate within cells. Nerve cells (neurons) in the brain and spinal cord (central nervous system) are particularly vulnerable to the damaging effects of free radicals and these cells die off when they are deprived of vitamin E. Nerve cell damage can lead to problems with movement and other features of ataxia with vitamin E deficiency.
Question: What are the genetic changes related to renal coloboma syndrome ?

Answer: Renal coloboma syndrome is caused by mutations in the PAX2 gene. The PAX2 gene provides instructions for making a protein that is involved in the early development of the eyes, ears, brain and spinal cord (central nervous system), kidneys, and genital tract. The PAX2 protein attaches (binds) to specific regions of DNA and regulates the activity of other genes. On the basis of this role, the PAX2 protein is called a transcription factor. After birth, the PAX2 protein is thought to protect against cell death during periods of cellular stress.  Mutations in the PAX2 gene lead to the production of a nonfunctional PAX2 protein that is unable to aid in development, causing incomplete formation of certain tissues. Why the kidneys and eyes are specifically affected by PAX2 gene mutations is unclear.  Approximately half of those affected with renal coloboma syndrome do not have an identified mutation in the PAX2 gene. In these cases, the cause of the disorder is unknown.
Question: What are the genetic changes related to McKusick-Kaufman syndrome ?

Answer: Mutations in the MKKS gene cause McKusick-Kaufman syndrome. This gene provides instructions for making a protein that plays an important role in the formation of the limbs, heart, and reproductive system. The protein's structure suggests that it may act as a chaperonin, which is a type of protein that helps fold other proteins. Proteins must be folded into the correct 3-dimensional shape to perform their usual functions in the body. Although the structure of the MKKS protein is similar to that of a chaperonin, some recent studies have suggested that protein folding may not be this protein's primary function. Researchers speculate that the MKKS protein also may be involved in transporting other proteins within the cell.  The mutations that underlie McKusick-Kaufman syndrome alter the structure of the MKKS protein. Although the altered protein disrupts the development of several parts of the body before birth, it is unclear how MKKS mutations lead to the specific features of this disorder.
Question: What are the genetic changes related to familial adenomatous polyposis ?

Answer: Mutations in the APC gene cause both classic and attenuated familial adenomatous polyposis. These mutations affect the ability of the cell to maintain normal growth and function. Cell overgrowth resulting from mutations in the APC gene leads to the colon polyps seen in familial adenomatous polyposis. Although most people with mutations in the APC gene will develop colorectal cancer, the number of polyps and the time frame in which they become malignant depend on the location of the mutation in the gene.  Mutations in the MUTYH gene cause autosomal recessive familial adenomatous polyposis (also called MYH-associated polyposis). Mutations in this gene prevent cells from correcting mistakes that are made when DNA is copied (DNA replication) in preparation for cell division. As these mistakes build up in a person's DNA, the likelihood of cell overgrowth increases, leading to colon polyps and the possibility of colon cancer.
Question: What to do for Anemia of Inflammation and Chronic Disease ?

Answer: - Anemia is a condition in which a person has a lower than normal number of red blood cells or the amount of hemoglobin in the red blood cells drops below normal, which prevents the bodys cells from getting enough oxygen.  - Anemia of inflammation and chronic disease (AI/ACD) is a type of anemia that commonly occurs with chronic illnesses, infections, cancer, or inflammatory disorders.  - AI/ACD typically develops slowly and, because it is usually mild, may cause few or no symptoms. Sometimes, AI/ACD can cause or contribute to fatigue, weakness, pale skin, a fast heartbeat, shortness of breath, and exercise intolerance.  - To diagnose AI/ACD, a health care provider orders a blood test called a complete blood count (CBC).  - AI/ACD often is not treated separately from the condition with which it occurs. In general, health care providers focus on treating the underlying illness.
Question: What are the complications of Urine Blockage in Newborns ?

Answer: When a defect in the urinary tract blocks the flow of urine, the urine backs up and causes the ureters to swell, called hydroureter, and hydronephrosis.
                
Hydronephrosis is the most common problem found during prenatal ultrasound of a baby in the womb. The swelling may be easy to see or barely detectable. The results of hydronephrosis may be mild or severe, yet the long-term outcome for the childs health cannot always be predicted by the severity of swelling. Urine blockage may damage the developing kidneys and reduce their ability to filter. In the most severe cases of urine blockage, where little or no urine leaves the babys bladder, the amount of amniotic fluid is reduced to the point that the babys lung development is threatened.
                
After birth, urine blockage may raise a childs risk of developing a UTI. Recurring UTIs can lead to more permanent kidney damage.
Question: What is (are) Kidney Disease ?

Answer: Instead of dialysis, some people with kidney failure -- including older adults -- may be able to receive a kidney transplant. This involves having a healthy kidney from another person surgically placed into your body. The new, donated kidney does the work that your two failed kidneys used to do. The donated kidney can come from an anonymous donor who has recently died, or from a living person -- usually a relative. But you might also be able to receive a kidney from an unrelated donor, including your spouse or a friend. (Watch the video to learn more about kidney transplantation. To enlarge the video, click the brackets in the lower right-hand corner. To reduce the video, press the Escape (Esc) button on your keyboard.) Kidney transplantation is a treatment for kidney failure -- not a cure. You will need to see your healthcare provider regularly. And you will need to take medications for as long as you have your transplant to suppress your immune system so it doesn't reject the transplanted kidney.
Question: What are the treatments for Depression ?

Answer: A bushy, wild-growing plant with yellow flowers, St John's wort has been used for centuries in many folk and herbal remedies. It is commonly used in Europe to treat mild depression, and it is a top-seller in the United States as well. In a study funded by the National Institutes of Health, the herb was found to be no more effective than a placebo (sugar pill) in treating adults suffering from major depression. Other research has shown that St. John's wort can interact unfavorably with other drugs. The herb interferes with certain drugs used to treat heart disease, depression, seizures, certain cancers, and organ transplant rejection. Because of these potential interactions, older adults should always consult with their doctors before taking any herbal supplement. Another product sold as a dietary supplement, S-adenosyl methionine (SAMe), has shown promise in controlled trials as helpful when added to an SSRI antidepressant that is only partially effective.
Question: What are the stages of Childhood Ependymoma ?

Answer: Key Points
                    - The area where the tumor is found and the childs age are used in place of a staging system to plan cancer treatment.    - The information from tests and procedures done to detect (find) childhood ependymoma is used to plan cancer treatment.
                
                
                    The area where the tumor is found and the childs age are used in place of a staging system to plan cancer treatment.
                    Staging is the process used to find out how much cancer there is and if cancer has spread. There is no standard staging system for childhood ependymoma. Treatment is based on where the cancer is in the body and the age of the child.
                
                
                    The information from tests and procedures done to detect (find) childhood ependymoma is used to plan cancer treatment.
                    Some of the tests used to detect childhood ependymoma are repeated after the tumor is removed by surgery. (See the General Information section.) This is to find out how much tumor remains after surgery.
Question: What is (are) Adrenal Gland Disorders ?

Answer: The adrenal glands are small glands located on top of each kidney. They produce hormones that you can't live without, including sex hormones and cortisol. Cortisol helps you respond to stress and has many other important functions.    With adrenal gland disorders, your glands make too much or not enough hormones. In Cushing's syndrome, there's too much cortisol, while with Addison's disease, there is too little. Some people are born unable to make enough cortisol.    Causes of adrenal gland disorders include       - Genetic mutations    - Tumors including pheochromocytomas    - Infections    - A problem in another gland, such as the pituitary, which helps to regulate the adrenal gland    - Certain medicines      Treatment depends on which problem you have. Surgery or medicines can treat many adrenal gland disorders.    NIH: National Institute of Child Health and Human Development
Question: What is (are) Tick Bites ?

Answer: If you spend time outdoors or have pets that go outdoors, you need to beware of ticks. Ticks are small bloodsucking parasites. Many species transmit diseases to animals and people. Some of the diseases you can get from a tick bite are Lyme disease, ehrlichiosis, Rocky Mountain spotted fever and tularemia.     Some ticks are so small that they can be difficult to see. Ticks may get on you if you walk through areas where they live, such as tall grass, leaf litter or shrubs.     Tick-borne diseases occur worldwide, including in your own backyard. To help protect yourself and your family, you should       -  Use a chemical repellent with DEET, permethrin or picaridin    -  Wear light-colored protective clothing     -  Tuck pant legs into socks     -  Avoid tick-infested areas     -  Check yourself, your children and your pets daily for ticks and carefully remove any ticks you find
Question: What is (are) Friedreich's Ataxia ?

Answer: Friedreich's ataxia is an inherited disease that damages your nervous system. The damage affects your spinal cord and the nerves that control muscle movement in your arms and legs. Symptoms usually begin between the ages of 5 and 15. The main symptom is ataxia, which means trouble coordinating movements. Specific symptoms include       - Difficulty walking    -  Muscle weakness    -  Speech problems    -  Involuntary eye movements    -  Scoliosis (curving of the spine to one side)    -  Heart palpitations, from the heart disease which can happen along with Friedreich's ataxia       People with Friedreich's ataxia usually need a wheelchair 15 to 20 years after symptoms first appear. In severe cases, people become incapacitated. There is no cure. You can treat symptoms with medicines, braces, surgery, and physical therapy.    NIH: National Institute of Neurological Disorders and Stroke
Question: Do you have information about Puberty

Answer: Summary : Puberty is the time in life when a boy or girl becomes sexually mature. It is a process that usually happens between ages 10 and 14 for girls and ages 12 and 16 for boys. It causes physical changes, and affects boys and girls differently.    In girls:       - The first sign of puberty is usually breast development.    - Then hair grows in the pubic area and armpits.    - Menstruation (or a period) usually happens last.       In boys:       - Puberty usually begins with the testicles and penis getting bigger.    - Then hair grows in the pubic area and armpits.    - Muscles grow, the voice deepens, and facial hair develops as puberty continues.       Both boys and girls may get acne. They also usually have a growth spurt (a rapid increase in height) that lasts for about 2 or 3 years. This brings them closer to their adult height, which they reach after puberty.     NIH: National Institute of Child Health and Human Development
Question: What is (are) Lyme disease ?

Answer: Lyme disease is the most common tickborne infectious disease in the United States. Early signs and symptoms of the condition include fever, chills, muscle pain, headache, and joint pain. As the condition progresses, affected people may experience heart problems, Bell's palsy, arthritis, abnormal muscle movement, speech problems and cognitive (thinking) abnormalities. Please visit the Center for Disease Control and Prevention's Web site for a more comprehensive list of symptoms. Lyme disease is caused by the bacterium Borrelia burgdorferi, which is transmitted to humans through the bite of infected blacklegged ticks. Certain features of the condition, including whether or not an affected person will develop medication-resistant chronic arthritis, is thought to be influenced by genetic factors (certain human leukocyte antigen genes). Treatment generally includes antibiotics to address the bacterial infection and other medications (i.e. pain medications) to relieve symptoms.
Question: What is (are) 11-beta-hydroxylase deficiency ?

Answer: Congenital adrenal hyperplasia (CAH) due to 11-beta-hydroxylase deficiency is one of a group of disorders (collectively called congenital adrenal hyperplasia) that affect the adrenal glands. In this condition, the adrenal glands produce excess androgens (male sex hormones). This condition is caused by mutations in the CYP11B1 gene and is inherited in an autosomal recessive pattern. There are two types, the classic form and the non-classic form. Females with the classic form have ambiguous external genitalia with normal internal reproductive organs. Males and females with the classic form have early development of their secondary sexual characteristics (precocious puberty). The early growth spurt can prevent growth later in adolescence and lead to short stature in adulthood. About two-thirds of individuals with the classic form have high blood pressure which develops in the first year of life.
Question: Is Autosomal recessive polycystic kidney disease inherited ?

Answer: How is autosomal recessive polycystic kidney disease inherited? Autosomal recessive polycystic kidney disease (ARPKD) is inherited in an autosomal recessive manner. This means that an affected individual has two gene alterations (mutations) in the PKHD1 gene, with one mutation inherited from each parent. Each parent, who has one altered copy of the gene, is referred to as a carrier. Carriers do not typically show signs and symptoms of the condition. When two carriers for an autosomal recessive condition have children, each child has a 25% (1 in 4) risk to have the condition, a 50% (1 in 2) risk to be an unaffected carrier like each of the parents, and a 25% chance to not have the condition and not be a carrier. This means that with each pregnancy, there is a 75% (3 in 4) chance to have an unaffected child.
Question: What is (are) Chondrodysplasia punctata 1, X-linked recessive ?

Answer: Chondrodysplasia punctata 1, X-linked recessive (CDPX1) is a genetic disorder present from birth that affects bone and cartilage development. On x-ray, affected infants have characteristic spots at the ends of their bones. These spots are called chondrodysplasia punctata or stippled epiphyses and typically disappear between age 2 and 3. Additional common features of CDPX1 are shortened fingers and a flat nose. Some people with this condition have breathing abnormalities, hearing loss, abnormalities of the spinal bones in the neck, and delayed intellectual development. CDPX1 is caused by changes in the ARSE gene, which is located on the X chromosome. This condition is inherited in an X-linked recessive manner and occurs almost exclusively in males. Most affected individuals have a normal lifespan, although some individuals experience complications that can be life-threatening.
Question: What causes Trisomy 18 ?

Answer: What causes Trisomy 18? In most cases, trisomy 18 is caused by having 3 copies of chromosome 18 in each cell in the body, instead of the usual 2 copies. The extra genetic material from the 3rd copy of the chromosome disrupts development, causing the characteristic signs and symptoms of the condition. About 5% of people with trisomy 18 have 'mosaic trisomy 18' (when there is an extra copy of the chromosome in only some of the body's cells). The severity of mosaic trisomy 18 depends on the number and locations of cells with the extra copy. Very rarely, an extra piece of chromosome 18 is attached to another chromosome; this is called translocation trisomy 18, or partial trisomy 18. If only part of the long (q) arm of chromosome 18 is present in 3 copies, the features may be less severe than in people with full trisomy 18.
Question: What is (are) Amyotrophic lateral sclerosis ?

Answer: Amyotrophic lateral sclerosis (ALS), also referred to as "Lou Gehrig's disease," is a progressive motor neuron disease which leads to problems with muscle control and movement. There are various types of ALS, which are distinguished by their signs and symptoms and their cause. Early symptoms may include muscle twitching, cramping, stiffness, or weakness, eventually followed by slurred speech and difficulty chewing or swallowing (dysphagia). As the disease progresses, individuals become weaker are are eventually wheelchair-dependent. Death often results from respiratory failure within 2 to 10 years after the onset of symptoms. Most affected individuals have a sporadic (not inherited) form of ALS; about 5-10% have a familial (inherited) form of the condition. Familial ALS may caused by mutations in any one of several genes and the pattern of inheritance varies depending on the gene involved. Treatment is generally supportive.
Question: What is (are) X-linked agammaglobulinemia ?

Answer: X-linked agammaglobulinema is a primary immunodeficiency characterized by very low levels of immunoglobulins (proteins made by the immune system to help fight infections). People affected by this condition generally begin developing frequent and recurrent bacterial infections from about 6 months of age. Commonly diagnosed infections include lung infections (pneumonia and bronchitis), middle ear infections, conjunctivitis, sinus infections, various skin infections, and infections that are associated with chronic diarrhea. X-linked agammaglobulinemia is caused by changes (mutations) in the BTK gene and is inherited in an X-linked recessive manner. Treatment aims to boost the immune system, which may be accomplished by administering immunoglobulins through a vein (IVIG) or subcutaneously (SCIG). Frequent infections are generally treated with antibiotics.
Question: What are the treatments for Nephrogenic diabetes insipidus ?

Answer: How might nephrogenic diabetes insipidus be treated? Management is usually best accomplished by a team of physicians and other healthcare professionals. The team may include a nutritionist, a pediatric (or adult) nephrologist or endocrinologist, and a clinical geneticist. The basis of management involves free access to drinking water and toilet facilities. Polyuria and polydipsia can be reduced up to 50% without disrupting appropriate levels of sodium in the blood through the use of thiazide diuretics hydrochlorothiazide, chlorothiazide) and/or other diuretics (i.e., potassium-sparing diuretic amiloride), dietary restriction of sodium, and nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin, which can potentially improve the ability of the body to concentrate urine and reduce urine output.
Question: how can hps be prevented for Hantavirus ?

Answer: Eliminate or minimize contact with rodents in your home, workplace, or campsite. If rodents don't find that where you are is a good place for them to be, then you're less likely to come into contact with them. Seal up holes and gaps in your home or garage. Place traps in and around your home to decrease rodent infestation. Clean up any easy-to-get food.
  
Recent research results show that many people who became ill with HPS developed the disease after having been in frequent contact with rodents and/or their droppings around a home or a workplace. On the other hand, many people who became ill reported that they had not seen rodents or rodent droppings at all. Therefore, if you live in an area where the carrier rodents are known to live, try to keep your home, vacation place, workplace, or campsite clean.
  
For more information on how you can prevent rodent infestations, the following information is available on the CDC Rodents site: