randomani/MedicalQnA-llama2 huggingface dataset:
This is a medical question of type : genetic changes 
 What are the genetic changes related to allergic asthma ? 
 The cause of allergic asthma is complex. It is likely that a combination of multiple genetic and environmental factors contribute to development of the condition. Doctors believe genes are involved because having a family member with allergic asthma or another allergic disorder increases a person's risk of developing asthma.  Studies suggest that more than 100 genes may be associated with allergic asthma, but each seems to be a factor in only one or a few populations. Many of the associated genes are involved in the body's immune response. Others play a role in lung and airway function.  There is evidence that an unbalanced immune response underlies allergic asthma. While there is normally a balance between type 1 (or Th1) and type 2 (or Th2) immune reactions in the body, many individuals with allergic asthma predominantly have type 2 reactions. Type 2 reactions lead to the production of immune proteins called IgE antibodies and the generation of other factors that predispose to bronchial hyperresponsiveness. Normally, the body produces IgE antibodies in response to foreign invaders, particularly parasitic worms. For unknown reasons, in susceptible individuals, the body reacts to an allergen as if it is harmful, producing IgE antibodies specific to it. Upon later encounters with the allergen, IgE antibodies recognize it, which stimulates an immune response, causing bronchoconstriction, airway swelling, and mucus production.  Not everyone with a variation in one of the allergic asthma-associated genes develops the condition; exposure to certain environmental factors also contributes to its development. Studies suggest that these exposures trigger epigenetic changes to the DNA. Epigenetic changes modify DNA without changing the DNA sequence. They can affect gene activity and regulate the production of proteins, which may influence the development of allergies in susceptible individuals.
This is a medical question of type : inheritance 
 Is allergic asthma inherited ? 
 Allergic asthma can be passed through generations in families, but the inheritance pattern is unknown. People with mutations in one or more of the associated genes inherit an increased risk of allergic asthma, not the condition itself. Because allergic asthma is a complex condition influenced by genetic and environmental factors, not all people with a mutation in an asthma-associated gene will develop the disorder.
This is a medical question of type : treatment 
 What are the treatments for allergic asthma ? 
 These resources address the diagnosis or management of allergic asthma:  - American Academy of Allergy Asthma and Immunology: Asthma Treatment and Management  - Genetic Testing Registry: Asthma, atopic  - Genetic Testing Registry: Asthma, susceptibility to   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
This is a medical question of type : information 
 What is (are) ovarian cancer ? 
 Ovarian cancer is a disease that affects women. In this form of cancer, certain cells in the ovary become abnormal and multiply uncontrollably to form a tumor. The ovaries are the female reproductive organs in which egg cells are produced. In about 90 percent of cases, ovarian cancer occurs after age 40, and most cases occur after age 60.  The most common form of ovarian cancer begins in epithelial cells, which are the cells that line the surfaces and cavities of the body. These cancers can arise in the epithelial cells on the surface of the ovary. However, researchers suggest that many or even most ovarian cancers begin in epithelial cells on the fringes (fimbriae) at the end of one of the fallopian tubes, and the cancerous cells migrate to the ovary.  Cancer can also begin in epithelial cells that form the lining of the abdomen (the peritoneum). This form of cancer, called primary peritoneal cancer, resembles epithelial ovarian cancer in its origin, symptoms, progression, and treatment. Primary peritoneal cancer often spreads to the ovaries. It can also occur even if the ovaries have been removed. Because cancers that begin in the ovaries, fallopian tubes, and peritoneum are so similar and spread easily from one of these structures to the others, they are often difficult to distinguish. These cancers are so closely related that they are generally considered collectively by experts.  In about 10 percent of cases, ovarian cancer develops not in epithelial cells but in germ cells, which are precursors to egg cells, or in hormone-producing ovarian cells called granulosa cells.  In its early stages, ovarian cancer usually does not cause noticeable symptoms. As the cancer progresses, signs and symptoms can include pain or a feeling of heaviness in the pelvis or lower abdomen, bloating, feeling full quickly when eating, back pain, vaginal bleeding between menstrual periods or after menopause, or changes in urinary or bowel habits. However, these changes can occur as part of many different conditions. Having one or more of these symptoms does not mean that a woman has ovarian cancer.  In some cases, cancerous tumors can invade surrounding tissue and spread to other parts of the body. If ovarian cancer spreads, cancerous tumors most often appear in the abdominal cavity or on the surfaces of nearby organs such as the bladder or colon. Tumors that begin at one site and then spread to other areas of the body are called metastatic cancers.  Some ovarian cancers cluster in families. These cancers are described as hereditary and are associated with inherited gene mutations. Hereditary ovarian cancers tend to develop earlier in life than non-inherited (sporadic) cases.  Because it is often diagnosed at a late stage, ovarian cancer can be difficult to treat; it leads to the deaths of about 140,000 women annually, more than any other gynecological cancer. However, when it is diagnosed and treated early, the 5-year survival rate is high.
This is a medical question of type : frequency 
 How many people are affected by ovarian cancer ? 
 Ovarian cancer affects about 12 in 100,000 women per year.
This is a medical question of type : inheritance 
 Is ovarian cancer inherited ? 
 Most cases of ovarian cancer are not caused by inherited genetic factors. These cancers are associated with somatic mutations that are acquired during a person's lifetime, and they do not cluster in families.  A predisposition to cancer caused by a germline mutation is usually inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to increase a person's chance of developing cancer. Although ovarian cancer occurs only in women, the mutated gene can be inherited from either the mother or the father. It is important to note that people inherit an increased likelihood of developing cancer, not the disease itself. Not all people who inherit mutations in these genes will ultimately develop cancer.  In many cases of ovarian cancer that clusters in families, the genetic basis for the disease and the mechanism of inheritance are unclear.
This is a medical question of type : treatment 
 What are the treatments for ovarian cancer ? 
 These resources address the diagnosis or management of ovarian cancer:  - Dana-Farber Cancer Institute  - Familial Ovarian Cancer Registry  - Fred Hutchinson Cancer Research Center  - Gene Review: Gene Review: BRCA1 and BRCA2 Hereditary Breast/Ovarian Cancer  - Genetic Testing Registry: Hereditary breast and ovarian cancer syndrome  - Genetic Testing Registry: Ovarian cancer  - Genomics Education Programme (UK): Hereditary Breast and Ovarian Cancer  - M.D. Anderson Cancer Center  - MedlinePlus Encyclopedia: BRCA1 and BRCA2 Gene Testing  - MedlinePlus Encyclopedia: CA-125 Blood Test  - Memorial Sloan-Kettering Cancer Center   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
This is a medical question of type : frequency 
 How many people are affected by multiple lentigines syndrome ? 
 Multiple lentigines syndrome is thought to be a rare condition; approximately 200 cases have been reported worldwide.
This is a medical question of type : genetic changes 
 What are the genetic changes related to multiple lentigines syndrome ? 
 Mutations in the PTPN11, RAF1, or BRAF genes cause multiple lentigines syndrome. Approximately 90 percent of individuals with multiple lentigines syndrome have mutations in the PTPN11 gene. RAF1 and BRAF gene mutations are responsible for a total of about 10 percent of cases. A small proportion of people with multiple lentigines syndrome do not have an identified mutation in any of these three genes. In these individuals, the cause of the condition is unknown.  The PTPN11, RAF1, and BRAF genes all provide instructions for making proteins that are involved in important signaling pathways needed for the proper formation of several types of tissue during development. These proteins also play roles in the regulation of cell division, cell movement (migration), and cell differentiation (the process by which cells mature to carry out specific functions).  Mutations in the PTPN11, RAF1, or BRAF genes lead to the production of a protein that functions abnormally. This abnormal functioning impairs the protein's ability to respond to cell signals. A disruption in the regulation of systems that control cell growth and division leads to the characteristic features of multiple lentigines syndrome.
This is a medical question of type : inheritance 
 Is multiple lentigines syndrome inherited ? 
 This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.
This is a medical question of type : treatment 
 What are the treatments for multiple lentigines syndrome ? 
 These resources address the diagnosis or management of multiple lentigines syndrome:  - Cincinnati Children's Hospital: Cardiomyopathies  - Gene Review: Gene Review: Noonan Syndrome with Multiple Lentigines  - Genetic Testing Registry: LEOPARD syndrome 1  - Genetic Testing Registry: LEOPARD syndrome 2  - Genetic Testing Registry: LEOPARD syndrome 3  - Genetic Testing Registry: Noonan syndrome with multiple lentigines  - MedlinePlus Encyclopedia: Hypertrophic Cardiomyopathy   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
This is a medical question of type : information 
 What is (are) congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency ? 
 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. The adrenal glands are located on top of the kidneys and produce a variety of hormones that regulate many essential functions in the body. In people with CAH due to 11-beta-hydroxylase deficiency, the adrenal glands produce excess androgens, which are male sex hormones.  There are two types of CAH due to 11-beta-hydroxylase deficiency, the classic form and the non-classic form. The classic form is the more severe of the two types.  Females with the classic form of CAH due to 11-beta-hydroxylase deficiency have external genitalia that do not look clearly male or female (ambiguous genitalia). However, the internal reproductive organs develop normally. Males and females with the classic form of this condition have early development of their secondary sexual characteristics such as growth of facial and pubic hair, deepening of the voice, appearance of acne, and onset of a growth spurt. The early growth spurt can prevent growth later in adolescence and lead to short stature in adulthood. In addition, approximately two-thirds of individuals with the classic form of CAH due to 11-beta-hydroxylase deficiency have high blood pressure (hypertension). Hypertension typically develops within the first year of life.  Females with the non-classic form of CAH due to 11-beta-hydroxylase deficiency have normal female genitalia. As affected females get older, they may develop excessive body hair growth (hirsutism) and irregular menstruation. Males with the non-classic form of this condition do not typically have any signs or symptoms except for short stature. Hypertension is not a feature of the non-classic form of CAH due to 11-beta-hydroxylase deficiency.
This is a medical question of type : frequency 
 How many people are affected by congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency ? 
 CAH due to 11-beta-hydroxylase deficiency accounts for 5 to 8 percent of all cases of congenital adrenal hyperplasia. It is estimated that CAH due to 11-beta-hydroxylase deficiency occurs in 1 in 100,000 to 200,000 newborns. This condition is more common in Moroccan Jews living in Israel, occurring in approximately 1 in 5,000 to 7,000 newborns. The classic form of CAH due to 11-beta-hydroxylase deficiency appears to be much more common than the non-classic form.
This is a medical question of type : genetic changes 
 What are the genetic changes related to congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency ? 
 Mutations in the CYP11B1 gene cause CAH due to 11-beta-hydroxylase deficiency. The CYP11B1 gene provides instructions for making an enzyme called 11-beta-hydroxylase. This enzyme is found in the adrenal glands, where it helps produce hormones called cortisol and corticosterone. Cortisol has numerous functions, such as maintaining blood sugar levels, protecting the body from stress, and suppressing inflammation. Corticosterone gets converted to the hormone aldosterone, which helps control blood pressure by maintaining proper salt and fluid levels in the body.  CAH due to 11-beta-hydroxylase deficiency is caused by a shortage (deficiency) of the 11-beta-hydroxylase enzyme. When 11-beta-hydroxylase is lacking, precursors that are used to form cortisol and corticosterone build up in the adrenal glands and are converted to androgens. The excess production of androgens leads to abnormalities of sexual development, particularly in females with CAH due to 11-beta-hydroxylase deficiency. A buildup in the precursors used to form corticosterone increases salt retention, leading to hypertension in individuals with the classic form of CAH due to 11-beta-hydroxylase deficiency.  The amount of functional 11-beta-hydroxylase enzyme that an individual produces typically determines the extent of abnormal sexual development. Individuals with the classic form of the condition usually have CYP11B1 gene mutations that result in the production of an enzyme with low levels of function or no function at all. Individuals with the non-classic form of the condition typically have CYP11B1 gene mutations that lead to the production of an enzyme with moderately reduced function. The severity of the signs and symptoms of sexual development do not appear to be related to the severity of the hypertension.
This is a medical question of type : inheritance 
 Is congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency inherited ? 
 This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
This is a medical question of type : treatment 
 What are the treatments for congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency ? 
 These resources address the diagnosis or management of congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency:  - Genetic Testing Registry: Deficiency of steroid 11-beta-monooxygenase  - MedlinePlus Encyclopedia: Congenital Adrenal Hyperplasia   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
This is a medical question of type : information 
 What is (are) adult polyglucosan body disease ? 
 Adult polyglucosan body disease is a condition that affects the nervous system. People with this condition have problems walking due to reduced sensation in their legs (peripheral neuropathy) and progressive muscle weakness and stiffness (spasticity). Damage to the nerves that control bladder function, a condition called neurogenic bladder, causes affected individuals to have progressive difficulty controlling the flow of urine. About half of people with adult polyglucosan body disease experience a decline in intellectual function (dementia).  People with adult polyglucosan body disease typically first experience signs and symptoms related to the condition between ages 30 and 60.
This is a medical question of type : frequency 
 How many people are affected by adult polyglucosan body disease ? 
 Adult polyglucosan body disease is a rare condition; although its exact prevalence is unknown, at least 50 affected individuals have been described in the medical literature.
This is a medical question of type : genetic changes 
 What are the genetic changes related to adult polyglucosan body disease ? 
 Mutations in the GBE1 gene cause adult polyglucosan body disease. The GBE1 gene provides instructions for making the glycogen branching enzyme. This enzyme is involved in the production of a complex sugar called glycogen, which is a major source of stored energy in the body. Most GBE1 gene mutations result in a shortage (deficiency) of the glycogen branching enzyme, which leads to the production of abnormal glycogen molecules. These abnormal glycogen molecules, called polyglucosan bodies, accumulate within cells and cause damage. Nerve cells (neurons) appear to be particularly vulnerable to the accumulation of polyglucosan bodies in people with this disorder, leading to impaired neuronal function.  Some mutations in the GBE1 gene that cause adult polyglucosan body disease do not result in a shortage of glycogen branching enzyme. In people with these mutations, the activity of this enzyme is normal. How mutations cause the disease in these individuals is unclear. Other people with adult polyglucosan body disease do not have identified mutations in the GBE1 gene. In these individuals, the cause of the disease is unknown.
This is a medical question of type : inheritance 
 Is adult polyglucosan body disease inherited ? 
 This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
This is a medical question of type : treatment 
 What are the treatments for adult polyglucosan body disease ? 
 These resources address the diagnosis or management of adult polyglucosan body disease:  - Gene Review: Gene Review: Adult Polyglucosan Body Disease  - Genetic Testing Registry: Polyglucosan body disease, adult  - MedlinePlus Encyclopedia: Neurogenic Bladder  - MedlinePlus Encyclopedia: Spasticity   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
This is a medical question of type : information 
 What is (are) cerebral cavernous malformation ? 
 Cerebral cavernous malformations are collections of small blood vessels (capillaries) in the brain that are enlarged and irregular in structure. These capillaries have abnormally thin walls, and they lack other support tissues, such as elastic fibers, which normally make them stretchy. As a result, the blood vessels are prone to leakage, which can cause the health problems related to this condition. Cavernous malformations can occur anywhere in the body, but usually produce serious signs and symptoms only when they occur in the brain and spinal cord (which are described as cerebral).  Approximately 25 percent of individuals with cerebral cavernous malformations never experience any related health problems. Other people with this condition may experience serious signs and symptoms such as headaches, seizures, paralysis, hearing or vision loss, and bleeding in the brain (cerebral hemorrhage). Severe brain hemorrhages can result in death. The location and number of cerebral cavernous malformations determine the severity of this disorder. These malformations can change in size and number over time.  There are two forms of the condition: familial and sporadic. The familial form is passed from parent to child, and affected individuals typically have multiple cerebral cavernous malformations. The sporadic form occurs in people with no family history of the disorder. These individuals typically have only one malformation.
This is a medical question of type : frequency 
 How many people are affected by cerebral cavernous malformation ? 
 Cerebral cavernous malformations affect about 0.5 percent of the population worldwide.
This is a medical question of type : genetic changes 
 What are the genetic changes related to cerebral cavernous malformation ? 
 Mutations in at least three genes, KRIT1 (also known as CCM1), CCM2, and PDCD10 (also known as CCM3), cause familial cerebral cavernous malformations.  The precise functions of these genes are not fully understood. Studies show that the proteins produced from these genes are found in the junctions connecting neighboring blood vessel cells. The proteins interact with each other as part of a complex that strengthens the interactions between cells and limits leakage from the blood vessels. Mutations in any of the three genes impair the function of the protein complex, resulting in weakened cell-to-cell junctions and increased leakage from vessels as seen in cerebral cavernous malformations.  Mutations in these three genes account for 85 to 95 percent of all cases of familial cerebral cavernous malformations. The remaining 5 to 15 percent of cases may be due to mutations in unidentified genes or to other unknown causes. Mutations in the KRIT1, CCM2, and PDCD10 genes are not involved in sporadic cerebral cavernous malformations. The cause of this form of the condition is unknown.
This is a medical question of type : inheritance 
 Is cerebral cavernous malformation inherited ? 
 This condition has an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In the familial form, an affected person inherits the mutation from one affected parent.  Most people with cerebral cavernous malformations have the sporadic form of the disorder. These cases occur in people with no history of the disorder in their family.
This is a medical question of type : treatment 
 What are the treatments for cerebral cavernous malformation ? 
 These resources address the diagnosis or management of cerebral cavernous malformation:  - Angioma Alliance: Imaging and Diagnostics  - Gene Review: Gene Review: Familial Cerebral Cavernous Malformation  - Genetic Testing Registry: Cerebral cavernous malformation  - Genetic Testing Registry: Cerebral cavernous malformations 1  - Genetic Testing Registry: Cerebral cavernous malformations 2  - Genetic Testing Registry: Cerebral cavernous malformations 3  - MedlinePlus Encyclopedia: Cerebral angiography   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care