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What agency is in charge of intelligence requirements?
|
Joint and National Intelligence Support to Military Operations
| 81,826 |
What is (are) Multiple pterygium syndrome Escobar type ?
|
Multiple pterygium syndrome, Escobar type is characterized by webbing of the neck, elbows, and/or knees, and joint contractures. Symptoms of Escobar syndrome are present from birth. It can be caused by mutations in the CHRNG gene. It tends to be inherited in an autosomal recessive fashion.
| 103,195 |
What are the genetic changes related to ankyloblepharon-ectodermal defects-cleft lip/palate syndrome ?
|
AEC syndrome is caused by mutations in the TP63 gene. This gene provides instructions for making a protein known as p63, which plays an essential role in early development. The p63 protein is a transcription factor, which means that it attaches (binds) to DNA and controls the activity of particular genes. The p63 protein turns many different genes on and off during development. It appears to be especially critical for the development of ectodermal structures, such as the skin, hair, teeth, and nails. Studies suggest that it also plays important roles in the development of the limbs, facial features, urinary system, and other organs and tissues. The TP63 gene mutations responsible for AEC syndrome interfere with the ability of p63 to turn target genes on and off at the right times. It is unclear how these changes lead to abnormal ectodermal development and the specific features of AEC syndrome.
| 95,154 |
What are the symptoms of Cataract microcornea syndrome ?
|
What are the signs and symptoms of Cataract microcornea syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Cataract microcornea 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) Cataract 90% Microcornea 90% Myopia 50% Corneal dystrophy 7.5% Iris coloboma 7.5% Nystagmus 7.5% Opacification of the corneal stroma 7.5% 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.
| 109,742 |
Why did Feynman go through a depression?
|
destruction of Hiroshima by the bomb
| 70,539 |
What was only an English translation of Latin Oriens and Orientalis, "the land of the rising sun"?
|
"east"
| 21,926 |
What is (are) Leber hereditary optic neuropathy ?
|
Leber hereditary optic neuropathy (LHON) is an inherited form of vision loss. Although this condition usually begins in a person's teens or twenties, rare cases may appear in early childhood or later in adulthood. For unknown reasons, males are affected much more often than females. This condition is caused by mutations in the MT-ND1, MT-ND4, MT-ND4L, and MT-ND6 genes.
| 109,504 |
What is (are) Rosacea ?
|
Rosacea is a long-term disease that affects your skin and sometimes your eyes. It causes redness and pimples. Rosacea is most common in women and people with fair skin. It most often affects middle-aged and older adults. In most cases, rosacea only affects the face. Symptoms can include - Frequent redness of the face, or flushing - Small, red lines under the skin - Acne - A swollen nose - Thick skin, usually on the forehead, chin, and cheeks - Red, dry, itchy eyes and sometimes vision problems No one knows what causes rosacea. You may be more likely to have it if you blush a lot or if rosacea runs in your family. Rosacea is not dangerous. There is no cure, but treatments can help. They include medicines and sometimes surgery. NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
| 117,976 |
What did the Taylor Report recommend to abolish from all stadiums?
|
standing terraces
| 77,766 |
What's the most recent generation of iPod Touch?
|
sixth
| 2,498 |
After Queen Victoria refuse to replace her ladies with wives of Tories, what did Sir Robert Peel do?
|
resigned his commission
| 37,347 |
In the years between 1918 and 1940 how many Estonian language books were printed?
|
23,868
| 15,912 |
When was Okinawa finally returned?
|
May 15, 1972
| 75,157 |
What language is the descendant of Sanskrit?
|
Prakrit
| 32,589 |
Due to lack of strategic and hard power, countries are excluded from what?
|
UN Security Council
| 74,260 |
Where was the Ptolemaic Kingdom located?
|
north-east Africa
| 38,440 |
What is the term when the mind is ready to penetrate and gain insight?
|
vipassanā
| 6,738 |
What is (are) Alagille syndrome ?
|
Alagille syndrome is a genetic disorder that can affect the liver, heart, and other parts of the body. One of the major features of Alagille syndrome is liver damage caused by abnormalities in the bile ducts. These ducts carry bile (which helps to digest fats) from the liver to the gallbladder and small intestine. In Alagille syndrome, the bile ducts may be narrow, malformed, and reduced in number (bile duct paucity). As a result, bile builds up in the liver and causes scarring that prevents the liver from working properly to eliminate wastes from the bloodstream. Signs and symptoms arising from liver damage in Alagille syndrome may include a yellowish tinge in the skin and the whites of the eyes (jaundice), itchy skin, and deposits of cholesterol in the skin (xanthomas). Alagille syndrome is also associated with several heart problems, including impaired blood flow from the heart into the lungs (pulmonic stenosis). Pulmonic stenosis may occur along with a hole between the two lower chambers of the heart (ventricular septal defect) and other heart abnormalities. This combination of heart defects is called tetralogy of Fallot. People with Alagille syndrome may have distinctive facial features including a broad, prominent forehead; deep-set eyes; and a small, pointed chin. The disorder may also affect the blood vessels within the brain and spinal cord (central nervous system) and the kidneys. Affected individuals may have an unusual butterfly shape of the bones of the spinal column (vertebrae) that can be seen in an x-ray. Problems associated with Alagille syndrome generally become evident in infancy or early childhood. The severity of the disorder varies among affected individuals, even within the same family. Symptoms range from so mild as to go unnoticed to severe heart and/or liver disease requiring transplantation. Some people with Alagille syndrome may have isolated signs of the disorder, such as a heart defect like tetralogy of Fallot, or a characteristic facial appearance. These individuals do not have liver disease or other features typical of the disorder.
| 109,356 |
Who was Zeus's sister?
|
Hera
| 42,509 |
What is (are) deafness-dystonia-optic neuronopathy syndrome ?
|
Deafness-dystonia-optic neuronopathy (DDON) syndrome, also known as Mohr-Tranebjrg syndrome, is characterized by hearing loss that begins early in life, problems with movement, impaired vision, and behavior problems. This condition occurs almost exclusively in males. The first symptom of DDON syndrome is hearing loss caused by nerve damage in the inner ear (sensorineural hearing loss), which begins in early childhood. The hearing impairment worsens over time, and most affected individuals have profound hearing loss by age 10. People with DDON syndrome typically begin to develop problems with movement during their teens, although the onset of these symptoms varies among affected individuals. Some people experience involuntary tensing of the muscles (dystonia), while others have difficulty coordinating movements (ataxia). The problems with movement usually worsen over time. Individuals with DDON syndrome have normal vision during childhood, but they may begin to develop an increased sensitivity to light (photophobia) or other vision problems during their teens. These people often have a slowly progressive reduction in the sharpness of vision (visual acuity) and become legally blind in mid-adulthood. People with this condition may also have behavior problems, including changes in personality and aggressive or paranoid behaviors. They also usually develop a gradual decline in thinking and reasoning abilities (dementia) in their forties. The lifespan of individuals with DDON syndrome depends on the severity of the disorder. People with severe cases have survived into their teenage years, while those with milder cases have lived into their sixties.
| 105,326 |
What are the treatments for CHST3-related skeletal dysplasia ?
|
These resources address the diagnosis or management of CHST3-related skeletal dysplasia: - Gene Review: Gene Review: CHST3-Related Skeletal Dysplasia - Genetic Testing Registry: Spondyloepiphyseal dysplasia with congenital joint dislocations 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
| 93,726 |
What does Hokkien mean?
|
Fujian province
| 39,663 |
What is (are) Parkinson's Disease ?
|
Lewy bodies are unusual deposits or clumps of the brain protein alpha-synuclein, along with other proteins, which are seen upon microscopic examination of the brain. Many brain cells of people with Parkinson's disease contain Lewy bodies. Researchers do not yet know why Lewy bodies form or what role they play in the development of Parkinson's disease. The clumps may prevent the cell from functioning normally, or they may actually be helpful, perhaps by keeping harmful proteins "locked up" so that the cells can function.
| 118,777 |
The ordered the Russian troops to leave the Principalities?
|
Tsar Nicholas I
| 52,052 |
How many tons of bombs had to be dropped to be considered a major attack?
|
more than 100 tons of bombs dropped
| 73,070 |
Who is considered to have been the one that founded Illuminationist philosophy?
|
Shahab al-Din Suhrawardi
| 79,241 |
Where can an MCU be embedded?
|
dedicated videoconferencing units
| 29,293 |
What are the treatments for Blepharophimosis, ptosis, and epicanthus inversus syndrome type 1 ?
|
How might Blepharophimosis syndrome type 1 be treated? Management of blepharophimosis syndrome type 1 requires the input of several specialists including a clinical geneticist, pediatric ophthalmologist, eye plastic (oculoplastic) surgeon, endocrinologist, reproductive endocrinologist, and gynecologist. Eyelid surgery should be discussed with an oculoplastic surgeon to decide on the method and timing that is best suited for the patient. Traditionally, surgical correction of the blepharophimosis, epicanthus inversus, and telecanthus (canthoplasty) is performed at ages three to five years, followed about a year later by ptosis correction (usually requiring a brow suspension procedure). If the epicanthal folds are small, a "Y-V canthoplasty" is traditionally used; if the epicanthal folds are severe, a "double Z-plasty" is used. Unpublished reports have indicated that advanced understanding of the lower eyelid position has allowed for more targeted surgery that results in a more natural appearance. For a general explanation of these procedures and to locate an eye-care professional visit the Foundation of the American Academy of Ophthalmology and the National Eye Institute websites. To locate a surgeon through the American Society of Ophthalmic Plastic & Reconstructive Surgery click here. Generally, premature ovarian failure (POF) is treated with hormone replacement therapy. There is no specific treatment for POF caused by blepharophimosis syndrome type 1. Hormone replacement therapy is generally estrogen and progesterone and sometimes also includes testosterone. Birth control pills are sometimes substituted for hormone replacement therapy. Although health care providers can suggest treatments for some of the symptoms of POF, currently there is no scientifically established treatment to restore fertility for women diagnosed with POF. Women with POF are encouraged to speak to a health care professional. If you wish to obtain more information and support, you can visit the International Premature Ovarian Failure Association.
| 114,558 |
Is cytochrome P450 oxidoreductase 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.
| 97,685 |
What did not exist through the entire classical music period?
|
the symphony
| 18,411 |
What causes Mitochondrial genetic disorders ?
|
What causes mitochondrial genetic disorders? Mitochondrial genetic disorders can be caused by changes (mutations) in either the mitochondrial DNA or nuclear DNA that lead to dysfunction of the mitochondria. Most DNA (hereditary material that is passed from parent to child) is packaged within the nucleus of each cell (known as nuclear DNA). However, mitochondria (the structures in each cell that produce energy) contain a small amount of their own DNA, which is known as mitochondrial DNA. When the mitochondria are not working properly, the body does not have enough energy to carry out its normal functions. This can lead to the variety of health problems associated with mitochondrial genetic disorders.
| 113,834 |
What are the symptoms of Syngnathia multiple anomalies ?
|
What are the signs and symptoms of Syngnathia multiple anomalies? The Human Phenotype Ontology provides the following list of signs and symptoms for Syngnathia multiple anomalies. 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 teeth 90% Aplasia/Hypoplasia affecting the eye 90% Choanal atresia 90% Cognitive impairment 90% Facial palsy 90% Iris coloboma 90% Microcephaly 90% Narrow mouth 90% Nystagmus 90% Respiratory insufficiency 90% Sacrococcygeal pilonidal abnormality 90% Short stature 90% Trismus 90% Vertebral segmentation defect 90% 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.
| 110,369 |
Santa Monica plans on water independence by what year?
|
2020
| 75,912 |
Women with red caps crowded around guillotines during the Reign of Terror to do what?
|
celebrate
| 72,639 |
What does the JEDEC EIA370 transistor number start with?
|
2N
| 74,575 |
What Babylonian ruler created formal law tables?
|
Hammurabi
| 52,316 |
Where has the Medieval Fair of Norman been held since 2003?
|
Reaves Park
| 60,767 |
What language has one of the most phonemic orthographies of all European languages?
|
Czech
| 54,246 |
What percentage of the Rajasthani GDP comes from tourism?
|
eight percent
| 69,140 |
Who failed to take advantage of the retreat?
|
local commanders
| 52,090 |
What is (are) Neuroacanthocytosis ?
|
Neuroacanthocytosis refers to a group of genetic conditions that are characterized by movement disorders and acanthocytosis (abnormal, spiculated red blood cells). Four syndromes are classified as neuroacanthocytosis: Chorea-acanthocytosis, McLeod syndrome, Huntington's disease-like 2 (HDL2), and panthothenate kinase-associated neurodegeneration (PKAN). Acanthocytosis may not always be observed in HDL2 and PKAN. These disorders are caused by different genetic mutations, and the signs and symptoms vary, but usually include chorea (involuntary, dance-like movements), parkinsonism (slowness of movement), dystonia (abnormal body postures), and problems walking. There may also be muscle weakness, involuntary movements of the face and tongue, tongue/lip biting (which is mostly characteristic of Chorea-acanthocytosis), as well as difficulty with speech and eating, cognitive impairment, psychiatric symptoms, and seizures. Individuals with McLeod syndrome often have cardiac problems. Many features of these disorders are due to degeneration of the basal ganglia, a part of the brain that controls movement. Additional disorders that are also known have neurologic symptoms, acanthocytosis, and either lipoprotein disorders or systemic findings. The diagnosis of neuroacanthocytosis is typically based on the symptoms and clinical observation, a review of family history, and the evaluation of specific laboratory and imaging studies.
| 88,385 |
Is tyrosinemia 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.
| 94,320 |
Was Hebb's thought of the relationship between short and long term memory true?
|
research showed this to be false
| 36,117 |
On what date did Gaddafi declare the beginning of a "Popular Revolution"?
|
16 April 1973
| 70,877 |
What is another name for walking stick insects?
|
Phasmatodea
| 64,917 |
Who did Jugurtha have to bribe in order for them to accept him as the new leader of Numidia?
|
the Romans
| 77,942 |
When did the nation reestablish itself ?
|
empire was revived in 1261
| 73,842 |
What type of Catholicism is Armenia's church part of?
|
Oriental Orthodox
| 85,291 |
What causes Angelman syndrome ?
|
What causes Angelman syndrome? Angelman syndrome is caused by a loss of function of a gene called UBE3A on chromosome 15. The exact mechanism that causes this loss of function is complex. People normally inherit one copy of the UBE3A gene from each parent. Both copies of this gene are turned on (active) in many of the body's tissues. In certain areas of the brain, however, only the copy inherited from a person's mother is active. This parent-specific gene activation is known as genomic imprinting. If the maternal copy of the UBE3A gene is lost because of a chromosomal change or a gene mutation, a person will have no active copies of the gene in some parts of the brain. Several different genetic mechanisms can inactivate or delete the maternal copy of the UBE3A gene. Most cases of Angelman syndrome occur when a segment of the maternal chromosome 15 containing this gene is deleted. In other cases, Angelman syndrome is caused by a mutation in the maternal copy of the UBE3A gene. In a small percentage of cases, a person with Angelman syndrome inherits two copies of chromosome 15 from his or her father, instead of one copy from each parent. This is called paternal uniparental disomy. Rarely, Angelman syndrome can also be caused by a chromosomal rearrangement called a translocation, or by a mutation or other defect in the region of DNA that controls activation of the UBE3A gene. These genetic changes can abnormally turn off (inactivate) UBE3A or other genes on the maternal copy of chromosome 15. The cause of Angelman syndrome is unknown in 10 to 15 percent of affected individuals. Changes involving other genes or chromosomes may be responsible for the condition in these individuals.
| 114,636 |
How many successive finishes did Walter Smith manage for the Everton FC?
|
three
| 28,726 |
Which country claims the Armenian Genocide didn't occur?
|
Turkey
| 76,989 |
Which is one of the tribes that spoke Insular Celtic?
|
Pictish (northern Britain)
| 79,607 |
What is another term for collective effervescence?
|
emotional energy
| 28,227 |
Where have cases in the Jehovah's Witnesses favor been heard outside of the U.S.?
|
Canada
| 85,533 |
Bronze and brass are examples of what?
|
substitutional alloys
| 49,846 |
What is (are) congenital cataracts, facial dysmorphism, and neuropathy ?
|
Congenital cataracts, facial dysmorphism, and neuropathy (CCFDN) is a rare disorder that affects several parts of the body. It is characterized by a clouding of the lens of the eyes at birth (congenital cataracts) and other eye abnormalities, such as small or poorly developed eyes (microphthalmia) and abnormal eye movements (nystagmus). Affected individuals, particularly males, often have distinctive facial features that become more apparent as they reach adulthood. These features include a prominent midface, a large nose, protruding teeth, and a small lower jaw. CCFDN causes progressive damage to the peripheral nerves, which connect the brain and spinal cord to muscles and sensory cells. This nerve damage is known as peripheral neuropathy. Weakness in the legs, followed by the arms, begins in the first few years of life, and as a result children with CCFDN have delayed development of motor skills such as standing and walking. In adolescence, affected individuals develop sensory abnormalities such as numbness and tingling, mainly in the legs. By adulthood they typically have significant difficulties with mobility. Muscle weakness can also lead to skeletal abnormalities such as hand and foot deformities and abnormal curvature of the spine. People with CCFDN may have problems with balance and coordination (ataxia), tremors, and difficulty with movements that involve judging distance or scale (dysmetria). Some have mild intellectual disability. Individuals with CCFDN have short stature, are typically underweight, and have reduced bone density. A complication called rhabdomyolysis occurs in some people with CCFDN, typically following a viral infection or, in rare cases, during or after surgery. Rhabdomyolysis is a breakdown of muscle tissue that results in severe muscle weakness. The destruction of muscle tissue releases a protein called myoglobin, which is processed by the kidneys and released in the urine (myoglobinuria). The presence of myoglobin causes the urine to be red or brown. The muscles may take up to a year to recover, and the episodes may worsen the muscle weakness caused by the neuropathy.
| 96,872 |
What agency maintains the Presidential Library system?
|
NARA
| 17,782 |
What is the name of the study done by composer Ryan Maguire?
|
The Ghost in the MP3
| 25,580 |
Who besides African Americans were victims of Tennessee's late-19th century electoral reform?
|
poor Whites
| 69,765 |
How to diagnose Autoimmune atrophic gastritis ?
|
How is autoimmune atrophic gastritis diagnosed? A diagnosis of autoimmune atrophic gastritis is generally not suspected until characteristic signs and symptoms are present. Additional testing can then be ordered to confirm the diagnosis. This generally includes: A biopsy of the affected tissue obtained through endoscopy Blood work that demonstrates autoantibodies against certain cells of the stomach
| 101,413 |
The most well supported theory on the origins of the Ashkenazim is one that details a Jewish migration through which modern day country?
|
through what is now Italy
| 35,602 |
What was the target percentage of public transport mode share that was set by the state government in 2006?
|
20%
| 31,590 |
What is the name of the dog with four eyes in Norse mythology?
|
Garmr
| 8,101 |
What habitat is the body louse specific to?
|
clothing
| 41,027 |
When is the earliest hieroglyghics date back?
|
3200 BC
| 83,074 |
For what does a strong presumption exist internationally that a head of state has acted within in entering into a treaty?
|
his proper authority
| 19,505 |
What did the Predictor calculate after it was pointed at a target?
|
the proper aim point automatically
| 32,375 |
Where did the drug traffickers come from?
|
Latin America
| 21,361 |
In what part of the website are Wayback Machine's rules regarding removing content?
|
FAQ
| 10,078 |
what research (or clinical trials) is being done for Cavernous Malformation ?
|
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. Studies of cerebral cavernous malformations (CCMs) show that alterations in the function of structural proteins may also give rise to vascular malformations. Currently there is no therapy to prevent the development or progression of CCMs. NINDS-funded scientists have developed an animal model that studies two of the familial genes related to the development of CCMs. Research shows that the protein signaling pathway Rhoa/ROCK, which allows cells to communicate regarding the formation of cell structure, is involved in blood vessel activity/ and the flow of molecules and cells into and out of blood vessels. These scientists hypothesize that blocking ROCK activity will inhibit CCM development and hemorrhage, and possibly create a therapy for these malformations.
| 115,184 |
How to diagnose Dopa-responsive dystonia ?
|
How is dopa-responsive dystonia diagnosed? Dopa-responsive dystonia (DRD) is diagnosed based on the signs and symptoms present, results of laboratory tests (sometimes including genetic testing), and response to therapy with levodopa. If DRD is suspected, a therapeutic trial with low doses of levodopa remains the most practical approach to the diagnosis. It is generally agreed that people with childhood-onset dystonia of unknown cause should be treated initially with levodopa. The characteristic symptoms and response to treatment are sufficient to establish the diagnosis for people with the most common form, autosomal dominant DRD. There is only one gene in which mutations are known to cause this form of DRD, but not all people with the disorder are found to have a mutation in the responsible gene. While finding a mutation may provide information about prognosis, it does not alter the treatment. Other types of laboratory tests, such as measuring specific substances or enzymes in the blood or cerebrospinal fluid (CSF), may be useful to support the diagnosis. For tyrosine hydroxylase deficiency, an autosomal recessive genetic cause of DRD, molecular genetic testing has confirmed the presence of mutations in all affected people to date. Specific laboratory tests performed on CSF help support the diagnosis but are not diagnostic on their own. For sepiapterin reductase deficiency, a very rare autosomal recessive form of DRD, there are distinctive findings in CSF and reduced or absent activity of sepiapterin reductase in fibroblasts. Molecular genetic testing can identify mutations in the responsible gene and confirm the diagnosis of this form of DRD. The major conditions that may have a similar presentation to DRD and are part of the differential diagnosis include early-onset parkinsonism, early-onset primary dystonia, and cerebral palsy or spastic paraplegia. People with specific questions about being evaluated for any form of dystonia should speak with a neurologist or other health care provider.
| 102,562 |
What did Wendell B. Blancke investigate at the end of the war?
|
Exploitation German Archives
| 53,588 |
Which Nigerian political party was mostly Islamic?
|
Nigerian People's Congress
| 52,933 |
What are the treatments for Joubert Syndrome ?
|
Treatment for Joubert syndrome is symptomatic and supportive. Infant stimulation and physical, occupational, and speech therapy may benefit some children. Infants with abnormal breathing patterns should be monitored. Screening for progressive eye, liver, and kidney complications associated with Joubert-related disorders should be performed on a regular basis.
| 114,970 |
the vinaya was recited by?
|
Upāli
| 6,921 |
What is (are) Tailbone Disorders ?
|
The tailbone is the small bone at the bottom of your backbone, or spine. Tailbone disorders include tailbone injuries, pain, infections, cysts and tumors. You rarely break your tailbone. Instead, most injuries cause bruises or pulled ligaments. A backward fall onto a hard surface, such as slipping on ice, is the most common cause of such injuries. Symptoms of various tailbone disorders include pain in the tailbone area, pain upon sitting, pain or numbness in the arms or legs due to pressure on nerves in the tailbone area, and a mass or growth you can see or feel.
| 93,172 |
What are the symptoms of Dehydrated hereditary stomatocytosis ?
|
What are the signs and symptoms of Dehydrated hereditary stomatocytosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Dehydrated hereditary stomatocytosis. 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) Cholelithiasis 5% Hemoglobinuria 5% Hepatitis 5% Hepatomegaly 5% Increased serum ferritin 5% Jaundice 5% Pallor 5% Splenomegaly 5% Autosomal dominant inheritance - Exercise-induced hemolysis - Increased red cell hemolysis by shear stress - Reticulocytosis - 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.
| 100,391 |
What is (are) Teenage Pregnancy ?
|
Most teenage girls don't plan to get pregnant, but many do. Teen pregnancies carry extra health risks to both the mother and the baby. Often, teens don't get prenatal care soon enough, which can lead to problems later on. They have a higher risk for pregnancy-related high blood pressure and its complications. Risks for the baby include premature birth and a low birth weight. If you're a pregnant teen, you can help yourself and your baby by - Getting regular prenatal care - Taking your prenatal vitamins for your health and to prevent some birth defects - Avoiding smoking, alcohol, and drugs - Using a condom, if you are having sex, to prevent sexually transmitted diseases that could hurt your baby
| 117,579 |
Who dispatched a telegram to the supreme headquarters prohibiting the execution of prisoners of war?
|
Tito
| 19,688 |
Whose offer to buy the paper was turned down?
|
Maxwell's offer
| 48,116 |
Are children or adolescents more likely to question assertions and less likely to accept facts?
|
adolescents
| 30,813 |
Which Navy was assumed not to be able to operate under German air superiority?
|
Royal
| 72,854 |
In what decade did computer hardware become able to handle a relational system?
|
1980s
| 76,385 |
What is (are) Spinocerebellar ataxia autosomal recessive 7 ?
|
Spinocerebellar ataxia autosomal recessive 7, also called SCAR7, is a slowly progressive hereditary form of spinocerebellar ataxia. Symptoms of SCAR7 can include difficulty walking and writing, speech difficulties (dysarthria), limb ataxia, and a decrease in the size of a region of the brain called the cerebellum (cerebellar atrophy). Of the few reported cases in the literature, some patients also had eye involvement that included nystagmus (in voluntary eye movements) and saccadic pursuit eye movements. Out of 5 affected siblings examined in a large Dutch family, 2 became wheelchair-dependent late in life. The severity of the symptoms varies from mild to severe. SCAR7 is caused by mutations in the TPP1 gene and is inherited in an autosomal recessive manner.
| 110,220 |
What are the treatments for Benign rolandic epilepsy (BRE) ?
|
What treatment is available for benign rolandic epilepsy? Although treatment is usually not necessary since the episodes are infrequent and are typically outgrown by puberty, anticonvulsants such as carbamazepine.
| 101,972 |
Who is at risk for Breast Cancer? ?
|
The risks of breast cancer screening tests include the following. - Finding breast cancer may not improve health or help a woman live longer. Screening may not help you if you have fast-growing breast cancer or if it has already spread to other places in your body. Also, some breast cancers found on a screening mammogram may never cause symptoms or become life-threatening. Finding these cancers is called overdiagnosis. Finding breast cancer may not improve health or help a woman live longer. Screening may not help you if you have fast-growing breast cancer or if it has already spread to other places in your body. Also, some breast cancers found on a screening mammogram may never cause symptoms or become life-threatening. Finding these cancers is called overdiagnosis. - False-negative test results can occur. Screening test results may appear to be normal even though breast cancer is present. A woman who receives a false-negative test result (one that shows there is no cancer when there really is) may delay seeking medical care even if she has symptoms. False-negative test results can occur. Screening test results may appear to be normal even though breast cancer is present. A woman who receives a false-negative test result (one that shows there is no cancer when there really is) may delay seeking medical care even if she has symptoms. - False-positive test results can occur. Screening test results may appear to be abnormal even though no cancer is present. A false-positive test result (one that shows there is cancer when there really isnt) is usually followed by more tests (such as biopsy), which also have risks. False-positive test results can occur. Screening test results may appear to be abnormal even though no cancer is present. A false-positive test result (one that shows there is cancer when there really isnt) is usually followed by more tests (such as biopsy), which also have risks. - Anxiety from additional testing may result from false positive results. In one study, women who had a false-positive screening mammogram followed by more testing reported feeling anxiety 3 months later, even though cancer was not diagnosed. However, several studies show that women who feel anxiety after false-positive test results are more likely to schedule regular breast screening exams in the future. Anxiety from additional testing may result from false positive results. In one study, women who had a false-positive screening mammogram followed by more testing reported feeling anxiety 3 months later, even though cancer was not diagnosed. However, several studies show that women who feel anxiety after false-positive test results are more likely to schedule regular breast screening exams in the future. - Mammograms expose the breast to radiation. Being exposed to radiation is a risk factor for breast cancer. The risk of breast cancer from radiation exposure is higher in women who received radiation before age 30 and at high doses. For women older than 40 years, the benefits of an annual screening mammogram may be greater than the risks from radiation exposure. Mammograms expose the breast to radiation. Being exposed to radiation is a risk factor for breast cancer. The risk of breast cancer from radiation exposure is higher in women who received radiation before age 30 and at high doses. For women older than 40 years, the benefits of an annual screening mammogram may be greater than the risks from radiation exposure. - There may be pain or discomfort during a mammogram. During a mammogram, the breast is placed between 2 plates that are pressed together. Pressing the breast helps to get a better x-ray of the breast. Some women have pain or discomfort during a mammogram. There may be pain or discomfort during a mammogram. During a mammogram, the breast is placed between 2 plates that are pressed together. Pressing the breast helps to get a better x-ray of the breast. Some women have pain or discomfort during a mammogram. Some women worry about radiation exposure, but the risk of any harm from a mammogram is actually quite small. The doses of radiation used are very low and considered safe. The exact amount of radiation used during a mammogram will depend on several factors. For instance, breasts that are large or dense will require higher doses to get a clear image. Learn more about the risks of breast cancer screening.
| 91,037 |
In addition to back stories and drama, what did Fuller add to the show?
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telephone voting
| 6,995 |
What are the symptoms of Odonto onycho dysplasia with alopecia ?
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What are the signs and symptoms of Odonto onycho dysplasia with alopecia? The Human Phenotype Ontology provides the following list of signs and symptoms for Odonto onycho dysplasia with alopecia. 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 fingernails 90% Alopecia 90% Aplasia/Hypoplasia of the eyebrow 90% Hypoplastic toenails 90% Microdontia 90% Palmoplantar keratoderma 90% Reduced number of teeth 90% 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.
| 109,865 |
Where was Kerry injured?
|
in the left arm above the elbow
| 68,818 |
How many consecutive years did American Idol been ranked number one in ratings?
|
eight
| 6,986 |
What was the purpose of Iman Crosson's video?
|
encourage young Americans to enroll
| 84,228 |
What nickname are residents of Mexico given that more reflects the Spanish influence of the city?
|
defeños
| 43,659 |
What did the UK, France and Israel intend to do to Nasser?
|
topple
| 61,448 |
What was the determination of the referendum?
|
separation
| 81,126 |
What is Uruguay's oldest theater?
|
The Solís Theatre
| 39,861 |
Barts and the London School of Dentistry if part of which university in the University of London Network?
|
Queen Mary
| 47,106 |
What are the treatments for hyperlysinemia ?
|
These resources address the diagnosis or management of hyperlysinemia: - Genetic Testing Registry: Hyperlysinemia - Genetic Testing Registry: Saccharopinuria 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
| 98,451 |
England left FIFA in 1928 and ultimately rejoined in what year?
|
1946
| 26,322 |
What are the genetic changes related to inclusion body myopathy with early-onset Paget disease and frontotemporal dementia ?
|
Mutations in the VCP gene cause IBMPFD. The VCP gene provides instructions for making an enzyme called valosin-containing protein, which has a wide variety of functions within cells. One of its most critical jobs is to help break down (degrade) proteins that are abnormal or no longer needed. Mutations in the VCP gene alter the structure of valosin-containing protein, disrupting its ability to break down other proteins. As a result, excess and abnormal proteins may build up in muscle, bone, and brain cells. The proteins form clumps that interfere with the normal functions of these cells. It remains unclear how damage to muscle, bone, and brain cells leads to the specific features of IBMPFD.
| 93,389 |
Who is at risk for Varicose Veins? ?
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Many factors may raise your risk for varicose veins, including family history, older age, gender, pregnancy, overweight or obesity, lack of movement, and leg trauma.
Family History
Having family members who have varicose veins may raise your risk for the condition. About half of all people who have varicose veins have a family history of them.
Older Age
Getting older may raise your risk for varicose veins. The normal wear and tear of aging may cause the valves in your veins to weaken and not work well.
Gender
Women tend to get varicose veins more often than men. Hormonal changes that occur during puberty, pregnancy, and menopause (or with the use of birth control pills) may raise a woman's risk for varicose veins.
Pregnancy
During pregnancy, the growing fetus puts pressure on the veins in the mother's legs. Varicose veins that occur during pregnancy usually get better within 3 to 12 months of delivery.
Overweight or Obesity
Being overweight or obese can put extra pressure on your veins. This can lead to varicose veins. For more information about overweight and obesity, go to the Health Topics Overweight and Obesity article.
Lack of Movement
Standing or sitting for a long time, especially with your legs bent or crossed, may raise your risk for varicose veins. This is because staying in one position for a long time may force your veins to work harder to pump blood to your heart.
Leg Trauma
Previous blood clots or traumatic damage to the valves in your veins can weaken their ability to move blood back to the heart, increasing the risk for varicose veins.
| 91,831 |
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