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Where was Charles Dickens employed as a child?

blacking factory

What American carrier was sunk in the Battle of the Coral Sea?

Lexington

What is (are) cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy ?

Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy, commonly known as CARASIL, is an inherited condition that causes stroke and other impairments. Abnormalities affecting the brain and other parts of the nervous system become apparent in an affected person's twenties or thirties. Often, muscle stiffness (spasticity) in the legs and problems with walking are the first signs of the disorder. About half of affected individuals have a stroke or similar episode before age 40. As the disease progresses, most people with CARASIL also develop mood and personality changes, a decline in thinking ability (dementia), memory loss, and worsening problems with movement. Other characteristic features of CARASIL include premature hair loss (alopecia) and attacks of low back pain. The hair loss often begins during adolescence and is limited to the scalp. Back pain, which develops in early to mid-adulthood, results from the breakdown (degeneration) of the discs that separate the bones of the spine (vertebrae) from one another. The signs and symptoms of CARASIL worsen slowly with time. Over the course of several years, affected individuals become less able to control their emotions and communicate with others. They increasingly require help with personal care and other activities of daily living; after a few years, they become unable to care for themselves. Most affected individuals die within a decade after signs and symptoms first appear, although few people with the disease have survived for 20 to 30 years.

What is the name of the mountaneous region along the Atlantic cost.

The Appalachian Highland

Who believes that the Soviet Unions was afraid of Germany?

Historian Werner Maser

How many people died as a result of the MVD and NAA clash in 1918?

five Armenians

From where may a converter be fed?

rotor circuit

Is hereditary cerebral amyloid angiopathy inherited ?

Hereditary cerebral amyloid angiopathy caused by mutations in the APP, CST3, or ITM2B gene is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. There is also a non-hereditary form of cerebral amyloid angiopathy that occurs in people with no history of the disorder in their family. The cause of this form of the condition is unknown. These cases are described as sporadic and are not inherited.

Where is the Ptolemaic Kingdom?

north-east Africa

How many users did Sony say might have been affected by the intrusion?

77 million

How many companies were started through Northwestern's Innovations and New Ventures Office?

12

What is the only medal Bermuda has ever won?

bronze medal in boxing.

Is Danon disease inherited ?

How is Danon disease inherited? Dannon disease is inherited in an X-linked fashion. Click here to visit the Centre for Genetics Education Web site to learn more about X linked inheritance.

What is (are) Richter syndrome ?

Richter syndrome is a rare condition in which chronic lymphocytic leukemia (CLL) changes into a fast-growing type of lymphoma. Symptoms of Richter syndrome can include fever, loss of weight and muscle mass, abdominal pain, and enlargement of the lymph nodes, liver, and spleen. Laboratory results may show anemia and low platelet counts (which can lead to easy bleeding and bruising).

What is (are) Ataxia Telangiectasia ?

Ataxia-telangiectasia is a rare, childhood neurological disorder that causes degeneration in the part of the brain that controls motor movements and speech. The first signs of the disease are unsteady walking and slurred speech, usually occurring during the first five years of life. Telangiectasias (tiny, red "spider" veins), which appear in the corners of the eyes or on the surface of the ears and cheeks, are characteristic of the disease, but are not always present and generally do not appear in the first years of life. About 35 percent of those with A-T develop cancer, most frequently acute lymphocytic leukemia or lymphoma. The most unusual symptom is an acute sensitivity to ionizing radiation, such as X-rays or gamma rays. Many individuals with A-T have a weakened immune system, making them susceptible to recurrent respiratory infections. Other features of the disease may include mild diabetes mellitus, premature graying of the hair, difficulty swallowing, and delayed physical and sexual development. Children with A-T usually have normal or above normal intelligence.

What is (are) adermatoglyphia ?

Adermatoglyphia is the absence of ridges on the skin on the pads of the fingers and toes, as well as on the palms of the hands and soles of the feet. The patterns of these ridges (called dermatoglyphs) form whorls, arches, and loops that are the basis for each person's unique fingerprints. Because no two people have the same patterns, fingerprints have long been used as a way to identify individuals. However, people with adermatoglyphia do not have these ridges, and so they cannot be identified by their fingerprints. Adermatoglyphia has been called the "immigration delay disease" because affected individuals have had difficulty entering countries that require fingerprinting for identification. In some families, adermatoglyphia occurs without any related signs and symptoms. In others, a lack of dermatoglyphs is associated with other features, typically affecting the skin. These can include small white bumps called milia on the face, blistering of the skin in areas exposed to heat or friction, and a reduced number of sweat glands on the hands and feet. Adermatoglyphia is also a feature of several rare syndromes classified as ectodermal dysplasias, including a condition called Naegeli-Franceschetti-Jadassohn syndrome/dermatopathia pigmentosa reticularis that affects the skin, hair, sweat glands, and teeth.

According to some, what was Ibn Sina trying to do regarding his works?

"re-Aristotelianise" Muslim philosophy

What does the Paradox of the Stone posit?

he is not omnipotent

What did this person also state about all of mankind in regards to wayward transgressions ?

his argument is that all men are sinners;

What are the symptoms of Muir-Torre syndrome ?

What are the signs and symptoms of Muir-Torre syndrome? Sebaceous adenoma is the most characteristic finding in people with Muir-Torre syndrome (MTS). Other types of skin tumors in affected people include sebaceous epitheliomas, sebaceous carcinomas (which commonly occur on the eyelids) and keratoacanthomas. Sebaceous carcinoma of the eyelid can invade the orbit of the eye and frequently metastasize, leading to death. Tumors at other sites can also metastasize, but are less likely to cause death. Common sites of keratocathomas include the face and the upper side of the hands, but they can occur anywhere on the body. The most common internal cancer in people with MTS is colorectal cancer, occurring in almost half of affected people. The second most common site is the genitourinary tract. Other cancers that may occur include breast cancer, lymphoma, leukemia (rarely), salivary gland tumors, lower and upper respiratory tract tumors, and chondrosarcoma. Intestinal polyps as well as various benign tumors may also occur. The Human Phenotype Ontology provides the following list of signs and symptoms for Muir-Torre 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) Adenoma sebaceum 90% Neoplasm of the colon 50% Neoplasm of the stomach 50% Hematological neoplasm 7.5% Neoplasm of the breast 7.5% Neoplasm of the liver 7.5% Ovarian neoplasm 7.5% Renal neoplasm 7.5% Salivary gland neoplasm 7.5% Uterine neoplasm 7.5% Autosomal dominant inheritance - Basal cell carcinoma - Benign gastrointestinal tract tumors - Benign genitourinary tract neoplasm - Breast carcinoma - Colon cancer - Colonic diverticula - Duodenal adenocarcinoma - Laryngeal carcinoma - Malignant genitourinary tract tumor - Sebaceous gland carcinoma - 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.

What did the clans people all have in common?

theoretically descending from a common ancestor

What is (are) Primary CNS Lymphoma ?

Key Points - Primary central nervous system (CNS) lymphoma is a disease in which malignant (cancer) cells form in the lymph tissue of the brain and/or spinal cord. - Having a weakened immune system may increase the risk of developing primary CNS lymphoma. - Tests that examine the eyes, brain, and spinal cord are used to detect (find) and diagnose primary CNS lymphoma. - Certain factors affect prognosis (chance of recovery) and treatment options. Primary central nervous system (CNS) lymphoma is a disease in which malignant (cancer) cells form in the lymph tissue of the brain and/or spinal cord. Lymphoma is a disease in which malignant (cancer) cells form in the lymph system. The lymph system is part of the immune system and is made up of the lymph, lymph vessels, lymph nodes, spleen, thymus, tonsils, and bone marrow. Lymphocytes (carried in the lymph) travel in and out of the central nervous system (CNS). It is thought that some of these lymphocytes become malignant and cause lymphoma to form in the CNS. Primary CNS lymphoma can start in the brain, spinal cord, or meninges (the layers that form the outer covering of the brain). Because the eye is so close to the brain, primary CNS lymphoma can also start in the eye (called ocular lymphoma).

What are the treatments for Alpha-1 Antitrypsin Deficiency ?

Alpha-1 antitrypsin (AAT) deficiency has no cure, but its related lung diseases have many treatments. Most of these treatments are the same as the ones used for a lung disease called COPD (chronic obstructive pulmonary disease). If you have symptoms related to AAT deficiency, your doctor may recommend: Medicines called inhaled bronchodilators (brong-ko-di-LA-tors) and inhaled steroids. These medicines help open your airways and make breathing easier. They also are used to treat asthma and COPD. Flu and pneumococcal (noo-mo-KOK-al) vaccines to protect you from illnesses that could make your condition worse. Prompt treatment of lung infections also can help protect your lungs. Pulmonary rehabilitation (rehab). Rehab involves treatment by a team of experts at a special clinic. In rehab, you'll learn how to manage your condition and function at your best. Extra oxygen, if needed. A lung transplant. A lung transplant may be an option if you have severe breathing problems. If you have a good chance of surviving the transplant surgery, you may be a candidate for it. Augmentation (og-men-TA-shun) therapy is a treatment used only for people who have AAT-related lung diseases. This therapy involves getting infusions of the AAT protein. The infusions raise the level of the protein in your blood and lungs. Not enough research has been done to show how well this therapy works. However, some research suggests that this therapy may slow the development of AAT deficiency in people who don't have severe disease. People who have AAT deficiency and develop related liver or skin diseases will be referred to doctors who treat those diseases. Future Treatments Researchers are working on possible treatments that will target the faulty AAT genes and replace them with healthy genes. These treatments are in the early stages of development. Researchers also are studying therapies that will help misshapen AAT proteins move from the liver into the bloodstream. They're also studying a type of augmentation therapy in which the AAT protein is inhaled instead of injected into a vein. If you're interested in new treatments, ask your doctor about ongoing clinical trials for AAT deficiency.

What is (are) Potocki-Shaffer syndrome ?

Potocki-Shaffer syndrome is a contiguous gene deletion syndrome associated with deletions in a specific region of chromosome 11 (11p11.2). The characteristic features of Potocki-Shaffer syndrome include openings in the two bones that form the top and sides of the skull (enlarged parietal foramina), multiple benign bone tumors called exostoses, intellectual disability, developmental delay, a distinctive facial appearance, autism and problems with vision and hearing. In some cases, individuals with the syndrome may have a defect in the heart, kidneys, or urinary tract. The features of Potocki-Shaffer syndrome result from the loss of several genes on the short (p) arm of chromosome 11. In particular, the deletion of a gene called ALX4 causes enlarged parietal foramina, while the loss of another gene, EXT2, causes the multiple exostoses. Another condition called WAGR syndrome is caused by a deletion of genetic material in the p arm of chromosome 11, specifically at position 11p13. Occasionally, a deletion is large enough to include the 11p11.2 and 11p13 regions. Individuals with such a deletion have signs and symptoms of both Potocki-Shaffer syndrome and WAGR syndrome. A referral to an early childhood intervention and developmental-behavioral specialist at the time of diagnosis and to have an evaluation for vision and hearing problems, as well as a full skeletal survey at the time of diagnosis or by age 3 years, whichever is later, is recommended.

From a PC, what application can you use to visit the PlayStation Store?

Media Go

What is the overwhelming ethnic majority in Nanjing?

Han nationality

What was Nasser negotiating in 1953?

British withdrawal from the Suez Canal

Which sector was the second largest?

the manufacturing and industrial sector

What format did adult comics begin to be published in?

prestige

What are the symptoms of Intravenous leiomyomatosis ?

What are the signs and symptoms of intravenous leiomyomatosis? IVL most often does not cause detectable signs or symptoms. In fact, they may be found by chance during surgery. When symptoms do arise, they can include abnormal uterine bleeding, lower abdominal tenderness, ad venous thrombosis. When IVL in the uterus is exposed to venous blood that flows to the heart, it usually grows slowly and may reach the heart undetected. When IVL reaches the heart, it can result in pulmonary embolisms, cardiac failure, fainting, and in some cases, sudden death. Most people do not experience symptoms until the IVL reaches the heart.

Obesity can cause resistance to which hormone?

leptin

What are the symptoms of Spondylometaphyseal dysplasia with cone-rod dystrophy ?

What are the signs and symptoms of Spondylometaphyseal dysplasia with cone-rod dystrophy? The Human Phenotype Ontology provides the following list of signs and symptoms for Spondylometaphyseal dysplasia with cone-rod dystrophy. 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 retinal pigmentation 90% Abnormality of color vision 50% Astigmatism 50% Hyperlordosis 50% Hypermetropia 50% Myopia 50% Nystagmus 50% Photophobia 50% Scoliosis 50% Visual impairment 50% Brachydactyly syndrome 7.5% Limitation of joint mobility 7.5% Abnormality of macular pigmentation - Autosomal recessive inheritance - Cone/cone-rod dystrophy - Coxa vara - Cupped ribs - Dental malocclusion - Femoral bowing - Hypoplastic inferior ilia - Joint stiffness - Metaphyseal cupping - Metaphyseal irregularity - Metaphyseal widening - Narrow greater sacrosciatic notches - Ovoid vertebral bodies - Postnatal growth retardation - Progressive visual loss - Recurrent otitis media - Rhizomelia - Severe platyspondyly - Short finger - Short metacarpal - Spondylometaphyseal dysplasia - Tibial bowing - 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.

What type of government did the Puritan settlers establish?

theocratic government

How many people ride the Mexico city subway system each day?

5 million people

What's the name of the comic book character modeled on Schwarzenegger?

the Governator

Who was Claude R Kirk

966 Claude R. Kirk, Jr. was elected as the first post-Reconstruction Republican governor, in an upset election

How much did the student body expand under Howard S. McDonald?

nearly five times

What three contributions to Atlantic City was Edward L. Bader known for?

construction, athletics and aviation

What causes Glucose-6-phosphate dehydrogenase deficiency ?

What causes glucose-6-phosphate dehydrogenase (G6PD) deficiency? Glucose-6-phosphate dehydrogenase (G6PD) deficiency is caused by mutations in the G6PD gene. This gene gives the body instructions to make an enzyme called G6PD, which is involved in processing carbohydrates. This enzyme also protects red blood cells from potentially harmful molecules called reactive oxygen species. Chemical reactions involving G6PD produce compounds that prevent reactive oxygen species from building up to toxic levels within red blood cells. Mutations in the G6PD gene lower the amount of G6PD or alter its structure, lessening its ability to play its protective role. As a result, reactive oxygen species can accumulate and damage red blood cells. Factors such as infections, certain drugs, or eating fava beans can increase the levels of reactive oxygen species, causing red blood cells to be destroyed faster than the body can replace them. This reduction of red blood cells causes the signs and symptoms of hemolytic anemia in people with G6PD deficiency.

How much did the television commercial "1984" cost?

US$1.5 million

How many people are affected by Ochoa syndrome ?

Ochoa syndrome is a rare disorder. About 150 cases have been reported in the medical literature.

Which consul was responsible for the reforms that allowed all citizens access to join the Roman army?

Gaius Marius

It has been known to snow even in what Southern city?

Athens

What is (are) fibrodysplasia ossificans progressiva ?

Fibrodysplasia ossificans progressiva (FOP) is a disorder in which muscle tissue and connective tissue such as tendons and ligaments are gradually replaced by bone (ossified), forming bone outside the skeleton (extra-skeletal or heterotopic bone) that constrains movement. This process generally becomes noticeable in early childhood, starting with the neck and shoulders and proceeding down the body and into the limbs. Extra-skeletal bone formation causes progressive loss of mobility as the joints become affected. Inability to fully open the mouth may cause difficulty in speaking and eating. Over time, people with this disorder may experience malnutrition due to their eating problems. They may also have breathing difficulties as a result of extra bone formation around the rib cage that restricts expansion of the lungs. Any trauma to the muscles of an individual with fibrodysplasia ossificans progressiva, such as a fall or invasive medical procedures, may trigger episodes of muscle swelling and inflammation (myositis) followed by more rapid ossification in the injured area. Flare-ups may also be caused by viral illnesses such as influenza. People with fibrodysplasia ossificans progressiva are generally born with malformed big toes. This abnormality of the big toes is a characteristic feature that helps to distinguish this disorder from other bone and muscle problems. Affected individuals may also have short thumbs and other skeletal abnormalities.

What spectrum of light is red within?

visible light

Which team did Barcelona beat to win the UEFA Super Cup?

Porto

What book was printed by Isaac Newton in 1687?

Philosophiæ Naturalis Principia Mathematica

What group was the main antagonist during the Chinese Civil War?

the Communists

Who apologized to Chopin for adding embellishments to a musical piece he perforemed that was written by Chopin?

Liszt

What are the genetic changes related to pachyonychia congenita ?

Mutations in several genes, including KRT6A, KRT6B, KRT6C, KRT16, and KRT17, can cause pachyonychia congenita. All of these genes provide instructions for making tough, fibrous proteins called keratins. These proteins form networks that provide strength and resilience to the tissues that make up the skin, hair, and nails. When pachyonychia congenita is caused by mutations in the KRT6A gene, it is classified as PC-K6a. Similarly, KRT6B gene mutations cause PC-K6b, KRT6C gene mutations cause PC-K6c, KRT16 gene mutations cause PC-K16, and KRT17 gene mutations cause PC-K17. Mutations in keratin genes alter the structure of keratin proteins, which prevents these proteins from forming strong, stable networks within cells. Without this network, skin cells become fragile and are easily damaged, making the skin less resistant to friction and minor trauma. Even normal activities such as walking can cause skin cells to break down, resulting in the formation of severe, painful blisters and calluses. Defective keratins also disrupt the growth and function of cells in the hair follicles and nails, resulting in the other features of pachyonychia congenita.

What is the name of the university's group service-learning expedition in Asia, Africa or Latin America?

Global Engagement Summer Institute

What do friendly short football tournaments have little of?

prestige

What did the Bells call the house completed in 1889?

The Lodge

What are the treatments for multiple sclerosis ?

These resources address the diagnosis or management of multiple sclerosis: - Gene Review: Gene Review: Multiple Sclerosis Overview - Multiple Sclerosis Association of America: Treatments for MS - Multiple Sclerosis International Federation: About MS--Diagnosis - National Multiple Sclerosis Society: Diagnosing Tools 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

which outsider parties considered unacceptable to work with?

far-right, far-left and regionalism

A team players layout is a what?

formation

What parts of the Bronx have more hills?

western

When did Canada gain independence from the United Kingdom?

1931

What actions of the Soviet Union did The United States oppose?

the Soviet Union fostered communist revolutionary movements,

What deepest part of the ocean was bacteria found?

Mariana Trench

When was the History of the Florentine People published?

1442

Ancestors of which tribes lived in Oklahoma?

Wichita and Caddo

What type of storm is a major threat to Charleston in the summer and early fall?

Hurricanes

What does the superscript m represent?

metastable isotope

What started competition between families for wealth?

Possession of livestock

Is vitelliform macular dystrophy inherited ?

Best disease is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person has one parent with the condition. The inheritance pattern of adult-onset vitelliform macular dystrophy is uncertain. Some studies have suggested that this disorder may be inherited in an autosomal dominant pattern. It is difficult to be sure, however, because many affected people have no history of the disorder in their family, and only a small number of affected families have been reported.

What Puerto Rican leader did the FBI spy on?

Pedro Albizu Campos

What is the function of Tyson Research Center?

a biological field station and research/education center.

How to diagnose Neonatal progeroid syndrome ?

How is neonatal progeroid syndrome diagnosed? A diagnosis of neonatal progeroid syndrome is made based on the presence of characteristic signs and symptoms. Rarely, a diagnosis may be suspected before birth if concerning features are viewed on ultrasound; however, most cases are diagnosed shortly after birth.

On average how many weekly hours did a domestic servant put in?

80

What is (are) Pigment-dispersion syndrome ?

Pigment-dispersion syndrome is an eye disorder that occurs when pigment granules that normally adhere to the back of the iris (the colored part of the eye) flake off into the clear fluid produced by the eye (aqueous humor). These pigment granules may flow towards the drainage canals of the eye, slowly clogging them and raising the pressure within the eye (intraocular pressure or IOP). This rise in eye pressure can cause damage to the optic nerve (the nerve in the back of the eye that carries visual images to the brain). If the optic nerve becomes damaged, pigment-dispersion syndrome becomes pigmentary glaucoma. This happens in about 30% of cases. Pigment-dispersion syndrome commonly presents between the second and fourth decades, which is earlier than other types of glaucoma. While men and women are affected in equal numbers, men develop pigmentary glaucoma up to 3 times more often than women. Myopia (nearsightedness) appears to be an important risk factor in the development of pigment-dispersion syndrome and is present in up to 80% of affected individuals. The condition may be sporadic or follow an autosomal dominant pattern of inheritance with reduced penetrance . At least one gene locus on chromosome 7 has been identified. Pigment-dispersion syndrome can be treated with eye drops or other medications. In some cases, laser surgery may be performed.

The evolution of air defence was in answer to the evolution of what?

aircraft

Who showed that q-glass could be produced from a melt?

NIST researchers

Is Thoracic outlet syndrome inherited ?

Are cervical ribs inherited? Cervical ribs are actually thought to be a common trait. It has been estimated that 1 to 2% of the population have a cervical rib. Cervical ribs can affect one or both sides of the neck, and may cause thoracic outlet syndrome by putting pressure on an artery. Currently, the cause of cervical ribs is not known. In general, both genetic and environmental factors are thought to be involved. There have been animal studies investigating the role of HOX genes in causing extra ribs. Studies have also suggested environmental exposures, such as maternal exposure to foreign chemicals or stress during pregnancy could play a role. Further research in this area is needed. There have been rare case reports of families with multiple members with cervical rib. In these families autosomal dominant inheritance was suspected. Click here to learn more about autosomal dominant inheritance. While we were unable to find recurrence risk data that might help inform your loved ones of their risk for cervical rib and thoracic outlet syndrome, we do suggest that your family members let their healthcare provider know of their family medical history. The Surgeon General's Family History Initiative's Family Health Portrait Tool, may be a helpful resource. You can use this tool to collect, record, and share your family health history information. http://www.hhs.gov/familyhistory/

In what year did Sharif become CM?

2009

What network aired the first season of American Idol?

Fox

What date did the torch relay event take place?

April 28.

What are the complications of Nephrotic Syndrome in Adults ?

The loss of different proteins from the body can lead to a variety of complications in people with nephrotic syndrome. Blood clots can form when proteins that normally prevent them are lost through the urine. Blood clots can block the flow of blood and oxygen through a blood vessel. Loss of immunoglobulinsimmune system proteins that help fight disease and infectionleads to an increased risk of infections. These infections include pneumonia, a lung infection; cellulitis, a skin infection; peritonitis, an abdominal infection; and meningitis, a brain and spine infection. Medications given to treat nephrotic syndrome can also increase the risk of these infections. Other complications of nephrotic syndrome include - hypothyroidisma condition in which the thyroid gland does not produce enough thyroid hormone to meet the bodys needs - anemiaa condition in which red blood cells are fewer or smaller than normal, which means less oxygen is carried to the bodys cells - coronary artery disease, also called coronary heart diseaseheart disease caused by narrowing of the arteries that supply blood to the heart - high blood pressure, also called hypertensiona condition in which blood flows through the blood vessels with a force greater than normal - acute kidney injurysudden and temporary loss of kidney function

The main gods of ancient Greece known as the what?

Dodekatheon

What ideals were Greek and Roman Classical architecture not based on?

religious or empirical ones

In what year did the concept of red and blue states become relatively fixed?

2000

Randomly chosen people from different groups may be more similar to each other than with members of their own what?

cluster

What is Lancashire's long and productive tradition?

music making

What are the treatments for Psoriasis ?

The goals of psoriasis treatment are to change the course of the disease by interfering with the increased production of skin cells, and to remove scales and smooth rough skin.

What are the symptoms of Pachydermoperiostosis ?

What are the signs and symptoms of Pachydermoperiostosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Pachydermoperiostosis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal cortical bone morphology 90% Abnormality of epiphysis morphology 90% Abnormality of the fontanelles or cranial sutures 90% Bone pain 90% Osteomyelitis 90% Seborrheic dermatitis 90% Abnormal hair quantity 50% Abnormality of the fingernails 50% Abnormality of the knees 50% Abnormality of the scalp 50% Abnormality of the tibia 50% Acne 50% Arthralgia 50% Arthritis 50% Clubbing of toes 50% Coarse facial features 50% Joint swelling 50% Limitation of joint mobility 50% Osteoarthritis 50% Osteolysis 50% Ptosis 50% Abnormality of the gastric mucosa 7.5% Anemia 7.5% Aseptic necrosis 7.5% Cerebral palsy 7.5% Deviation of finger 7.5% Gastrointestinal hemorrhage 7.5% Genu varum 7.5% Growth hormone excess 7.5% Gynecomastia 7.5% Hepatomegaly 7.5% Impaired temperature sensation 7.5% Malabsorption 7.5% Neoplasm of the lung 7.5% Neoplasm of the skin 7.5% Palmoplantar keratoderma 7.5% Reduced bone mineral density 7.5% Scoliosis 7.5% Short palm 7.5% Splenomegaly 7.5% Arthropathy - Autosomal dominant inheritance - Autosomal recessive inheritance - Clubbing - Clubbing of fingers - Congenital onset - Cutis gyrata of scalp - Disproportionate tall stature - Eczematoid dermatitis - High palate - Hyperhidrosis - Large fontanelles - Long clavicles - Osteolytic defects of the phalanges of the hand - Osteopenia - Osteoporosis - Palmoplantar hyperkeratosis - Patent ductus arteriosus - Pectus excavatum - Periosteal thickening of long tubular bones - Redundant skin - Thickened calvaria - Thickened skin - Wormian bones - 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.

What is (are) Pressure Sores ?

Pressure sores are areas of damaged skin caused by staying in one position for too long. They commonly form where your bones are close to your skin, such as your ankles, back, elbows, heels and hips. You are at risk if you are bedridden, use a wheelchair, or are unable to change your position. Pressure sores can cause serious infections, some of which are life-threatening. They can be a problem for people in nursing homes. You can prevent the sores by - Keeping skin clean and dry - Changing position every two hours - Using pillows and products that relieve pressure Pressure sores have a variety of treatments. Advanced sores are slow to heal, so early treatment is best.

What branch of the US military was born in Philadelphia?

United States Marine Corps

What are the treatments for cyclic neutropenia ?

These resources address the diagnosis or management of cyclic neutropenia: - Gene Review: Gene Review: ELANE-Related Neutropenia - Genetic Testing Registry: Cyclical neutropenia - Seattle Children's Hospital 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

Where is the Royal Basilica of the Hungarian kings?

Székesfehérvár

What are the treatments for Townes-Brocks syndrome ?

Is there treatment for Townes-Brocks syndrome? Treatment is directed towards the specific symptoms, including immediate surgical intervention for imperforate anus; surgery for severe malformations of the hands; routine management of congenital heart defects; hemodialysis and possibly kidney transplantation for end-stage renal disease (ESRD); and early treatment of hearing loss. In addition, regular monitoring of renal function in individuals with and without renal anomalies is suggested.

In what year was the contract of Sven-Göran Eriksson terminated?

2006

When did English Freemasonry arrive in France?

the 1720s

What is the meaning of federalism?

as a political movement, and of what constitutes a 'federalist', varies with country and historical context

What languages does Hamp say are similar to Armenian?

Greek and Ancient Macedonian

What are the genetic changes related to PRICKLE1-related progressive myoclonus epilepsy with ataxia ?

PRICKLE1-related progressive myoclonus epilepsy with ataxia is caused by mutations in the PRICKLE1 gene. This gene provides instructions for making a protein called prickle homolog 1, whose function is unknown. Studies suggest that it interacts with other proteins that are critical for brain development and function. Mutations in the PRICKLE1 gene alter the structure of prickle homolog 1 and disrupt its ability to interact with other proteins. However, it is unclear how these changes lead to movement problems, seizures, and the other features of PRICKLE1-related progressive myoclonus epilepsy with ataxia.

Where was the 62nd AES Convention held?

Brussels

Between 1939 and 1949, how many military officers and personnel were trained on the Evanston and Chicago campuses?

nearly 50,000

What is (are) Pemphigus ?

Pemphigus is an autoimmune disorder. If you have it, your immune system attacks healthy cells in your skin and mouth, causing blisters and sores. No one knows the cause. Pemphigus does not spread from person to person. It does not appear to be inherited. But some people's genes put them more at risk for pemphigus. Pemphigoid is also an autoimmune skin disease. It leads to deep blisters that do not break easily. Pemphigoid is most common in older adults and may be fatal for older, sick patients. Doctors diagnose pemphigus with a physical exam, a biopsy, and blood tests. The treatment of pemphigus and pemphigoid is the same: one or more medicines to control symptoms. These may include - Steroids, which reduce inflammation - Drugs that suppress the immune system response - Antibiotics to treat associated infections NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases

When was the Holy Viaticum for the dying authorised?

1212

During the Migrations period Germans would encounter what group in the south?

Celts