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Econometric studies have shown that this effect cannot be explained by a variety of alternative factors, including differential trends across areas, changing crop prices, shifts in certain educational and health policies and the effect of malaria eradication. No significant contemporaneous results were found for adults who should have benefited less from the intervention owing to their substantially lower (prior) infection rates. The program nearly eradicated hookworm and would flourish afterward with new funding as the Rockefeller Foundation International Health Division.The RFs hookworm campaign in Mexico showed how science and politics play a role in developing health policies. It brought together government officials, health officials, public health workers, Rockefeller officials and the community. This campaign was launched to eradicate hookworms in Mexico. Although the campaign did not focus on long-term treatments, it did set the terms of the relationship between Mexico and the Rockefeller Foundation. The scientific knowledge behind this campaign helped shape public health policies, improved public health and built a strong relationship between US and Mexico.In the 1920s, hookworm eradication reached the Caribbean and Latin America, where great mortality was reported among people in the West Indies towards the end of the 18th century, as well as through descriptions sent from Brazil and various other tropical and sub-tropical regions. Treatments
Treatment in the early 20th century relied on the use of Epsom salt to reduce protective mucus, followed by thymol to kill the worms. By the 1940s, tetrachloroethylene was the leading method. | "Spinraza access by country". TreatSMA. 18 October 2018. Retrieved 2019-05-28. | 0-1
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Recurrent silent strokes, with or without clinical strokes, often lead to cognitive decline and overt subcortical dementia. A case of CADASIL presenting as schizophreniform organic psychosis has been reported. Pathophysiology
The underlying pathology of CADASIL is progressive hypertrophy of the smooth muscle cells in blood vessels. Autosomal dominant mutations in the Notch 3 gene (on the long arm of chromosome 19) cause an abnormal accumulation of Notch 3 at the cytoplasmic membrane of vascular smooth muscle cells both in cerebral and extracerebral vessels, seen as granular osmiophilic deposits on electron microscopy. Leukoencephalopathy follows. Depending on the nature and position of each mutation, a consensus significant loss of betasheet structure of the Notch3 protein has been predicted using in silico analysis. Diagnosis
MRIs show hypointensities on T1-weighted images and hyperintensities on T2-weighted images, usually multiple confluent white matter lesions of various sizes, are characteristic. These lesions are concentrated around the basal ganglia, peri-ventricular white matter, and the pons, and are similar to those seen in Binswanger disease. These white matter lesions are also seen in asymptomatic individuals with the mutated gene. While MRI is not used to diagnose CADASIL, it can show the progression of white matter changes even decades before onset of symptoms.The definitive test is sequencing the whole Notch 3 gene, which can be done from a sample of blood. However, as this is quite expensive and CADASIL is a systemic arteriopathy, evidence of the mutation can be found in small and medium-size arteries. Therefore, skin biopsies are often used for the diagnosis. | Tagraxofusp, sold under the brand name Elzonris, is an anti-cancer medication for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN). It was approved for use in the United States in 2018, and after a second review, in the EU in January 2021. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication.Tagraxofusp is a fusion protein consisting of interleukin 3 (IL-3) fused to diphtheria toxin. The fusion protein readily kills cultured pDC by binding to their IL-3 receptors to thereby gain entrance to the cells and then blocking these cells protein synthesis (due to its diphtheria toxin portion inhibiting eukaryotic elongation factor 2). Society and culture
Legal status
In July 2020, the European Medicines Agency (EMA) recommended the refusal of the marketing authorization for tagraxofusp. The Agency was concerned that due to the design of the study and the small number of participants, it was not possible to be sure how effective the medicine was in treating blastic plasmacytoid dendritic cell neoplasm. In addition, the medicine could cause capillary leak syndrome (an unpredictable, potentially life-threatening side effect due to increased permeability of small blood vessels), which had led to some fatal outcomes.On 12 November 2020, the Committee for Medicinal Products for Human Use (CHMP) of the EMA adopted a positive opinion following a re-examination procedure, recommending the granting of a marketing authorization for the medicinal product Elzonris, intended for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN). Tagraxofusp was approved for medical use in the European Union in January 2021. | 0-1
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Mutations in the ASS gene reduce the activity of the enzyme, which disrupts the urea cycle and prevents the body from processing nitrogen effectively. Excess nitrogen, in the form of ammonia, and other byproducts of the urea cycle, accumulate in the bloodstream, leading to the characteristic features of type I citrullinemia. Type II
The symptoms of type II citrullinemia (Online Mendelian Inheritance in Man (OMIM): 605814 and Online Mendelian Inheritance in Man (OMIM): 603471) usually appear during adulthood and mainly affect the central nervous system. Characteristic features include confusion, abnormal behaviors (such as aggression, irritability, and hyperactivity), seizures, and coma. Specific investigation like decrease citrulline level , increase ammonium ion . These symptoms can be life-threatening, and are known to be triggered by certain medications, infections, and alcohol intake in people with this type.Type II citrullinemia may also develop in people who had a liver disorder called neonatal cholestasis during infancy. This condition blocks the flow of bile and prevents the body from processing certain nutrients properly. In many cases, the symptoms resolve within a year. Years or even decades later, however, some of these people develop the characteristic features of adult type II citrullinemia.Type II citrullinemia is primarily found in the Japanese population, where it occurs in an estimated one in 100,000 to 230,000 individuals. Type II has also been reported in people from East Asian and Middle Eastern populations. Mutations in the SLC25A13 gene are responsible for type II citrullinemia. | Citrullinemia is an autosomal recessive urea cycle disorder that causes ammonia and other toxic substances to accumulate in the blood.Two forms of citrullinemia have been described, both having different signs and symptoms, and are caused by mutations in different genes. Citrullinemia belongs to a class of genetic diseases called urea cycle disorders. The urea cycle is a sequence of chemical reactions taking place in the liver. These reactions process excess nitrogen, generated when protein is used for energy by the body, to make urea, which is excreted by the kidneys. Diagnosis
Type I
Type I citrullinemia (Online Mendelian Inheritance in Man (OMIM): 215700, also known as classic citrullinemia) usually becomes evident in the first few days of life. Affected infants typically appear normal at birth, but as ammonia builds up in the body, they develop a lack of energy (lethargy), poor feeding, vomiting, seizures, and loss of consciousness. These medical problems can be life-threatening in many cases. A milder form of type I citrullinemia is less common in childhood or adulthood. Some people with gene mutations that cause type I citrullinemia never experience signs and symptoms of the disorder. Investigation for diagnosis of citrullinemia type l elevated citrulline .Type I citrullinemia is the most common form of the disorder, affecting about one in 57,000 births worldwide. Mutations in the ASS gene cause type I citrullinemia. The enzyme made by this gene, argininosuccinate synthetase (EC 6.3.4.5), is responsible for one step of the urea cycle. | 11
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Fungal spores may be viewed directly on hair shafts. This technique identifies a fungal infection in about 40%–70% of the infections, but cannot identify the species of dermatophyte. Culture test: This is the most effective, but also the most time-consuming, way to determine if ringworm is on a pet. In this test, the veterinarian collects hairs from the pet, or else collects fungal spores from the pets hair with a toothbrush, or other instrument, and inoculates fungal media for culture. These cultures can be brushed with transparent tape and then read by the veterinarian using a microscope, or can be sent to a pathological lab. The three common types of fungi which commonly cause pet ringworm can be identified by their characteristic spores. These are different-appearing macroconidia in the two common species of Microspora, and typical microconidia in Trichophyton infections.Identifying the species of fungi involved in pet infections can be helpful in controlling the source of infection. M. canis, despite its name, occurs more commonly in domestic cats, and 98% of cat infections are with this organism. It can also infect dogs and humans, however. T. mentagrophytes has a major reservoir in rodents, but can also infect pet rabbits, dogs, and horses. M. gypseum is a soil organism and is often contracted from gardens and other such places. Besides humans, it may infect rodents, dogs, cats, horses, cattle, and swine. | The lesions are located on the head, neck, tail, and perineum. The typical lesion is a round, whitish crust. Multiple lesions may coalesce in "map-like" appearance. Clinical dermatophytosis is also diagnosed in sheep, dogs, cats, and horses. Causative agents, besides Trichophyton verrucosum, are T. mentagrophytes, T. equinum, Microsporum gypseum, M. canis, and M. nanum.Dermatophytosis may also be present in the holotype of the Cretaceous eutriconodont mammal Spinolestes, suggesting a Mesozoic origin for this disease. Diagnosis
Ringworm in pets may often be asymptomatic, resulting in a carrier condition which infects other pets. In some cases, the disease only appears when the animal develops an immunodeficiency condition. Circular bare patches on the skin suggest the diagnosis, but no lesion is truly specific to the fungus. Similar patches may result from allergies, sarcoptic mange, and other conditions. Three species of fungi cause 95% of dermatophytosis in pets: these are Microsporum canis, Microsporum gypseum, and Trichophyton mentagrophytes. Veterinarians have several tests to identify ringworm infection and identify the fungal species that cause it:
Woods test: This is an ultraviolet light with a magnifying lens. Only 50% of M. canis will show up as an apple-green fluorescence on hair shafts, under the UV light. The other fungi do not show. The fluorescent material is not the fungus itself (which does not fluoresce), but rather an excretory product of the fungus which sticks to hairs. Infected skin does not fluoresce. Microscopic test: The veterinarian takes hairs from around the infected area and places them in a staining solution to view under the microscope. | 11
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The loss of function mutation results in a phenotype that is different from that of a gain of function mutation, and these phenotypes are associated with two different forms of type 4 hemochromatosis. Loss-of-function mutations are more frequent and are associated with type 4A hemochromatosis. These mutations lead to a defect in the localization of ferroportin. Gain-of-function mutations are associated with type 4B and lead to production of ferroportin that resists negative regulation by hepcidin.Unlike other forms of hemochromatosis, which have a recessive pattern of inheritance, type 4 is an autosomal dominant disorder. The dominant inheritance pattern occurs in hemochromatosis type 4 because ferroportin is multimeric. Consequently, mutant ferroportin can associate with wild-type ferroportin in multimers and interfere with the function of normal ferroportin proteins. Pathophysiology
In normal iron regulation, iron is absorbed in the intestine, and ferroportin transports iron from the cells of the intestinal lining into the bloodstream. Iron in the bloodstream is then bound by transferrin, which carries the iron to target cells. Iron is stored in cells and blood serum in a protein called ferritin. Reticuloendothelial macrophages, which can phagocytose red blood cells, are important in the iron recycling process. Ferroportin is upregulated in the reticuloendothelial macrophages after phagocytosis occurs so that iron from the degraded red blood cells can be released into the bloodstream and transported to other types of cells as needed. Hepcidin, a protein synthesized in the liver in response to iron or inflammation, is a regulator of ferroportin expression. | Common noninfectious tenosynovitis are: stenosing tenosynovitis, intersection syndrome, extensor pollicis longus (EPL) tenosynovitis, de Quervains and fourth compartment tenosynovitis. Diagnosis
Diagnosis of tenosynovitis is typically made clinically after a thorough patient history and physical exam. Aspirated fluid can also be cultured to identify the infectious organism. X-rays are typically unremarkable but can help rule out a broken bone or a foreign body
Treatment
The mainstay of treatment for infectious tenosynovitis includes symptom relief, antibiotic therapy, and surgery. Early recognition of the disease with early initiation of antibiotics are important for better range of movement of the affected finger. Minimally invasive procedures into the flexor tendon sheath such as catheter irrigation give better outcomes (74% chance of good outcome) when compared to open surgery (26% chance of good outcome). However, wound irrigation with antibiotics has no clear benefits. Most infectious tenosynovitis cases should be managed with tendon sheath irrigation and drainage, with or without debridement of surrounding necrotic tissue, along with treatment with broad-spectrum antibiotics. In severe cases, amputation may even be necessary to prevent the further spread of infection. Following surgical intervention, antibiotic therapy is continued and adjusted based on the results of the fluid culture. Prognosis
The earlier the condition is identified, the better the chance of getting full range of motion of the finger. However, finger stiffness, Boutonniere deformity, deep space infection, tendon necrosis, adhesions, persistent infection, and need for amputation of the finger can occur. Tendon adhesion and finger stiffness are caused by the violation of the flexor tendon sheath. | 0-1
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The difference between Verrutop and other acid treatments is that it does not damage the surrounding skin. Another product available over-the-counter that can aid in wart removal is silver nitrate in the form of a caustic pencil, which is also available at drug stores. In a placebo-controlled study of 70 patients, silver nitrate given over nine days resulted in clearance of all warts in 43% and improvement in warts in 26% one month after treatment compared to 11% and 14%, respectively, in the placebo group. The instructions must be followed to minimize staining of skin and clothing. Occasionally, pigmented scars may develop. Procedures
Keratolysis, of dead surface skin cells usually using salicylic acid, blistering agents, immune system modifiers ("immunomodulators"), or formaldehyde, often with mechanical paring of the wart with a pumice stone, blade etc. Electrodesiccation
Cryosurgery or cryotherapy, which involves freezing the wart (generally with liquid nitrogen), creating a blister between the wart and epidermal layer after which the wart and the surrounding dead skin fall off. An average of 3 to 4 treatments are required for warts on thin skin. Warts on calloused skin like plantar warts might take dozens or more treatments. Surgical curettage of the wart
Laser treatment – often with a pulse dye laser or carbon dioxide (CO2) laser. Pulse dye lasers (wavelength 582 nm) work by selective absorption by blood cells (specifically hemoglobin). CO2 lasers work by selective absorption by water molecules. Pulse dye lasers are less destructive and more likely to heal without scarring. | Bepotastine (Talion, Bepreve) is a 2nd generation antihistamine. It was approved in Japan for use in the treatment of allergic rhinitis and urticaria/pruritus in July 2000 and January 2002, respectively. It is currently marketed in the United States as an eye drop under the brand-name Bepreve, by ISTA Pharmaceuticals, a subsidiary of Bausch + Lomb. Pharmacology
Bepotastine is available as an ophthalmic solution and oral tablet. It is a direct H1-receptor antagonist that inhibits the release of histamine from mast cells. The ophthalmic formulation has shown minimal systemic absorption, between 1 and 1.5% in healthy adults. Common side effects are eye irritation, headache, unpleasant taste, and nasopharyngitis. The main route of elimination is urinary excretion, 75-90% excreted unchanged. Marketing history
It is marketed in Japan by Tanabe Seiyaku under the brand name Talion. Talion was co-developed by Tanabe Seiyaku and Ube Industries, the latter of which discovered bepotastine. In 2001, Tanabe Seiyaku granted Senju, now owned by Allergan, exclusive worldwide rights, with the exception of certain Asian countries, to develop, manufacture and market bepotastine for ophthalmic use. Senju, in turn, has granted the United States rights for the ophthalmic preparation to ISTA Pharmaceuticals. Sales and patents
In 2011, ISTA pharmaceuticals experienced a 2.4% increase in net revenues from 2010, which was driven by the sales of Bepreve. Their net revenue for 2011 was $160.3 million. ISTA Pharmaceuticals was acquired by Bausch & Lomb in March 2012 for $500 million. Bausch & Lomb hold the patent for bepotastine besilate (https://www.accessdata.fda.gov/scripts/cder/ob/docs/temptn.cfm. | 0-1
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Mepacrine may also be used for refractory cases.Probiotics, when given in combination with the standard treatment, has been shown to assist with clearance of Giardia.During pregnancy, paromomycin is the preferred treatment drug because of its poor intestinal absorption, resulting in less exposure to the fetus. Alternatively, metronidazole can be used after the first trimester as there has been wide experience in its use for trichomonas in pregnancy. Prognosis
In people with a properly functioning immune system, infection may resolve without medication. A small portion, however, develop a chronic infection. People with an impaired immune system are at higher risk of chronic infection. Medication is an effective cure for nearly all people although there is growing drug-resistance.Children with chronic giardiasis are at risk for failure to thrive as well as more long-lasting sequelae such as growth stunting. Up to half of infected people develop a temporary lactose intolerance leading symptoms that may mimic a chronic infection. Some people experience post-infectious irritable bowel syndrome after the infection has cleared. Giardiasis has also been implicated in the development of food allergies. This is thought to be due to its effect on intestinal permeability. Epidemiology
In some developing countries Giardia is present in 30% of the population. In the United States it is estimated that it is present in 3–7% of the population.The number of reported cases in the United States in 2018 was 15,584. All states that classify giardiasis as a notifiable disease had cases of giardiasis. | The degree to which malabsorption occurs in symptomatic and asymptomatic cases is highly varied.The species Giardia intestinalis uses enzymes that break down proteins to attack the villi of the brush border and appears to increase crypt cell proliferation and crypt length of crypt cells existing on the sides of the villi. On an immunological level, activated host T lymphocytes attack endothelial cells that have been injured in order to remove the cell. This occurs after the disruption of proteins that connect brush border endothelial cells to one another. The result is increased intestinal permeability.There appears to be a further increase in programmed enterocyte cell death by Giardia intestinalis, which further damages the intestinal barrier and increases permeability. There is significant upregulation of the programmed cell death cascade by the parasite, and, furthermore, substantial downregulation of the anti-apoptotic protein Bcl-2 and upregulation of the proapoptotic protein Bax. These connections suggest a role of caspase-dependent apoptosis in the pathogenesis of giardiasis.Giardia protects its own growth by reducing the formation of the gas nitric oxide by consuming all local arginine, which is the amino acid necessary to make nitric oxide. Arginine starvation is known to be a cause of programmed cell death, and local removal is a strong apoptotic agent. Host defense
Host defense against Giardia consists of natural barriers, production of nitric oxide, and activation of the innate and adaptive immune systems. Natural barriers
Natural barriers defend against parasite entering the hosts body. Natural barriers consist of mucus layers, bile salt, proteases, and lipases. | 11
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Signs and symptoms
Common symptoms include:
dyspnea (shortness of breath)Signs include:
tachycardia (a heart rate exceeding the normal resting rate)
continuous "machine-like" (also described as "rolling-thunder" and "to-and-fro") heart murmur (usually from aorta to pulmonary artery, with higher flow during systole and lower flow during diastole)
cardiomegaly (enlarged heart, reflecting ventricular dilation and volume overload)
left subclavicular thrill
bounding pulse
widened pulse pressure
increased cardiac output
increased systolic pressure
poor growth
differential cyanosis, i.e. cyanosis of the lower extremities but not of the upper body.People with patent ductus arteriosus typically present in good health, with normal respirations and heart rate. If the PDA is moderate or large, widened pulse pressure and bounding peripheral pulses are frequently present, reflecting increased left ventricular stroke volume and diastolic run-off of blood into the (initially lower-resistance) pulmonary vascular bed. Eisenmenger physiology is pulmonary hypertension due to a left-to-right shunt. Prominent suprasternal and carotid pulsations may be noted secondary to increased left ventricular stroke volume. Risk factors
Known risk factors include:
Preterm birth
Congenital rubella syndrome
Chromosomal abnormalities (e.g., Down syndrome)
Genetic conditions such as Loeys–Dietz syndrome (would also present with other heart defects), Wiedemann–Steiner syndrome, and CHARGE syndrome. Fetal Alcohol Spectrum Disorder
Diagnosis
PDA is usually diagnosed using noninvasive techniques. Echocardiography (in which sound waves are used to capture the motion of the heart) and associated Doppler studies are the primary methods of detecting PDA. | Drugs such as alprostadil, a PGE-1 analog, can be used to keep a PDA open until the primary defect is corrected surgically. Prognosis
If left untreated, the disease may progress from left-to-right shunt (acyanotic heart) to right-to-left shunt (cyanotic heart), called Eisenmengers syndrome. Pulmonary hypertension is a potential long-term outcome, which may require a heart and/or lung transplant. Another complication of PDA is intraventricular hemorrhage. History
Robert Edward Gross, MD performed the first successful ligation of a patent ductus arteriosus on a seven-year-old girl at Childrens Hospital Boston in 1938. Adult
Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis. See also
George Alexander Gibson
References
External links
Patent Ductus Arteriosus Causes from US Department of Health and Human Services
Patent Ductus Arteriosus from Merck
Patent ductus arteriosus information for parents. | 11
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Bitlis has hot, dry summers and cold, very snowy winters. Economy
Historically, Bitlis produced wheat, which the British, in 1920, described as being "particularly excellent." However, poor trade routes in the area during the early 20th century meant that the wheat was mainly produced and used by locals. During this time, the British stated that the people of Bitlis were unable to use all of the wheat they produced, and most was "left to rot in the underground storehouses." Notable individuals
Badh ibn Dustak (died 991), Kurdish tribal leader
Arakel Paghishetsi (1380-1454) Armenian musician, hymnologist
Hovhannes Paghishetsi (1678-1741) 49th Armenian patriarch of Constantinople
Vardan Paghishetsi (?? ?-1705) Armenian chronographer
Vardan Paghishetsi (16th century) Armenian medieval illuminatorThe city was the home of the sixteenth century Kurdish historian, Sherefxan Bedlisi (also: Sharaf al-Din Bitlisi), author of the Sharafnameh, and who was also an appointed prince of the Persian and later Ottoman Empires. Hosam al-Din Ali Bitlisi was a Kurdish Sufi author. He was the father of the noted historian Idris Bitlisi. Ottoman administrator and Kurdish religious scholar and author Idris-i Bitlisi is claimed to have been born in Bitlis also. He was instrumental in conquest, Ottomanization and administration of Ottoman lands from Urfa, Mardin to Egypt. Said Nursi (Nurs, Bitlis, 1877) notable Kurdish Sunni Muslim Theologian. Writer of the Risale-i-Nur collection used as the foundation of movements such as the Nurcu in Turkey and the Gulenist movement founded by Fetullah Gulen. Fuat Sezgin (Bitlis, 1924), a prominent Historian of Science, Orientalist was born in Bitlis. He is the author and editor of numerous publications. | Parametritis (also known as pelvic cellulitis) is an infection of the parametrium (connective tissue adjacent to the uterus). It is considered a form of pelvic inflammatory disease. References
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1p36 deletion syndrome is a congenital genetic disorder characterized by moderate to severe intellectual disability, delayed growth, hypotonia, seizures, limited speech ability, malformations, hearing and vision impairment, and distinct facial features. The symptoms may vary, depending on the exact location of the chromosomal deletion.The condition is caused by a genetic deletion (loss of a segment of DNA) on the outermost band on the short arm (p) of chromosome 1. It is one of the most common deletion syndromes. It is estimated that the syndrome occurs in one in every 5,000 to 10,000 births. Signs and symptoms
There are a number of signs and symptoms characteristic of monosomy 1p36, but no one individual will display all of the possible features. In general, children will exhibit failure to thrive and global delays. Developmental and behavioral
Most young children with 1p36 deletion syndrome have delayed development of speech and motor skills. Speech is severely affected, with many children learning only a few words or having no speech at all. Behavioral problems are also common, and include temper outbursts, banging or throwing objects, striking people, screaming episodes, and self-injurious behavior (wrist biting, head striking/banging). A significant proportion of affected people are on the autism spectrum, and many exhibit stereotypy. Neurologic
Most people with 1p36 deletion syndrome have some structural abnormality of the brain, and approximately half have epilepsy or other seizures. Almost all children exhibit some degree of hypotonia. Common structural brain abnormalities include agenesis of the corpus callosum, cerebral cortical atrophy, gait abnormalities, and ventriculomegaly. | The breakpoints for 1p36 deletion syndrome have been variable and are most commonly found from 1p36.13 to 1p36.33. 40 percent of all breakpoints occur 3 to 5 million base pairs from the telomere. The size of the deletion ranges from approximately 1.5 million base pairs to greater than 10 million.Most deletions in chromosome 1p36 are de novo mutations. 20% of patients with 1p36 deletion syndrome inherit the disease from one parent who carries a balanced or symmetrical translocation. Diagnosis
1p36 deletion syndrome is usually suspected based on the signs and symptoms and confirmed by fluorescence in situ hybridization (FISH). Chromosomal microarray or karyotype analysis may also be used to diagnose 1p36 deletion. Treatment
There is no cure for 1p36 deletion syndrome, and treatment is focused on relieving symptoms of the disease. Of particular importance are appropriate medication for endocrine and neurologic manifestations, such as anti-seizure medications. Feeding difficulties can be managed with specialized assistive devices or with a gastrostomy (feeding) tube. Epidemiology
1p36 deletion syndrome is the most common terminal deletion syndrome in humans. It occurs in between 1 in 5000 and 1 in 10000 live births. And only 100 cases have been reported since 1981. == References == | 11
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Occurrence of morphine in other Papaverales and Papaveraceae, as well as in some species of hops and mulberry trees has not been confirmed. Morphine is produced most predominantly early in the life cycle of the plant. Past the optimum point for extraction, various processes in the plant produce codeine, thebaine, and in some cases negligible amounts of hydromorphone, dihydromorphine, dihydrocodeine, tetrahydro-thebaine, and hydrocodone (these compounds are rather synthesized from thebaine and oripavine). In the brain of mammals, morphine is detectable in trace steady-state concentrations. The human body also produces endorphins, which are chemically related endogenous opioid peptides that function as neuropeptides and have similar effects to morphine. Human biosynthesis
Morphine is an endogenous opioid in humans that can be synthesized by and released from various human cells, including white blood cells. CYP2D6, a cytochrome P450 isoenzyme, catalyzes the biosynthesis of morphine from codeine and dopamine from tyramine along the biosynthetic pathway of morphine in humans. The morphine biosynthetic pathway in humans occurs as follows:L-tyrosine → para-tyramine or L-DOPA → dopamine → (S)-norlaudanosoline → (S)-reticuline → 1,2-dehydroretinulinium → (R)-reticuline → salutaridine → salutaridinol → thebaine → neopinone → codeinone → codeine → morphine (S)-Norlaudanosoline (also known as tetrahydropapaveroline) can also be synthesized from 3,4-dihydroxyphenylacetaldehyde (DOPAL), a metabolite of L-DOPA and dopamine. Urinary concentrations of endogenous codeine and morphine have been found to significantly increase in individuals taking L-DOPA for the treatment of Parkinsons disease. Biosynthesis in the opium poppy
Morphine is biosynthesized in the opium poppy from the tetrahydroisoquinoline reticuline. It is converted into salutaridine, thebaine, and oripavine. | The elimination half-life of morphine is approximately 120 min, though there may be slight differences between men and women. Morphine can be stored in fat, and, thus, can be detectable even after death. Morphine can cross the blood–brain barrier, but, because of poor lipid solubility, protein binding, rapid conjugation with glucuronic acid and ionization, it does not cross easily. Heroin, which is derived from morphine, crosses the blood–brain barrier more easily, making it more potent. Extended-release
There are extended-release formulations of orally administered morphine whose effect last longer, which can be given once per day. Brand names for this formulation of morphine include Avinza, Kadian, MS Contin and Dolcontin. For constant pain, the relieving effect of extended-release morphine given once (for Kadian) or twice (for MS Contin) every 24 hours is roughly the same as multiple administrations of immediate release (or "regular") morphine. Extended-release morphine can be administered together with "rescue doses" of immediate-release morphine as needed in case of breakthrough pain, each generally consisting of 5% to 15% of the 24-hour extended-release dosage. Detection in body fluids
Morphine and its major metabolites, morphine-3-glucuronide and morphine-6-glucuronide, can be detected in blood, plasma, hair, and urine using an immunoassay. Chromatography can be used to test for each of these substances individually. Some testing procedures hydrolyze metabolic products into morphine before the immunoassay, which must be considered when comparing morphine levels in separately published results. Morphine can also be isolated from whole blood samples by solid phase extraction (SPE) and detected using liquid chromatography-mass spectrometry (LC-MS). | 11
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Physical therapy
An evidence-based guideline produced by the American Academy of Orthopedic Surgeons assigned various grades of recommendation to physical therapy and other nonsurgical treatments. One of the primary issues with physiotherapy is that it attempts to reverse (often) years of pathology inside the carpal tunnel. Self-myofascial ligament stretching can be an easy, do-at-home, treatment to help alleviate symptoms. Self-myofascial stretching involves stretching the carpal ligament for 30 seconds, 6 times a day for about 6 weeks. Many patients report improvements in symptoms such as pain, function, and nerve conduction. Practitioners caution that any physiotherapy such as myofascial release may take weeks of persistent application to effectively manage carpal tunnel syndrome.Again, some claim that pro-active ways to reduce stress on the wrists, which alleviates wrist pain and strain, involve adopting a more ergonomic work and life environment. For example, some have claimed that switching from a QWERTY computer keyboard layout to a more optimised ergonomic layout such as Dvorak was commonly cited as beneficial in early CTS studies; however, some meta-analyses of these studies claim that the evidence that they present is limited.Tendon and nerve gliding exercises appear to be useful in carpal tunnel syndrome.A randomized control trial published in 2017 sought to examine the efficacy of manual therapy techniques for the treatment of carpal tunnel syndrome. The study included a total of 140 individuals diagnosed with carpal tunnel syndrome and the patients were divided into two groups. One group received treatment that consisted of manual therapy. | As expected, visual field testing in cone dystrophy usually reveals a central scotoma. In cases with the typical bulls-eye appearance, there is often relative central sparing.Because of the wide spectrum of fundus changes and the difficulty in making the diagnosis in the early stages, electroretinography (ERG) remains the best test for making the diagnosis. Abnormal cone function on the ERG is indicated by a reduced single-flash and flicker response when the test is carried out in a well-lit room (photopic ERG). The relative sparing of rod function in cone dystrophy is evidenced by a normal scotopic ERG, i.e. when the test is carried out in the dark. In more severe or longer standing cases, the dystrophy involves a greater proportion of rods with resultant subnormal scotopic records. Since cone dystrophy is hereditary and can be asymptomatic early on in the disease process, ERG is an invaluable tool in the early diagnosis of patients with positive family histories. Cone dystrophy in general usually occurs sporadically. Hereditary forms are usually autosomal dominant, and instances of autosomal recessive and X-linked inheritance also occur. In the differential diagnosis, other macular dystrophies as well as the hereditary optic atrophies must be considered. Fluorescent angiography, ERG, and color vision tests are important tools to help facilitate diagnosis in early stages. Treatment
Though there is no treatment for cone dystrophy, certain supplements may help in delaying the progression of the disease. | 0-1
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The most recent prevalence report out of England in 2006 is 10.9 per 100,000. References
== External links == | After splinting the teeth to eliminate the mobility, the cause of the mobility (in other words, the loss of clinical attachment and bone) must be managed; this is achieved through surgical periodontal procedures such as soft tissue and bone grafts, as well as restoration of edentulous areas. As with primary occlusal trauma, treatment may include either a removable prosthesis or implant-supported crown or bridge. References
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A description of the miserable living standards of the mill workers in England in 1844 was given by Fredrick Engels in The Condition of the Working Class in England in 1844. In the preface to the 1892 edition, Engels noted that the extreme poverty he had written about in 1844 had largely disappeared. David Ames Wells also noted that living conditions in England had improved near the end of the 19th century and that unemployment was low. The scarcity and the high price of labor in the US in the 19th century was well documented by contemporary accounts, as in the following:
"The laboring classes are comparatively few in number, but this is counterbalanced by, and indeed, may be one of the causes of the eagerness by which they call in the use of machinery in almost every department of industry. Wherever it can be applied as a substitute for manual labor, it is universally and willingly resorted to.... It is this condition of the labor market, and this eager resort to machinery wherever it can be applied, to which, under the guidance of superior education and intelligence, the remarkable prosperity of the United States is due." Scarcity of labor was a factor in the economics of slavery in the United States. As new territories were opened and federal land sales were conducted, land had to be cleared and new homesteads established. Hundreds of thousands of immigrants annually came to the US and found jobs digging canals and building railroads. | Thyroid hormone resistance (also resistance to thyroid hormone (RTH), and sometimes Refetoff syndrome) describes a rare syndrome in which the thyroid hormone levels are elevated but the thyroid stimulating hormone (TSH) level is not suppressed, or not completely suppressed as would be expected. The first report of the condition appeared in 1967. Essentially this is decreased end organ responsiveness to thyroid hormones. A new term "impaired sensitivity to thyroid hormone" has been suggested in March 2014 by Refetoff et al. Presentation
The syndrome can present with variable symptoms, even between members of the same family harboring the same mutation. Typically most or all tissues are resistant to thyroid hormone, so despite raised measures of serum thyroid hormone the individual may appear euthyroid (have no symptoms of over- or underactivity of the thyroid gland). The most common symptoms are goiter and tachycardia. It has also been linked to some cases of attention deficit hyperactivity disorder (ADHD), although the majority of people with that diagnosis have no thyroid problems. An association with depression has been proposed. Causes
Normal thyroid hormone function requires normal thyroid hormone transport across cell membrane, appropriate deiodination, thyroid hormone nuclear receptor, thyroid hormone response elements, co-activators, co-repressors, and normal histone acetylation. | 0-1
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Death can occur either due to myocardial infarction secondary to blood clot formation in a coronary artery aneurysm or to rupture of a large coronary artery aneurysm. Death is most common two to 12 weeks after the onset of illness.Many risk factors predicting coronary artery aneurysms have been identified, including persistent fever after IVIG therapy, low hemoglobin concentrations, low albumin concentrations, high white-blood-cell count, high band count, high CRP concentrations, male sex, and age less than one year. Coronary artery lesions resulting from Kawasaki disease change dynamically with time. Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms. Narrowing of the coronary artery, which occurs as a result of the healing process of the vessel wall, often leads to significant obstruction of the blood vessel and the heart not receiving enough blood and oxygen. This can eventually lead to heart muscle tissue death, i.e., myocardial infarction (MI).MI caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the main cause of death from Kawasaki disease. The highest risk of MI occurs in the first year after the onset of the disease. MI in children presents with different symptoms from those in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children. | Vitamin deficiency is the condition of a long-term lack of a vitamin. When caused by not enough vitamin intake it is classified as a primary deficiency, whereas when due to an underlying disorder such as malabsorption it is called a secondary deficiency. An underlying disorder may be metabolic – as in a genetic defect for converting tryptophan to niacin – or from lifestyle choices that increase vitamin needs, such as smoking or drinking alcohol. Government guidelines on vitamin deficiencies advise certain intakes for healthy people, with specific values for women, men, babies, the elderly, and during pregnancy or breastfeeding. Many countries have mandated vitamin food fortification programs to prevent commonly occurring vitamin deficiencies.Conversely, hypervitaminosis refers to symptoms caused by vitamin intakes in excess of needs, especially for fat-soluble vitamins that can accumulate in body tissues.The history of the discovery of vitamin deficiencies progressed over centuries from observations that certain conditions – for example, scurvy – could be prevented or treated with certain foods having high content of a necessary vitamin, to the identification and description of specific molecules essential for life and health. During the 20th century, several scientists were awarded the Nobel Prize in Physiology or Medicine or the Nobel Prize in Chemistry for their roles in the discovery of vitamins. Defining deficiency
A number of regions have published guidelines defining vitamin deficiencies and advising specific intakes for healthy people, with different recommendations for women, men, infants, the elderly, and during pregnancy and breast feeding including Japan, the European Union, the United States, and Canada. | 0-1
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Clinical significance
Anything arising from the intervertebral disc may be termed discogenic in particular when referring to associated pain as discogenic pain. Herniation
A spinal disc herniation, commonly referred to as a slipped disc, can happen when unbalanced mechanical pressures substantially deform the anulus fibrosus, allowing part of the nucleus to obtrude. These events can occur during peak physical performance, during traumas, or as a result of chronic deterioration (typically accompanied with poor posture), and has been associated with a Propionbacterium acnes infection. Both the deformed anulus and the gel-like material of the nucleus pulposus can be forced laterally or posteriorly, distorting local muscle function and putting pressure on the nearby nerve. This can give symptoms typical of nerve root entrapment, which can vary between paresthesia, numbness, chronic and/or acute pain, either locally or along the dermatome served by the entrapped nerve, loss of muscle tone and decreased homeostatic performance. The disc is not physically slipped; it bulges, usually in just one direction. Another kind of herniation, of the nucleus pulposus, can happen as a result of the formation of Schmorls nodes on the intervertebral disc. This is referred to as vertical disc herniation. Degeneration
Before age 40, approximately 25% of people show evidence of disc degeneration at one or more levels. Beyond age 40, more than 60% of people show evidence of disc degeneration at one or more levels on magnetic resonance imaging (MRI). These degenerative changes are a normal part of the ageing process and do not correlate to pain. | Similar symptoms were noted at the siege of Acre by Crusaders. Coincidental to, or dependent on, the appearance of a gonorrhea epidemic, several changes occurred in European medieval society. Cities hired public health doctors to treat affected patients without right of refusal. Pope Boniface rescinded the requirement that physicians complete studies for the lower orders of the Catholic priesthood.Medieval public health physicians in the employ of their cities were required to treat prostitutes infected with the "burning", as well as lepers and other epidemic patients. After Pope Boniface completely secularized the practice of medicine, physicians were more willing to treat a sexually transmitted disease. Research
A vaccine for gonorrhea has been developed that is effective in mice. It will not be available for human use until further studies have demonstrated that it is both safe and effective in the human population. Development of a vaccine has been complicated by the ongoing evolution of resistant strains and antigenic variation (the ability of N. gonorrhoeae to disguise itself with different surface markers to evade the immune system).As N. gonorrhoeae is closely related to N. meningitidis and they have 80–90% homology in their genetic sequences some cross-protection by meningococcal vaccines is plausible. A study published in 2017 showed that MeNZB group B meningococcal vaccine provided a partial protection against gonorrhea. The vaccine efficiency was calculated to be 31%. References
External links
Gonorrhea at Curlie
"Gonorrhea – CDC Fact Sheet" | 0-1
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Pyromania is generally harder to treat in adults, often due to lack of cooperation by the patient. Treatment usually consists of more medication to prevent stress or emotional outbursts, in addition to long-term psychotherapy. In adults, however, the recovery rate is generally poor, and if an adult does recover, it usually takes a longer period of time. History
Pyromania was thought in the 1800s to be a concept involved with moral insanity and moral treatment, but had not been categorized under impulse control disorders. Pyromania is one of the four recognized types of arson, alongside burning for profit, to cover up an act of crime and for revenge. Pyromania is the second most common type of arson. Common synonyms for pyromaniacs in colloquial English include firebug (US) and fire raiser (UK), but these also refer to arsonists. Pyromania is a rare disorder with an incidence of less than one percent in most studies; also, pyromaniacs hold a very small proportion of psychiatric hospital admissions. Pyromania can occur in children as young as age three, though such cases are rare. Only a small percentage of children and teenagers arrested for arson are child pyromaniacs. A preponderance of the individuals are male; one source states that ninety percent of those diagnosed with pyromania are male. Based on a survey of 9,282 Americans using the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, impulse-control problems such as gambling, pyromania and compulsive shopping collectively affect 9% of the population. | Pyromania moved from the DSM-4 chapter "Impulse-Control Disorders Not Otherwise Specified," to the chapter "Disruptive, impulse-control, and conduct disorders" in DSM-5. Signs and symptoms
According to DSM-5, there are six signs of pyromania. Pyromania is mainly categorized by the purposeful setting of fire, tension or arousal before a fire is set, interest in or attraction to fire, and pleasure or relief after setting a fire. These fires not set for personal gain, are not meant to express anger or conceal illegal activity, are not in support of sociopolitical ideologies, are not in response to delusions, and are not signs of intellectual disability. For diagnosis, the setting of fire should not be better explained by a conduct disorder, manic episode, or a personality disorder (antisocial personality disorder). ICD-11 also adds substance abuse to this list. According to ICD-11, signs of fire setting may occur "in response to feelings of depressed mood, anxiety, boredom, loneliness, or other negative affective states." Those with pyromania exhibit problems in social environments and learning disabilities. Women pyromaniacs "often report histories of exposure to trauma, including sexual abuse, and self-harm." Episodic fire setting may become more intense and violent over time, becoming potentially chronic if untreated. Causes
Most studied cases of pyromania occur in children and teenagers. There is a range of causes, but an understanding of the different motives and actions of fire setters can provide a platform for prevention. Common causes of pyromania can be broken down into two main groups: individual and environmental. | 11
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This includes:
15-20% of patients with neurofibromatosis 1 (NF1)
25% of patients with mutations in one of the RAS family of oncogenes (only in their leukemia cells)
Another 35% of patients with a mutation in a gene called PTPN11 (again, only in their leukemia cells). Diagnosis
The following criteria are required in order to diagnose JMML:All 4 of the following:
No Philadelphia chromosome or BCR/ABL fusion gene. Peripheral blood monocytosis >1 x 109/L. Less than 20% blasts (including promonocytes) in the blood and bone marrow (blast count is less than 2% on average)
SplenomegalyAt least one of:
Mutation in RAS or PTPN11
Diagnosis of neurofibromatosis 1
Chromosome 7 monosomyOr two or more of the following criteria:
Hemoglobin F increased for age. Immature granulocytes and nucleated red cells in the peripheral blood. White blood cell count >10 x 109/L. Clonal chromosomal abnormality (e.g., monosomy 7). Granulocyte-macrophage colony-stimulating factor (GM-CSF) hypersensitivity of myeloid progenitors in vitro.These criteria are identified through blood tests and bone marrow tests. The differential diagnosis list includes infectious diseases like Epstein–Barr virus, cytomegalovirus, human herpesvirus 6, histoplasma, mycobacteria, and toxoplasma, which can produce similar symptoms. | Hydrocodone/aspirin (INNs) is an oral combination drug formulation of the opioid analgesic hydrocodone and the nonsteroidal anti-inflammatory drug (NSAID) aspirin that is used in the treatment of chronic and acute pain. It is sold under brand names including Alor 5/500, Azdone, Damason-P, Lortab ASA, and Panasal 5/500. Adverse effects
See also
Hydrocodone/paracetamol
Hydrocodone/ibuprofen
Oxycodone/aspirin
== References == | 0-1
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Metabolic abnormalities
Insufficient selenium, vitamin D or sunlight exposure, or vitamin B6. Gastrointestinal causes: the distal digestive tract secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohns disease, ulcerative colitis, Whipples disease and celiac sprue can all cause hypomagnesemia. Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant. Other
Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines. Malabsorption
Acute pancreatitis
Fluoride poisoning
Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications. Pathophysiology
Magnesium is a co-factor in over 300 functions in the body regulating many kinds of biochemical reactions. It is involved in protein synthesis, muscle and nerve functioning, bone development, energy production, the maintenance of normal heart rhythm, and the regulation of glucose and blood pressure, among other important roles. Low magnesium intake over time can increase the risk of illnesses, including high blood pressure and heart disease, diabetes mellitus type 2, osteoporosis, and migraines.There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. Magnesium has several effects:
Potassium
Potassium channel efflux is inhibited by magnesium. Thus hypomagnesemia results in an increased excretion of potassium in kidney, resulting in a hypokalaemia. | Replacement by mouth is appropriate for people with mild symptoms, while intravenous replacement is recommended for people with severe effects.Numerous oral magnesium preparations are available. In two trials of magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was less bioavailable than magnesium citrate, chloride, lactate or aspartate. Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate forms.Intravenous magnesium sulfate (MgSO4) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma. Food
Food sources of magnesium include leafy green vegetables, beans, nuts, and seeds. Epidemiology
The condition is relatively common among people in hospital. History
Magnesium deficiency in humans was first described in the medical literature in 1934. Plants
Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants dry matter and is necessary for normal plant growth. Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency, as does aluminium toxicity.Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll. Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal chlorosis, or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. | 11
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Significant complications of the operation include bleeding, heart problems (heart attack, arrhythmias), stroke, infections (often pneumonia) and injury to the kidneys. Uses
Coronary artery bypass surgery aims to prevent death from coronary artery disease and improve quality of life by relieving angina. Indications for surgery are based on studies examining the pros and cons of CABG in various subgroups of patients (depending on the anatomy of the lesions or how well heart is functioning) with CAD and comparing it with other therapeutic strategies, most importantly percutaneous coronary intervention (PCI). Coronary artery disease
Coronary artery disease is caused when coronary arteries of the heart accumulate atheromatic plaques, causing stenosis in one or more arteries and place myocardium at risk of myocardial infarction. CAD can occurs in any of the major vessels of coronary circulation, which are Left Main Stem, Left Ascending Artery, Circumflex artery, and Right Coronary Artery and their branches. CAD can be asymptomatic for some time- causing no trouble, can produce chest pain when patient is exercising, or can produce angina even at rest. The former is called stable angina, while the latter unstable angina. Worse, it can manifest as a myocardial infarction, in (which the blood flow to a part of myocardium is blocked. If the blood flow is not restored within a few hours, either spontaneously or by medical intervention, the specific part of the myocardium becomes necrotic (dies) and is replaced by a scar. | It has also been noted that the timing of the operation, plays a role in survival, it is preferable to delay the surgery if possible (6 hours in cases of nontransmural MI, 3 days in cases of transmural MI)CABG of coronary lesions is also indicated in mechanical complications of an infarction (ventricular septal defect, papillary muscle rupture or myocardial rupture) should be addressed There are no absolute contraindications of CABG but severe disease of other organs such as liver or brain, limited life expectancy, fragility should be taken into consideration when planning the treatment path of a patient. Other cardiac surgery
CABG is also performed when a patient is to undergo another cardiac surgical procedure, most commonly for valve disease, and at angiography a significant lesion of the coronaries is found. CABG can be employed in other situations other than atheromatic disease of native heart arteries, like for the dissection of coronary arteries (where a rupture of the coronary layers creates a pseudo-lumen and diminishes blood delivery to the heart) caused e.g. by pregnancy, tissue diseases as Enhler-Danlos, Marfan Syndrome, cocaine abuse or Percutaneous Coronary Intervention). A coronary aneurysm is another reason for CABG, for a thrombus might develop within the vessel, and possibly travel further. CABG vs PCI
CABG and percutaneous coronary intervention (PCI) are the two modalities the medical community has to revascularize stenotic lesions of the cardiac arteries. | 11
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Zinc was regularly imported to Europe from the Orient in the 17th and early 18th centuries, but was at times very expensive. Isolation
Metallic zinc was isolated in India by 1300 AD, much earlier than in the West. Before it was isolated in Europe, it was imported from India in about 1600 CE. Postlewayts Universal Dictionary, a contemporary source giving technological information in Europe, did not mention zinc before 1751 but the element was studied before then.Flemish metallurgist and alchemist P. M. de Respour reported that he had extracted metallic zinc from zinc oxide in 1668. By the start of the 18th century, Étienne François Geoffroy described how zinc oxide condenses as yellow crystals on bars of iron placed above zinc ore that is being smelted. In Britain, John Lane is said to have carried out experiments to smelt zinc, probably at Landore, prior to his bankruptcy in 1726.In 1738 in Great Britain, William Champion patented a process to extract zinc from calamine in a vertical retort-style smelter. His technique resembled that used at Zawar zinc mines in Rajasthan, but no evidence suggests he visited the Orient. Champions process was used through 1851.German chemist Andreas Marggraf normally gets credit for discovering pure metallic zinc, even though Swedish chemist Anton von Swab had distilled zinc from calamine four years previously. In his 1746 experiment, Marggraf heated a mixture of calamine and charcoal in a closed vessel without copper to obtain a metal. This procedure became commercially practical by 1752. | Contraindications
Calcipotriol/betamethasone dipropionate is contraindicated in patients with hypersensitivity to either glucocorticoids or vitamin D or disorders in calcium metabolism. This drug is also contraindicated for patients with erythrodermic, exfoliative, or pustular psoriasis. Adverse effects
A number of clinical studies have been conducted to investigate possible adverse events of this fixed combination corticosteroid and vitamin D analog. Safety and tolerability of calcipotriol/betamethasone dipropionate (Cal/BD) ointment has been assessed in a combined total of 2448 patients, exposed to treatment for 4 or 8 weeks (median weekly dose of 24.5 g). The most common adverse events for patients receiving Cal/BD were pruritus (3.1%), headache (2.8%), and nasopharyngitis (2.3%). Lesional/perilesional adverse events, defined as an adverse event located ≤2 cm from the lesional border, were reported by 8.7% of patients treated with Cal/BD ointment. Median time to onset of lesional/perilesional adverse events was 7 days.Adverse events during treatment with the foam formulation have been evaluated in three 4-week randomized, multicenter, prospective vehicle- and/or active-controlled clinical trials of subjects with plaque psoriasis. The median weekly dose was 24.8 g. Application site irritation, application site pruritus (itching), folliculitis (inflammation of hair follicles), skin hypopigmentation (loss of skin color), hypercalcemia (increased blood calcium levels), urticaria, and exacerbation of psoriasis were reported in <1% of subjects. Local long-term adverse effects of continuous steroid exposure may include skin atrophy, stretch marks, telangiectasia (spider veins), dryness, local infections, and miliaria ("prickly heat"). | 0-1
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Congenital toxoplasmosis may lead to hydrocephalus, seizures, lymphadenopathy, hepatosplenomegaly, rash, and fever. However, retinochoroiditis is the most common manifestation, occurring in 3/4 of cases. In congenital toxoplasmosis, the disease is bilateral in 65–85% of cases and involves the macula in 58%. Chronic or recurrent maternal infection during pregnancy is not thought to confer a risk of congenital toxoplasmosis because maternal immunity protects against fetal transmission. In contrast, pregnant women without serologic evidence of prior exposure to Toxoplasma should take sanitary precautions such as having someone else clean and maintain litter boxes and avoiding undercooked meats. Diagnosis
In most instances, the diagnosis of toxoplasmic retinochoroiditis is made clinically on the basis of the appearance of the characteristic lesion on eye examination. Seropositivity (positive blood test result) for Toxoplasma is very common and therefore not useful in diagnosis; however, a negative result i.e. absence of antibodies is often used to rule out disease. Others believe that serology is useful to confirm active toxoplasmic retinochoroiditis, not only by showing positivity but by also showing a significant elevation of titers: The mean IgG values were 147.7 ± 25.9 IU/ml for patients with active disease versus 18.3 ± 20.8 IU/ml for normal individuals.Antibodies against Toxoplasma:
IgG : appear within the first 2 weeks after infection, typically remain detectable for life, albeit at low levels;and may cross the placenta. IgM : rise early during the acute phase of the infection, typically remain detectable for less than 1 year, and do not cross the placenta. | It has been suggested that in the absence of exposure to cold and damp, COVID-19 should be considered as a possible cause of chilblains.In a study at the dermatology department of Saint-Louis Hospital in Paris, researchers found that most of their study participants carried high levels of autoantibodies, proteins generated by the immune system that inadvertently attack the bodys own tissues. Compared with healthy individuals, the participants showed high activity of proteins called type 1 interferons, which switch on pathogen-fighting genes in immune cells. See also
Equestrian perniosis
Erythrocyanosis crurum
Raynauds disease
References
External links
DermAtlas 1683395337
Cold stress, National Institute for Occupational Safety and Health | 0-1
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Verapamil, sold under various trade names, is a calcium channel blocker medication used for the treatment of high blood pressure, angina (chest pain from not enough blood flow to the heart), and supraventricular tachycardia. It may also be used for the prevention of migraines and cluster headaches. It is given by mouth or by injection into a vein.Common side effects include headache, low blood pressure, nausea, and constipation. Other side effects include allergic reactions and muscle pains. It is not recommended in people with a slow heart rate or heart failure. It is believed to cause problems for the fetus if used during pregnancy. It is in the non–dihydropyridine calcium channel blocker family of medications.Verapamil was approved for medical use in the United States in 1981. It is on the World Health Organizations List of Essential Medicines. Verapamil is available as a generic medication. Long acting formulations exist. In 2019, it was the 141st most commonly prescribed medication in the United States, with more than 4 million prescriptions. Medical uses
Verapamil is used for controlling ventricular rate in supraventricular tachycardia and migraine headache prevention. It is a class-IV antiarrhythmic and more effective than digoxin in controlling ventricular rate. Verapamil is not listed as a first line agent by the guidelines provided by JAMA in JNC-8. However, it may be used to treat hypertension if patient has co-morbid atrial fibrillation or other types of arrhythmia.Verapamil is also used intra-arterially to treat cerebral vasospasm. Verapamil is used to treat the condition cluster headache. | A vanishing twin, also known as twin resorption, is a fetus in a multigestation pregnancy that dies in utero and is then partially or completely reabsorbed. In some instances, the dead twin is compressed into a flattened, parchment-like state known as fetus papyraceus.Vanishing twins occur in up to one of every eight multifetus pregnancies and may not even be known in most cases. "High resorption rates, which cannot be explained on the basis of the expected abortion rate, suggest intense fetal competition for space, nutrition, or other factors during early gestation, with frequent loss or resorption of the other twin(s). "In pregnancies achieved by in vitro fertilization, "it frequently happens that more than one amniotic sac can be seen in early pregnancy, whereas a few weeks later there is only one to be seen and the other has vanished." See also
Chimera (genetics)
Mosaicism
Parasitic twin
References
Further reading
External links
Vanishing twin at eMedicine.com
50 articles about vanishing twin phenomenon in PubMed | 0-1
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Peer support groups have tentative evidence of benefit. There is also some evidence indicating benefits in community-based overdose education and naloxone distribution programs. Buprenorphine and methadone can help decrease drug cravings. Combining pharmacologic treatments with behavioral therapy, such as support or recovery groups, can increase likelihood of overcoming addiction and reduce the risk of an opioid overdose. Individuals diagnosed with opioid dependence should be prescribed naloxone to prevent overdose and should be directed to one of treatment options available, such as needle exchange programs and treatment centers. A naloxone prescription is also recommended when risk factors for opioid overdose are present such as history of overdose, substance use disorder, or higher doses of opioids. Brief motivational interviewing can also be performed and has been shown to improve peoples motivation to change their behavior. Despite these opportunities, the dissemination of prevention interventions in the US has been hampered by the lack of coordination and sluggish federal government response.In the United States, 49 states and the District of Columbia have expanded naloxone access at a pharmacy level via standing order, protocol order, naloxone-specific collaborative practice agreement, or pharmacist prescriptive authority. Treatments
In people who have overdosed on opioids, basic life support and naloxone are recommended as soon as possible. Naloxone is effective at reversing the cause, rather than just the symptoms, of an opioid overdose. Compared to adults, children often need larger doses of naloxone per kilogram of body weight.Programs to provide drug users and their caregivers with naloxone are recommended. | Among those who refuse to go to hospital following reversal, the risks of a poor outcome in the short term appear to be low. Other efforts to prevent deaths from overdose include increasing access to naloxone and treatment for opioid dependence.Drug use contributes to 500,000 deaths worldwide, with opioid overdose resulting in approximately 115,000 of these deaths in 2018. This is up from 18,000 deaths in 1990. In 2018, approximately 269 million people had engaged in drug usage at least once, 58 million of which used opioids. Drug use disorders have affected around 35.6 million people worldwide in 2018. The WHO estimates that 70% of deaths due to drug use are in relation to opioids, with 30% being due to overdose. It is believed that the opioid epidemic has partly been caused due to assurances that prescription opioids were safe, by the pharmaceutical industry in the 1990s. This led to unwarranted trust and a subsequent heavy reliance on opioids. Though there are treatment interventions which can effectively reduce the risk of overdose in people with opioid dependence, less than 10% of affected individuals receive it. Signs and symptoms
Opiate overdose symptoms and signs can be referred to as the "opioid overdose triad": decreased level of consciousness, pinpoint pupils and respiratory depression. Other symptoms include seizures and muscle spasms. Sometimes an opiate overdose can lead to such a decreased level of consciousness such that the person will not wake up. | 11
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In addition, corticosteroid side effects can include weight gain, weakening of the surrounding tissues, and even osteoporosis, with regular use. Cellular based therapy may have a role in future injection based treatments, though there is no current research proving the effectiveness of these therapies. Surgical treatment
If medicine or physical therapy is ineffective or abnormal structures are found, surgery may be recommended. Surgical treatment is rarely necessary unless intra-articular pathology is present. In patients with persistently painful iliopsoas symptoms surgical release of the contracted iliopsoas tendon has been used since 1984. Iliopsoas and iliotibial band lengthening can be done arthroscopically. Postop, these patients will usually undergo extensive physical therapy; regaining full strength may take up to 9–12 months. Rehabilitation
Patients may require intermittent NSAID therapy or simple analgesics as they progress in activities. If persistent pain caused by bursitis continues, a corticosteroid injection may be beneficial. Physical therapy, or athletic training therapy, and rehabilitation
Both active and passive stretching exercises that include hip and knee extension should be the focus of the program. Stretching the hip into extension and limiting excessive knee flexion avoids placing the rectus femoris in a position of passive insufficiency, thereby maximizing the stretch to the iliopsoas tendon. Strengthening exercises for the hip flexors may also be an appropriate component of the program. A non-steroidal anti-inflammatory drug regimen as well as activity modification or activity progression (or both) may be used. Once symptoms have decreased a maintenance program of stretching and strengthening can be initiated. | Popping during external snapping hip (lateral-extra articular), occurs when the thickened posterior aspect of the ITB or the anterior gluteus maximus rubs over the greater trochanter as the hip is extended. Internal snapping hip (medial-extra articular) is usually described by the patient as a snapping or locking of the hip with an audible snap and occurs when the iliopsoas tendon snaps over underlying bony prominences. Almost half of patients with internal snapping hip also have inter-articular pathology. Intra-articular
The causes of intra-articular snapping hip syndrome seem to be broadly similar to those of the extra-articular type, but often include an underlying mechanical problem in the lower extremity. The pain associated with the internal variety tends to be more intense and therefore more debilitating than with the external variety. Intra-articular snapping hip syndrome is often indicative of injury such as a torn acetabular labrum, ligamentum teres tears, loose bodies, articular cartilage damage, or synovial chondromatosis (cartilage formations in the synovial membrane of the joint). Diagnostic
Ultrasound during hip motion may visualize tendon subluxation and any accompanying bursitis when evaluating for iliopsoas involvement in medial extra-articular cases. MRI can sometimes identify intra-articular causes of snapping hip syndrome. Treatment
This condition is usually curable with appropriate treatment, or sometimes it heals spontaneously. If it is painless, there is little cause for concern. | 11
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Early diagnosis is important since these people can be placed on antibiotics to ward off infections before they occur. Small groups of CGD patients may also be affected by McLeod syndrome because of the proximity of the two genes on the same X-chromosome. Atypical infections
People with CGD are sometimes infected with organisms that usually do not cause disease in people with normal immune systems. Among the most common organisms that cause disease in CGD patients are:
Bacteria (particularly those that are catalase-positive)Staphylococcus aureus. Serratia marcescens. Listeria species. E. coli. Klebsiella species. Pseudomonas cepacia, a.k.a. Burkholderia cepacia. Nocardia. Fungi
Aspergillus species. Aspergillus has a propensity to cause infection in people with CGD and of the Aspergillus species, Aspergillus fumigatus seems to be most common in CGD. Candida species.Patients with CGD can usually resist infections of catalase-negative bacteria but are susceptible to catalase-positive bacteria. Catalase is an enzyme that catalyzes the breakdown of hydrogen peroxide in many organisms. In infections caused by organisms that lack catalase (catalase-negative), the host with CGD is successfully able to "borrow" hydrogen peroxide being made by the organism and use it to fight off the infection. In infections by organisms that have catalase (catalase-positive), this "borrowing mechanism" is unsuccessful because the enzyme catalase first breaks down any hydrogen peroxide that would be borrowed from the organism. Therefore in the CGD patient, hydrogen peroxide cannot be used to make oxygen radicals to fight infection, leaving the patient vulnerable to infection by catalase-positive bacteria. | Dialysis disequilibrium syndrome (DDS) is the collection of neurological signs and symptoms, attributed to cerebral edema, during or following shortly after intermittent hemodialysis or CRRT.Classically, DDS arises in individuals starting hemodialysis due to end-stage chronic kidney disease and is associated, in particular, with "aggressive" (high solute removal) dialysis. However, it may also arise in fast onset, i.e. acute kidney failure in certain conditions. Symptoms and signs
Diagnosis of mild DDS is often complicated by other dialysis complications such as malignant hypertension, uremia, encephalopathy, subdural hemorrhage, hyper- and hypoglycaemia, or electrolyte imbalances. Presentation of moderate and severe DDS requires immediate identification and treatment as the condition can result in severe neurological issues and death.1. Headache
2. Nausea
3. Dizziness
4. Confusion
5. Visual disturbance
6. Tremor
7. Seizures
8. Coma
Causes
The cause of DDS is currently not well understood. There are two theories to explain it; the first theory postulates that urea transport from the brain cells is slowed in chronic kidney disease, leading to a large urea concentration gradient, which results in reverse osmosis. The second theory postulates that organic compounds are increased in uremia to protect the brain and result in injury by, like in the first theory, reverse osmosis. More recent studies on rats noted that brain concentrations of organic osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus attributed to osmotic effects related to a high urea gradient between plasma and brain. | 0-1
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Unlikely: No evidence of CNS damage. Structural
Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts. Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most people, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.Evidence of a CNS structural impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional impairments are highly likely.During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain. During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth. | Mechanism of action
For its use in cancer, its mechanism of action is unknown, but on a cellular level, laboratory tests show that tretinoin forces APL cells to differentiate and stops them from proliferating; in people there is evidence that it forces the primary cancerous promyelocytes to differentiate into their final form, allowing normal cells to take over the bone marrow. Recent study shows that ATRA inhibits and degrades active PIN1.For its use in acne, tretinoin (along with other retinoids) are vitamin A derivatives that act by binding to two nuclear receptor families within keratinocytes: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). These events contribute to the normalization of follicular keratinization and decreased cohesiveness of keratinocytes, resulting in reduced follicular occlusion and microcomedone formation. The retinoid-receptor complex competes for coactivator proteins of AP-1, a key transcription factor involved in inflammation. Retinoids also down-regulate expression of toll-like receptor (TLR)-2, which has been implicated in the inflammatory response in acne. Moreover, tretinoin and retinoids may enhance the penetration of other topical acne medications.The combination of the 10% benzoyl peroxide and light results in more than 50% degradation of tretinoin in about 2 hours and 95% in 24 hours. This lack of stability in the presence of light and oxidizing agents has led to the development of novel formulations of the drug. When microencapsulated tretinoin is exposed to benzoyl peroxide and light only 1% degradation takes place in about 4 hours and only 13% after 24 hours. Biosynthesis
Tretinoin is synthesized from beta-carotene. | 0-1
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Hypoventilation (also known as respiratory depression) occurs when ventilation is inadequate (hypo meaning "below") to perform needed respiratory gas exchange. By definition it causes an increased concentration of carbon dioxide (hypercapnia) and respiratory acidosis. Hypoventilation is not synonymous with respiratory arrest, in which breathing ceases entirely and death occurs within minutes due to hypoxia and leads rapidly into complete anoxia, although both are medical emergencies. Hypoventilation can be considered a precursor to hypoxia and its lethality is attributed to hypoxia with carbon dioxide toxicity. Causes
Hypoventilation may be caused by:
A medical condition such as stroke affecting the brainstem
Voluntary breath-holding or underbreathing, for example, hypoventilation training or the Buteyko method. Medication or drugs, typically when taken in accidental or intentional overdose. Opioids and benzodiazepines in particular are known to cause respiratory depression. Examples of opioids include pharmaceuticals such as oxycodone and hydromorphone and examples of benzodiazepines include lorazepam and alprazolam. Hypocapnia, which stimulates hypoventilation
Obesity; see Obesity hypoventilation syndrome
Chronic mountain sickness, a mechanism to conserve energy. Medications
As a side effect of medicines or recreational drugs, hypoventilation may become potentially life-threatening. Many different central nervous system (CNS) depressant drugs such as ethanol, benzodiazepines, barbiturates, GHB, sedatives, and opioids produce respiratory depression when taken in large or excessive doses, or mixed with other depressants. Strong opiates (namely fentanyl, heroin, and morphine), barbiturates, and certain benzodiazepines (such as alprazolam) are known for depressing respiration. In an overdose, an individual may cease breathing entirely (go into respiratory arrest) which is rapidly fatal without treatment. | Potassium citrate (also known as tripotassium citrate) is a potassium salt of citric acid with the molecular formula K3C6H5O7. It is a white, hygroscopic crystalline powder. It is odorless with a saline taste. It contains 38.28% potassium by mass. In the monohydrate form, it is highly hygroscopic and deliquescent. As a food additive, potassium citrate is used to regulate acidity, and is known as E number E332. Medicinally, it may be used to control kidney stones derived from uric acid or cystine. Synthesis
Potassium citrate can be synthesized by the neutralization of citric acid which is achieved by the addition of potassium bicarbonate, potassium carbonate or potassium hydroxide to it. The solution can then be filtered and the solvent can be evaporated till granulation. Uses
Potassium citrate is rapidly absorbed when given by mouth, and is excreted in the urine. Since it is an alkaline salt, it is effective in reducing the pain and frequency of urination when these are caused by highly acidic urine. It is used for this purpose in dogs and cats, but is chiefly employed as a non-irritating diuretic. Potassium citrate is an effective way to treat/manage gout and arrhythmia, if the patient is hypokalemic. It is widely used to treat urinary calculi (kidney stones), and is often used by patients with cystinuria. | 0-1
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Acids, alcohols and gases are usually detected in these tests when bacteria are grown in selective liquid or solid media.The isolation of enzymes from infected tissue can also provide the basis of a biochemical diagnosis of an infectious disease. For example, humans can make neither RNA replicases nor reverse transcriptase, and the presence of these enzymes are characteristic., of specific types of viral infections. The ability of the viral protein hemagglutinin to bind red blood cells together into a detectable matrix may also be characterized as a biochemical test for viral infection, although strictly speaking hemagglutinin is not an enzyme and has no metabolic function.Serological methods are highly sensitive, specific and often extremely rapid tests used to identify microorganisms. These tests are based upon the ability of an antibody to bind specifically to an antigen. The antigen, usually a protein or carbohydrate made by an infectious agent, is bound by the antibody. This binding then sets off a chain of events that can be visibly obvious in various ways, dependent upon the test. For example, "Strep throat" is often diagnosed within minutes, and is based on the appearance of antigens made by the causative agent, S. pyogenes, that is retrieved from a patients throat with a cotton swab. Serological tests, if available, are usually the preferred route of identification, however the tests are costly to develop and the reagents used in the test often require refrigeration. | Ospemifene (brand names Osphena and Senshio produced by Shionogi) is an oral medication indicated for the treatment of dyspareunia – pain during sexual intercourse – encountered by some women, more often in those who are post-menopausal. Ospemifene is a selective estrogen receptor modulator (SERM) acting similarly to an estrogen on the vaginal epithelium, building vaginal wall thickness which in turn reduces the pain associated with dyspareunia. Dyspareunia is most commonly caused by "vulvar and vaginal atrophy. "The medication was approved by the FDA in February 2013 and by the European Commission for marketing in the EU in January 2015. Medical uses
Ospemifene is used to treat dyspareunia. In the US it is indicated for the treatment of moderate to severe dyspareunia, a symptom of vulvar and vaginal atrophy (VVA), due to menopause. In the EU it is indicated for the treatment of moderate to severe symptomatic VVA in post-menopausal women who are not candidates for local vaginal oestrogen therapy. Contraindications
Women with "undiagnosed abnormal genital bleeding; known or suspected estrogen-dependent neoplasia; active or history of deep vein thrombosis; pulmonary embolism; arterial thromboembolic disease; and are or may become pregnant" or "with known or suspected breast cancer or those with extreme hepatic impairment" should not take ospemifene. This is not a full list of contraindications. Side effects
Side effects associated with ospemifene include vaginal discharge, hot flashes, and diaphoresis. More serious adverse effects are similar to those of estrogens and estrogen receptor modulators. | 0-1
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Although they are illegal for personal use in many jurisdictions, Tasers have been marketed to the general public. Other electroshock weapons such as stun guns, stun batons ("cattle prods"), and electroshock belts administer an electric shock by direct contact. Electric fences are barriers that use electric shocks to deter animals or people from crossing a boundary. The voltage of the shock may have effects ranging from uncomfortable, to painful or even lethal. Most electric fencing is used today for agricultural fencing and other forms of animal control purposes, though it is frequently used to enhance security of restricted areas, and there exist places where lethal voltages are used. Torture
Electric shocks are used as a method of torture, since the received voltage and current can be controlled with precision and used to cause pain and fear without always visibly harming the victims body. Electrical torture has been used in war and by repressive regimes since the 1930s. The United States Army is known to have used electrical torture during World War II. During the Algerian War electrical torture was used by French military forces. Amnesty International published a statement that Russian military forces in Chechnya tortured local women with electric shocks by attaching wires onto their breasts.The parrilla (Spanish for grill) is a method of torture whereby the victim is strapped to a metal frame and subjected to electric shock. It has been used in a number of contexts in South America. | Acute eosinophilic leukemia (AEL) is a rare subtype of acute myeloid leukemia with 50 to 80 percent of eosinophilic cells in the blood and marrow. It can arise de novo or may develop in patients having the chronic form of a hypereosinophilic syndrome. Patients with acute eosinophilic leukemia have a propensity for developing bronchospasm as well as symptoms of the acute coronary syndrome and/or heart failure due to eosinophilic myocarditis and eosinophil-based endomyocardial fibrosis. Hepatomegaly and splenomegaly are more common than in other variants of AML. Diagnosis
A specific histochemical reaction, cyanide-resistant peroxidase, permits identification of leukemic blast cells with eosinophilic differentiation and diagnosis of acute eosinoblastic leukemia in some cases of AML with few identifiable eosinophils in blood or marrow. Treatment and prognosis
when there is eosinophilia with increased immature precursors along with blasts; one need to identify lineage of blasts. As per old FAB classification most of the time blast lineage will be myeloid and may fall in M4EO of FAB classification. This entity need treatment like acute myeloid leukemia. However more rarely Eosinophilic leukemia may have underlying lymphoid blasts with t(5;14) (IL3;IGH). with this gene fusion and eosinophilic cytokine comes under control of immunoglobulin heavy chain (IgH) locus. This entity need treatment as ALL. Overall prognosis is not dependent on eosinophilia but underlying lineage and genetic abnormalities. References
== External links == | 0-1
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The trend, starting in archaeology and spreading to anthropology reached its height in the late half of the 20th century. However, some newer research in archaeology and bioarchaeology may provide evidence that violence within and among groups is not a recent phenomenon. According to the book "The Bioarchaeology of Violence" violence is a behavior that is found throughout human history.Lawrence H. Keeley at the University of Illinois writes in War Before Civilization that 87% of tribal societies were at war more than once per year, and that 65% of them were fighting continuously. He writes that the attrition rate of numerous close-quarter clashes, which characterize endemic warfare, produces casualty rates of up to 60%, compared to 1% of the combatants as is typical in modern warfare. "Primitive Warfare" of these small groups or tribes was driven by the basic need for sustenance and violent competition.Fry explores Keeleys argument in depth and counters that such sources erroneously focus on the ethnography of hunters and gatherers in the present, whose culture and values have been infiltrated externally by modern civilization, rather than the actual archaeological record spanning some two million years of human existence. Fry determines that all present ethnographically studied tribal societies, "by the very fact of having been described and published by anthropologists, have been irrevocably impacted by history and modern colonial nation states" and that "many have been affected by state societies for at least 5000 years. "The relatively peaceful period since World War II is known as the Long Peace. | Cambridge University Press; 2010 [cited October 17, 2011]. ISBN 978-0521731690. Nazaretyan, A.P. (2007). Violence and Non-Violence at Different Stages of World History: A view from the hypothesis of techno-humanitarian balance. In: History & Mathematics. Moscow: KomKniga/URSS. pp. 127–48. ISBN 978-5484010011. External links
Violence prevention at World Health Organization
Violence prevention at Centers for Disease Control and Prevention
Violence prevention at American Psychological Association
World Report on Violence Against Children Archived 2016-01-11 at the Wayback Machine at Secretary-General of the United Nations
Hidden in Plain Sight: A statistical analysis of violence against children Archived 2017-11-15 at the Wayback Machine at UNICEF
Heat and Violence | 11
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Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment, in general, has positive outcomes. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the persons severity, needs and support of family and friends. Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting. : 97 Evidence does not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke. Moderate quality evidence does indicate naming performance improvements for nouns but not verbs using tDCSSpecific treatment techniques include the following:
Copy and recall therapy (CART) – repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming
Visual communication therapy (VIC) – the use of index cards with symbols to represent various components of speech
Visual action therapy (VAT) – typically treats individuals with global aphasia to train the use of hand gestures for specific items
Functional communication treatment (FCT) – focuses on improving activities specific to functional tasks, social interaction, and self-expression
Promoting aphasics communicative effectiveness (PACE) – a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy, the focus is on pragmatic communication rather than treatment itself. | Evolocumab (trade name Repatha) is a monoclonal antibody medication designed for the treatment of hyperlipidemia. Evolocumab is a fully human monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation and its inhibition thereby enhances the livers ability to remove LDL-C, or "bad" cholesterol, from the blood. Mechanism
Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface. In the absence of PCSK9, there are more LDL receptors on the surface of liver cells to remove LDL-C from the blood. History
Amgen submitted a biologics license application (BLA) for evolocumab to the FDA in August 2014. The FDA approved evolocumab injection on 27 August 2015, for some patients who are unable to get their LDL cholesterol under control with current treatment options. The European Commission approved it in July 2015. Evolocumab received approval from Health Canada on September 10, 2015. Amgen reported approval by Health Canada in a press release on September 15, 2015.Regeneron Pharmaceuticals and Amgen had each filed for patent protection on their monoclonal antibodies against PCSK9 and the companies ended up in patent litigation in the U.S. In March 2016 a district court found that Regenerons drug alirocumab infringed Amgens patents; Amgen then requested an injunction barring Regeneron and Sanofi from marketing alirocumab, which was granted in January 2017. The judge gave Regeneron and Sanofi 30 days to appeal before the injunction went into effect.Results of the FOURIER trial were published in March 2017. | 0-1
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As a result, gonadotropin and sex hormone levels are only partially suppressed when elagolix is taken once per day. In addition, the degree of suppression can be dose-dependently adjusted as needed, for instance with higher-dose twice-daily administration to achieve greater hormonal suppression. Because of its short duration in the body, the effects of elagolix are rapidly reversible upon discontinuation. In addition, due to its partial and incomplete suppression of estradiol levels, the side effects of elagolix, such as hot flashes and decreased BMD, are lower than with first-generation GnRH modulators. In clinical trials, elagolix produced dose-dependent decreases in gonadotropin, estradiol, and progesterone levels in women. Median levels of estradiol were partially suppressed to 42 pg/mL (follicular phase levels) with 150 mg once daily and were fully or near-fully suppressed to 12 pg/mL (postmenopausal levels) with 200 mg twice daily. In a 21-day study in premenopausal women, the effects of elagolix on FSH levels were found to be maximal at a dosage of 300 mg twice per day or above, whereas its effects on LH and estradiol levels were maximal at a dosage of 200 mg twice per day or above. Levels of progesterone were maintained at anovulatory levels (<2 ng/mL) across the 21-day study period at dosages of elagolix of 100 mg twice per day and above. A dosage of elagolix of 400 mg twice per day appears to produce no greater suppression in gonadotropin or estradiol levels than a dosage of 300 mg twice per day in premenopausal women. | Suppression of gonadotropin and sex hormone levels with elagolix occurs rapidly, within hours, and upon discontinuation of elagolix, gonadotropin and sex hormone levels remain suppressed for at least 12 hours, but show recovery within 24 to 48 hours. As a consequence of its suppression of gonadotropin and sex hormone levels, elagolix inhibits ovulation in women. Over the course of three menstrual cycles, the ovulation rate with elagolix was 50% at 150 mg once daily and 32% at 200 mg twice daily. Because ovulation is triggered by a surge in estradiol levels at mid-cycle, estrogen exposure during elagolix therapy might be greater around this time in some women.In addition to its activity as a GnRH antagonist, elagolix is a weak to moderate inducer of CYP3A and an inhibitor of P-glycoprotein. As a result, elagolix may affect the metabolism and/or transport of other medications, and this may contribute to drug interactions with elagolix. Pharmacokinetics
Elagolix is taken by the oral route of administration, in contrast to other GnRH modulators. The oral bioavailability of elagolix in humans is not described in the Food and Drug Administration (FDA) label for the medication, but in animal research elagolix showed a low oral bioavailability of 5.8% in rats and 11% in monkeys. Following administration, elagolix is rapidly absorbed, with peak concentrations occurring after 0.5 to 1.5 hours. The drug accumulation ratio of elagolix at 150 mg once per day is 0.98 and at 200 mg twice per day is 0.89, indicating that it is not accumulated in the body with continuous administration. | 11
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The pilot study was conducted only on men. Diagnosis
Nocturia diagnosis requires knowing the patients nocturnal urine volume (NUV). The ICS defines NUV as “the total volume of urine passed between the time the individual goes to bed with the intention of sleeping and the time of waking with the intention of rising.” Thus, NUV excludes the last void before going to bed, but includes the first morning void if the urge to urinate woke the patient. The amount of sleep a patient gets, and the amount they intend to get, are also considered in a diagnosis.As with any patient, a detailed history of the problem is required to establish what is normal for that patient. The principal diagnostic tool for nocturia is the voiding bladder diary. Based on information recorded in the diary, a physician can classify the patient as having global polyuria, nocturnal polyuria, or bladder storage problems. A voiding bladder diary should record:
number of voids
timing of voids
volume voided
volume and time of fluid intakePatients should include the first morning void in the NUV. However, the first morning void is not included with the number of nightly voids. Causes
Polyuria
Polyuria is excessive or an abnormally large production or passage of urine. Increased production and passage of urine may also be termed diuresis. Polyuria is usually viewed as a symptom or sign of another disorder (not a disease by itself), but it can be classed as a disorder, at least when its underlying causes are not clear. | Piperacillin/tazobactam, sold under the brand name Zosyn among others, is a combination medication containing the antibiotic piperacillin and the β-lactamase inhibitor tazobactam. The combination has activity against many Gram-positive and Gram-negative bacteria including Pseudomonas aeruginosa. It is used to treat pelvic inflammatory disease, intra-abdominal infection, pneumonia, cellulitis, and sepsis. It is given by injection into a vein.Common adverse effects include headache, trouble sleeping, rash, nausea, constipation, and diarrhea. Serious adverse effects include Clostridium difficile infection and allergic reactions including anaphylaxis. Those who are allergic to other β-lactam are more likely to be allergic to piperacillin/tazobactam. Use in pregnancy or breastfeeding appears to generally be safe. It usually results in bacterial death through blocking their ability to make a cell wall.Piperacillin/tazobactam was approved for medical use in the United States in 1993. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. Medical uses
Its main uses are in intensive care medicine (pneumonia, peritonitis), some diabetes-related foot infections, and empirical therapy in febrile neutropenia (e.g., after chemotherapy). The drug is administered intravenously every 6 or 8 hr, typically over 3–30 min. It may also be administered by continuous infusion over four hours. Prolonged infusions are thought to maximize the time that serum concentrations are above the minimum inhibitory concentration (MIC) of the bacteria implicated in infection. | 0-1
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Obstetrics
Fentanyl is sometimes given intrathecally as part of spinal anesthesia or epidurally for epidural anaesthesia and analgesia. Because of fentanyls high lipid solubility, its effects are more localized than morphine, and some clinicians prefer to use morphine to get a wider spread of analgesia. It is widely used in obstetrical anesthesia because of its short time to action peak (about 5 min. ), the rapid termination of its effect after a single dose, and the occurrence of relative cardiovascular stability. In obstetrics, the dose must be closely regulated in order to prevent large amounts of transfer from mother to fetus. At high doses, the drug may act on the fetus to cause postnatal respiratory distress. For this reason, shorter acting agents such as alfentanyl or remifentanil may be more suitable in the context of inducing general anaesthesia. Pain management
The bioavailability of intranasal fentanyl is about 70–90%, but with some imprecision due to clotted nostrils, pharyngeal swallow, and incorrect administration. For both emergency and palliative use, intranasal fentanyl is available in doses of 50, 100, and 200 µg. In emergency medicine, safe administration of intranasal fentanyl with a low rate of side effects and a promising pain-reducing effect was demonstrated in a prospective observational study in about 900 out-of-hospital patients.In children, intranasal fentanyl is useful for the treatment of moderate and severe pain and is well tolerated. Chronic pain
It is also used in the management of chronic pain including cancer pain. Often, transdermal patches are used. | Occupational contamination
In France, the last two victims of variant Creutzfeldt-Jakob disease, who died in 2019 and 2021, were research technicians at the National Research Institute for Agriculture, Food and the Environment (INRAE). Emilie Jaumain, who died in 2019, at the age of 33, had been the victim of a work accident in 2010, during which she had pricked herself with a tool contaminated with infected brain. The efficacy of this route of contamination has been unambiguously demonstrated in primates. Pierrette C., who died in 2021, had been victim of the same type of work accident. After her diagnosis, a moratorium was initiated in all French laboratories on research activities on infectious prions. In March 2022, INRAE recognized the occupational cause of these two deaths. This raises serious questions about the safety of personnel in these laboratories. Indeed, inspections have noted serious failures in the protection of agents in the face of this deadly risk, and the long incubation period of this disease leads to fears of new cases in the future, hence great concern. Other causes
Eating other types of brains such as those from squirrels is not recommended as one person contracted vCJD from eating the brain of a squirrel. Mechanism
Despite the consumption of contaminated beef in the UK being high, vCJD has infected a small number of people. One explanation for this can be found in the genetics of people with the disease. | 0-1
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It is thought to do so by causing oxidative damage to liver cells, resulting in oxidized species of uroporphyrinogen that inhibit the activity of hepatic UROD. It is also felt to increase the uptake of iron in liver cells, leading to further oxidation of uroporphyrinogen by the release of activated oxygen species. Additionally, exposure to chlorinated cyclic hydrocarbons can lead to a deficiency in the activity of uroporphyrinogen decarboxylase, causing the buildup of excess uroporphyrinogen. Additionally, alcohol has been shown to increase the activity of the delta-aminolevulinic acid synthetase (ALA synthetase), the rate-limiting enzymatic step in heme synthesis in the mitochondria, in rats. Therefore, alcohol consumption may increase the production of uroporphyrinogen, exacerbating symptoms in individuals with porphyria cutanea tarda. Diagnosis
While the most common symptom of PCT is the appearance of skin lesions and blistering, their appearance is not conclusive. Laboratory testing commonly reveals high levels of uroporphyrinogen in the urine, clinically referred to as uroporphyrinogenuria. Additionally, testing for common risk factors such as hepatitis C and hemochromatosis is strongly suggested, as their high prevalence in patients with PCT may require additional treatment. If clinical appearance of PCT is present, but laboratories are negative, the diagnosis of pseudoporphyria should be seriously considered. Classification
Some sources divide PCT into two types: sporadic and familial. Other sources include a third type, but this is less common. | "Azilsartan medoxomil". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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As of 2020, early evidence indicates that a third cause of FSHD2 is mutation in both copies of the LRIF1 gene, which encodes the protein ligand-dependent nuclear receptor-interacting factor 1 (LRIF1). LRIF1 is known to interact with the SMCHD1 protein. As of 2019, there are presumably additional mutations at other unidentified genetic locations that can cause FSHD2.Mutation of a single allele of SMCHD1 or DNMT3B can cause disease. Mutation of both copies LRIF1 has been tentatively shown to cause disease in a single person as of 2020. As in FSHD1, a 4qA allele must be present for disease to result. However, unlike the D4Z4 array, the genes implicated in FSHD2 are not in proximity with the 4qA allele, and so they are inherited independently from the 4qA allele, resulting in a digenic inheritance pattern. For example, one parent without FSHD can pass on an SMCHD1 mutation, and the other parent, also without FSHD, can pass on a 4qA allele, bearing a child with FSHD2. Two ends of a disease spectrum
Initially, FSHD1 and FSHD2 were described as two separate genetic causes of the same disease. However, they can also be viewed not as distinct causes, but rather as risk factors. | Camila is the Portuguese and Spanish form of the given name Camilla and may refer to:
Film and television
Camila (TV series), a Mexican telenovela from 1998
Camila (film), a 1984 Argentine film by María Luisa Bemberg
Music
Camila (band), Mexican band
Camila (album), Camila Cabellos debut studio album released 2018
"Camila, Camila", a song by Brazilian rock band Nenhum de Nós
Other uses
Camila (Pontus), a town of ancient Pontus, in Anatolia
Camila Martins Pereira (born 1994), Brazilian footballer known by the mononym Camila
Camila, brand name of a progestogen-only pill containing norethisterone (norethindrone)
See also
Camilla (disambiguation)
Camilla (born 1947), Queen consort of Charles III of the United Kingdom | 0-1
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Negative symptoms include alogia (lack of speech), blunted affect (reduced intensity of outward emotional expression), avolition (lack of motivation), and anhedonia (inability to experience pleasure). Negative symptoms can be more lasting and more debilitating than positive symptoms of psychosis. Mood symptoms are of mania, hypomania, mixed episode, or depression, and tend to be episodic rather than continuous. A mixed episode represents a combination of symptoms of mania and depression at the same time. Symptoms of mania include elevated or irritable mood, grandiosity (inflated self-esteem), agitation, risk-taking behavior, decreased need for sleep, poor concentration, rapid speech, and racing thoughts. Symptoms of depression include low mood, apathy, changes in appetite or weight, disturbances in sleep, changes in motor activity, fatigue, guilt or feelings of worthlessness, and suicidal thinking. DSM-5 states that if a patient only experiences psychotic symptoms during a mood episode, their diagnosis is Mood Disorder with Psychotic Features and not Schizophrenia or Schizoaffective Disorder. If the patient experiences psychotic symptoms without mood symptoms for longer than a two-week period, their diagnosis is either Schizophrenia or Schizoaffective Disorder. If mood disorder episodes are present for the majority and residual course of the illness and up until the diagnosis, the patient can be diagnosed with Schizoaffective Disorder. Causes
A combination of genetic and environmental factors are believed to play a role in the development of schizoaffective disorder. | Pathology
Adrenal tumors are often not biopsied prior to surgery, so diagnosis is confirmed on examination of the surgical specimen by a pathologist. Grossly, ACCs are often large, with a tan-yellow cut surface, and areas of hemorrhage and necrosis. On microscopic examination, the tumor usually displays sheets of atypical cells with some resemblance to the cells of the normal adrenal cortex. The presence of invasion and mitotic activity help differentiate small cancers from adrenocortical adenomas. Several relatively rare variants of ACC include:
Oncocytic adrenal cortical carcinoma
Myxoid adrenal cortical carcinoma
Carcinosarcoma
Adenosquamous adrenocortical carcinoma
Clear cell adrenal cortical carcinoma
Differential diagnosis
Differential diagnosis includes:
Adrenocortical adenoma
Renal cell carcinoma
Pheochromocytoma
Hepatocellular carcinomaAdrenocortical carcinomas are most commonly distinguished from adrenocortical adenomas (their benign counterparts) by the Weiss system, as follows:
Total score indicates:
0-2: Adrenocortical adenoma
3: Undetermined
4-9: Adrenocortical carcinoma
Treatment
The only curative treatment is complete surgical excision of the tumor, which can be performed even in the case of invasion into large blood vessels, such as the renal vein or inferior vena cava. The 5-year survival rate after successful surgery is 50–60%, but unfortunately, many patients are not surgical candidates. Radiation therapy and radiofrequency ablation may be used for palliation in patients who are not surgical candidates. Minimally invasive surgical techniques remain controversial due to the absence of long-term data, with a particular concern for rates of recurrence and peritoneal carcinomatosis.Chemotherapy regimens typically include the drug mitotane, an inhibitor of steroid synthesis, which is toxic to cells of the adrenal cortex, as well as standard cytotoxic drugs. | 0-1
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Pediatricians, allergists and ophthalmologists are among the first to see or identify a child as having tics, although the majority of tics are first identified by the childs parents. Coughing, blinking, and tics that mimic unrelated conditions such as asthma are commonly misdiagnosed. In the UK, there is an average delay of three years between symptom onset and diagnosis. Differential diagnosis
Tics that may appear to mimic those of Tourettes—but are associated with disorders other than Tourettes—are known as tourettism and are ruled out in the differential diagnosis for Tourette syndrome. The abnormal movements associated with choreas, dystonias, myoclonus, and dyskinesias are distinct from the tics of Tourettes in that they are more rhythmic, not suppressible, and not preceded by an unwanted urge. Developmental and autism spectrum disorders may manifest tics, other stereotyped movements, and stereotypic movement disorder. The stereotyped movements associated with autism typically have an earlier age of onset; are more symmetrical, rhythmical and bilateral; and involve the extremities (for example, flapping the hands).If another condition might better explain the tics, tests may be done; for example, if there is diagnostic confusion between tics and seizure activity, an EEG may be ordered. An MRI can rule out brain abnormalities, but such brain imaging studies are not usually warranted. Measuring thyroid-stimulating hormone blood levels can rule out hypothyroidism, which can be a cause of tics. If there is a family history of liver disease, serum copper and ceruloplasmin levels can rule out Wilsons disease. The typical age of onset of TS is before adolescence. | Relation to other psychiatric disorders
Depersonalization exists as both a primary and secondary phenomenon, although making a clinical distinction appears easy, it is not absolute. The most common comorbid disorders are depression and anxiety, although cases of depersonalization disorder without symptoms of either do exist. Comorbid obsessive and compulsive behaviours may exist as attempts to deal with depersonalization, such as checking whether symptoms have changed and avoiding behavioural and cognitive factors that exacerbate symptoms. Many people with personality disorders such as schizoid personality disorder, schizotypal personality disorder, and borderline personality disorder will have high chances of having depersonalization disorder. History
The word depersonalization itself was first used by Henri Frédéric Amiel in The Journal Intime. The 8 July 1880 entry reads:
I find myself regarding existence as though from beyond the tomb, from another world; all is strange to me; I am, as it were, outside my own body and individuality; I am depersonalized, detached, cut adrift. Is this madness? Depersonalization was first used as a clinical term by Ludovic Douglas in 1898 to refer to "a state in which there is the feeling or sensation that thoughts and acts elude the self and become strange; there is an alienation of personality – in other words a depersonalization". This description refers to personalization as a psychical synthesis of attribution of states to the self.Early theories of the cause of depersonalization focused on sensory impairment. | 0-1
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A phase I clinical research study to test the safety and efficacy of a combination chemotherapy regimen consisting of methotrexate, L-asparaginase, idarubicin, and dexamethasone followed by allogenic or autologous bone marrow transplantation in 26 participants newly diagnosed with BPDCN is planned but not yet in its recruiting phase.While few studies have reported on the treatment of BPDCN that has recurred following initial therapy, donor lymphocyte infusions coupled with alternative chemotherapy treatments have induced second complete or partial remissions in a few patients. Tagraxofusp-erzs
Tagraxofusp-erzs (trade name Elzonris; formerly SL-401 and DT388-IL3) was approved in the United States in December 2018 for the treatment of BPDCN. Tagraxofusp-erzs is a fusion protein consisting of interleukin 3 (i.e. IL-3) fused to diphtheria toxin. The fusion protein readily kills cultured pDC by binding to their IL-3 receptors to thereby gain entrance to the cells and then blocking these cells protein synthesis (due to diphtheria toxin-mediated inhibition of eukaryotic elongation factor 2). Prognosis
Due to the high rates of recurrence following initial therapy and the short overall survival times of individuals with BPDCN, prognosis of the disease is poor. However, further study of treatment regimens that include intrathecal chemotherapy and hematological stem cell transplantation in initial treatment regimens (see previous section) and newer non-chemotherapeutic drug treatments (see next section) may improve this situation. Research
UCART123
UCART123 are chimeric T cell receptor-bearing cells, i.e. T lymphocytes engineered to bear a monoclonal antibody that directs them to attack and kill BPDCN cells. | CD123), CLEC4C, and Neuropilin, and 5) failure to express certain marker proteins that are commonly expressed by myeloid, lymphoid, and NK cell lineages.Blastic plasmacytoid dendritic cell neoplasm typically arises after the serial acquisition of multiple genetic abnormalities in pDC or their precursor cells. Inactivating mutations (i.e. mutations which cause the gene to make no or a less active product) in the TET2 gene are the most common genetic abnormality in the disease, occurring in 32–67% of all BPDCN cases and often accompanied by mutations in either the NPM1 or SRSF2 gene. Numerous other genetic abnormalities are associated with the disease: 1) mutations in NRAS, ASXL1, and TP53; 2) deletions of the CDKN2A-ARF-CDKN2B locus on the short arm of chromosome 9, CDKN1B locus on the short arm of chromosome 12, RB1 locus on the long arm of chromosome 13, or NRC1 locus on the long arm of chromosome 5; 3) fusions of KMT2A on the long arm of chromosome 11 with MLLT1 on the short arm of chromosome 10, SUPT3H on the short arm of chromosome with MYC on the long arm of chromosome 8, or KMT2A on the long arm of chromosome 11 with MLLT1 on the long arm of chromosome 19; and 4) duplication or loss of entire chromosomes, particularly chromosomes 9, 13, or 15. Laboratory studies indicate that malignant pDC have a pathologically overactive NF-κB pathway that promotes their survival and production of various cytokines) that stimulate their own proliferation. | 11
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Venous spread may occur when intra-abdominal or thoracic pressure increases and venous flow is retrograde which then allows tumor cells in the systemic venous system to enter the vertebral venous system. Centripetal migration from systemic tumors along perineural, invasion of nerve space, or perivascular spaces. Malignant cells can migrate along spinal or cranial nerve epineurium-perineurium, invade the subpial space, and travel along blood vessels into the endoneurial space, or invade the nerve parenchyma.Infiltration happens most often at the base of the brain, dorsal surface, and especially at the cauda equina, which is largely due to the effect of gravity. Once in the CSF, malignant cells can extend along the membrane surfaces or spread freely in the CSF and attach to other locations. These cells have the ability to penetrate the pial membrane and invade the spinal cord and cranial nerves. Infiltration to spinal cord
Infiltration from the subarachnoid space into the spinal cord occurs primarily along the perivascular tissues that surround blood vessels at the brain entrance. Infiltration from the anterior median fissure, a 3mm deep furrow on the anterior side of the spinal cord, to the anterior horn of the spinal cord, the ventral grey matter of the spinal cord, is found along the central artery. | Dorsal radiculopathy which is secondary ascending degeneration of the posterior funiculus may also occur due to malignant cells collecting or a presence of tumor which cause compression of the nerve. Tumor cell proliferation is observed around nerve roots as well as loss of myelinated nerve fibers and axonal swelling. In areas of tumor cells, infiltration of macrophages is observed. Nerve root infiltration has shown positive correlation with meningeal dissemination. Infiltration of the spinal cord parenchyma is found with destruction of the pia mater. Tumor cell infiltration is associated with spongy changes in the white matter of the spinal cord beneath the pia mater with demyelination, axonal swelling, and macrophage infiltration. Transverse necrosis of the spinal cord is usually marked with bleeding from tumor growth in the subarachnoid space and is the result of compression by the hematoma in the subarachnoid space. From primary cancer to the meninges
NM is a secondary cancer meaning that it is the result of neoplastic cells that have metastasized from a primary cancer site. These cancers develop an enzyme that is able to break down blood vessels at a microscopic level. These cells enter the blood vessels and travel across the body. Once the brain is reached, they break down the blood–brain barrier to enter the Cerebrospinal Fluid (CSF). There the cancerous cells seed and disseminate into the leptomeninges which are composed of the arachnoid and the pia. | 11
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Though community members have shown support though writing opinion pieces.In late January 2019, the New York Times reported rising housing prices to be a major factor in the increasing homelessness in New Zealand so that "smaller markets like Tauranga, a coastal city on the North Island with a population of 128,000, had seen an influx of people who had left Auckland in search of more affordable housing. Average property values in Tauranga had risen to $497,000 from $304,000 in the last five years, and Demographia now rated it among the 10 least affordable cities in the world — along with famously expensive locales such as Hong Kong, San Francisco, Sydney and Vancouver, British Columbia. "In mid August 2019, the Associate Housing Minister Kris Faafoi and Social Development Minister Carmel Sepuloni announced that the Government would be launching a NZ$54 million program to tackle homelessness in New Zealand. This includes investing $31 million over the next four years for 67 intensive case managers and navigators to work with homeless people and a further $16 million for the Sustaining Tenancies Programme. This funding complements the Governments Housing First programme. Russia and the USSR
After the abolition of serfdom in Russia in 1861, major cities experienced a large influx of former peasants who sought jobs as industrial workers in rapidly developing Russian industry. These people often lived in harsh conditions, sometimes renting a room shared between several families. There also was a large number of shelterless homeless. | Non-white people are also overrepresented in homeless populations, with such groups two and one-half times more likely to be homeless in the U.S. The median age of homeless people is approximately 35. Statistics for developed countries
In 2005, an estimated 100 million people worldwide were homeless. The following statistics indicate the approximate average number of homeless people at any one time. Each country has a different approach to counting homeless people, and estimates of homelessness made by different organizations vary wildly, so comparisons should be made with caution. European Union: 3,000,000 (UN-HABITAT 2004)
England: 11,580 single households were assessed as rough sleeping at the point of approach in 2021, up 39% from 2019–20, with 119,400 households owed a prevention duty in 2020–21
Scotland: 27,571 households were assessed as homeless in 2020/21, a decrease of 13% compared to 2019/20
Canada: 150,000
Australia: On census night in 2006 there were 105,000 people homeless across Australia, an increase from the 99,900 Australians who were counted as homeless in the 2001 census
United States: The HUD 2018 Annual Homeless Assessment Report (AHAR) to Congress reports that in a single night, roughly 553,000 people were experiencing homelessness in the United States. According to HUDs July 2010 fifth Homeless Assessment Report to Congress, in a single night in January 2010, single-point analysis reported to HUD showed 649,917 people experiencing homelessness. This number had increased from January 2009s 643,067. The unsheltered count increased by 2.8 percent while the sheltered count remained the same. | 11
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Expansion of mosquito habitats
Deforestation, and projects involving housing, agriculture and water can incidentally expand mosquito habitats. Economic necessity, disasters and conflicts, are known to affect the migration of people, which can also contribute to the movement of mosquitoes and hence risk of malaria. Failure to take this into account has previously resulted in failed attempts to control malaria. Air traffic and global warming
With an increase in air traffic volume, higher climate temperatures and humidity, the summers of temperate climates are potentially favourable for mosquitoes. Should temperatures rise in Europe and the United States as a result of global climate change, conditions may become more ideal for mosquito survival, potentially leading to a rise in isolated outbreaks of airport and imported malaria. Uninfected mosquitoes that arrive by flight may also live for long in enough as to feed on an infected person, which could also result in the transmission of malaria in non-endemic countries. Airports, air routes and aircraft
Airports
The highest risk of airport malaria in Europe is from western and central Africa. A number of species have been found in these Western European airports, particularly Anopheles gambiae which breeds in Africas rainy season during summer, when conditions in Europe are more favourable for its survival.When the cabin and cargo hold doors are opened, ground personnel working on airstrips are at risk. Also, those who manipulate and open containers in warehouses, stores or the post office are exposed to bites of the mosquitoes which have travelled in containers. | Association for Genitourinary Medicine (UK) and the Medical Society for the Study of Venereal Diseases (UK), 2001. External links
Zoons Balanitis at eMedicine
Dermatological atlas | 0-1
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As a result, VIP induces an increase in vaginal blood flow accompanied by an increase in vaginal lubrication. The findings suggest that VIP may participate in the control of the local physiological changes observed during sexual arousal: genital vasodilation and increase in vaginal lubrication. Vaginal dryness
Insufficient lubrication or vaginal dryness can cause dyspareunia, which is a type of sexual pain disorder. While vaginal dryness is considered an indicator for sexual arousal disorder, vaginal dryness may also result from insufficient excitement and stimulation or from hormonal changes caused by menopause (potentially causing atrophic vaginitis), pregnancy, or breast-feeding. Irritation from contraceptive creams and foams can also cause dryness, as can fear and anxiety about sexual intimacy. Vaginal dryness can also be a symptom of Sjögren syndrome (SS), a chronic autoimmune disorder in which the body destroys moisture-producing glands. Certain medications, including some over-the-counter antihistamines, as well as life events such as pregnancy, lactation, menopause, aging or diseases such as diabetes, will inhibit lubrication. Medicines with anticholinergic or sympathomimetic effects will dry out the mucosal or "wet" tissues of the vagina. Such medicines include many common drugs for allergenic, cardiovascular, psychiatric, and other medical conditions. Oral contraceptives may also increase or decrease vaginal lubrication. Older women produce less vaginal lubrication and reduced estrogen levels may be associated with increased vaginal dryness. Artificial lubricants
When a woman is experiencing vaginal dryness before sexual activity, sexual intercourse may be uncomfortable or painful for her. | A personal lubricant can be applied to the vaginal opening, the penis, or both, to augment the naturally produced lubrication and prevent or reduce the discomfort or pain. More rarely, a vaginal suppository may be inserted prior to intercourse. Oil-based lubricants can weaken latex and reduce the effectiveness of condoms, latex gloves, or dental dams as either forms of birth control or for protection from sexually transmitted diseases, so water- or silicone-based lubricants are often used instead. The use of an artificial lubricant can make sexual intercourse less painful for a woman, but does not address the underlying cause of the vaginal dryness itself. Both canola oil and mineral oil are recommended by the American Society for Reproductive Medicine as fertility-preserving types of personal lubricant. Dry sex
Some people practice dry sex, which involves the removal of vaginal lubrication in some way. The rationale for the practice seems to be for cleansing purposes and to enhance the sexual pleasure of the penetrating partner. However, besides making sexual intercourse painful for the female, the practice is believed to increase the risk of transmitting sexually transmitted diseases for both partners, such as HIV, whose risk of transmission is increased by lacerations in the vaginal tissue resulting from the lack of lubrication. See also
References
External links
Mayo Clinic - Vaginal dryness | 11
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Furthermore, pharmacological data (e.g., the probable efficacy of the opioid antagonist, naltrexone, in the treatment of both kleptomania and substance use disorders) could present additional support for a joint relationship between kleptomania and substance use disorders. Based on the idea that kleptomania and substance use disorders may share some etiological features, it could be concluded that kleptomania would react optimistically to the same treatments. As a matter of fact, certain non-medical treatment methods that are successful in treating substance use are also accommodating in treating kleptomania. Obsessive-compulsive disorder
Kleptomania is frequently thought of as being a part of obsessive-compulsive disorder (OCD), since the irresistible and uncontrollable actions are similar to the frequently excessive, unnecessary, and unwanted rituals of OCD. Some individuals with kleptomania demonstrate hoarding symptoms that resemble those with OCD. Prevalence rates between the two disorders do not demonstrate a strong relationship. Studies examining the comorbidity of OCD in subjects with kleptomania have inconsistent results, with some showing a relatively high co-occurrence (45%-60%) while others demonstrate low rates (0%-6.5%). Similarly, when rates of kleptomania have been examined in subjects with OCD, a relatively low co-occurrence was found (2.2%-5.9%). Pyromania
Pyromania, another impulse disorder, has many ties to kleptomania. Many pyromaniacs begin fires alongside petty stealing which often appears similar to kleptomania. Treatment
Although the disorder has been known to psychologists for a long time, the cause of kleptomania is still ambiguous. Therefore, a diverse range of therapeutic approaches have been introduced for its treatment. These treatments include: psychoanalytic oriented psychotherapy, behavioral therapy, and pharmacotherapy. | == References == | 0-1
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Names
It is also known as hydroxydaunorubicin and hydroxydaunomycin.It is sold under a number of different brand names, including Adriamycin PFS, Adriamycin RDF, or Rubex. Formulations
Doxorubicin is photosensitive, and containers are often covered by an aluminum bag and/or brown wax paper to prevent light from affecting it. Doxorubicin is also available in liposome-encapsulated forms as Doxil (pegylated form), Myocet (nonpegylated form), and Caelyx, which are also given by intravenous injection.The FDA approved the first generic version of Doxil, made by Sun, in February 2013. Research
Combination therapy experiments with sirolimus (rapamycin) and doxorubicin have shown promise in treating Akt-positive lymphomas in mice.Further, the release of photo-activated adriamycin with the aid of nanoporous optical antenna resulted in significant anti-cancer effect in MCF-7 breast cancer cells. In 2006, animal research coupling a murine monoclonal antibody with doxorubicin created an immunoconjugate that was able to eliminate HIV-1 infection in mice. Antimalarial activity
There is some evidence for antimalarial activity for doxorubicin and similar compounds. In 2009, a compound similar in structure to doxorubicin was found to inhibit plasmepsin II, an enzyme unique to the malarial parasite Plasmodium falciparum. The pharmaceutical company GlaxoSmithKline (GSK) later identified doxorubicin in a set of compounds that inhibit parasite growth
Fluorescence
Doxorubicin is also known to be fluorescent. This has often been used to characterize doxorubicin concentrations, and has opened the possibility of using the molecule as a theranostic agent. However, there are significant limitations, as doxorubicins fluorescence spectrum is known to depend on a variety of factors, including the pH of the environment, solvent dielectric constant and others. | The same can occur with elements in food, such as calcium, which impacts both heme and non-heme iron absorption. Absorption of iron is better at a low pH (i.e. an acidic environment), and absorption is decreased if there is a simultaneous intake of antacids. Many other substances decrease the rate of non-heme iron absorption. One example is tannins from foods such as tea and phytic acid. Because iron from plant sources is less easily absorbed than the heme-bound iron of animal sources, vegetarians and vegans should have a somewhat higher total daily iron intake than those who eat meat, fish or poultry.Taken after a meal, there are fewer side effects but there is also less absorption because of interaction and pH alteration. Generally, an interval of 2–3 hours between the iron intake and that of other drugs seems advisable, but is less convenient for patients and can impact on compliance. History
The first pills were commonly known as Blauds pills, which were named after P. Blaud of Beaucaire, the French physician who introduced and started the use of these medications as a treatment for patients with anemia. Administration
By mouth
Iron can be supplemented by mouth using various forms, such as iron(II) sulfate. This is the most common and well studied soluble iron salt sold under brand names such as Feratab, Fer-Iron, and Slow-FE. It is in complex with gluconate, dextran, carbonyl iron, and other salts. Ascorbic acid, vitamin C, increases the absorption of non-heme sources of iron.Heme iron polypeptide (HIP) (e.g. | 0-1
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West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. In about 80% of infections people have few or no symptoms. About 20% of people develop a fever, headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent.West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease. Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, but it otherwise does not spread directly between people. Risks for severe disease include being over 60 years old and having other health problems. Diagnosis is typically based on symptoms and blood tests.There is no human vaccine. The best way to reduce the risk of infection is to avoid mosquito bites. Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. When mosquitoes cannot be avoided, mosquito repellent, window screens, and mosquito nets reduce the likelihood of being bitten. There is no specific treatment for the disease; pain medications may reduce symptoms.The virus was discovered in Uganda in 1937, and was first detected in North America in 1999. WNV has occurred in Europe, Africa, Asia, Australia, and North America. | Calan may refer to
Calan (band), a Welsh band
Calan, Morbihan, a town in Brittany, France
Calan, a trade name for the drug Verapamil
Călan, a town in Hunedoara County, Romania
Alline Calandrini (born 1988), known as Calan, a Brazilian footballer | 0-1
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Among the many classified mitochondrial diseases, those involving dysfunctional COX assembly are thought to be the most severe.The vast majority of COX disorders are linked to mutations in nuclear-encoded proteins referred to as assembly factors, or assembly proteins. These assembly factors contribute to COX structure and functionality, and are involved in several essential processes, including transcription and translation of mitochondrion-encoded subunits, processing of preproteins and membrane insertion, and cofactor biosynthesis and incorporation.Currently, mutations have been identified in seven COX assembly factors: SURF1, SCO1, SCO2, COX10, COX15, COX20, COA5 and LRPPRC. Mutations in these proteins can result in altered functionality of sub-complex assembly, copper transport, or translational regulation. Each gene mutation is associated with the etiology of a specific disease, with some having implications in multiple disorders. Disorders involving dysfunctional COX assembly via gene mutations include Leigh syndrome, cardiomyopathy, leukodystrophy, anemia, and sensorineural deafness. Histochemistry
The increased reliance of neurons on oxidative phosphorylation for energy facilitates the use of COX histochemistry in mapping regional brain metabolism in animals, since it establishes a direct and positive correlation between enzyme activity and neuronal activity. This can be seen in the correlation between COX enzyme amount and activity, which indicates the regulation of COX at the level of gene expression. COX distribution is inconsistent across different regions of the animal brain, but its pattern of its distribution is consistent across animals. This pattern has been observed in the monkey, mouse, and calf brain. One isozyme of COX has been consistently detected in histochemical analysis of the brain. | Untreated bowel infarction quickly leads to life-threatening infection and sepsis, and may be fatal.The only treatment for bowel infarction is immediate surgical repair and eventually removal of the dead bowel segment.Patients who have undergone extensive resection of the small bowel may develop malabsorption, indicating the need for dietary supplements. Additional images
See also
Adhesions
Ischemic colitis
Volvulus
References
== External links == | 0-1
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Rh deficiency syndrome is a type of hemolytic anemia that involves erythrocytes whom membranes are deficient in Rh antigens. It is considered a rare condition. See also
List of hematologic conditions
RHAG
References
== External links == | A cirsoid aneurysm, also referred to as an arteriovenous hemangioma is the dilation of a group of blood vessels due to congenital malformations with arterio venous (AV) shunting. "Cirsoid" means resembling a varix. They are most common on the head or neck.Cirsoid aneurysms appear as nodules or papules. Histologically, they are composed of both thick- and thin-walled blood vessels. == References == | 0-1
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Procedural
Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy. Similar conditions
Congestion of the mucosa in other parts of the gastrointestinal tract can also be seen in portal hypertension. When the condition involves the colon, it is termed portal hypertensive colopathy. References
== External links == | Kaposis sarcoma (KS) is a type of cancer that can form masses in the skin, in lymph nodes, in the mouth, or in other organs. The skin lesions are usually painless, purple and may be flat or raised. Lesions can occur singly, multiply in a limited area, or may be widespread. Depending on the sub-type of disease and level of immune suppression, KS may worsen either gradually or quickly. KS is caused by a combination of immune suppression (such as due to HIV/AIDS) and infection by Human herpesvirus 8 (HHV8 – also called KS-associated herpesvirus (KSHV)).Four sub-types are described: classic, endemic, immunosuppression therapy-related (also called iatrogenic), and epidemic (also called AIDS-related). Classic KS tends to affect older men in regions where KSHV is highly prevalent (Mediterranean, Eastern Europe, Middle East), is usually slow-growing, and most often affects only the legs. Endemic KS is most common in Sub-Saharan Africa and is more aggressive in children, while older adults present similarly to classic KS. Immunosuppression therapy-related KS generally occurs in people following organ transplantation and mostly affects the skin. Epidemic KS occurs in people with AIDS and many parts of the body can be affected. KS is diagnosed by tissue biopsy, while the extent of disease may be determined by medical imaging.Treatment is based on the sub-type, whether the condition is localized or widespread, and the persons immune function. Localized skin lesions may be treated by surgery, injections of chemotherapy into the lesion, or radiation therapy. Widespread disease may be treated with chemotherapy or biologic therapy. | 0-1
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As per a study of six narcoleptic patients it was found that L-dopa improved vigilance and performance as evaluated by the AVS and the FCRTT, while the capacity to fall asleep rapidly remained unchanged as evaluated by the MSLT. It raises the hypothesis that dopamine may play a role in the physiopathology of excessive daytime sleepiness of this condition. Carnitine
Carnitine, has also been shown to improve narcolepsy symptoms (including daytime sleepiness) by increasing fatty-acid oxidation. Abnormally low levels of acylcarnitine have been observed in patients with narcolepsy. These same low levels have been associated with primary hypersomnia in general in mouse studies. "Mice with systemic carnitine deficiency exhibit a higher frequency of fragmented wakefulness and rapid eye movement (REM) sleep, and reduced locomotor activity." Administration of acetyl-L-carnitine was shown to improve these symptoms in mice. A subsequent human trial found that narcolepsy patients given L-carnitine spent less total time in daytime sleep than patients who were given placebo. See also
References
== External links == | Pharmacology
Pharmacodynamics
(R)-Etomidate is tenfold more potent than its (S)-enantiomer. At low concentrations (R)-etomidate is a modulator at GABAA receptors containing β2 and β3 subunits. At higher concentrations, it can elicit currents in the absence of GABA and behaves as an allosteric agonist. Its binding site is located in the transmembrane section of this receptor between the beta and alpha subunits (β+α−). β3-containing GABAA receptors are involved in the anesthetic actions of etomidate, while the β2-containing receptors are involved in some of the sedation and other actions that can be elicited by this drug. Pharmacokinetics
At the typical dose, anesthesia is induced for the duration of about 5–10 minutes, though the half-life of drug metabolism is about 75 minutes, because etomidate is redistributed from the plasma to other tissues. Onset of action: 30–60 seconds
Peak effect: 1 minute
Duration: 3–5 minutes; terminated by redistribution
Distribution: Vd: 2–4.5 L/kg
Protein binding: 76%
Metabolism: Hepatic and plasma esterases
Half-life distribution: 2.7 minutes
Half-life redistribution: 29 minutes
Half-life elimination: 2.9 to 5.3 hours
Metabolism
Etomidate is highly protein-bound in blood plasma and is metabolised by hepatic and plasma esterases to inactive products. It exhibits a biexponential decline. Formulation
Etomidate is usually presented as a clear colourless solution for injection containing 2 mg/ml of etomidate in an aqueous solution of 35% propylene glycol, although a lipid emulsion preparation (of equivalent strength) has also been introduced. Etomidate was originally formulated as a racemic mixture, but the R form is substantially more active than its enantiomer. It was later reformulated as a single-enantiomer drug, becoming the first general anesthetic in that class to be used clinically. | 0-1
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These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia.Studies have tested the use of melatonin, high dosage vitamins, and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current rate of people for those taking antipsychotic drugs. Tentative evidence supports the use of vitamin E for prevention. Treatment
Valbenazine was approved by the FDA for tardive dyskinesia in April 2017. Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders (e.g. Huntingtons chorea). Deutetrabenazine, an isotopic isomer of tetrabenazine, was approved by the FDA for tardive dyskinesia in August 2017. Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials, but the overall evidence for its effectiveness is considered "weak." Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage. Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia. As of 2018 evidence is insufficient to support the use of benzodiazepines, baclofen, progabide, sodium valproate, gaboxadol, or calcium channel blockers (e.g. diltiazem). Epidemiology
Tardive dyskinesia most commonly occurs in people with psychiatric conditions who are treated with antipsychotic medications for many years. | This can be seen in people who are experiencing the classic signs of pericarditis but then show signs of relief, and progress to show signs of cardiac tamponade which include decreased alertness and lethargy, pulsus paradoxus (decrease of at least 10 mmHg of the systolic blood pressure upon inspiration), low blood pressure (due to decreased cardiac index), (jugular vein distention from right sided heart failure and fluid overload), distant heart sounds on auscultation, and equilibration of all the diastolic blood pressures on cardiac catheterization due to the constriction of the pericardium by the fluid.In such cases of cardiac tamponade, EKG or Holter monitor will then depict electrical alternans indicating wobbling of the heart in the fluid filled pericardium, and the capillary refill might decrease, as well as severe vascular collapse and altered mental status due to hypoperfusion of body organs by a heart that can not pump out blood effectively.The diagnosis of tamponade can be confirmed with trans-thoracic echocardiography (TTE), which should show a large pericardial effusion and diastolic collapse of the right ventricle and right atrium. Chest X-ray usually shows an enlarged cardiac silhouette ("water bottle" appearance) and clear lungs. Pulmonary congestion is typically not seen because equalization of diastolic pressures constrains the pulmonary capillary wedge pressure to the intra-pericardial pressure (and all other diastolic pressures). Causes
Infectious
Pericarditis may be caused by viral, bacterial, or fungal infection. In the developed world, viruses are believed to be the cause of about 85% of cases. | 0-1
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Due to its rarity and to the fact that genetic diagnosis has been used only in recent years, in the past NF-1 was in some cases confused with Legius syndrome, another syndrome with vaguely similar symptoms, including cafe-au-lait spots.NF-1 is an age specific disease; most signs of NF-1 are visible after birth (during infancy), but many symptoms of NF-1 occur as the person ages and has hormonal changes. NF-1 was formerly known as von Recklinghausen disease, after the researcher (Friedrich Daniel von Recklinghausen) who first documented the disorder.The severity of NF-1 varies widely, and little is known about what causes a person to have a more severe or less severe case. Even within the same family (as there is a 50% chance that a parent will pass their condition to their offspring), levels of severity can vary enormously. However, 60% of people with NF-1 have mild cases, with few symptoms that have very little effect in their day-to-day lives. 20% of NF-1 patients have moderate cases, with several symptoms that have little more than cosmetic effects. The other 20% have severe cases with several symptoms that affect the persons quality of life. Even in this last group, symptoms are rarely life-threatening. Signs and symptoms
The following is a list of conditions and complications associated with NF-1, and, where available, age range of onset and progressive development, occurrence percentage of NF-1 population, method of earliest diagnosis, and treatments and related medical specialties. | Amlodipine/celecoxib, sold under the brand name Consensi, is a fixed-dose combination medication used to treat both hypertension and osteoarthritis at the same time in adults. It contains amlodipine besylate and celecoxib. It is taken by mouth.The most common side effects include edema, abdominal pain, diarrhea, dyspepsia, flatulence, peripheral edema, accidental injury, dizziness, pharyngitis, rhinitis, sinusitis, upper respiratory tract infection, and rash.It was approved for medical use in the United States in May 2018. Medical uses
Amlodipine/celecoxib is indicated for use in adults for whom treatment with amlodipine for hypertension and celecoxib for osteoarthritis are appropriate. History
Amlodipine/celecoxib was approved for use in the United States in May 2018. References
External links
"Amlodipine mixture with celecoxib". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Methadone users in detox also find more luck in therapy because they dont have to deal with constant opioid cravings or the severity of acute withdrawal symptoms. Advantages of methadone include:
Reduction in infectious disease due to the cessation of opiate misuse, especially injection drug abuse
Reduction in illegal crime due to the cessation in illicit drug usage
Overall increase in quality of life
Improved social functioning
More attendance in alcohol therapy since withdrawal symptoms arent a diversionMethadone replacement therapy will also help people achieve stabilization early on in their rehabilitation. People should devote 100% of their time to recovery, helping them to solve the underlying problems that lead to their opiate addiction. They will get a career and start to find a better balance in their lives. It also enables parents to continue raising their children in a safe home environment. When their conditions improve and they want to refrain from taking methadone, they must be properly weaned off the medication, which must be done under medical observation. Although other medication-assisted therapies for opiate addiction, such as buprenorphine, are available, methadone is often seen as the most promising alternative for people who are heavily addicted to opiates. Methadone has a number of serious side effects, including:
Slowed breathing
Sexual dysfunction
Nausea
Vomiting
Restlessness
Itchy eyesDosages can be adjusted after 1–2 days, or another medication may be recommended for your situation if you experience side effects. Lung and breathing complications are possible long-term side effects of methadone use. Methadone, as an opiate, has the potential to be addictive. | Congenital
Congenital conditions that are implicated in VFP include neurological disorders like hydrocephalus and Arnold-Chiari malformation, dysmorphic neurological disorders such as Moebius syndrome or Goldenhar Syndrome, anatomical abnormalities such as a tracheoesophageal fistula, vascular anomalies (e.g. vascular ring) affecting the vocal mechanism, syndromes affecting brainstem function or atrophic diseases such as Charcot-Marie-Tooth.In the absence of imaging, either invasive (e.g. laryngoscopy) or non-invasive (e.g. computed tomography scan), congenital VFP can be detected in infants through the presence of stridor (i.e. a high-pitched wheezing resulting from a blockage in the larynx or trachea), difficulties feeding, an abnormal sounding cry or excessive hoarseness.Recovery from congenital VFP varies and is reliant on the severity of the condition. Some cases of VFP recover spontaneously, often within the first year. If the paresis is persistent, surgical options such as vocal fold injections or tracheotomy can be taken into consideration. Infection
Many viral infections have been reported as a cause for VF paresis, including herpes simplex virus, Epstein-Barr virus, Varicella-Zoster, cytomegalovirus, HIV, West Nile virus, and upper respiratory infection. Bacterial infections have also been reported to cause VF paresis, such as syphilis and Lyme disease. Tumors
When abnormal cells group together in the body, they are said to form a tumor. Tumors can be either malignant (cancerous) or benign (non-cancerous). Tumors may lead to paralysis of the vocal folds when they affect the recurrent laryngeal nerves (RLNs) either directly or indirectly:
RLN paralysis can be caused by tumors of the thyroid, lung, esophagus, and mediastinum. | 0-1
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Birth-control pills and hormone replacement therapy also can trigger melasma. The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone treatment.Genetic predisposition is also a major factor in determining whether someone will develop melasma. People with the Fitzpatrick skin type III or greater from African, Asian, or Hispanic descent are at a much higher risk than others. In addition, women with a light brown skin type who are living in regions with intense sun exposure are particularly susceptible to developing this condition.The incidence of melasma also increases in patients with thyroid disease. It is thought that the overproduction of melanocyte-stimulating hormone brought on by stress can cause outbreaks of this condition. Other rare causes of melasma include allergic reaction to medications and cosmetics. Addisons disease
Melasma suprarenale (Latin - above the kidneys) is a symptom of Addisons disease, particularly when caused by pressure or minor injury to the skin, as discovered by FJJ Schmidt of Rotterdam in 1859. Diagnosis
Types
The two different kinds of melasma are epidermal and dermal. Epidermal melasma results from melanin pigment that is elevated in the suprabasal layers of the epidermis.Dermal melasma occurs when the dermal macrophages have an elevated melanin level. Melasma is usually diagnosed visually or with assistance of a Woods lamp (340 - 400 nm wavelength). Under Woods lamp, excess melanin in the epidermis can be distinguished from that of the dermis. | Cutaneous diphtheria is an infection of the skin by Corynebacterium diphtheriae. : 265 It is also known as "desert sore". See also
Diphtheria
Skin lesion
== References == | 0-1
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With these parameters, DAS28 is calculated as:
D
A
S
28
=
0.56
×
T
E
N
28
+
0.28
×
S
W
28
+
0.70
×
ln
(
E
S
R
)
+
0.014
×
S
A
{\displaystyle DAS28=0.56\times {\sqrt {TEN28}}+0.28\times {\sqrt {SW28}}+0.70\times \ln(ESR)+0.014\times SA}
From this, the disease activity of the affected person can be classified as follows:
It is not always a reliable indicator of treatment effect. | Disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the progression of disease. Biological DMARDs may be used when disease does not respond to other treatments. However, they may have a greater rate of adverse effects. Surgery to repair, replace, or fuse joints may help in certain situations.RA affects about 24.5 million people as of 2015. This is between 0.5 and 1% of adults in the developed world with 5 and 50 per 100,000 people newly developing the condition each year. Onset is most frequent during middle age and women are affected 2.5 times as frequently as men. It resulted in 38,000 deaths in 2013, up from 28,000 deaths in 1990. The first recognized description of RA was made in 1800 by Dr. Augustin Jacob Landré-Beauvais (1772–1840) of Paris. The term rheumatoid arthritis is based on the Greek for watery and inflamed joints. Signs and symptoms
RA primarily affects joints, but it also affects other organs in more than 15–25% of cases. Associated problems include cardiovascular disease, osteoporosis, interstitial lung disease, infection, cancer, feeling tired, depression, mental difficulties, and trouble working. Joints
Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. | 11
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This type of meningitis is usually caused by viruses but it may be due to bacterial infection that has already been partially treated, when bacteria disappear from the meninges, or pathogens infect a space adjacent to the meninges (e.g. sinusitis). Endocarditis (an infection of the heart valves which spreads small clusters of bacteria through the bloodstream) may cause aseptic meningitis. Aseptic meningitis may also result from infection with spirochetes, a group of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). Meningitis may be encountered in cerebral malaria (malaria infecting the brain) or amoebic meningitis, meningitis due to infection with amoebae such as Naegleria fowleri, contracted from freshwater sources. Bacterial
The types of bacteria that cause bacterial meningitis vary according to the infected individuals age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and bacteria that normally inhabit the digestive tract such as Escherichia coli (carrying the K1 antigen). Listeria monocytogenes (serotype IVb) can be contracted when consuming improperly prepared food such as dairy products, produce and deli meats, and may cause meningitis in the newborn. Older children are more commonly affected by Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination). | Other signs include the presence of positive Kernigs sign or Brudziński sign. Kernigs sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernigs sign, pain limits passive extension of the knee. A positive Brudzinskis sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernigs sign and Brudzinskis sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely.Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash, which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjunctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. | 11
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Nervous may refer to:
nervousness
Nervous system, a network of cells in an animals body that coordinates movement and the senses
Nervous tissue, the cells of the nervous system that work in aggregate to transmit signals
Music
"Nervous" (Gene Summers song), 1958; covered by several performers
"Nervous" (Gavin James song), 2016
"Nervous" (Shawn Mendes song), 2018
"Nervous", a song by K.Flay from Solutions, 2019
"Nervous", a song by L Devine, 2018
"Nervous", a song by Nick Jonas from Spaceman, 2021
Nervous Records, a UK record label
Nervous Records (US), a US record label
See also
"Nervousness", a song by the Gigolo Aunts from Tales from the Vinegar Side
Nervous Norvus (1912–1968), the performing name of Jimmy Drake
Nervous shark, a species of requiem shark
All pages with titles beginning with Nervous | People with anorexia are, in general, highly perfectionistic and most have obsessive compulsive personality traits which may facilitate sticking to a restricted diet. It has been suggested that patients with anorexia are rigid in their thought patterns, and place a high level of importance upon being thin.A risk factor for anorexia is trauma. Although the prevalence rates vary greatly, between 37% and 100%, there appears to be a link between traumatic events and eating disorder diagnosis. Approximately 72% of individuals with anorexia report experiencing a traumatic event prior to the onset of eating disorder symptoms, with binge-purge subtype reporting the highest rates. There are many traumatic events that may be risk factors for development of anorexia, the first identified traumatic event predicting anorexia was childhood sexual abuse. However, other traumatic events, such as physical and emotional abuse have also been found to be risk factors. Interpersonal, as opposed to non-interpersonal trauma, has been seen as the most common type of traumatic event, which can encompass sexual, physical, and emotional abuse. Individuals who experience repeated trauma, like those who experience trauma perpetrated by a caregiver or loved one, have increased symptom severity of anorexia and a greater prevalence of comorbid psychiatric diagnoses.In individuals with anorexia, the prevalence rates for those who also qualify for a PTSD diagnosis ranges from 4% to 52% in non-clinical samples to 10% to 47% in clinical samples. | 0-1
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Those with THC in their system are from three to seven times more likely to be the cause of the accident than those who had not used either cannabis or alcohol, although its role is not necessarily causal because THC stays in the bloodstream for days to weeks after intoxication.Some immediate undesired side effects include a decrease in short-term memory, dry mouth, impaired motor skills, reddening of the eyes, dizziness, feeling tired and vomiting. Some users may experience an episode of acute psychosis, which usually abates after six hours, but in rare instances, heavy users may find the symptoms continuing for many days.Legalization has increased the rates at which children are exposed to cannabis, particularly from edibles. While the toxicity and lethality of THC in children is not known, they are at risk for encephalopathy, hypotension, respiratory depression severe enough to require ventilation, somnolence and coma. Fatality
Cannabis is suspected of being a potential, and under-reported, contributory factor or direct cause in cases of sudden death, due to the strain it can place on the cardiovascular system. Multiple deaths have been attributed to cannabinoid hyperemesis syndrome.A 16-month survey of Oregon and Alaska emergency departments found a report of the death of an adult who had been admitted for acute cannabis toxicity. Long-term
Psychological effects
A 2015 meta-analysis found that, although a longer period of abstinence was associated with smaller magnitudes of impairment, both retrospective and prospective memory were impaired in cannabis users. The authors concluded that some, but not all, of the deficits associated with cannabis use were reversible. | Novartis also notes the influence of position and preference on US Centers for Medicare & Medicaid formularies in expanding their market value.Nepafenac, Nevanac, and Ilevro are all absent from the 2016 Annual Report issued from Novartis. Intellectual property
There are currently seven U.S. patents filed that are directly associated with the modernized formulations of nepafenac, all stemming from Novartis. There are three patents associated with Nevanac that are still active and four associated with Ilevro. The earliest patent related to the modern formulations of nepafenac was approved on June 11, 2002, after being filed in 1999, by Bahram Asgharian. A patent was filed by Warren Wong, associated with Alcon, Inc. based out of Fort Worth, Texas, on December 2, 2005, for aqueous suspensions of nepafenac. Another patent for a nepafenac-based drug was filed on May 8, 2006, by Geoffrey Owen, Amy Brooks, and Gustav Graff. A patent was filed by Masood A. Chowhan and Huagang Chen on February 9, 2007, and approved on May 24, 2011, followed closely by a patent filed by Warren Wong on September 23, 2010, and approved on December 6, 2011. Masood A. Chowhan, Malay Ghosh, Bahram Asgharian, and Wesley Wehsin Han filed another patent on December 1, 2010, and approved on December 30, 2014. The most recent patent was filed by Masood A. Chowhan, Malay Ghosh, Bahram Asgharian, and Wesley Weshin Han on November 12, 2014, and approved on May 30, 2017. | 0-1
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Wernickes aphasia, also known as receptive aphasia, sensory aphasia or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernickes aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits (i.e. hemiparesis) do not occur in individuals with Wernickes aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernickes aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits. Like many acquired language disorders, Wernickes aphasia can be experienced in many different ways and to many different degrees. Patients diagnosed with Wernickes aphasia can show severe language comprehension deficits; however, this is dependent on the severity and extent of the lesion. Severity levels may range from being unable to understand even the simplest spoken and/or written information to missing minor details of a conversation. Many diagnosed with Wernickes aphasia have difficulty with repetition in words and sentences and/or working memory.Wernickes aphasia was named after German physician Carl Wernicke, who is credited with discovering the area of the brain responsible for language comprehension (Wernickes area). Signs and symptoms
The following are common symptoms seen in patients with Wernickes aphasia:
Impaired comprehension: deficits in understanding (receptive) written and spoken language. | The social implication of viewing aging as a disease could be profound, though this classification is not yet widespread. Lepers were people who were historically shunned because they had an infectious disease, and the term "leper" still evokes social stigma. Fear of disease can still be a widespread social phenomenon, though not all diseases evoke extreme social stigma. Social standing and economic status affect health. Diseases of poverty are diseases that are associated with poverty and low social status; diseases of affluence are diseases that are associated with high social and economic status. Which diseases are associated with which states vary according to time, place, and technology. Some diseases, such as diabetes mellitus, may be associated with both poverty (poor food choices) and affluence (long lifespans and sedentary lifestyles), through different mechanisms. The term lifestyle diseases describes diseases associated with longevity and that are more common among older people. For example, cancer is far more common in societies in which most members live until they reach the age of 80 than in societies in which most members die before they reach the age of 50. Language of disease
An illness narrative is a way of organizing a medical experience into a coherent story that illustrates the sick individuals personal experience. People use metaphors to make sense of their experiences with disease. The metaphors move disease from an objective thing that exists to an affective experience. The most popular metaphors draw on military concepts: Disease is an enemy that must be feared, fought, battled, and routed. | 0-1
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Constipation is also common in individuals with muscular and myotonic dystrophy.Systemic diseases that may present with constipation include celiac disease and systemic sclerosis.Constipation has a number of structural (mechanical, morphological, anatomical) causes, namely through creating space-occupying lesions within the colon that stop the passage of stool, such as colorectal cancer, strictures, rectocoles, anal sphincter damage or malformation and post-surgical changes. Extra-intestinal masses such as other malignancies can also lead to constipation from external compression.Constipation also has neurological causes, including anismus, descending perineum syndrome, and Hirschsprungs disease. In infants, Hirschsprungs disease is the most common medical disorder associated with constipation. Anismus occurs in a small minority of persons with chronic constipation or obstructed defecation.Spinal cord lesions and neurological disorders such as Parkinsons disease and pelvic floor dysfunction can also lead to constipation. Chagas disease may cause constipation through the destruction of the myenteric plexus. Psychological
Voluntary withholding of the stool is a common cause of constipation. The choice to withhold can be due to factors such as fear of pain, fear of public restrooms, or laziness. When a child holds in the stool a combination of encouragement, fluids, fiber, and laxatives may be useful to overcome the problem. Early intervention with withholding is important as this can lead to anal fissures. Congenital
A number of diseases present at birth can result in constipation in children. They are as a group uncommon with Hirschsprungs disease (HD) being the most common. | Low fiber intake, inadequate amounts of fluids, poor ambulation or immobility, or medications can contribute to constipation. Once the presence of constipation is identified based on a culmination of the symptoms described above, then the cause of constipation should be figured out. Separating non-life-threatening from serious causes may be partly based on symptoms. For example, colon cancer may be suspected if a person has a family history of colon cancer, fever, weight loss, and rectal bleeding. Other alarming signs and symptoms include family or personal history of inflammatory bowel disease, age of onset over 50, change in stool caliber, nausea, vomiting, and neurological symptoms like weakness, numbness and difficulty urinating. Examination
A physical examination should involve at least an abdominal exam and rectal exam. Abdominal exam may reveal an abdominal mass if there is significant stool burden and may reveal abdominal discomfort. Rectal examination gives an impression of the anal sphincter tone and whether the lower rectum contains any feces or not. Rectal examination also gives information on the consistency of the stool, the presence of hemorrhoids, blood and whether any perineal irregularities are present including skin tags, fissures, anal warts. Physical examination is done manually by a physician and is used to guide which diagnostic tests to order. Diagnostic tests
Functional constipation is common and does not warrant diagnostic testing. Imaging and laboratory tests are typically recommended for those with alarm signs or symptoms.The laboratory tests performed depends on the suspected underlying cause of the constipation. | 11
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The doctor may inject into the patients bloodstream a contrast agent, which causes vascular tissues to stand out against other tissues, so that information about blood supply and vascular anomalies is easier to gather. Treatment
Treatment depends on the underlying cause. In general, exercise, particularly of the aerobic type, is effective for preventing ED during midlife. Counseling can be used if the underlying cause is psychological, including how to lower stress or anxiety related to sex. Medications by mouth and vacuum erection devices are first-line treatments,: 20, 24 followed by injections of drugs into the penis, as well as penile implants. : 25–26 Vascular reconstructive surgeries are beneficial in certain groups. Treatments, other than surgery, do not fix the underlying physiological problem, but are used as needed before sex. Medications
The PDE5 inhibitors sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis) are prescription drugs which are taken by mouth. : 20–21 As of 2018, sildenafil is available in the UK without a prescription. Additionally, a cream combining alprostadil with the permeation enhancer DDAIP has been approved in Canada as a first line treatment for ED. Penile injections, on the other hand, can involve one of the following medications: papaverine, phentolamine, and prostaglandin E1, also known as alprostadil. In addition to injections, there is an alprostadil suppository that can be inserted into the urethra. Once inserted, an erection can begin within 10 minutes and last up to an hour. Medications to treat ED may cause a side effect called priapism. | This type of device is sometimes referred to as penis pump and may be used just prior to sexual intercourse. Several types of FDA approved vacuum therapy devices are available under prescription. When pharmacological methods fail, a purpose-designed external vacuum pump can be used to attain erection, with a separate compression ring fitted to the base of the penis to maintain it. These pumps should be distinguished from other penis pumps (supplied without compression rings) which, rather than being used for temporary treatment of impotence, are claimed to increase penis length if used frequently, or vibrate as an aid to masturbation. More drastically, inflatable or rigid penile implants may be fitted surgically. Surgery
Often, as a last resort, if other treatments have failed, the most common procedure is prosthetic implants which involves the insertion of artificial rods into the penis. : 26 Some sources show that vascular reconstructive surgeries are viable options for some people. Alternative medicine
The Food and Drug Administration (FDA) does not recommend alternative therapies to treat sexual dysfunction. Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of ED, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products. The FDA has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant. | 11
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Also, it speeds healing of nerve damage (and minimizes the extent of recent nerve trauma). Deferoxamine may modulate expression and release of inflammatory mediators by specific cell types. Research
Deferoxamine is being studied as a treatment for spinal cord injury and intracerebral hemorrhage. It is also used to induce hypoxia-like environment in mesenchymal stem cells. See also
Chelation therapy
== References == | Genetics
Originally believed to be inherited in an X-linked recessive fashion, gerodermia osteodysplastica is now known to display strictly autosomal recessive inheritance. This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.It has been associated with SCYL1BP1. Diagnosis
Differential diagnosis
Many features of gerodermia osteodysplastica (GO) and another autosomal recessive form of cutis laxa, wrinkly skin syndrome (WSS, Online Mendelian Inheritance in Man (OMIM): 278250), are similar to such an extent that both disorders were believed to be variable phenotypes of a single disorder.Several delineating factors, however, suggest that gerodermia osteodysplastica and wrinkly skin syndrome are distinct entities, but share the same clinic spectrum.While the prevailing feature of wrinkly, loose skin is more localized with GO, it is usually systemic, yet eases in severity with age during the course of WSS. Also, as the fontanelles ("soft spots") are usually normal on the heads of infants with GO, they are often enlarged in WSS infants.While WSS is associated with mutations of genes on chromosomes 2, 5, 7, 11 and 14; GO has been linked to mutations in the protein GORAB. | 0-1
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Earthquakes may cause landslips to dam rivers, which collapse and cause floods.The terrain below the Sarez Lake in Tajikistan is in danger of catastrophic flooding if the landslide dam formed by the earthquake, known as the Usoi Dam, were to fail during a future earthquake. Impact projections suggest the flood could affect roughly 5 million people. Major earthquakes
One of the most devastating earthquakes in recorded history was the 1556 Shaanxi earthquake, which occurred on 23 January 1556 in Shaanxi, China. More than 830,000 people died. Most houses in the area were yaodongs—dwellings carved out of loess hillsides—and many victims were killed when these structures collapsed. The 1976 Tangshan earthquake, which killed between 240,000 and 655,000 people, was the deadliest of the 20th century.The 1960 Chilean earthquake is the largest earthquake that has been measured on a seismograph, reaching 9.5 magnitude on 22 May 1960. Its epicenter was near Cañete, Chile. The energy released was approximately twice that of the next most powerful earthquake, the Good Friday earthquake (27 March 1964), which was centered in Prince William Sound, Alaska. The ten largest recorded earthquakes have all been megathrust earthquakes; however, of these ten, only the 2004 Indian Ocean earthquake is simultaneously one of the deadliest earthquakes in history. Earthquakes that caused the greatest loss of life, while powerful, were deadly because of their proximity to either heavily populated areas or the ocean, where earthquakes often create tsunamis that can devastate communities thousands of kilometers away. | The differences in travel time from the epicenter to the observatory are a measure of the distance and can be used to image both sources of earthquakes and structures within the Earth. Also, the depth of the hypocenter can be computed roughly. P-wave speed
Upper crust soils and unconsolidated sediments: 2–3 km (1.2–1.9 mi) per second
Upper crust solid rock: 3–6 km (1.9–3.7 mi) per second
Lower crust: 6–7 km (3.7–4.3 mi) per second
Deep mantle: 13 km (8.1 mi) per second. S-waves speed
Light sediments: 2–3 km (1.2–1.9 mi) per second in
Earths crust:4–5 km (2.5–3.1 mi) per second
Deep mantle: 7 km (4.3 mi) per second
Seismic wave arrival
As a consequence, the first waves of a distant earthquake arrive at an observatory via the Earths mantle. On average, the kilometer distance to the earthquake is the number of seconds between the P- and S-wave times 8. Slight deviations are caused by inhomogeneities of subsurface structure. By such analysis of seismograms, the Earths core was located in 1913 by Beno Gutenberg. S-waves and later arriving surface waves do most of the damage compared to P-waves. P-waves squeeze and expand the material in the same direction they are traveling, whereas S-waves shake the ground up and down and back and forth. Earthquake location and reporting
Earthquakes are not only categorized by their magnitude but also by the place where they occur. The world is divided into 754 Flinn–Engdahl regions (F-E regions), which are based on political and geographical boundaries as well as seismic activity. | 11
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In 2004, 3M obtained FDA approval to market imiquimod as a treatment for superficial basal cell carcinoma.In 2006, 3M sold its pharmaceutical business in the Americas to Graceway Pharmaceuticals, its European pharmaceutical business to Meda AB, and its pharmaceutical business in other territories to two private equity firms.Graceway declared bankruptcy in 2011, after the expiration of the patents on imiquimod, and its assets, including the rights to imiquimod branding and approvals in the Americas, were purchased by Medicis Pharmaceutical.Imiquimod 5% was approved for medical use in the European Union in September 1998. Imiquimod 3.75% was approved for medical use in the European Union in August 2012.As of 2015, imiquimod is generic and is available worldwide under many brands. Research
One randomized double-blind Phase III clinical study found clearance of genital warts (an FDA-approved indication) improved from 9% with placebo to 24.9% with 3.75% imiquimod cream applied for up to eight weeks.Imiquimod has been tested for treatment of molluscum contagiosum. Two large randomized controlled trials, however, found no evidence of effectiveness of imiquimod in treating children with molluscum contagiosum, and concerning adverse effects were also noted. These disprove earlier anecdotal claims and smaller, less reliable studies.Imiquimod has also been tested for treatment of vulvar intraepithelial neoplasia, vaginal intraepithelial neoplasia, common warts (a 2012 Cochrane review found no randomized controlled trials), plantar warts, warts in people with suppressed immune systems, flat warts on face and neck, and warts under and around fingernails and toenails. | The adrenergic substances released by the sympathetic nervous system can also bind to and influence various immunological cells, further providing a connection between the systems. The HPA axis ultimately results in the release of cortisol, which generally has immunosuppressive effects. However, the effect of stress on the immune system is disputed, and various models have been proposed in an attempt to account for both the supposedly "immunodeficiency" linked diseases and diseases involving hyper activation of the immune system. One model proposed to account for this suggests a push towards an imbalance of cellular immunity(Th1) and humoral immunity(Th2). The proposed imbalance involved hyperactivity of the Th2 system leading to some forms of immune hypersensitivity, while also increasing risk of some illnesses associated with decreased immune system function, such as infection and cancer. Effects of chronic stress
Chronic stress is a term sometimes used to differentiate it from acute stress. Definitions differ, and may be along the lines of continual activation of the stress response, stress that causes an allostatic shift in bodily functions, or just as "prolonged stress". For example, results of one study demonstrated that individuals who reported relationship conflict lasting one month or longer have a greater risk of developing illness and show slower wound healing. Similarly, the effects that acute stressors have on the immune system may be increased when there is perceived stress and/or anxiety due to other events. For example, students who are taking exams show weaker immune responses if they also report stress due to daily hassles. | 0-1
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Problem gambling or ludomania is repetitive gambling behavior despite harm and negative consequences. Problem gambling may be diagnosed as a mental disorder according to DSM-5 if certain diagnostic criteria are met. Pathological gambling is a common disorder that is associated with both social and family costs. The DSM-5 has re-classified the condition as an addictive disorder, with those affected exhibiting many similarities to those who have substance addictions. The term gambling addiction has long been used in the recovery movement. Pathological gambling was long considered by the American Psychiatric Association to be an impulse-control disorder rather than an addiction. However, data suggest a closer relationship between pathological gambling and substance use disorders than exists between PG and obsessive-compulsive disorder, largely because the behaviors in problem gambling and most primary substance use disorders (i.e. those not resulting from a desire to "self-medicate" for another condition such as depression) seek to activate the brains reward mechanisms while the behaviors characterizing obsessive-compulsive disorder are prompted by overactive and misplaced signals from the brains fear mechanisms.Problem gambling is an addictive behavior with a high comorbidity with alcohol problems. A common tendency shared by people who have a gambling addiction is impulsivity. Signs and symptoms
Research by governments in Australia led to a universal definition for that country which appears to be the only research-based definition not to use diagnostic criteria: "Problem gambling is characterized by many difficulties in limiting money and/or time spent on gambling which leads to adverse consequences for the gambler, others, or for the community." | Problem gambling is often associated with increased suicidal ideation and attempts compared to the general population.Early onset of problem gambling may increase lifetime risk of suicide. Both comorbid substance use and comorbid mental disorders increase the risk of suicide in people with problem gambling. A 2010 Australian hospital study found that 17% of suicidal patients admitted to the Alfred Hospitals emergency department were problem gamblers. Mechanisms
Biology
According to the Illinois Institute for Addiction Recovery, evidence indicates that pathological gambling is an addiction similar to chemical addiction. It has been observed that some pathological gamblers have lower levels of norepinephrine than normal gamblers. According to a study conducted by Alec Roy, formerly at the National Institute on Alcohol Abuse and Alcoholism, norepinephrine is secreted under stress, arousal, or thrill, so pathological gamblers gamble to make up for their under-dosage.Studies have compared pathological gamblers to substance addicts, concluding that addicted gamblers display more physical symptoms during withdrawal.Deficiencies in serotonin might also contribute to compulsive behavior, including a gambling addiction. There are three important points discovered after these antidepressant studies:
Antidepressants can reduce pathological gambling in case when there is an effect on serotonergic reuptake inhibitors and 5-HT1/5-HT2 receptor antagonists. Pathological gambling, as the part of obsessive-compulsive disorder, requires the higher doses of antidepressants as is usually required for depressive disorders. | 11
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Flossing daily and using interdental brushes (if the space between teeth is large enough), as well as cleaning behind the last tooth, the third molar, in each quarter
Using an antiseptic mouthwash: Chlorhexidine gluconate-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis. Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve to monitor the persons oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.Clinical trials show that smoking cessation abd dietary improvements improve disease outcomes.Typically, dental hygienists (or dentists) use special instruments to clean (debride) teeth below the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to prevent any further progress of established periodontitis. Studies show that after such a professional cleaning (periodontal debridement), microbial plaque tends to grow back to precleaning levels after about three to four months. Nonetheless, the continued stabilization of a persons periodontal state depends largely, if not primarily, on the persons oral hygiene at home, as well as on the go. Without daily oral hygiene, periodontal disease will not be overcome, especially if the person has a history of extensive periodontal disease. Management
The cornerstone of successful periodontal treatment starts with establishing excellent oral hygiene. This includes twice-daily brushing with daily flossing. Also, the use of an interdental brush is helpful if space between the teeth allows. | (The Time song) (1990)
"Shake" (EliZe song) (2004)
"Shake" (Ying Yang Twins song) (2005)
"Shake" (Jesse McCartney song) (2010)
"Shake" (Little Boots song) (2011)
"Shake" (Flavour Nabania song) (2012)
"Shake" (CNBLUE song) (2017)
"Shake" (1981), by GQ
"Shake" (1993), from the album Concentration by Machines of Loving Grace
"Shake" (1999), by Double
"Shake" (2009), by Chae Yeon
"Shake" (2009), from The Alesha Show: The Encore by Alesha Dixon
"Shake" (2013), by Victoria Justice
"Shake" (2013), from Lets Be Still by The Head and the Heart
Shakin (Eddie Money song)
Shakin (Sawyer Brown song)
"Shakin", a song on the 2000 album Thirteen Tales from Urban Bohemia by The Dandy Warhols
"The Shake" (Kisschasy song)
"The Shake" (Neal McCoy song)
Other
Camera shake, an effect fixed with image stabilization
Shake (company), a legal document startup
Shake (software), an image-compositing package produced by Apple Inc
Shake (unit), an informal unit of time equal to ten nanoseconds
SHAKE algorithm, a time integration algorithm for molecular dynamics simulation
See also
Earthquake
The Shake (disambiguation)
Shake It (disambiguation)
Shaked (surname)
Shaken (disambiguation)
Shaker (disambiguation)
Shakes (disambiguation)
Shock (disambiguation)
Shook (disambiguation)
All pages with titles beginning with Shake
All pages with titles containing Shake | 0-1
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Sens 1981 essay Poverty and Famines: An Essay on Entitlement and Deprivation played a prominent part in forging the new consensus.In 2007 and 2008, rapidly increasing food prices caused a global food crisis. Food riots erupted in several dozen countries; in at least two cases, Haiti and Madagascar, this led to the toppling of governments. A second global food crisis unfolded due to the spike in food prices of late 2010 and early 2011. Fewer food riots occurred, due in part to greater availability of food stock piles for relief. However, several analysts argue the food crisis was one of the causes of the Arab Spring. Efforts since the global 2008 crisis
In the early 21st century, the attention paid to the problem of hunger by the leaders of advanced nations such as those that form the G8 had somewhat subsided. Prior to 2009, large scale efforts to fight hunger were mainly undertaken by governments of the worst affected countries, by civil society actors, and by multilateral and regional organizations. In 2009, Pope Benedict published his third encyclical, Caritas in Veritate, which emphasised the importance of fighting against hunger. The encyclical was intentionally published immediately before the July 2009 G8 Summit to maximise its influence on that event. | Endometritis is inflammation of the inner lining of the uterus (endometrium). Symptoms may include fever, lower abdominal pain, and abnormal vaginal bleeding or discharge. It is the most common cause of infection after childbirth. It is also part of spectrum of diseases that make up pelvic inflammatory disease.Endometritis is divided into acute and chronic forms. The acute form is usually from an infection that passes through the cervix as a result of an abortion, during menstruation, following childbirth, or as a result of douching or placement of an IUD. Risk factors for endometritis following delivery include Caesarean section and prolonged rupture of membranes. Chronic endometritis is more common after menopause. The diagnosis may be confirmed by endometrial biopsy. Ultrasound may be useful to verify that there is no retained tissue within the uterus.Treatment is usually with antibiotics. Recommendations for treatment of endometritis following delivery includes clindamycin with gentamicin. Testing for and treating gonorrhea and chlamydia in those at risk is also recommended. Chronic disease may be treated with doxycycline. Outcomes with treatment are generally good.Rates of endometritis are about 2% following vaginal delivery, 10% following scheduled C-section, and 30% with rupture of membranes before C-section if preventive antibiotics are not used. The term "endomyometritis" may be used when inflammation of the endometrium and the myometrium is present. The condition is also relatively common in other animals such as cows. Symptoms
Symptoms may include fever, lower abdominal pain, and abnormal vaginal bleeding or discharge. Types
Acute endometritis
Acute endometritis is characterized by infection. | 0-1
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Such psychosis (when diagnosed as such), is often considered "premenstrual exacerbation" or "menstrual psychosis", or postpartum psychosis. Childbirth may trigger the disorder in some women. Approximately 1 in 10,000 women experience brief psychotic disorder shortly after childbirth. Diagnosis
The symptoms must not be caused by schizophrenia, schizoaffective disorder, delusional disorder, or mania in bipolar disorder. They must also not be caused by a drug (such as amphetamines) or medical condition (such as a brain tumor). Differential diagnosis
There are general medical causes of brief psychosis that should be considered during evaluation, including postnatal depression, HIV and AIDS, malaria, syphilis, Alzheimers disease, Parkinsons disease, hypoglycaemia (an abnormally low level of glucose in the blood), lupus, multiple sclerosis, brain tumor, SARS-CoV-2 (COVID-19) infection and pediatric autoimmune neuropsychiatric disorders (PANS). Epidemiology
The exact incidence and prevalence of brief psychotic disorder is not known, but it is generally considered uncommon. Internationally, it occurs twice as often in women than men, and even more often in women in the United States. It typically occurs in the late 30s and early 40s. Approximately 1 in 10,000 women experience brief psychotic disorder shortly after childbirth. History
Otto Fenichel noted how such short psychotic breaks were more common in World War II than in World War I, in the wake of traumatic shocks: he considered in such cases that "enough preconscious attention remains to re-establish the contact with reality as soon as it becomes bearable again". BPD in Film/TV/Media
BPD and its symptoms were featured in the Kevin Spacey and Daniel Wu-starring film Inseparable. | S. mansoni was first noted by Theodor Maximillian Bilharz in Egypt in 1851, while discovering S. haematobium. Sir Patrick Manson identified it as unique species in 1902. Louis Westenra Sambon gave the name Schistosomum mansoni in 1907 in honour of Manson. Structure
Adult
Schistosomes, unlike other trematodes, are long and cylindrical worms and are sexually dimorphic. The male S. mansoni is approximately 1 cm long (0.6–1.1 cm) and is 0.1 cm wide. It is white, and it has a funnel-shaped oral sucker at its anterior end followed by a second pediculated ventral sucker. The external part of the worm is composed of a double bilayer, which is continuously renewed as the outer layer, known as the membranocalyx, and is shed continuously. The tegument bears a large number of small tubercules. The suckers have small thorns in their inner part as well as in the buttons around them. The male genital apparatus is composed of 6 to 9 testicular masses, situated dorsally. There is one deferent canal beginning at each testicle, which is connected to a single deferent that dilates into a reservatory, the seminal vesicle, located at the beginning of the gynaecophoric canal. The copula happens through the coaptation of the male and female genital orifices.The female has a cylindrical body, longer and thinner than the males (1.2 to 1.6 cm long by 0.016 cm wide). It has the general appearance of a roundworm. The female parasite is darker, and it looks gray. | 0-1
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Dermatographic urticaria is a skin disorder and one of the most common types of urticaria, affecting 2–5% of the population. Signs and symptoms
The condition manifests as an allergic-like reaction, causing a warm red wheal to appear on the skin. As it is often the result of scratches, involving contact with other materials, it can be confused with an allergic reaction, when in fact it is the act of being scratched that causes a wheal to appear. These wheals are a subset of urticaria (hives), and appear within minutes, in some cases accompanied by itching. The first outbreak of urticaria can lead to other reactions on body parts not directly stimulated, scraped, or scratched. In a normal case, the swelling will decrease without treatment within 15–30 minutes, but, in extreme cases, itchy red welts may last anywhere from a few hours to days. Causes
Symptoms are thought to be the result of histamine being released by mast cells on the surface of the skin. Despite the lack of antigens, histamine causes the skin to swell in affected areas. If the membrane that surrounds the mast cells is too weak it will easily and rapidly break down under physical pressure, which then causes an allergic-like reaction.Symptoms can be caused or induced by:
The underlying cause of dermographism is not known, and it can last for many years without relief. The condition may subside and be effectively cured; however, it is often a lifelong ailment. | It is not a life-threatening disease, and it is not contagious.Dermographism may occur in mastocytosis (systemic mast cell proliferation). Diagnosis
This condition is diagnosed by a health care provider writing or drawing on the patients skin with a tongue depressor or other implement, to see whether a red wheal appears soon afterwards. Treatment
Dermographism can be treated by substances which prevent histamine from causing the reaction (i.e. an antihistamine). These may need to be given as a combination of H1 antagonists, or possibly with an H2-receptor antagonist such as cimetidine. Over-the-counter vitamin C, 1000 mg daily, increases histamine degradation and removal.Refraining from taking hot baths or showers may help if the condition is generalized (i.e. all over), as well as possibly for localized cases (i.e. in a specific area). If taking hot showers helps, it may be a condition called shower eczema. If it affects mainly the head, it may be psoriasis. In rare cases, allergy tests may uncover substances the patient is allergic to.While cromoglycate, which prevents histamine from being released from mast cells, is used topically in rhinitis and asthma, it is not effective orally for treating chronic urticaria. See also
Triple response of Lewis
References
== External links == | 11
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Disopyramide decreases the inhomogeneity between infarcted and normal myocardium refractory periods; in addition to lengthening the refractory period. This decreases the chance of re-entry depolarization, because signals are more likely to encounter tissue in a refractory state which cannot be excited. This provides a possible treatment for atrial and ventricular fibrillation, as it restores pacemaker control of the tissue to the SA and AV nodes. Obstructive hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, occurring in 1:500 individuals in the general population. It is estimated that there are 600,000 individuals in the United States with hypertrophic cardiomyopathy. The most common variant of HCM presents with left ventricular (LV) intracavitary obstruction due to systolic anterior motion of the mitral valve, and mitral-septal contact, diagnosed readily with echocardiography. Pharmacologic treatment with negative inotropic drugs is first-line therapy. Beta-blockers are used first, and while they improve symptoms of shortness of breath, chest pain and exercise intolerance, they do not reduce resting LV intraventricular pressure gradients and often are inadequate to control symptoms. Many investigators and clinicians believe that disopyramide controlled release is the most potent agent available for reducing resting pressure gradients and improving symptoms. Disopyramide has been actively used for more than 30 years. Disopyramide administration for obstructive HCM has a IB recommendation in the 2020 American Heart Association/American College of Cardiology Foundation guidelines for treatment of obstructive HCM. A IB treatment recommendation indicates that a treatment is recommended, and may be useful, and beneficial. | See also
Actisomide
References
External links
Disopyramide on RxList | 11
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Gene therapy
idecabtagene vicleucel (Abecma) – first cell-based gene therapy was approved by FDA in 2021 for the treatment of adults with relapsed or refractory multiple myeloma who have received at least four prior therapies
ciltacabtagene autoleucel (Carvykti) was approved for medical use in the United States in February 2022. Ciltacabtagene autoleucel is indicated for the treatment of adults with relapsed or refractory multiple myeloma after four or more prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monoclonal antibody. Other measures
In addition to direct treatment of the plasma cell proliferation, bisphosphonates (e.g., pamidronate or zoledronic acid) are routinely administered to prevent fractures; they have also been observed to have a direct antitumor effect even in people without known skeletal disease. If needed, red blood cell transfusions or erythropoietin can be used for management of anemia. Side effects
Chemotherapies and stem cell transplants can cause unwanted bleedings and may require platelet transfusions. It was seen that platelet transfusions for people undergoing a chemotherapy or a stem cell transplantation for the prevention of bleeding events had different effects on the number of participants with a bleeding event, the number of days on which a bleeding occurred, the mortality secondary to bleeding and the number of platelet transfusions depending on the way they were used (therapeutic, depending on a threshold, different dose schedules or prophylactic). | Occupancy of the serotonin transporter with vortioxetine in young men was found to be highest in the raphe nucleus with median occupancies of 25%, 53%, and 98% after 9 days of administration with 2.5, 10, and 60 mg/day vortioxetine. In another study, serotonin transporter occupancy in men was 50%, 65%, and ≥80% for 5, 10, and 20 mg/day vortioxetine.Based on its clinical efficacy (e.g., at 5 mg/day), it appears that vortioxetine may produce antidepressant effects at SERT occupancy as low as 50%. This is in apparent contrast to SSRIs and SNRIs, which appear to require a minimum of 70 to 80% occupancy for antidepressant efficacy. These findings are suggestive that the antidepressant effects of vortioxetine may be mediated by serotonin receptor interactions in addition to serotonin reuptake inhibition. A study found no significant occupancy of the 5-HT1A receptor with vortioxetine at 30 mg/day for 9 days, which suggests that at least this specific serotonin receptor may not be involved in the clinical pharmacology of vortioxetine. However, methodological concerns were noted that may limit the interpretability of this result. Occupancy of other serotonin receptors like 5-HT3 and 5-HT7 by vortioxetine in humans does not seem to have been studied. In relation to the preceding, the contribution of serotonin receptor interactions to the antidepressant effects of vortioxetine is unknown and remains to be established. | 0-1
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Signs and symptoms
The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure (ICP). By contrast, chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with Hakims triad (Adams triad).Symptoms of increased ICP may include headaches, vomiting, nausea, papilledema, sleepiness, or coma. With increased levels of CSF, there have been cases of hearing loss due to CSF creating pressure on the auditory pathways or disrupting the communication of inner ear fluid. Elevated ICP of different etiologies have been linked to sensorineural hearing loss (SNHL). Transient SNHL has been reported after the loss of CSF with shunt surgeries. Hearing loss is a rare but well-known sequela of procedures resulting in CSF loss. Elevated ICP may result in uncal or tonsillar herniation, with resulting life-threatening brain stem compression.Hakims triad of gait instability, urinary incontinence, and dementia is a relatively typical manifestation of the distinct entity normal-pressure hydrocephalus. Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located). The symptoms depend on the cause of the blockage, the persons age, and how much brain tissue has been damaged by the swelling.In infants with hydrocephalus, CSF builds up in the central nervous system (CNS), causing the fontanelle (soft spot) to bulge and the head to be larger than expected. | Pharmacology
Mechanism of action (eye drops)
It is a nucleoside analogue, a modified form of deoxyuridine, similar enough to be incorporated into viral DNA replication, but the –CF3 group added to the uracil component blocks base pairing, thus interfering with viral DNA replication. Pharmacokinetics (eye drops)
Trifluridine passes the cornea and is found in the aqueous humour. Systemic absorption is negligible. Pharmacokinetics (oral)
Pharmacokinetic data of oral trifluridine have only been evaluated in combination with tipiracil, which significantly affects biotransformation of the former. At least 57% of trifluridine are absorbed from the gut, and highest blood plasma concentrations are reached after two hours in cancer patients. The substance has no tendency to accumulate in the body. Plasma protein binding is over 96%. Trifluridine is metabolised by the enzyme thymidine phosphorylase to 5-trifluoromethyl-2,4(1H,3H)-pyrimidinedione (FTY), and also by glucuronidation. Elimination half-life is 1.4 hours on the first day and increases to 2.1 hours on the twelfth day. It is mainly excreted via the kidneys.Tipiracil causes Cmax (highest blood plasma concentrations) of trifluridine to increase 22-fold, and its area under the curve 37-fold, by inhibiting thymidine phosphorylase. Chemistry
The substance is a white crystalline powder. It is freely soluble in methanol and acetone; soluble in water, ethanol, 0.01 M hydrochloric acid, and 0.01 M sodium hydroxide; sparingly soluble in isopropyl alcohol and acetonitrile; slightly soluble in diethyl ether; and very slightly soluble in isopropyl ether. References
External links
Costin D, Dogaru M, Popa A, Cijevschi I (2004). "Tratamentul cu trifluridină în infecția oculară herpetică" [Trifluridine therapy in herpetic in keratitis]. | 0-1
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About 70% of survivors show residual neurological deficits, but some survivors have shown surprisingly little deficit considering the magnitude of the white matter affected.This disease has been occasionally associated with ulcerative colitis and Crohns disease, malaria, sepsis associated with immune complex deposition, methanol poisoning, and other underlying conditions. Also anecdotal association with MS has been reportedLaboratory studies that support diagnosis of AHL are: peripheral leukocytosis, cerebrospinal fluid (CSF) pleocytosis associated with normal glucose and increased protein. On magnetic resonance imaging (MRI), lesions of AHL typically show extensive T2-weighted and fluid-attenuated inversion recovery (FLAIR) white matter hyperintensities with areas of hemorrhages, significant edema, and mass effect. Treatment
No controlled clinical trials have been conducted on ADEM treatment, but aggressive treatment aimed at rapidly reducing inflammation of the CNS is standard. The widely accepted first-line treatment is high doses of intravenous corticosteroids, such as methylprednisolone or dexamethasone, followed by 3–6 weeks of gradually lower oral doses of prednisolone. Patients treated with methylprednisolone have shown better outcomes than those treated with dexamethasone. Oral tapers of less than three weeks duration show a higher chance of relapsing, and tend to show poorer outcomes. Other anti-inflammatory and immunosuppressive therapies have been reported to show beneficial effect, such as plasmapheresis, high doses of intravenous immunoglobulin (IVIg), mitoxantrone and cyclophosphamide. | Poorer outcomes are associated with unresponsiveness to steroid therapy, unusually severe neurological symptoms, or sudden onset. Children tend to have more favorable outcomes than adults, and cases presenting without fevers tend to have poorer outcomes. The latter effect may be due to either protective effects of fever, or that diagnosis and treatment is sought more rapidly when fever is present. ADEM can progress to MS. It will be considered MS if some lesions appear in different times and brain areas
Motor deficits
Residual motor deficits are estimated to remain in about 8 to 30% of cases, the range in severity from mild clumsiness to ataxia and hemiparesis. Neurocognitive
Patients with demyelinating illnesses, such as MS, have shown cognitive deficits even when there is minimal physical disability. Research suggests that similar effects are seen after ADEM, but that the deficits are less severe than those seen in MS. A study of six children with ADEM (mean age at presentation 7.7 years) were tested for a range of neurocognitive tests after an average of 3.5 years of recovery. All six children performed in the normal range on most tests, including verbal IQ and performance IQ, but performed at least one standard deviation below age norms in at least one cognitive domain, such as complex attention (one child), short-term memory (one child) and internalizing behaviour/affect (two children). Group means for each cognitive domain were all within one standard deviation of age norms, demonstrating that, as a group, they were normal. | 11
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Galactosemia (British galactosaemia, from Greek γαλακτόζη + αίμα, meaning galactose + blood, accumulation of galactose in blood) is a rare genetic metabolic disorder that affects an individuals ability to metabolize the sugar galactose properly. Galactosemia follows an autosomal recessive mode of inheritance that confers a deficiency in an enzyme responsible for adequate galactose degradation. Friedrich Goppert (1870–1927), a German physician, first described the disease in 1917, with its cause as a defect in galactose metabolism being identified by a group led by Herman Kalckar in 1956. Galactosemia was the second disorder found to be detectable through newborn screening methods by Robert Guthrie.Its incidence is about 1 per 60,000 births for people of European ancestry. In other populations the incidence rate differs. Galactosaemia is about one hundred times more common (1:480 births) in the Irish Traveller population. Symptoms
Adults
Infants
Infants may appear asymptomatic at birth, however, upon ingestion of galactose a few days later (via breast and/or formula feeding), children start to experience life-threatening symptoms, which include:
poor feeding, and weight gain
vomiting and diarrhea
hepatocellular damage
lethargy, and hypotoniaProgression of this acute neonatal toxicity syndrome may include the development of sepsis, cataracts, and even pseudotumor cerebri (which may cause a bulging of fontanelle). Cause
Lactose in food (such as dairy products) is broken down by the enzyme lactase into glucose and galactose. | A galactosemia test is a blood test (from the heel of the infant) or urine test that checks for three enzymes that are needed to change galactose sugar that is found in milk and milk products into glucose, a sugar that the human body uses for energy. A person with galactosemia doesnt have one of these enzymes. This causes high levels of galactose in the blood or urine.Affected children can have serious, irreversible effects or even die within days from birth. It is important that newborns be screened for metabolic disorders without delay. Galactosemia can even be detected through NBS before any ingestion of galactose-containing formula or breast milk. Detection of the disorder through NBS does not depend on protein or lactose ingestion, and, therefore, it should be identified on the first specimen unless the infant has been transfused. A specimen should be taken prior to transfusion. The enzyme is prone to damage if analysis of the sample is delayed or exposed to high temperatures. The routine NBS is accurate for detection of galactosemia. Two screening tests are used to screen infants affected with galactosemia—the Beutlers test and the Hill test. The Beutlers test screens for galactosemia by detecting the level of enzyme of the infant. Therefore, the ingestion of formula or breast milk does not affect the outcome of this part of the NBS, and the NBS is accurate for detecting galactosemia prior to any ingestion of galactose. | 11
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This increase is due in part to a rise in the numbers of older mothers and of multiple births, where preeclampsia occurs more frequently. For example, in 1998 birth rates among women ages 30 to 44 and the number of births to women ages 45 and older were at the highest levels in three decades, according to the National Center for Health Statistics. Furthermore, between 1980 and 1998, rates of twin births increased about 50 percent overall and 1,000 percent among women ages 45 to 49; rates of triplet and other higher-order multiple births jumped more than 400 percent overall, and 1,000 percent among women in their 40s. == References == | Millipede burns are a cutaneous condition caused by some millipedes that secrete a toxic liquid that causes a brownish pigmentation or burn when it comes into contact with the skin. Some millipedes produce quinones in their defensive secretions, which have been reported to cause brown staining of the skin. See also
Centipede bite
Skin lesion
References
== External links == | 0-1
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Other uses
Bupropion is not effective in the treatment of cocaine dependence, but it is showing promise in reducing drug use in light methamphetamine users. Based on studies indicating that bupropion lowers the level of the inflammatory mediator TNF-alpha, there have been suggestions that it might be useful in treating inflammatory bowel disease, psoriasis, and other autoimmune conditions, but very little clinical evidence is available. Bupropion is not effective in treating chronic low back pain. Available forms
Bupropion is available as an oral tablet in a number of different formulations. It is formulated mostly as the hydrochloride salt but also to a lesser extent as the hydrobromide salt. The available forms of bupropion hydrochloride include IR (instant-release) tablets (50, 75, 100 mg), SR (sustained-release) tablets (50, 100, 150, 200 mg), and XL (extended-release) tablets (150, 300, 450 mg). The only marketed form of bupropion hydrobromide is Aplenzin, an extended-release oral tablet (174, 348, 522 mg). In addition to single-drug formulations, bupropion is formulated in combinations including naltrexone/bupropion (Contrave; 8 mg/90 mg extended-release tablets) and dextromethorphan/bupropion (Auvelity; 45 mg/105 mg tablets). Contraindications
The drug label advises that bupropion should not be prescribed to individuals with epilepsy or other conditions that lower the seizure threshold, such as anorexia nervosa, bulimia nervosa, benzodiazepine or alcohol withdrawal. It should be avoided in individuals who are taking monoamine oxidase inhibitors (MAOIs). When switching from MAOIs to bupropion, it is important to include a washout period of about two weeks between the medications. | A study administering ganirelix to healthy adult females (n=15) found the mean (SD) elimination half-life (t1/2) to be 16.2(1.6) hours, volume of distribution/absolute bioavailability (Vd/F) 76.5(10.3) liters, maximum serum concentration (Cmax) 11.2(2.4) ng/mL, and the time until maximum concentration (tmax) 1.1(0.2) hours. One 250 µg injection of ganirelix resulted in a mean absolute bioavailability of 91.1%. Chemistry
Ganirelix is derived from GnRH, with amino acid substitutions made at positions 1, 2, 3, 6, 8, and 10. History
The European Commission gave marketing authorization for ganirelix throughout the European Union to N.V. Organon in May 2000. See also
Gonadotropin-releasing hormone receptor § Antagonists
References
External links
"Ganirelix". Drug Information Portal. U.S. National Library of Medicine. "Ganirelix acetate". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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This process does not require the presence of androgen, nor a functional androgen receptor.Until around the seventh week of development, the embryo has indifferent sex accessory ducts, which consist of two pairs of ducts: the Müllerian ducts and the Wolffian ducts. Sertoli cells within the testes secrete anti-Müllerian hormone around this time to suppress the development of the Müllerian ducts, and cause their degeneration. Without this anti-Müllerian hormone, the Müllerian ducts develop into the female internal genitalia (uterus, cervix, fallopian tubes, and upper vaginal barrel). Unlike the Müllerian ducts, the Wolffian ducts will not continue to develop by default. In the presence of testosterone and functional androgen receptors, the Wolffian ducts develop into the epididymides, vasa deferentia, and seminal vesicles. If the testes fail to secrete testosterone, or the androgen receptors do not function properly, the Wolffian ducts degenerate. Masculinization of the male external genitalia (the penis, penile urethra, and scrotum), as well as the prostate, are dependent on the androgen dihydrotestosterone. Testosterone is converted into dihydrotestosterone by the 5-alpha reductase enzyme. If this enzyme is absent or deficient, then dihydrotestosterone is not created, and the external male genitalia do not develop properly. As is the case with the internal male genitalia, a functional androgen receptor is needed for dihydrotestosterone to regulate the transcription of target genes involved in development. | Moreover, a third of the remaining chronic cases will usually remit during follow-up observation, and another third will end up with only mild thrombocytopenia (defined as a platelet count above 50,000). A number of immune related genes and polymorphisms have been identified as influencing predisposition to ITP, with FCGR3a-V158 allele and KIRDS2/DL2 increasing susceptibility and KIR2DS5 shown to be protective.ITP is usually chronic in adults and the probability of durable remission is 20–40 percent. The male to female ratio in the adult group varies from 1:1.2 to 1.7 in most age ranges (childhood cases are roughly equal for both sexes) and the median age of adults at the diagnosis is 56–60. The ratio between male and female adult cases tends to widen with age. In the United States, the adult chronic population is thought to be approximately 60,000—with women outnumbering men approximately 2 to 1, which has resulted in ITP being designated an orphan disease.The mortality rate due to chronic ITP varies but tends to be higher relative to the general population for any age range. In a study conducted in Great Britain, it was noted that ITP causes an approximately 60 percent higher rate of mortality compared to sex- and age-matched subjects without ITP. This increased risk of death with ITP is largely concentrated in the middle-aged and elderly. Ninety-six percent of reported ITP-related deaths were individuals 45 years or older. No significant difference was noted in the rate of survival between males and females. | 0-1
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Diagnosis requires identifying the mold in the affected tissue by biopsy and confirming it with a fungal culture. Because the causative fungi occur all around, a culture alone is not decisive. Tests may also include culture and direct detection of the fungus in lung fluid, blood, serum, plasma and urine. Blood tests include a complete blood count to look specifically for neutropenia. Other blood tests include iron levels, blood glucose, bicarbonate, and electrolytes. Endoscopic examination of the nasal passages may be needed. Imaging
Imaging is often performed, such as CT scan of lungs and sinuses. Signs on chest CT scans, such as nodules, cavities, halo signs, pleural effusion and wedge-shaped shadows, showing invasion of blood vessels, may suggest a fungal infection, but do not confirm mucormycosis. A reverse halo sign in a person with a blood cancer and low neutrophil count, is highly suggestive of mucormycosis. CT scan images of mucormycosis can be useful to distinguish mucormycosis of the orbit and cellulitis of the orbit, but images may appear identical to those of aspergillosis. MRI may also be useful. Currently (when? ), MRI with gadolinium contrast is the investigation of choice in rhinoorbito cerebral mucormycosis. Culture and biopsy
To confirm the diagnosis, biopsy samples can be cultured. Culture from biopsy samples does not always give a result as the organism is very fragile. To precisely identify the species requires an expert. The appearance of the fungus under the microscope will determine the genus and species. | In anatomy, the precordium or praecordium is the portion of the body over the heart and lower chest.Defined anatomically, it is the area of the anterior chest wall over the heart. It is therefore usually on the left side, except in conditions like dextrocardia, where the individuals heart is on the right side. In such a case, the precordium is on the right side as well. The precordium is naturally a cardiac area of dullness. During examination of the chest, the percussion note will therefore be dull. In fact, this area only gives a resonant percussion note in hyperinflation, emphysema or tension pneumothorax. Precordial chest pain can be an indication of a variety of illnesses, including costochondritis and viral pericarditis. See also
Precordial thump
Precordial examination
Commotio cordis
Hyperdynamic precordium
Precordial catch syndrome
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In vitro studies have found a potential for acid rebound to occur due to antacid overuse, however the significance of this finding has been called into question. Properties of antacids
When an excess amount of acid is produced in the stomach, the natural mucous barrier that protects the lining of the stomach can degrade, leading to pain and irritation. There is also potential for the development of acid reflux, which can cause pain and damage to the esophagus. Antacids contain alkaline ions that chemically neutralize stomach gastric acid, reducing damage to the stomach lining and esophagus, and relieving pain. Some antacids also inhibit pepsin, an enzyme that can damage the esophagus in acid reflux.Antacids do not directly inhibit acid secretion, and thus are distinct from acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors. Antacids do not kill the bacteria Helicobacter pylori, which causes most ulcers. Interactions
Antacids are known to interact with several oral medications, including fluoroquinolone and tetracycline antibiotics, iron, itraconazole, and prednisone. Metal chelation is responsible for some of these interactions (e.g. fluoroquinolones, tetracyclines), leading to decreased absorption of the chelated drug. Some interactions may be due to the pH increase observed in the stomach following antacid ingestion, leading to increased absorption of weak acids, and decreased absorption of weak bases. | Antacids also cause an increase in pH of the urine (alkalization), which may cause increased blood concentrations of weak bases, and increased excretion of weak acids.A proposed method to mitigate the effects of stomach acidity and chelation on drug absorption is to space out the administration of antacids with interacting medications, however this method has not been well studied for drugs affected by urine alkalization.There are concerns regarding interactions between delayed-release tablets and antacids, as antacids may increase the stomach pH to a point at which the coating of the delayed-release tablet will dissolve, leading to degradation of the drug if it is pH sensitive. Formulations
Antacids may be formulated with other active ingredients such as simethicone to control gas, or alginic acid to act as a physical barrier to acid. Liquids
Several liquid antacid preparations are marketed. Common liquid preparations include milk of magnesia and magnesium/aluminum combinations. A potential advantage of using a liquid preparation over a tablet is that liquids may provide quicker relief, however this may coincide with a shorter duration of action. Tablets
Chewable tablets
Chewable tablets are one of the most common forms of antacids, and are readily available over-the-counter. Upon reaching the stomach, the tablet powder will dissolve in the stomach acid, allowing the cations to be released and neutralize excess stomach acid. Common salts available in tablet form include those of calcium, magnesium, aluminum, and sodium.Some common brand are Tums, Gaviscon chewable tablets and Maalox chewable tablets. | 11
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The mean patient age was 62 years in one series (range 18 to 90 years).The mean age varies by etiology category; patients with giant cell arteritis (GCA) are older (mean 78 years, range 50 to 82 years), while those with PION in the setting of spine surgery are younger on average.There is a higher than expected prevalence of atherosclerotic risk factors and comorbid vascular disease, especially in patients with nonarteritic (idiopathic) PION, with 87 percent of patients having at least one risk factor for, or one other manifestation of, atherosclerotic vascular disease. While anterior ischemic optic neuropathy (AION) appears to be more common than PION after cardiac surgery, PION is relatively more common in cases of spine surgery. References
Further reading
Luneau K, Newman NJ, Biousse V (November 2008). "Ischemic optic neuropathies". The Neurologist. 14 (6): 341–54. doi:10.1097/NRL.0b013e318177394b. PMID 19008740. S2CID 8445417. Remigio D, Wertenbaker C (2000). "Post-operative bilateral vision loss". Survey of Ophthalmology. 44 (5): 426–32. doi:10.1016/S0039-6257(00)00107-7. PMID 10734242. Buono LM, Foroozan R, Savino PJ, Danesh-Meyer HV, Stanescu D (June 2003). "Posterior ischemic optic neuropathy after hemodialysis". Ophthalmology. 110 (6): 1216–8. doi:10.1016/S0161-6420(03)00257-4. PMID 12799249. == External links == | Alora may refer to:
Alora (gastropod), a genus of wentletraps in the family Epitoniidae
Alora (drug), a brand name for transdermal Estradiol
Álora, a town in southern Spain | 0-1
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Individuals with this symptom of CBD often lose the ability to speak as the disease progresses. Psychiatric and cognitive disorders
Psychiatric problems associated with CBD often present as a result of the debilitating symptoms of the disease. Prominent psychiatric and cognitive conditions cited in individuals with CBD include dementia, depression, and irritability, with dementia forming a key feature that sometimes leads to the misdiagnosis of CBD as another cognitive disorder such as Alzheimers disease (AD). Frontotemporal dementia can be an early feature. Molecular features
Neuropathological findings associated with CBD include the presence of astrocytic abnormalities within the brain and improper accumulation of the protein tau (referred to as tauopathy). Astroglial inclusions
Postmortem histological examination of the brains of individuals diagnosed with CBD reveal unique characteristics involving the astrocytes in localized regions. The typical procedure used in the identification of these astroglial inclusions is the Gallyas-Braak staining method. This process involves exposing tissue samples to a silver staining material which marks for abnormalities in the tau protein and astroglial inclusions. Astroglial inclusions in CBD are identified as astrocytic plaques, which present as annularly displays of blurry outgrowths from the astrocyte. A recent study indicated that produces a high density of astrocytic plaques in the anterior portion of the frontal lobe and in the premotor area of the cerebral cortex. Tauopathy
The protein tau is an important microtubule-associated protein (MAP), and is typically found in neuronal axons. However, malfunctioning of the development of the protein can result in unnatural, high-level expression in astrocytes and glial cells. | Hot tub folliculitis (pseudomonal folliculitis) is a common type of folliculitis, a condition which causes inflammation of hair follicles. : 272 This condition is caused by an infection of hair follicles by a non-pathogenic strain of the bacterium Pseudomonas aeruginosa. The bacterium is commonly found in hot tubs, water slides, and rarely in swimming pools. Children are more prone because they typically stay in the water longer than adults. Hot tub folliculitis appears on the skin in the form of a rash, roughly resembling chicken pox and then develops further to appear as a pimple. Hot tub folliculitis can be extremely painful and/or itchy, and left alone without scratching will go away much more quickly. If the rash is aggravated, it can stay, worsen, and spread, lasting for months. By that time, it is much more difficult to treat. In an immunocompetent person, the rash is self-limited and will usually resolve after about 7 to 10 days but the condition can leave a hyperpigmented lesion that goes away after a few months.Normally, the rash does not need specific treatment and will go away on its own. Antibiotics may be prescribed in some cases. If the rash continues to appear longer than the 7- to 10-day time period, a physician should be consulted. Folliculitis that is not treated properly could worsen and cause abscesses. See also
Skin lesion
== References == | 0-1
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A common complication of the surgery is hemorrhage and the loss of blood. There is also the possibility of the hemangioma reoccurring after its removal. Additionally, the risk of a stroke or death is also possible.Treatments for cerebral cavernous hemangiomas include radiosurgery or microsurgery. The treatment approach depends on the site, size and symptoms present, as well as the history of hemorrhage from the lesion. Microsurgery is generally preferred if the cerebral cavernous hemangioma is superficial in the central nervous system, or the risk of damage to surrounding tissue from irradiation is too high. Additionally, a large hemorrhage with deterioration of the patient or intractable symptoms (such as seizures or coma) are further indications for microsurgical intervention. Gamma-knife radiation is the favored mechanism of radiosurgery. It provides a precise radiation dose to the cerebral cavernous hemangioma while relatively sparing the surrounding tissue. These treatment approaches for cavernous hemangiomas in other regions of the body have limited research. Prognosis
A few studies have worked on providing details related to the outlook of disease progression. Two studies show that each year 0.5% of people who have never had bleeding from their brain cavernoma, but had symptoms of seizures, were affected by bleeding. In contrast, patients who have had bleeding from their brain cavernoma in the past had a higher risk of being affected by subsequent bleeding. The statistics for this are very broad, ranging from 4–23% a year. | Systemic therapies include itraconazole (200 mg daily for seven days) and fluconazole (150 to 300 mg weekly dose for 2 to 4 weeks) that are preferred to oral ketoconazole which is no longer approved due to its potential hepatotoxic sides effects. The single-dose regimens and pulse therapy regimens can be made more effective by having the patient exercise 1–2 hours after the dose, to induce sweating. The sweat is allowed to evaporate, and showering is delayed for a day, leaving a film of the medication on the skin. Epidemiology
This skin disease commonly affects adolescents and young adults, especially in warm and humid climates. The yeast is thought to feed on skin oils (lipids), as well as dead skin cells. Infections are more common in people who have seborrheic dermatitis, dandruff, and hyperhidrosis. References
External links
Media related to Tinea versicolor at Wikimedia Commons | 0-1
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This is associated with the development of dyspnea, fever, weight gain, peripheral edema and is treated with dexamethasone. The etiology of retinoic acid syndrome has been attributed to capillary leak syndrome from cytokine release from the differentiating promyelocytes.The monoclonal antibody, gemtuzumab ozogamicin, has been used successfully as a treatment for APL, although it has been withdrawn from the US market due to concerns regarding potential toxicity of the drug and it is not currently marketed in Australia, Canada or the UK. Given in conjunction with ATRA, it produces a response in around 84% of patients with APL, which is comparable to the rate seen in patients treated with ATRA and anthracycline-based therapy. It produces less cardiotoxicity than anthracycline-based treatments and hence may be preferable in these patients. Maintenance therapy
After stable remission was induced, the standard of care previously was to undergo 2 years of maintenance chemotherapy with methotrexate, mercaptopurine and ATRA. A significant portion of patients relapsed without consolidation therapy. In the 2000 European APL study, the 2-year relapse rate for those that did not receive consolidation chemotherapy (ATRA not included) therapy was 27% compared to 11% in those that did receive consolidation therapy (p<0.01). Likewise in the 2000 US APL study, the survival rates in those receiving ATRA maintenance was 61% compared to just 36% without ATRA maintenance.However, recent research on consolidation therapy following ATRA-ATO, which became the standard treatment in 2013, has found that maintenance therapy in low-risk patients following this therapy may be unnecessary, although this is controversial. | Most deaths following remission are from other causes, such as second malignancies, which in one study occurred in 8% of patients. In this study, second malignancies accounted for 41% of deaths, and heart disease, 29%. Survival rates were 88% at 6.3 years and 82% at 7.9 years.In another study, 10-year survival rate was estimated to be approximately 77%. Epidemiology
Acute promyelocytic leukemia represents 10–12% of AML cases. The median age is approximately 30–40 years, which is considerably younger than the other subtypes of AML (70 years), however in elderly population APL has peculiar characteristics. Incidence is higher among individuals of Latin American or South European origin. It can also occur as a secondary malignancy in those that receive treatment with topoisomerase II inhibitors (such as the anthracyclines and etoposide) due to the carcinogenic effects of these agents, with patients with breast cancer representing the majority of such patients. Around 40% of patients with APL also have a chromosomal abnormality such as trisomy 8 or isochromosome 17 which do not appear to impact on long-term outcomes. References
External links
Sanz, Miguel A.; Grimwade, David; Tallman, Martin S.; Lowenberg, Bob; Fenaux, Pierre; Estey, Elihu H.; Naoe, Tomoki; Lengfelder, Eva; Büchner, Thomas; Döhner, Hartmut; Burnett, Alan K.; Lo-Coco, Francesco (2009). "Management of acute promyelocytic leukemia: Recommendations from an expert panel on behalf of the European Leukemia Net". Blood. 113 (9): 1875–1891. doi:10.1182/blood-2008-04-150250. hdl:1765/18239. PMID 18812465. PDQ Adult Treatment Editorial Board (2002–2020). "Adult Acute Myeloid Leukemia Treatment (PDQ®): Patient Version". Adult Acute Myeloid Leukemia Treatment (PDQ®). National Cancer Institute (US). PMID 26389377. | 11
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Lymphangioleiomyomatosis (LAM) is a rare, progressive and systemic disease that typically results in cystic lung destruction. It predominantly affects women, especially during childbearing years. The term sporadic LAM is used for patients with LAM not associated with tuberous sclerosis complex (TSC), while TSC-LAM refers to LAM that is associated with TSC. Signs and symptoms
The average age of onset is the early to mid 30s. Exertional dyspnea (shortness of breath) and spontaneous pneumothorax (lung collapse) have been reported as the initial presentation of the disease in 49% and 46% of patients, respectively.Diagnosis is typically delayed 5 to 6 years. The condition is often misdiagnosed as asthma or chronic obstructive pulmonary disease. The first pneumothorax, or lung collapse, precedes the diagnosis of LAM in 82% of patients. The consensus clinical definition of LAM includes multiple symptoms:
Fatigue
Cough
Coughing up blood (rarely massive)
Chest pain
Chylous complications arising from lymphatic obstruction, including
Chylothorax
Chylous ascites
Chylopericardium
Chyloptysis
Chyluria
Chyle in vaginal discharge
Chyle in stool. Angiomyolipomas (fatty kidney tumors) are present in about 30% of patients with sporadic LAM and up to 90% of patients with TSC-LAM. Angiomyolipomas can sometimes spontaneously bleed, causing pain or low blood pressure. Cystic lymphangiomas or lymph nodes with hypodense centers, which mimic necrotizing lymphomas, ovarian or renal cancers, or other malignancies can occur in the retroperitoneum, pelvis or mediastinum.Lung destruction in LAM is a consequence of diffuse infiltration by neoplastic smooth muscle-like cells that invade all lung structures including the lymphatics, airway walls, blood vessels and interstitial spaces. | Tolmetin is a nonsteroidal anti-inflammatory drug (NSAID) of the heterocyclic acetic acid derivative class. It is used primarily to reduce hormones that cause pain, swelling, tenderness, and stiffness in conditions such as osteoarthritis and rheumatoid arthritis, including juvenile rheumatoid arthritis. In the United States it is marketed as Tolectin and comes as a tablet or capsule. Clinical trials
Tolmetin is applicable in the treatment of rheumatoid arthritis, osteoarthrosis, pain, and ankylosing spondylitis. Mechanism of action
Although the mechanism of action of tolmetin is unknown, research involving humans and animals has shown that tolmetin does not achieve anti-inflammatory response by stimulation of the adrenal or pituitary gland, but it has shown tolmetin restrains prostaglandin synthetase in vitro and reduces plasma levels of prostaglandin E, possibly causing the anti-inflammatory response. When tested in rats, tolmetin prevented experimentally stimulated polyarthritis and reduced inflammation. In patients with rheumatoid arthritis or osteoarthritis tolmetin restrained disease activity as efficiently as aspirin and indometacin, although the occurrence of mild gastrointestinal adverse effects and tinnitus was lower in patients treated with tolmetin than it was with aspirin-treated patients and the occurrence of adverse effects of the central nervous system was lower with tolmetin than it was with indometacin. Side effects
Tolmetin can increase the risk of heart or circulatory conditions such as heart attacks and strokes. It should not be taken shortly before or after coronary artery bypass surgery. Tolmetin can also increase the risk of gastrointestinal conditions such as perforation or bleeding, which is fatal. | 0-1
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Colorectal cancer diagnosed in a person with one or more first-degree relative with colorectal cancer or Lynch syndrome associated tumour diagnosed under age 50
5. Person with colorectal cancer and two or more first- or second-degree relatives with colorectal cancer or Lynch syndrome associated cancer diagnosed at any age.It is important to note that these clinical criteria can be difficult to use in practice and clinical criteria used alone misses between 12 and 68 percent of Lynch syndrome cases. Surgery
Prophylactic hysterectomy and salpingo-oophorectomy (removal of the uterus, Fallopian tubes, and ovaries to prevent cancer from developing) can be performed before ovarian or endometrial cancer develops. Treatment
Surgery remains the front-line therapy for HNPCC. Patients with Lynch syndrome who develop colorectal cancer may be treated with either a partial colectomy or total colectomy with ileorectal anastomosis. Due to increased risk of colorectal cancer following partial colectomy and similar quality of life after both surgeries, a total colectomy may be a preferred treatment for HNPCC, especially in younger patients.There is an ongoing controversy over the benefit of 5-fluorouracil-based adjuvant therapies for HNPCC-related colorectal tumours, particularly those in stages I and II. Anti-PD-1 antibody therapy can be effective.Checkpoint blockade with anti-PD-1 therapy is now preferred first line therapy for advanced Microsatellite-Instability–High colorectal cancer. Epidemiology
Though the exact prevalence of Lynch syndrome-causing mutations in the general population remain unknown, recent studies estimate the prevalence to be 1 in 279 individuals, or 0.35%. | Purple glove syndrome (PGS) is a poorly understood skin disease in which the extremities become swollen, discoloured and painful. PGS is potentially serious, and may require amputation. PGS is most common among elderly patients and those receiving multiple large intravenous doses of the epilepsy drug phenytoin. Compartment syndrome is a complication of PGS. Cause
Purple glove syndrome is caused by the intravenous anticonvulsant phenytoin. This medication has many already established neurological side effects, however glove syndrome is a rare, but very serious adverse effect that may lead to limb amputations. This may occur due to the administration of phenytoin with or without extravasation. The defining characteristic is a purplish to black discoloration of the extremity followed by peripheral edema and pain distal to the site of infusion. Onset is generally seen within the first few hours of administration. The true pathology of purple glove syndrome is not fully elucidated, however it is believed to be due to the crystallization of phenytoin within the blood and extravasates into the surrounding interstitium. Another mechanism may be due to the disruption of endothelial transcellular junctions followed by leaking of phenytoin into the surround soft tissues. Diagnosis
Treatment
Doctors recommend discontinuing the use of phenytoin. The application of heat can help to relieve pain. Oral phenytoin can also result in development of purple glove syndrome. References
External links
FDA: Potential Signals of Serious Risks/New Safety Information Identified by the Adverse Event Reporting System (AERS) -- January - March 2008 | 0-1
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More than 25 squamous epithelial cells at low power magnification exam under the microscope strongly suggest salivary contamination. Sputum samples have been used to quantify the degree of airway inflammation in human diseases such as asthma. Specifically, this work has demonstrated that a subgroup of severe asthma patients has airway inflammation that is resistant to treatment with corticosteroids.When a sputum specimen is plated out in microbiology, it is best to get the portion of the sample that almost looks like yellow pus onto the swab. If there is any blood in the sputum, this should also be on the swab. Microbiological sputum samples are used to look for infections, such as Moraxella catarrhalis, Mycobacterium tuberculosis, Streptococcus pneumoniae, and Haemophilus influenzae. Other pathogens can also be found. Purulent sputum contains pus, composed of white blood cells, cellular debris, dead tissue, serous fluid, and viscous liquid (mucus). Purulent sputum is typically yellow or green. It is seen in cases of pneumonia, bronchiectasis, lung abscess, or an advanced stage of bronchitis. Interpretation
Sputum can be (when examined by the naked eye):
Bloody (hemoptysis)
Blood-streaked sputum –an indicator of possible inflammation of the throat (larynx and/or trachea) or bronchi; lung cancer; other bleeding erosions, ulcers, or tumors of the lower airway. Pink sputum – it indicates sputum evenly mixed with blood from alveoli and/or small peripheral bronchi as is seen in potential pulmonary edema. Massive blood – an indicator of possible cavitary tuberculosis or tumor such as lung cancer, or lung abscess; bronchiectasis; lung infarction; pulmonary embolism. | Red, jelly-like sputum - an indicator of possible pneumonia caused by Klebsiella. Green or greenish colored - indicative of potential longstanding respiratory infection (green from degenerative changes in cell debris) as in pneumonia, ruptured lung abscess, chronic infectious bronchitis, and infected bronchiectasis or cystic fibrosis. Rust colored – usually caused by pneumococcal bacteria (in pneumonia), pulmonary embolism, lung cancer or pulmonary tuberculosis. Brownish –potential indicator of chronic bronchitis (greenish/yellowish/brown); chronic pneumonia (whitish-brown); tuberculosis; lung cancer. Yellow, yellowish purulent – an indicator of the sample containing pus. "The sputum color of patients with acute cough and no underlying chronic lung disease does not imply therapeutic consequences such as prescription of antibiotics." The color can provide hints as to effective treatment in chronic bronchitis patients:A yellow-greenish (mucopurulent) color suggests that treatment with antibiotics can reduce symptoms. The green color is caused by degenerating neutrophil verdoperoxidase. Whitish gray sputum color against a white color background (such as a white sink surface) tends to indicate either a specimen from someone who is dehydrated, and/or from an older person, and/or a specimen with a mixed, modest number of eosinophils and maybe some acute inflammatory neutrophil cells (this last choice tends to suggest chronic allergic bronchitis). A white, milky, or opaque (mucoid) appearance means that antibiotics are less likely to be effective in treatment because the likelihood is greater of a viral infection or allergy (even asthma...thick sputum) than of antibiotic-responsive micro-organisms. Foamy white – may come from earlier-phase pulmonary edema. Frothy pink – may indicate more severe pulmonary edema. | 11
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By 1954, it was found that the mutant hemoglobin was highly prevalent in West Africa. In 1960, Vernon Ingram and J. A. Hunt at the University of Cambridge discovered that the mutation was a single amino acid replacement of glutamic acid with lysine. References
External links
Hemoglobin+C at the US National Library of Medicine Medical Subject Headings (MeSH)
Hemoglobin+C+Disease at the US National Library of Medicine Medical Subject Headings (MeSH) | There is very low quality evidence indicating that doxycycline use may be associated with an increased risk of indigestion, photosensitivity, vomiting, and yeast infections, when compared with mefloquine and atovaquone-proguanil. Causal prophylaxis
Causal prophylactics target not only the blood stages of malaria, but the initial liver stage as well. This means that the user can stop taking the drug seven days after leaving the area of risk. Malarone and primaquine are the only causal prophylactics in current use. Regimens
Specific regimens are recommended by the WHO, UK HPA and CDC for prevention of P. falciparum infection. HPA and WHO advice are broadly in line with each other (although there are some differences). CDC guidance frequently contradicts HPA and WHO guidance. These regimens include:
doxycycline 100 mg once daily (started one day before travel, and continued for four weeks after returning);
mefloquine 250 mg once weekly (started two-and-a-half weeks before travel, and continued for four weeks after returning);
atovaquone/proguanil (Malarone) 1 tablet daily (started one day before travel, and continued for 1 week after returning). Can also be used for therapy in some cases.In areas where chloroquine remains effective:
chloroquine 300 mg once weekly, and proguanil 200 mg once daily (started one week before travel, and continued for four weeks after returning);
hydroxychloroquine 400 mg once weekly (started one to two weeks before travel and continued for four weeks after returning)What regimen is appropriate depends on the person who is to take the medication as well as the country or region travelled to. | 0-1
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Unconsciousness, such as due to the ingestion of excessive doses of central depressants like alcohol or opioids, can result in ischemia of the extremities due to unusual body positions that prevent normal circulation
Pathophysiology
Ischemia results in tissue damage in a process known as ischemic cascade. The damage is the result of the build-up of metabolic waste products, inability to maintain cell membranes, mitochondrial damage, and eventual leakage of autolyzing proteolytic enzymes into the cell and surrounding tissues. Restoration of blood supply to ischemic tissues can cause additional damage known as reperfusion injury that can be more damaging than the initial ischemia. Reintroduction of blood flow brings oxygen back to the tissues, causing a greater production of free radicals and reactive oxygen species that damage cells. It also brings more calcium ions to the tissues causing further calcium overloading and can result in potentially fatal cardiac arrhythmias and also accelerates cellular self-destruction. The restored blood flow also exaggerates the inflammation response of damaged tissues, causing white blood cells to destroy damaged cells that may otherwise still be viable. Treatment
Early treatment is essential to keep the affected organ viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularization, or partial amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. | Alfentanil (R-39209, trade name Alfenta, Rapifen in Australia) is a potent but short-acting synthetic opioid analgesic drug, used for anaesthesia in surgery. It is an analogue of fentanyl with around one-fourth to one-tenth the potency, one-third the duration of action, and an onset of action four times faster than that of fentanyl. Alfentanil has a pKa of approximately 6.5, which leads to a very high proportion of the drug being uncharged at physiologic pH, a characteristic responsible for its rapid onset. It is an agonist at mu opioid receptors. While alfentanil tends to cause fewer cardiovascular complications than other similar drugs such as fentanyl and remifentanil, it tends to give stronger respiratory depression and so requires careful monitoring of breathing and vital signs. Almost exclusively used by anesthesia providers during portions of a case where quick, fast-acting (though not long-lasting) pain control is needed (as, for example, during nerve blocks), alfentanil is administered by the parenteral (injected) route for fast onset and precise control of dosage. Discovered at Janssen Pharmaceutica in 1976, alfentanil is classified as a Schedule II drug in the United States.Side effects of fentanyl analogs are similar to those of fentanyl itself and include itching, nausea and potentially life-threatening respiratory depression. Fentanyl analogs have killed hundreds of people throughout Europe and the former Soviet republics since the most recent resurgence in use began in Estonia in the early 2000s, and novel derivatives continue to appear. References
External links
Medline Plus Patient Information - 09/01/2010
https://www.fda.gov/Drugs/DevelopmentApprovalProcess/DevelopmentResources/DrugInteractionsLabeling/ucm093664.htm February 2017
Genf interaction table- https://www.hug.ch/sites/interhug/files/structures/pharmacologie_et_toxicologie_cliniques/carte_cytochromes_2016_final.pdf February 2017 | 0-1
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Trigeminal neuralgia (TN or TGN), also called Fothergill Disease, Tic Douloureux, or Trifacial Neuralgia is a long-term pain disorder that affects the trigeminal nerve, the nerve responsible for sensation in the face and motor functions such as biting and chewing. It is a form of neuropathic pain. There are two main types: typical and atypical trigeminal neuralgia. The typical form results in episodes of severe, sudden, shock-like pain in one side of the face that lasts for seconds to a few minutes. Groups of these episodes can occur over a few hours. The atypical form results in a constant burning pain that is less severe. Episodes may be triggered by any touch to the face. Both forms may occur in the same person. It is regarded as one of the most painful disorders known to medicine, and often results in depression.The exact cause is unknown, but believed to involve loss of the myelin of the trigeminal nerve. This might occur due to compression from a blood vessel as the nerve exits the brain stem, multiple sclerosis, stroke, or trauma. Less common causes include a tumor or arteriovenous malformation. It is a type of nerve pain. Diagnosis is typically based on the symptoms, after ruling out other possible causes such as postherpetic neuralgia.Treatment includes medication or surgery. The anticonvulsant carbamazepine or oxcarbazepine is usually the initial treatment, and is effective in about 90% of people. Side effects are frequently experienced that necessitate drug withdrawal in as many as 23% of patients. | Ocular melanosis (OM) is a blue-gray and/or brown lesion of the conjunctiva that can be separated into benign conjunctival epithelial melanosis (BCEM) and primary acquired melanosis (PAM), of which the latter is considered a risk factor for uveal melanoma. The disease is caused by an increase of melanocytes in the iris, choroid, and surrounding structures. Overproduction of pigment by these cells can block the trabecular meshwork through which fluid drains from the eye. The increased fluid in the eye leads to increased pressure, which can lead to glaucoma. In humans, this is sometimes known as pigment dispersion syndrome. Benign Conjunctival Epithelial Melanosis
BCEM, also referred to as conjunctival hypermelanosis, complexion-associated melanosis, or racial melanosis, is a non-cancerous lesion of the conjunctiva that is more commonly found in dark-skinned individuals (over 90% of lesions are found in black persons and around 5% in white persons). It is due to excess production of melanin in the setting of a normal number of melanocytes in the conjunctiva. It appears very early in life and the pattern does not seem to change upon reaching adulthood. There can be asymmetrical involvement of the eyes, and lesions are usually described as flat, brown, and patchy areas of pigmentation. Primary Acquired Melanosis
PAM is a potentially cancerous lesion of the conjunctiva, which has a higher risk of transforming into a malignant melanoma in white persons. Nearly 75% of all melanomas that arise from the conjunctiva have been found to have occurred in the setting of PAM. | 0-1
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One-day cricket
an abbreviated form of the game, with just one innings per team, usually with a limited number of overs and played over one day. One Day International (ODI)
a match between two national sides limited to 50 overs per innings, played over at most one day. One down
a batsman who bats at No. 3 i.e. when the team is "down by one wicket", a crucial position in the teams batting innings. One short
when a batsman fails to make contact with the ground beyond the popping crease, and turns back for an additional run. Opener
1. an opening batsman
2. an opening bowler
Opening batsman
One of the two batsmen who are in at the start of the innings. They must face the opening bowlers and new ball, so require good defensive technique to avoid getting out, especially in a timed match. In a limited overs match an opening batsman must also score quickly during the power play. Opening bowler
One of the two bowlers who begin the innings using the new ball. They are usually the fastest or most aggressive bowlers in the side. Opposite number
A player on the other team who plays the same role. Often used for captains and wicket keepers. Orthodox
1. shots played in the accepted "textbook" manner, and batsmen who play in this manner. 2. see left-arm orthodox spin. Out
1. the state of a batsman who has been dismissed. | Dead bat
A defensive shot with the bat held in a loose grip and/or angled towards the ground. If the ball strikes the bat it loses momentum and falls quickly to the ground. Used to reduce the chance of being caught off an edge. Dead rubber
A match played in a series after one side has gained an unassailable lead, e.g. has already won 3 matches in a 5-match series, or in a tournament if both teams have already qualified (or failed to qualify) for the subsequent rounds. The term is used disparagingly to imply that the match is of lesser importance, but some regard the concept as outdated. Death bowler
A bowler who specialises in delivering the death overs at the end of a limited overs match. Because batsmen usually play very aggressively in this period, a death bowler must be particularly skilled at variations which are difficult to score from and/or unexpected by the batsman, such as yorkers and slower balls. Death overs
(or slog overs)
The final few overs of an innings in a limited overs match. Because only runs matter in determining the result, a batting side with wickets in hand will bat very aggressively in this period, seeking to hit every delivery for a boundary, even if it risks a dismissal. Typically the batting strike rate is highest in this period, and the bowlers economy is poorest. Death rattle
The sound of the ball breaking the wicket when a batsman is out bowled. Debenture
a certificate of loan agreement, used by some professional clubs to raise funding. | 11
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Generally, stopping antipsychotics for people with dementia does not cause problems, even in those who have been on them a long time.N-methyl-D-aspartate (NMDA) receptor blockers such as memantine may be of benefit but the evidence is less conclusive than for AChEIs. Due to their differing mechanisms of action memantine and acetylcholinesterase inhibitors can be used in combination however the benefit is slight.An extract of Ginkgo biloba known as EGb 761 has been widely used for treating mild to moderate dementia and other neuropsychiatric disorders. Its use is approved throughout Europe. The World Federation of Biological Psychiatry guidelines lists EGb 761 with the same weight of evidence (level B) given to acetylcholinesterase inhibitors, and mementine. EGb 761 is the only one that showed improvement of symptoms in both AD and vascular dementia. EGb 761 is seen as being able to play an important role either on its own or as an add-on particularly when other therapies prove ineffective. EGb 761 is seen to be neuroprotective; it is a free radical scavenger, improves mitochondrial function, and modulates serotonin and dopamine levels. Many studies of its use in mild to moderate dementia have shown it to significantly improve cognitive function, activities of daily living, neuropsychiatric symptoms, and quality of life. However, its use has not been shown to prevent the progression of dementia.While depression is frequently associated with dementia, the use of antidepressants such as selective serotonin reuptake inhibitors (SSRIs) do not appear to affect outcomes. | The bacteria invade nerve tissue in the brain, increasing the permeability of the blood–brain barrier and promoting the onset of Alzheimers. Individuals with a plethora of tooth plaque risk cognitive decline. Poor oral hygiene can have an adverse effect on speech and nutrition, causing general and cognitive health decline. Oral viruses
Herpes simplex virus (HSV) has been found in more than 70% of those aged over 50. HSV persists in the peripheral nervous system and can be triggered by stress, illness or fatigue. High proportions of viral-associated proteins in amyloid plaques or neurofibrillary tangles (NFTs) confirm the involvement of HSV-1 in Alzheimers disease pathology. NFTs are known as the primary marker of Alzheimers disease. HSV-1 produces the main components of NFTs. Diet
Diet is seen to be a modifiable risk factor for the development of dementia. Thiamine deficiency is identified to increase the risk of Alzheimers disease in adults. The role of thiamine in brain physiology is unique and essential for the normal cognitive function of older people. Many dietary choices of the elderly population, including the higher intake of gluten-free products, compromise the intake of thiamine as these products are not fortified with thiamine.The Mediterranean and DASH diets are both associated with less cognitive decline. A different approach has been to incorporate elements of both of these diets into one known as the MIND diet. These diets are generally low in saturated fats while providing a good source of carbohydrates, mainly those that help stabilize blood sugar and insulin levels. | 11
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They are more rigid, demonstrating sharp edges, fractures, and broken-off ends.Waxy casts are broad casts, which is a more general term to describe the wider cast product of a dilated duct. It is seen in chronic kidney failure. In nephrotic syndrome many additional types of cast exist including broad and waxy casts if the condition is chronic (this is referred to as a telescopic urine with the presence of many casts). Fatty casts
Formed by the breakdown of lipid-rich epithelial cells, these are hyaline casts with fat globule inclusions, yellowish-tan in color. If cholesterol or cholesterol esters are present, they are associated with the "Maltese cross" sign under polarized light. They are pathognomonic for high urinary protein nephrotic syndrome. Pigment casts
Formed by the adhesion of metabolic breakdown products or drug pigments, these casts are so named due to their discoloration. Pigments include those produced endogenously, such as hemoglobin in hemolytic anemia, myoglobin in rhabdomyolysis, and bilirubin in liver disease. Drug pigments, such as phenazopyridine, may also cause cast discoloration. Crystal casts
Though crystallized urinary solutes, such as oxalates, urates, or sulfonamides, may become enmeshed within a ketanaline cast during its formation, the clinical significance of this occurrence is not felt to be great. Cellular casts
Red blood cell casts
The presence of red blood cells within the cast is always pathological and is strongly indicative of granulomatosis with polyangiitis, systemic lupus erythematosus, post-streptococcal glomerulonephritis, or Goodpastures syndrome. They can also be associated with renal infarction and subacute bacterial endocarditis. | Clinical trial number NCT03070392 for "Safety and Efficacy of IMCgp100 Versus Investigator Choice in Advanced Uveal Melanoma" at ClinicalTrials.gov | 0-1
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In the 1990s, the National Institute of Mental Health (NIMH) found that up to 7% of adolescents who develop major depressive disorder may commit suicide as young adults. Such statistics demonstrate the importance of interventions by family and friends, the importance of early diagnosis, and treatment by medical staff, in order to prevent suicide amongst at-risk youth. However, some data showed an opposite conclusion. Most depression symptoms are reported more frequently by females; such as sadness (reported by 85.1% of women and 54.3% of men) and crying (approximately 63.4% of women and 42.9% of men). Women have a higher probability to experience depression than men with the prevalences of 19.2% and 13.5% respectively. Risk factor
Risk factors for adolescent depression include female sex, a family history of depression, a personal history of trauma, family conflict, minority sexual orientation, or having a chronic medical illness. There tends to be higher prevalence rates and more severe symptoms in adolescent girls when compared to adolescent boys. These higher rates are also applicable in older adolescents when compared to younger adolescents. This may be due to hormonal fluctuations may that make adolescent women to be more vulnerable to depression. The fact that increased prevalence of depression correlates with hormonal changes in women, particularly during puberty, suggests that female hormones may be a trigger for depression. The gender gap in depression between adolescent men and women is mostly due to young womens lower levels of positive thinking, need for approval, and self-focusing negative conditions. | Sebaceoma (also known as a "sebaceous epithelioma") is a cutaneous condition that appears as a yellow or orange papule. : 662
See also
Sebaceous carcinoma
Sebaceous adenoma
Skin lesion
== References == | 0-1
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Fexinidazole is a medication used to treat African trypanosomiasis (sleeping sickness) caused by Trypanosoma brucei gambiense. It is effective against both first and second stage disease. Some evidence also supports its use in Chagas disease. It is taken by mouth.Common side effects include nausea, vomiting, headache, and trouble sleeping. Other side effects may include QT prolongation, psychosis, and low white blood cells. It is unclear if use during pregnancy or breast feeding is safe. Fexinidazole is in the antiparasitic and the nitroimidazole family of medications. It is believed to work by turning on certain enzymes within the parasites that result in their death.Fexinidazole was first described in 1978. It was given a positive opinion by the European Medicines Agency in 2018. It is on the World Health Organizations List of Essential Medicines. Development for sleeping sickness was funded by the Drugs for Neglected Diseases initiative in collaboration with Sanofi. Fexinidazole was approved for medical use in the United States in July 2021. Medical use
Sleeping sickness
A trial in Africa found fexinidazole to be 91% effective at treating sleeping sickness. Though less effective than nifurtimox with eflornithine in severe disease, fexinidazole has the benefit that it can be taken by mouth.Fexinidazole is the first drug candidate for the treatment of advanced-stage sleeping sickness in thirty years. Other
It has activity against Trypanosoma cruzi, Tritrichomonas foetus, Trichomonas vaginalis, Entamoeba histolytica, and Trypanosoma brucei. It has not been found to be useful for visceral leishmaniasis. Mechanism of action
The biologically relevant active metabolites in vivo are the sulfoxide and sulfone. | Some scientists speculate that some forms of essential myoclonus may be a type of epilepsy with no known cause. Juvenile myoclonic epilepsy (JME) usually consists of jerking and muscle twitches of the upper extremities. This may include the arms, shoulders, elbows, and very rarely, the legs. JME is among the most common types of epilepsy and can affect one of every 14 people with the disease. These seizures typically occur shortly after waking up. Onset for JME can be seen around puberty for most patients. Administration of medications that also treat multiple seizure types is usually the most effective form of treatment. Lennox-Gastaut syndrome (LGS), or childhood epileptic encephalopathy, is a rare epileptic disorder accounting for 1–4% of childhood epilepsies. The syndrome has much more severe symptoms ranging from multiple seizures daily, learning disabilities, abnormal findings in electroencephalogram (EEG). Earlier age of seizure onset is correlated with higher risk of cognitive impairment. Progressive myoclonus epilepsy (PME) is a group of diseases characterized by myoclonus, epileptic seizures, tonic-clonic seizures, and other serious symptoms such as trouble walking or speaking. These rare disorders often get worse over time and can be fatal. Studies have identified at least three forms of PME. Lafora disease is inherited as an autosomal recessive disorder, meaning that the disease occurs only when a child inherits two copies of a defective gene, one from each parent. Lafora disease is characterized by myoclonus, epileptic seizures, and dementia (progressive loss of memory and other intellectual functions). | 0-1
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To prevent secondary complications(conditions that occur in the course of a disease as a result), physiotherapy is recommended. Prior to birth recognition of an affected fetus during pregnancy requires a plan involving multiple medical disciplines for a safe delivery for both mother and infant and to allow for an evaluation and possible treatment for hydrocephalus shortly after birth.Hydrocephalus: Surgery should be performed as needed, to shunt cerebrospinal fluid (CSF) in order to reduce pressure inside the head (intracranial pressure). Intellectual Disability: The development of the individual should be monitored since the development outcomes are variable among affected individuals, educational programs are needed for these individuals. Adducted Thumbs: Surgical procedures are generally not required, a splint may reduce the degree of the adduction, and in milder cases tendon transfer may improve the thumb function.Spastic paraplegia: Currently there are no specific treatments to prevent or reduce neural degeneration. Treatments aim to reduce symptoms and improving balance, strength, and agility. Individuals should be evaluated periodically by a neurologist and physiatrist to evaluate progress made and to develop treatment strategies to maximize walking ability and reduce symptoms. The General guidelines for follow-up and treatment can be followed while monitoring the neurologic features of the condition. Treatment for spastic paraplegia usually involves exercise to: (1) improve and maintain cardiovascular fitness (The hearts ability to supply oxygen to the tissues) (2) reverse the reduced functional capacity (3) improve the mechanics of walking, and gait in general (4) Improve the individuals independence and sense of control. | Amniocentesis provides a sample of amniotic fluid that can be used to screen for sequence variants or chromosomal variants, whereas samples obtained through chorionic villus sampling can only be used to detect major chromosomal abnormalities (such as trisomy 21), making chorionic villous sampling less relevant in the context of diagnosing L1 syndrome (which is often caused by sequence variants). Amniocentesis (typically performed between 15 and 18 weeks of pregnancy) has a 1% risk of complications for mother and fetus, including miscarriage, while chorionic villus sampling (typically performed between 10 and 12 weeks of pregnancy) has a 2% risk of complications including miscarriage. Mothers carrying a fetus with suspected L1 syndrome will often elect to undergo amniocentesis despite its risk, rather than waiting to pursue lower-risk genetic testing after their child is born, because prenatal diagnostic results can inform considerations to terminate the pregnancy.For any child born with multiple physical abnormalities, the first-line diagnostic test is chromosomal microarray. Management
To know the extent of the disease and the required needs of an individual diagnosed with L1 syndrome, some tests are recommended, including: Head imaging study, Complete neurologic evaluation, Developmental evaluation, Evaluation for Hirschsprung disease if there is a history of constipation, Consultation with a clinical geneticist and/or genetic counselor. A proper management of the manifestations of the L1 syndrome involves a multidisciplinary(involving a team specialized in more than one medical fields) approach involving a team that works within these fields: pediatrics, child neurology, neurosurgery, rehabilitation, and clinical genetics. | 11
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Iron overload or haemochromatosis (also spelled hemochromatosis in American English) indicates increased total accumulation of iron in the body from any cause and resulting organ damage. The most important causes are hereditary haemochromatosis (HH or HHC), a genetic disorder, and transfusional iron overload, which can result from repeated blood transfusions. Signs and symptoms
Organs most commonly affected by haemochromatosis include the liver, heart, and endocrine glands.Haemochromatosis may present with the following clinical syndromes:
liver: chronic liver disease and cirrhosis of the liver. heart: heart failure, cardiac arrhythmia. hormones: diabetes (see below) and hypogonadism (insufficiency of the sex hormone producing glands) which leads to low sex drive and/or loss of fertility in men and loss of menstrual cycle in women. metabolism: diabetes in people with iron overload occurs as a result of selective iron deposition in islet beta cells in the pancreas leading to functional failure and cell death. skeletal: arthritis, from calcium pyrophosphate deposition in joints leading to joint pains. The most commonly affected joints are those of the hands, particularly the knuckles of the second and third fingers. skin: melanoderma (darkening or bronzing of the skin).The skins deep tan color, in concert with insulin insufficiency due to pancreatic damage, is the source of a nickname for this condition: "bronze diabetes" (for more information, see the history of haemochromatosis). Causes
The term haemochromatosis was initially used to refer to what is now more specifically called haemochromatosis type 1 (or HFE-related hereditary haemochromatosis). | Beckers nevus (also known as "Beckers melanosis", "Beckers pigmentary hamartoma", "nevoid melanosis", and "pigmented hairy epidermal nevus") is a benign skin disorder predominantly affecting males. : 687 The nevus can be present at birth, but more often shows up around puberty. It generally first appears as an irregular pigmentation (melanosis or hyperpigmentation) on the torso or upper arm (though other areas of the body can be affected), and gradually enlarges irregularly, becoming thickened and often hairy (hypertrichosis). The nevus is due to an overgrowth of the epidermis, pigment cells (melanocytes), and hair follicles. This form of nevus was first documented in 1948 by American dermatologist Samuel William Becker (1894–1964). Clinical information
Medical knowledge and documentation of this disorder is poor, likely due to a combination of factors including recent discovery, low prevalence, and the more or less aesthetic nature of the effects of the skin disorder. Thus the pathophysiology of Beckers nevus remains unclear. While it is generally considered an acquired rather than congenital disorder, there exists at least one case report documenting what researchers claim is a congenital Beckers nevus with genetic association: a 16-month-old boy with a hyperpigmented lesion on his right shoulder whose father has a similar lesion on his right shoulder. Prevalence
The most extensive study to date, a 1981 survey of nearly 20,000 French males aged 17 to 26, served to disprove many commonly held beliefs about the disorder. In the French study, 100 subjects were found to have Beckers nevi, revealing a prevalence of 0.52%. | 0-1
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At the end of the 1990s came an increased distrust of the concept of "sick building". A dissertation at the Karolinska Institutet in Stockholm 1999 questioned the methodology of previous research, and a Danish study from 2005 showed these flaws experimentally. It was suggested that sick building syndrome was not really a coherent syndrome and was not a disease to be individually diagnosed, but a collection of as many as to dozen semi related diseases. In 2006 the Swedish National Board of Health and Welfare recommended in the medical journal Läkartidningen that "sick building syndrome" should not be used as a clinical diagnosis. Thereafter, it has become increasingly less common to use terms such as "sick buildings" and "sick building syndrome" in research. However, the concept remains alive in popular culture and is used to designate the set of symptoms related to poor home or work environment engineering. "Sick building" is therefore an expression used especially in the context of workplace health. Sick building syndrome made a rapid journey from media to courtroom where professional engineers and architects became named defendants and were represented by their respective professional practice insurers. Proceedings invariably relied on expert witnesses, medical and technical experts along with building managers, contractors and manufacturers of finishes and furnishings, testifying as to cause and effect. Most of these actions resulted in sealed settlement agreements, none of these being dramatic. | The World Health Organization created a 484-page tome on indoor air quality back in 1984 when SBS was attributed only to non-organic causes, and suggested that the book might form a basis for legislation or litigation.Case studies can contribute to a better understanding and management of sick building syndrome. Sick building causes are frequently pinned down to flaws in the heating, ventilation, and air conditioning (HVAC) systems. However, there have been inconsistent findings on whether air conditioning systems result in SBS or not.More recently, sick building was confirmed as a vector for the transmission of SARS in 2003. Norovirus has also been linked with buildings because of "the small inoculum required to produce infection (<100 viral particles), prolonged viral shedding, and its ability to survive in the environment." Many norovirus outbreaks have been traced back to cruise ships with food service in unsanitary conditions, or filthy personal hygiene around the toilet. Signs and symptoms
Human exposure to aerosols has been documented to give rise to a variety of adverse health effects. Building occupants complain of symptoms such as sensory irritation of the eyes, nose, or throat; neurotoxic or general health problems; skin irritation; nonspecific hypersensitivity reactions; infectious diseases; and odor and taste sensations. Exposure to poor lighting conditions has led to general malaise.Extrinsic allergic alveolitis has been associated with the presence of fungi and bacteria in the moist air of residential houses and commercial offices. | 11
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Preventing Hearing Loss Caused by Chemical (Ototoxicity) and Noise Exposure Safety and Health Information Bulletin (SHIB). U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. doi:10.26616/NIOSHPUB2018124 (8 March 2018). Publication No. 2018-124. Themann, Christa L.; Morata, Thais; Afanuh, Susan (27 September 2019). "Using Total Worker Health® concepts to address hearing health". U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. Cincinnati, OH. doi:10.26616/NIOSHPUB2019155. S2CID 242864449. Retrieved 4 March 2020. Publication No. 2019-155
World Report on Hearing. World Health Organization. 3 March 2021. World report archived on 10 June 2022. | Dysfunction is caused when the tumor compresses the normal kidney parenchyma.The mesenchymal component may include cells showing rhabdomyoid differentiation or malignancy (rhabdomyosarcomatous Wilms).Wilms tumors may be separated into two prognostic groups based on pathologic characteristics:
Favorable – Contains well developed components mentioned above
Anaplastic – Contains diffuse anaplasia (poorly developed cells)
Molecular biology and related conditions
Mutations of the WT1 gene which is located on the short arm of chromosome 11 (11p13) are observed in approximately 20% of Wilms tumors, the majority of them being inherited from the germline, while a minority are acquired somatic mutations. In addition at least half of the Wilms tumors with mutations in WT1 also carry acquired somatic mutations in CTNNB1, the gene encoding the proto-oncogene beta-catenin. This latter gene is found on short arm of chromosome 3 (3p22.1). Most cases do not have mutations in any of these genes. An association with H19 has been reported. H19 is a long noncoding RNA located on the short arm of chromosome 11 (11p15.5). Diagnosis
The majority of people with Wilms tumor present with an asymptomatic abdominal mass which is noticed by a family member or healthcare professional. Renal tumors can also be found during routine screening in children who have known predisposing clinical syndromes. The diagnostic process includes taking a medical history, a physical exam, and a series of tests including blood, urine, and imaging tests.Once Wilms tumor is suspected, an ultrasound scan is usually done first to confirm the presence of an intrarenal mass. | 0-1
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In Hungarian, gonosz szem means "evil eye", but more widespread is the expression szemmelverés (lit. "beating with eye"), which refers to the supposed/alleged act of harming one by an evil look
In Irish, the term drochshúil is used for the evil eye, being a compound of droch (bad, poor, evil, ill) and súil (eye). This can also be used to refer to someone with weak eyesight. In Indonesian the word dengki refers to evil eye. In Italian, the word malocchio (pronounced [maˈlɔkkjo]) refers to the evil eye. In Japanese it is known as "邪視" ("jashi"). In Kurdish, it is called "Çav pîs/Chaw pis/ چاو پیس"
In Lithuanian evil eye is known as "pikta akis", while act of evil watching is called "nužiūrėjimas" (noun), "nužiūrėti" (verb). In Malay, it is called mata jahat, meaning literally "bad/evil eye". In Malayalam it is known as kannu veykkuka – to cast an evil eye while "kannu peduka" means to be on the receiving end of the malefic influence. "kannu dosham" refers to a bad effect caused by an evil eye. In Maltese it is known as "l-għajn". It is a common symbol for warding off evil intentions. | Signs and symptoms
Genetics
Costello syndrome is caused by any of at least five different mutations in the HRAS gene on chromosome 11. This gene provides instructions for making a protein, H-Ras, that helps control cell growth and division. Mutations that cause Costello syndrome lead to the production of an H-Ras protein that is permanently active. Instead of triggering cell growth in response to particular signals from outside the cell, the overactive protein directs cells to grow and divide constantly. This unchecked cell division may predispose those affected to the development of benign and malignant tumors. It remains unclear how mutations in HRAS cause other features of Costello syndrome, but many of the signs and symptoms may result from cell overgrowth and abnormal cell division.HRAS is a proto-oncogene in which somatic mutations in healthy people can contribute to cancer. Whereas children with Costello syndrome typically have a mutation in HRAS in every cell of their bodies, an otherwise healthy person with a tumor caused in part by HRAS mutation will only have mutant HRAS within the tumor. The test for the mutation in cancer tumors can also be used to test children for Costello syndrome.Costello syndrome is inherited in an autosomal dominant manner, which means one copy of the altered gene is sufficient to cause the disorder. Almost all cases have resulted from new mutations, and occur in people with no history of the disorder in their family. This condition is rare; as of 20 April 2007, 200 to 300 cases have been reported worldwide. | 0-1
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