text:
Schistosomiasis

Schistosomiasis, also known as snail fever, bilharzia, and Katayama fever, is a disease caused by parasitic flatworms called schistosomes. The urinary tract or the intestines may be infected. Symptoms include abdominal pain, diarrhea, bloody stool, or blood in the urine. Those who have been infected for a long time may experience liver damage, kidney failure, infertility, or bladder cancer. In children, it may cause poor growth and learning difficulties.

The disease is spread by contact with fresh water contaminated with the parasites. These parasites are released from infected freshwater snails. The disease is especially common among children in developing countries, as they are more likely to play in contaminated water. Schistosomiasis is also common among women, who can have greater exposure through daily chores that involve water, such as washing clothes and fetching water. Other high-risk groups include farmers, fishermen, and people using unclean water during daily living. It belongs to the group of helminth infections. Diagnosis is by finding eggs of the parasite in a person's urine or stool. It can also be confirmed by finding antibodies against the disease in the blood.

Methods of preventing the disease include improving access to clean water and reducing the number of snails. In areas where the disease is common, the medication praziquantel may be given once a year to the entire group. This is done to decrease the number of people infected, and consequently, the spread of the disease. Praziquantel is also the treatment recommended by the World Health Organization (WHO) for those who are known to be infected.

Schistosomiasis affected about 236.6 million people worldwide in 2019. An estimated 4,400 to 200,000 people die from it each year. The disease is most commonly found in Africa, Asia, and South America. Around 700 million people, in more than 70 countries, live in areas where the disease is common. In tropical countries, schistosomiasis is second only to malaria among parasitic diseases with the greatest economic impact. Schistosomiasis is listed as a neglected tropical disease.

Signs and symptoms

Many individuals do not experience symptoms. If symptoms do appear, they usually take 4–6 weeks from the time of infection. The first symptom of the disease may be a general feeling of illness. Within 12 hours of infection, an individual may complain of a tingling sensation or light rash, commonly referred to as "swimmer's itch", due to irritation at the point of entrance. The rash that may develop can mimic scabies and other types of rashes.

The manifestations of schistosomal infection vary over time as the cercariae, and later adult worms and their eggs, migrate through the body. If eggs migrate to the brain or spinal cord, seizures, paralysis, or spinal-cord inflammation are possible.

Acute Infection
Manifestation of acute infection from schistosoma include cercarial dermatitis (hours to days) and acute systemic schistosomiasis (2–8 weeks) which can include symptoms of fever, myalgia, a cough, bloody diarrhea, chills, or lymph node enlargement. Some patients may also experience dyspnea and hypoxia associated with the development of pulmonary infiltrates.

Cercarial dermatitis
The first potential reaction is an itchy, maculopapular rash that results from cercariae penetrating the skin within the first 12 hours to days of cercarial skin penetration. The first time a non-sensitized person is exposed, the rashes are usually mild with an associated prickling sensation that quickly disappear on its own since this is a type of hypersensitivity reaction. In sensitized people who have previously been infected, the rash can develop into itchy, red, raised lesions (papules) with some turning into fluid-filled lesions (vesicles). Previous infections with cercariae causes a faster developing and worse presentation of dermatitis due to the stronger immune response. The round bumps are usually one to three centimeters across. Because people living in affected areas have often been repeatedly exposed, acute reactions are more common in tourists and migrants. The rash can occur between the first few hours and a week after exposure, and they normally resolve on their own in around 7–10 days. For human schistosomiasis, a similar type of dermatitis called "swimmer's itch" can also be caused by cercariae from animal trematodes that often infect birds. Cercarial dermatitis is not contagious and can not be transmitted from person-to-person.

Symptoms may include:
 * Flat, red rash
 * Small red, raised pimples
 * Small red blisters
 * Prickling or tingling sensation, burning, itching of the skin

Scratching the rash can lead to secondary bacterial infection of the skin, thus it is important to refrain from scratching. Some common treatments for itching include corticosteroid cream, anti-itch lotion, application of cool compresses to rash, bathing in Epsom salts or baking soda, and in severe itching cases, prescription strength cream and lotions. Oral antihistamines can also help relieve the itching.

Acute schistosomiasis (Katayama fever)
Acute schistosomiasis (Katayama fever) may occur weeks or months (around 2–8 weeks) after the initial infection as a systemic reaction against migrating schistosomulae as they pass through the bloodstream through the lungs to the liver and also against the antigens of eggs. Similarly to swimmer's itch, Katayama fever is more commonly seen in people with their first infection such as migrants and tourists, and it is associated with heavy infection. It is seen, however, in native residents of China infected with S. japonicum. S. japonicum can cause acute schistosomiasis in chronically infected population, and it can lead to a more severe form of acute schistosomiasis.

Symptoms may include: Acute schistosomiasis usually self-resolves in 2–8 weeks in most cases., but a small proportion of people have persistent weight loss, diarrhea, diffuse abdominal pain, and rash.
 * Dry cough with changes on chest X-ray
 * Fever
 * Fatigue
 * Muscle aches
 * Headache
 * Malaise
 * Abdominal pain
 * Diarrhea
 * Enlargement of both the liver and the spleen
 * Hives

Complications may include:

Neurological side effects may include Cardiac side effects may include
 * Spinal cord inflammation (transverse myelitis) may occur if worms or eggs travel to the spinal cord during this acute phase of infection.
 * Headaches
 * Disturbances of sensorium
 * Hemiplegia
 * Tetraplegia
 * Visual impairment
 * Ataxia/ speech impairment
 * Motor paralysis

 * Myocarditis
 * Pericarditis
 * Asymptomatic myocardial ischemia

Treatment may include:
 * Corticosteroid such as prednisone is used to alleviate the hypersensitivity reaction and reduce inflammation
 * Praziquantel can be administered to kill the adult schistosomes to prevent chronic infection in addition to corticosteroid therapy. It is not effective to recent infection as it only targets the adult worms, but not the premature schistosomulae. Therefore, a repeat treatment of praziquantel several weeks after initial infection may be warranted. It is recommended to treat with praziquantel 4–6 weeks after initial exposure since it targets adult worms. For Acute Schistosomiasis(AS) Praziquantel is ineffective on schistosomulae above 7 days and does not prevent the chronic phase of the disease. Too early of treatment can worsen symptoms of AS. In some cases, this worsening of symptoms can be life-threatening by causing encephalitis related to vasculitis, myocarditis, or pulmonary events.
 * Oxamniquine (50 mg/kg once) can be administer at the early phase of schistosomiasis. It is more effective in against schistsomulae than praziquantel but only with S.mansoni. This prevents the occurrence of chronic S.mansoni infection and egg-laying stage.
 * Artemeter is an artemisin derivative efficient against schistosomulae aged 7-21 days. only reduced S.mansoni infection by 50% in exposed children

Chronic infection
In long-established disease, adult worms lay eggs that can cause inflammatory reactions. The eggs secrete proteolytic enzymes that help them migrate to the bladder and intestines to be shed. The enzymes also cause an eosinophilic inflammatory reaction when eggs get trapped in tissues or embolize to the liver, spleen, lungs, or brain. The long-term manifestations are dependent on the species of schistosome, as the adult worms of different species migrate to different areas. Many infections are mildly symptomatic, with anemia and malnutrition being common in endemic areas.

Intestinal schistosomiasis
The worms of S. mansoni and S. japonicum migrate to the veins of the gastrointestinal tract and liver. Eggs in the gut wall can lead to pain, blood in the stool, and diarrhea (especially in children). Severe disease can lead to narrowing of the colon or rectum.

In intestinal schistosomiasis, eggs become lodged in the intestinal wall during their migration from the mesenteric venules to the intestinal lumen, and the trapped eggs cause an immune system reaction called a granulomatous reaction. They mostly affect the large bowel and rectum, and involvement of the small bowel is more rare. This immune response can lead to obstruction of the colon and blood loss. The infected individual may have what appears to be a potbelly. There is a strong correlation between morbidity of intestinal schistosomiasis and the intensities of infection. In cases of light infections, symptoms may be mild and can go unrecognized. The most common species to cause intestinal schistosomiasis are S. mansoni and S. japonicum, however, S. mekongi and S. intercalatum can also cause this disease.

Symptoms may include:
 * Abdominal pain and discomfort
 * Loss of appetite
 * Mucous diarrhea with or without gross blood
 * Blood in feces that is not visibly present (fecal occult blood)
 * Abdominal distention

Complications may include: Approximately 10-50% of people living in endemic regions of S. mansoni and S. japonicum develop intestinal schistosomiasis. S. mansoni infection epidemiologically overlaps with high HIV prevalence in Sub-Saharan Africa, where gastrointestinal schistosomiasis has been linked to increased HIV transmission.
 * Intestinal polyps
 * Intestinal ulcers
 * Iron deficient anemia
 * Fistula
 * Bowel strictures (narrowing of colon or rectum)
 * Protein-losing enteropathy
 * Partial or complete bowel obstruction
 * Appendicitis (rare)

Hepatosplenic schistosomiasis
Eggs also migrate to the liver leading to fibrosis in 4 to 8% of people with chronic infection, mainly those with long-term heavy infection.

Eggs can become lodged in the liver, leading to portal hypertension, splenomegaly, the buildup of fluid in the abdomen, and potentially life-threatening dilations or swollen areas in the esophagus or gastrointestinal tract that can tear and bleed profusely (esophageal varices). This condition can be separated into two distinct phases: inflammatory hepatic schistosomiasis (early inflammatory reaction) and chronic hepatic schistosomiasis. Most common species to cause this condition are S. mansoni, S. japonicum, and S. mekongi.

Inflammatory hepatic schistosomiasis
 * This condition occurs mainly in children and adolescents due to early immune reaction to eggs trapped within the periportal and presinusoidal spaces of the liver creating numerous granulomas. Liver function is not affected, and the severity of liver and spleen enlargement is correlated to the intensity of the infection. It is characterized by an enlarged left lobe of the liver with a sharp edge and enlarged spleen with nodules. The enlargement of liver and spleen is usually mild, but in severe cases, they can enlarge to the level of the belly button and even into the pelvis.

Chronic (fibrotic) hepatic schistosomiasis
 * This is a late stage liver disease that occurs mainly in young and middle-aged adults who have been chronically infected with a heavy infection and whose immune regulation of fibrosis is not functioning properly. It affects only a small proportion of people who are infected. Liver function and liver architecture are not affected unlike cirrhosis. The pathogenesis of this disease is caused by deposition of collagen and extracellular matrix proteins within the periportal space, which leads to liver portal fibrosis and enlarged fibrotic portal tracts (Symmer's pipe stem fibrosis). The periportal fibrosis physically compress the portal vein leading to portal hypertension (increased portal venous pressure), increased pressure of the splenic vein, and subsequent enlargement of the spleen. Portal hypertension can also increase the pressure in portosystemic anastomoses (vessel connections between the portal circulation and systemic circulation) leading to esophageal varices and caput medusae. These portosystemic anastomoses also allows a pathway for the eggs to travel to locations such as the lungs, spinal cord, or brain. Co-infection with hepatitis is common in regions endemic to schistosomiasis with hepatitis B or hepatitis C, and co-infection with hepatitis C is associated with more rapid liver deterioration and worse outcome. Fibrotic hepatic schistosomiasis caused by S. mansoni usually develops in around 5–15 years, while it can take less time for S. japonicum.
 * Symptoms may include:
 * Esophageal varices (can cause life-threatening esophageal variceal bleed)
 * Ascites (end-stage)
 * Caput medusae
 * Enlarged spleen and liver
 * Complications may include:
 * Neuroschistosomiasis due to portosystemic anastomoses from portal hypertension
 * Pulmonary Schistosomiasis due to portosystemic anastomoses from portal hypertension

Pulmonary schistosomiasis
Portal hypertension secondary to hepatosplenic schistosomiasis can cause vessel connections between the portal (liver and gut) circulation and systemic circulation to develop, which creates a pathway for the eggs and worms to travel to the lungs. The eggs can be deposited around the alveolar capillary beds and causes granulomatous inflammation of the pulmonary arterioles followed by fibrosis. This leads to high blood pressure in the pulmonary circulation system (pulmonary hypertension), increased pressure in the right heart, enlargement of the pulmonary artery and right atria, and thickening of the right ventricular wall.

Symptoms of pulmonary hypertension may include:
 * Shortness of breath
 * Chest pain
 * Feeling tired
 * Fainting during physical exertion

Urogenital schistosomiasis

The worms of S. haematobium migrate to the veins around the bladder and ureters where they reproduce. S. haematobium can produce up to 3000 eggs per day, these eggs migrate from the veins to the bladder and ureter lumens, but up to 50 percent of them can become trapped in the surrounding tissues causing granulomatous inflammation, polyps formation, and ulceration of bladder, ureter, and genital tract tissues. This can lead to blood in the urine 10 to 12 weeks after infection. Over time, fibrosis can lead to obstruction of the urinary tract, hydronephrosis, and kidney failure. Bladder cancer diagnosis and mortality are generally elevated in affected areas; efforts to control schistosomiasis in Egypt have led to decreases in the bladder cancer rate. The risk of bladder cancer appears to be especially high in male smokers, perhaps due to chronic irritation of the bladder lining allowing it to be exposed to carcinogens from smoking.

In women, genitourinary disease can also include genital lesions that may lead to increased rates of HIV transmission. If lesions involve the fallopian tubes or ovaries, it may lead to infertility. If the reproductive organs in male are affected, there could be blood in the sperm.

Urinary symptoms may include: Genital symptoms may include:
 * Blood in the urine - blood is usually seen at the end of a urine stream (most common symptom)
 * Painful urination
 * Increase frequency of urination
 * Protein in the urine
 * Secondary urinary tract infection
 * Secondary kidney infection
 * Calcification of the bladder wall
 * Inflammation and ulceration of uterine cervix, vagina, or vulva
 * Blood in the sperm
 * Infertility in female

Kidney function is unaffected in many cases, and the lesions are reversible with proper treatment to eliminate the worms.

Neuroschistosomiasis
Central nervous system lesions occur occasionally due to inflammation and granuloma development around eggs or worms that find their way to the brain or spinal cord through the circulatory system, and they can potentially develop irreversible scarring without proper treatment. Cerebral granulomatous disease may be caused by S. japonicum eggs in the brain during both the acute and chronic phase of the disease. Communities in China affected by S. japonicum have rates of seizures eight times higher than baseline. Cerebral granulomatous infection may also be caused by S. mansoni. In situ egg deposition following the anomalous migration of the adult worm, which appears to be the only mechanism by which Schistosoma can reach the central nervous system in people with schistosomiasis. The destructive action on the nervous tissue and the mass effect produced by a large number of eggs surrounded by multiple, large granulomas in circumscribed areas of the brain characterize the pseudotumoral form of neuroschistosomiasis and are responsible for the appearance of clinical manifestations: headache, hemiparesis, altered mental status, vertigo, visual abnormalities, seizures, and ataxia. Similarly, granulomatous lesions from S. mansoni and S. haematobium eggs in the spinal cord can lead to transverse myelitis (inflammation of the spinal cord) with flaccid paraplegia. In cases with advanced hepatosplenic and urinary schistosomiasis, the continuous embolization of eggs from the portal mesenteric system (S. mansoni) or portal mesenteric-pelvic system (S. haematobium) to the brain, results in a sparse distribution of eggs associated with scant periovular inflammatory reaction, usually with little or no clinical significance.

Spinal cord inflammation (transverse myelitis) symptoms may include:
 * Paralysis of the lower extremities
 * Loss of bowel or urinary control
 * Loss of sensation below the level of the lesion
 * Pain below the level of the lesion

Cerebral granulomatous infection symptoms may include: Corticosteroids are used to prevent permanent neurological damage from the inflammatory response to the eggs, and sometimes anticonvulsants are needed to stop the seizures. Corticosteroids are given prior to administration of praziquantel.
 * Seizures
 * Headaches
 * Motor impairment
 * Sensory impairment
 * Cerebellar symptoms
 * Unsteady gait
 * Inability to stand or sit without support
 * Uncoordinated movements
 * Scanning speech
 * Irregular eye movements

Transmission and life cycle
Infected Schistosoma individuals release eggs into water via their fecal material or urine. A collection of stool samples under a microscope will show the eggs of S. intercalatum, S. mansori, and S. japonicum. Looking at a urine sample under a microscope would reveal the eggs of S. haematobium and rarely, the eggs of S. mansori. After larvae hatch from these eggs, the larvae infect a very specific type of freshwater snail. For example, in S. haematobium and S. intercalatum it is snails of the genus Bulinus, in S. mansoni it is Biomphalaria, and in S. japonicum it is Oncomelania. The schistosome larvae undergo the next phase of their lifecycles in these snails, spending their time reproducing and developing. Once this step has been completed, the parasite leaves the snail and enters the water column. The parasite can live in the water for only 48 hours without a mammalian host. Once a host has been found, the worm enters its blood vessels. For several weeks, the worm remains in the vessels, continuing its development into its adult phase. When maturity is reached, mating occurs and eggs are produced. Eggs enter the bladder/intestine and are excreted through urine and feces and the process repeats. If the eggs do not get excreted, they can become engrained in the body tissues and cause a variety of problems such as immune reactions and organ damage. While transmission typically occurs only in countries where the freshwater snails are native, a case in Germany was reported where a man got schistosomiasis from an infected snail in his aquarium.

Humans encounter larvae of the schistosome parasite when they enter contaminated water while bathing, playing, swimming, washing, fishing, or walking through the water.

Life cycle
The life cycle stages: Schistosomes can live an average of 3–5 years, and the eggs can survive for more than 30 years after infection.
 * 1) The excretion of schistosome eggs in urine or feces depending on species
 * 2) The hatching of the eggs leading to release of the free-swimming, ciliated larvae called miracidia
 * 3) Miracidia find and penetrate the snails, which are the intermediate hosts (specific species of snails is dependent on the species of schistosoma)
 * 4) Within the snails, two successive generations of sporocysts occur
 * 5) Sporocysts give rise to the infective free-swimming larvae with forked tails called cercariae, and they leave the snails to enter the water
 * 6) Cercariae find the human hosts and penetrate their skin
 * 7) Upon entrance into the human hosts, cercariae lose their tails and become schistosomulae
 * 8) The schistosomulae travel to the lungs and heart via the venous circulation
 * 9) They migrate to the portal venous system of the liver where they mature into the adult form with two separate sexes
 * 10) The adult male and female are paired together, exit the liver via portal venous system, and travel to the venous systems of the intestines or bladder (species dependent) and produce eggs
 * 11) S. japonicum - superior mesenteric veins (but can also inhabit inferior mesenteric veins)
 * 12) S. mansoni - inferior mesenteric veins (but can also inhabit superior mesenteric veins)
 * 13) S. haematobium - vesicular and pelvic venous plexus of the bladder (occasionally rectal venules)
 * 14) S. intercalatum and S. guineensis - inferior mesenteric plexus (lower portion of the bowels compared to S. mansoni)

Other hosts
Schistosomiasis is also a concern of cattle husbandry and mice. O-methyl-threonine is weakly effective in mouse schistosomiasis but is not in use.

Pathogenesis
The infectious stage starts when the free-swimming larval form of the schistosome, cercariae, penetrates the human skin using their suckers, proteolytic enzymes, and tail movements; the cercariae transformed into schistosomulae by losing its tail and subsequently travels to the heart and lungs through venous system until it eventually reach the liver where it will mature into the adult form. The diseases caused by the schistomes are characterized into acute schistosomiasis and chronic schistosomiasis, and they can vary dependent on the species of schistosome.

Acute infection
 * Minutes to days after initial infection:
 * Cercerial dermatitis (Swimmer's itch) - swimmer's itch is caused by a localized allergic reaction at the sites of skin penetration by the cercariae causing an inflammatory reaction that is characterized by itchy red pimples and blisters.
 * Few weeks to months after initial infection:
 * Acute Schistosomiasis (Katayama's Fever) - the exact pathophysiology of this disease remains unknown. It has been hypothesized to be caused by a systemic immune response due to immune complex formation (Type III hypersensivity) with the foreign antigens on the migratory schistosomula and the eggs, and the subsequent deposition of these complexes on various tissues leading to activation of an autoimmune response. Acute schistosomiasis caused by S. mansoni and S. haematobium generally affect people who have been infected for the first time such as tourists visiting endemic regions. In contrast, cases of acute schistosomiasis caused by S. japonicum can occur in reinfection to population who reside in endemic regions, and they occur in higher incidences and can have worse prognosis. It was proposed that the large amount of egg antigens released by S. japonicum interact with antibodies leading to the formation of high volume of immune complexes, which cause enlargement of the lymph tissues. This sequence of events can lead to clinical manifestation of fever, enlargement of spleen and liver due to fibrosis, portal hypertension, and death.

Chronic infection

The clinical manifestations of chronic infection is mainly caused by immune reaction to the eggs entrapment within tissues resulting in granuloma formation and chronic inflammation. Adult worms live together in pairs (one male and female), sexually reproduce, and lay eggs in the veins around the intestines and bladder depending on the species, and these eggs can rupture the wall of the veins to escape to the surrounding tissues. The eggs make their way through the tissues to the intestinal or bladder lumen with help of proteolytic enzymes, however, a large amount of eggs are unable to finish their journey and remained stuck within the tissues where they can elicit an immune response. The miracidia in these eggs can then release antigens that stimulate an inflammatory immune response. The miracidia within the eggs live for around 6–8 weeks before they die and stop releasing the antigens. The granulomatous response is a cellular immune response mediated by CD4+ T cells, neutrophils, eosinophils, lymphocytes, macrophages, and monocytes, and this chronic inflammatory response elicited by the eggs can cause fibrosis, tissue destruction, and granuloma nodules that disrupt the functions of the organs involved. Th1 helper cell response is prominent releasing cytokines such as IFN-γ during the early phases of infection, and it transitions to Th2 response leading to increase in level of IgE, IL-4, and eosinophils as egg production progresses. In chronic infections, the Th2 response shifts to increasing the level of IL-10, IL-13, and IgG4, which reverses the progression of the granulomas and lead to collagen deposition at the sites of the granulomas. The specific clinical symptoms and severity of the disease this causes depends on the type of schistosome infection, duration of infection, number of eggs, and the organ at which the eggs are deposited. The amount of eggs entrapped in the tissues will continue to increase if the schistosoma are not eliminated.

Identification of eggs in stools
Diagnosis of infection is confirmed by the identification of eggs in stools. Eggs of S. mansoni are about 140 by 60 μm in size and have a lateral spine. The diagnosis is improved through the use of the Kato-Katz technique, a semiquantitative stool examination technique. Other methods that can be used are enzyme-linked immunosorbent assay, circumoval precipitation test, and alkaline phosphatase immunoassay.

Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected. Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Because eggs may be passed intermittently or in small numbers, their detection is enhanced by repeated examinations or concentration procedures, or both. In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique. Eggs can be found in the urine in infections with S. haematobium (recommended time for collection: between noon and 3 PM) and with S. japonicum. Quantification is possible by using filtration through a nucleopore filter membrane of a standard volume of urine followed by egg counts on the membrane. Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may demonstrate eggs when stool or urine examinations are negative.

Identification of microhematuria in urine using urine reagent strips is more accurate than circulating antigen tests in the identification of active schistosomiasis in endemic areas.

Antibody detection
Antibody detection can be useful to indicate schistosome infection in people who have traveled to areas where schistosomiasis is common and in whom eggs cannot be demonstrated in fecal or urine specimens. Test sensitivity and specificity vary widely among the many tests reported for the serologic diagnosis of schistosomiasis and are dependent on both the type of antigen preparations used (crude, purified, adult worm, egg, cercarial) and the test procedure.

At the U.S. Centers for Disease Control and Prevention, a combination of tests with purified adult worm antigens is used for antibody detection. All serum specimens are tested by FAST-ELISA using S. mansoni adult microsomal antigen. A positive reaction (greater than 9 units/μL serum) indicates infection with Schistosoma species. Sensitivity for S. mansoni infection is 99%, 95% for S. haematobium infection, and less than 50% for S. japonicum infection. Specificity of this assay for detecting schistosome infection is 99%. Because test sensitivity with the FAST-ELISA is reduced for species other than S. mansoni, immunoblots of the species appropriate to the person's travel history are also tested to ensure detection of S. haematobium and S. japonicum infections. Immunoblots with adult worm microsomal antigens are species-specific, so a positive reaction indicates the infecting species. The presence of antibody is indicative only of schistosome infection at some time and cannot be correlated with clinical status, worm burden, egg production, or prognosis. Where a person has traveled can help determine which Schistosoma species to test for by immunoblot.

In 2005, a field evaluation of a novel handheld microscope was undertaken in Uganda for the diagnosis of intestinal schistosomiasis by a team led by Russell Stothard from the Natural History Museum of London, working with the Schistosomiasis Control Initiative, London.

Molecular diagnostics
Polymerase chain reaction (PCR) based testing is accurate and rapid. However, it is not frequently used in countries where the disease is common due to the cost of the equipment and the technical expertise required to run the tests. Using a microscope to detect eggs costs about US$0.40 per test whereas PCR is about $US 7 per test as of 2019. Loop-mediated isothermal amplification are being studied as they are lower cost. LAMP testing is not commercially available as of 2019.

Laboratory testing
S. haematobium screening in the community can be done by using urine dip-stick to check for hematuria, and the stool guaiac test can be used to test for blood in the stool for potential S. mansoni and S. japonicum infection. For travelers or migrants in endemic regions, complete blood count with differential can be used to identify a high level of eosinophil in the blood, which could be indicative of an acute infection. Liver function test can be ordered if hepatosplenic schistosomiasis is suspected, and a subsequent hepatitis test panel can be ordered if liver function test is abnormal.

Like most parasitic infections, schistosomiasis will usually cause significant eosinophilia that can be identified on a complete blood count with differential.

Tissue biopsy
If other diagnostic methods of schistosomiasis have failed to detect the infection, but there is still a high suspicion for schistosomiasis, tissue biopsy from the rectum, bladder, and liver can be obtained to look for schistosome eggs within the tissue samples.

Imaging
Imaging modalities such as X-rays, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) can be utilized to evaluate for severity of schistosomiasis and damages of the infected organs. For example, X-ray and CT scans of the chest can be used to detect lesions in the lungs from pulmonary schistosomiasis, and pelvic X-ray can reveal calcification of the bladder in chronic urinary schistosomiasis. Ultrasound may be used to look for abnormalities in the liver and spleen in hepatosplenic schistosomiasis, and CT scan of the liver is a good tool to look for calcification in the liver associated with S. japonicum infection. CT scan can also be used to assess damages from the schistosomiasis infection in the intestinal, urogenital, and central nervous system. MRI is used to evaluate schistosomiasis of the central nervous system, liver, and genital.

PET/CT scan that identifies tissues with higher metabolic activity have been used to help diagnose schistosomiasis in rare cases. This is due to the high level of inflammation caused by the schistosomal eggs, which increases the metabolic rate of the surrounding tissues.

Prevention
Many countries are working towards eradicating the disease. The World Health Organization is promoting these efforts. In some cases, urbanization, pollution, and the consequent destruction of snail habitat have reduced exposure, with a subsequent decrease in new infections. The elimination of snail populations using molluscicides had been attempted to prevent schistosomiasis in the past, but it was an expensive process that often only reduced but did not eliminate the snail population. The drug praziquantel is used for prevention in high-risk populations living in areas where the disease is common. The Centers for Disease Control and Prevention advises avoiding drinking or coming into contact with contaminated water in areas where schistosomiasis is common.

A 2014 review found tentative evidence that increasing access to clean water and sanitation reduces schistosome infection.

Other important preventive measures include hygiene education leading to behavioral change and sanitary engineering to ensure safe water supply.

Preventive anthelminthic administration
For schistosomiasis control, the World Health Organization recommends preventive anthelminthic administration, which is the treatment of an entire affected population and the periodic treatment of all groups at high risk of acquiring schistosomiasis by using Praziquantel. In 2019, 44.5% of people with schistosomiasis were treated globally, and 67.2% of school-aged children needing preventive chemotherapy received treatment.

Snails, dams, and prawns
For many years from the 1950s onwards, vast dams and irrigation schemes were constructed, causing a massive rise in water-borne infections from schistosomiasis. The detailed specifications laid out in various United Nations documents since the 1950s could have minimized this problem. Irrigation schemes can be designed to make it hard for the snails to colonize the water and to reduce the contact with the local population. Even though guidelines on how to design these schemes to minimise the spread of the disease had been published years before, the designers were unaware of them. The dams appear to have reduced the population of the large migratory prawn Macrobrachium, which eats the snails. After the construction of fourteen large dams, greater increases in schistosomiasis occurred in the historical habitats of native prawns than in other areas. Further, at the 1986 Diama Dam on the Senegal River, restoring prawns upstream of the dam reduced both snail density and the human schistosomiasis reinfection rate.

Integrated strategy in China
In China, the national strategy for schistosomiasis control has shifted three times since it was first initiated: transmission control strategy (from mid-1950s to early 1980s), morbidity control strategy (from mid-1980s to 2003), and the "new integrated strategy" (2004 to present). The morbidity control strategy focused on synchronous chemotherapy for humans and bovines and the new strategy developed in 2004 intervenes in the transmission pathway of schistosomiasis, mainly including replacement of bovines with machines, prohibition of grazing cattle in the grasslands, improving sanitation, installation of fecal-matter containers on boats, praziquantel drug therapy, snail control, and health education. A 2018 review found that the "new integrated strategy" was highly effective to reduce the rate of S. japonicum infection in both humans and the intermediate host snails and reduced the infection risk by 3–4 times relative to the conventional strategy.

Treatment

Two drugs, praziquantel and oxamniquine, are available for the treatment of schistosomiasis. They are considered equivalent in relation to efficacy against S. mansoni and safety. Because of praziquantel's lower cost per treatment, and oxaminiquine's lack of efficacy against the urogenital form of the disease caused by S. haematobium, in general praziquantel is considered the first option for treatment. Praziquantel can be safely used in pregnant women and young children. The treatment objective is to cure the disease and to prevent the evolution of the acute to the chronic form of the disease. All cases of suspected schistosomiasis should be treated regardless of presentation because the adult parasite can live in the host for years.

Schistosomiasis is treatable by taking by mouth a single dose of the drug praziquantel annually.

Praziquantel only eliminates the adult schistosomes, but it is not effective in killing the eggs and immature worms. Live eggs can be excreted by the infected individuals for weeks after treatment with praziquantel. The immature worms can survive and grow up to be adult schistosomes after praziquantel therapy. Thus, it is important to have repeated schistosomiasis testing of the stool and/or urine around 4–6 weeks after praziquantel therapy. Treatment of praziquantel may be repeated to ensure complete elimination of the parasite.

The WHO has developed guidelines for community treatment based on the impact the disease has on children in villages in which it is common:
 * When a village reports more than 50 per cent of children have blood in their urine, everyone in the village receives treatment.
 * When 20 to 50 percent of children have bloody urine, only school-age children are treated.
 * When fewer than 20 percent of children have symptoms, mass treatment is not implemented.

Other possible treatments include a combination of praziquantel with metrifonate, artesunate, or mefloquine. A Cochrane review found tentative evidence that when used alone, metrifonate was as effective as praziquantel. Mefloquine, which has previously been used to treat and prevent malaria, was recognised in 2008–2009 to be effective against schistosomes.

Historically, antimony potassium tartrate remained the treatment of choice for schistosomiasis until the development of praziquantel in the 1980s.

Post-treatment monitoring Osteopontin (OPN) is a promising tool for monitoring praziquantel efficacy and post-treatment fibrosis regression as (OPN) expression is modulated by S. mansoni egg antigens and its levels correlate with severity of schistosomiasis fibrosis and portal hypertension in mice and humans. Praziquantel pharmacotherapy reduces systemic OPN levels and liver collagen content in mice.

Epidemiology

The disease is found in tropical countries in Africa, the Caribbean, eastern South America, Southeast Asia, and the Middle East. S. mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East. S. mekongi and S. intercalatum are found locally in Southeast Asia and central West Africa, respectively.

The disease is endemic in about 75 developing countries and mainly affects people living in rural agricultural and peri-urban areas.

Infection estimates
In 2010, approximately 238 million people were infected with schistosomiasis, 85 percent of whom live in Africa. An earlier estimate from 2006 had put the figure at 200 million people infected. As of the latest WHO record, 236.6 million people were infected in 2019. In many of the affected areas, schistosomiasis infects a large proportion of children under 14 years of age. An estimated 600 to 700 million people worldwide are at risk from the disease because they live in countries where the organism is common. In 2012, 249 million people were in need of treatment to prevent the disease. This likely makes it the most common parasitic infection with malaria second and causing about 207 million cases in 2013.

S. haematobium, the infectious agent responsible for urogenital schistosomiasis, infects over 112 million people annually in Sub-Saharan Africa alone. It is responsible for 32 million cases of dysuria, 10 million cases of hydronephrosis, and 150,000 deaths from kidney failure annually, making S. haematobium the world's deadliest schistosome.

Deaths
Estimates regarding the number of deaths vary. Worldwide, the Global Burden of Disease Study issued in 2010 estimated 12,000 direct deaths while the WHO in 2014 estimated more than 200,000 annual deaths related to schistosomiasis. Another 20 million have severe consequences from the disease. It is the most deadly of the neglected tropical diseases.

History
The most ancient evidence of schistosomiasis dates back to more than 6,000 years ago. Studies conducted on human skeletal remains found in northern Syria (5800–4000 BC) demonstrated evidence of a terminal spined schistosome from the pelvic sediment of skeletal remains. Even though this evidence comes from the Middle East, it has been suggested that the 'cradle' of schistosomes lies in the region of the African Great Lakes, an area in which both the parasites and their intermediate hosts are in an active state of evolution. Subsequently, it is believed that schistosomiasis spread to Egypt as a result of the importation of monkeys and slaves during the reign of the fifth dynasty of the Pharaohs (ca. 2494–2345 BC).

Schistosomiasis is known as bilharzia or bilharziosis in many countries, after German physician Theodor Bilharz, who first described the cause of urinary schistosomiasis in 1851.

The first physician who described the entire disease cycle was the Brazilian parasitologist Pirajá da Silva in 1908. The earliest case known of infection was discovered in 2014, belonging to a child who lived 6,200 years ago.

The disease was a common cause of death for Egyptians in the Greco-Roman Period.

In 2016, more than 200 million people needed treatment, but only 88 million people were actually treated for schistosomiasis.

Etymology
Schistosomiasis is named for the genus of parasitic flatworm Schistosoma, a term which means 'split body'. The name Bilharzia comes from Theodor Bilharz, a German pathologist working in Egypt in 1851 who first discovered these worms. The name Katayama disease comes from the Katayama district of Hiroshima Prefecture in Japan, where schistosomiasis was once endemic.

Society and culture
Schistosomiasis is endemic in Egypt, exacerbated by the country's dam and irrigation projects along the Nile. From the late 1950s through the early 1980s, infected villagers were treated with repeated injections of tartar emetic. Epidemiological evidence suggests that this campaign unintentionally contributed to the spread of hepatitis C via unclean needles. Egypt has the world's highest hepatitis C infection rate, and the infection rates in various regions of the country closely track the timing and intensity of the anti-schistosomiasis campaign.

By the early 20th century, schistosomiasis' symptom of blood in the urine was seen as a male version of menstruation in Egypt and was thus viewed as a rite of passage for boys.

Among human parasitic diseases, schistosomiasis ranks second behind malaria in terms of socio-economic and public health importance in tropical and subtropical areas.

Research
A proposed vaccine against S. haematobium infection called "Bilhvax" underwent a phase 3 clinical trial among children in Senegal. The results, reported in 2018, showed that it was not effective despite provoking some immune response. Using CRISPR gene editing technology, researchers decreased the symptoms due to schistosomiasis in an animal model.

Using thromboelastography, researchers at Tufts University observed that murine blood incubated by adult worms for 1 hour has a coagulation profile similar to that of patients that have hemophilia or on anti-coagulant drugs, suggesting that schistosomes could possess anti-coagulant properties. Inhibiting schistosome activity in blood coagulation could potentially serve as a therapeutic option for schistosomiasis.

title: Schistosomiasis


text:
Mortality rate

Mortality rate, or death rate, is a measure of the number of deaths (in general, or due to a specific cause) in a particular population, scaled to the size of that population, per unit of time. Mortality rate is typically expressed in units of deaths per 1,000 individuals per year; thus, a mortality rate of 9.5 (out of 1,000) in a population of 1,000 would mean 9.5 deaths per year in that entire population, or 0.95% out of the total. It is distinct from "morbidity", which is either the prevalence or incidence of a disease, and also from the incidence rate (the number of newly appearing cases of the disease per unit of time).

An important specific mortality rate measure is the crude death rate, which looks at mortality from all causes in a given time interval for a given population. , for instance, the CIA estimates that the crude death rate globally will be 7.7 deaths per 1,000 people in a population per year. In a generic form, mortality rates can be seen as calculated using $$(d/p) \cdot 10^n$$, where d represents the deaths from whatever cause of interest is specified that occur within a given time period, p represents the size of the population in which the deaths occur (however this population is defined or limited), and $$10^n$$is the conversion factor from the resulting fraction to another unit (e.g., multiplying by $$10^3$$to get mortality rate per 1,000 individuals).

Crude death rate, globally
The crude death rate is defined as "the mortality rate from all causes of death for a population," calculated as the "total number of deaths during a given time interval" divided by the "mid-interval population", per 1,000 or 100,000; for instance, the population of the U.S. was around 290,810,000 in 2003, and in that year, approximately 2,419,900 deaths occurred in total, giving a crude death (mortality) rate of 832 deaths per 100,000. , the CIA estimates the U.S. crude death rate will be 8.3 per 1,000, while it estimates that the global rate will be 7.7 per 1,000.

According to the World Health Organization, the ten leading causes of death, globally, in 2016, for both sexes and all ages, were as presented in the table below.

Crude death rate, per 100,000 population Mortality rate is also measured per thousand. It is determined by how many people of a certain age die per thousand people. Decrease of mortality rate is one of the reasons for increase of population. Development of medical science and other technologies has resulted in the decrease of mortality rate in all the countries of the world for some decades. In 1990, the mortality rate of children under five years of age was 144 per thousand, but in 2015 the child mortality rate was 38 per thousand.
 * 1) Ischaemic heart disease, 126
 * 2) Stroke, 77
 * 3) Chronic obstructive pulmonary disease, 41
 * 4) Lower respiratory infections, 40
 * 5) Alzheimer's disease and other dementias, 27
 * 6) Trachea, bronchus, and lung cancers, 23
 * 7) Diabetes mellitus, 21
 * 8) Road injury, 19
 * 9) Diarrhoeal diseases, 19
 * 10) Tuberculosis, 17

Related measures of mortality
Other specific measures of mortality include:

For any of these, a "sex-specific mortality rate" refers to "a mortality rate among either males or females", where the calculation involves both "numerator and denominator... limited to the one sex".

Use in epidemiology
In most cases there are few if any ways to obtain exact mortality rates, so epidemiologists use estimation to predict correct mortality rates. Mortality rates are usually difficult to predict due to language barriers, health infrastructure related issues, conflict, and other reasons. Maternal mortality has additional challenges, especially as they pertain to stillbirths, abortions, and multiple births. In some countries, during the 1920s, a stillbirth was defined as "a birth of at least twenty weeks' gestation in which the child shows no evidence of life after complete birth". In most countries, however, a stillbirth was defined as "the birth of a fetus, after 28 weeks of pregnancy, in which pulmonary respiration does not occur".

Census data and vital statistics
Ideally, all mortality estimation would be done using vital statistics and census data. Census data will give detailed information about the population at risk of death. The vital statistics provide information about live births and deaths in the population. Often, either census data and vital statistics data is not available. This is common in developing countries, countries that are in conflict, areas where natural disasters have caused mass displacement, and other areas where there is a humanitarian crisis

Household surveys
Household surveys or interviews are another way in which mortality rates are often assessed. There are several methods to estimate mortality in different segments of the population. One such example is the sisterhood method, which involves researchers estimating maternal mortality by contacting women in populations of interest and asking whether or not they have a sister, if the sister is of child-bearing age (usually 15) and conducting an interview or written questions about possible deaths among sisters. The sisterhood method, however, does not work in cases where sisters may have died before the sister being interviewed was born.

Orphanhood surveys estimate mortality by questioning children are asked about the mortality of their parents. It has often been criticized as an adult mortality rate that is very biased for several reasons. The adoption effect is one such instance in which orphans often do not realize that they are adopted. Additionally, interviewers may not realize that an adoptive or foster parent is not the child's biological parent. There is also the issue of parents being reported on by multiple children while some adults have no children, thus are not counted in mortality estimates.

Widowhood surveys estimate adult mortality by responding to questions about the deceased husband or wife. One limitation of the widowhood survey surrounds the issues of divorce, where people may be more likely to report that they are widowed in places where there is the great social stigma around being a divorcee. Another limitation is that multiple marriages introduce biased estimates, so individuals are often asked about first marriage. Biases will be significant if the association of death between spouses, such as those in countries with large AIDS epidemics.

Sampling
Sampling refers to the selection of a subset of the population of interest to efficiently gain information about the entire population. Samples should be representative of the population of interest. Cluster sampling is an approach to non-probability sampling; this is an approach in which each member of the population is assigned to a group (cluster), and then clusters are randomly selected, and all members of selected clusters are included in the sample. Often combined with stratification techniques (in which case it is called multistage sampling), cluster sampling is the approach most often used by epidemiologists. In areas of forced migration, there is more significant sampling error. Thus cluster sampling is not the ideal choice.

Mortality statistics
Causes of death vary greatly between developed and less developed countries; see also list of causes of death by rate for worldwide statistics.

According to Jean Ziegler (the United Nations Special Rapporteur on the Right to Food for 2000 to March 2008), mortality due to malnutrition accounted for 58% of the total mortality in 2006: "In the world, approximately 62 million people, all causes of death combined, die each year. In 2006, more than 36 million died of hunger or diseases due to deficiencies in micronutrients".

Of the roughly 150,000 people who die each day across the globe,  about two thirds—100,000 per day—die of age-related causes. In industrialized nations, the proportion is much higher, reaching 90%.

Economics
Scholars have stated that there is a significant relationship between a low standard of living that results from low income; and increased mortality rates. A low standard of living is more likely to result in malnutrition, which can make people more susceptible to disease and more likely to die from these diseases. A lower standard of living may lead to as a lack of hygiene and sanitation, increased exposure to and the spread of disease, and a lack of access to proper medical care and facilities. Poor health can in turn contribute to low and reduced incomes, which can create a loop known as the health-poverty trap. Indian economist and philosopher Amartya Sen has stated that mortality rates can serve as an indicator of economic success and failure.

Historically, mortality rates have been adversely affected by short term price increases. Studies have shown that mortality rates increase at a rate concurrent with increases in food prices. These effects have a greater impact on vulnerable, lower-income populations than they do on populations with a higher standard of living.

In more recent times, higher mortality rates have been less tied to socio-economic levels within a given society, but have differed more between low and high-income countries. It is now found that national income, which is directly tied to standard of living within a country, is the largest factor in mortality rates being higher in low-income countries.

Preventable mortality
These rates are especially pronounced for children under 5 years old, particularly in lower-income, developing countries. These children have a much greater chance of dying of diseases that have become mostly preventable in higher-income parts of the world. More children die of malaria, respiratory infections, diarrhea, perinatal conditions, and measles in developing nations. Data shows that after the age of 5 these preventable causes level out between high and low-income countries.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Mortality rate


text:
Talk:Thorium

 * A guide on how to add a reference to this article and fall in line with the general referencing style

Write a reference as you usually would in a template that is most appropriate for your reference: cite book, cite journal, cite web, cite report. Please use,  ,  ,  , etc.; also, please add   if there are more than three authors. Please use initials instead of complete first names, the longer range notation for page numbers (1234–5678; 1234−1567; 123–145; 123–124), and the dmy date format ("1 January 1970"). Add author links if possible (via ).

The following reference should look like this:

 * in the text near the claim.

(please do not archive this message; it is a general instruction and is meant to remain untagged)

Use in cavity magnetrons filaments (used in microwave ovens)
The page on cavity magnetrons states Thorium is used in the filaments of the magnetron. It would be interesting to find references to support this and to mention it under the applications for / uses of Thorium.

Thoria used in Vacuum Tubes
In the early 1920, the use of Thoria was discovered to improve Vacuum Tubes, see the following https://archive.org/details/70yearsofradiotu00stok/mode/2up?q=thoria 2600:8803:7D00:5B10:312D:2FED:8211:778B (talk) 00:47, 14 July 2024 (UTC)

 * Thanks, I included that ref and used it to correct some erroneous content. Johnjbarton (talk) 02:35, 14 July 2024 (UTC)

title: Talk:Thorium


text:
Talk:Cerium

Tarnishes rapidly or slowly?
"Immediately after lanthanum, the 4f orbitals suddenly contract and are lowered in energy to the point that they participate readily in chemical reactions;"

Isn't this the exact opposite of what you want to say? The lanthanide contraction makes the 4f orbitals less likely to participate in chemical reactions, not more likely,72.200.200.2 (talk) 02:31, 5 April 2019 (UTC)
 * Well, I have corrected it since then (actually it happens already at La, not after La), but the point is correct: up till barium 4f is too high up to participates. At the early lanthanides it contracts and is lowered to the point that allows ready participation. Then as you progress through the lanthanide series they contract further than that and it becomes harder and harder to use them until ytterbium. At lutetium it becomes impossible. Double sharp (talk) 12:38, 26 January 2021 (UTC)

How hard is cerium? It cannot simultaneously be soft enough to cut with a knife and have a hardness similar to silver.
In the first paragraph I read: and it is soft enough to be cut with a steel kitchen knife

And in the "Physical" section I read: It is a ductile metal with a hardness similar to that of silver. I know silver cannot be cut with a knife. This statement has a credible citation labelled with the number 5.

I don't personally have any metallic cerium to try, but one or the other of these statements is true, but not both. I would tend to go with the one that has the citation, rather than the one labelled "citation needed". — Preceding unsigned comment added by Frostybeard (talk • contribs) 08:20, 22 January 2022 (UTC)

Section on Ce+4 not existing
I've removed this section: Despite the common name of cerium(IV) compounds, the Japanese spectroscopist Akio Kotani wrote "there is no genuine example of cerium(IV)". The reason for this can be seen in the structure of ceria itself, which always contains some octahedral vacancies where oxygen atoms would be expected to go and could be better considered a non-stoichiometric compound with chemical formula CeO2−x. Furthermore, each cerium atom in ceria does not lose all four of its valence electrons, but retains a partial hold on the last one, resulting in an oxidation state between +3 and +4. Even supposedly purely tetravalent compounds such as CeRh3, CeCo5, or ceria itself have X-ray photoemission and X-ray absorption spectra more characteristic of intermediate-valence compounds. The 4f electron in cerocene,, is poised ambiguously between being localized and delocalized and this compound is also considered intermediate-valent. because the sources do not appear to endorse it. And I can't find the opening quote anywhere. Jo-Jo Eumerus (talk) 21:27, 23 January 2022 (UTC)
 * Pinging Double Sharp who added this section a few years ago; perhaps they can clarify. Jo-Jo Eumerus (talk) 21:31, 23 January 2022 (UTC)
 * It is right there. From the transcript in the RSC podcast: Indeed the great Japanese spectroscopist Akio Kotani once wrote that 'there is no genuine example of Cerium 4'. (That's how you say "Ce(IV)" out loud; presumably whoever wrote the transcript was not aware of this.) For ceria, we have from that source: Ceria is also very hard which has made it a useful roche or polish for lens. If you happen to want to grind or polish your own telescope, then cerium dioxide is probably what you will use. But what makes the oxide really interesting is it misbehaves. Although the formula may appear to be CeO2, one cerium 2 oxygens in reality the compound always has slightly less than 2 oxygens; the surface is peppered with defects, gaps where an oxygen atom should be and the degree of imperfection varies.
 * For cerocene, the Nature source reads Another fun aspect of element 58 engendered by its redox activity is the somewhat unconventional and controversial electronic structures of its compounds, such as cerocene (Ce(C8H8)2), an 8-fold symmetric, eclipsed sandwich complex. The most accurate picture of the valence at its cerium cation has remained somewhat ambiguous. Energy decomposition analysis suggests a strong ionic interaction between the cerium centre and each cyclooctatetraene ring, and X-ray absorption spectroscopy indicates that cerocene has a ground state that is strongly multiconfigurational — so much so that the compound is now described as 'intermediate valent'. It is trapped between configurations of Ce(III) and Ce(IV) character that are quantum-mechanically admixed and comprise a strongly stabilized open-shell singlet ground state. ... The simultaneous local/non-local character of the 4f-electron in cerocene is reminiscent of f-element superconductors' behaviour, and investigations on cerium compounds can provide insight on how local behaviour gives rise to exotic materials properties. I'd do the same for the last source about the intermetallics, but I'd have to quote quite a lot of it.
 * In fairness, I cannot find where Kotani originally wrote that. However, I somehow doubt the Royal Society of Chemistry would've made it completely up. Double sharp (talk) 22:00, 23 January 2022 (UTC)
 * Double sharp (talk) 22:13, 23 January 2022 (UTC)
 * Thanks for solving this; the problem with using audio sources is that they are harder to use. I am not sure that I would interpret the sources as implying Furthermore, each cerium atom in ceria does not lose all four of its valence electrons, but retains a partial hold on the last one, resulting in an oxidation state between +3 and +4, however; as far as I know a non stoichiometric compound is a different thing from "partial hold" and -ocene compounds to my understanding often have charge-valence peculiarities. Incidentally, even after solving this issue I see there are other uncited sentences, stubby paragraphs and unsourced paragraphs here. Perhaps this should be sent to a good article review. Jo-Jo Eumerus (talk) 10:21, 24 January 2022 (UTC)
 * That bit is in the RSC podcast too: But if you take an even closer look at Ceria it becomes more confusing. At first sight it looks like a no-brainer. Cerium looses 4 electrons handing them over to the surrounding oxygen leaving aside defects, this means it has a 4+ oxidation state. But on very close inspection with x-ray spectroscopy its clear that the cerium hangs on to at least some of those four electrons and its true oxidation state is in a quantum mechanical limbo some where between 3 and 4.
 * I admit I haven't really kept a close eye on this article since I pushed it to GA in 2016; if you feel it should be sent to GAR, please feel free to do so. :) I see that most of the cn tags are for stuff about applications and biology; unfortunately the sources I have access to at the moment are mostly on chemistry, so I may not be able to fix them, but I can try looking. Double sharp (talk) 11:47, 24 January 2022 (UTC)
 * OK, I'll proceed. Jo-Jo Eumerus (talk) 16:37, 24 January 2022 (UTC)

Omission of use of cerium in grinding optics
The article appears to omit the widespread use of cerium oxide as a polishing agent for the manufacture of accurate lenses and mirrors. A suspension of cerium oxide particles is used instead of much harder silicon carbide or even harder diamond grains on the surface of a tool made with polishing pitch, especially in hand polishing, because you want a hardness closer to the softness of the glass surface being polished, to avoid the over-removal of glass from the surface being polished. David Spector (talk) 19:48, 12 November 2022 (UTC)

Source verification: Greenwood and Earnshaw (1997). Chemistry of the Elements (2nd ed.)
Does anyone have access to the Greenwood and Earnshaw ref? I would like to verify: The measured abundances of less common elements varies widely with the location tested. Consequently comparisons of "relative abundance" are often meaningless. Nevertheless wikipedia editors like to read the tables of abundance and draw their own conclusions.
 * "Cerium is the most abundant of all the lanthanides, "
 * "Thus, despite its position as one of the so-called rare-earth metals, cerium is actually not rare at all."
 * any comparison of abundance to the abundance of other elements similar to the one in the article.

Tnanks! Johnjbarton (talk) 15:55, 14 April 2024 (UTC)

 * Sure! According to G&E pg. 1229,
 * So, I guess it answers the second and third bullet points and indirectly the first (I guess?).  141 Pr  {contribs} 16:09, 14 April 2024 (UTC)
 * So, I guess it answers the second and third bullet points and indirectly the first (I guess?).  141 Pr  {contribs} 16:09, 14 April 2024 (UTC)

title: Talk:Cerium


text:
Jeu de paume

Jeu de paume (, ; originally spelled jeu de paulme; lit. '"palm game"'), nowadays known as real tennis, (US) court tennis or (in France) courte paume, is a ball-and-court game that originated in France. It was an indoor precursor of tennis played without racquets, and so "game of the hand", though these were eventually introduced. It is a former Olympic sport, and has the oldest ongoing annual world championship in sport, first established over 250 years ago. The term also refers to the court on which the game is played and its building, which in the 17th century was sometimes converted into a theatre.

History

In the earliest versions of the game, the players hit the ball with their hands, as in palla, volleyball, Fives, or certain varieties of pelota. Jeu de paume, or jeu de paulme as it was formerly spelled, literally means "palm game". In time, gloves replaced bare hands. Even when paddle-like bats, and finally racquets, became standard equipment for the game by the late 17th century, the name did not change. It became known as "tennis" in English (see History of tennis), and later "real tennis" after the derived game of lawn tennis became the more widely known sport.

The term is used in France today to denote the game of tennis on a court in which the ancient or modern game might be played. The indoor version is sometimes called jeu de courte paume or just courte paume ("short palm") to distinguish it from the outdoor version, longue paume ("long palm"), played on a field of variable length.

At the 1908 Summer Olympics, jeu de paume was a medal event: American Jay Gould II won the gold medal.

Since 1740, jeu de paume has been the subject of an amateur world championship, held each year in September. It is the oldest active trophy in international sport.

Hand

 * Fistball
 * Fives
 * Frisian handball
 * Pallone
 * Basque pelota
 * Gaelic handball
 * Hoodae

Various other forms of handball may be related to one degree or another; this is generally difficult to ascertain with certainty, and some, like the Mesoamerican ballgame clearly have an independent origin.

Racquet
Various other racquet games (squash, badminton, etc.) may be related to one degree or another.
 * Real tennis
 * Longue paume (outdoor version of jeu de paume without net)
 * Lawn tennis (what is usually meant by the term "tennis" today)

Basket

 * Jai alai, a variation of Basque pelota using a hand-held basket known as a cesta or xistera.

Cultural references
Étienne Pasquier, a writer and a historian, published an essay regarding jeu de paume in his Recherches; late 16th century. Pasquier was addicted to the sport.

The Galerie nationale du Jeu de Paume, a museum of contemporary art, is housed in a former court on the north side of the Tuileries park in the centre of Paris.

The painter Jacques-Louis David's famous sketch, le Serment du jeu de paume ('the Tennis Court Oath') now hangs in the court of the Palace of Versailles. It depicts a seminal moment of the French Revolution, when, on 20 June 1789, deputies of the Estates-General met at the court and vowed that they would not disband before the proclamation of a formal Constitution for France.

Le Jeu de Paume is a moral ode published in 1791 by André Chénier.

In the 1981 film The French Lieutenant's Woman, socialite Charles Smithson (Jeremy Irons) is seen playing jeu de paume in London.

In the Agatha Christie's Poirot TV series episode "Death in the Clouds", Poirot mentions that tennis, considered an English game, originated in 11th-century France as jeu de paume.

The 2014 Whitney Biennial exhibition featured the premiere of the stop-motion film Jeu de Paume by Joshua Mosley.

title: Jeu de paume


text:
Calimero

Calimero is an animated television series about a charming but hapless anthropomorphized chicken; the only black one in a family of yellow chickens. He wears half of his egg shell still on his head. Calimero originally appeared on the Italian television show Carosello on July 14, 1963, and soon became a popular icon in Italy.

The characters were created by the animation studio Organizzazione Pagot and originated as a series of animated advertisements for Miralanza AVA soap products shown throughout Italy. The creators of the main character were Nino Pagot, Toni Pagot and Ignazio Colnaghi. At the end of each episode, it turns out that Calimero is not actually black, but only very dirty, and becomes white after being washed by the advertised soap products.

The characters were later licensed in Japan as an anime series twice, titled Calimero (カリメロ). The first was made by Toei Animation and ran from October 15, 1972, to September 30, 1975; the second, with new settings and characters, was made in 1992. Altogether, 99 Japanese episodes were made (47 in the 1972 Toei series, and 52 in the 1992 Toei series). The series mostly consists of the many adventures of Calimero and his friends as they solve mysteries and make documentaries. However, their adventures usually get them into quite a bit of trouble. The second series was never renewed for a second season. English dubbed versions for the first two anime series were never officially released, though dubbed pilot episodes do exist. However, the series did come out in other languages. The original 1970s shorts and the third CGI series were released in English, however. The first series was also broadcast on European networks such as TROS (The Netherlands), ZDF and RTL II (Germany) or TVE (Spain).

A third animation series about the character, in computer animation, premiered in TF1 in 2013. The production team includes France’s Gaumont Animation, rights owner Calidra, Italy’s Studio Campedelli and Japanese partners TV Tokyo and Kodansha. The series also aired on several other TV channels, including on Disney Junior in the United Kingdom and Australia.

1974 series

 * Calimero (カリメロ) – The hero of the show.
 * Priscilla (プリシラ) – Calimero's girlfriend, a shy bird with common sense.
 * Peter Jobatta (ピーター ジョバッタ) –
 * Buta (ブータ) –
 * Deppa (デッパ) –
 * Calimero's mother (カリメロの母) –
 * Calimero's father (カリメロの父) –
 * Mr. Owl (フクロウ先生) –

1992 series

 * Calimero –
 * Priscilla –
 * Peter (ピーター) –
 * Giuliano (Peanut in English dub pilot) (ジュリアーノ) –
 * Susie (スージー) – a wealthy girl duck.
 * Roshita (ロシータ) –
 * Pepe (ペペ) –

2013 series

 * Calimero - Voiced by: Rachel Berger (English) / Fanny Bloc (French) / Ayaka Asai (Japanese)
 * Priscilla -Voiced by: Naïke Fauveau (French) / Rumi Ōkubo (Japanese)
 * Giuliano (Valeriano in UK English dub)- Voiced by Georges de Vitis (French) / Kokoro Kikuchi (Japanese)
 * Peter (Pierrot in UK English dub) - Voiced by: Pascal Sellem (French) / Tōru Sakurai (Japanese)
 * Susie - Voiced by: Ren Kato (Japanese)
 * Pepe - Voiced by: Tōmoyuki Maruyama (Japanese)

Mobile game
A mobile game titled Calimero's Village was released for iOS and Android in 2015 by BulkyPix.

Impact in popular culture
The main character in the anime series has had a lasting impact in the vocabulary of some countries, either because of his looks, with an egg shell on his head, or because of his frequent complaining about being unfairly treated by others:

 * Calimero is the name and subject of a Welsh language song by the band Super Furry Animals
 * French singer Brigitte Fontaine collaborated with the band Stereolab on a song of the same name
 * In the Netherlands and Belgium, the term "" is used to denote people who are staunchly convinced that their position as an underdog is due to their smaller size, either literally or symbolically, which covers up for their own shortcomings. Often the character's lines from the show are cited, "They are big and I is [sic] small and that is not fair, oh no!" (translated back from Dutch, with intentional error).
 * The slang nickname during the 1970s and 1980s for military policemen in the Israeli Army was Calimero, due to their egg-shaped white helmet; the same was the case in Spain, where calimero was also a name for a type of helmet for motorbikers.
 * In parts of Yugoslavia, the Polski Fiat 126p was nicknamed Kalimero in reference to the character.
 * Italian luxury fashion house Bottega Veneta introduced the "Kalimero" bucket bag in 2022, taking inspiration from the bindle that the character carries.

title: Calimero