Ganga and Jamuna Mondal (born Ayara and Jayara Ratun, 1969 or 1970), known professionally as The Spider Girls and The Spider Sisters, are conjoined twins from a Bengali family in Basirhat, West Bengal, India.

In Chinese alchemy, elixir poisoning refers to the toxic effects from elixirs of immortality that contained metals and minerals such as mercury and arsenic. The official "Twenty-Four Histories" record numerous Chinese emperors, nobles, and officials who ironically died from taking elixirs in order to prolong their lifespans. The first emperor to die from elixir poisoning was likely Qin Shi Huang (d. 210 BCE) and the last was Yongzheng (d. 1735). Despite common knowledge that immortality potions could be deadly, fangshi and Daoist alchemists continued the elixir-making practice for two millennia.

They work at the travelling "Dreamland Circus" in India. Their "act" consists of them sitting on a charpoy in a tent, with paying spectators allowed entry to view and converse with them. In 2009, they were reported to have earned GBP26 for five hours a night. They are married to a single man named Gadadhar, a carnival worker.

Heat alert programs should be developed for implementation when hotter than normal temperatures, or a heat wave occurs.

International Organization for Standardization helps set standards for monitoring environments, analyzing data, and interpreting results.

The etymology of English elixir derives from Medieval Latin "", from Arabic ("al-ʾiksīr"), probably from Ancient Greek ("xḗrion" "a desiccative powder for wounds"). "Elixir" originated in medieval European alchemy meaning "A preparation by the use of which it was sought to change metals into gold" (elixir stone or philosopher's stone) or "A supposed drug or essence with the property of indefinitely prolonging life" (elixir of life). The word was figuratively extended to mean "A sovereign remedy for disease. Hence adopted as a name for quack medicines" (e.g., Daffy's Elixir) and "The quintessence or soul of a thing; its kernel or secret principle". In modern usage, "elixir" is a pharmaceutical term for "A sweetened aromatic solution of alcohol and water, serving as a vehicle for medicine" ("Oxford English Dictionary", 2nd ed., 2009). Outside of Chinese cultural contexts, English "elixir poisoning" usually refers to accidental contamination, such as the 1937 Elixir sulfanilamide mass poisoning in the United States.

"Dān" 丹 "cinnabar; vermillion; elixir; alchemy" is the keyword for Chinese immortality elixirs. The red mineral cinnabar ("dānshā" 丹砂 lit. "cinnabar sand") was anciently used to produce the pigment vermilion ("zhūhóng" 朱紅) and the element mercury ("shuǐyín" 水銀 "watery silver" or "gǒng" 汞).

According to the "ABC Etymological Dictionary of Old Chinese", the etymology of Modern Standard Chinese "dān" from Old Chinese "*tān" (< *"tlan" ?) 丹 "red; vermillion; cinnabar", "gān" 矸 in "dāngān" 丹矸 from *"tân-kân" (< *"tlan-klan" ?) "cinnabar; vermillion ore", and "zhān" from *"tan" 旃 "a red flag" derive from Proto-Kam-Sui *"h-lan" "red" or Proto-Sino-Tibetan *"tja-n" or *"tya-n" "red". The *"t-" initial and *"t-" or *"k-" doublets indicate that Old Chinese borrowed this item. (Schuessler 2007: 204).

Although the word "dan" 丹 "cinnabar; red" frequently occurs in oracle script from the late Shang Dynasty (ca. 1600-1046 BCE) and bronzeware script and seal script from the Zhou Dynasty (1045-256 BCE), paleographers disagree about the graphic origins of the logograph 丹 and its ancient variants 𠁿 and 𠕑. Early scripts combine a 丶 dot or ⼀ stroke (depicting a piece of cinnabar) in the middle of a surrounding frame, which is said to represent:

- "jǐng" 井 "well" represents the mine from which the cinnabar is taken" ("Shuowen Jiezi")

- "the crucible of the Taoist alchemists" (Léon Wieger )

- "the contents of a square receptacle" (Bernhard Karlgren)

- "placed in a tray or palette to be used as red pigment" (Wang Hongyuan 王宏源)

- "mineral powder on a stretched filter-cloth" (Needham and Lu).

Many Chinese elixir names are compounds of "dan", such as "jīndān" 金丹 (with "gold") meaning "golden elixir; elixir of immortality; potable gold" and "xiāndān" 仙丹 (with "Daoist immortal") "elixir of immortality; panacea", and "shéndān" 神丹 (with "spirit; god") "divine elixir". "Bùsǐ zhī yào" 不死之藥 "drug of deathlessness" was another early name for the elixir of immortality. Chinese alchemists would "liàndān" 煉丹 (with "smelt; refine") "concoct pills of immortality" using a "dāndǐng" 丹鼎 (with "tripod cooking vessel; cauldron") "furnace for concocting pills of immortality". In addition, the ancient Chinese believed that other substances provided longevity and immortality, notably the "língzhī" 靈芝 ""Ganoderma" mushroom".

The transformation from chemistry-based "waidan" 外丹 "external elixir/alchemy" to physiology-based "neidan" 內丹 "internal elixir/alchemy" gave new analogous meanings to old terms. The human body metaphorically becomes a "ding" "cauldron" in which the adept forges the Three Treasures (essence, life-force, and spirit) within the "jindan" Golden Elixir within the "dāntián" 丹田 (with "field") "lower part of the abdomen".

In early China, alchemists and pharmacists were one in the same. Traditional Chinese Medicine also used less concentrated cinnabar and mercury preparations, and "dan" means "pill; medicine" in general, for example, "dānfāng" 丹方 semantically changed from "prescription for elixir of immortality" to "medical prescription". "Dan" was lexicalized into medical terms such as " dānjì" 丹劑 "pill preparation" and "dānyào" 丹藥 "pill medicine".

The Chinese names for immortality elixirs have parallels in other cultures and languages, for example, Indo-Iranian "soma" or "haoma", Sanskrit "amrita", and Greek "ambrosia".

A formal diagnose of any type of echinococcosis requires a combination of tools that involve imaging techniques, histopathology, or nucleic acid detection and serology. For cystic echinococcosis diagnosis, imaging is the main method—while serology tests (such as indirect hemogglutination, ELISA (enzyme linked immunosorbent assay), immunoblots or latex agglutination) that use antigens specific for "E. granulosus" verify the imaging results. The imaging technique of choice for cystic echinococcosis is ultrasonography, since it is not only able to visualize the cysts in the body's organs, but it is also inexpensive, non-invasive and gives instant results. In addition to ultrasonography, both MRI and CT scans can and are often used although an MRI is often preferred to CT scans when diagnosing cystic echinococcosis since it gives better visualization of liquid areas within the tissue.

"'Conjoined twins" are identical twins joined in utero. An extremely rare phenomenon, the occurrence is estimated to range from 1 in 49,000 births to 1 in 189,000 births, with a somewhat higher incidence in Southeast Asia and Africa. Approximately half are stillborn, and an additional one-third die within 24 hours. Most live births are female, with a ratio of 3:1.

Two contradicting theories exist to explain the origins of conjoined twins. The more generally accepted theory is "fission", in which the fertilized egg splits partially. The other theory, no longer believed to be the basis of conjoined twinning, is fusion, in which a fertilized egg completely separates, but stem cells (which search for similar cells) find like-stem cells on the other twin and fuse the twins together. Conjoined twins share a single common chorion, placenta, and amniotic sac, although these characteristics are not exclusive to conjoined twins as there are some monozygotic but non-conjoined twins who also share these structures in utero.

The most famous pair of conjoined twins was Chang and Eng Bunker (Thai: อิน-จัน, In-Chan) (1811–1874), Thai brothers born in Siam, now Thailand. They traveled with P.T. Barnum's circus for many years and were labeled as the Siamese twins. Chang and Eng were joined at the torso by a band of flesh, cartilage, and their fused livers. In modern times, they could have been easily separated. Due to the brothers' fame and the rarity of the condition, the term "Siamese twins" came to be used as a synonym for conjoined twins.

As with cystic echinococcosis, ultrasonography is the imaging technique of choice for alveolar echinococcosis and is usually complemented by CT scans since CT scans are able to detect the largest number of lesions and calcifications that are characteristic of alveolar echinococcosis. MRIs are also used in combination with ultrasonography though CT scans are preferred. Like cystic echinococcosis, imaging is the major method used for the diagnosis of alveolar echinococcosis while the same types of serologic tests (except now specific for "E. multilocularis" antigens) are used to verify the imaging results. It is also important to note that serologic tests are more valuable for the diagnosis of alveolar echinococcosis than for cystic echinococcosis since they tend to be more reliable for alveolar echinococcosis since more antigens specific for "E. multilocularis" are available. In addition to imaging and serology, identification of "E. multilocularis" infection via PCR or a histological examination of a tissue biopsy from the patient is another way to diagnose alveolar echinococcosis.

Growth stunting is identified by comparing measurements of children's heights to the World Health Organization 2006 growth reference population: children who fall below the fifth percentile of the reference population in height for age are defined as stunted, regardless of the reason. The lower than fifth percentile corresponds to less than two standard deviations of the WHO Child Growth Standards median.

As an indicator of nutritional status, comparisons of children's measurements with growth reference curves may be used differently for populations of children than for individual children. The fact that an individual child falls below the fifth percentile for height for age on a growth reference curve may reflect normal variation in growth within a population: the individual child may be short simply because both parents carried genes for shortness and not because of inadequate nutrition. However, if substantially more than 5% of an identified child population have height for age that is less than the fifth percentile on the reference curve, then the population is said to have a higher-than-expected prevalence of stunting, and malnutrition is generally the first cause considered.

The diagnosis of neurocysticercosis is mainly clinical, based on a compatible presentation of symptoms and findings of imaging studies.

There are currently only two donor-funded non-governmental organizations that focus exclusively on NTDs: the Schistosomiasis Control Initiative and Deworm the World. Despite under-funding, many neglected diseases are cost-effective to treat and prevent. The cost of treating a child for infection of soil transmitted helminths and schistosomes (some of the main causes of neglected diseases), is less than US$0.50 per year, when administered as part of school-based mass deworming by Deworm the World. This programme is recommended by Giving What We Can and the Copenhagen Consensus Centre as one of the most efficient and cost-effective solutions. The efforts of Schistosomiasis Control Initiative to combat neglected diseases include the use of rapid-impact packages: supplying schools with packages including four or five drugs, and training teachers in how to administer them.

Neuroimaging with CT or MRI is the most useful method of diagnosis. CT scan shows both calcified and uncalcified cysts, as well as distinguishing active and inactive cysts. Cystic lesions can show ring enhancement and focal enhancing lesions. Some cystic lesions, especially the ones in ventricles and subarachnoid space may not be visible on CT scan, since the cyst fluid is isodense with cerebrospinal fluid (CSF). Thus diagnosis of extraparenchymal cysts usually relies on signs like hydrocephalus or enhanced basilar meninges. In such cases CT scan with intraventricular contrast or MRI can be used. MRI is more sensitive in detection of intraventricular cysts.

Three main things are needed to reduce stunting:

- a kind of environment where political commitment can thrive (also called an "enabling environment")

- applying several nutritional modifications or changes in a population on a large scale which have a high benefit and a low cost

- a strong foundation that can drive change (food security, empowerment of women and a supportive health environment through increasing access to safe water and sanitation).

To prevent stunting, it is not just a matter of providing better nutrition but also access to clean water, improved sanitation (hygienic toilets) and hand washing at critical times (summarised as "WASH"). Without provision of toilets, prevention of tropical intestinal diseases, which may affect almost all children in the developing world and lead to stunting will not be possible.

Studies have looked at ranking the underlying determinants in terms of their potency in reducing child stunting and found in the order of potency:

- percent of dietary energy from non-staples (greatest impact)

- access to sanitation and women's education

- access to safe water

- women's empowerment as measured by the female-to-male life expectancy ratio

- per capita dietary energy supply

Three of these determinants should receive attention in particular: access to sanitation, diversity of calorie sources from food supplies, and women's empowerment. A study by the Institute of Development Studies has stressed that: "The first two should be prioritized because they have strong impacts yet are farthest below their desired levels".

The goal of UN agencies, governments and NGO is now to optimise nutrition during the first 1000 days of a child's life, from pregnancy to the child's second birthday, in order to reduce the prevalence of stunting. The first 1000 days in a child's life are a crucial "window of opportunity" because the brain develops rapidly, laying the foundation for future cognitive and social ability. Furthermore, it is also the time when young children are the most at risk of infections that lead to diarrhoea. It is the time when they stop breast feeding (weaning process), begin to crawl, put things in their mouths and become exposed to faecal matter from open defecation and environmental enteropathies.

Biotechnology companies in the developing world have targeted neglected tropical diseases due to need to improve global health.

Mass drug administration is considered a possible method for eradication, especially for lymphatic filariasis, onchocerciasis, and trachoma, although drug resistance is a potential problem. According to Fenwick, Pfizer donated 70 million doses of drugs in 2011 to eliminate trachoma through the International Trachoma Initiative. Merck has helped The African Programme for the Control of Onchocerciasis (APOC) and Oncho Elimination Programme for the Americas to greatly diminished the effect of Onchocerciasis by donating ivermectin. Merck KGaA pledged to give 200 million tablets of praziquantel over 10 years, the only cure for schistosomiasis. GlaxoSmithKline has donated two billion tablets of medicine for lymphatic filariasis and pledged 400 million deworming tablets per year for five years in 2010. Johnson & Johnson has pledged 200 million deworming tablets per year. Novartis has pledged leprosy treatment, EISAI pledged two billion tablets to help treat lymphatic filariasis.

MJD can be diagnosed by recognizing the symptoms of the disease and by taking a family history. Physicians ask patients questions about the kind of symptoms relatives with the disease had, the progression and harshness of symptoms, and the ages of onset in family members.

Presymptomatic diagnosis of MJD can be made with a genetic test. The direct detection of the genetic mutation responsible for MJD has been available since 1995. Genetic testing looks at the number of CAG repeats within the coding region of the MJD/ATXN3 gene on chromosome 14. The test will show positive for MJD if this region contains 61-87 repeats, as opposed to the 12-44 repeats found in healthy individuals. A limitation to this test is that if the number of CAG repeats in an individual being tested falls between the healthy and pathogenic ranges (45-60 repeats), then the test cannot predict whether an individual will have MJD symptoms.

Specific helminths can be identified through microscopic examination of their eggs (ova) found in faecal samples. The number of eggs is measured in units of eggs per gram. However, it does not quantify mixed infections, and in practice, is inaccurate for quantifying the eggs of schistosomes and soil-transmitted helmiths. Sophisticated tests such as serological assays, antigen tests, and molecular diagnosis are also available; however, they are time-consuming, expensive and not always reliable.

For basic diagnosis, specific helminths can be generally identified from the faeces, and their eggs microscopically examined and enumerated using fecal egg count method. However, there are certain limitations such as the inability to identify mixed infections, and on clinical practice, the technique is inaccurate and unreliable.

A novel effective method for egg analysis is the Kato-Katz technique. It is a highly accurate and rapid method for "A. lumbricoides" and "T. trichiura"; however not so much for hookworm, which could be due to fast degeneration of the rather delicate hookworm eggs.

There are five sub-types of MJD that are characterized by the age of onset and range of symptoms.

The sub-types illustrate a wide variety of symptoms that patients can experience. However, assigning individuals to a specific sub-type of the disease is of limited clinical significance.

- Type I is distinguished by arrival between the ages of 10 and 30 and represents approximately 13% of individuals. It usually has fast development and severe rigidity and dystonia.

- Type II is the most common sub-type (approximately 57% of individuals with MJD ) and typically begins between 20 and 50 years of age . It has an intermediate progression and causes symptoms that include spasticity, exaggerated reflex responses and spastic gait, ataxia and upper motor neuron signs.

- Type III MJD has a slow progression. Patients typically have an onset between the ages of 40 and 70 and represent approximately 30% of MJD patients. Symptoms include muscle twitching, tingling, cramps, unpleasant sensations such as numbness, pain in the feet, hands and limbs and muscle atrophy. Nearly all patients experience a decline in their vision such as blurred vision, double vision, inability to control eye movements, and loss of capability to distinguish color. Some patients also experience Parkinsonian symptoms.

- Type IV is distinguished by Parkinsonian symptoms that respond particularly well to levodopa treatment.

- Type V appears to resemble Hereditary Spastic Paraplegia; however, more research is needed to conclude the relationship between Type V MJD and hereditary spastic paraplegia.

Poverty and disease are tied closely together, with each factor aiding the other. Many diseases that primarily affect the poor serve to also deepen poverty and worsen conditions. Poverty also significantly reduces people's capabilities making it more difficult to avoid poverty related diseases.

The majority of diseases and related mortality in poor countries is due to preventable, treatable diseases for which medicines and treatment regimes are readily available. Poverty is in many cases the single dominating factor in higher rates of prevalence of these diseases. Poor hygiene, ignorance in health-related education, non-availability of safe drinking water, inadequate nutrition and indoor pollution are factors exacerbated by poverty.

Just the big three PRDs — TB, AIDS/HIV and Malaria — account for 18% of diseases in poor countries. The disease burden of treatable childhood diseases in high-mortality, poor countries is 5.2% in terms of disability-adjusted life years but just 0.2% in the case of advanced countries.

In addition, infant mortality and maternal mortality are far more prevalent among the poor. For example, 98% of the 11,600 daily maternal and neonatal deaths occur in developing countries.

Together, diseases of poverty kill approximately 14 million people annually. Gastroenteritis with its associated diarrhea results in about 1.8 million deaths in children yearly with most of these in the world's poorest nations.

At the global level, the three primary poverty-related diseases (PRDs) are AIDS, malaria, and tuberculosis. Developing countries account for 95% of the global AIDS prevalence and 98% of active tuberculosis infections. Furthermore, 90% of malaria deaths occur in sub-Saharan Africa. Together, these three diseases account for 10% of global mortality.

Treatable childhood diseases are another set which have disproportionately higher rates in poor countries despite the availability of cures for decades. These include measles, pertussis and polio.

Three other diseases, measles, pneumonia, and diarrheal diseases, are also closely associated with poverty, and are often included with AIDS, malaria, and tuberculosis in broader definitions and discussions of diseases of poverty.

Painful red swelling of the hands and feet in a patient receiving chemotherapy is usually enough to make the diagnosis. The problem can also arise in patients after bone marrow transplants, as the clinical and histologic features of PPE can be similar to cutaneous manifestations of acute (first 3 weeks) graft-versus-host disease. It is important to differentiate PPE, which is benign, from the more dangerous graft-versus-host disease. As time progresses, patients with graft-versus-host disease progress to have other body parts affected, while PPE is limited to hands and feet. Serial biopsies every 3 to 5 days can also be helpful in differentiating the two disorders (Crider et al., 1986).

The most important determinant of the neurodiagnostic procedures is the state of the child at the time of first medical attendance:

(1) The child has a brief or lengthy seizure of Panayiotopoulos syndrome but fully recovers prior to arriving in the accident and emergency department or being seen by a physician. A child with the distinctive clinical features of Panayiotopoulos syndrome, particularly ictus emeticus and lengthy seizures, may not need any investigations other than EEG. However, because approximately 10% to 20% of children with similar seizures may have brain pathology, an MRI may be needed.

(2) The child with a typical lengthy seizure of Panayiotopoulos syndrome partially recovers while still in a postictal stage, tired, mildly confused, and drowsy on arrival to the accident and emergency department or when seen by a physician. The child should be kept under medical supervision until fully recovered, which usually occurs after a few hours of sleep. Then guidelines are the same as in (1) above.

(3) The child is brought to the accident and emergency department or is seen by a physician while ictal symptoms continue. This is the most difficult and challenging situation. There may be dramatic symptoms accumulating in succession, which demand rigorous and experienced evaluation. The seizure may be very dramatic, with symptoms accumulating in succession, convulsions may occur and a child who becomes unresponsive and flaccid demands rigorous and experienced evaluation. The most prominent acute disorders in the differential diagnosis include encephalitis or an encephalopathic state from causes such as infections, metabolic derangement (either inborn error or others such as hypoglycaemia), raised intracranial pressure and so forth. A history of a previous similar seizure is reassuring and may prevent further procedures.

Electroencephalography (EEG). EEG is the only investigation with abnormal results, usually showing multiple spikes in various brain locations (Figure). There is marked variability of interictal EEG findings from normal to multifocal spikes that also change significantly in serial EEGs. Occipital spikes are common but not necessary for diagnosis. Frontal or centrotemporal spikes may be the only abnormality. Generalised discharges may happen alone or together with focal spikes. A few children have consistently normal EEG, including sleep EEG. EEG abnormalities may persist for many years after clinical remission. Conversely, spikes may appear only once in successive EEGs. Series of EEGs of the same child may present with all of the above variations from normal to very abnormal. EEG abnormalities do not appear to determine clinical manifestations, duration, severity, and frequency of seizures or prognosis.

There are now significant reports of ictal EEGs in 20 cases, which objectively document the seizures of Panayiotopoulos syndrome and their variable localisation at onset. All these recorded seizures occurred while the children were asleep. The onset of the electrical ictal discharge was mainly occipital (7 cases) or frontal (7 cases)and consisted of rhythmic monomorphic decelerating theta or delta activity with small spikes. The first clinical manifestation which appeared long (1–10 minutes) after the electrical onset, usually consisted of opening of the eyes as if the children were waking from sleep. At this stage, usually the children responded, often correctly, to simple questions. On many occasions, tachycardia was the first objective sign when ||ECG|| was recorded. Vomiting was a common ictal symptom occurring at any stage of the seizures but not as the first clinical manifestation. Seizures associated with ictal vomiting did not have any particular localization or lateralization. Vomiting occurred mainly when the ictal discharges were more diffuse than localized. Sometimes only retching without vomiting occurred, and on a few occasions, vomiting did not occur. Other autonomic manifestations included mydriasis, pallor, cyanosis, tachypnea, hypersalivation, and perspiration at various stages of the ictus. Of non-autonomic manifestations, deviation of eyes to the right or left occurred before or after vomiting without any apparent EEG localisation; it was present in seizures starting from the occipital or frontal regions.

Magnetoencephalography (MEG). The multifocal nature of epileptogenicity in Panayiotopoulos syndrome has been also documented with MEG, which revealed that the main epileptogenic areas are along the parietal-occipital, the calcarine, or the central (rolandic) sulci. Patients with frontal spikes were significantly older than patients with spikes on rolandic, parieto-occipital, or calcarine sulci. Follow-up MEG demonstrated shifting localization or disappearance of MEG spikes.

Prevention and control measures to prevent soil-transmitted helminthiasis are the following: availability of clean water for personal and domestic uses, improved access to sanitation which includes the use of properly functioning and clean toilets by all community members, education on personal hygiene such as hand washing and hygienic and safe food preparation; eliminating the use of untreated human faeces as fertilizer.

As the symptoms become prominent, the child will visit their pediatrician or family doctor to confirm whether or not the child has Panner Disease. When the child visits the doctor, the doctor will seek information about the child’s age, sports participation, activity level, and what the child’s dominant arm is. The affected elbow will be compared to the healthy elbow and any differences between the two will be noted. The location of where the pain is in the elbow, and the child’s range of motion and extension will also be determined to make an accurate diagnosis. To check the child’s range of motion and extension limitation the child will be asked to move the arm of the affected elbow in various directions. The movement of the arm in various directions will allow the doctor to conclude how good the child is able to move the arm and the doctor will be able to determine if there is pain caused by the various directions of movement.

To confirm the diagnosis, an x-ray or MRI scan will be done. The radiograph will enable the doctor to visualize irregularities and see the shape of the capitellum and also visualize the growth plate. In Panner Disease, the capitellum may appear flat and the bone growth plate will look irregular and fragmented. The areas where bone breakdown has occurred can also be visualized on the radiograph. When the patient undergoes a MRI scan any irregularities of the capitellum will able to be visualized, and the bone will be able to be visualized in more detail to determine the extent of swelling, if any. In the MRI results for Panner disease, there will be a decreased signal intensity of the capitellum on a T1 series and increased signal intensity on a T2 series.