Lucio Godina (March 8, 1908 – November 24, 1936) and Simplicio Godina (March 8, 1908 - December 8, 1936) were pygopagus conjoined twins from the island of Samar in the Philippines.

At the age of 21 they married Natividad and Victorina Matos, who were identical twins. They performed in various sideshow acts, including in an orchestra on Coney Island and in dance with their wives.

After Lucio died of rheumatic fever in New York City, doctors operated to separate him from Simplicio. Simplicio survived the operation, but died shortly thereafter due to spinal meningitis.

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.

Electric shock is also used as a medical therapy, under carefully controlled conditions:

- Electroconvulsive therapy or ECT is a psychiatric therapy for mental illness. The objective of the therapy is to induce a seizure for therapeutic effect. There is no conscious sensation of the electric shock because of the anesthesia used beforehand. Convulsive therapy was introduced in 1934 by Hungarian neuropsychiatrist Ladislas J. Meduna who, believing mistakenly that schizophrenia and epilepsy were antagonistic disorders, induced seizures first with camphor and then metrazol (cardiazol). The first patient was treated by Lucio Bini and Ugo Cerlettiin. ECT is generally administered three times a week for about 8-12 treatments.

- As a surgical tool for cutting or coagulation. An "Electrosurgical Unit" (or ESU) uses high currents (e.g. 10 amperes) at high frequency (e.g. 500 kHz) with various schemes of amplitude modulation to achieve the desired result - cut or coagulate - or both. These devices are safe when used correctly.

- As a treatment for fibrillation or irregular heart rhythms: see defibrillator and cardioversion.

- As a method of pain relief: see Transcutaneous Electrical Nerve Stimulator (more commonly referred to as a TENS unit).

- As an aversive punishment for conditioning of developmentally delayed individuals with severe behavioral problems. This controversial skin-shock method is employed only at the Judge Rotenberg Educational Center, a special needs school in Massachusetts.

- As a treatment for Hyperhidrosis with the device called iontophoresis

- As part of electrodiagnosis diagnostic tests including nerve conduction studies and electromyography.

- For genetic engineering and gene delivery using a non-viral vector system electroporation

Mild electric shocks are also used for entertainment, especially as a practical joke for example in such devices as a shocking pen or a shocking gum. However devices such as a joy buzzer and most other machines in amusement parks today only use vibration that feels somewhat like an electric shock to someone not expecting it.

Patients have an essentially normal life expectancy but require regular medical follow-up.

Diagnosis often can be made through clinical examination and urine tests (excess mucopolysaccharides are excreted in the urine). Enzyme assays (testing a variety of cells or body fluids in culture for enzyme deficiency) are also used to provide definitive diagnosis of one of the mucopolysaccharidoses. Prenatal diagnosis using amniocentesis and chorionic villus sampling can verify if a fetus either carries a copy of the defective gene or is affected with the disorder. Genetic counseling can help parents who have a family history of the mucopolysaccharidoses determine if they are carrying the mutated gene that causes the disorders.

Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.

Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. and or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.

Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.

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".

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.

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.

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

Seven distinct clinical types and numerous subtypes of the mucopolysaccharidoses have been identified. Although each mucopolysaccharidosis (MPS) differs clinically, most patients generally experience a period of normal development followed by a decline in physical and/or mental function. (Note: MPS-V and MPS-VIII are no longer in use as designations for any disease.)

A karyotype is done to diagnose XXYY syndrome. Treatment consists of medications, behavioral therapies and intensive community support.

The diagnostic criteria for Dorian Gray syndrome are:

- Signs of dysmorphophobia

- Arrested development (inability to mature)

- Using at least two different medical-lifestyle products and services:

- Hair-growth restoration (e.g. finasteride)

- Antiadiposita to lose weight (e.g. orlistat)

- Anti-impotence drugs (e.g. sildenafil)

- Anti-depressant drugs (e.g. fluoxetine)

- Cosmetic dermatology (e.g. laser resurfacing)

- Cosmetic surgery (e.g. a face-lift, liposuction)

Making a correct diagnosis for a genetic and rare disease is often times very challenging. So the doctors and other healthcare professions rely on the person’s medical history, the severity of the symptoms, physical examination and lab tests to make and confirm a diagnosis.

There is a possibility of interpreting the symptoms of PWS with other conditions such as AVMs and or AVFs. This is because AVMs and AVFs also involve the characteristic overgrowth in soft tissue, bone and brain. Also PWS can be misdiagnosed with Klippel–Trenaunay syndrome (KTS). However, KTS consists of the following: triad capillary malformation, venous malformation, and lymphatic malformation.

Usually a specific set of symptoms such as capillary and arteriovenous malformations occur together and this is used to distinguish PWS from similar conditions. Arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs) are caused by RASA1 mutations as well. Therefore, if all the other tests (discussed below) fail to determine PWS, which is highly unlikely, genetic testing such as sequence analysis and gene-targeted deletion/duplication analysis can be performed to identify possible RASA1 gene mutations.

But PWS can be distinguished from other conditions because of its defining port-wine stains that are large, flat and pink. The port-wine stains and physical examination are enough to diagnose PWS. But additional testing is necessary to determine the extent of the PWS syndrome. The following tests may be ordered by physicians to help determine the appropriate next steps: MRI, ultrasound, CT/CAT scan, angiogram, and echocardiogram.

MRI: This is a high-resolution scan that is used to identify the extent of the hypertrophy or overgrowth of the tissues. This can also be used to identify other complications that may arise a result of hypertrophy.

Ultrasound: this can be necessary to examine the vascular system and determine how much blood is actually flowing through the AVMs.

CT/CAT scan: this scan is especially useful for examining the areas affected by PWS and is helpful for evaluating the bones in the overgrown limb.

Angiogram: an angiogram can also be ordered to get a detailed look at the blood vessels in the affected or overgrown limb. In this test an interventional radiologist injects a dye into the blood vessels that will help see how the blood vessels are malformed.

Echocardiogram: depending on the intensity of the PWS syndrome, an echo could also be ordered to check the condition of the heart.

And PWS often requires a multidisciplinary care. Depending on the symptoms, patients are dependent on: dermatologists, plastic surgeons, general surgeons, interventional radiologists, orthopedists, hematologists, neurosurgeons, vascular surgeons and cardiologists. Since the arteriovenous and capillary malformations cannot be completely reconstructed and depending on the extent and severity of the malformations, these patients may be in the care of physicians for their entire lives.

In most of the reported cases, the treatment options were very similar. Plasmapheresis alone or in combination with steroids, sometimes also with thymectomy and azathioprine, have been the most frequently used therapeutic approach in treating Morvan’s Syndrome. However, this does not always work, as failed response to steroids and to subsequently added plasmapheresis have been reported. Intravenous immunoglobulin was effective in one case.

In one case, the dramatic response to high-dose oral prednisolone together with pulse methylprednisolone with almost complete disappearance of the symptoms within a short period should induce consideration of corticosteroids.

In another case, the subject was treated with haloperidol (6 mg/day) with some improvement in the psychomotor agitation and hallucinations, but even high doses of carbamazepine given to the subject failed to improve the spontaneous muscle activity. Plasma Exchange (PE) was initiated, and after the third such session, the itching, sweating, mental disturbances, and complex nocturnal behavior improved and these symptoms completely disappeared after the sixth session, with improvement in insomnia and reduced muscle twitching. However, one month after the sixth PE session, there was a progressive worsening of insomnia and diurnal drowsiness, which promptly disappeared after another two PE sessions.

In one case there high dose steroid treatment resulted in a transient improvement, but aggressive immuno-suppressive therapy with cyclophosphamide was necessary to control the disease and result in a dramatic clinical improvement.

In another case, the subject was treated with prednisolone (1 mg/kg body weight) with carbamazepine, propanolol, and amitriptyline. After two weeks, improvement with decreased stiffness and spontaneous muscle activity and improved sleep was observed. After another 7–10 days, the abnormal sleep behavior disappeared completely.

In another case, symptomatic improvement with plasmapheresis, thymectomy, and chronic immunosuppression provide further support for an autoimmune or paraneoplastic basis.

Although thymectomy is believed to be a key element in the proposed treatment, there is a reported case of Morvan’s Syndrome presenting itself post-thymectomy.

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.

The time workers spend in hot environments should be limited, with an increase of recovery time spent in cool environments. Use of more efficient procedures and tools is beneficial to reducing metabolic demands of the job. Heat tolerance may be increased by implementing a heat tolerance plan and increasing physical fitness. Employees should be trained to recognize and treat the early signs and symptoms of heat illnesses, and employers should provide cool water for employees.

Being an extremely rare disease, it is unknown as to what exactly causes Panner Disease. It is believed that the disease may be brought on by continuous overuse of the elbow and that puts pressure on the elbow and also strains the elbow in children during the period of rapid bone growth. The overuse of the elbow can be due to the involvement in sports such as baseball, handball, and gymnastics where these sports involve throwing or putting a lot of pressure on the joints. These repeated activities cause microtraumas and results in the affected elbow being swollen, irritated, and in pain. Panner Disease results when the blood supply to the capitellum is disrupted and therefore the cells within the growth plate of the capitellum die and it becomes flat due to the softening and collapsing of the surrounding bone. To prevent future instances of Panner Disease the child is instructed to cease all physical and sports activities that involve the use of the affected elbow until the symptoms are relieved.

The causes for PWS are either genetic or unknown. Some cases are a direct result of the RASA1 gene mutations. And individuals with RASA1 can be identified because this genetic mutation always causes multiple capillary malformations. PWS displays an autosomal dominant pattern of inheritance. This means that one copy of the damaged or altered gene is sufficient to elicit PWS disorder. In most cases, PWS can occur in people that have no family history of the condition. In such cases the mutation is sporadic. And for patients with PWS with the absence of multiple capillary mutations, the causes are unknown.

According to Boston’s Children Hospital, no known food, medications or drugs can cause PWS during pregnancy. PWS is not transmitted from person to person. But it can run in families and can be inherited. PWS effects both males and females equally and as of now no racial predominance is found

At the moment, there are no known measures that can be taken in order to prevent the onset of the disorder. But Genetic Testing Registry can be great resource for patients with PWS as it provides information of possible genetic tests that could be done to see if the patient has the necessary mutations. If PWS is sporadic or does not have RASA1 mutation then genetic testing will not work and there is not a way to prevent the onset of PWS.

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.

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.

The diagnosis is based on the biochemical findings (increased concentrations of lysine, arginine and ornithine in urine and low concentrations of these amino acids in plasma, elevation of urinary orotic acid excretion after protein-rich meals, and inappropriately high concentrations of serum ferritin and lactate dehydrogenase isoenzymes) and the screening of known mutations of the causative gene from a DNA sample.

Immunosuppressive therapies, encompassing corticosteroids, azathioprine, methotrexate and more recently, rituximab, are the mainstay of therapy. Other treatments include PE, IVIG, and thymectomy. Patients reportedly exhibited a heterogenous response to immunomodulation.

Antiepileptics can be used for symptomatic relief of peripheral nerve hyperexcitability. Indeed, some patients have exhibited a spontaneous remission of symptoms.

Islamophobia is an intense fear or hatred of, or prejudice against, the Islamic religion or Muslims, especially when seen as a geopolitical force or the source of terrorism.

The term was first used in the early 20th century and it emerged as a neologism in the 1970s, then it became increasingly salient during the 1980s and 1990s, and it reached public policy prominence with the report by the Runnymede Trust's Commission on British Muslims and Islamophobia (CBMI) entitled "Islamophobia: A Challenge for Us All" (1997). The introduction of the term was justified by the report's assessment that "anti-Muslim prejudice has grown so considerably and so rapidly in recent years that a new item in the vocabulary is needed".

The causes and characteristics of Islamophobia are still debated. Some commentators have posited an increase in Islamophobia resulting from the September 11 attacks, some from multiple terror attacks in Europe and the United States, while others have associated it with the increased presence of Muslims in the United States and in the European Union. Some people also question the validity of the term. The academics S. Sayyid and Abdoolkarim Vakil maintain that Islamophobia is a response to the emergence of a distinct Muslim public identity globally, the presence of Muslims is in itself not an indicator of the degree of Islamophobia in a society. Sayyid and Vakil maintain that there are societies where virtually no Muslims live but many institutionalized forms of Islamophobia still exist in them.