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Krista and Tatiana Hogan (born October 25, 2006) are Canadians who are conjoined craniopagus twins. They are joined at the head (the top, back, and sides). They were born in Vancouver, British Columbia and are the only unseparated ones of that type currently alive in Canada. They live with their mother, Felicia Simms, in Vernon, British Columbia and often travel to Vancouver for care at BC Children's Hospital and Sunny Hill Health Centre for Children.
Based on statistics, the twins were given a 20% chance of survival at birth . At birth at B.C. Women's Hospital & Health Centre, they were described as "wriggly, vigorous and very vocal." They weighed twelve and a half pounds, not six and a half pounds as reported by some media outlets, when they were born by caesarean section.
Anastasia and Tatiana Dogaru
born August 29, 2004) are craniopagus conjoined twins. They were scheduled to begin the first of several surgeries to separate them at Rainbow Babies and Children's Medical Center in Cleveland, Ohio. However, in August 2007 the surgery was called off as too dangerous.
The twins were born in Rome, Italy to Romanian parents, Alin Dogaru, a Byzantine Catholic priest, and Claudia Dogaru, a nurse. Their mother heard about the successful separation of Egyptian-born twins who were also joined at the head and hoped her children could also be successfully separated. The Dogaru family — who also have an older daughter, Maria, and younger son Theodor — were brought to north Texas by the World Craniofacial Foundation to have Anastasia and Tatiana evaluated for possible separation.
The girls are currently developing normally for their age and speak both Romanian and English. They get around with Anastasia leading the way and Tatiana following. The top of Tatiana's head is attached to the back of Anastasia's. Anastasia, whose kidneys don't function, relies on her sister's kidneys, and Tatiana on her sister's circulatory system. The girls also share blood flow to the back of the brain and some brain matter. Doctors estimated the twins had only a 50 percent chance of surviving the surgery. There were also risks of complications, such as brain damage, but the girls also risk early death if they remain conjoined. Their parents believed separation would give them their best chance at living a normal life.
In May 2007, doctors used a catheter to insert wire coils into the veins of the two girls, successfully redirecting their blood flow. It was the first time the procedure was attempted in conjoined twins. Doctors pushed back the first of the planned separation surgeries to June 2007 while studying the complex circulatory system of the twins, but, in August of that year, decided it was too risky.
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.
Craniopagus twins are conjoined twins that are fused at the cranium. This condition occurs in about 10–20 babies in every million births in the United States. Among this small group, cephalic conjoining, or craniopagus twinning, represents the rarest of congenital abnormalities, accounting for 2–6% of all conjoined twins. Additionally, conjoined twins are genetically identical and always share the same sex. The union in craniopagus twins may occur on any portion of the Calvary, but does not include either the face or the foramen magnum. The thorax and abdomen are separate and each twin has its own umbilicus and umbilical cord. The union may involve the entire diameter of the head or only a small portion. This suggests that although there are many different kinds of vulnerabilities already known in the scientific community, there are an infinite number of variations that can occur. Most of these variations are based on the rotation of one twin's skull to the other and the different phenotype sub-groups of craniopagus twins are based on all these rotational conformations. Each of these factors (rotation, spot of union) affects the development of the brain, the vascular system within the brain and overall wellness of life both of the twins have outside the womb. Relatively few craniopagus twins survive the perinatal period – approximately 40% of conjoined twins are stillborn and an additional 33% die within the immediate perinatal period, usually from organ abnormalities and failure. However 25% of craniopagus twins survive and can be considered for a surgical separation and several attempts occur yearly worldwide. In the last-half century, many advances in medicine including brain imaging, neuro-anesthesia and neurosurgical techniques have proven that a successful outcome is possible following separation of total craniopagus twins.
The causes of childhood obesity can be based on both a combination of individual choices and socio-environmental adaptions with genetic factors playing an important role also.
The medical condition of being overweight or obesity is defined as "abnormal or excessive fat accumulation that may impair health". It is measured through the Body Mass Index (BMI), defined as a person's weight, in kilograms, divided by the square of the person's height, in meters. If an individual has a BMI of 25–29, he or she is overweight. Having a BMI of 30 or more means an individual is obese. The greater the BMI, the greater the risk of chronic diseases as a result of obesity. These diseases include cardiovascular diseases, diabetes, musculoskeletal disorders, cancer, and premature death.
One reason that poverty produces such high rates of fistula cases is the malnutrition that exists in such areas. Lack of money and access to proper nutrition, as well as vulnerability to diseases that exist in impoverished areas because of limited basic health care and disease prevention methods, cause inhabitants of these regions to experience stunted growth. Sub-Saharan Africa is one such environment where the shortest women have on average lighter babies and more difficulties during birth when compared with full-grown women. This stunted growth causes expectant mothers to have skeletons unequipped for proper birth, such as an underdeveloped pelvis. This weak and underdeveloped bone structure increases the chances that the baby will get stuck in the pelvis during birth, cutting off circulation and leading to tissue necrosis. Because of the correlation between malnutrition, stunted growth, and birthing difficulties, maternal height can at times be used as a measure for expected labor difficulties.
Genetics, according to the Australian Health Survey plays a primary role in determining obesity. In 2011/2012 it was recorded that 90% of the Australian population had inherited their obese tendencies due to the epigenetic modifications of their mothers during pregnancy. Interchanging closely with the genetic factor, the environment and individual temptations are also highlighted as contributing causes to the worldwide epidemic. The genetic configuration influences the tendencies to become overweight, and diet and physical activity determines to what extent those tendencies are elaborated.
High levels of poverty also lead to low levels of education among impoverished women concerning maternal health. This lack of information in combination with obstacles preventing rural women to easily travel to and from hospitals lead many to arrive at the birthing process without prenatal care. This can cause a development of unplanned complications that may arise during home births, in which traditional techniques are used. These techniques often fail in the event of unplanned emergencies, leading women to go to hospital for care too late, desperately ill, and therefore vulnerable to the risks of anesthesia and surgery that must be used on them. In a study of women who had prenatal care and those who had unbooked emergency births, “the death rate in the booked-healthy group was as good as that in many developed countries, [but] the death rate in the unbooked emergencies was the same as the death rate in England in the 16th and 17th centuries.” In this study, 62 unbooked emergency women were diagnosed with obstetric fistulae out of 7,707 studied, in comparison to three diagnosed booked mothers out of 15,020 studied. In addition, studies find that education is associated with lower desired family size, greater use of contraceptives, and increased use of professional medical services. Educated families are also more likely to be able to afford health care, especially maternal healthcare.
The MONICA Project, sponsored by the World Health Organization, discovered that 30% of the population in the Arab World is overweight or obese, including adolescents and adults. This percentage is smaller for North African countries than oil-producing countries, but is still a prevalent trend. The spread of the Western lifestyle, defined as "the intake of attractive energy dense food with undesirable composition, increased consumption of animal fats and sugars and reduced consumption of dietary fiber, along with a lack of sufficient physical activity", is one of the leading causes. Specifically in the Arabian Peninsula, "physical activity of the population has significantly diminished with the availability of housemaids, private cars, television, and sophisticated household appliances. In addition, the types of food and fat intake have changed...".
Other common factors, besides a sedentary lifestyle and unhealthy food choices, across the Arab world include urbanization, technology, and a cultural appreciation of female plumpness and the practice of "leblouh" ("fattening").
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.
Though heart disease is not exclusive to the poor, there are aspects of a life of poverty that contribute to its development. This category includes coronary heart disease, stroke and heart attack. Heart disease is the leading cause of death worldwide and there are disparities of morbidity between the rich and poor. Studies from around the world link heart disease to poverty. Low neighborhood income and education were associated with higher risk factors. Poor diet, lack of exercise and limited (or no) access to a specialist were all factors related to poverty, though to contribute to heart disease.
Both low income and low education were predictors of coronary heart disease, a subset of cardiovascular disease. Of those admitted to hospital in the United States for heart failure, women and African Americans were more likely to reside in lower income neighborhoods. In the developing world, there is a 10 fold increase in cardiac events in the black and urban populations.
There is most likely a link between children's linear growth and household sanitation practices. The ingestion of high quantities of fecal bacteria by young children through putting soiled fingers or household items in the mouth leads to intestinal infections. This affect children's nutritional status by diminishing appetite, reducing nutrient absorption, and increasing nutrient losses.
The diseases recurrent diarrhoea and intestinal worm infections (helminthiasis) which are both linked to poor sanitation have been shown to contribute to child stunting. The evidence that a condition called environmental enteropathy also stunts children is not conclusively available yet, although the link is plausible and several studies are underway on this topic. Environmental enteropathy is a syndrome causing changes in the small intestine of persons and can be brought on due to lacking basic sanitary facilities and being exposed to faecal contamination on a long-term basis.
Research on a global level has found that the proportion of stunting that could be attributed to five or more episodes of diarrhoea before two years of age was 25%. Since diarrhoea is closely linked with water, sanitation and hygiene (WASH), this is a good indicator for the connection between WASH and stunted growth. To what extent improvements in drinking water safety, toilet use and good handwashing practices contribute to reduce stunting depends on the how bad these practices were prior to interventions.
Poor maternal nutrition during pregnancy and breastfeeding can lead to stunted growth of their children. Women who are underweight or anemic during pregnancy, are more likely to have stunted children which perpetuates the inter-generational transmission of stunting.
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".
The exact nature of how conjoined twins develop inutero remains unclear. Embryologists have traditionally attributed identical twinning as "splitting or fission" of either the inner cell mass of pleuripotential cells or early embryonic disc at 13–14 days of gestation just before the primitive streak. Some theorists suggested that conjoined twins develop as a result of the failed fusion of a single fertilized ovum. However a new hypothesis suggests that cranial fusion occurs between two separate embryos prior to the end of the 4th week of gestation. This is able to happen because the cranial neuropore is still open which is responsible for the ultimate fusion and formation of the brain stem and central nervous system. Furthermore, this secondary fusion of embryonic discs could implicate that intact skin will not fuse to other intact skin, including the ectoderm of the embryo. This means that two embryonic discs could only unite in locations where the ectoderm is absent. Moreover, the fusion occurs from neural folds of two separate, dorsally oriented embryonic discs, and the union can occur only after the ectoderm is disrupted to allow the neural and surface ectodermal layers to separate from each other.
The union in craniopagus twins may happen at any portion of the calvarium. The juncture can involve either the entire diameter of the head or any portion of the head and can be positioned at a multitude of rotational angles. In fact, craniopagus twins are rarely found in a symmetrical union. Apart from this, the vertebral axes may have a straight line. Despite this, the angle of the vertebrae is the ultimate dictator in how the individuals heads actually face. The majority of twins face either the same way or the exact opposite direction.
Many reviews suggest a practical four-category system that breaks down the craniopagus twins on the basis of vertical or angular configuration or on the basis if there were shared dural venous sinuses. This scheme was applied to 64 cases and has adequately described sets of twins for over the last 86 years.
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.
Heat-related illnesses from occupational heat stress have several risk factors. Some of these factors include high temperatures, humidity, radiant heat sources, limited air movement, metabolic heat from physical exertion of energy, not drinking enough fluids, personal protective equipment and clothing, physical condition and health problems, medications, pregnancy, lack of acclimatization, advanced age, having a previous heat-related illness and others.
In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.
Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.
Heat alert programs should be developed for implementation when hotter than normal temperatures, or a heat wave occurs.
While moderate to severe traumatic brain injury is a risk for ALS, it is unclear if mild traumatic brain injury increases rates.
In 1994 the National Institute for Occupational Safety and Health (NIOSH) reported a nonsignificant increase in nervous system disorders due to four cases of ALS among National Football League (NFL) players. It was unclear if this was due to chance or not. Another study from 2012 also found a possible increase in ALS in NFL football players. An older study did not find an increased risk among high school football players. A 2007 review found an increased risk among soccer players. ALS may also occur more often among the US military veterans however the reason is unknown. This may be due to head injury.
After the 2012 report was released, some NFL players involved in the legal settlement with the NFL complained that the NFL, which initially agreed to pay $765 million, was not doing enough to help players. The judge in the case concurred, and the NFL then agreed to pay an unlimited amount of damages for players found to have ALS, Parkinson's disease, Alzheimer's disease and dementia.
Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.
Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.
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.
Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).