<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Starvation and explain in detail? [/INST] Starvation is a severe deficiency in caloric energy intake, below the level needed to maintain an organisms life. It is the most extreme form of malnutrition. In humans, prolonged starvation can cause permanent organ damage and eventually, death. The term inanition refers to the symptoms and effects of starvation. Starvation may also be used as a means of torture or execution.
According to the World Health Organization (WHO), hunger is the single gravest threat to the worlds public health. The WHO also states that malnutrition is by far the biggest contributor to child mortality, present in half of all cases. Undernutrition is a contributory factor in the death of 3.1 million children under five every year. Figures on actual starvation are difficult to come by, but according to the Food and Agriculture Organization, the less severe condition of undernourishment currently affects about 842 million people, or about one in eight (12.5%) people in the world population.The bloated stomach represents a form of malnutrition called kwashiorkor. The exact pathogenesis of kwashiorkor is not clear, as initially it was thought to relate to diets high in carbohydrates (e.g. maize) but low in protein. While many patients have low albumin, this is thought to be a consequence of the condition. Possible causes such as aflatoxin poisoning, oxidative stress, immune dysregulation, and altered gut microbiota have been suggested. Treatment can help mitigate symptoms such as the pictured weight loss and muscle wasting, however prevention is of utmost importance.Without any food, humans usually die in around 2 months. There was a surprising case when someone survived 382 days. Lean people can usually survive with a loss of up to 18% of their body mass. Obese people can tolerate more, possibly over 20%. Females survive longer than males.

Signs and symptoms
The following are some of the symptoms of starvation:

Changes in behaviour or mental status
The beginning stages of starvation impact mental status and behaviours. These symptoms show up as irritable mood, fatigue, trouble concentrating, and preoccupation with food thoughts. People with those symptoms tend to be easily distracted and have no energy.

Physical signs
As starvation progresses, the physical symptoms set in. The timing of these symptoms depends on age, size, and overall health. It usually takes days to weeks, and includes weakness, fast heart rate, shallow breaths that are slowed, thirst, and constipation. There may also be diarrhea in some cases. The eyes begin to sink in and glass over. The muscles begin to become smaller and muscle wasting sets in. One prominent sign in children is a swollen belly. Skin loosens and turns pale in color, and there may be swelling of the feet and ankles.

Weakened immune system
Symptoms of starvation may also appear as a weakened immune system, slow wound healing, and poor response to infection. Rashes may develop on the skin. The body directs any nutrients available to keeping organs functioning.

Other symptoms
Other effects of starvation may include:

Anemia
Gallstones
Hypotension
Stomach disease
Cardiovascular and respiratory diseases
Irregular or absent menstrual periods in women
Kidney disease or failure
Electrolyte imbalance
Emaciation
Oliguria

Stages of starvation
The symptoms of starvation show up in three stages. Phase one and two can show up in anyone that skips meals, diets, and goes through fasting. Phase three is more severe, can be fatal, and results from long-term starvation.
Phase one: When meals are skipped, the body begins to maintain blood sugar levels by producing glycogen in the liver and breaking down stored fat and protein. The liver can provide glycogen for the first few hours. After that, the body begins to break down fat and protein. The body uses Fatty acids as an energy source for muscles but lowers the amount of glucose sent to the brain. Another chemical that comes from fatty acids is glycerol. It can be used as glucose for energy but eventually runs out.
Phase two: Phase two can last for weeks at a time. In this phase, the body mainly uses stored fat for energy. The breakdown occurs in the liver and turns fat into ketones. After fasting for one week, the brain will use these ketones and any available glucose. Using ketones lowers the need for glucose, and the body slows the breakdown of proteins.
Phase three: By this point, the fat stores are gone, and the body begins to turn to stored protein for energy. This means it needs to break down muscle tissues full of protein; the muscles break down very quickly. Protein is essential for cells to work correctly, and when it runs out, the cells can no longer function.
The cause of death due to starvation is usually an infection or the result of tissue breakdown. This is due to the body becoming unable to produce enough energy to fight off bacteria and viruses. The final stage of starvation includes signals like hair color loss, skin flaking, swelling in the extremities, and a bloated belly. Even though they may feel hunger, people in the final stage of starvation usually cannot eat enough food to recover.

Causes
The body expends more energy than it takes in. This imbalance can arise from one or more medical conditions or circumstantial situations, which can include:
Medical reasons

Anorexia nervosa
Bulimia nervosa
Eating disorder, not otherwise specified
Celiac disease
Coma
Major depressive disorder
Diabetes mellitus
Digestive disease
Constant vomitingCircumstantial causes

Child, elder, or dependant abuse
Famine for any reason, such as political strife and war
Hunger striking
Excessive fasting
Poverty
Torture

Biochemistry
With a typical high-carbohydrate diet, the human body relies on free blood glucose as its primary energy source. Glucose can be obtained directly from dietary sugars and by the breakdown of other carbohydrates. In the absence of dietary sugars and carbohydrates, glucose is obtained from the breakdown of stored glycogen. Glycogen is a readily-accessible storage form of glucose, stored in notable quantities in the liver and skeletal muscle.
After the exhaustion of the glycogen reserve, and for the next two to three days, fatty acids become the principal metabolic fuel. At first, the brain continues to use glucose. If a non-brain tissue is using fatty acids as its metabolic fuel, the use of glucose in the same tissue is switched off.  Thus, when fatty acids are being broken down for energy, all of the remaining glucose is made available for use by the brain.After two or three days of fasting, the liver begins to synthesize ketone bodies from precursors obtained from fatty acid breakdown. The brain uses these ketone bodies as fuel, thus cutting its requirement for glucose. After fasting for three days, the brain gets 30% of its energy from ketone bodies. After four days, this may increase to 70% or more. Thus, the production of ketone bodies cuts the brains glucose requirement from 80 g per day to 30 g per day, about 35% of normal, with 65% derived from ketone bodies. But of the brains remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). This still leaves a deficit of about 10 g of glucose per day that must be supplied from another source; this other source will be the bodys own proteins.
After exhaustion of fat stores, the cells in the body begin to break down protein. This releases alanine and lactate produced from pyruvate, which can be converted into glucose by the liver. Since much of human muscle mass is protein, this phenomenon is responsible for the wasting away of muscle mass seen in starvation. However, the body is able to choose which cells will break down protein and which will not. About 2–3 g of protein has to be broken down to synthesize 1 g of glucose; about 20–30 g of protein is broken down each day to make 10 g of glucose to keep the brain alive. However, this number may decrease the longer the fasting period is continued, in order to conserve protein.
Starvation ensues when the fat reserves are completely exhausted and protein is the only fuel source available to the body. Thus, after periods of starvation, the loss of body protein affects the function of important organs, and death results, even if there are still fat reserves left. In a leaner person, the fat reserves are depleted faster, and the protein, sooner, therefore death occurs sooner.) Ultimately, the cause of death is in general cardiac arrhythmia or cardiac arrest, brought on by tissue degradation and electrolyte imbalances. Conditions like metabolic acidosis may also kill starving people.

Prevention
Starvation can be caused by factors beyond the control of the individual. The Rome Declaration on World Food Security outlines several policies aimed at increasing food security and, consequently, preventing starvation. These include:

Poverty reduction
Prevention of wars and political instability
Food aid
Agricultural sustainability
Reduction of economic inequalitySupporting farmers in areas of food insecurity through such measures as free or subsidized fertilizers and seeds increases food harvest and reduces food prices.

Treatment
Patients that suffer from starvation can be treated, but this must be done cautiously to avoid refeeding syndrome. Rest and warmth must be provided and maintained. Food can be given gradually in small quantities. The quantity of food can be increased over time. Proteins may be administered intravenously to raise the level of serum proteins.  For worse situations, hospice care and opioid medications can be used.

Organizations
Many organizations have been highly effective at reducing starvation in different regions. Aid agencies give direct assistance to individuals, while political organizations pressure political leaders to enact more macro-scale policies that will reduce famine and provide aid.

Statistics
According to estimates by the Food and Agriculture Organization, between 720 and 811 million people were affected by hunger globally in 2020.  This was a decrease from estimated 925 million in 2010 and roughly 1 billion in 2009. In 2007, 923 million people were reported as being undernourished, an increase of 80 million since 1990–92.
An estimated 820 million people did not have enough to eat in 2018, up from 811 million in the previous year, which is the third year of increase in a row.As the definitions of starving and malnourished people are different, the number of starving people is different from that of malnourished. Generally, far fewer people are starving than are malnourished.
The proportion of malnourished and starving people in the world has been more or less continually decreasing for at least several centuries. This is due to an increasing supply of food and to overall gains in economic efficiency. In 40 years, the proportion of malnourished people in the developing world has been more than halved. The proportion of starving people has decreased even faster.

Capital punishment
Historically, starvation has been used as a death sentence. From the beginning of civilization to the Middle Ages, people were immured, and died for want of food.
In ancient Greco-Roman societies, starvation was sometimes used to dispose of guilty upper-class citizens, especially erring female members of patrician families. In the year 31, Livilla, the niece and daughter-in-law of Tiberius, was discreetly starved to death by her mother for her adulterous relationship with Sejanus and for her complicity in the murder of her own husband, Drusus the Younger.
Another daughter-in-law of Tiberius, named Agrippina the Elder (a granddaughter of Augustus and the mother of Caligula), also died of starvation, in 33 AD; however, it is unclear if her starvation was self-inflicted.
A son and daughter of Agrippina were also executed by starvation for political reasons; Drusus Caesar, her second son, was put in prison in 33 AD, and starved to death by orders of Tiberius (he managed to stay alive for nine days by chewing the stuffing of his bed); Agrippinas youngest daughter, Julia Livilla, was exiled on an island in 41 by her uncle, Emperor Claudius, and her death by starvation was arranged by the empress Messalina.
It is also possible that Vestal Virgins were starved when found guilty of breaking their vows of celibacy.
Ugolino della Gherardesca, his sons, and other members of his family were immured in the Muda, a tower of Pisa, and starved to death in the thirteenth century. Dante, his contemporary, wrote about Gherardesca in his masterpiece The Divine Comedy.
In Sweden in 1317, King Birger of Sweden imprisoned his two brothers for a coup they had staged several years earlier (Nyköping Banquet). According to legend they died of starvation a few weeks later, since their brother had thrown the prison key in the castle moat.
In Cornwall in the UK in 1671, John Trehenban from St Columb Major was condemned to be starved to death in a cage at Castle An Dinas for the murder of two girls.
The Makah, a Native American tribe inhabiting the Pacific Northwest near the modern border of Canada and the United States, practiced death by starvation as a punishment for slaves.

Concentration camps and ghettos
Many of the prisoners in the Nazi concentration camps were murdered through deliberate maltreatment, disease, starvation, and overwork, or were executed as unfit for labor. Many occupants of ghettos in eastern Europe also starved to death, most notoriously in the Warsaw Ghetto in German-occupied Poland. Prisoners were transported in inhumane conditions by rail freight cars, in which many died before reaching their destination. The prisoners were confined to the cattle cars for days or even weeks, with little or no food or water. Many died of dehydration in the intense heat of summer or froze to death in winter. Nazi concentration camps in Europe from 1933 to 1945 deliberately underfed prisoners, who were at the same time forced to perform heavy labour. Their diet was restricted to watery vegetable soup and a little bread, with little to no dietary fats, proteins or other essential nutrients. Such treatment led to loss of body tissues, and when prisoners became skeletal, the so-called Muselmann were murdered by gas or bullets when examined by camp doctors.

Starvation was also used as a punishment where victims were locked into a small cell until dead, a process which could take many days.
Saint Maximilian Kolbe, a martyred Polish friar, underwent a sentence of starvation in Auschwitz concentration camp in 1941. Ten prisoners had been condemned to death by starvation in the wake of a successful escape from the camp. Kolbe volunteered to take the place of a man with a wife and children. After two weeks of starvation, Kolbe and three other inmates remained alive; they were then executed with injections of phenol.

See also
References
Further reading

Online books, and library resources in your library and in other libraries about Starvation
U.N. Chief: Hunger Kills 17,000 Kids Daily - by CNN
Wilson, DE; Zeikus, R; Chan, IF (Apr 1987) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Platinosis and explain in detail? [/INST] Platinosis is an allergy-like reaction to exposure to soluble salts of platinum.
The symptoms of platinosis may include asthma, dermatitis, dyspnea, conjunctival vasodilatation, and rhinopharyngitis.
The symptoms are progressive, sometimes taking months to years to appear.  Platinosis is usually associated with workers in industries related to platinum production.
The effects are permanent.
Halogeno-platinum compounds are among the most potent respiratory and skin sensitisers known, therefore it is vital that exposure via the skin and by breathing contaminated air is carefully controlled.
In practice, the compounds mainly responsible for platinum sensitisation are typically the soluble, ionic, platinum-chloro compounds such as ammonium hexachloroplatinate and tetrachloroplatinate, and hexachloroplatinic acid. Other ionic halogeno compounds are also sensitisers, the order of allergenicity being Cl > Br > I.
Neutral compounds such as cis-platin and ammine and nitro complexes such as [Pt(NH3)4]Cl2, K2[Pt(NO2)4] and platinum nitrate are not considered to be allergenic; neither is the metal.

See also
Heavy metal poisoning

References
Parrot, Jl; Hébert, R; Saindelle, A; Ruff, F (Nov 1969). "Platinum and platinosis. Allergy and histamine release due to some platinum salts". Archives of Environmental Health. 19 (5): 685–91. doi:10.1080/00039896.1969.10666910. PMID 4187030.
Saindelle, A; Ruff, F; Hébert, R; Parrot, Jl (Oct 1968). "A new histamine liberator: chloroplatinate. An occupational allergy: platinosis" [A new histamine liberator: chloroplatinate. An occupational allergy: platinosis]. Revue Française dAllergologie (in French). 8 (4): 205–14. doi:10.1016/S0370-4688(68)80018-3. PMID 4180839.
Parrot, Jl; Saindelle, A; Ruff, F (Dec 1967). "Platinum and platinosis. Histamine release by some platinum salts and platinum allergy" [Platinum and platinosis. Histamine release by some platinum salts and platinum allergy]. La Presse Médicale (in French) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pemphigus and explain in detail? [/INST] Pemphigus ( or ) is a rare group of blistering autoimmune diseases that affect the skin and mucous membranes. The name is derived from the Greek root pemphix, meaning "pustule".In pemphigus, autoantibodies form against desmoglein, which forms the "glue" that attaches adjacent epidermal cells via attachment points called desmosomes. When autoantibodies attack desmogleins, the cells become separated from each other and the epidermis becomes detached, a phenomenon called acantholysis. This causes blisters that slough off and turn into sores. In some cases, these blisters can cover a large area of the skin.Originally, the cause of this disease was unknown, and "pemphigus" was used to refer to any blistering disease of the skin and mucosa.  In 1964, researchers found that the blood of patients with pemphigus contained antibodies to the layers of skin that separate to form the blisters. In 1971, an article investigating the autoimmune nature of this disease was published.

Types
The several types of pemphigus (pemphigus vulgaris, pemphigus foliaceus, intraepidermal neutrophilic IgA dermatosis, and paraneoplastic pemphigus) vary in severity. Skin lesions caused by pemphigus can lead to fatal infections, so treatment is extremely important.

Pemphigus vulgaris (PV - ICD-10 L10.0) is the most common form of the disorder and occurs when antibodies attack desmoglein 3. Sores often originate in the mouth, making eating difficult and uncomfortable. Although PV may occur at any age, it is most common among people between 40 and 60. It is more frequent among Ashkenazi Jews. Rarely, it is associated with myasthenia gravis.  Nail disease may be the only finding and has prognostic value in management.
Pemphigus foliaceus (PF) is the least severe of the three varieties. Desmoglein 1, the protein that is targeted by the autoantibodies, is enriched in the upper skin layers. PF is characterized by crusty sores that often begin on the scalp, and may move to the chest, back, and face. Mouth sores do not occur. This form is also frequent among Ashkenazi Jews. It is not as painful as PV, and is often misdiagnosed as dermatitis or eczema
Intraepidermal neutrophilic IgA dermatosis is characterized histologically by intraepidermal bullae with neutrophils, some eosinophils, and acantholysis.
The least common and most severe type of pemphigus is paraneoplastic pemphigus (PNP). This disorder is a complication of cancer, usually lymphoma or Castlemans disease. It may precede the diagnosis of the tumor. Painful sores appear on the mouth, lips, and the esophagus. In this variety of pemphigus, the disease process often involves the lungs, causing bronchiolitis obliterans (constrictive bronchiolitis). Though much less frequent, it is still found the most in the Ashkenazi Jewish population. Complete removal of and/or cure of the tumor may improve the skin disease, but lung damage is generally irreversible.
Endemic pemphigus foliaceus includes fogo selvagem, the new variant of endemic pemphigus foliaceus in El Bagre, Colombia, and the Tunisian endemic pemphigus in North Africa.Hailey-Hailey disease, also called familial benign pemphigus, is an inherited skin disease, not an autoimmune disease, so it is not considered part of the pemphigus group of diseases.

Diagnosis
Pemphigus defines a group of autoimmune intraepithelial blistering diseases that are characterized by loss of normal cell-cell adhesion (acantholysis), and by the presence of pathogenic (predominantly IgG) autoantibodies reacting against epithelial adhesion molecules. Pemphigus is further divided in two major subtypes: pemphigus vulgaris (PV) and pemphigus foliaceus (PF). However, several other disorders such as IgA pemphigus, IgE pemphigus, pemphigus herpetiformis, drug-induced pemphigus, Senear Usher syndrome, and endemic pemphigus foliaceus exist, and are recognized by a dermatologist from the appearance and distribution of the skin lesions. It is also commonly diagnosed by specialists practicing otolaryngology- head and neck surgery, periodontists, oral and maxillofacial surgeons, and eye doctors, as lesions can affect the eyes and mucous membranes of the oral cavity. Intraorally, it resembles the more common diseases lichen planus and mucous membrane pemphigoid. Definitive diagnosis requires examination of a skin or mucous membrane biopsy by a dermatopathologist or oral pathologist. The skin biopsy is taken from the edge of a blister, prepared for histopathology and examined with a microscope. The pathologist looks for an intraepidermal vesicle caused by the breaking apart of epidermal cells (acantholysis). Thus, the superficial (upper) portion of the epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister. This bottom layer of cells is said to have a "tombstone" appearance.
Definitive diagnosis also requires the demonstration of antidesmoglein autoantibodies by direct immunofluorescence on the skin biopsy. These antibodies appear as IgG deposits along the desmosomes between epidermal cells, a pattern reminiscent of chicken wire. Antidesmoglein antibodies can also be detected in a blood sample using the ELISA technique.

Classification
Pemphigus is a group of autoimmune blistering diseases that may be classified into these types:
Pemphigus vulgaris
Pemphigus vegetans
Pemphigus vegetans of Hallopeau
Pemphigus vegetans of Neumann
Pemphigus foliaceus, of which there several forms:
Pemphigus erythematosus or Senear–Usher Syndrome
Endemic pemphigus foliaceus with its three variants, Fogo Selvagem, the new variant endemic pemphigus Foliaeus and Tunisian endemic pemphigus foliaceus
Paraneoplastic pemphigus
IgA pemphigus, of which there several forms:
Subcorneal pustular dermatosis
Intraepidermal neutrophilic IgA dermatosis
Drug induced pemphigus

Treatment
If not treated, pemphigus can be fatal, usually from overwhelming opportunistic infection of lesions. The most common treatment is the administration of oral steroids, especially prednisone, often in high doses. The side effects of corticosteroids may require the use of so-called steroid-sparing or adjuvant drugs. One of the most dangerous side effects of high-dosage steroid treatments is intestinal perforations, which may lead to sepsis. Steroids and other medications being taken to treat pemphigus may also mask the effects of the perforations. Patients on high dosages of oral steroids should closely monitor their gastrointestinal health. As lesions are usually terribly painful, pain medication likely complicate and exacerbate the gastrointestinal issues caused by steroids.

Treatment options
Topical steroids, such as clobetasol
Intralesional injection of steroids, such as dexamethasone
Immunosuppressant drugs, such as CellCept (mycophenolic acid): In recent years, adjuvant drugs, especially biologics, have shown great promise </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mohr–Tranebjærg syndrome and explain in detail? [/INST] Mohr–Tranebjærg syndrome (MTS) is a rare X-linked recessive syndrome also known as deafness–dystonia syndrome and caused by mutation in the TIMM8A gene. It is characterized by clinical manifestations commencing with early childhood onset hearing loss, followed by adolescent onset progressive dystonia or ataxia, visual impairment from early adulthood onwards and dementia from the 4th decade onwards. The severity of the symptoms may vary, but they progress usually to severe deafness and dystonia and sometimes are accompanied by cortical deterioration of vision and mental deterioration.

Signs and Symptoms
Mohr-Tranebjærg is characterized by a variety of symptoms affecting hearing loss. In the span of a subject with Mohr-Tranebjærg, by the age of early childhood, around 18 months, the development of quickly progressive prelingual or postlingual sensorineural hearing loss. The presence of auditory symptoms is characterized by preserved oto-acoustic emissions, abnormal auditory brain stem response, poor speech, and worsening in auditory symptoms even with auditory devices. Also, neuropsychological manifestations, possibly consisting of personality changes, paranoia, and mild intellectual deficit could emerge. During adolescence, there is a possibility that a slowly progressive movement disorder, similar to gegenhalten, dystonia, or ataxia could develop. Patients with Mohr-Tranebjærg experience reduced visual acuity, photophobia, acquired color vision defect and central scotomas developing at around 20 years of age, and leading to more severe blindness by age 30 or 40.The first symptom of DDON syndrome is hearing loss caused by nerve damage in the inner ear (sensorineural hearing loss), which begins in early childhood. The hearing impairment worsens over time, and most affected individuals have profound hearing loss by age 10.Individuals with Mohr Tranebjærg syndrome have normal vision during childhood, but they may develop vision problems due to breakdown of the nerves that carry information from the eyes to the brain (optic atrophy). Affected individuals can develop an increased sensitivity to light (photophobia) or other vision problems beginning in adolescence. Their sharpness of vision (visual acuity) slowly worsens, often leading to legal blindness in mid-adulthood.

Genetics
This condition is caused by mutations in the TIMM8A gene. This gene is located on the long arm of X chromosome (Xq22).
The protein encoded by this gene localizes to the intermembrane space in mitochondria where it functions in the import of nuclear encoded proteins into the mitochondrial inner membrane. How this produces the clinical picture is not yet clear.
The pattern of inheritance is X-linked recessive. Where the female is a carrier, male offspring have a 50 percent chance of inheriting the disease and female offspring have a 50 percent chance of being a carrier. Where the male is affected, male offspring do not inherit the pathogenic mutation and females are obligate carriers.TIMM8A is also referred to as DDP. Koehler determined the function of the DDP gene and concluded that the Mohr-Tranebjaerg syndrome is a novel type of mitochondrial disease that is most likely caused by a defective mitochondrial protein-import system.

Diagnosis
A combination of hearing impairment and recurrent infections due to XLA in a male patient should elicit sequencing of the TIMM8A gene. Neuroimaging is employed to verify the presence of cerebral atrophy. In cases of suspected CGS; testing for XLA is possible.

Differential diagnosis
This is long and includes

Arts syndrome
Autosomal recessive nonsyndromic sensorineural deafness type DFNB
Friedreich ataxia
MELAS syndrome
Mitochondrial DNA depletion syndrome (encephalomyopathic form with methylmalonic aciduria)
McLeod neuroacanthocytosis syndrome
Pendred syndrome
Usher syndrome type 1 and 2
Wolfram syndrome
X-linked spinocerebellar ataxia type 3 and 4

Treatment
Symptomatic Treatment
The treatment for Mohr-Tranebjærg vary depending on the symptoms and the evolution of these symptoms over time </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pelvic fracture and explain in detail? [/INST] A pelvic fracture is a break of the bony structure of the pelvis. This includes any break of the sacrum, hip bones (ischium, pubis, ilium), or tailbone. Symptoms include pain, particularly with movement. Complications may include internal bleeding, injury to the bladder, or vaginal trauma.Common causes include falls, motor vehicle collisions, a vehicle hitting a pedestrian, or a direct crush injury. In younger people significant trauma is typically required while in older people less significant trauma can result in a fracture. They are divided into two types: stable and unstable. Unstable fractures are further divided into anterior posterior compression, lateral compression, vertical shear, and combined mechanism fractures. Diagnosis is suspected based on symptoms and examination with confirmation by X-rays or CT scan. If a person is fully awake and has no pain of the pelvis medical imaging is not needed.Emergency treatment generally follows advanced trauma life support. This begins with efforts to stop bleeding and replace fluids. Bleeding control may be achieved by using a pelvic binder or bed-sheet to support the pelvis. Other efforts may include angiographic embolization or preperitoneal packing. After stabilization, the pelvis may require surgical reconstruction.Pelvic fractures make up around 3% of adult fractures. Stable fractures generally have a good outcome. The risk of death with an unstable fracture is about 15%, while those who also have low blood pressure have a risk of death approaching 50%. Unstable fractures are often associated with injuries to other parts of the body.

Signs and symptoms
Symptoms include pain, particularly with movement.

Complications
Complications are likely to result in cases of excess blood loss or puncture to certain organs, possibly leading to shock. Swelling and bruising may result, more so in high-impact injuries. Pain in the affected areas may differ where severity of impact increases its likelihood and may radiate if symptoms are aggravated when one moves around.

Causes
Common causes include falls, motor vehicle collisions, a vehicle hitting a pedestrian, or a direct crush injury. In younger people significant trauma is typically required while in older people less significant trauma can result in a fracture.

Pathophysiology
The bony pelvis consists of the ilium (i.e., iliac wings), ischium, and pubis, which form an anatomic ring with the sacrum. Disruption of this ring requires significant energy. When it comes to the stability and the structure of the pelvis, or pelvic girdle, understanding its function as support for the trunk and legs helps to recognize the effect a pelvic fracture has on someone. The pubic bone, the ischium and the ilium make up the pelvic girdle, fused together as one unit. They attach to both sides of the spine and circle around to create a ring and sockets to place hip joints. Attachment to the spine is important to direct force into the trunk from the legs as movement occurs, extending to ones back. This requires the pelvis to be strong enough to withstand pressure and energy. Various muscles play important roles in pelvic stability. Because of the forces involved, pelvic fractures frequently involve injury to organs contained within the bony pelvis. In addition, trauma to extra-pelvic organs is common. Pelvic fractures are often associated with severe hemorrhage due to the extensive blood supply to the region. The veins of the presacral pelvic plexus are particularly vulnerable. Greater than 85 percent of bleeding due to pelvic fractures is venous or from the open surfaces of the bone.

Diagnosis
If a person is fully awake and has no pain in the pelvis, medical imaging of the pelvis is not needed.

Classification
Pelvic fractures are most commonly described using one of two classification systems. The different forces on the pelvis result in different fractures. Sometimes they are determined based on stability or instability.

Tile classification
The Tile classification system is based on the integrity of the posterior sacroiliac complex.In type A injuries, the sacroiliac complex is intact. The pelvic ring has a stable fracture that can be managed nonoperatively.
Type B injuries are caused by either external or internal rotational forces resulting in partial disruption of the posterior sacroiliac complex. These are often unstable.
Type C injuries are characterized by complete disruption of the posterior sacroiliac complex and are both rotationally and vertically unstable. These injuries are the result of great force, usually from a motor vehicle crash, fall from a height or severe compression.

Young-Burgess classification
The Young-Burgess classification system is based on mechanism of injury: anteroposterior compression type I, II and III, lateral
compression types I, II and III, and vertical shear, or a combination of forces.
Lateral compression (LC) fractures involve transverse fractures of the pubic rami, either ipsilateral or contralateral to a posterior injury.

Grade I – Associated sacral compression on side of impact
Grade II – Associated posterior iliac ("crescent") fracture on side of impact
Grade III – Associated contralateral sacroiliac joint injuryThe most common force type, lateral compression (LC) forces, from side-impact automobile accidents and pedestrian injuries, can result in an internal rotation. The superior and inferior pubic rami may fracture anteriorly, for example. Injuries from shear forces, like falls from above, can result in disruption of ligaments or bones. When multiple forces occur, it is called combined mechanical injury (CMI). The best imaging modality to use for this classification is probably a pelvic CT scan.

Open book fracture
One specific kind of pelvic fracture is known as an open book fracture. This is often the result of a heavy impact to the groin (pubis), a common motorcycling accident injury. In this kind of injury, the left and right halves of the pelvis are separated at front and rear, the front opening more than the rear, i.e. like an open book that falls to the ground and splits in the middle. Depending on the severity, this may require surgical reconstruction before rehabilitation.  Forces from an anterior or posterior direction, like head-on car accidents, usually cause external rotation of the hemipelvis, an “open-book” injury. Open fractures have an increased risk of infection and hemorrhaging from vessel injury, leading to higher mortality.

Prevention
As the human body ages, the bones become weaker and brittle and are therefore more susceptible to fractures. Certain precautions are crucial in order to lower the risk of getting pelvic fractures. The most damaging is one from a car accident, cycling accident, or falling from a high building which can result in a high energy injury.  This can be very dangerous because the pelvis supports many internal organs and can damage these organs. Falling is one of the most common causes of pelvic fracture. Therefore, proper precautions should be taken to prevent this from happening.

Treatment
A pelvic fracture is often complicated and treatment can be a long and painful process </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Injury of axillary nerve and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Acromion and explain in detail? [/INST] In human anatomy, the acromion (from Greek: akros, "highest", ōmos, "shoulder", plural: acromia) is a bony process on the scapula (shoulder blade). Together with the coracoid process it extends laterally over the shoulder joint.  The acromion is a continuation of the scapular spine, and hooks over anteriorly.  It articulates with the clavicle (collar bone) to form the acromioclavicular joint.

Structure
The acromion forms the summit of the shoulder, and is a large, somewhat triangular or oblong process, flattened from behind forward, projecting at first lateralward, and then curving forward and upward, so as to overhang the glenoid fossa. It starts from the base of acromion which marks its projecting point emerging from the spine of scapula.

Surfaces
Its superior surface, directed upward, backward, and lateralward, is convex, rough, and gives attachment to some fibers of the deltoideus, and in the rest of its extent is subcutaneous.  Its inferior surface is smooth and concave.

Borders
Its lateral border is thick and irregular, and presents three or four tubercles for the tendinous origins of the deltoid.  Its medial border, shorter than the lateral, is concave, gives attachment to a portion of the trapezius, and presents about its center a small oval surface for articulation with the acromial end of the clavicle.

Variation
There are three morphologically distinct types of acromia and a correlation between these morphologies and rotator cuff tear:

Os acromiale
The acromion has four ossification centers called (from tip to base) pre-acromion, meso-acromion, meta-acromion, and basi-acromion.  In most cases, the first three fuse at 15–18 years, whereas the base part fuses to the scapular spine at 12 years.  However, in between 1% and 15% of cases, this osseous union fails and the acromion remains separate as an accessory bone. This condition is referred to as os acromiale, but rarely causes pain.  Earlier estimates of its prevalence were as low as 1.4%, and this higher estimate was made by Sammarco in the year 2000, based on radiographic and anatomical studies.Four types of os acromiale can be distinguished:
A non-union between the meso- and meta-acromia, the most common or typical os acromiale
A non-union between the pre- and meso-acromia
A non-union between the pre- and meso-acromia; and between the meso- and meta-acromia, atypical
A non-union between the pre- and meso-acromia; between the pre- and meso-acromia; and between the meta- and basi-acromiaThis feature was common in skeletons recovered from the Mary Rose shipwreck: it is thought that in those men, much archery practice from childhood on with the mediaeval war bow (which needs a pull three times as strong as the modern standard Olympic bow) pulled at the acromion so much that it prevented bony fusion of the acromion with the scapula.
Although historically regarded as an incidental finding, the os acromiale may occasionally produce symptoms from subacromial impingement or instability at the site of non-union.  In people with symptoms of  os acromiale, dynamic ultrasound sometimes shows hypermobility in the area during shoulder movement, or graded compression with the probe.

In other animals
The acromion process of bats (Mammalia: Chiroptera) is particularly elongated compared to that of  humans.
Turtles have an acromion that forms the anterior part of the triradiate pectoral girdle (together with the coracoid and scapula).  In this highly specialized endoskeletal structure, the scapula is a dorsal (directed upwards) process attached to the first rib; the coracoid is a posteroventral (directed backward and down) process; and the acromion is a medioventral (directed inwards and down) process (also known as the prescapular process) located at the base of the scapula.  This had led to some controversy regarding the evolutionary origin of turtles, because in both pareiasaurs and non-mammalian therapsids the acromion is located at the dorsal tip of the scapula.
In modern turtles, the acromion projects ventrally and articulates with the plastron (the flat lower part of the shell), but it evolved in a common ancestor of pareiasaurs and turtles long before the plastron.  In these primitive ancestors, the acromion projected forward to form a strong and flexible articulation between the shoulder girdle and the clavicle.  Notwithstanding these changes, the acromion of turtles retains its original function, to support the shoulder girdle and increase stride length.

Additional images
Notes
 This article incorporates text in the public domain from page 203 of the 20th edition of Grays Anatomy (1918)

Habermeyer, Peter; Magosch, Petra; Lichtenberg, Sven (2006). Classifications and Scores of the Shoulder. Heidelberg: Springer. ISBN 978-3-540-24350-2.
Lee, Michael S. Y. (January 22, 1996). "The Homologies and Early Evolution of the Shoulder Girdle in Turtles". Proc. R. Soc. Lond. B. 263 (1366): 111–117. doi:10.1098/rspb.1996.0018. S2CID 84529868.
Rieppel, Olivier; Reisz, Robert R. (1999). "The Origin and Early Evolution of Turtles" </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Brachymetacarpia and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypergonadism and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sebaceoma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Riddoch syndrome and explain in detail? [/INST] The Riddoch syndrome is a term coined by Zeki and Ffytche (1998) in a paper published in Brain. The term acknowledges the work of George Riddoch who was the first to describe a condition in which a form of visual impairment, caused by lesions in the occipital lobe, leaves the sufferer blind but able to distinguish visual stimuli with specific characteristics when these appear in the patients blind field. The most common stimuli that can be perceived consciously are the presence and direction of fast moving objects (moving at a speed in excess of 10 degrees per second); in his work these moving objects were described as "vague and shadowy" </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Magnesium deficiency and explain in detail? [/INST] Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body. It can result in multiple symptoms. Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus. Complications may include seizures or cardiac arrest such as from torsade de pointes. Those with low magnesium often have low potassium.Causes include low dietary intake, alcoholism, diarrhea, increased urinary loss, poor absorption from the intestines, and diabetes mellitus. A number of medications may also cause low magnesium, including proton pump inhibitors (PPIs) and furosemide. The diagnosis is typically based on finding low blood magnesium levels (hypomagnesemia). Normal magnesium levels are between 0.6 and 1.1 mmol/L (1.46–2.68 mg/dL) with levels less than 0.6 mmol/L (1.46 mg/dL) defining hypomagnesemia. Specific electrocardiogram (ECG) changes may be seen.Treatment is with magnesium either by mouth or intravenously. For those with severe symptoms, intravenous magnesium sulfate may be used. Associated low potassium or low calcium should also be treated. The condition is relatively common among people in hospitals.

Signs and symptoms
Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Magnesium plays an important role in carbohydrate metabolism and its deficiency may worsen insulin resistance, a condition that often precedes diabetes, or may be a consequence of insulin resistance.People being treated on an intensive care unit (ICU) who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.

Causes
Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of magnesium, reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor – many people consume diets high in refined foods such as white bread and polished rice which have been stripped of magnesium-rich plant fiber.Magnesium deficiency is not uncommon in hospitalized patients. Up to 12% of all people admitted to hospital, and as high as 60–65% of people in an intensive care unit, have hypomagnesemia.About 57% of the US population does not meet the US RDA for dietary intake of magnesium. The kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used, or in chronic alcoholism, levels may drop.
Low levels of magnesium in blood may be due to not enough magnesium in the diet, the intestines not absorbing enough magnesium, or the kidneys excreting too much magnesium. Deficiencies may be due to the following conditions:

Medications
Loop and thiazide diuretic use (the most common cause of hypomagnesemia)
Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia.
Long term, high dosage use of proton-pump inhibitors such as omeprazole
Other drugs
Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively increasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.
Adrenergics, displace magnesium into the cell
Cisplatin, stimulates kidney excretion
Ciclosporin, stimulates kidney excretion
Mycophenolate mofetil

Genetics
Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB, BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the distal convoluted tubule of the kidney.
Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as magnesium and calcium) in the thick ascending limb of Henles loop of the kidney is impaired. This results in loss of magnesium and calcium in the urine.
Mitochondriopathies, such as caused by mutations in SARS2, MT-TI or as seen with Kearns-Sayre syndrome.
Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of magnesium in the distal convoluted tubule.

Metabolic abnormalities
Insufficient selenium, vitamin D or sunlight exposure, or vitamin B6.
Gastrointestinal causes: the distal digestive tract secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohns disease, ulcerative colitis, Whipples disease and celiac sprue can all cause hypomagnesemia.
Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant.

Other
Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.
Malabsorption
Acute pancreatitis
Fluoride poisoning
Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.

Pathophysiology
Magnesium is a co-factor in over 300 functions in the body regulating many kinds of  biochemical reactions. It is involved in protein synthesis, muscle and nerve functioning, bone development, energy production, the maintenance of normal heart rhythm, and the regulation of glucose and blood pressure, among other important roles. Low magnesium intake over time can increase the risk of illnesses, including high blood pressure and heart disease, diabetes mellitus type 2, osteoporosis, and migraines.There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. Magnesium has several effects:

Potassium
Potassium channel efflux is inhibited by magnesium. Thus hypomagnesemia results in an increased excretion of potassium in kidney, resulting in a hypokalaemia. This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.In this light, hypomagnesemia is frequently the cause of hypokalaemic patients failing to respond to potassium supplementation. Thus, clinicians should ensure that both magnesium and potassium is replaced when deficient. Patients with diabetic ketoacidosis should have their magnesium levels monitored to ensure that the serum loss of potassium, which is driven intracellularly by insulin administration, is not exacerbated by additional urinary losses.

Calcium
Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Thus hypomagnesemia results in an increased intracellular calcium level. This inhibits the release of  parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.

Arrhythmia
Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in cardiac myocytes, the muscles cells of the heart. A lack of magnesium inhibits reuptake of potassium, causing a decrease in intracellular potassium. This decrease in intracellular potassium results in a tachycardia.

Pre-eclampsia
Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. Magnesium increases prostaglandins, decreases thromboxane, and decreases angiotensin II, microvascular leakage, and vasospasm through its function similar to calcium channel blockers. Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.

Asthma
Magnesium exerts a bronchodilatatory effect, probably by antagonizing calcium-mediated bronchoconstriction.

Neurological effects
reducing electrical excitation
modulating release of acetylcholine
antagonising N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system and thus providing neuroprotection from excitoxicity.

Diabetes mellitus
Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11.0 and 47.7%.
Magnesium deficiency is strongly associated with high glucose and insulin resistance, which indicate that it is common in poorly controlled diabetes. Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications. Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile.  However, their effect on cardiovascular risk in diabetes are to be determined.

Homeostasis
Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll (chloroplasts), cocoa derivatives, nuts, wheat, seafood, and meat. It is absorbed primarily in the duodenum of the small intestine. The rectum and sigmoid colon can absorb magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.The body contains 21–28 grams of magnesium (0.864–1.152 mol). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium.The majority of serum magnesium is bound to chelators, including proteins and citrate. Roughly 33% is bound to proteins, and 5–10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7–2.3 mg/dL (0.69–0.94 mmol/L).
The kidneys regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys daily, of which 5% (120 mg) is excreted through urine. The loop of Henle is the major site for magnesium homeostasis, and 60% is reabsorbed.
Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists, serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.

Diagnosis
Magnesium deficiency is not easy to directly measure. Typically the diagnosis is based on finding low blood magnesium levels (hypomagnesemia). Specifically by finding a plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dL). Severe disease generally has a level of less than 0.50 mmol/L (1.25 mg/dL).Magnesium deficiency (or depletion) refers to low total body levels of magnesium which is usually determined by finding low blood levels (hypomagnesemia). Hypomagnesemia refers only to blood levels of magnesium. Either of magnesium deficiency and hypomagnesemia can be present without the other.

Electrocardiogram
The electrocardiogram (ECG) change may show a tachycardia with a prolonged QT interval. Other changes may include prolonged PR interval, ST segment depression, flipped T waves, and long QRS duration.

Treatments
Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Replacement by mouth is appropriate for people with mild symptoms, while intravenous replacement is recommended for people with severe effects.Numerous oral magnesium preparations are available. In two trials of magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was less bioavailable than magnesium citrate, chloride, lactate or aspartate. Magnesium citrate has been reported as more bioavailable than oxide or amino-acid chelate forms.Intravenous magnesium sulfate (MgSO4) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma.

Food
Food sources of magnesium include leafy green vegetables, beans, nuts, and seeds.

Epidemiology
The condition is relatively common among people in hospital.

History
Magnesium deficiency in humans was first described in the medical literature in 1934.

Plants
Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants dry matter and is necessary for normal plant growth. Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency, as does aluminium toxicity.Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll. Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Folliculitis and explain in detail? [/INST] Folliculitis is the infection and inflammation of one or more hair follicles. The condition may occur anywhere on hair-covered skin. The rash may appear as pimples that come to white tips on the face, chest, back, arms, legs, buttocks, or head.Although acne can often involve superficial infection and inflammation of some hair follicles, the condition of those follicles is usually not called folliculitis, as that term is usually reserved for the separate set of disease entities comprising infected and inflamed hair follicles with causes other than acne.

Signs and symptoms
Rash (reddened skin area)
Itching skin
Pimples or pustules located around a hair or follicle; may be confused with chicken pox
May crust over
Typically occur on neck, armpit, or groin
May present as genital lesions
Spreading from leg to arm to body through improper treatment with antibiotics

Complications
This condition can develop into a more severe skin condition, such as cellulitis or abscess.

Causes
Most carbuncles, boils, and other cases of folliculitis are infected with Staphylococcus aureus.Folliculitis starts with the introduction of a skin pathogen to a hair follicle. Hair follicles can also be damaged by friction from clothing, an insect bite, blockage of the follicle, shaving, or braids that are very tight and close to the scalp. The damaged follicles are then infected by Staphylococcus spp. Folliculitis can affect people of all ages.Iron-deficiency anemia is sometimes associated with chronic cases.

Bacterial
Staphylococcus aureus folliculitis
Hot-tub folliculitis is caused by the bacterium Pseudomonas aeruginosa.  The folliculitis usually occurs after sitting in a hot tub that was not properly cleaned before use.  Symptoms are found around the body parts that sit in the hot tub - the legs, hips, chest, buttocks, and surrounding areas.  Symptoms are amplified around regions that were covered by wet clothing, such as bathing suits.
Sycosis vulgaris, sycosis barbae, or barbers itch is a staphylococcal infection of the hair follicles in the bearded area of the face, usually the upper lip. Shaving aggravates the condition.
Gram-negative folliculitis may appear after prolonged acne treatment with antibiotics.

Fungal
Tinea barbae is similar to barbers itch, but the infection is caused by the fungus T </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Urtica dioica and explain in detail? [/INST] Urtica dioica, often known as common nettle, burn nettle, stinging nettle (although not all plants of this species sting) or nettle leaf, or just a nettle or stinger, is a herbaceous perennial flowering plant in the family Urticaceae. Originally native to Europe, much of temperate Asia and western North Africa, it is now found worldwide, including New Zealand and  North America. The species is divided into six subspecies, five of which have many hollow stinging hairs called trichomes on the leaves and stems, which act like hypodermic needles, injecting histamine and other chemicals that produce a stinging sensation upon contact ("contact urticaria", a form of contact dermatitis).The plant has a long history of use as a source for traditional medicine, food, tea, and textile raw material in ancient (such as Saxon) and modern societies.

Description
Urtica dioica is a dioecious, herbaceous, perennial plant, 3 to 7 feet (0.9 to 2 metres) tall in the summer and dying down to the ground in winter. It has widely spreading rhizomes and stolons, which are bright yellow, as are the roots. The soft, green leaves are 1 to 6 inches (30 to 200 mm) long and are borne oppositely on an erect, wiry, green stem. The leaves have a strongly serrated margin, a cordate base, and an acuminate tip with a terminal leaf tooth longer than adjacent laterals. It bears small, greenish or brownish, numerous flowers in dense axillary inflorescences.
The leaves and stems are very hairy with non-stinging hairs, and in most subspecies, also bear many stinging hairs (trichomes or spicules), whose tips come off when touched, transforming the hair into a needle that can inject several chemicals causing a painful sting or paresthesia, giving the species its common names: stinging nettle, burn-nettle, burn-weed, or burn-hazel.

Taxonomy
The taxonomy of Urtica species has been confused, and older sources are likely to use a variety of systematic names for these plants. Formerly, more species were recognised than are now accepted. However, at least six clear subspecies of U. dioica are described, some formerly classified as separate species:

U. dioica subsp. dioica (European stinging nettle), from Europe, Asia, and northern Africa, has stinging hairs.
U. dioica subsp. galeopsifolia (fen nettle or stingless nettle), from Europe, does not have stinging hairs.
U. dioica subsp. afghanica, from southwestern and central Asia, sometimes has stinging hairs or is sometimes hairless.
U. dioica subsp. gansuensis, from eastern Asia (China), has stinging hairs.
U. dioica subsp. gracilis (Ait.) Selander (American stinging nettle), from North America, has stinging hairs and is monoecious.
U. dioica subsp. holosericea (Nutt.) Thorne (hoary stinging nettle), from North America, has stinging hairs and is monoecious.Other species names formerly accepted as distinct by some authors but now regarded as synonyms of one or other subspecies include U. breweri, U. californica, U. cardiophylla, U. lyalli, U. major, U. procera, U. serra, U. strigosissima, U. trachycarpa, and U. viridis.

Etymology
Urtica is derived from a Latin word meaning sting.Dioica (δίοικος) is derived from Greek, meaning of two houses (having separate staminate and pistillate plants; dioecious).

Distribution and habitat
U. dioica is considered to be native to Europe, much of temperate Asia and western North Africa. It is abundant in northern Europe and much of Asia, usually found in the countryside. It is less widespread in southern Europe and north Africa, where it is restricted by its need for moist soil, but is still common. It has been introduced to many other parts of the world. In North America, it is widely distributed in Canada and the United States, where it is found in every province and state except for Hawaii, and also can be found in northernmost Mexico. It grows in abundance in the Pacific Northwest, especially in places where annual rainfall is high. The European subspecies has been introduced into Australia, North America and South America.In Europe, nettles have a strong association with human habitation and buildings. The presence of nettles may indicate the site of a long-abandoned building, and can also indicate soil fertility. Human and animal waste may be responsible for elevated levels of phosphate and nitrogen in the soil, providing an ideal environment for nettles.

Ecology
Nettles are the larval food plant for several species of butterflies, such as the peacock butterfly, comma (Polygonia c-album), and the small tortoiseshell. It is also eaten by the larvae of some moths including angle shades, buff ermine, dot moth, the flame, the gothic, grey chi, grey pug, lesser broad-bordered yellow underwing, mouse moth, setaceous Hebrew character, and small angle shades. The roots are sometimes eaten by the larva of the ghost moth (Hepialus humuli).
It is a known host to the pathogenic fungus Phoma herbarum.Stinging nettle is particularly found as an understory plant in wetter environments, but it is also found in meadows. Although nutritious, it is not widely eaten by either wildlife or livestock, presumably because of the sting. It spreads by abundant seeds and also by rhizomes, and is often able to survive and re-establish quickly after fire.

Cultivation
Field
Sowing and planting
Three cultivation techniques can be used for the stinging nettle: 1) direct sowing, 2) growing seedlings in nurseries with subsequent transplantation and 3) vegetative propagation via stolons or head cuttings.
Direct sowing: The seedbed should have a loose and fine structure, but should be reconsolidated using a packer roller imminently prior to sowing. Sowing time can be either in autumn or in spring. Seed density should be 6 kilograms/hectare with row spacing of 30 cm (12 in) and 42–50 cm in autumn and spring, respectively. The disadvantage of direct sowing is that it usually leads to incomplete plant coverage. This drawback can be mitigated by covering the seedbed with a transparent perforated foil in order to improve seed germination. Further, weed control can be problematic as the stinging nettle has a slow seedling development time.
Growing seedlings: For this technique pre-germinated seeds are sown between mid-/end-February and beginning of April and grown in nurseries. Seedlings are grown in tuffs with 3–5 plants/tuff and a seed density of 1.2–1.6 kg/1000 tuffs. A fastened germination is achieved by alternating high temperature during daytime (30 °C for 8 h) and lower temperature during nighttime (20 °C for 16 h). Before transplanting, the seedlings should be fertilized and acclimated to cold temperatures. Transplantation should start around Mid-April with row spacing of 42–50 cm (17–20 in) and plant spacing within rows of 25–30 cm.
Vegetative propagation: Stolons (with several buds) of 10 cm should be planted from mid-April in a depth of 5–7 cm (2–2+3⁄4 in). Head cuttings are grown in nurseries starting between mid-May and mid-June. Growing tips with two leaf pairs are cut from the mother plant and treated with root-growth inducing hormones. Transplantation can be delayed in comparison to the growing seedling technique.

Greenhouse
The stinging nettle can also be grown in controlled-environment agriculture systems, such as soil-less medium cultivations or aeroponics, which may achieve higher yields, standardize quality, and reduce harvesting costs and contamination.

Sting and treatment
Urtica dioica produces its inflammatory effect on skin (stinging, burning sensation often called "contact urticaria") both by impaling the skin via spicules – causing mechanical irritation – and by biochemical irritants, such as histamine, serotonin, and acetylcholine, among other chemicals. Anti-itch drugs, usually in the form of creams containing antihistamines or hydrocortisone, may provide relief from nettle dermatitis. The term, contact urticaria, has a wider use in dermatology, involving dermatitis caused by various skin irritants and pathogens.Docks, especially the broad-leaf dock (Rumex obtusifolius) often grow in similar environments to stinging nettles and are regarded as a folk remedy to counteract the sting of a nettle, although there is no evidence of any chemical effect. It may be that the act of rubbing a dock leaf against a nettle sting acts as a distracting counterstimulation, or that belief in the docks effect provides a placebo effect.

Uses
Culinary
U. dioica has a flavour similar to spinach when cooked. Young plants were harvested by Native Americans and used as a cooked plant in spring when other food plants were scarce. Soaking stinging nettles in water or cooking removes the stinging chemicals from the plant, which allows them to be handled and eaten without injury. After the stinging nettle enters its flowering and seed-setting stages, the leaves develop gritty particles called cystoliths, which can irritate the kidneys and urinary tract.: 106–107   Cystoliths are made of calcium carbonate, and will not dissolve when boiled.  Leaves harvested post-flowering must have their cystoliths broken down by acid, as in the fermentation process. In its peak season, nettle contains up to 25% protein, dry weight, which is high for a leafy green vegetable. The leaves are also dried and may then be used to make a herbal tea, as can also be done with the nettles flowers.
Nettles can be used in a variety of recipes, such as polenta, pesto, and purée. Nettle soup is a common use of the plant, particularly in Northern and Eastern Europe.
Nettles are sometimes used in cheesemaking, such as for Cornish Yarg and as a flavouring in varieties of Gouda.Nettles are used in Montenegro, Serbia and Bosnia and Hercegovina as part of the dough filling for the börek pastry. The top baby leaves are selected and simmered, and then mixed with other ingredients such as herbs and rice, before being used as a filling between dough layers. Similarly, in Greece the tender leaves are often used, after simmering, as a filling for hortopita, which is similar to spanakopita, but with wild greens rather than spinach for filling.Young nettles can also be used to make an alcoholic drink.

Competitive eating
In the UK, an annual World Nettle Eating Championship draws thousands of people to Dorset, where competitors attempt to eat as much of the raw plant as possible. Competitors are given 60 cm (24 in) stalks of the plant, from which they strip the leaves and eat them. Whoever strips and eats the most stinging nettle leaves in a fixed time is the winner. The competition dates back to 1986, when two neighbouring farmers attempted to settle a dispute about which had the worst infestation of nettles, and one of them said, "Ill eat any nettle of yours thats longer than mine."

Traditional medicine
As Old English stiðe, nettle is one of the nine plants invoked in the pagan Anglo-Saxon Nine Herbs Charm, recorded in 10th century traditional medicine. Nettle was believed to be a galactagogue – a substance that promotes lactation. Urtication, or flogging with nettles is the process of deliberately applying stinging nettles to the skin to provoke inflammation. An agent thus used was considered to be a rubefacient (something that causes redness), used as a folk remedy for treating rheumatism.

Chastisement
In indigenous justice systems in Ecuador, urtication was used as punishment for severe crimes in 2010. The sentenced perpetrator of a crime was flogged with stinging nettle, in public, naked, whilst being showered with freezing cold water.

Textiles and fibre
Nettle stems contain a bast fibre that has been traditionally used for the same purposes as linen and is produced by a similar retting process. Unlike cotton, nettles grow easily without pesticides. The fibres are coarser, however.Historically, nettles have been used to make clothing for almost 3,000 years, as ancient nettle textiles from the Bronze Age have been found in Denmark. It is widely believed that German Army uniforms were almost all made from nettle during World War I due to a potential shortage of cotton, although there is little evidence to support this. More recently, companies in Austria, Germany, and Italy have started to produce commercial nettle textiles.The fibre content in nettle shows a high variability and reaches from below 1% to 17%. Under middle-European conditions, stems yield typically between 45 and 55 dt / ha (decitons per hectare), which is comparable to flax stem yield. Due to the variable fibre content, the fibre yields vary between 0.2 and 7 dt / ha, but the yields are normally in the range between 2 and 4 dt / ha. Fibre varieties are normally cloning varieties and therefore planted from vegetative propagated plantlets. Direct seeding is possible, but leads to great heterogeneity in maturity.Nettles may be used as a dye-stuff, producing yellow from the roots, or yellowish green from the leaves.

Feed
Nutrient contents
Fresh leaves contain approximately 82.4% water, 17.6% dry matter, 5.5% protein, 0.7 to 3.3% fat, and 7.1% carbohydrates. Mature leaves contain about 40% α- linolenic acid, a valuable omega-3 acid. For exact fatty acid contents see Table 1. Seeds contain much more fatty acid than leaves.
Minerals (Ca, K, Mg, P, Si, S, Cl) and trace elements (Ti, 80 ppm, Mn, Cu, Fe) contents depend mostly on the soil and the season.Carotenoids can be found primarily in the leaves, where different forms of lutein, xanthophyll and carotene are present (Table 2). Some carotenes are precursors of vitamin A (retinol), their retinol equivalents RE or retinol activity equivalents per g dry weight are 1.33 for mature leaves and 0.9 for young leaves. Nettle contains much less carotenes and retinol than carrots, which contain 8.35 RE per g fresh weight. Depending on the batch and the leave and stem content, nettle contains only traces of zeaxanthin or between 20–60 mg/kg of dry matter. Nettle contains ascorbic acid (vitamin C), riboflavin (vitamin B2), pantothenic acid, vitamin K1 and tocopherols (vitamin E). The highest vitamin contents can be found in the leaves.

Poultry: Egg yolk colouring in laying hens
In laying hens, nettle can be used as an egg yolk colorant instead of artificial pigments or other natural pigments (derived from marigold for yellow). Nettle has high carotenoid contents, especially lutein, β-carotene and zeaxanthin, of which lutein and zeaxanthin act as yellow pigments. Feeding as little as 6.25 g dry nettle per kg feed is as effective as the synthetic pigments to colour the egg yolk. Feeding nettle has no detrimental effect on the performance of the laying hens or on the general quality of eggs.

Ruminants
Ruminants avoid fresh stinging nettles; however, if the nettles are wilted or dry, voluntary intake can be high.

Use in agriculture / horticulture
In the European Union and United Kingdom, nettle extract can be used as a insecticide, fungicide, and acaricide under Basic Substance regulations. As an insecticide nettle extract can be used for the control of codling moth, diamondback moth, and spider mites. As a fungicide, it can be used for the control of Pythium root rot, powdery mildew, early blight, late blight, Septoria blight, Alternaria leaf spot, and grey mould.

Gardening
Nettles have a number of other uses in the vegetable garden, including the potential for encouraging beneficial insects. Since nettles prefer to grow in phosphorus-rich and nitrogen rich soils that have recently been disturbed (and thus aerated), the growth of nettles is an indicator that an area has high fertility (especially phosphate and nitrate), and thus is an indicator to gardeners as to the quality of the soil.Nettles contain nitrogenous compounds, so are used as a compost activator or can be used to make a liquid fertilizer, which although low in phosphate, is useful in supplying magnesium, sulphur, and iron. They are also one of the few plants that can tolerate, and flourish in, soils rich in poultry droppings.
The stinging nettle is the red admiral caterpillars primary host plant and can attract migrating red admiral butterflies to a garden. U. dioica can be a troubling weed, and mowing can increase plant density. Regular and persistent tilling will greatly reduce its numbers, and the use of herbicides such as 2,4-D and glyphosate are effective control measures.

Culture
In Great Britain and Ireland, U. dioica and the annual nettle Urtica urens are the only common stinging plants and have found a place in several figures of speech in the English language. Shakespeares Hotspur urges that "out of this nettle, danger, we pluck this flower, safety" (Henry IV, Part 1, Act II Scene 3). The figure of speech "to grasp the nettle" probably originated from Aesops fable "The Boy and the Nettle". In Seán OCaseys Juno and the Paycock, one of the characters quotes Aesop "Gently touch a nettle and itll sting you for your pains/Grasp it as a lad of mettle and soft as silk remains". The metaphor may refer to the fact that if a nettle plant is grasped firmly rather than brushed against, it does not sting so readily, because the hairs are crushed down flat and do not penetrate the skin so easily.In the German language, the idiom sich in die Nesseln setzen, or to sit in nettles, means to get into trouble.
In Hungarian, the idiom csalánba nem üt a mennykő, the lightning bolt does not strike into nettles, alludes to the belief that bad people escape trouble or the devil looks after his own. The same idiom exists in the Serbian language – неће гром у коприве. In Dutch, a netelige situatie means a predicament. In French, the idiom faut pas pousser mémé dans les orties (do not push granny into the nettles) means that we should be careful not to abuse a situation. The name urticaria for hives comes from the Latin name of nettle (Urtica, from urere, to burn).
The English word nettled, meaning irritated or angry, is derived from nettle.There is a common idea in Great Britain that the nettle was introduced by the Romans. The idea was mentioned by William Camden in his book Britannia of 1586. However, in 2011, an early Bronze Age burial cist on Whitehorse Hill, Dartmoor, Devon was excavated. The cist dated from between 1730 and 1600 BC. It contained various high value beads as well as fragments of a sash made from nettle fibre. It is possible that the sash was traded from mainland Europe, but perhaps more probable that it was locally made.

See also
Nettles in folklore

References
Further reading
Elliott, C. (1997). "Rash Encounters". Horticulture </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ornithine aminotransferase deficiency and explain in detail? [/INST] Ornithine aminotransferase deficiency (also known as gyrate atrophy of the choroid and retina) is an inborn error of ornithine metabolism, caused by decreased activity of the enzyme ornithine aminotransferase.  Biochemically, it can be detected by elevated levels of ornithine in the blood.  Clinically, it presents initially with poor night vision, which slowly progresses to total blindness.  It is believed to be inherited in an autosomal recessive manner.  Approximately 200 known cases have been reported in the literature.  The incidence is highest in Finland, estimated at 1:50,000.Research suggests there can be some adverse effect on muscles and also the brain. The cause of this is somewhat unclear but may relate to very low levels of creatine often found in this population.
Treatment may include vitamin B6, lysine or dramatic dietary change to minimise arginine from patients diet. Research has indicated that these treatments may be somewhat effective in lowering ornithine blood concentration levels in some patients, either in combination or individually.  Vitamin B6 has been found to be very effective in a small proportion of patients.

Presentation
Quite often, the presenting symptom of ornithine aminotransferase (OAT) deficiency is myopia which progresses to night blindness.  The onset of myopia is often in early childhood.  Ophthalmological findings in affected individuals include constricted visual fields, posterior subcapsular cataracts (can begin in late teens), elevated dark adaptation thresholds and decreased or absent electroretinographic responses </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Valsalva retinopathy and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nelsons syndrome and explain in detail? [/INST] Nelsons syndrome is a disorder that occurs in about one in four patients who have had both adrenal glands removed to treat Cushings disease. In patients with pre-existing adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, loss of adrenal feedback following bilateral adrenalectomy can trigger the rapid growth of the tumor, leading to visual symptoms (e.g. bitemporal hemianopsia) and hyperpigmentation. The severity of the disease is dependent upon the effect of ACTH release on the skin, pituitary hormone loss from mass compression, as well as invasion into surrounding structures around the pituitary gland.The first case of Nelsons syndrome was reported in 1958 by Dr. Don Nelson. Within the past ten to twenty years, improvements have been made with identification and care for patients with Cushings disease. Techniques such as pituitary radiation therapy, ACTH assay, transsphenoidal pituitary surgery, higher resolution MRIs, and sampling of the inferior petrosal sinus have allowed physicians to pursue routes for Cushings syndrome therapy prior to consideration of bilateral adrenalectomy.Nelsons syndrome is also referred to as post adrenalectomy syndrome, a possible result of adrenalectomy performed for Cushings disease.

Symptoms and signs
The common symptoms include:
hyper-pigmentation of the skin
visual disturbances
headaches
abnormally high levels of beta-MSH and ACTH
abnormal enlargements of the pituitary gland,
interruption of menstrual cycles in women

Cause
Common causes include bilateral adrenalectomy for the treatment of Cushings disease, and hypopituitarism. The onset of the disease can occur up to 24 years after a bilateral adrenalectomy has been performed, with an average of up to 15 years after. A preventative measure that can be utilized is prophylactic radiotherapy when a bilateral adrenalectomy is being performed in order to prevent Nelsons syndrome from manifesting. Screening can also be done with the help of an MRI in order to visualize the pituitary for tumors. If tumors are not present then an MRI should be performed at intervals. Hyper-pigmentation and fasting ACTH levels within plasma above 154 pmol/L are predictive of Nelsons syndrome after an adrenalectomy. Risk factors include being younger in age and pregnancy.

Mechanism
After a bilateral adrenalectomy is performed cortisol levels are no longer normal. This increases CRH production because it is not suppressed within the hypothalamus anymore. The increased CRH levels promote the growth of the tumor. Mutations with genes and with the glucocorticoid receptor can affect the tumor as well. Furthermore, differences between Nelson syndrome and Cushings disease have been studied. Particularly Nelsons syndrome differs from Cushings disease due to the following: secretions from the tumors, replacement of glucocorticoids, and injury to the hypothalamus due to radiation therapy utilized on the patient. The pathophysiology of Nelsons syndrome is not understood very well. Corticotrophinomas are generated from corticotroph cells. Expression of functional CRH and vasopressin V3 receptors increase in number. Additionally, there are two isoforms of glucocorticoid receptors. Heterozygosity loss in the glucocorticoid receptor can occur in the tumors present from Nelsons syndrome. Overall, not all patients that have had a total bilateral adrenalectomy develop Nelsons syndrome, which makes the mechanism harder to understand for such a rare disease. It is not clear whether the adrenalectomy or reduced cortisol secretion causes aggressive tumor growth.

Diagnosis
Common diagnostic techniques include:
MRIs
CAT scans
blood samples.Blood samples are assessed for the absence or presence of aldosterone and cortisol. Physical examinations are also useful in patients in order to examine vision, skin pigmentation, how the body replaces steroids, and the cranial nerves. Recent advancements in high-resolution MRIs allow for adenomas to be detected during the early stages of Nelson syndrome. Physical examination including height, weight, vital signs, blood pressure, eye examination, thyroid examination, abdominal examination, neurological examination, skin examination and pubertal staging needs to be assessed. Through blood pressure and pulse readings can indicate hypothyroidism and adrenal insufficiency. Hyper-pigmentation, hyporeflexia, and loss of vision can also indicate Nelsons syndrome when assessed together. Specifically for a child who might have Nelsons syndrome, the patient should be questioned about the symptoms of the disease, and well as symptoms of other diseases to narrow down which disease the patient presents with. The patient should be questioned about how often and to what degree headaches, visual disturbances, and symptoms associated with pituitary malfunction occur. Additionally, adrenal steroid replacement should be assessed.

Treatment
Common treatments for Nelsons syndrome include radiation or surgical procedure. Radiation allows for the limitation of the growth of the pituitary gland and the adenomas. If the adenomas start to affect the surrounding structures of the brain, then a micro-surgical technique can be adapted in order to remove the adenomas in a transsphenoidal (bone at base of the skull) process. Death may result with development of a locally aggressive pituitary tumor </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Retinal dysplasia and explain in detail? [/INST] Retinal dysplasia is an eye disease affecting the retina of animals and, less commonly, humans.  It is usually a nonprogressive disease and can be caused by viral infections, drugs, vitamin A deficiency, or genetic defects.  Retinal dysplasia is characterized by folds or rosettes (round clumps) of the retinal tissue.

Retinal dysplasia in dogs
Most cases of retinal dysplasia in dogs are hereditary.  It can involve one or both retinas.  Retinal dysplasia can be focal, multifocal, geographic, or accompanied by retinal detachment </s>