<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 Selenium and explain in detail? [/INST] Selenium is a chemical element with the symbol Se and atomic number 34. It is a nonmetal (more rarely considered a metalloid) with properties that are intermediate between the elements above and below in the periodic table, sulfur and tellurium, and also has similarities to arsenic. It seldom occurs in its elemental state or as pure ore compounds in the Earths crust. Selenium – from Greek selḗnē (σελήνη Moon) – was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium (named for the Earth).
Selenium is found in metal sulfide ores, where it partially replaces the sulfur. Commercially, selenium is produced as a byproduct in the refining of these ores, most often during production. Minerals that are pure selenide or selenate compounds are known but rare. The chief commercial uses for selenium today are glassmaking and pigments. Selenium is a semiconductor and is used in photocells. Applications in electronics, once important, have been mostly replaced with silicon semiconductor devices. Selenium is still used in a few types of DC power surge protectors and one type of fluorescent quantum dot.
Although trace amounts of selenium are necessary for cellular function in many animals, including humans, both elemental selenium and (especially) selenium salts are toxic in even small doses, causing selenosis. Selenium is listed as an ingredient in many multivitamins and other dietary supplements, as well as in infant formula, and is a component of the antioxidant enzymes glutathione peroxidase and thioredoxin reductase (which indirectly reduce certain oxidized molecules in animals and some plants) as well as in 3 deiodinase enzymes. Selenium requirements in plants differ by species, with some plants requiring relatively large amounts and others apparently not requiring any.

Characteristics
Physical properties
Selenium forms several allotropes that interconvert with temperature changes, depending somewhat on the rate of temperature change. When prepared in chemical reactions, selenium is usually an amorphous, brick-red powder. When rapidly melted, it forms the black, vitreous form, usually sold commercially as beads. The structure of black selenium is irregular and complex and consists of polymeric rings with up to 1000 atoms per ring. Black Se is a brittle, lustrous solid that is slightly soluble in CS2. Upon heating, it softens at 50 °C and converts to gray selenium at 180 °C; the transformation temperature is reduced by presence of halogens and amines.The red α, β, and γ forms are produced from solutions of black selenium by varying the evaporation rate of the solvent (usually CS2). They all have a relatively low, monoclinic crystal symmetry (space group 14) and contain nearly identical puckered Se8 rings with different arrangements, as in sulfur. The eight atoms of a ring are not equivalent (i.e. they are not mapped one onto another by any symmetry operation), and in fact in the γ-monoclinic form, half the rings are in one configuration (and its mirror image) and half in another. The packing is most dense in the α form. In the Se8 rings, the Se-Se distance varies depending on where the pair of atoms is in the ring, but the average is 233.5 pm, and the Se-Se-Se angle is on average 105.7° . Other selenium allotropes may contain Se6 or Se7 rings.The most stable and dense form of selenium is gray and has a chiral hexagonal crystal lattice (space group 152 or 154 depending on the chirality) consisting of helical polymeric chains, where the Se-Se distance is 237.3 pm and Se-Se-Se angle is 103.1° . The minimum distance between chains is 343.6 pm. Gray Se is formed by mild heating of other allotropes, by slow cooling of molten Se, or by condensing Se vapor just below the melting point. Whereas other Se forms are insulators, gray Se is a semiconductor showing appreciable photoconductivity. Unlike the other allotropes, it is insoluble in CS2. It resists oxidation by air and is not attacked by nonoxidizing acids. With strong reducing agents, it forms polyselenides. Selenium does not exhibit the changes in viscosity that sulfur undergoes when gradually heated.

Optical properties
Owing to its use as a photoconductor in flat-panel x-ray detectors (see below), the optical properties of amorphous selenium (α-Se) thin films have been the subject of intense research.

Isotopes
Selenium has seven naturally occurring isotopes. Five of these, 74Se, 76Se, 77Se, 78Se, 80Se, are stable, with 80Se being the most abundant (49.6% natural abundance). Also naturally occurring is the long-lived primordial radionuclide 82Se, with a half-life of 9.2×1019 years. The non-primordial radioisotope 79Se also occurs in minute quantities in uranium ores as a product of nuclear fission. Selenium also has numerous unstable synthetic isotopes ranging from 64Se to 95Se; the most stable are 75Se with a half-life of 119.78 days and 72Se with a half-life of 8.4 days. Isotopes lighter than the stable isotopes primarily undergo beta plus decay to isotopes of arsenic, and isotopes heavier than the stable isotopes undergo beta minus decay to isotopes of bromine, with some minor neutron emission branches in the heaviest known isotopes.

Chemical compounds
Selenium compounds commonly exist in the oxidation states −2, +2, +4, and +6.

Chalcogen compounds
Selenium forms two oxides: selenium dioxide (SeO2) and selenium trioxide (SeO3). Selenium dioxide is formed by the reaction of elemental selenium with oxygen:

            Se

              8

          +
          8

            O

              2

          ⟶
          8

            SeO

              2

    {\displaystyle {\ce {Se8 + 8 O2 -> 8 SeO2}}}
  It is a polymeric solid that forms monomeric SeO2 molecules in the gas phase. It dissolves in water to form selenous acid, H2SeO3. Selenous acid can also be made directly by oxidizing elemental selenium with nitric acid:

          3

          Se
          +
          4

            HNO

              3

          +

            H

              2

          O
          ⟶
          3

            H

              2

            SeO

              3

          +
          4

          NO

    {\displaystyle {\ce {3 Se + 4 HNO3 + H2O -> 3 H2SeO3 + 4 NO}}}
  Unlike sulfur, which forms a stable trioxide, selenium trioxide is thermodynamically unstable and decomposes to the dioxide above 185 °C:

          2

            SeO

              3

          ⟶
          2

            SeO

              2

          +

            O

              2

    {\displaystyle {\ce {2 SeO3 -> 2 SeO2 + O2}}}
   (ΔH = −54 kJ/mol)Selenium trioxide is produced in the laboratory by the reaction of anhydrous potassium selenate (K2SeO4) and sulfur trioxide (SO3).Salts of selenous acid are called selenites. These include silver selenite (Ag2SeO3) and sodium selenite (Na2SeO3).
Hydrogen sulfide reacts with aqueous selenous acid to produce selenium disulfide:

            H

              2

            SeO

              3

          +
          2

            H

              2

          S
          ⟶

            SeS

              2

          +
          3

            H

              2

          O

    {\displaystyle {\ce {H2SeO3 + 2 H2S -> SeS2 + 3 H2O}}}
  Selenium disulfide consists of 8-membered rings. It has an approximate composition of SeS2, with individual rings varying in composition, such as Se4S4 and Se2S6. Selenium disulfide has been used in shampoo as an antidandruff agent, an inhibitor in polymer chemistry, a glass dye, and a reducing agent in fireworks.Selenium trioxide may be synthesized by dehydrating selenic acid, H2SeO4, which is itself produced by the oxidation of selenium dioxide with hydrogen peroxide:

            SeO

              2

          +

            H

              2

            O

              2

          ⟶

            H

              2

            SeO

              4

    {\displaystyle {\ce {SeO2 + H2O2 -> H2SeO4}}}
  Hot, concentrated selenic acid can react with gold to form gold(III) selenate.

Halogen compounds
Iodides of selenium are not well known. The only stable chloride is selenium monochloride (Se2Cl2), which might be better known as selenium(I) chloride; the corresponding bromide is also known. These species are structurally analogous to the corresponding disulfur dichloride. Selenium dichloride is an important reagent in the preparation of selenium compounds (e.g. the preparation of Se7). It is prepared by treating selenium with sulfuryl chloride (SO2Cl2). Selenium reacts with fluorine to form selenium hexafluoride:

            Se

              8

          +
          24

            F

              2

          ⟶
          8

            SeF

              6

    {\displaystyle {\ce {Se8 + 24 F2 -> 8 SeF6}}}
  In comparison with its sulfur counterpart (sulfur hexafluoride), selenium hexafluoride (SeF6) is more reactive and is a toxic pulmonary irritant.
Some of the selenium oxyhalides, such as selenium oxyfluoride (SeOF2) and selenium oxychloride (SeOCl2) have been used as specialty solvents.

Selenides
Analogous to the behavior of other chalcogens, selenium forms hydrogen selenide, H2Se. It is a strongly odiferous, toxic, and colorless gas. It is more acidic than H2S. In solution it ionizes to HSe−. The selenide dianion Se2− forms a variety of compounds, including the minerals from which selenium is obtained commercially. Illustrative selenides include mercury selenide (HgSe), lead selenide (PbSe), zinc selenide (ZnSe), and copper indium gallium diselenide (Cu(Ga,In)Se2). These materials are semiconductors. With highly electropositive metals, such as aluminium, these selenides are prone to hydrolysis:

            Al

              2

            Se

              3

          +
          3

            H

              2

          O
          ⟶

            Al

              2

            O

              3

          +
          3

            H

              2

          Se

    {\displaystyle {\ce {Al2Se3 + 3 H2O -> Al2O3 + 3 H2Se}}}
  Alkali metal selenides react with selenium to form polyselenides, Se2−n, which exist as chains.

Other compounds
Tetraselenium tetranitride, Se4N4, is an explosive orange compound analogous to tetrasulfur tetranitride (S4N4). It can be synthesized by the reaction of selenium tetrachloride (SeCl4) with [((CH3)3Si)2N]2Se.Selenium reacts with cyanides to yield selenocyanates:

          8

          KCN
          +

            Se

              8

          ⟶
          8

          KSeCN

    {\displaystyle {\ce {8 KCN + Se8 -> 8 KSeCN}}}

Organoselenium compounds
Selenium, especially in the II oxidation state, forms stable bonds to carbon, which are structurally analogous to the corresponding organosulfur compounds. Especially common are selenides (R2Se, analogues of thioethers), diselenides (R2Se2, analogues of disulfides), and selenols (RSeH, analogues of thiols). Representatives of selenides, diselenides, and selenols include respectively selenomethionine, diphenyldiselenide, and benzeneselenol. The sulfoxide in sulfur chemistry is represented in selenium chemistry by the selenoxides (formula RSe(O)R), which are intermediates in organic synthesis, as illustrated by the selenoxide elimination reaction. Consistent with trends indicated by the double bond rule, selenoketones, R(C=Se)R, and selenaldehydes, R(C=Se)H, are rarely observed.

History
Selenium (Greek σελήνη selene meaning "Moon") was discovered in 1817 by Jöns Jacob Berzelius and Johan Gottlieb Gahn. Both chemists owned a chemistry plant near Gripsholm, Sweden, producing sulfuric acid by the lead chamber process. The pyrite from the Falun Mine created a red precipitate in the lead chambers which was presumed to be an arsenic compound, so the pyrites use to make acid was discontinued. Berzelius and Gahn wanted to use the pyrite and they also observed that the red precipitate gave off a smell like horseradish when burned. This smell was not typical of arsenic, but a similar odor was known from tellurium compounds. Hence, Berzeliuss first letter to Alexander Marcet stated that this was a tellurium compound. However, the lack of tellurium compounds in the Falun Mine minerals eventually led Berzelius to reanalyze the red precipitate, and in 1818 he wrote a second letter to Marcet describing a newly found element similar to sulfur and tellurium. Because of its similarity to tellurium, named for the Earth, Berzelius named the new element after the Moon.In 1873, Willoughby Smith found that the electrical resistance of grey selenium was dependent on the ambient light. This led to its use as a cell for sensing light. The first commercial products using selenium were developed by Werner Siemens in the mid-1870s. The selenium cell was used in the photophone developed by Alexander Graham Bell in 1879. Selenium transmits an electric current proportional to the amount of light falling on its surface. This phenomenon was used in the design of light meters and similar devices. Seleniums semiconductor properties found numerous other applications in electronics. The development of selenium rectifiers began during the early 1930s, and these replaced copper oxide rectifiers because they were more efficient. These lasted in commercial applications until the 1970s, following which they were replaced with less expensive and even more efficient silicon rectifiers.
Selenium came to medical notice later because of its toxicity to industrial workers. Selenium was also recognized as an important veterinary toxin, which is seen in animals that have eaten high-selenium plants. In 1954, the first hints of specific biological functions of selenium were discovered in microorganisms by biochemist, Jane Pinsent. It was discovered to be essential for mammalian life in 1957. In the 1970s, it was shown to be present in two independent sets of enzymes. This was followed by the discovery of selenocysteine in proteins. During the 1980s, selenocysteine was shown to be encoded by the codon UGA. The recoding mechanism was worked out first in bacteria and then in mammals (see SECIS element).

Occurrence
Native (i.e., elemental) selenium is a rare mineral, which does not usually form good crystals, but, when it does, they are steep rhombohedra or tiny acicular (hair-like) crystals. Isolation of selenium is often complicated by the presence of other compounds and elements.
Selenium occurs naturally in a number of inorganic forms, including selenide, selenate, and selenite, but these minerals are rare. The common mineral selenite is not a selenium mineral, and contains no selenite ion, but is rather a type of gypsum (calcium sulfate hydrate) named like selenium for the moon well before the discovery of selenium. Selenium is most commonly found as an impurity, replacing a small part of the sulfur in sulfide ores of many metals.In living systems, selenium is found in the amino acids selenomethionine, selenocysteine, and methylselenocysteine. In these compounds, selenium plays a role analogous to that of sulfur. Another naturally occurring organoselenium compound is dimethyl selenide.Certain soils are selenium-rich, and selenium can be bioconcentrated by some plants. In soils, selenium most often occurs in soluble forms such as selenate (analogous to sulfate), which are leached into rivers very easily by runoff. Ocean water contains significant amounts of selenium.Typical background concentrations of selenium do not exceed 1 ng/m3 in the atmosphere; 1 mg/kg in soil and vegetation and 0.5 μg/L in freshwater and seawater.Anthropogenic sources of selenium include coal burning, and the mining and smelting of sulfide ores.

Production
Selenium is most commonly produced from selenide in many sulfide ores, such as those of copper, nickel, or lead. Electrolytic metal refining is particularly productive of selenium as a byproduct, obtained from the anode mud of copper refineries. Another source was the mud from the lead chambers of sulfuric acid plants, a process that is no longer used. Selenium can be refined from these muds by a number of methods. However, most elemental selenium comes as a byproduct of refining copper or producing sulfuric acid. Since its invention, solvent extraction and electrowinning (SX/EW) production of copper produces an increasing share of the worldwide copper supply. This changes the availability of selenium because only a comparably small part of the selenium in the ore is leached with the copper.Industrial production of selenium usually involves the extraction of selenium dioxide from residues obtained during the purification of copper. Common production from the residue then begins by oxidation with sodium carbonate to produce selenium dioxide, which is mixed with water and acidified to form selenous acid (oxidation step). Selenous acid is bubbled with sulfur dioxide (reduction step) to give elemental selenium.About 2,000 tonnes of selenium were produced in 2011 worldwide, mostly in Germany (650 t), Japan (630 t), Belgium (200 t), and Russia (140 t), and the total reserves were estimated at 93,000 tonnes. These data exclude two major producers: the United States and China. A previous sharp increase was observed in 2004 from $4–$5 to $27/lb. The price was relatively stable during 2004–2010 at about US$30 per pound (in 100 pound lots) but increased to $65/lb in 2011. The consumption in 2010 was divided as follows: metallurgy – 30%, glass manufacturing – 30%, agriculture – 10%, chemicals and pigments – 10%, and electronics – 10%. China is the dominant consumer of selenium at 1,500–2,000 tonnes/year.

Applications
Fertilizers
Researchers found that application of selenium fertilizer to lettuce crops decreased the accumulation of lead and cadmium. Peaches and pears given a foliar selenium spray contained higher levels of selenium and also stayed firm and ripe longer when in storage. In low doses, selenium has shown a beneficial effect on plant resistance to various environmental stress factors including drought, UV-B, soil salinity, and cold or hot temperatures. However, it can damage plants at higher doses.

Manganese electrolysis
During the electrowinning of manganese, the addition of selenium dioxide decreases the power necessary to operate the electrolysis cells. China is the largest consumer of selenium dioxide for this purpose. For every tonne of manganese, an average 2 kg selenium oxide is used.

Glass production
The largest commercial use of Se, accounting for about 50% of consumption, is for the production of glass. Se compounds confer a red color to glass. This color cancels out the green or yellow tints that arise from iron impurities typical for most glass. For this purpose, various selenite and selenate salts are added. For other applications, a red color may be desired, produced by mixtures of CdSe and CdS.

Alloys
Selenium is used with bismuth in brasses to replace more toxic lead. The regulation of lead in drinking water applications such as in the US with the Safe Drinking Water Act of 1974, made a reduction of lead in brass necessary. The new brass is marketed under the name EnviroBrass. Like lead and sulfur, selenium improves the machinability of steel at concentrations around 0.15%. Selenium produces the same machinability improvement in copper alloys.

Lithium–selenium batteries
The lithium–selenium (Li–Se) battery is one of the most promising systems for energy storage in the family of lithium batteries. The Li–Se battery is an alternative to the lithium–sulfur battery, with an advantage of high electrical conductivity.

Solar cells
Selenium was the basis of the very first solar cells, with the first example of rooftop solar being a selenium cell from 1884. Such cells were later used in battery-free light meters for photography. Copper indium gallium selenide is a material used in solar cells.

Photoconductors
Amorphous selenium (α-Se) thin films have found application as photoconductors in flat panel x-ray detectors. These detectors use amorphous selenium to capture and convert incident x-ray photons directly into electric charge.

Rectifiers
Selenium rectifiers were first used in 1933. Their use continued into the 1990s.

Other uses
Small amounts of organoselenium compounds have been used to modify the catalysts used for the vulcanization for the production of rubber.The demand for selenium by the electronics industry is declining. Its photovoltaic and photoconductive properties are still useful in photocopying, photocells, light meters and solar cells. Its use as a photoconductor in plain-paper copiers once was a leading application, but in the 1980s, the photoconductor application declined (although it was still a large end-use) as more and more copiers switched to organic photoconductors. Though once widely used, selenium rectifiers have mostly been replaced (or are being replaced) by silicon-based devices. The most notable exception is in power DC surge protection, where the superior energy capabilities of selenium suppressors make them more desirable than metal-oxide varistors.
Zinc selenide was the first material for blue LEDs, but gallium nitride dominates that market. Cadmium selenide was an important component in quantum dots. Sheets of amorphous selenium convert X-ray images to patterns of charge in xeroradiography and in solid-state, flat-panel X-ray cameras. Ionized selenium (Se+24) is one of the active mediums used in X-ray lasers.Selenium is a catalyst in some chemical reactions, but it is not widely used because of issues with toxicity. In X-ray crystallography, incorporation of one or more selenium atoms in place of sulfur helps with multiple-wavelength anomalous dispersion and single wavelength anomalous dispersion phasing.Selenium is used in the toning of photographic prints, and it is sold as a toner by numerous photographic manufacturers. Selenium intensifies and extends the tonal range of black-and-white photographic images and improves the permanence of prints.75Se is used as a gamma source in industrial radiography.

Pollution
In high concentrations, selenium acts as an environmental contaminant.  Sources of pollution include waste materials from certain mining, agricultural, petrochemical, and industrial manufacturing operations.  In Belews Lake North Carolina, 19 species of fish were eliminated from the lake due to 150–200 μg Se/L wastewater discharged from 1974 to 1986 from a Duke Energy coal-fired power plant.  At the Kesterson National Wildlife Refuge in California, thousands of fish and waterbirds were poisoned by selenium in agricultural irrigation drainage.
Substantial physiological changes may occur in fish with high tissue concentrations of selenium. Fish affected by selenium may experience swelling of the gill lamellae, which impedes oxygen diffusion across the gills and blood flow within the gills. Respiratory capacity is further reduced due to selenium binding to hemoglobin. Other problems include degeneration of liver tissue, swelling around the heart, damaged egg follicles in ovaries, cataracts, and accumulation of fluid in the body cavity and head. Selenium often causes a malformed fish fetus which may have problems feeding or respiring; distortion of the fins or spine is also common. Adult fish may appear healthy despite their inability to produce viable offspring.
Selenium is bioaccumulated in aquatic habitats, which results in higher concentrations in organisms than the surrounding water. Organoselenium compounds can be concentrated over 200,000 times by zooplankton when water concentrations are in the 0.5 to 0.8 μg Se/L range. Inorganic selenium bioaccumulates more readily in phytoplankton than zooplankton. Phytoplankton can concentrate inorganic selenium by a factor of 3000.  Further concentration through bioaccumulation occurs along the food chain, as predators consume selenium rich prey. It is recommended that a water concentration of 2 μg Se/L be considered highly hazardous to sensitive fish and aquatic birds. Selenium poisoning can be passed from parents to offspring through the egg, and selenium poisoning may persist for many generations. Reproduction of mallard ducks is impaired at dietary concentrations of 7 μg Se/L. Many benthic invertebrates can tolerate selenium concentrations up to 300 μg/L of Se in their diet.Selenium pollution might impact some aquatic systems and may be caused by anthropogenic factors such as farming runoff and industrial processes. Fish are a major source of protein for humans, people who eat more fish are generally healthier than those who eat less, indicating selenium pollution does not appear to be a problem, although it might be useful to be aware that selenium has a potential effect on humans.Bioaccumulation of selenium in aquatic environments causes fish kills depending on the species in the affected area. There are, however, a few species that have been seen to survive these events and tolerate the increased selenium. It has also been suggested that season could have an impact on the harmful effects of selenium on fish.Selenium poisoning of water systems may result whenever new agricultural run-off courses through dry lands. This process leaches natural soluble selenium compounds (such as selenates) into the water, which may then be concentrated in wetlands as the water evaporates. Selenium pollution of waterways also occurs when selenium is leached from coal flue ash, mining and metal smelting, crude oil processing, and landfill. High selenium levels in waterways were found to cause congenital disorders in oviparous species, including wetland birds and fish. Elevated dietary methylmercury levels can amplify the harm of selenium toxicity in oviparous species.

Biological role
Although it is toxic in large doses, selenium is an essential micronutrient for animals. In plants, it occurs as a bystander mineral, sometimes in toxic proportions in forage (some plants may accumulate selenium as a defense against being eaten by animals, but other plants, such as locoweed, require selenium, and their growth indicates the presence of selenium in soil).Selenium is a component of the unusual amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for reduction of antioxidant enzymes, such as glutathione peroxidases and certain forms of thioredoxin reductase found in animals and some plants (this enzyme occurs in all living organisms, but not all forms of it in plants require selenium).
The glutathione peroxidase family of enzymes (GSH-Px) catalyze certain reactions that remove reactive oxygen species such as hydrogen peroxide and organic hydroperoxides:

2 GSH + H2O2----GSH-Px → GSSG + 2 H2OThe thyroid gland and every cell that uses thyroid hormone use selenium, which is a cofactor for the three of the four known types of thyroid hormone deiodinases, which activate and then deactivate various thyroid hormones and their metabolites; the iodothyronine deiodinases are the subfamily of deiodinase enzymes that use selenium as the otherwise rare amino acid selenocysteine. (Only the deiodinase iodotyrosine deiodinase, which works on the last breakdown products of thyroid hormone, does not use selenium.)Selenium may inhibit Hashimotos disease, in which the bodys own thyroid cells are attacked as foreign. A reduction of 21% on TPO antibodies is reported with the dietary intake of 0.2 mg of selenium.Increased dietary selenium reduces the effects of mercury toxicity, although it is effective only at low to modest doses of mercury. Evidence suggests that the molecular mechanisms of mercury toxicity includes the irreversible inhibition of selenoenzymes that are required to prevent and reverse oxidative damage in brain and endocrine tissues. An antioxidant, selenoneine, which is derived from selenium and has been found to be present in the blood of bluefin tuna, is the subject of scientific research regarding its possible roles in inflammatory and chronic diseases, methylmercury detoxification, and oxidative damages. It seems as though when mercury levels in a marine fish rise, so do the selenium levels. To the knowledge of researchers, there are no reports of mercury levels exceeding that of selenium levels in ocean fish.

Evolution in biology
From about three billion years ago, prokaryotic selenoprotein families drive the evolution of selenocysteine, an amino acid. Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea, and eukaryotes as selenocysteine, where selenoprotein peroxiredoxins protect bacterial and eukaryotic cells against oxidative damage. Selenoprotein families of GSH-Px and the deiodinases of eukaryotic cells seem to have a bacterial phylogenetic origin. The selenocysteine-containing form occurs in species as diverse as green algae, diatoms, sea urchins, fish, and chickens. Selenium enzymes are involved in the small reducing molecules glutathione and thioredoxin. One family of selenium-bearing molecules (the glutathione peroxidases) destroys peroxide and repairs damaged peroxidized cell membranes, using glutathione. Another selenium-bearing enzyme in some plants and in animals (thioredoxin reductase) generates reduced thioredoxin, a dithiol that serves as an electron source for peroxidases and also the important reducing enzyme ribonucleotide reductase that makes DNA precursors from RNA precursors.Trace elements involved in GSH-Px and superoxide dismutase enzymes activities, i.e. selenium, vanadium, magnesium, copper, and zinc, may have been lacking in some terrestrial mineral-deficient areas. Marine organisms retained and sometimes expanded their selenoproteomes, whereas the selenoproteomes of some terrestrial organisms were reduced or completely lost. These findings suggest that, with the exception of vertebrates, aquatic life supports selenium use, whereas terrestrial habitats lead to reduced use of this trace element. Marine fishes and vertebrate thyroid glands have the highest concentration of selenium and iodine. From about 500 million years ago, freshwater and terrestrial plants slowly optimized the production of "new" endogenous antioxidants such as ascorbic acid (vitamin C), polyphenols (including flavonoids), tocopherols, etc. A few of these appeared more recently, in the last 50–200 million years, in fruits and flowers of angiosperm plants. In fact, the angiosperms (the dominant type of plant today) and most of their antioxidant pigments evolved during the late Jurassic period.The deiodinase isoenzymes constitute another family of eukaryotic selenoproteins with identified enzyme function. Deiodinases are able to extract electrons from iodides, and iodides from iodothyronines. They are, thus, involved in thyroid-hormone regulation, participating in the protection of thyrocytes from damage by H2O2 produced for thyroid-hormone biosynthesis. About 200 million years ago, new selenoproteins were developed as mammalian GSH-Px enzymes.

Nutritional sources of selenium
Dietary selenium comes from meat, nuts, cereals and mushrooms. Brazil nuts are the richest dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs).The US Recommended Dietary Allowance (RDA) of selenium for teenagers and adults is 55 µg/day. Selenium as a dietary supplement is available in many forms, including multi-vitamins/mineral supplements, which typically contain 55 or 70 µg/serving. Selenium-specific supplements typically contain either 100 or 200 µg/serving.
In June 2015, the US Food and Drug Administration (FDA) published its final rule establishing the requirement of minimum and maximum levels of selenium in infant formula.The selenium content in the human body is believed to be in the 13–20 mg range.

Indicator plant species
Certain species of plants are considered indicators of high selenium content of the soil because they require high levels of selenium to thrive. The main selenium indicator plants are Astragalus species (including some locoweeds), princes plume (Stanleya sp.), woody asters (Xylorhiza sp.), and false goldenweed (Oonopsis sp.)

Detection in biological fluids
Selenium may be measured in blood, plasma, serum, or urine to monitor excessive environmental or occupational exposure, to confirm a diagnosis of poisoning in hospitalized victims, or investigate a suspected case of fatal overdose. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Both organic and inorganic forms of selenium are largely converted to monosaccharide conjugates (selenosugars) in the body prior to elimination in the urine. Cancer patients receiving daily oral doses of selenothionine may achieve very high plasma and urine selenium concentrations.

Toxicity
Although selenium is an essential trace element, it is toxic if taken in excess. Exceeding the Tolerable Upper Intake Level of 400 micrograms per day can lead to selenosis. This 400 µg Tolerable Upper Intake Level is based primarily on a 1986 study of five Chinese patients who exhibited overt signs of selenosis and a follow up study on the same five people in 1992. The 1992 study actually found the maximum safe dietary Se intake to be approximately 800 micrograms per day (15 micrograms per kilogram body weight), but suggested 400 micrograms per day to avoid creating an imbalance of nutrients in the diet and to accord with data from other countries. In China, people who ingested corn grown in extremely selenium-rich stony coal (carbonaceous shale) have suffered from selenium toxicity. This coal was shown to have selenium content as high as 9.1%, the highest concentration in coal ever recorded.Signs and symptoms of selenosis include a garlic odor on the breath, gastrointestinal disorders, hair loss, sloughing of nails, fatigue, irritability, and neurological damage. Extreme cases of selenosis can exhibit cirrhosis of the liver, pulmonary edema, or death. Elemental selenium and most metallic selenides have relatively low toxicities because of low bioavailability. By contrast, selenates and selenites have an oxidant mode of action similar to that of arsenic trioxide and are very toxic. The chronic toxic dose of selenite for humans is about 2400 to 3000 micrograms of selenium per day. Hydrogen selenide is an extremely toxic, corrosive gas. Selenium also occurs in organic compounds, such as dimethyl selenide, selenomethionine, selenocysteine and methylselenocysteine, all of which have high bioavailability and are toxic in large doses.
On 19 April 2009, 21 polo ponies died shortly before a match in the United States Polo Open. Three days later, a pharmacy released a statement explaining that the horses had received an incorrect dose of one of the ingredients used in a vitamin/mineral supplement compound that had been incorrectly prepared by a compounding pharmacy. Analysis of blood levels of inorganic compounds in the supplement indicated the selenium concentrations were 10 to 15 times higher than normal in the blood samples, and 15 to 20 times higher than normal in the liver samples. Selenium was later confirmed to be the toxic factor.

In fish and other wildlife, selenium is necessary for life, but toxic in high doses. For salmon, the optimal concentration of selenium is about 1 microgram selenium per gram of whole body weight. Much below that level, young salmon die from deficiency; much above, they die from toxic excess.The Occupational Safety and Health Administration (OSHA) has set the legal limit (permissible exposure limit) for selenium in the workplace at 0.2 mg/m3 over an 8-hour workday. The National Institute for Occupational Safety and Health (NIOSH) has set a Recommended exposure limit (REL) of 0.2 mg/m3 over an 8-hour workday. At levels of 1 mg/m3, selenium is immediately dangerous to life and health.

Deficiency
Selenium deficiency can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, and in those of advanced age (over 90). Also, people dependent on food grown from selenium-deficient soil are at risk. Although New Zealand soil has low levels of selenium, adverse health effects have not been detected in the residents.Selenium deficiency, defined by low (<60% of normal) selenoenzyme activity levels in brain and endocrine tissues, occurs only when a low selenium level is linked with an additional stress, such as high exposures to mercury or increased oxidant stress from vitamin E deficiency.Selenium interacts with other nutrients, such as iodine and vitamin E. The effect of selenium deficiency on health remains uncertain, particularly in relation to Kashin-Beck disease. Also, selenium interacts with other minerals, such as zinc and copper. High doses of Se supplements in pregnant animals might disturb the Zn:Cu ratio and lead to Zn reduction; in such treatment cases, Zn levels should be monitored. Further studies are needed to confirm these interactions.In the regions (e.g </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 Parry–Romberg syndrome and explain in detail? [/INST] Parry–Romberg syndrome (PRS)  is a rare disease characterized by progressive shrinkage and degeneration of the tissues beneath the skin, usually on only one side of the face (hemifacial atrophy) but occasionally extending to other parts of the body. An autoimmune mechanism is suspected, and the syndrome may be a variant of localized scleroderma, but the precise cause and pathogenesis of this acquired disorder remains unknown. It has been reported in the literature as a possible consequence of sympathectomy. The syndrome has a higher prevalence in females and typically appears between 5 and 15 years of age.
In addition to the connective tissue disease, the condition is sometimes accompanied by neurological, ocular and oral symptoms. The range and severity of associated symptoms and findings are highly variable.

Signs and symptoms
Skin and connective tissues
Initial facial changes usually involve the area of the face covered by the temporal or buccinator muscles. The disease progressively spreads from the initial location, resulting in atrophy of the skin and its adnexa, as well as underlying subcutaneous structures such as connective tissue, (fat, fascia, cartilage, bones) and/or muscles of one side of the face. The mouth and nose are typically deviated towards the affected side of the face.The process may eventually extend to involve tissues between the nose and the upper corner of the lip, the upper jaw, the angle of the mouth, the area around the eye and brow, the ear, and/or the neck. The syndrome often begins with a circumscribed patch of scleroderma in the frontal region of the scalp which is associated with a loss of hair and the appearance of a depressed linear scar extending down through the midface on the affected side. This scar is referred to as a "coup de sabre" lesion because it resembles the scar of a wound made by a sabre, and is indistinguishable from the scar observed in frontal linear scleroderma.In 20% of cases, the hair and skin overlying affected areas may become hyperpigmented or hypopigmented with patches of unpigmented skin. In up to 20% of cases the disease may involve the ipsilateral (on the same side) or contralateral (on the opposite side) neck, trunk, arm, or leg. The cartilage of the nose, ear and larynx can be involved. The disease has been reported to affect both sides of the face in 5 to 10% of cases.Symptoms and physical findings usually become apparent during the first or early during the second decade of life. The average age of onset is nine years of age, and the majority of individuals experience symptoms before 20 years of age. The disease may progress for several years before eventually going into remission (abruptly ceasing).

Neurological
Neurological abnormalities are common. Roughly 45% of people with Parry–Romberg syndrome also have trigeminal neuralgia (severe pain in the tissues supplied by the ipsilateral trigeminal nerve, including the forehead, eye, cheek, nose, mouth and jaw) and/or migraine (severe headaches that may be accompanied by visual abnormalities, nausea and vomiting).10% of affected individuals develop a seizure disorder as part of the disease. The seizures are typically Jacksonian in nature (characterized by rapid spasms of a muscle group that subsequently spread to adjacent muscles) and occur on the side contralateral to the affected side of the face. Half of these cases are associated with abnormalities in both the gray and white matter of the brain—usually ipsilateral but sometimes contralateral—that are detectable on magnetic resonance imaging (MRI) scan.

Ocular
Enophthalmos (recession of the eyeball within the orbit) is the most common eye abnormality observed in Parry–Romberg syndrome. It is caused by a loss of subcutaneous tissue around the orbit. Other common findings include drooping of the eyelid (ptosis), constriction of the pupil (miosis), redness of the conjunctiva, and decreased sweating (anhidrosis) of the affected side of the face. Collectively, these signs are referred to as Horners syndrome. Other ocular abnormalities include ophthalmoplegia (paralysis of one or more of the extraocular muscles) and other types of strabismus, uveitis, and heterochromia of the iris.

Oral
The tissues of the mouth, including the tongue, gingiva, teeth and soft palate are commonly involved in Parry–Romberg syndrome. 50% of affected individuals develop dental abnormalities such as delayed eruption, dental root exposure, or resorption of the dental roots on the affected side. 35% have difficulty or inability to normally open the mouth or other jaw symptoms, including temporomandibular joint disorder and spasm of the muscles of mastication on the affected side. 25% experience atrophy of one side of the upper lip and tongue.

Causes
The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Further, the National Organization for Rare Disorders has stated there is currently no evidence that Parry–Romberg syndrome is genetic or that it can be passed on to children. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.

Diagnosis
Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset. Oligoclonal bands and an elevated IgG index may be found in 50% of the patients.

Management
Medical
Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Surgical
Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Epidemiology
Parry–Romberg syndrome appears to occur randomly and for unknown reasons. Prevalence is higher in females than males, with a ratio of roughly 3:2. The condition is observed on the left side of the face about as often as on the right side.

History
The disease was first described in 1825 by Caleb Hillier Parry (1755–1822), in a collection of his medical writings which were published posthumously by his son Charles Henry Parry (1779–1860). It was described a second time in 1846 by Moritz Heinrich Romberg (1795–1873) and Eduard Heinrich Henoch (1820–1910). German neurologist Albert Eulenburg (1840–1917) was the first to use the descriptive title "progressive hemifacial atrophy" in 1871.

See also
Hemifacial microsomia
List of cutaneous conditions
Trigeminal trophic lesion

References
Further reading
Karim A, Laghmari M, Ibrahimy W, Essakali HN, Mohcine Z (October 2005). "[Neuroretinitis, Parry-Romberg syndrome, and scleroderma]". Journal Français dOphtalmologie (in French). 28 (8): 866–70. doi:10.1016/S0181-5512(05)81008-3. PMID 16249769.
Lakhani PK, David TJ (February 1984). "Progressive hemifacial atrophy with scleroderma and ipsilateral limb wasting (Parry-Romberg syndrome)". Journal of the Royal Society of Medicine. 77 (2): 138–9. doi:10.1177/014107688407700215. PMC 1439690. PMID 6737396.
Larner AJ, Bennison DP (September 1993). "Some observations on the aetiology of progressive hemifacial atrophy ("Parry-Romberg syndrome")". Journal of Neurology, Neurosurgery, and Psychiatry. 56 (9): 1035–6. doi:10.1136/jnnp.56.9.1035-a. PMC 489747. PMID 8410030.
Miller MT, Spencer MA (1995). "Progressive hemifacial atrophy. A natural history study". Transactions of the American Ophthalmological Society. 93: 203–15, discussion 215–7. PMC 1312058. PMID 8719679.
Pinheiro TP, Silva CC, Silveira CS, Botelho PC, Pinheiro MD, Pinheiro JJ (March 2006) </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 Trichosporonosis 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 Granulocytosis 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 Saddle nose 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 Millipede burn 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 Hernia and explain in detail? [/INST] A hernia is the abnormal exit of tissue or an organ, such as the bowel, through the wall of the cavity in which it normally resides. Various types of hernias can occur, most commonly involving the abdomen, and specifically the groin. Groin hernias are most commonly of the inguinal type but may also be femoral. Other types of hernias include hiatus, incisional, and umbilical hernias. Symptoms are present in about 66% of people with groin hernias. This may include pain or discomfort in the lower abdomen, especially with coughing, exercise, or urinating or defecating. Often, it gets worse throughout the day and improves when lying down. A bulge may appear at the site of hernia, that becomes larger when bending down. Groin hernias occur more often on the right than left side. The main concern is bowel strangulation, where the blood supply to part of the bowel is blocked. This usually produces severe pain and tenderness in the area. Hiatus, or hiatal hernias often result in heartburn but may also cause chest pain or pain while eating.Risk factors for the development of a hernia include smoking, chronic obstructive pulmonary disease, obesity, pregnancy, peritoneal dialysis, collagen vascular disease and previous open appendectomy, among others. Predisposition to hernias is genetic and occur more often in certain families. Deleterious mutations causing predisposition to hernias seem to have dominant inheritance (especially for men). It is unclear if groin hernias are associated with heavy lifting. Hernias can often be diagnosed based on signs and symptoms. Occasionally, medical imaging is used to confirm the diagnosis or rule out other possible causes. The diagnosis of hiatus hernias is often by endoscopy.Groin hernias that do not cause symptoms in males do not need to be repaired. Repair, however, is generally recommended in women due to the higher rate of femoral hernias, which have more complications. If strangulation occurs, immediate surgery is required. Repair may be done by open surgery or laparoscopic surgery. Open surgery has the benefit of possibly being done under local anesthesia rather than general anesthesia. Laparoscopic surgery generally has less pain following the procedure. A hiatus hernia may be treated with lifestyle changes such as raising the head of the bed, weight loss and adjusting eating habits. The medications H2 blockers or proton pump inhibitors may help. If the symptoms do not improve with medications, a surgery known as laparoscopic Nissen fundoplication may be an option.About 27% of males and 3% of females develop a groin hernia at some point in their lives. Inguinal, femoral and abdominal hernias were present in 18.5 million people and resulted in 59,800 deaths in 2015. Groin hernias occur most often before the age of 1 and after the age of 50. It is not known how commonly hiatus hernias occur, with estimates in North America varying from 10% to 80%. The first known description of a hernia dates back to at least 1550 BC, in the Ebers Papyrus from Egypt.

Signs and symptoms
By far the most common hernias develop in the  abdomen when a weakness in the abdominal wall evolves into a localized hole, or "defect", through which adipose tissue, or abdominal organs covered with peritoneum, may protrude. Another common hernia involves the spinal discs and causes sciatica. A hiatus hernia occurs when the stomach protrudes into the mediastinum through the esophageal opening in the diaphragm.
Hernias may or may not present with either pain at the site, a visible or palpable lump, or in some cases more vague symptoms resulting from pressure on an organ that has become "stuck" in the hernia, sometimes leading to organ dysfunction. Fatty tissue usually enters a hernia first, but it may be followed or accompanied by an organ.
Hernias are caused by a disruption or opening in the fascia, or fibrous tissue, which forms the abdominal wall. It is possible for the bulge associated with a hernia to come and go, but the defect in the tissue will persist.
Symptoms and signs vary depending on the type of hernia. Symptoms may or may not be present in some inguinal hernias. In the case of reducible hernias, a bulge in the groin or in another abdominal area can often be seen and felt. When standing, such a bulge becomes more obvious. Besides the bulge, other symptoms include pain in the groin that may also include a heavy or dragging sensation, and in men, there is sometimes pain and swelling in the scrotum around the testicular area.Irreducible abdominal hernias or incarcerated hernias may be painful, but their most relevant symptom is that they cannot return to the abdominal cavity when pushed in. They may be chronic, although painless, and can lead to strangulation (loss of blood supply), obstruction (kinking of intestine), or both. Strangulated hernias are always painful and pain is followed by tenderness. Nausea, vomiting, or fever may occur in these cases due to bowel obstruction. Also, the hernia bulge, in this case, may turn red, purple or dark and pink.
In the diagnosis of abdominal hernias, imaging is the principal means of detecting internal diaphragmatic and other nonpalpable or unsuspected hernias. Multidetector CT (MDCT) can show with precision the anatomic site of the hernia sac, the contents of the sac, and any complications. MDCT also offers clear detail of the abdominal wall allowing wall hernias to be identified accurately.

Complications
Complications may arise post-operation, including rejection of the mesh that is used to repair the hernia. In the event of a mesh rejection, the mesh will very likely need to be removed. Mesh rejection can be detected by obvious, sometimes localized swelling and pain around the mesh area. Continuous discharge from the scar is likely for a while after the mesh has been removed.
A surgically treated hernia can lead to complications such as inguinodynia, while an untreated hernia may be complicated by:

Inflammation
Obstruction of any lumen, such as bowel obstruction in intestinal hernias
Strangulation
Hydrocele of the hernial sac
Hemorrhage
Autoimmune problems
Irreducibility or incarceration, in which it cannot be reduced, or pushed back into place, at least not without very much external effort. In intestinal hernias, this also substantially increases the risk of bowel obstruction and strangulation.

Causes
Causes of hiatus hernia vary depending on each individual. Among the multiple causes, however, are the mechanical causes which include: improper heavy weight lifting, hard coughing bouts, sharp blows to the abdomen, and incorrect posture.Furthermore, conditions that increase the pressure of the abdominal cavity may also cause hernias or worsen the existing ones. Some examples would be: obesity, straining during a bowel movement or urination (constipation, enlarged prostate), chronic lung disease, and also, fluid in the abdominal cavity (ascites).Also, if muscles are weakened due to poor nutrition, smoking, and overexertion, hernias are more likely to occur.
The physiological school of thought contends that in the case of inguinal hernia, the above-mentioned are only an anatomical symptom of the underlying physiological cause. They contend that the risk of hernia is due to a physiological difference between patients who have hernia and those who do not, namely the presence of aponeurotic extensions from the transversus abdominis aponeurotic arch.Abdominal wall hernia may occur due to trauma. If this type of hernia is due to blunt trauma it is an emergency condition and could be associated with various solid organs and hollow viscus injuries.

Diagnosis
Inguinal
By far the most common hernias (up to 75% of all abdominal hernias) are inguinal hernias, which are further divided into the more common indirect inguinal hernia (2/3, depicted here), in which the inguinal canal is entered via a congenital weakness at its entrance (the internal inguinal ring), and the direct inguinal hernia type (1/3), where the hernia contents push through a weak spot in the back wall of the inguinal canal. Inguinal hernias are the most common type of hernia in both men and women. In some selected cases, they may require surgery.
There are special cases where a direct and indirect hernia appear together. A pantaloon hernia (or saddlebag hernia) is a combined direct and indirect hernia when the hernial sac protrudes on either side of the inferior epigastric vessels.
Additionally, though very rare, two or more indirect hernias may appear together such as in a double indirect hernia.

Femoral
Femoral hernias occur just below the inguinal ligament, when abdominal contents pass into the weak area at the posterior wall of the femoral canal. They can be hard to distinguish from the inguinal type (especially when ascending cephalad): however, they generally appear more rounded, and, in contrast to inguinal hernias, there is a strong female preponderance in femoral hernias. The incidence of strangulation in femoral hernias is high. Repair techniques are similar for femoral and inguinal hernia.
A Coopers hernia is a femoral hernia with two sacs, the first being in the femoral canal, and the second passing through a defect in the superficial fascia and appearing almost immediately beneath the skin.

Umbilical
They involve protrusion of intra-abdominal contents through a weakness at the site of passage of the umbilical cord through the abdominal wall.
Umbilical hernias in adults are largely acquired, and are more frequent in obese or pregnant women. Abnormal decussation of fibers at the linea alba may be a contributing factor.

Incisional
An incisional hernia occurs when the defect is the result of an incompletely healed surgical wound. When these occur in median laparotomy incisions in the linea alba, they are termed ventral hernias. These can be the most frustrating and difficult to treat, as the repair utilizes already attenuated tissue. These occur in about 13% of people at 2 years following surgery.

Diaphragmatic
Higher in the abdomen, an (internal) "diaphragmatic hernia" results when part of the stomach or intestine protrudes into the chest cavity through a defect in the diaphragm.
A hiatus hernia is a particular variant of this type, in which the normal passageway through which the esophagus meets the stomach (esophageal hiatus) serves as a functional "defect", allowing part of the stomach to (periodically) "herniate" into the chest. Hiatus hernias may be either "sliding", in which the gastroesophageal junction itself slides through the defect into the chest, or non-sliding (also known as para-esophageal), in which case the junction remains fixed while another portion of the stomach moves up through the defect. Non-sliding or para-esophageal hernias can be dangerous as they may allow the stomach to rotate and obstruct. Repair is usually advised.
A congenital diaphragmatic hernia is a distinct problem, occurring in up to 1 in 2000 births, and requiring pediatric surgery. Intestinal organs may herniate through several parts of the diaphragm, posterolateral (in Bochdaleks triangle (lumbocostal triangle), resulting in a Bochdalek hernia), or anteromedial-retrosternal (in the cleft of foramina of Morgagni (sternocostal triangle), resulting in a Morgagnis hernia).

Other hernias
Since many organs or parts of organs can herniate through many orifices, it is very difficult to give an exhaustive list of hernias, with all synonyms and eponyms. The above article deals mostly with "visceral hernias", where the herniating tissue arises within the abdominal cavity. Other hernia types and unusual types of visceral hernias are listed below, in alphabetical order:

Abdominal wall hernias:
Umbilical hernia
Epigastric hernia: a hernia through the linea alba above the umbilicus.
Spigelian hernia, also known as spontaneous lateral ventral hernia
Amyands hernia: containing the appendix vermiformis within the hernia sac
Brain herniation, sometimes referred to as brain hernia, is a potentially deadly side effect of very high intracranial pressure that occurs when a part of the brain is squeezed across structures within the skull.
Broad ligament hernia, of the uterus.
Double indirect hernia: an indirect inguinal hernia with two hernia sacs, without a concomitant direct hernia component (as seen in a pantaloon hernia).
Hiatus hernia: a hernia due to "short oesophagus" — insufficient elongation — stomach is displaced into the thorax
Littres hernia: a hernia involving a Meckels diverticulum. It is named after the French anatomist Alexis Littré (1658–1726).
Lumbar hernia: a hernia in the lumbar region (not to be confused with a lumbar disc hernia), contains the following entities:
Petits hernia: a hernia through Petits triangle (inferior lumbar triangle). It is named after French surgeon  Jean Louis Petit (1674–1750).
Grynfeltts hernia: a hernia through Grynfeltt-Lesshaft triangle (superior lumbar triangle). It is named after physician Joseph Grynfeltt (1840–1913).
Maydls hernia: two adjacent loops of small intestine are within a hernial sac with a tight neck. The intervening portion of bowel within the abdomen is deprived of its blood supply and eventually becomes necrotic.
Obturator hernia: hernia through obturator canal
Parastomal hernias, which is when tissue protrudes adjacent to a stoma tract.
Paraumbilical hernia: a type of umbilical hernia occurring in adults
Perineal hernia: a perineal hernia protrudes through the muscles and fascia of the perineal floor. It may be primary but usually is acquired following perineal prostatectomy, abdominoperineal resection of the rectum, or pelvic exenteration.
Properitoneal hernia: rare hernia located directly above the peritoneum, for example, when part of inguinal hernia projects from the deep inguinal ring to the preperitoneal space.
Richters hernia: a hernia involving only one sidewall of the bowel, which can result in bowel strangulation leading to perforation through ischaemia without causing bowel obstruction or any of its warning signs. It is named after German surgeon August Gottlieb Richter (1742–1812).
Sliding hernia: occurs when an organ drags along part of the peritoneum, or, in other words, the organ is part of the hernia sac. The colon and the urinary bladder are often involved. The term also frequently refers to sliding hernias of the stomach.
Sciatic hernia: this hernia in the greater sciatic foramen most commonly presents as an uncomfortable mass in the gluteal area. Bowel obstruction may also occur. This type of hernia is only a rare cause of sciatic neuralgia.
Sports hernia: a hernia characterized by chronic groin pain in athletes and a dilated superficial inguinal ring.
Tibialis anterior hernia: can present as a bulge in the shins. Pain on rest, walking, or during exercise may occur. The bulge can typically not be present unless pressure or flexing of the leg occurs.
Velpeau hernia: a hernia in the groin in front of the femoral blood vessels

Treatment
Truss
The benefits of the use of an external device to maintain reduction of the hernia without repairing the underlying defect (such as hernia trusses, trunks, belts, etc.) are unclear.

Surgery
Surgery is recommended for some types of hernias to prevent complications such as obstruction of the bowel or strangulation of the tissue, although umbilical hernias and hiatus hernias may be watched, or are treated with medication. Most abdominal hernias can be surgically repaired, but surgery has complications. Time needed for recovery after treatment is reduced if hernias are operated on laparoscopically. However, open surgery can be done sometimes without general anesthesia. Robot-assisted hernia surgery has also recently gained popularity as safe alternatives to open surgery.
Uncomplicated hernias are principally repaired by pushing back, or "reducing", the herniated tissue, and then mending the weakness in muscle tissue (an operation called herniorrhaphy). If complications have occurred, the surgeon will check the viability of the herniated organ and remove part of it if necessary.
Muscle reinforcement techniques often involve synthetic materials (a mesh prosthesis). The mesh is placed either over the defect (anterior repair) or under the defect (posterior repair). At times staples are used to keep the mesh in place. These mesh repair methods are often called "tension free" repairs because, unlike some suture methods (e.g., Shouldice), muscle is not pulled together under tension </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 Enamel-renal syndrome 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 Congenital nephrotic syndrome and explain in detail? [/INST] Congenital nephrotic syndrome is a rare kidney disease which manifests in infants during the first 3 months of life, and is characterized by high levels of protein in the urine (proteinuria), low levels of protein in the blood, and swelling. This disease is primarily caused by genetic mutations which result in damage to components of the glomerular filtration barrier and allow for leakage of plasma proteins into the urinary space.

Signs and symptoms
Urine protein loss leads to total body swelling (generalized edema) and abdominal distension in the first several weeks to months of life. Fluid retention may lead to cough (from pulmonary edema), ascites, and widened cranial sutures and fontanelles. High urine protein loss can lead to foamy appearance of urine. Infants may be born prematurely with low birth weight, and have meconium stained amniotic fluid or a large placenta.

Complications
Frequent, severe infections: urinary loss of immunoglobulins
Malnutrition and poor growth
Blood clots (hypercoagulability): imbalance of plasma coagulation factors from urine protein loss
Hypothyroidism: urinary loss of thyroid-binding protein
Poor bone health associated with vitamin D deficiency: urinary loss of vitamin D binding protein
Acute kidney injury
Chronic kidney disease and ultimately end-stage kidney disease

Causes
Primary (genetic) causes
Mutations in the following five genes account for greater than 80% of the genetic causes of congenital nephrotic syndrome:
NPHS1 (Finnish Type): The gene NPHS1 encodes for the protein nephrin. This genetic variant is characterized by severe protein loss in the first several days to weeks of life. Fin-major and Fin-minor were the first two main genetic mutations identified in Finnish newborns, however, numerous mutations have now been identified in patients all over the world from various ethnic groups.  NPHS1 mutations are the most common cause of primary congenital nephrotic syndrome, accounting for 40-80% of cases.
NPHS2: This gene encodes for the protein podocin. Patients with this genetic mutation develop nephrotic syndrome in the first few weeks of infancy, but can also manifest symptoms later in life. Urinary protein loss is less severe when compared with the Finnish type. Both nephrin and podocin play important roles in the structure and function of the podocyte filtration slit diaphragm and disease involvement is typically limited to the kidneys
WT1: The Wilms tumor suppressor gene regulates the expression of many genes involved in kidney and urogenital development. Mutations lead to several types of developmental syndromes, including Denys-Drash syndrome, Frasier syndrome, WAGR syndrome (Wilms tumor, aniridia, genitourinary abnormalities, and intellectual disability), and isolated nephrotic syndrome in infants. Depending on the specific syndrome, patients are at risk for Wilms and other tumors, genital abnormalities, and nephrotic syndrome.
LAMβ2 (Pierson syndrome): This gene encodes for the protein laminin β2, which helps attach podocytes to the glomerular basement membrane. Patients with Pierson syndrome have eye abnormalities, including nonreactive narrowing of the pupils (microcoria), and neurologic deficits.
PLCε1: Codes for the enzyme Phospholipase Cε1, which is expressed in podocytes.

Secondary Causes
Congenital infections: syphilis, cytomegalovirus, toxoplasmosis, rubella, human immunodeficiency virus (HIV), malaria, hepatitis B
Immunologic: maternal systemic lupus erythematosus

Diagnosis
An examination reveals massive fluid retention and generalized swelling. Abnormal sounds are heard when listening to the heart and lungs with a stethoscope. Blood pressure may be high. The patient may have signs of malnutrition.A urinalysis reveals large amounts of protein and sometimes small amounts of blood in the urine. Kidney function may be normal in the first weeks or months of life. Laboratory studies show low serum levels of protein (albumin) and immunoglobulins, and elevated levels of triglycerides and cholesterol. Blood work may also show thyroid and vitamin D deficiency. Kidneys on ultrasound imaging may appear enlarged and brighter (hyperechoic). The disorder can be screened during pregnancy by finding elevated levels of alpha-fetoprotein on a routine sampling of amniotic fluid.Indication for kidney biopsy remains unclear as histologic findings do no reveal the cause of congenital nephrotic syndrome, but findings may help in developing treatment strategies. Findings on light microscopy can vary from minimal change nephropathy to focal segmental glomerulosclerosis or diffuse mesanigial sclerosis. Electron microscopy shows podocyte disruption (loss of foot processes or slit diaphragm).Genetic analysis and infectious workup are needed to determine the precise cause of congenital nephrotic syndrome. Understanding the underlying cause can assist in disease management, prognosis, and genetic counseling.

Treatment
Genetic forms of nephrotic syndrome are typically resistant to steroid and other immunosuppressive treatment. Goals of therapy are to control urinary protein loss and swelling, provide good nutrition to allow the child to grow, and prevent complications. Early and aggressive treatment is required to control the disorder.
Patients with severe urine protein loss require albumin infusions help replace protein loss and diuretic medications help rid the body of excess fluid. For patients with mild to moderate urine protein losses, ACE inhibitor medications (like Captopril and others) and non-steroidal anti-inflammatory drugs (like indomethacin) are used to slow the spilling of protein (albumin) in the urine. Removal of the kidneys (one at the time or both) can decrease protein loss and limit the number of albumin infusions needed. Infants with WT1 mutations will undergo bilateral kidney removal to prevent development of Wilms tumor.Antibiotics may be needed to control infections. Immunizations are recommended after kidney removal but prior to transplantation. Patients may also take iron supplements, potassium chloride, thyroxine and other vitamins to replenish what minerals the kidneys have leaked out. Anticoagulants (such as aspirin, dipyridamole, and warfarin) are used to prevent clot formation.Dietary modifications may include the restriction of sodium and use of dietary supplements as appropriate for the nature and extent of malnutrition. Fluids may be restricted to help control swelling. Children with this disease require diets high in calories and protein, and many patients require a feeding tube (nasogastric tube or gastrostomy tube (g-tube)) for medication and/or feeds. Some patients develop oral aversions and will use the tube for all feeds </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 Ichthyosis hystrix and explain in detail? [/INST] Ichthyosis hystrix is a group of rare skin disorders in the ichthyosis family of skin disorders characterized by massive hyperkeratosis with an appearance like spiny scales. This term is also used to refer to a type of epidermal nevi with extensive bilateral distribution.

Types
Ichthyosis hystrix, Curth-Macklin type
The symptoms of ichthyosis hystrix Curth-Macklin are similar to epidermolytic hyperkeratosis (NPS-2 type) but there is no blistering and the hyperkeratosis is verrucous or spine-like </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 Klatskin tumor and explain in detail? [/INST] A Klatskin tumor (or hilar cholangiocarcinoma) is a cholangiocarcinoma (cancer of the biliary tree) occurring at the confluence of the right and left hepatic bile ducts. The disease was named after Gerald Klatskin, who in 1965 described 15 cases and found some characteristics for this type of cholangiocarcinoma

Cause
The cause of cholangiocarcinoma has not been defined. A number of pathologic conditions, however, resulting in either acute or chronic biliary tract epithelial injury may predispose to malignant change. Primary sclerosing cholangitis, an idiopathic inflammatory condition of the biliary tree, has been associated with the development of cholangiocarcinoma in up to 40% of patients. Congenital biliary cystic disease, such as choledochal cysts or Carolis disease, has also been associated with malignant transformation in up to 25% of cases. These conditions appear to be related to an anomalous pancreatico-biliary duct junction and, perhaps, are related to the reflux of pancreatic secretions into the bile duct. Chronic biliary tract parasitic infection, seen commonly in Southeast Asia due to Clonorchis sinensis and Opisthorchis viverrini, has also been identified as a risk factor. Although gallstones and cholecystectomy are not thought to be associated with an increased incidence of cholangiocarcinoma, hepatolithiasis and choledocholithiasis may predispose to malignant change. Further, industrial exposure to asbestos and nitrosamines, and the use of the radiologic contrast agent, Thorotrast (thorium dioxide), are considered to be risk factors for the development of cholangiocarcinoma.

Diagnosis
Levels of the tumor markers carbohydrate antigen 19-9 (CA 19–9), carcinoembryonic antigen (CEA) and CA 125 are abnormally high in the bloodstreams of patients with intrahepatic cholangiocarcinoma and Klatskin tumor. The serum CA 19–9 in particular may be very high. The ultrasonography (and the use of Doppler modes) permit definitive diagnosis of a large number of lesions and the involvement of hepatic hilum, but it is less sensitive than CT or MRI in detecting focal lesions. Ultrasonography always detects dilatation of the bile ducts, but more rarely the tumor itself.Magnetic resonance cholangiopancreatography (MRCP) is a good non-invasive alternative to these other procedure </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 Speech delay and explain in detail? [/INST] Speech delay, also known as alalia, refers to a delay in the development or use of the mechanisms that produce speech. Speech – as distinct from language – is the actual process of making sounds, using such organs and structures as the lungs, vocal cords, mouth, tongue, teeth, etc.  Language delay refers to a delay in the development or use of the knowledge of language.
Because language and speech are two independent stages, they may be individually delayed. For example, a child may be delayed in speech (i.e., unable to produce intelligible speech sounds), but not delayed in language. In this case, the child would be attempting to produce an age appropriate amount of language, but that language would be difficult or impossible to understand. Conversely, since a child with a language delay typically has not yet had the opportunity to produce speech sounds, it is likely to have a delay in speech as well.

Signs and symptoms
The warning signs of early speech delay are categorized into age-related milestones, beginning at the age of 12 months and continuing through early adolescence.At the age of 12 months, there is cause for concern if the child is not able to do the following:

Using gestures such as waving good-bye and pointing at objects
Practicing the use of several different consonant sounds
Vocalizing or communicating needsBetween the ages of 15 and 18 months children are at a higher risk for speech delay if they are displaying the following:

Not saying "momma" and "dada"
Not reciprocating when told "no", "hello", and "bye"
Does not have a one to three word vocabulary at 12 months and up to 15 words by 18 months
Is unable to identify body parts
Displaying difficulties imitating sounds and actions
Shows preference to gestures over verbalizationAdditional signs of speech delay after the age of 2 years and up to the age of 4 include the following:

Inability to spontaneously produce words and phrases
Inability to follow simple directions and commands
Cannot make two word connections
Lacks consonant sounds at the beginning or end of words
Is difficult to understand by close family members
Is not able to display the tasks of common household objects
Is unable to form simple 2 to 3 word sentences

Effects
Studies show that children diagnosed with speech delay are more likely to present with behavioral and social emotional problems both in childhood and as adults.  Decreased receptive language, reading, and learning skills are common side effects for children that have a speech delay and do not receive adequate intervention.  Similar studies suggest that children with speech delays are more likely to have a difficult time communicating and bonding with peers, which could have negative effects on their psychosocial health later in life.

Causes
At times, speech delay and impairment is caused by a physical disruption in the mouth such as a deformed frenulum, lips, or palate.  If the motion or ability to form words and appropriate sounds is disrupted, the child may be slow to pick up words and lack the ability to shape their mouth and tongue in the formation of words.Other more serious concerns are those that can be caused by oral-motor issues.  Oral-motor dysfunction refers to a lack or delay in the area of the brain that speech is formed and created and communicated to the mouth and tongue. While speech may be the only concern, this disorder can be highlighted with feeding issues as well.Children that are having speech delay disorders could have the following characteristics (Shriberg 1982):

Speech mechanism in which speech is associated with hearing, motor speech and craniofacial malfunction
Cognitive-linguistic aspects in which the impairment is associated with the childs intellectual, receptive, expressive and linguistic ability.
Psychosocial issues in which the impairment is associated with caregiver, school environment, and the childs self behaviors such as aggression and maturityThe many other causes of speech delay include bilingual children with phonological disorders, autism spectrum conditions, childhood apraxia, auditory processing disorder, prematurity, cognitive impairment and hearing loss.   In addition, when children are addicted to screens, they arent stimulated to be involved in conversations, causing speech delays. Broomfield and Dodds (2004a) found out after survey that 6.4% of children who are perfectly normal showed speech difficulty while they lacked these disorders will often show early signs and are at times identified as "at risk" when the speech delay is diagnosed.
In the case of speech delay in a child with autism, there may not be a physiological cause such as an oral-motor issue or hearing loss. The child may prefer to communicate using non-spoken language or use a nonverbal communication method. Studies show that early interventions may help a child with cerebral palsy, autism spectrum disorder or Down syndrome acquire language skills necessary for social communication to a certain degree.

Therapies and treatments
After the initial diagnosis of speech delay, a hearing test will be administered to ensure that hearing loss or deafness is not an underlying cause of the delay.  If a child has successfully completed the hearing test, the therapy or therapies used will be determined. There are many therapies available for children that have been diagnosed with a speech delay, and for every child, the treatment and therapies needed vary with the degree, severity, and cause of the delay. While speech therapy is the most common form of intervention, many children may benefit from additional help from occupational and physical therapies as well </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 Sialidosis and explain in detail? [/INST] Mucolipidosis type I (ML I) is an inherited lysosomal storage disease that results from a deficiency of the enzyme alpha-N -acetyl neuraminidase (sialidase). The lack of this enzyme results in an abnormal accumulation of complex carbohydrates known as mucopolysaccharides, and of fatty substances known as mucolipids. Both of these substances accumulate in bodily tissues.

Presentation
Symptoms of ML I are either present at birth or develop within the first year of life. In many infants with ML I, excessive swelling throughout the body is noted at birth. These infants are often born with coarse facial features, such as a flat nasal bridge, puffy eyelids, enlargement of the gums, and excessive tongue size (macroglossia). Many infants with ML I are also born with skeletal malformations such as hip dislocation. Infants often develop sudden involuntary muscle contractions (called myoclonus) and have red spots in their eyes (cherry red spots) </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 Neonatal jaundice and explain in detail? [/INST] Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. Other symptoms may include excess sleepiness or poor feeding. Complications may include seizures, cerebral palsy, or kernicterus.In most of cases there is no specific underlying disorder (physiologic). In other cases it results from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders (pathologic). A bilirubin level more than 34 μmol/L (2 mg/dL) may be visible. Concerns, in otherwise healthy babies, occur when levels are greater than 308 μmol/L (18 mg/dL), jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two weeks, or the baby appears unwell. In those with concerning findings further investigations to determine the underlying cause are recommended.The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause. Treatments may include more frequent feeding, phototherapy, or exchange transfusions. In those who are born early more aggressive treatment tends to be required. Physiologic jaundice generally lasts less than seven days. The condition affects over half of babies in the first week of life. Of babies that are born early about 80% are affected. Globally over 100,000 late-preterm and term babies die each year as a result of jaundice.

Sign and symptoms
Bronze baby syndrome (dark pigmentation of skin).
The primary symptom is yellowish discoloration of the white part of the eyes and skin in a newborn baby. Other symptoms may include excess sleepiness or poor feeding.A bilirubin level more than 34 μmol/L (2 mg/dL) may be visible. For the feet to be affected level generally must be over 255 μmol/L (15 mg/dL).

Complications
Prolonged hyperbilirubinemia (severe jaundice) can result in chronic bilirubin encephalopathy (kernicterus).  Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus.Infants with kernicterus may have a fever or seizures. High pitched crying is an effect of kernicterus.Exchange transfusions performed to lower high bilirubin levels are an aggressive treatment.

Causes
In newborns, jaundice tends to develop because of two factors—the breakdown of fetal hemoglobin as it is replaced with adult hemoglobin and the relatively immature metabolic pathways of the liver, which are unable to conjugate and so excrete bilirubin as quickly as an adult. This causes an accumulation of bilirubin in the blood (hyperbilirubinemia), leading to the symptoms of jaundice.If the neonatal jaundice is not resolved with simple phototherapy, other causes such as biliary atresia, Progressive familial intrahepatic cholestasis, bile duct paucity, Alagille syndrome, alpha 1-antitrypsin deficiency, and other pediatric liver diseases should be considered. The evaluation for these will include blood work and a variety of diagnostic tests.  Prolonged neonatal jaundice is serious and should be followed up promptly.Severe neonatal jaundice may indicate the presence of other conditions contributing to the elevated bilirubin levels, of which there are a large variety of possibilities (see below).  These should be detected or excluded as part of the differential diagnosis to prevent the development of complications.  They can be grouped into the following categories:

Unconjugated
Hemolytic
Intrinsic causes of hemolysis
Membrane conditions
Spherocytosis
Hereditary elliptocytosis
Enzyme conditions
Glucose-6-phosphate dehydrogenase deficiency (also called G6PD deficiency)
Pyruvate kinase deficiency
Globin synthesis defect
sickle cell disease
Alpha-thalassemia, e.g. HbH disease

Extrinsic causes of hemolysis
Systemic conditions
Sepsis
Arteriovenous malformation
Alloimmunity (The neonatal or cord blood gives a positive direct Coombs test and the maternal blood gives a positive indirect Coombs test)
Hemolytic disease of the newborn (ABO)
Rh disease
Hemolytic disease of the newborn (anti-Kell)
Hemolytic disease of the newborn (anti-Rhc)
Other blood type mismatches causing hemolytic disease of the newborn

Non-hemolytic causes
Breastfeeding jaundice
Breast milk jaundice
Cephalohematoma
Polycythemia
Urinary tract infection
Sepsis
Hypothyroidism
Gilberts syndrome
Crigler–Najjar syndrome
High GI obstruction (Pyloric stenosis, Bowel obstruction)

Conjugated (Direct)
Liver causes
Infections
Sepsis
Hepatitis A
Hepatitis B
TORCH infections
Metabolic
Galactosemia
Alpha 1-antitrypsin deficiency, which is commonly missed, and must be considered in DDx
Cystic fibrosis
Dubin–Johnson syndrome
Rotor syndrome
Drugs
Total parenteral nutrition
Idiopathic

Post-liver
Biliary atresia or bile duct obstruction
Alagille syndrome
Choledochal cyst

Non-organic causes
Breastfeeding jaundice
"Breastfeeding jaundice" (or "lack of breastfeeding jaundice") is caused by insufficient breast milk intake, resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines. Usually occurring in the first week of life, most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production.

Breast milk jaundice
Whereas breastfeeding jaundice is a mechanical problem, breast milk jaundice is a biochemical occurrence and the higher bilirubin possibly acts as an antioxidant. Breast milk jaundice occurs later in the newborn period, with the bilirubin level usually peaking in the sixth to 14th days of life. This late-onset jaundice may develop in up to one third of healthy breastfed infants.
The gut is sterile at birth and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugated bilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is called enterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk. Breast milk also contains glucoronidase which will increase deconjugation and enterohepatic recirculation of bilirubin.
The breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood. However, these results have not been supported by subsequent studies.
An enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin.

Physiological jaundice
Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods.
Phase oneTerm infants - jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to 204 μmol/L (12 mg/dL).
Preterm infants - jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to 255 μmol/L (15 mg/dL).Phase two - bilirubin levels decline to about 34 μmol/L (2 mg/dL) for two weeks, eventually mimicking adult values.Preterm infants - phase two can last more than one month.
Exclusively breastfed infants - phase two can last more than one month.Mechanisms involved in physiological jaundice include:

Relatively low activity of the enzyme glucuronosyltransferase which normally converts unconjugated bilirubin to conjugated bilirubin that can be excreted into the gastrointestinal tract. Before birth, this enzyme is actively down-regulated, since bilirubin needs to remain unconjugated in order to cross the placenta to avoid being accumulated in the fetus. After birth, it takes some time for this enzyme to gain function.
Shorter life span of fetal red blood cells, being approximately 80 to 90 days in a full term infant, compared to 100 to 120 days in adults.
Relatively low conversion of bilirubin to urobilinogen by the intestinal flora, resulting in relatively high absorption of bilirubin back into the circulation.

Diagnosis
Diagnosis is often by measuring the serum bilirubin level in the blood. In those who are born after 35 weeks and are more than a day old transcutaneous bilirubinometer may also be used. The use of an icterometer, a piece of transparent plastic painted in five transverse strips of graded yellow lines, is not recommended.

Transcutaneous bilirubinometer
This is hand held, portable and rechargeable but expensive. When pressure is applied to the photoprobe, a xenon tube generates a strobe light, and this light passes through the subcutaneous tissue. The reflected light returns through the second fiber optic bundle to the spectrophotometric module. The intensity of the yellow color in this light, after correcting for the hemoglobin, is measured and instantly displayed in arbitrary units.

Pathological jaundice
Any of the following features suggests pathological jaundice:
Clinical jaundice appearing in the first 24 hours or greater than 14 days of life.
Increases in the level of total bilirubin by more than 8.5 μmol/L (0.5 mg/dL) per hour or (85 μmol/L) 5 mg/dL per 24 hours.
Total bilirubin more than 331.5 μmol/L (19.5 mg/dL) (hyperbilirubinemia).
Direct bilirubin more than 34 μmol/L (2.0 mg/dL).The signs which help detect pathological jaundice are the presence of intrauterine growth restriction, stigma of intrauterine infections (e.g. cataracts, small head, and enlargement of the liver and spleen), cephalohematoma, bruising, signs of bleeding in the brains ventricles. History of illness is noteworthy. Family history of jaundice and anemia, family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection (fever, rash or lymphadenopathy), maternal drugs (e.g. sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency) are suggestive of pathological jaundice in neonates.

Treatment
The bilirubin levels for initiative of phototherapy varies depends on the age and health status of the newborn </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 Sprue 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 Occupational acne and explain in detail? [/INST]  </s>