Persius/hicric huggingface dataset:
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Weight loss resort
A weight loss resort is a for various spas, resorts and retreats offering weight loss programs for adults. A pejorative term, perhaps more widely used, is fat farm.

# History
Weight loss resorts have existed in the United States in large numbers since the 1950s. Some of these achieved their touted weight loss through forced low-calorie diets and exercise, and were criticized as "quick fixes" that did not result in long-term weight loss.

## Recent
Many modern weight loss resorts, particularly luxury resorts, take an approach geared more towards encouraging a healthy lifestyle and eating behavior than just achieving short-term weight loss. Programs like yoga, mediation and deep-breathing exercises may be offered in addition to traditional exercise. Many offer the chance to consult with medical doctors, physical therapists, nutritionists, personal trainers, even acupuncturists and life coaches.  Other programs may teach attendees how to cook or select healthy meals.
Some are more similar to medical centers and take a clinical approach, such as Clinique La Prairie and the Cooper Wellness Program in Dallas, Texas.
Prices at these luxury resorts can be quite expensive, some cost over $3,000 a week.
Celebrities such as Oprah Winfrey and Michael Moore are sometimes mocked for going to weight loss resorts.
X-linked recessive
X-linked recessive is a mode of inheritance in which a mutation in a gene on the X chromosome causes the phenotype to be expressed only (1) in males (who are necessarily hemizygous for the gene mutation because they have only one X chromosome) and (2) in females who are homozygous for the gene mutation (i.e., they have a copy of the gene mutation on each of their two X chromosomes).
X-linked inheritance means that the gene causing the trait or the disorder is located on the X chromosome. Females have two X chromosomes, while males have one X and one Y chromosome. Carrier females who have only one copy of the mutation do not usually express the phenotype, although differences in X chromosome inactivation can lead to varying degrees of clinical expression in carrier females since some cells will express one X allele and some will express the other.  The current estimate of sequenced X-linked genes is 499 and the total including vaguely defined traits is 983

# Sex Differences In Phenotype and Frequency
In humans, generally "men are affected and women are carriers" for two reasons. The first is the simple statistical fact that if the X-chromosomes is a population carry a particular X-linked mutation at a frequency of 'f' (for example, 1%) then that will be the frequency that men are likely to express the mutation (since thay have only one X, while women will express it at a frequency of f2 (for example 1% - 1% = 0.01%) since they have two X's and hence two chances to get the normal allele.  Thus, X-linked mutations tend to be rare in women.  The second reason for female rarity is that women who express the mutation must have two X chromosomes that carry the trait and they necessarily got one from their father, who would have also expressed the trait because he only had one X chromosome in the first place.  If the trait lowers the probability of fathering a child or induces the father to only have children with women who aren't carriers (so as not to create daughters who are carriers rather than expressers and then only if no genetic screening is used) then women become even less likely to express the trait than the statistical prediction of f2 .

# Examples
Red-Green color blindness is a classic example of an X-linked trait because it is easy to explain the phenotype and it's relatively common  (7% to 10% of men are carriers making the above calculations predict 0.49% to 1% for women).  It's commonness is possibly attributable to it not being a serious disability in most cases and an actual advantage in some situation (for example, not being distracted by some of the color in color based camouflage).  Hemophilia A is another famous example because it was found in European royal families who intermarried and were famous enough that their pedigrees could be established and offered in textbooks as a "famous example" of an X-linked trait that had been documented in history books before mendelian genetics was understood.
Traits or diagnoses known or suspected to be X-linked (at least in some forms of the diagnosis) are:
Xenon hexafluoride
Xenon hexafluoride is the chemical compound with the formula XeF6.  This colorless crystalline compound is one of the three binary fluorides of xenon, the other two being XeF2 and XeF4.  All are exergonic and stable at normal temperatures.  XeF6 is the strongest fluorinating agent of the series.
Xenon hexafluoride can be prepared by long-term heating of XeF2 at about 300 degrees and pressure 6 MPa.

# Structure
The structure of XeF6 required several years to establish in contrast to the cases of xenon difluoride and xenon tetrafluoride. In the gas phase it adopts a slightly distorted octahedral geometry. It lacks perfect octahedral symmetry, as predicted by VSEPR theory due to the presence of six fluoride ligands and one lone pair of electrons.  According to Konrad Seppelt, the Associate Professor of Chemistry at the University of Heidelberg, "the structure is best described in terms of a mobile electron pair that moves over the faces and edges of the octahedron and thus distorts it in a dynamic manner.".
NMR spectra of129Xe19F6 indicate that it is tetrameric: four equivalent xenon atoms are arranged in a tetrahedron surrounded by a fluctuating array of 24 fluorine atoms that interchange positions in a "cogwheel mechanism".

# Reactions
Xenon hexafluoride hydrolyzes stepwise, ultimately affording xenon trioxide:
XeF6 serves as a Lewis acid, binding one and two fluoride anions:
The two other binary fluorides do not form such stable adducts with fluoride.  The salt Rb2XeF8 is among the most robust xenon compounds, decomposing only above 400 C.
Y-chromosomal Adam
In human genetics, Y-chromosomal Adam (Y-mrca) is the patrilineal human most recent common ancestor (mrca) from whom all Y chromosomes in living men are descended. Y-chromosomal Adam is thus the male counterpart of Mitochondrial Eve (the mt-mrca), the matrilineal human most recent common ancestor, from whom all mitochondrial DNA in living humans is descended.
By analyzing DNA from people in all regions of the world, geneticist Spencer Wells has concluded that all humans alive today are descended from a single man who lived in Africa around 60,000 years ago.

# Time frame
Y-chromosomal Adam probably lived between 60,000 and 90,000 years ago, judging from molecular clock and genetic marker studies. While their descendants certainly became close intimates, Y-chromosomal Adam and mitochondrial Eve are separated by at least 30,000 years, or possibly a thousand generations.  This is due to the differences found in male and female reproductive strategies.
The more recent age of the Y-mrca compared to the mt-mrca corresponds to a larger statistical dispersion of the probability distribution for a Paleolithic man to have living descendants compared to that of a Paleolithic woman. While fertile women had more or less equally distributed chances of giving birth to a certain number of fertile descendants, chances for fertile men varied more widely, with some fathering no children and others fathering many, with multiple women.
Y-chromosomal Adam is not the same individual at all points in human history; the Y-mrca of all humans alive today is different from the one for humans alive at some point in the remote past or future: as male lines die out, a more recent individual becomes the new Y-mrca. In times of rapid population growth, patrilineal lines are less likely to die out than during a population bottleneck.

# Naming
Y-chromosomal Adam is named after the Adam of the Genesis account of creation as a metaphor only.
The name may seem to imply that Y-chromosomal Adam was the only living male of his time; he was not. "Y-Adam" is not even a single fixed individual but a title that continually passes on to more recent individuals as time goes on.
Jacobsen syndrome
Jacobsen Syndrome, also known as 11q deletion, is a rare congenital disorder resulting from deletion of a terminal region of chromosome 11 that includes band 11q24.1. It can cause mild mental retardation, a distinctive facial appearance, and a variety of physical problems including heart defects and a bleeding disorder. The syndrome was first identified by Danish physician Petra Jacobsen in 1973, and is believed to occur in approximately 1 out of every 100,000 births.

# Physical Characteristics
- Closely-set eyes caused by trigonocephaly
- Folding of the skin near the eye (epicanthus)
- Short, upturned nose (anteverted nostrils)
- Thin lips that curve inward
- Displaced receding chin (retrognathia)
- Low-set, misshapen ears
- Permanent upward curvature of the pinkie and ring fingers (bilateral camptodactyly)
- Hammer toes
In addition, patients tend to be shorter than average and have poor psychomotor skills.

# Outlook
Patients with this disorder can often live relatively normal lives within the limitations of their disability, although this varies from person to person, and congenital heart disease that does not manifest itself until adulthood is common. There is a greater incidence of various forms of cancer among Jacobsen patients. The vast majority of patients have a bleeding disorder called Paris-Trousseau Syndrome, which causes reduced blood platelet counts and an impairment of platelets' normal blood clotting function. Platelet counts increase during childhood and can eventually reach normal levels, but many patients still have poor clotting due to abnormalities in platelet function. Unless their platelet function has been tested and shown to be normal, Jacobsen patients should be assumed to have a bleeding disorder.
The majority of Jacobsen syndrome cases are not familial in nature, resulting from a spontaneous mutation occurring in a single parental gamete. However, some instances of familial disease resulting from local chromosome fragility or an unbalanced translocation have been described.

# Sources
- 11q.org - Note: PDF file
- Orthoseek - Specializes in pediatric orthopedics and pediatric sports medicine
it:Sindrome di Jacobsen
Hypoglossal nerve

# Overview
The hypoglossal nerve is the twelfth cranial nerve (XII). The nerve arises from the hypoglossal nucleus and emerges from the medulla oblongata in the preolivary sulcus separating the olive and the pyramid. It then passes through the hypoglossal canal.  On emerging from the hypoglossal canal, it gives off a small meningeal branch and picks up a branch from the anterior ramus of C1.  It spirals behind the vagus nerve and passes between the internal carotid artery and internal jugular vein lying on the carotid sheath.  After passing deep to the posterior belly of the digastric muscle, it passes to the submandibular region to enter the tongue.
It supplies motor fibres to all of the muscles of the tongue, except the palatoglossus muscle which is innervated by the vagus nerve (X).

# Testing the hypoglossal nerve
To test the function of the nerve, a person is asked to poke out their tongue. If there is a loss of function on one side (unilateral paralysis) the tongue will point towards the affected side.
The strength of the tongue can be tested by getting the person to poke the inside of their cheek, and feeling how strongly they can push a finger pushed against their cheek - a more elegant way of testing than directly touching the tongue.
The tongue can also be looked at for signs of lower motor neuron disease, such as fasciculation and atrophy.
Ipsilateral paralysis/pareisis of the tongue, results in contralateral curvature of the tongue (toward the unimpaired side of the mouth).

# Additional images
- Veins of the tongue. The hypoglossal nerve has been displaced downward in this preparation.
- Section of the medulla oblongata at about the middle of the olive.
- Diagram showing the course of the arcuate fibers.
- Transverse section passing through the sensory decussation.
- Hind- and mid-brains; postero-lateral view.
- Upper part of medulla spinalis and hind- and mid-brains; posterior aspect, exposed in situ.
- Plan of hypoglossal nerve.
- The mouth cavity.
16S ribosomal RNA
The 16S rRNA is a 1542 nt long component of the small prokaryotic ribosomal subunit (30S) and is known to interact with the 50S subunit in both P and A site. The 3' end contains the anti-Shine-Dalgarno sequence which binds upstream to the AUG start codon on the mRNA.

# Universal Primers
It is used for phylogenetic studies as it is highly conserved, in fact the primers are called universal (or quasi-universal as it does not pick up some recently discovered hydrothermal archaea species though).
16S rRNA Forward 	AGA GTT TGA TCC TGG CTC AG
16S rRNA Reverse 	ACG GCT ACC TTG TTA CGA CTT
Mitochondrial and chloroplastic rRNA is picked up, but not that of Nanoarchaeota.
-  Schluenzen F, Tocilj A, Zarivach R;  et al. (2000). "Structure of functionally activated small ribosomal subunit at 3.3 angstroms resolution". Cell. 102 (5): 61523. PMID 11007480. Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
-  Huber H, Hohn MJ, Rachel R, Fuchs T, Wimmer VC, Stetter KO (2002). "A new phylum of Archaea represented by a nanosized hyperthermophilic symbiont". Nature. 417 (6884): 637. doi:10.1038/417063a. PMID 11986665. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)
3-Iodothyronamine
3-iodothyronamine (T1AM) is an endogenous thyronamine. T1AM is a high-affinity ligand for the trace amine-associated receptor TAAR1 (TAR1, TA1), a G protein-coupled receptor.
 In rodents, T1AM causes a rapid drop in body temperature when injected.
T1AM may be part of a signaling pathway to modulate cardiac function as the compound can induce negative inotropic effects and decrease cardiac output.
Triple X syndrome

# Overview
Triple X syndrome is a form of chromosomal variation characterized by the presence of an extra X chromosome in each cell of a human female. The condition is also known as triplo-X, trisomy X, XXX syndrome, and 47,XXX aneuploidy. Triple X results during division of a parent's reproductive cells, which occurs about once in every 1,000 births. People with trisomy X do not exhibit any symptoms and cannot be distinguished from normal XX females unless karyotyping is performed.

# Etiology
Triple X syndrome is not inherited, but usually occurs as a quite random event during the formation of reproductive cells (ovum and sperm). An error in cell division called nondisjunction can result in reproductive cells with additional chromosomes. For example, an oocyte or sperm cell may gain an extra copy of the X chromosome as a result of the nondisjunction. If one of these cells contributes to the genetic makeup of a child, the child will have an extra X chromosome in each of her cells. In some cases, trisomy X occurs during cell division in early embryonic development.
Some females with triple X syndrome have an extra X chromosome in only some of their cells. These cases are called 46,XX/47,XXX mosaics.

# Symptoms
Due to inactivation and formation of a Barr body in all female cells, only one X chromosome is active at any time in a female cell.  Thus, triple X syndrome most often causes no unusual physical features of medical problems.  Females with the condition are usually taller than average, and their weight may be low in comparison to their height.  They may have menstrual irregularities,and, although rarely exhibiting severe mental impariments, have an increased risk of learning disabilities, delayed speech, and language skills.
A similar range of body types and characteristics are present in both triple X and Klinefelter's syndrome. These include a lanky/youthful appearance, non-affectedness, or varying degrees of androgyny.  The additional X chromosome can come from either the maternal or paternal side.  Although body types and characteristics are distinguishable in triple X, the condition is verified only by karyotype testing.
Most woman with triple X have normal sexual development and are able to conceive children. A few may experience an early onset of menstruation.  Triple X woman are rarely diagnosed, apart from pre-natal testing methods, such as amniocentesis.  Most medical professionals do not regard the condition a disability. However, such status can be sought by parents for early intervention treatment if mild delays are present.

# Incidence
Triple X syndrome occurs in  around 1 in 1,000 girls. On average, five to ten girls with triple X syndrome are born in the United States each day.

# First case
The first published report of a woman with a 47,XXX karyotype was by Patricia A. Jacobs, et al. at Western General Hospital in Edinburgh, Scotland, in 1959. It was found in a 35-year-old, 5 ft. 9 in. (176 cm) tall, 128 lb. (58.2 kg) woman who had premature ovarian failure at age 19; her mother was age 41 and her father was 40 at the time of her conception.
Bromodeoxyuridine
Bromodeoxyuridine (5-bromo-2-deoxyuridine, BrdU) is a synthetic nucleoside which is an analogue of thymidine. BrdU is commonly used in the detection of proliferating cells in living tissues.
BrdU can be incorporated into the newly synthesized DNA of replicating cells (during the S phase of the cell cycle), substituting for thymidine during DNA replication. Antibodies specific for BrdU can then be used to detect the incorporated chemical (see immunohistochemistry), thus indicating cells that were actively replicating their DNA. Binding of the antibody requires denaturation of the DNA, usually by exposing the cells to acid or heat.
Because BrdU can replace thymidine during DNA replication, it can cause mutations, and its use is therefore potentially a health hazard.
ATP citrate lyase
ATP citrate lyase is an enzyme that in animals represents an important step in fatty acid biosynthesis.  ATP citrate lyase is important in that, by converting citrate to acetyl CoA, it links the metabolism of carbohydrates, which yields citrate as an intermediate, and the production of fatty acids, which requires acetyl CoA.
In plants, ATP citrate lyase generates cytosolic acetyl-CoA precursor of thousands of specialized metabolites including waxes, sterols, and polyketides.

# Function
ATP citrate lyase is the primary enzyme responsible for the synthesis of cytosolic acetyl-CoA in many tissues. The enzyme is a tetramer of apparently identical subunits.  The product, acetyl-CoA, in animals serves several important biosynthetic pathways, including lipogenesis and cholesterogenesis. It is activated by insulin. 
In plants, ATP citrate lyase generates the acetyl-CoA for cytosolically-synthesized metabolites.   (Acetyl-CoA is not transported across subcellular membranes of plants.) These include: elongated fatty acids (used in seed oils, membrane phospholipids, the ceramide moiety of sphingolipids, cuticle, cutin, and suberin); flavonoids; malonic acid; acetylated phenolics, alkaloids, isoprenoids, anthocyanins, and sugars; and, mevalonate-derived isoprenoids (e.g., sesquiterpenes, sterols, brassinosteroids); malonyl and acyl-derivatives (d-amino acids, malonylated flavonoids, acylated, prenylated and malonated proteins).  De novo fatty acid biosynthesis in plants is plastidic, thus ATP citrate lyase is not important for this pathway.
ATP-citrate lyase is responsible for catalyzing the conversion of citrate and CoA into acetyl-CoA and oxaloacetate, along with the hydrolysis of ATP.

# Reaction
In the presence of ATP and Coenzyme A, citrate lyase catalyzes the cleavage of citrate to yield acetyl CoA, oxaloacetate, ADP, and orthophosphate:
This enzyme was formerly listed as EC 4.1.3.8.

# Location
The enzyme is cytosolic in plants and animals.

# Structure
The enzyme is composed of two subunits in green plants (including Chlorophyceae, Marchantimorpha, Bryopsida, Pinaceae, monocotyledons, and eudicots), species of fungi, Glaucophytes, Chlamydomonas, and prokaryotes.
Animal ACL enzymes are homomeric, presumably an evolutionary fusion of the ACLA and ACLB genes probably occurred early in the evolutionary history of this kingdom.
A structure of truncated human ATP citrate lyase was determined using X-ray diffraction to a resolution of 2.10 A.