Persius/hicric huggingface dataset:
How to create a user page

# What is a user page?
Every user account on WikiDoc has an identity page called the user page. This page serves as a way to introduce individual users to the editing community. Unlike most pages that have standard convention, this page is the one place you can express your creativity.

# How do I find my user page?
Your user page can be accessed at the top right corner of every page.
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# How can I personalize my user page?
There are lots of ways you can personalize your page!
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Below is a template for how to code a user page for all of these. If you copy the code below and paste it to your page, you can replace the information with your own.
At the top right click on 'edit source' to input the template.
Human accelerated regions
Human accelerated regions (HARs), first described in August 2006, are a set of 49 segments of the human genome which are conserved throughout vertebrate evolution but are strikingly different in humans. They are named HAR1 through HAR49 according to their degree of difference between humans and chimpanzees (HAR1 showing the largest degree of human-chimpanzee differences of the 49). Found by scanning through giant genomic databases of multiple species, some of these highly mutated areas are thought to have contributed to the development of human neuroanatomy, language, and complex thought.
Several of the HARs encompass genes known to produce proteins important in neurodevelopment. HAR1 is an 118 base pair stretch found on the long arm of chromosome 20 overlapping with part of the RNA genes HAR1F and HAR1R. HAR1F is active in the developing human brain. The HAR1 sequence is found (and conserved) in chickens and chimpanzees but is not present in fish or frogs that have been studied. There are 18 base pair mutations different between humans and chimpanzees, far more than expected by its history of conservation.

# Sources and notes
-  Pollard K. et al. An RNA gene expressed during cortical development evolved rapidly in humans. Advanced electronic publishing. Nature. August 16, 2006. PMID 16915236 supplement

# Further reading
- Scientists Identify Gene Difference Between Humans and Chimps, Scientific American, 17 August 2006
- Researchers Identify Human DNA on the Fast Track, Howard Hughes Medical Institute website, 16 August 2006.
- What made us human? - PDF of Katherine Pollard's lecture.
Human parainfluenza virus

# Overview
Human parainfluenza virus is an enveloped, single stranded negative sense RNA virus with four distinct serotypes. The virus genome consists of approximately 15,000 nucleotides used to encode six structural proteins; they function to attach, enter, and fuse with the host cell, forming a complex with the RNA genome. Human parainfluenza virus is a member of the paramyxoviridae family. It is a member of one of two genuses depending on the serotype: Respirovirus or Rubulavirus. Human parainfluenza virus infects the body by infiltrating white blood cells. It is transmitted through respiratory droplets through the air, as well as physical contact with an infected individual or contaminated physical surface.

# Microbiological Characteristics
- Human parainfluenza virus (HPIV) is an enveloped, single stranded negative sense RNA virus.
- Human parainfluenza virus is comprised of four distinct serotypes:
HPIV-1
HPIV-2
HPIV-3
HPIV-4
- HPIV-1
- HPIV-2
- HPIV-3
- HPIV-4
- The human parainfluenza virus genome consists of approximately 15,000 nucleotides used to encode the following six structural proteins:.
- Human parainfluenza virus is a member of the paramyxoviridae family.
- The genus for human parainfluenza virus depends on its serotype:
Respirovirus: HPIV-1 & HPIV-3
Rubulavirus: HPIV-2 & HPIV-4
- Respirovirus: HPIV-1 & HPIV-3
- Rubulavirus: HPIV-2 & HPIV-4

# Transmission
- Human parainfluenza virus is primarily transmitted by the following:
Airborne respiratory droplets from coughing and sneezing
Close physical contact with an infected individual
Physical contact with a contaminated surface
- Airborne respiratory droplets from coughing and sneezing
- Close physical contact with an infected individual
- Physical contact with a contaminated surface

# Virology
- Human parainfluenza virus infiltrates histiocytes, lymphocytes, plasma cells, and neutrophils white blood cells..
HPIV fuses with the white blood cells through the glycoproteins hemagglutinin-neuraminidase and fusion protein.
Upon fusion, the HPIV nucleocapsid is expelled into the recipient cell cytoplasm.
Viral transcription occurs through virus-specific RNA-dependent RNA polymerase.
The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the following:
Positive-sense RNA strand
Negative-sense RNA strand
The negative-sense RNA strand is encapsidated by nucleoprotein and is then used for further transcription and replication.
- HPIV fuses with the white blood cells through the glycoproteins hemagglutinin-neuraminidase and fusion protein.
- Upon fusion, the HPIV nucleocapsid is expelled into the recipient cell cytoplasm.
- Viral transcription occurs through virus-specific RNA-dependent RNA polymerase.
- The viral mRNAs are translated into viral proteins, leading to the replication of the genome into the following:
Positive-sense RNA strand
Negative-sense RNA strand
- Positive-sense RNA strand
- Negative-sense RNA strand
- The negative-sense RNA strand is encapsidated by nucleoprotein and is then used for further transcription and replication.
Hyper-IgM syndrome type 1
Hyper IgM Syndrome Type 1 is the X-linked variant of the Hyper-IgM syndrome. The affected individuals are virtually always male, because males only have one X chromosome, received from their mothers. Their mothers are not symptomatic, even though they are carriers of the allele, because the trait is recessive. Male offspring of these women have a 50% chance of inheriting their mother's mutant allele.

# Pathogenesis
This variant of the hyper-IgM syndrome is caused by mutation of the CD40LG gene. The genetic locus for this gene is Xq26. This gene codes for the CD40 ligand, which is expressed on T cells. When the CD40 ligand binds CD40 on B cells, then the B cell switches from producing IgM to producing IgA or IgG.
In these patients a biopsy of a ganglion may show poor development of structural and germinal centers because of the lack of activation of B cells by the T cells in them.

# Signs & Symptoms
A patient presenting with Hyper IgM syndrome may be affected by simple infectious organisms in exposed regions like the respiratory system. Vaccination against pathogenic organisms may not help these individuals, because vaccinating them does not properly stimulate production of antibodies. Symptoms can include:
- Fever (recurrent infections)
- Low counts of IgA, IgG and IgE antibodies
- CD40L not reactive in T cells

# Treatment
Patients presenting with this disease undergo antibiotic treatment and gammaglobulin transfusions. Antibiotics are used to fight off the pathogenic organisms, and the gammaglobulin helps provide a normal balance of antibodies to fight the infection.
OMIM: 308230
Hyper-IgM syndrome type 2
In medicine, Hyper IgM Syndrome Type 2 is a rare disease.
Unlike other hyper-IgM syndromes, the Type 2 patients identified thus far did not present with a history of opportunistic infections. One would expect opportunistic infections in any immunodeficiency syndrome. The putative genetic lesion is in the AICDA gene found at 12p13. The patients have three common findings :
- the absence of immunoglobulin class switch recombination
- the lack of immunoglobulin somatic hypermutations, and
- lymph node hyperplasia caused by the presence of giant germinal centers.
Hyper IgM Syndrome Type 1
Synonyms and keywords: X-linked hyperimmunoglobulin M syndrome

# Overview
Hyper IgM Syndrome Type 1 is the X-linked variant of the Hyper-IgM syndrome. The affected individuals are virtually always male, because males only have one X chromosome, received from their mothers. Their mothers are not symptomatic, even though they are carriers of the allele, because the trait is recessive. Male offspring of these women have a 50% chance of inheriting their mother's mutant allele.

# Pathogenesis
This variant of the hyper-IgM syndrome is caused by mutation of the CD40LG gene. The genetic locus for this gene is Xq26. This gene codes for the CD40 ligand, which is expressed on T cells. When the CD40 ligand binds CD40 on B cells, then the B cell switches from producing IgM to producing IgA or IgG.
In these patients a biopsy of a ganglion may show poor development of structural and germinal centers because of the lack of activation of B cells by the T cells in them.

# Signs & Symptoms
A patient presenting with Hyper IgM syndrome may be affected by simple infectious organisms in exposed regions like the respiratory system. Vaccination against pathogenic organisms may not help these individuals, because vaccinating them does not properly stimulate production of antibodies. Symptoms can include:
- Fever (recurrent infections)
- Low counts of IgA, IgG and IgE antibodies
- CD40L not reactive in T cells

# Treatment
Patients presenting with this disease undergo antibiotic treatment and gammaglobulin transfusions. Antibiotics are used to fight off the pathogenic organisms, and the gammaglobulin helps provide a normal balance of antibodies to fight the infection.
OMIM: 308230
Hypophosphatemia overview

# Overview
Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which create a high phosphorus demand by cells, removing phosphate from the blood (refeeding syndrome).
Because a decrease in phosphate in the blood is sometimes associated with an increase in phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used interchangeably; however, this is improper since there exist many causes of hypophosphatemia besides overexcretion and phosphaturia, and in fact the most common causes of hypophosphatemia are not associated with phosphaturia.

# Treatment

## Medical Therapy
Standard intravenous preparations of potassium phosphate are available and are routinely used in malnurished patients and alcoholics. Oral supplementation also is useful where no intravenous treatment is available. Historically one of the first demonstrations of this was in concentration camp victims who died soon after being re-fed: it was observed that those given milk (high in phosphate) had a higher survival rate than those who did not get milk.
Hypophyseal portal system
The hypophyseal portal system (or hypothalamo-hypophyseal portal system) is the system of blood vessels that links the hypothalamus and the anterior pituitary. It allows endocrine communication between the two structures. The anterior pituitary receives releasing and inhibitory hormones in the blood. Using these the anterior pituitary is able to fulfill its function of regulating the other endocrine glands.
It is one of only a few portal systems of circulation in the body; that is, it involves two capillary beds connected by venules.

# Hormone transport
mechanism for hormone transport via hypothalamoportal vessels:
- cells regulated by different nuclei in hypothalamus, ie: neurons that release neurotransmitters as hormones in the connective link between the pituitary and the brain. Hypothalamic hormones stimulate the release of the respective hormone from the anterior pituitary gland.
- ligands (in this case, hormones released by the hypothalamus to activate hormone release from the anterior pituitary) are picked up by blood vessels then taken to anterior pituitary where they are broken down and released back into blood vessels
- before they are broken down, hypothalamoportal vessel acts as local route for blood flow directly from hypothalamus to anterior pituitary.
IMITREX spray description

# Description
IMITREX Nasal Spray contains sumatriptan, a selective 5-HT1B/1D receptor agonist. Sumatriptan is chemically designated as 3--N-methyl-indole-5-methanesulfonamide, and it has the following structure:
The empirical formula is C14H21N3O2S, representing a molecular weight of 295.4. Sumatriptan is a white to off-white powder that is readily soluble in water and in saline.
Each IMITREX Nasal Spray contains 5 or 20 mg of sumatriptan in a 100-L unit dose aqueous buffered solution containing monobasic potassium phosphate NF, anhydrous dibasic sodium phosphate USP, sulfuric acid NF, sodium hydroxide NF, and purified water USP. The pH of the solution is approximately 5.5. The osmolality of the solution is 372 or 742 mOsmol for the 5- and 20-mg IMITREX Nasal Spray, respectively.
IMITREX tablet overdosage

# Overdosage
Patients in clinical trials (N = 670) received single oral doses of 140 to 300 mg without significant adverse reactions. Volunteers (N = 174) received single oral doses of 140 to 400 mg without serious adverse reactions.
Overdose in animals has been fatal and has been heralded by convulsions, tremor, paralysis, inactivity, ptosis, erythema of the extremities, abnormal respiration, cyanosis, ataxia, mydriasis, salivation, and lacrimation.
The elimination half-life of sumatriptan is approximately 2.5 hours 	, and therefore monitoring of patients after overdose with IMITREX Tablets should continue for at least 12 hours or while symptoms or signs persist.
It is unknown what effect hemodialysis or peritoneal dialysis has on the serum concentrations of sumatriptan.
Identical ancestors point
In genetic genealogy, the identical ancestors point (IAP) is that point in a given population's past where each individual alive turned out to be either the ancestor of every individual alive now, or to have no living descendants at all. This point lies further in the past than the population's most recent common ancestor (MRCA).
The MRCA had many contemporary companions of both sexes.  Many of these contemporaries left direct descendants, but not all of them left an unbroken link of descendants all the way down to today's population.  That is, some contemporaries are ancestors of no one in current population.  The rest of  contemporaries of MRCA may claim ancestry over a subset of current population, but not the entirety of current population.
Because ancestors of MRCA are by definition also common ancestors, the farther we push back in time, the more common ancestors we find, from this single MRCA.  Eventually we will reach a point in the past where all humans can be divided into two groups: those who left no descendants today and those who are common ancestors of all living humans today.  This point in time is termed the identical ancestors point. Even though each living person receives genes in dramatically different proportions from these ancestors from the identical ancestors point, all living people share exactly the same set of ancestors from this point back, all the way to the very first single-celled organism.
The identical ancestors point for Homo sapiens has been estimated to between 15,000 and 5,000 years ago, with an estimate of the human MRCA living about 2,000 to 5,000 years ago, that is, estimating the IAP to be about three times as distant as the MRCA.  Note that both the matrilineal and the patrilineal human mrcas are far more remote still, dating to some 150,000 and 90,000 years ago, respectively.
It is incorrect to assume that the MRCA and his/her ancestors passed all their genes down to every person alive today.  Because of sexual reproduction, at every generation, an ancestor only passes half of his or her genes to the next generation. The percentage of genes inherited from the MRCA becomes smaller and smaller at every successive generation, as genes inherited from contemporaries of MRCA are interchanged via sexual reproduction.
Incomplete gamma function
In mathematics, the gamma function is defined by a definite integral. The incomplete gamma function is defined as an integral function of the same integrand. There are two varieties of the incomplete gamma function: the upper incomplete gamma function is for the case that the lower limit of integration is variable (ie where the "upper" limit is fixed), and the lower incomplete gamma function can vary the upper limit of integration.
The upper incomplete gamma function is defined as:
The lower incomplete gamma function is defined as:

# Properties
In both cases a is a complex parameter, such that the real part of a is positive.
By integration by parts we can find that
Since the ordinary gamma function is defined as
we have
Furthermore,
and
Also
where Ei is the exponential integral, erf is the error function, and erfc is the complementary error function, erfc(x) = 1  erf(x).

# Regularized Gamma functions
Two related functions are the regularized Gamma functions:

# Connection with Kummer's confluent hypergeometric function
It is easily shown that, when the real part of z is positive,
\gamma(a,z) = \int_0^z e^{-t}t^{a-1} dt = a^{-1} z^a e^{-z} M(1,a+1,z),
where M(1, a+1, z) is Kummer's confluent hypergeometric function. Since the series
M(1, a+1, z) = 1 + \frac{1}{(a+1)}z + \frac{1}{(a+1)(a+2)}z^2 + \frac{1}{(a+1)(a+2)(a+3)}z^3 + \cdots
has an infinite radius of convergence, we may take
\gamma(a,z) = a^{-1} z^a e^{-z} M(1,a+1,z)\,
as the definition of (a, z) for all complex z. In this light, the lower incomplete gamma function (a, z) is an entire function of the complex variable z. Since the gamma function (z) is a meromorphic function with simple poles at {0, 1, 2, ...}, we may define the meromorphic upper incomplete gamma function as
\Gamma(a, z) = \Gamma(a) - \gamma(a, z). \,
For the actual computation of numerical values, the continued fraction of Gauss provides a useful expansion:
\frac{a e^z}{z^a} \gamma(a, z) = \cfrac{1}{1 - \cfrac{z}{a+1 + \cfrac{z}{a+2 - \cfrac{(a+1)z}
{a+3 + \cfrac{2z}{a+4 - \cfrac{(a+2)z}{a+5 + \cfrac{3z}{a+6 - \ddots}}}}}}}.
This continued fraction converges for all complex z, provided only that a is not a negative integer.
Medial palpebral arteries

# Overview
The medial palpebral arteries (internal palpebral arteries), two in number, superior and inferior, arise from the ophthalmic, opposite the pulley of the Obliquus superior; they leave the orbit to encircle the eyelids near their free margins, forming a superior and an inferior arch, which lie between the Orbicularis oculi and the tarsi.
The superior palpebral anastomoses, at the lateral angle of the orbit, with the zygomaticoorbital branch of the temporal artery and with the upper of the two lateral palpebral branches from the lacrimal artery.
The inferior palpebral anastomoses, at the lateral angle of the orbit, with the lower of the two lateral palpebral branches from the lacrimal and with the transverse facial artery, and, at the medial part of the lid, with a branch from the angular artery.
From this last anastomoses a branch passes to the nasolacrimal duct, ramifying in its mucous membrane, as far as the inferior meatus of the nasal cavity.

# Additional images
- Bloodvessels of the eyelids, front view.
Inferior phrenic arteries
The inferior phrenic arteries are two small vessels, which supply the diaphragm but present much variety in their origin.
They may arise separately from the front of the aorta, immediately above the celiac artery, or by a common trunk, which may spring either from the aorta or from the celiac artery. Sometimes one is derived from the aorta, and the other from one of the renal arteries; they rarely arise as separate vessels from the aorta.
They diverge from one another across the crura of the diaphragm, and then run obliquely upward and lateralward upon its under surface.
- The left phrenic passes behind the esophagus, and runs forward on the left side of the esophageal hiatus.
- The right phrenic passes behind the inferior vena cava, and along the right side of the foramen which transmits that vein.
Near the back part of the central tendon each vessel divides into a medial and a lateral branch.
- The medial branch curves forward, and anastomoses with its fellow of the opposite side, and with the musculophrenic and pericardiacophrenic arteries.
- The lateral branch passes toward the side of the thorax, and anastomoses with the lower intercostal arteries, and with the musculophrenic. The lateral branch of the right phrenic gives off a few vessels to the inferior vena cava; and the left one, some branches to the esophagus.
Each vessel gives off superior suprarenal branches to the suprarenal gland of its own side. The spleen and the liver also receive a few twigs from the left and right vessels respectively.
Intercalation (chemistry)
In chemistry, intercalation is the reversible inclusion of a molecule (or group) between two other molecules (or groups). Examples include DNA intercalation and in graphite intercalation compounds.

# DNA intercalation
There are several ways molecules - in this case, also known as "ligands" - can interact with DNA. Ligands may interact with DNA by covalently binding, electrostatically binding, or intercalating. Intercalation occurs when ligands of an appropriate size and chemical nature fit themselves in between base pairs of DNA.  These ligands are mostly polycyclic, aromatic, and planar, and therefore often make good nucleic acid stains. Intensively studied DNA intercalators include ethidium bromide, proflavine, daunomycin, doxorubicin, and thalidomide.  DNA intercalators are used in chemotherapeutic treatment to inhibit DNA replication in rapidly growing cancer cells.
In order for an intercalator to fit between base pairs, the DNA must dynamically open a space between its base pairs by unwinding. The degree of unwinding varies depending on the intercalator, for example, ethidium cation (the ionic form of ethidium bromide found in aqueous solution) unwinds DNA by about 26 while proflavine unwinds it by about 17. This unwinding causes the base pairs to separate, or "rise", creating an opening of about 0.34 nm (3.4 A). This unwinding induces local structural changes to the DNA strand, such as lengthening of the DNA strand, or twisting of the base pairs. These structural modifications can lead to functional changes, often to the inhibition of transcription and replication and DNA repair processes, which makes intercalators potent mutagens.  For this reason, DNA intercalators are often carcinogenic, such as the exo (but not the endo) 8,9 epoxide of aflatoxin B1, acridines such as proflavine or quinacrine, or ethidium bromide.
Intercalation as a mechanism of interaction between cationic, planar, polycyclic aromatic systems of the correct size (on the order of a base pair) was first proposed by Leonard Lerman in 1961. One proposed mechanism of intercalation is as follows: in aqueous isotonic solution, the cationic intercalator is attracted electrostatically to the polyanionic DNA. The ligand displaces a sodium and/or magnesium cation that always surround DNA (to balance its charge) and forms a weak electrostatic bond with the outer surface of DNA. From this position, the ligand may then slide into the hydrophobic environment found between the base pairs and away from the hydrophilic outer environment surrounding the DNA. The base pairs transiently form such openings due to energy absorbed during collisions with solvent molecules.

# Notes
-  Richards, A.D. & Rodgers, A. (2007). Synthetic metallomolecules as agents for the control of DNA structure. Chem. Soc. Rev. 36 471-483. Link