Persius/hicric huggingface dataset:
Interleukin 22
Interleukin-22 (IL-22) is protein that in humans is encoded by the IL22 gene.

# Structure
IL-22 is an -helical cytokine. IL-22 binds to a heterodimeric cell surface receptor composed of IL-10R2 and IL-22R1 subunits. IL-22R is expressed on tissue cells, and it is absent on immune cells.
Crystallization is possible if the N-linked glycosylation sites are removed in mutants of IL-22 bound with high-affinity cell-surface receptor sIL-22R1. The crystallographic asymmetric unit contained two IL-22-sIL-22R1 complexes.

# Function
IL-22 a member of a group of cytokines called the IL-10 family or IL-10 superfamily (including IL-19, IL-20, IL-24, and IL-26), a class of potent mediators of cellular inflammatory responses. It shares use of IL-10R2 in cell signaling with other members of this family, IL-10, IL-26, IL-28A/B and IL-29. IL-22 is produced by activated NK and T cells and initiates innate immune responses against bacterial pathogens especially in epithelial cells such as respiratory and gut epithelial cells. IL-22 along with IL-17 is rapidly produced by splenic LTi-like cells  and also produced by Th17 cells and likely plays a role in the coordinated response of both adaptive innate immune systems, autoimmunity and tissue regeneration.
IL-22 biological activity is initiated by binding to a cell-surface complex composed of IL-22R1 and IL-10R2 receptor chains and further regulated by interactions with a soluble binding protein, IL-22BP, which shares sequence similarity with an extracellular region of IL-22R1 (sIL-22R1). IL-22 and IL-10 receptor chains play a role in cellular targeting and signal transduction to selectively initiate and regulate immune responses. IL-22 can contribute to immune disease through the stimulation of inflammatory responses, S100s and defensins.  IL-22 also promotes hepatocyte survival in the liver and epithelial cells in the lung and gut similar to IL-10. In some contexts, the pro-inflammatory versus tissue-protective functions of IL-22 are regulated by the often co-expressed cytokine IL-17A 

# Target tissue
Targets of this cytokine are mostly non-hematopoietic cells such as hepatocytes, keratinocytes, and lung and intestinal epithelial cells. Pancreatic islets also express high levels of IL-22 receptor. It has been shown to induce islet beta cell regeneration.

# Signaling
IL-22, signals through the interferon receptor-related proteins CRF2-4 and IL-22R. It forms cell surface complexes with IL-22R1 and IL-10R2 chains resulting in signal transduction through receptor, IL-10R2. The IL-22/IL-22R1/IL-10R2 complex activates intracellular kinases (JAK1, Tyk2, and MAP kinases) and transcription factors, especially STAT3. It can induce IL-20 and IL-24 signaling when IL-22R1 pairs with IL-20R2.
Interleukin 23
Interleukin-23 (IL-23) is a heterodimeric cytokine composed of an IL12B (IL-12p40) subunit (that is shared with IL12) and the IL23A (IL-23p19) subunit. A functional receptor for IL-23 (the IL-23 receptor) has been identified and is composed of IL-12R 1 and IL-23R.

# Discovery
IL-23 was first described by Robert Kastelein and colleagues at the DNAX research institute using a combination of computational, biochemical and cellular  immunology approaches.

# Function
Prior to the discovery of IL-23, IL-12 had been proposed to represent a key mediator of inflammation in mouse models of inflammation. However, many studies aimed at assessing the role of IL-12 had blocked the activity of IL-12p40, and were therefore not as specific as thought. Studies which blocked the function of IL-12p35 did not produce the same results as those targeting IL-12p40 as would have been expected if both subunits formed part of IL-12 only.
The discovery of an additional potential binding partner for IL-12p40 led to a reassessment of this role for IL-12. Seminal  studies in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, showed that IL-23 was responsible for the inflammation observed, not IL-12 as previously thought. Subsequently, IL-23 was shown to facilitate development of inflammation in numerous other models of immune pathology where IL-12 had previously been implicated including models of arthritis, intestinal inflammation, and psoriasis. Ustekinumab, a monoclonal antibody directed against this cytokine, is used clinically to treat certain autoimmune conditions.
Interleukin 25
Interleukin-25 (IL-25)  also known as interleukin-17E (IL-17E)  is a protein that in humans is encoded by the IL25 gene.

# Function
IL-25 is a cytokine that shares the sequence similarity with IL-17. This cytokine can induce NF-B activation, and stimulate the production of IL-8. Both this cytokine and IL17B are ligands for the cytokine receptor IL17RB. Studies of the similar gene in mice suggested that this cytokine may be a proinflammatory cytokine favoring Th2-type immune response. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.
IL-25 is a cytokine that belongs to the IL-17 cytokine family and is secreted by type 2 helper T cells (Th2) and mast cells.

# Clinical significance
IL-25 induces the production of other cytokines, including IL-4, IL-5 and IL-13 in multiple tissues, which stimulate the expansion of eosinophils.  This cytokine is an important molecule controlling immunity of the gut and has been implicated in chronic inflammation associated with the gastrointestinal tract. IL-25 can kill some types of breast cancer cells.
Further, the IL-25 gene has been identified in a chromosomal region associated with (autoimmune deleted, IBD not defined as autoimmune) diseases of the gut such as inflammatory bowel disease (IBD), although no direct evidence suggests that IL-25 plays any role in this disease.
IL-25 has potent antitumor activity in vivo in several human cancers including melanoma, breast, lung, colon, and pancreatic cancers, suggesting the potential clinical use of IL-17E as an anticancer agent.
Interleukin 26
Interleukin-26 (IL-26) is a protein that in humans is encoded by the IL26 gene.
IL-26 is a 171-amino acid protein, which is similar in amino acid sequence to interleukin 10.  It was originally called AK155 and is composed of a signal sequence, 6 helices, and 4 conserved cysteine residues. IL-26 is expressed in certain herpesvirus-transformed T cells but not in primary stimulated T cells. IL-26 signals through a receptor complex comprising two distinct proteins called IL-20 receptor 1 and IL-10 receptor 2. By signaling through this receptor complex, IL-26 induces rapid phosphorylation of the transcription factors STAT1 and STAT3, which enhance IL-10 and IL-8 secretion and as expression of the CD54 molecule on the surface of epithelial cells.

# Role
Interleukin 26 (IL-26), is a natural human antimicrobial that promotes immune sensing of bacterial and host cell death. IL-26, a human TH17 cellderived cytokine, is a cationic amphipathic protein that kills extracellular bacteria via membrane-pore formation. Furthermore, TH17 cellderived IL-26 formed complexes with bacterial DNA and self-DNA released by dying bacteria and host cells. The IL-26DNA complexes triggered the production of type I interferon by plasmacytoid dendritic cells via activation of Toll-like receptor 9, but independently of the IL-26 receptor.
Interleukin 32
Interleukin 32 (Il32) is a protein that in humans is encoded by the IL32 gene.

# Function
This gene encodes a member of the cytokine family. The protein contains a tyrosine sulfation site, 3 potential N-myristoylation sites, multiple putative phosphorylation sites, and an RGD cell-attachment sequence. Expression of this protein is increased after the activation of T-cells by mitogens or the activation of NK cells by IL-2. This protein induces the production of TNF-alpha from macrophage cells. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
Interleukin 32 (IL-32) is a pro-inflammatory cytokine that can induce cells of the immune system (such as monocytes and macrophages) to secrete inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-) and IL-6. In addition, it can also induce the production of chemokines such as IL-8 and MIP-2 / CXCL2.
IL-32 can also support osteoclast differentiation but not osteoclast activation by regulating the MAPK/ERK pathway and the actin cytoskeleton.
Intramolecular
Intramolecular in chemistry describes a process or characteristic limited within the structure of a single molecule; a property or phenomenon limited to the extent of a single molecule.

# Examples
- intramolecular hydride transfer (transfer of a hydride ion from one part to another within the same molecule)
- intramolecular hydrogen bond (a hydrogen bond formed between two functional groups of the same molecule)
In intramolecular organic reactions, two reaction sites are contained within a single molecule. This creates a very high effective concentration (resulting in high reaction rates) and therefore many intramolecular reactions take place that would not occur as an intermolecular reaction between two compounds.
Examples of intramolecular reactions are the Smiles rearrangement, the Dieckmann condensation and the Madelung synthesis.

# Molecular tethers
In a niche concept called molecular tethers otherwise intermolecular reactions can be made temporarily intramolecular by anchoring both reactions by a tether with all the advantages associated to it. Popular choices of tether contain a carbonate ester, boronic ester,  silyl ether or a silyl acetal link (silicon tethers) which are fairly inert in many organic reactions yet can be cleaved by specific reagents.  Main hurdle for this strategy to work is selecting the proper length for the tether and making sure reactive groups have an optimal orientation with respect to each other.  An examples is a Pauson-Khand reaction of a alkene and an alkyne tethered together via a silyl ether 
Pauson-Khand silicon tether
In this particular reaction the tether angle bringing the reactive groups together is effectively reduced by placing isopropyl groups on the  silicon atom via the Thorpe-Ingold effect. No reaction takes place when these bulky groups are replaced by smaller methyl groups.
Another example is a photochemical cycloaddition with two alkene groups tethered through a silicon acetal group (racemic, the other enantiomer not depicted) which is subsequently cleaved by TBAF yielding the endo-diol.
Without the tether the exo isomer forms .
Ionic strength
The ionic strength, I, of a solution is a function of the concentration of all ions present in a solution.
 I_c = \begin{matrix}\frac{1}{2}\end{matrix}\sum_{{\rm B}=1}^{n} c_{\rm B}z_{\rm B}^{2} 
where cB is the  molar concentration of ion B (mol dm-3), zB is the charge number of that ion, and the sum is taken over all ions in the solution. For a 1:1 electrolyte such as sodium chloride, the ionic strength is equal to the concentration, but for MgSO4 the ionic strength is four times higher. Generally multivalent ions contribute strongly to the ionic strength.
For example the ionic strength of a mixed 0.0050M Na2SO4 + 0.0020M NaCl solution is :
I= 1/2(2*((+1)2 *0.005) + (+1)2 *0.0020 + (-2)2 *0.005 + (-1)2 *0.002)
=0.017M
Because in non-ideal solutions volumes are no longer strictly additive it is often preferable to work with molality (mol/kg H2O ) rather than amount concentration. In that case, ionic strength is defined as:
 I_m = \begin{matrix}\frac{1}{2}\end{matrix}\sum_{{\rm B}=1}^{n} m_{\rm B}z_{\rm B}^{2} 

# Importance
The ionic strength plays a central role in the Debye-Huckel theory that describes the strong deviations from ideality typically encountered in ionic solutions. It is also important for the theory of Double Layer (interfacial) and related Electrokinetic phenomena and Electroacoustic phenomena in colloids and other heterogeneous systems. That is, the Debye length, which is the inverse of the Debye parameter  kappa , is inversely proportional to the square root of the ionic strength. Debye length is characteristic of the Double layer thickness. Increasing the concentration or valence of the counterions compresses the double layer and increases the electrical potential gradient.

# Ionic replacement
The rate coefficient or rate constant of a chemical reaction is the coefficient that precedes reactant concentrations in a simple rate equation. 
For a chemical reaction n A + m  B  n ' C + m ' D, with rate equation:
In the study of solution reaction kinetics it is often desirable to change the concentration of an active species without changing the ionic strength, because the latter affects the value of the rate constant k. This can often be done by replacement. If, for example, the  is to be lowered, the solution is diluted with a solution containing the same concentration of a non-active species of equal charge e.g. SO42- rather than just solvent. This produces a solution with a lower  but of the same ionic strength.
Ipodate sodium

# Overview
Ipodate sodium (sodium iopodate) is an iodine-containing radiopaque contrast media used for X-rays.  The drug is given orally and the resulting contrast allows for easy resolution of the bile duct and gall bladder. The drug goes by the trade name Oragrafin or Gastrografin.

# Other uses
Although not FDA approved, ipodate sodium has been used to treat Graves' disease and thyroid storm, an extreme form of hyperthyroidism.

## Graves' disease
Long-term treatment of Graves' disease with ipodate sodium (500 mg, daily) given by mouth reduced levels of T3 and T4 in the patients.  This was done with minimal side effects, indicating possible clinical usefulness.  Iodine uptake was also noted to return to normal within seven days, indicating control with ipodate with rapid follow up treatment with 131I is feasible.

## Thyroid Storm
In emergency situations, ipodate can be administered for thyroid storm. As the ipodate is metabolized, it releases iodine into circulation, helping bring the T3 and T4 levels back down.  Ipodate also inhibits the conversion of T4 to T3 (which is more potent).  It is not considered a first-line approach, as potassium iodide and beta blockers have less potential for side-effects. Ipodate sodium lacks FDA approval for this use.
Iron(II) oxide
Iron(II) oxide, also known as ferrous oxide or ferrous iron, is one of the iron oxides. It is a black-colored powder with the chemical formula FeO.  It consists of the chemical element iron in the oxidation state of 2 bonded to oxygen. Its mineral form is known as wustite. The latter term is often used synonymously to ferrous oxide. Iron(II) oxide is an example of a non-stoichiometric compound and the ratio of the elements iron and oxygen can vary due to crystallographic vacancies.
Iron (II) oxide is also very unstable and it easily susceptible to corroding into Iron (III) Oxide.
Iron(II) oxide should not be confused with rust, which usually consists of hydrated iron(III) oxide (ferric oxide).
Iron(II) oxide is used as a pigment. It is FDA-approved for use in cosmetics and it is used in some tattoo inks.
Irregular bone

# Overview
The irregular bones are such as, from their peculiar form, cannot be grouped as long bone, short bone, flat bone or sesamoid bone. Irregular bones serve some unique purpose in the body of combining: (1) protection of nervous tissue (such as the vertebrae protect the spinal cord), (2) affording multiple anchor points for skeletal muscle attachment (as with the sacrum), and maintaining pharynx and trachea support, and tongue attachment (such as the hyoid bone).
They consist of cancellous tissue enclosed within a thin layer of compact bone.
The irregular bones are: the vertebr, sacrum, coccyx, temporal, sphenoid, ethmoid, zygomatic, maxilla, mandible, palatine, inferior nasal concha, and hyoid.

# Reference
- Stedman's Online Medical Dictionary, 27th Edition
Isocyanic acid
Isocyanic acid is an inorganic compound with the formula HNCO, discovered in 1830 by Liebig and Wohler.  This colourless substance is volatile and poisonous, with a boiling point of 23.5 C.  Isocyanic acid is the simplest stable chemical compound that contains carbon, hydrogen, nitrogen, and oxygen, the four most commonly-found elements in organic chemistry and biology.

# Preparation and reactions
Isocyanic acid can be made by protonation of the cyanate anion, such as from salts like potassium cyanate, by either gaseous hydrogen chloride or acids such as oxalic acid.
HNCO also can be made by the high-temperature thermal decomposition of cyanuric acid, a trimer.
Isocyanic acid hydrolyses to carbon dioxide and ammonia:
At sufficiently high concentrations, isocyanic acid oligomerizes to give cyanuric acid and cyamelide, a polymer.  These species usually are easily separated from liquid- or gas-phase reaction products.  Dilute solutions of isocyanic acid are stable in inert solvents, e.g. ether and chlorinated hydrocarbons.
Isocyanic acid reacts with amines to give ureas:
HNCO adds across electron-rich double bonds, such as vinylethers, to give the corresponding isocyanates.

# Isomers
Low-temperature photolysis of solids containing HNCO has been shown to make H-O-CN, cyanic acid, which is a tautomer of isocyanic acid.  Pure cyanic acid has not been isolated, and isocyanic acid is the predominant form in all solvents. Note that sometimes information presented for cyanic acid in reference books is actually for isocyanic acid.
Cyanic and isocyanic acids are isomers of fulminic acid (H-C=N-O), an unstable compound.
Isothiocyanate
Isothiocyanate is the chemical group  -N=C=S, formed by substituting sulfur for oxygen in the isocyanate group. Allyl isothiocyanate is a chemical compound found in mustard oil that is responsible for its pungency. It is used for amino acid sequencing in Edman degradation.

# Reactions
Isothiocyanates generally act as electrophiles with the carbon atom as the electrophilic center.

# Biological Activity
Isothiocyanates, such as phenethyl isothiocyanate (PEITC) and sulforaphane, have been shown to inhibit carcinogenesis and tumorigensis and as such are useful chemopreventive agents against the development and proliferation of cancers. They work on a variety of levels. Most notably, they have been shown to inhibit carcinogenesis through inhibition of cytochrome P450 enzymes, which oxidise compounds such as benzopyrene and other polycyclic aromatic hydrocarbons (PAHs)into more polar epoxy-diols which can then cause mutation and induce cancer development. Phenethyl isothiocyanate (PEITC) has been shown to induce apoptosis in certain cancer cell lines, and in some cases, is even able to induce apoptosis in cells that are resistant to some currently used chemotherapeutic drugs. For example, in drug resistant leukemia cells which produce the powerful apoptosis inhibitor protein BCl-2.
Tympanic nerve
The tympanic nerve (nerve of Jacobson) is a branch of the glossopharyngeal nerve found near the ear.

# Path
It arises from the petrous ganglion, and ascends to the tympanic cavity through a small canal on the under surface of the petrous portion of the temporal bone on the ridge which separates the carotid canal from the jugular fossa.
In the tympanic cavity it divides into branches which form the tympanic plexus and are contained in grooves upon the surface of the promontory.
Jacobson's nerve contains both sensory and secretory fibers.
- Sensory fibers supply the middle ear and parasympathetic secretory fibers serve the parotid gland.
- The secretory fibers enter the otic ganglion.
The postganglionic parasympathetic fibers are then distributed via the auriculotemporal nerve (branch of the trigeminal nerve) to the parotid gland.

# Clinical significance
This nerve may be involved by paraganglioma, in this location referred to as glomus jugulare or glomus tympanicum tumours.

# Additional images
- Sympathetic connections of the otic and superior cervical ganglia.
Jacqui Jackson
Jacqui Jackson is the single parent of seven children, three adolescent girls and four boys.  All four boys are on the autism spectrum. Jackson and her family appeared in a BBC documentary, My Family and Autism, screened in 2003.  A drama called Magnificent 7 featuring Helena Bonham Carter as Maggia character based on Jacqui Jacksonwas screened by BBC Two in 2005.  Jackson lives in Blackpool, Lancashire, England.

# Family life
Jackson's sons are:
- Matthew - the oldest child in the family.  Matthew was born prematurely and has dyslexia and developmental dyspraxia.
- Luke - diagnosed with Asperger syndrome and dyspraxia. Luke wrote a book called Freaks, Geeks and Asperger's Syndrome about his life with the condition which was published when he was 13.
- Joe - has ADHD
- Ben - the youngest child in the family.  Ben was born prematurely and is autistic.
Jackson also has three daughters named Rachel, Sarah and Anna.

# Education
Jackson has a first class honours degree in social science from the Open University and is studying towards a PhD at Coventry University in sensory issues in autistic children.

# Books
- Multicoloured Mayhem, Jessica Kingsley Publishers, 2003, ISBN 1-84310-171-8
- Damned Hard Day: Living with AD/HD, Jessica Kingsley Publishers, 2005, ISBN 1-84310-296-X
Jane E. Henney
Jane E. Henney is an American physician who was the first woman to serve as commissioner of the U.S. Food and Drug Administration.  Appointed by President Bill Clinton, she served at the FDA between 1998 and 2001.  Previously she had worked at the FDA from 1992 to 1994 as deputy commissioner for operations under then commissioner David Aaron Kessler, MD and then at the University of New Mexico (UNM), where she was vice president of the health sciences center.
Jane Henney was born in Woodburn, Indiana. Henney received her undergraduate training at Manchester College, an MD degree from Indiana University School of Medicine and did postgraduate work at The University of Texas M. D. Anderson Cancer Center in Houston, Texas. Trained as a medical oncologist, she joined the National Cancer Institute (NCI) at the National Institutes of Health (NIH) in 1976, working in the Cancer Therapy and Evaluation Program.  She is married to James Robert Graham III, MD, who also has had a distinguished career as a physician-leader. After leaving the FDA she joined the board of directors of the pharmaceutical company Astrazeneca.
She was named senior vice president and provost for health affairs at the University of Cincinnati in 2003.