Persius/hicric huggingface dataset:
2,5-Dimethoxy-4-iodoamphetamine
DOI or 2,5-dimethoxy-4-iodoamphetamine is a psychedelic hallucinogenic drug and a substituted amphetamine of the phenethylamine family. Despite being a substituted amphetamine it is not a stimulant. DOI has a stereocenter and R-(-)-DOI is the more active stereoisomer. In neuroscience research, -R-(-)-DOI is used as a radioligand and indicator of the presence of 5-HT2A serotonin receptors.
When ingested recreationally, DOI is active at a dosage of 1.5 - 3.0 mg (orally) and has a duration of 16 - 30 hours (approximately twice as long as LSD). DOI's effects have been compared to LSD, although there are differences that experienced users can distinguish.  Besides the longer duration, the trip tends to be more energetic than an LSD trip, with more body load and a different subjective visual experience. The after effects include residual stimulation and difficulty sleeping, which, depending on the dose, may persist for days. It is often sold as a substitute for LSD, or even sold falsely as LSD, which may be dangerous because DOI does not have the same established safety profile as LSD. Although there have been no known deaths due to DOI ingestion, it is relatively new on the recreational scene so long-term effects are not known.

# Pharmacology
The hallucinogenic effect of DOI is mediated by its partial agonistic activity at the 5-HT2A serotonin receptor, but DOI also has a high binding affinity for the 5-HT2B and the 5-HT2C serotonin receptors. DOI is often used as a tool compound in research when studying the 5-HT2 receptor family.
The solubility of DOI-hydrochloride in H2O is 10 mg/ml, and in ethanol 2 mg/ml (source: www.sigmaaldrich.com MSDS)

# History
DOI was first synthesized by Alexander Shulgin.  The radioactive iodine-125 form of DOI was first developed in the lab of David E. Nichols.
British Police recently reported that 3 young men had taken ill, reportedly, after taking DOI at a rave in Biggleswade, near Milton Keynes, and warned others who had taken it to seek medical attention.  This would appear to the first indication that DOI has found more widespread use as a recreational drug in the UK.
24-Dehydrocholesterol reductase
24-Dehydrocholesterol reductase is a protein that in humans is encoded by the DHCR24 gene.
This gene encodes a flavin adenine dinucleotide (FAD)-dependent oxidoreductase, which catalyzes the reduction of the delta-24 double bond of sterol intermediates during cholesterol biosynthesis. The protein contains a leader sequence that directs it to the endoplasmic reticulum membrane. Missense mutations in this gene have been associated with desmosterolosis. Also, reduced expression of the gene occurs in the temporal cortex of Alzheimer disease patients and overexpression has been observed in adrenal gland cancer cells.

# Model organisms
Model organisms have been used in the study of DHCR24 function. A conditional knockout mouse line, called Dhcr24tm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program  a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty-six tests were carried out on mutant mice and two significant abnormalities were observed. Few homozygous mutant embryos were identified during gestation, and none survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice and no further abmornalities were observed.
Three-center four-electron bond
The 3-center-4-electron bond is a model used to explain bonding in hypervalent molecules such as phosphorus pentafluoride, sulfur hexafluoride, the xenon fluorides, and the hydrogen difluoride ion. It is also known as the Pimentel-Rundle three-center model after the work published by  George C. Pimentel in 1951, which built on concepts developed earlier by Robert E. Rundle for electron-deficient bonding.
The model considers bonding of three colinear atoms. For example in XeF2, the linear F-Xe-F subunit is described by a set of three molecular orbitals  (MOs) derived from colinear p-orbitals on each atom. The Xe-F bonds result from the combination of a filled p orbital in the central atom (Xe) with two half-filled p orbitals on the axial atoms (F), resulting in a filled bonding orbital, a filled non-bonding orbital, and an empty antibonding orbital. The two lower energy MO's are doubly occupied. The HOMO is localized on the two terminal atoms.  This localization of charge is accommodated by the fact that the terminal ligands are highly electronegative in hypervalent molecules.  The molecules PF5 and SF4 are described, according to this model, as having one 3-center-4-electron bond as well as three and two other more conventionally described bonds, respectively.  In SF6 and in the xenon fluorides, all bonds are described with the 3-center-4-electron model.
The bonding in XeF2 can also be shown qualitatively using resonant Lewis structures as shown below:
In this representation, the octet rule is not broken, the bond orders are 1/2, and there is increased electron density in the fluorine atoms. These results are consistent with the molecular orbital picture discussed above.
Older models for explaining hypervalency invoked d orbitals.  As of 2008, these models still appear in some beginning level college texts; however, quantum chemical calculations suggest that d-orbital participation is negligible due to the large energy difference between the relevant p (filled) and d (empty) orbitals. Furthermore, a distinction should be made between "d orbitals" in the valence bond sense and "d functions" that are included in the QM calculation as polarization functions. The 3-center-4-electron bonding model has the advantage of dispensing with the need for d orbitals, which has led to its acceptance.
3-hydroxyacyl-CoA dehydrogenase
In enzymology, a 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35) is an enzyme that catalyzes the chemical reaction
Thus, the two substrates of this enzyme are (S)-3-hydroxyacyl-CoA and NAD+, whereas its 3 products are 3-oxoacyl-CoA, NADH, and H+.
This enzyme belongs to the family of oxidoreductases, to be specific those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor.

# Isozymes
In humans, the following genes encode proteins with 3-hydroxyacyl-CoA dehydrogenase activity:
- HADH  Hydroxyacyl-Coenzyme A dehydrogenase
- HSD17B10  3-Hydroxyacyl-CoA dehydrogenase type-2
- EHHADH  Peroxisomal bifunctional enzyme
- HSD17B4  Peroxisomal multifunctional enzyme type 2

# Function
3-Hydroxyacyl CoA dehydrogenase is classified as an oxidoreductase. It is involved in fatty acid metabolic processes. Specifically it catalyzes the third step of beta oxidation; the oxidation of L-3-hydroxyacyl CoA by NAD+. The reaction converts the hydroxyl group into a keto group.
The end product is 3-ketoacyl CoA.

# Metabolic pathways
This enzyme participates in 8 metabolic pathways:
- fatty acid elongation in mitochondria
- fatty acid metabolism
- valine, leucine and isoleucine degradation
- lysine degradation
- tryptophan metabolism
- benzoate degradation via coa ligation
- butanoate metabolism
- caprolactam degradation

# Nomenclature
The systematic name of this enzyme class is (S)-3-hydroxyacyl-CoA:NAD+ oxidoreductase. Other names in common use include:
- 1-specific DPN-linked beta-hydroxybutyric dehydrogenase
- 3-hydroxyacetyl-coenzyme A dehydrogenase
- 3-hydroxyacyl coenzyme A dehydrogenase
- 3-hydroxybutyryl-CoA dehydrogenase
- 3-hydroxyisobutyryl-CoA dehydrogenase
- 3-keto reductase
- 3-L-hydroxyacyl-CoA dehydrogenase
- 3beta-hydroxyacyl coenzyme A dehydrogenase
- beta-hydroxy acid dehydrogenase
- beta-hydroxyacyl CoA dehydrogenase
- beta-hydroxyacyl dehydrogenase
- beta-hydroxyacyl-coenzyme A synthetase
- beta-hydroxyacylcoenzyme A dehydrogenase
- beta-hydroxybutyrylcoenzyme A dehydrogenase
- beta-keto-reductase
- beta-ketoacyl-CoA reductase
- L-3-hydroxyacyl CoA dehydrogenase
- L-3-hydroxyacyl coenzyme A dehydrogenase

# Structural studies
As of 20 January 2010, 22 structures have been solved for this class of enzymes, with PDB accession codes 1F0Y, 1F12, 1F14, 1F17, 1F67, 1GZ6, 1IKT, 1IL0, 1LSJ, 1LSO, 1M75, 1M76, 1S9C, 1WDK, 1WDL, 1WDM, 1ZBQ, 1ZCJ, 2D3T, 2HDH, 3HAD, and 3HDH.
3-Hydroxysteroid dehydrogenase
3-Hydroxysteroid dehydrogenase (3-HSD or aldo-keto reductase family 1 member C4) is an enzyme that in humans is encoded by the AKR1C4 gene. It is known to be necessary for the synthesis of the endogenous neurosteroids allopregnanolone, THDOC, and 3-androstanediol. It is also known to catalyze the reversible conversion of 3-androstanediol (5-androstane-3,17-diol) to dihydrotestosterone (DHT, 5-androstan-17-ol-3-one) and vice versa.

# Function
This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the bioreduction of chlordecone, a toxic organochlorine pesticide, to chlordecone alcohol in liver. This gene shares high sequence identity with three other gene members and is clustered with those three genes at 10p15-p14 on chromosome 10.

# Clinical significance
Various antidepressants, including the SSRIs fluoxetine, fluvoxamine, sertraline, and paroxetine, the SNRI venlafaxine, and mirtazapine, have been found to activate certain 3-HSD enzymes, resulting in a selective facilitation of 5-dihydroprogesterone conversion into allopregnanolone. This action has been implicated in their effectiveness in affective disorders, and has resulted in them being described as selective brain steroidogenic stimulants (SBSSs).
5-Methoxy-diisopropyltryptamine
5-methoxy-diisopropyltryptamine, also known as 5-methoxy-N,N-diisopropyltryptamine, 5-MeO-DiPT, foxy methoxy, or just foxy,  is a tryptamine that is used recreationally as a psychedelic.  5-MeO-DiPT is orally active, and dosages between 620 mg are commonly reported.  Many users note an unpleasant body load accompanies higher dosages.  5-MeO-DiPT is also taken by insufflation, or sometimes it is smoked or injected.  Some users also report sound distortion, also noted with the related drug, DiPT.

# Effects
Erowid reports the following effects:

### Positive
- Mood lift, euphoria
- Intensification of tactile sensations, smell, etc
- Sexually interesting
- Emotionally opening

### Neutral
- Feelings of body & muscle energy, buzzing
- Auditory distortions, pitch shifts
- Visual distortions, open and closed-eye patterning, movement trails, shifting colors
- Physical and mental stimulation

### Negative
- Possible stomach discomfort, gas & vomiting
- Possible minor jaw-clenching
- Possible Diarrhea
- Anxious stimulation
- Muscle tension / discomfort
- Possible insomnia for 4-12 hours after peak
- Possible male impotence for duration of drug's effects during higher doses

# Legality
5-MeO-DIPT has been illegal in Germany since September 1999, Greece since February 2003, Denmark since February 2004, Sweden since October 2004, Japan since April 2005, and Singapore since early 2006.
On April 4, 2003, the United States DEA added both 5-MeO-DiPT and AMT to Schedule I of the Controlled Substances Act under "emergency scheduling" procedures. The drugs were officially placed into Schedule I on September 29, 2004.
Prior to its prohibition in the U.S., 5-MeO-DIPT was sold online alongside psychoactive analogues like DIPT, DPT, and 5-MeO-DMT, none of which have yet been expressly outlawed in that country. However, in July 2004, Operation Web Tryp was concluded, confirming that U.S. Federal law enforcement intends to prosecute sale of these analogs of 5-MeO-DIPT. Previous prosecutions under the Federal Analog Act have met, on occasion, with failure, given some court rulings regarding possible unconstitutional vagueness regarding what substances are properly considered 'analogs'; such issues may be addressed on appeal.
AH receptor-interacting protein
AH receptor-interacting protein (AIP) also known as aryl-hydrocarbon receptor-interacting protein, immunophilin homolog ARA9, or HBV X-associated protein 2 (XAP-2) is a protein that in humans is encoded by the AIP gene. The protein is a member of FKBP family.

# Function
AIP may play a positive role in aryl hydrocarbon receptor-mediated signalling possibly by influencing its receptivity for ligand and/or its nuclear targeting. AIP is the cellular negative regulator of the hepatitis B virus (HBV) X protein. Further, it's been known to suppress antiviral signaling and the induction of type I interferon by targeting IRF7, a key player in the antiviral signal pathways.

# Role in disease
AIP mutations may be the cause of a familial form of acromegaly, familial isolated pituitary adenoma (FIPA). Somatotropinomas (i.e. GH-producing pituitary adenomas), sometimes associated with prolactinomas, are present in most AIP mutated patients.

# Interactions
AIP has been shown to interact with the aryl hydrocarbon receptor, peroxisome proliferator-activated receptor alpha and the aryl hydrocarbon receptor nuclear translocator. Further, it has shown that AIP can interact with IRF7 to exert its novel function of negatively regulating antiviral signal pathways.
Ablepharon macrostomia syndrome

# Overview
Ablepharon macrostomia syndrome (AMS) is an extremely rare autosomal recessive genetic disorder characterized by malformations of the skull, skin, fingers and genitals. Affected individuals may also have malformations of the nipples and abdominal wall.
Younger individuals might experience language difficulties, and in some instances mental retardation is known.

# Genetics
File:Autorecessive.svg
It has been suggested that Ablepharon Macrostomia Syndrome is inherited as an autosomal recessive genetic trait.
Abacavir lamivudine description

# Description
EPZICOM: EPZICOM Tablets contain the following 2 synthetic nucleoside analogues: abacavir sulfate (ZIAGEN, also a component of TRIZIVIR) and lamivudine (also known as EPIVIR or 3TC) with inhibitory activity against HIV-1.
EPZICOM Tablets are for oral administration. Each orange, film-coated tablet contains the active ingredients 600 mg of abacavir as abacavir sulfate and 300 mg of lamivudine, and the inactive ingredients magnesium stearate, microcrystalline cellulose, and sodium starch glycolate. The tablets are coated with a film (OPADRY orange YS-1-13065-A) that is made of FD&C Yellow No. 6, hypromellose, polyethylene glycol 400, polysorbate 80, and titanium dioxide.
Abacavir Sulfate: The chemical name of abacavir sulfate is (1S,cis)-4--2-cyclopentene-1-methanol sulfate (salt) (2:1). Abacavir sulfate is the enantiomer with 1S, 4R absolute configuration on the cyclopentene ring. It has a molecular formula of (C14H18N6O)2H2SO4 and a molecular weight of 670.76 daltons. It has the following structural formula:
Abacavir sulfate is a white to off-white solid with a solubility of approximately 77 mg/mL in distilled water at 25C.
In vivo, abacavir sulfate dissociates to its free base, abacavir. All dosages for abacavir sulfate are expressed in terms of abacavir.
Lamivudine: The chemical name of lamivudine is (2R,cis)-4-amino-1-(2-hydroxymethyl-1,3-oxathiolan-5-yl)-(1H)-pyrimidin-2-one. Lamivudine is the (-)enantiomer of a dideoxy analogue of cytidine. Lamivudine has also been referred to as (-)2,3-dideoxy, 3-thiacytidine. It has a molecular formula of C8H11N3O3S and a molecular weight of 229.3 daltons. It has the following structural formula:
Lamivudine is a white to off-white crystalline solid with a solubility of approximately 70 mg/mL in water at 20C.
Acoustic Targeted Drug Delivery

# Background
Acoustic Targeted Drug Delivery ATDD is a method that uses ultrasound energy to enhance the transport of molecules into and/or across specific tissues. Generally this class of ultrasound energy falls under the class of therapeutic ultrasound, and ranges in ultrasonic frequencies of 1-20MHz and Sound intensitys of 0-30 watts/cm2
 The use of ATDD  in conjunction with local drug delivery by injection, topical application and convection enhanced delivery shows promise to significantly enhance the treatment of various diseases in the human body by specifically targeting the drug into the tissue. 

# How ATDD works
Focused ultrasound similar to High intensity focused ultrasound, but at much lower powers is applied to tissues in conjunction with the local application of pharmological agent. The ultrasound source (or transducer) is pulsed on and off, and moved in a defined pattern to sonicate the tissue of interest. The pulsing of the ultrasound serves two purposes 1. to agitate the tissue matrix by extending and compressing it, and 2. to keep the tissue from absorbing to much energy and ablating it (or causing necrosis). The manual movement of the transducer allows for control of the sonicated volume of tissue and where the drug may penetrate more readily.
ATDD may be applied:
- Geometrically, for example with a lens or with a spherically curved transducer.
- Electronically, by adjusting the relative phases of elements in an array of transducers (a "phased array"). By dynamically adjusting the electronic signals to the elements of a phased array, the beam can be steered to different locations, and aberrations due to tissue structures can be corrected.

# ATDD and topical drug delivery
Acyclovir clinical pharmacology

# Clinical Pharmacology
Pharmacokinetics:
The pharmacokinetics of acyclovir after oral administration have been evaluated in healthy volunteers and in immunocompromised patients with herpes simplex or varicella-zoster virus infection. Acyclovir pharmacokinetic parameters are summarized in Table 1.
In one multiple-dose, crossover study in healthy subjects (n = 23), it was shown that increases in plasma acyclovir concentrations were less than dose proportional with increasing dose, as shown in Table 2. The decrease in bioavailability is a function of the dose and not the dosage form.
There was no effect of food on the absorption of acyclovir (n = 6); therefore, ZOVIRAX Capsules, Tablets, and Suspension may be administered with or without food.
The only known urinary metabolite is 9-guanine.

## Special Populations
Adults With Impaired Renal Function: The half-life and total body clearance of acyclovir are dependent on renal function. A dosage adjustment is recommended for patients with reduced renal function (see DOSAGE AND ADMINISTRATION).
Geriatrics: Acyclovir plasma concentrations are higher in geriatric patients compared with younger adults, in part due to age-related changes in renal function. Dosage reduction may be required in geriatric patients with underlying renal impairment (see PRECAUTIONS: Geriatric Use).
Pediatrics: In general, the pharmacokinetics of acyclovir in pediatric patients is similar to that of adults. Mean half-life after oral doses of 300 mg/m2 and 600 mg/m2 in pediatric patients aged 7 months to 7 years was 2.6 hours (range 1.59 to 3.74 hours).

## Drug Interactions
Coadministration of probenecid with intravenous acyclovir has been shown to increase the mean acyclovir half-life and the area under the concentration-time curve. Urinary excretion and renal clearance were correspondingly reduced.
Adenine nucleotide translocator
Adenine nucleotide translocator (ANT), also known as the ADP/ATP translocase, exchanges free ATP with free ADP across the inner mitochondrial membrane. ANT is the most abundant protein in the inner mitochondrial membrane. It belongs to mitochondrial carrier family.

# Function
ANT has long been thought to function asymmetrically as a homodimer of subunits in the inner mitochondrial membrane. The dimer was thought to be a gated pore through which ADP and ATP were exchanged between the mitochondrial matrix and the cytoplasm.  The dimer hypothesis was first challenged when the three-dimensional structure of ANT was discovered to be a monomer.  Further work has shown that ANT functions as a monomer in detergents and in mitochondrial membranes.
ANT transports the free, i.e. deprotonated, non-Magnesium, non-Calcium bound forms of ADP and ATP, in a 1:1 ratio. It is fully reversible, and its directionality is governed by the concentrations of its substrates (ADP and ATP inside and outside mitochondria), the chelators of the adenine nucleotides, and the mitochondrial membrane potential. The relationship of these parameters can be expressed by an equation solving for the 'reversal potential of the ANT" (Erev_ANT), a value of the mitochondrial membrane potential at which no net transport of adenine nucleotides takes place by the ANT. The ANT and the F0-F1 ATP synthase are not necessarily in directional synchrony.
Apart from exchange of ADP and ATP across the inner mitochondrial membrane, the ANT also exhibits an intrinsic uncoupling activity
ANT is an important modulatory but not structural component of the mitochondrial permeability transition pore which can open and lead to cell death through apoptosis or necrosis.

# Types
In humans, there exist three paraologous ANT isoforms:
- SLC25A4  found primarily in heart and skeletal muscle
- SLC25A5  primarily expressed in fibroblasts
- SLC25A6  primarily express in liver
Auricular branch of vagus nerve
The auricular branch of the vagus nerve is often termed the Alderman's nerve or Arnold's nerve. The latter name is an eponym for Friedrich Arnold.

# Path
It arises from the jugular ganglion, and is joined soon after its origin by a filament from the petrous ganglion of the glossopharyngeal; it passes behind the internal jugular vein, and enters the mastoid canaliculus on the lateral wall of the jugular fossa.
Traversing the substance of the temporal bone, it crosses the facial canal about 4 mm. above the stylomastoid foramen, and here it gives off an ascending branch which joins the facial nerve.
The nerve reaches the surface by passing through the tympanomastoid fissure between the mastoid process and the tympanic part of the temporal bone, and divides into two branches:
- one joins the posterior auricular nerve.
- the other is distributed to the skin of the back of the auricula and to the posterior part of the external acoustic meatus.

# Clinical significance
This nerve may be involved by the glomus jugulare tumour.
Alfred Sommer (ophthalmologist)
Alfred (Al) Sommer is a prominent American ophthalmologist and academic at the Johns Hopkins University Bloomberg School of Public Health.

# Biography
Sommer was born in 1942 in New York City and graduated from Union College in Schenectady, New York in 1963. Sommer has an MD from Harvard Medical School (1967) and an MHS from the Johns Hopkins School of Hygiene and Public Health (1973).  He is professor of Epidemiology and International Health, as well as Ophthalmology (at the Johns Hopkins School of Medicine). He was dean of the Johns Hopkins Bloomberg School of Public Health from 1990-2005.
His research interests include outcomes assessment, child survival, epidemiology of visual disorders, glaucoma, vitamin A deficiency, blindness prevention strategies, cost-benefit analysis, the growing interface between medicine and public health, and clinical guidelines.
He was a recipient of the Danone International Prize for Nutrition in 2001 and the Albert Lasker Award for Clinical Medical Research in 1997.
In the 1970s, Sommer and his colleagues determined that children who were deficient in vitamin A deficiency were at greater risk of dying from childhood illnesses like measles and diarrhea. He further went on to prove that vitamin A supplementation could reduce child mortality from 23 to 34 percent. 
Sommer's vitamin A research was featured in the 2005 PBS documentary Rx for Survival.