Persius/hicric huggingface dataset:
Zolmitriptan overdosage

# Overdosage
There is no experience with acute overdose of zolmitriptan. Clinical study subjects who received single 50 mg oral doses of zolmitriptan commonly experienced sedation.
There is no specific antidote to zolmitriptan. In cases of severe intoxication, intensive care procedures are recommended, including establishing and maintaining a patent airway, ensuring adequate oxygenation and ventilation, and monitoring and support of the cardiovascular system.
The elimination half-life of zolmitriptan is 3 hours ; therefore, monitor patients after overdose with zolmitriptan for at least 15 hours or until symptoms or signs resolve. It is unknown what effect hemodialysis or peritoneal dialysis has on the plasma concentrations of zolmitriptan.
16 Personality Factors
The 16 Personality Factors, measured by the 16PF Questionnaire, were multivariately-derived by psychologist Raymond Cattell.
Below is a table outlining this model.

# Raymond Cattell's 16 Personality Factors
Cattell referred to these 16 factors as primary factors, as opposed to the so-called "Big Five" factors which he considered global factors. All of the primary factors correlate with global factors and could therefore be considered subfactors within them.

# Origins
In 1936 Gordon Allport and H.S. Odbert hypothesized that:
This statement has become known as the Lexical Hypothesis.
Allport and Odbert had worked through two of the most comprehensive dictionary|dictionaries of the English language available at the time, and extracted 18,000 personality-describing words. From this gigantic list they extracted 4500 personality-describing adjectives which they considered to describe observable and relatively permanent traits.
In 1946 Raymond Cattell used the emerging technology of computers to analyse the Allport-Odbert list. He organized the list into 181 clusters and asked subjects to rate people whom they knew by the adjectives on the list. Using factor analysis Cattell generated twelve factors, and then included four factors which he thought ought to appear. The result was the hypothesis that individuals describe themselves and each other according to sixteen different, independent factors.
With these sixteen factors as a basis, Cattell went on to construct the 16PF Personality Questionnaire, which remains in use by universities and businesses for research, personnel selection and the like. Although subsequent research has failed to replicate his results, and it has been shown that he retained too many factors, the current 16PF takes these findings into account and is considered to be a very good test. In 1963, W.T. Norman replicated Cattells work and suggested that five factors would be sufficient.
17-Hydroxypregnenolone

# Overview
17-Hydroxypregnenolone (also 17-OH-pregnenolone and  17-hydroxypregnenolone), is a C21 steroid that is obtained by hydroxylation of pregnenolone at the C17 position.  This step is performed by the mitochondrial cytochrome P450 enzyme 17-hydroxylase (CYP17A1)  that is present in the adrenal and gonads. Peak levels are reached in humans at the end of puberty and then decline. High levels are also achieved during pregnancy.

# Prohormone
17-OH-pregnenolone  is considered a prohormone in the formation of dehydroepiandrosterone (DHEA), itself a prohomone of the sex steroids.
This conversion is mediated by the enzyme 17,20 lyase . As such 17-OH-pregenolone represents an intermediary in the delta-5-pathway that leads from pregnenolone to DHEA. 17-hydroxypregneolone is also converted to 17-hydroxyprogesterone, a prohomone for glucocorticosteroids and androstenedione through the activity of 3-hydroxysteroid dehydrogenase.

# Neurohormone
There is some evidence that 17-OH-pregnenolone may have activity as a neurohormone.

# Clinical use
Measurements of 17-OH-pregnenolone are useful in the diagnosis of certain forms of congenital adrenal hyperplasia.
In patients with congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency 17-OH-pregnenolone is increased, while in patients with congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency levels are low to absent.
2-Arachidonoylglycerol
2-Arachidonoylglycerol (2-AG) is an endocannabinoid, an endogenous agonist of the CB1 receptor. It is an ester formed from the omega-6 fatty acid arachidonic acid and glycerol.

# Discovery
2-AG was a known chemical compound but its occurrence in mammals and its affinity for the cannabinoid receptors were first described in 1994-1995. A research group at Teikyo University reported the affinity of 2-AG for the cannabinoid receptors in 1994-1995, but the isolation of 2-AG in the canine gut was first reported in 1995 by the research group of Raphael Mechoulam at the Hebrew University of Jerusalem, which additionally characterized its pharmacological properties in vivo.

# Occurrence
2-AG, unlike anandamide (another endocannabinoid), is present at relatively high levels in the central nervous system; it is the most abundant molecular species of monoacylglycerol found in mouse and rat brain (~5-10 nmol/g tissue). Detection of 2-AG in brain tissue is complicated by the relative ease of its isomerization to 1-AG during standard lipid extraction conditions.
It has been found in maternal bovine and human milk.

# Pharmacology
Unlike anandamide, formation of 2-AG is calcium-dependent and is mediated by the activities of phospholipase C (PLC) and diacylglycerol lipase (DAGL). 2-AG acts as a full agonist at the CB1 receptor. At a concentration of 0.3 nM, 2-AG induces a rapid, transient increase in intracellular free calcium in NG108-15 neuroblastoma X glioma cells through a CB1 receptor-dependent mechanism. 2-AG is hydrolyzed in vitro by monoacylglycerol lipase (MAGL), fatty acid amide hydrolase (FAAH), and the uncharacterized serine hydrolase enzymes ABHD6 and ABHD12. The exact contribution of each of these enzymes to the termination of 2-AG signaling in vivo is unknown, though it is estimated that MAGL is responsible for ~85% of this activity.
2q37 deletion syndrome
2q37 deletion syndrome is a disorder caused by the deletion of a small piece of chromosome 2 in which one or more of 3 sub-bands, 2q37.1, 2q37.2, and 2q37.3, of the last band of one of the chromosome 2s long arms are deleted. The first report of this disorder was in 1989.

# Symptoms
The earliest signs and symptoms occur in newborns and consist of hypotonia, but show up in youth as developmental delays, low muscle tone, learning disabilities, being overweight, autism-like symptoms, seizures, eczema, asthma, chest and ear infections, and abnormalities in face, hands, and feet such as brachydactyly.
Autism-like symptoms consist of odd obsessions, repetitive behavior, poor use of eye contact, impaired speech, poor understanding of others emotions, idiosyncratic use of words or phrases.
People with this disorder also tend to have a characteristic appearance, including prominent forehead, thin, highly arched eyebrows, depressed nasal bridge, full cheeks, deficient nasal alae and prominent columella, thin upper lip, and various minor anomalies of the pinnae.
Heart, brain, gastrointestinal, and kidney problems such as Wilms tumor and , hernias, spinal curvatures, Osteopenia, hearing and sight difficulties can also occur.

# Diagnosis
Techniques used to diagnose this disorder are fluorescence in situ hybridization (FISH) and microarrays. FISH uses fluorescent dyes to visualize sections under a microscope, but some changes are too small to see. Microarray comparative genomic hybridization (array CGH) shows changes in small amounts DNA on chromosomes.

# Treatment
Therapy can help developmental delays, as well as physiotherapy for the low muscle tone. Exercise and healthy eating can reduce weight gain. Treatments are available for seizures, eczema, asthma, infections, and certain bodily ailments.

# Prognosis
While only a few adults have been reported with 2q37 microdeletion syndrome, it is predicted that this number will rise as various research studies continue to demonstrate that most with the disorder do not have a shortened life span.
Acetylcholine receptor
An acetylcholine receptor (abbreviated AChR) is an integral membrane protein that responds to the binding of the neurotransmitter acetylcholine.

# Classification
Like other transmembrane receptors, acetylcholine receptors are classified according to their "pharmacology", or according to their relative affinities and sensitivities to different molecules.  Although all acetylcholine receptors, by definition, respond to acetylcholine, they respond to other molecules as well.
- nicotinic acetylcholine receptors (nAChR, also known  as "ionotropic" acetylcholine receptors) are particularly responsive to nicotine
- muscarinic acetylcholine receptors (mAChR, also known as "metabotropic" acetylcholine receptors) are particularly responsive to muscarine.

# Receptor types
Molecular biology has shown that the nicotinic and muscarinic receptors belong to distinct protein superfamilies.

## nAChR
The nAChRs are ligand-gated ion channels, and, like other members of the "cys-loop" ligand-gated ion channel superfamily, are composed of five protein subunits symmetrically arranged like staves around a barrel. The subunit composition is highly variable across different tissues. Each subunit contains four regions named M1, M2, M3, and M4, which span the membrane and consist of approximately 20 amino acids.  The M2 region, which sits closest to the pore lumen, forms the pore lining.
Binding of acetylcholine to the N termini of each of the two alpha subunits results in the 15 rotation of all M2 helices. The cytoplasm side of the nAChR receptor has rings of high negative charge that determine the specific cation specificity of the receptor and remove the hydration shell often formed by ions in aqueous solution. In the intermediate region of the receptor, within the pore lumen, valine and leucine residues (Val 255 and Leu 251) define a hydrophobic region which the dehydrated ion must pass through.
nAChR is found at the edges of junctional folds at the neuromuscular junction on the postsynaptic side, and is activated by acetylcholine release across the synapse. The diffusion of Na+ and K+ across the receptor causes depolarization, the end-plate potential, that opens voltage-gated sodium channels, which allows for firing of the action potential and potentially muscular contraction.

## mAChR
In contrast, the mAChRs are not ion channels, but belong instead to the superfamily of G-protein-coupled receptors that activate other ionic channels via a second messenger cascade.

# Role in health and disease
Nicotinic acetylcholine receptors can be blocked by curare and toxins present in the venoms of snakes and shellfishes, like -bungarotoxin. Drugs such as the neuromuscular blocking agents bind reversibly to the nicotinic receptors in the neuromuscular junction and are used routinely in anaesthesia.
Nicotinic receptors are the primary mediator of the effects of nicotine. In myasthenia gravis, the receptor is targeted by antibodies, leading to muscle weakness. 
Muscarinic acetylcholine receptors can be blocked by the drugs atropine and scopolamine.
Azobisisobutyronitrile

# Overview
Azobisisobutyronitrile is a toxic compound often used as a foamer in plastics and rubber and as a radical initiator. It is commonly known as AIBN. Its most common chemical reaction is one of decomposition,  eliminating a molecule of nitrogen gas to form two 2-cyanoprop-2-yl radicals:
These radicals can be used to to initiate free radical polymerizations and other radical reactions. For instance a mixture of styrene and maleic anhydride in toluene will react if heated, forming the polystyrene polymer, only very slowly unless an initiator such an AIBN is present. Another example of a radical reaction that can be initiated by AIBN is the anti-Markovnikov hydrohalogenation of alkenes.
AIBN is safer to use than benzoyl peroxide (another radical initiator) because the risk of explosion is far smaller. However, it is considered a flammable solid.  
It is soluble in methanol and ethanol, but is insoluble in water. It can explode if dissolved in acetone.
AIBN is highly toxic. Wear a respirator/dust mask, protective gloves, & safety glasses when handling AIBN.
Several water-soluble azo initiators similar to AIBN are manufactured by DuPont and Wako.
Aldehyde dehydrogenase

# Overview
Aldehyde dehydrogenases are a group of enzymes that catalyse the oxidation (dehydrogenation) of aldehydes.  Multiple forms exist in mammals in the cytosol, mitochondria and endoplasmic reticulum.  They have been classified as Class 1 (cytosolic), Class 2 (mitochondrial) and Class 3 (tumour and other isozymes).  In all three classes constitutive and inducible forms exist.
The overall reaction catalysed by the aldehyde dehydrogenases is:
Aldehyde dehydrogenases have a broad substrate specificity.  Oxidation of aldehydes is considered to be generally a detoxification reaction, removing the electrophilic products of alcohol oxidation.
For example, alcohol dehydrogenase oxidizes ethanol to acetaldehyde, responsible for some hangover symptoms, and acetaldehyde dehydrogenase detoxifies this to acetic acid.  Similarly aldehyde dehydrogenase detoxifies acrolein, the hepatotoxic metabolite formed from allyl alcohol.  However, in the case of 2-butoxyethanol, alcohol and aldehyde dehydrogenases sequentially catalyse the formation of the hematotoxic metabolite, 2-butoxyacetic acid.
Aldehyde dehydrogenases can also behave as esterases, hydrolyzing esters such as para-nitrophenyl acetate.
A deficiency in these enzymes or a polymorphism which renders the enzyme inactive results in alcohol intolerance. Consumption of alcohol results in allergy-like symptoms including nasal congestion and flushing. This is most common of East Asian decent, and about 50% of Chinese, Korean and Japanese are somewhat alcohol intolerant. These symptoms are sometimes referred to as oriental flushing syndrome
-r 'asian flush'.

# Genes
- ALDH1A1, ALDH1A2, ALDH1A3, ALDH1B1, ALDH1L1, ALDH1L2
- ALDH2
- ALDH3A1, ALDH3A2, ALDH3B1, ALDH3B2
- ALDH4A1
- ALDH5A1
- ALDH6A1
- ALDH7A1
- ALDH8A1
- ALDH9A1
- ALDH16A1
- ALDH18A1
Antinuclear antibodies

# Overview
Anti-nuclear antibodies are antibodies directed against the cell nucleus. They are raised in several conditions, usually in an auto-immune condition where the immune system makes antibodies to fight its own body. Normally a test (see External Links) is administered in people with many arthritic type symptoms or skin rashes to exclude systemic lupus erythematosus(SLE). The rashes could be over both cheeks and shaped like a butterfly, or a wolf. They are known to affect almost any part of the body including kidneys and brain.

# Interpreting Test Results
- A high ANA titer may indicate systemic lupus erythematosus (SLE). SLE can be present with titers from 1 to 40 and higher. Almost all people with SLE have a high ANA titer. However, most people with a high ANA titer do not have SLE. Only about one-third of people who are referred to a rheumatologist for high ANA titers are diagnosed with SLE. Other conditions may cause a high ANA titer. About 30% to 40% of people with rheumatoid arthritis have a high ANA titer. 
- Many conditions may result in a high ANA titer. These conditions include autoimmune diseases, such as scleroderma, Sjogren's syndrome, juvenile rheumatoid arthritis, and myositis. Other conditions with a high ANA titer include Raynaud's syndrome, viral infections, and liver disease. Although an ANA titer may help support a diagnosis for these conditions, it is not used by itself to confirm a diagnosis. A thorough medical history, physical examination, and other tests are needed to confirm a suspected autoimmune disease.
- Some apparently healthy individuals have high levels of antinuclear antibodies. For instance, some people with a family history of autoimmune disease may have a high ANA titer. The higher the titer, however, the more likely it is that the person has an autoimmune disease.
- Positive ANA is also commonly seen in Sjogren's Syndrome, the second most common auto-immune disease (more common than Lupus)

# Differential Diagnosis
- Advanced age
- Chronic active hepatitis
- Cirrhosis
- Drugs
- HIV infection
- Mixed Connective Tissue Disease
- Multiple Sclerosis
- Necrotizing vasculitis
- Periarteritis nodosa
- Pregnant women
- Pulmonary Fibrosis
- Raynaud's Disease
- Rheumatoid Arthritis
- Silicone gel implants
- Sjogren's Syndrome
- Subacute bacterial endocarditis
- Systemic Lupus Erythematosus
- Tuberculosis
- Diabetes Mellitus (Type I)
Analysis of covariance

# Overview
Analysis of covariance (ANCOVA) is a general linear model with one continuous explanatory variable and one or more factors. ANCOVA is a merger of ANOVA and regression for continuous variables. ANCOVA tests whether certain factors have an effect after removing the variance for which quantitative predictors (covariates) account. The inclusion of covariates can increase statistical power because it accounts for some of the variability.

# Assumptions
As any statistical procedure, ANCOVA makes certain assumptions about the data entered into the model. Only if these assumptions are met, at least approximately, ANCOVA will yield valid results. Specifically, ANCOVA, just like ANOVA, assumes that the dependent variable is normally distributed and homoscedastic. Further, since ANCOVA is a regression-based method, the relationship of the dependent variable to the independent variable(s) must be linear in the parameters, as in regression analysis.

# Power considerations
While the inclusion of a covariate into a ANOVA generally increases statistical power by accounting for some of the variance in the dependent variable and thus increasing the ratio of variance explained by the independent variables, adding a covariate into ANOVA also reduces the degrees of freedom (see below). Accordingly, adding a covariate which accounts for very little variance in the dependent variable might actually reduce power.

# ANCOVA vs. block design
While for block design, subjects are first separated into homogeneous groups (blocks) based on the concomitant variable  and those within a given block are then randomly assigned into the different treatment groups; for ANCOVA, Subjects are measured on the covariate(s) and are randomly assigned into the different treatment groups without regard for their scores/values on the covariate(s). Block design control the effect of covariates by design, and ANCOVA control the effect of covariate through statistical analysis (statistical control)
Antepartum haemorrhage
For patient information on Placental abruption, click here
For patient information on Placenta previa, click here
Synonyms and keywords:  Antepartum hemorrhage; APH

# Overview
In obstetrics, antepartum haemorrhage  is bleeding from the vagina during pregnancy from twenty weeks gestational age to term.
It should be considered a medical emergency (regardless of whether there is pain) and medical attention should be sought immediately, as if it is left untreated it can lead to death of the mother and/or fetus.
Bleeding without pain is most frequently bloody show, which is benign; however, it may also be placenta previa (in which both the mother and fetus are in danger).  Painful APH is most frequently placental abruption.

# Causes
- Bloody show (benign) - most common cause of APH
- Placental abruption - most common pathological cause
- Placenta previa - second most common pathological cause
- Vasa previa - often difficult to diagnose, frequently leads to fetal demise
- Uterine rupture
- Bleeding from the lower genital tract
Cervical bleeding - cervicitis, cervical neoplasm, cervical polyp
Bleeding from the vagina itself - trauma, neoplasm
- Cervical bleeding - cervicitis, cervical neoplasm, cervical polyp
- Bleeding from the vagina itself - trauma, neoplasm
- Bleeding that may be confused with vaginal bleeding
GI bleed - hemorrhoids, inflammatory bowel disease
Urinary tract bleed - urinary tract infection
- GI bleed - hemorrhoids, inflammatory bowel disease
- Urinary tract bleed - urinary tract infection

# Related Chapters
- Obstetrical hemorrhage
Retinoic acid syndrome
Synonyms and keywords: APML differentiation syndrome; APL differentiation syndrome

# Overview
Retinoic acid syndrome (RAS) is a potentially life-threatening complication observed in patients with acute promyelocytic leukemia (APML) and first thought to be specifically associated with all-trans retinoic acid (ATRA) (also known as tretinoin) treatment.  Subsequently it was recognized that so-called RAS appeared in APML patients who had been treated with another highly efficacious drug, arsenic trioxide, and yet did not appear in patients treated with tretinoin for other disorders.  These facts and others support the notion that RAS depends on the presence of the malignant promyelocytes.  This has led to the growing deprecation of the term 'retinoic acid syndrome' and to an increasing use of the term differentiation syndrome to signify this APML treatment complication.

# Pathophysiology
Several mechanisms have been speculated including a capillary leak syndrome from cytokine release from the differentiating myeloid cells. Mediation by cathepsin G has also been suggested.

# Causes
The etiology of RAS remains unclear.  Alternatively, all-trans retinoic acid (ATRA) and arsenic trioxide may cause the maturing myeloid cells to acquire the ability to infiltrate organs such as the lung.

# Diagnosis

## Symptoms
The syndrome is characterized by dyspnea, fever, weight gain, hypotension, and pulmonary infiltrates.

## Laboratory Findings
An elevated white count is sometimes associated with this syndrome, but is not a prerequisite.

# Treatment
The treatment of RAS usually involves administering dexamethasone IV, with the dosage usually 10 mg BID for ten days. It is important for patients to discontinue the use of tretinoin due to the elevation of WBC and possible low blood oxygen.
Once RAS has resolved, pro-differentiation chemotherapy can be resumed.