Persius/hicric huggingface dataset:
Viral gastroenteritis overview

# Overview
Gastroenteritis is the inflammation of the stomach and the small and large intestines. Viral gastroenteritis is an infection caused by a variety of viruses that results in vomiting or diarrhea. It is often called the "stomach flu," although it is not caused by the influenza viruses.

# Causes
Many different viruses can cause gastroenteritis, including rotaviruses, noroviruses, adenovirus type 40 or 41, sapoviruses, and astroviruses. Viral gastroenteritis is not caused by bacteria (such as Salmonella or Escherichia coli) or parasites (such as Giardia), or by medications or other medical conditions, although the symptoms may be similar.

# Diagnosis

## Laboratory Findings
Rotavirus infection can be diagnosed by laboratory testing of a stool specimen. Tests to detect other viruses that cause gastroenteritis are not in routine use, but the viral gastroenteritis unit at the CDC can assist with special analysis upon request.

# Treatment

## Medical Therapy
The most important aspect of treating viral gastroenteritis in children and adults is to prevent dehydration. This treatment should begin at home. A physician may give specific instructions about what kinds of fluid to give. CDC recommends that families with infants and young children keep a supply of oral rehydration solution (ORS) at home at all times and use the solution when diarrhea first occurs in the child. Medications, including antibiotics (which have no effect on viruses) and other treatments, should be avoided unless specifically recommended by a physician.

# Diagnosis

## Primary Prevention
Currently, there is a licensed rotavirus vaccine available that protects against severe diarrhea from rotavirus infection in infants and young children. Studies into a norovirus vaccine are underway.
Persons can reduce their chance of getting infected by frequent handwashing, prompt disinfection of contaminated surfaces with household chlorine bleach-based cleaners, and prompt washing of soiled articles of clothing. If food or water is thought to be contaminated, it should be avoided.
Voriconazole contraindications

# Contraindications
VFEND is contraindicated in patients with known hypersensitivity to voriconazole or its excipients. There is no information regarding cross-sensitivity between VFEND (voriconazole) and other azole antifungal agents. Caution should be used when prescribing VFEND to patients with hypersensitivity to other azoles.
Coadministration of terfenadine, astemizole, cisapride, pimozide or quinidine with VFEND is contraindicated because increased plasma concentrations of these drugs can lead to QT prolongation and rare occurrences of torsade de pointes .
Coadministration of VFEND with sirolimus is contraindicated because VFEND significantly increases sirolimus concentrations .
Coadministration of VFEND with rifampin, carbamazepine and long-acting barbiturates is contraindicated because these drugs are likely to decrease plasma voriconazole concentrations significantly.
Coadministration of VFEND with high-dose ritonavir (400 mg q12h) is contraindicated because ritonavir (400 mg q12h) significantly decreases plasma voriconazole concentrations. Coadministration of voriconazole and low-dose ritonavir (100 mg q12h) should be avoided, unless an assessment of the benefit/risk to the patient justifies the use of voriconazole.
Coadministration of VFEND with rifabutin is contraindicated since VFEND significantly increases rifabutin plasma concentrations and rifabutin also significantly decreases voriconazole plasma concentrations .
Coadministration of VFEND with ergot alkaloids (ergotamine and dihydroergotamine) is contraindicated because VFEND may increase the plasma concentration of ergot alkaloids, which may lead to ergotism.
Coadministration of VFEND with St. John's Wort is contraindicated because this herbal supplement may decrease voriconazole plasma concentration.
Wells score for DVT (original)

# Overview

# Wells Score Calculator for DVT
This handy calculator computes the pre-test probability of deep vein thrombosis (DVT) using Wells criteria.
Check all boxes that apply to your patient:
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score -= 2;}
document.forms.value = score;
if(score <= 0){document.forms.value = "Low probability of DVT: Prevalence = 5%, Consider checking D-dimer";}
if(score == 1 || score == 2){document.forms.value = "Moderate probability of DVT: Prevalence = 17%, Consider checking D-dimer";}
if(score >= 3){document.forms.value = "High probability of DVT: Prevalence = 53%, Consider imaging of the deep veins";}

# Interpretation
The interpretation of the score is as follows:
- Score 3: High pretest probability (Prevalence of DVT - 75%)
- Score 1-2: Moderate pretest probability (Prevalence of DVT - 17%)
- Score 0: Low pretest probability (Prevalence of DVT - 3%)

# Limitations of Wells Score
- The accuracy of the Wells rule, though useful in secondary and tertiary care centers, has not been properly validated for use in primary care patients with the suspicion of DVT.
- The performance of the Wells score was decreased when evaluating elderly patients, patients with a prior DVT, or patients having other comorbidities. These results may be equivalent to what is found in a primary care setting. Also, it should be highlighted that Wells criteria is an additional tool to diagnosis rather than being a stand-alone test.
Xanthoma (patient information)
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# What is Xanthoma?
Xanthoma is a skin condition in which fat builds up under the surface of the skin.

# What are the symptoms of Xanthoma?
A xanthoma looks like a sore or bump under the skin. It's usually flat, soft to the touch, and yellow in color. It has sharp, distinct edges.

# What causes Xanthoma?
Xanthomas are common, particularly among older adults and people with high blood lipids.
Xanthomas vary in size. Some are very small, while others are bigger than 3 inches in diameter. They may appear anywhere on the body, but are most often seen on the elbows, joints, tendons, knees, hands, feet, or buttocks.
They may be a sign of a medical condition that involves an increase in blood lipids. Such conditions include:
- Certain cancers
- Diabetes
- Inherited metabolic disorders such as familial hypercholesterolemia
- Primary biliary cirrhosis
Xanthelasma palpebra, a common type of xanthoma that appears on the eyelids and may occur without any underlying medical condition, is not necessarily associated with elevated cholesterol or lipids.

# Who is at risk for Xanthoma?
Older adults and people with high blood lipids are at risk for xanthoma.

# How do I know I have Xanthoma?
Your health care provider will examine the skin. Usually, a diagnose of xanthoma can be made by looking at your skin. A biopsy of the growth will show a fatty deposit.
You may have blood tests done to check lipid levels, liver function, and for diabetes.

# When to seek urgent medical care
Call your health care provider if xanthomas develop. They may indicate an underlying disorder that needs treatment.

# Treatment options
If you have a disease that causes increased blood lipids, treating the condition may help reduce the development of xanthomas.
If the growth bothers you, your doctor may remove it. However, xanthomas may come back after surgery.

# Where to find medical care for Xanthoma
Directions to Hospitals Treating Xanthoma

# What to expect (Outlook/Prognosis)
The growth is non-cancerous and painless, but may be a sign of another medical condition.

# Possible complications
The growth may cause a change in how you look. This is called cosmetic disfiguring.

# Sources
Zinc dependent phospholipase C
Zinc dependent prokaryotic phospholipases C  is a family of bacterial phospholipases C, some of which are also known as alpha toxins.
Bacillus cereus contains a monomeric phospholipase C EC 3.1.4.3 (PLC) of 245 amino-acid residues. Although PLC prefers to acton phosphatidylcholine, it also shows weak catalytic activity with sphingomyelin and phosphatidylinositol. Sequence studies have shown the protein to be similar both to alpha toxin fromClostridium perfringens and Clostridium bifermentans, a phospholipase C involved in haemolysis and cell rupture, and to lecithinase from Listeria monocytogenes, which aids cell-to-cell spread by breaking down the 2-membrane vacuoles that surround the bacterium during transfer.
Each of these proteins is a zinc-dependent enzyme, binding 3 zinc ions per molecule. The enzymes catalyse the conversion of phosphatidylcholine and water to 1,2-diacylglycerol and choline phosphate.
In Bacillus cereus, there are nine residues known to be involved in binding the zinc ions: 5 His, 2 Asp, 1 Glu and 1 Trp. These residues are all conserved in the Clostridium alpha-toxin.
Zolmitriptan contraindications

# Contraindications
Zolmitriptan is contraindicated in patients with:
- Ischemic coronary artery disease (angina pectoris, history of myocardial infarction, or documented silent ischemia), other significant underlying cardiovascular disease, or coronary artery vasospasm including Prinzmetals angina 
- Wolff-Parkinson-White syndrome or arrhythmias associated with other cardiac accessory conduction pathway disorders 
- History of stroke, transient ischemic attack (TIA), or history of hemiplegic or basilar migraine because these patients are at a higher risk of stroke 
- Peripheral vascular disease (PVD) 
- Ischemic bowel disease 
- Uncontrolled hypertension 
- Recent use (i.e., within 24 hours) of another 5-HT1 agonist, ergotamine-containing medication, or ergot-type medication (such as dihydroergotamine or methysergide) 
- Concurrent administration of a monoamine oxidase (MAO)-A inhibitor or recent use of a MAO-A inhibitor (that is within 2 weeks) 
- Known hypersensitivity to zolmitriptan (angioedema and anaphylaxis seen)
Zolmitriptan drug interactions

# Drug Interactions

### 7.1 Ergot-containing Drugs
Ergot-containing drugs have been reported to cause prolonged vasospastic reactions. Because these effects may be additive, use of ergotamine-containing or ergot-type medications (like dihydroergotamine or methysergide) and zolmitriptan within 24 hours of each other is contraindicated .

### 7.2 MAO-A Inhibitors
MAO-A inhibitors increase the systemic exposure of zolmitriptan and its active N-desmethyl metabolite. Therefore, the use of zolmitriptan in patients receiving MAO-A inhibitors is contraindicated .

### 7.3 5-HT1B/1D agonists
Concomitant use of other 5-HT1B/1D agonists (including triptans) within 24 hours of zolmitriptan treatment is contraindicated because the risk of vasospastic reactions may be additive .

### 7.4 Selective Serotonin Reuptake Inhibitors and Serotonin Norepinephrine Reuptake Inhibitors
Cases of life-threatening serotonin syndrome have been reported during co-administration of triptans and selective serotonin reuptake inhibitors (SSRIs) or serotonin norepinephrine reuptake inhibitors (SNRIs) .

### 7.5 Cimetidine
Following administration of cimetidine, the half-life and blood levels of zolmitriptan and its active N-desmethyl metabolite were approximately doubled . If cimetidine and zolmitriptan are used concomitantly, limit the maximum single dose of zolmitriptan to 2.5 mg, not to exceed 5 mg in any 24-hour period .
Zori Stalker Williams syndrome

# Overview
Zori Stalker Williams syndrome is a rare syndrome associated with a range of diseases and symptoms such as Pectus excavatum, macrocephaly and dysplastic nails, familial short stature, developmental delay and distinctive facies. Further signs are known to be associated with this syndrome.
The name originates from the researchers who first defined and noticed the syndrome and its clinical signs.
It is believed that the syndrome is inherited in an autosomal dominant pattern, though there has been no new research undertaken for this rare disease.
ACES (nutritional supplement)
Antioxidant supplements with varying amounts of carotene(s) for (pro) vitamin A, vitamin C, vitamin E and Selenium are known by the acronym, ACES. The commercial ACES formulas are a first generation, high potency, combined antioxidant that vary in component concentrations, specific components or source, and their ratio according to manufacturer and are available as both tablet and capsule.
Beta-carotene, one of over 600 carotenoids, has been the most common ingredient for vitamin A activity in ACES formulas.  Ascorbic acid and ascorbates are the common ingredients to deliver vitamin C activity.  Vitamin E content has commonly varied among d,l-alpha-tocopheryl acetate (all-rac alpha-tocopheryl acetate), d-alpha-tocopheryl acetate, d-alpha-tocopheryl succinate, and d-alpha-tocopherol.  Selenium content has been delivered as selenate, selenium containing nutritional yeast and selenium containing organic forms such as L-Selenomethionine and L-selenium-methylselenocysteine, again varying with manufacturer.  More recent ACES formulas may use mixed natural carotene sources that include other carotenes such as zeaxanthin, alpha carotene, cryptoxanthin, lutein and lycopene.  Mixed tocopherols with varied proportions of R,R,R-alpha-tocopherol, R,R,R-beta-tocopherol, R,R,R-gamma-tocopherol and R,R,R-delta-tocopherol are other suitable sources of vitamin E content in ACES formulas.
Popularly known as "ACES" in the 1980s during a period of rapid commercial growth and public awareness, these formulas have frequently expanded and differentiated by adding minor amounts other antioxidants such as lipoic acid, pycnogenol, coenzyme Q-10, N-acetyl cysteine, as well as other nutrients that again vary with manufacturer, and are often simply referred to as super antioxidants or a branded, proprietary trade name.
Various ACES formulations will typically contain 10,000-25,000 IU carotenes, 250 mg - 1000 mg vitamin C, 200-400 IU alpha-tocopherol, and 50 mcg- 200 mcg selenium content per serving of one to three units (tablet or capsule), as well as other nutrients in more recent antioxidant formulations.
AIR synthetase (FGAM cyclase)
AIR synthetase is the fifth enzyme in the de novo synthesis of purine nucleotides. It catalyzes the reaction to form 5-aminoimidizole ribonucleotide (AIR) from formylglycinamidine-ribonucleotide FGAM. This reaction closes the ring and produces a 5-membered imidazole ring of the purine nucleus (AIR). AIR synthetase catalyzes the transfer of the oxygen of the formyl group to phosphate. It is a sequential mechanism in which ATP binds first to the enzyme and ADP is released last. This enzyme hydrolyzes ATP to activate the oxygen of the amide in order to carry out a nucleophilic attack by a nitrogen. The enzyme contains 388 amino acids and has an estimated molecular mass of 40.4 kDa.

# Purine Synthesis
Purines are one of the two types of nitrogenous heterocyclic bases, which are one of the three components of the nucleotides that make up nucleic acids. Synthesis can be de novo or salvage - AIR synthetase is a component of the de novo pathway. The first committed step of the de novo pathway begins with phosphoribose pyrophosphate (PRPP) and the end product is inosine monophospate (IMP). IMP is eventually converted to either AMP or GMP purines. The purine ring structure is composed by the attachment of 1 or 2 atoms at a time to the ribose sugar. The de novo pathway tends to be conserved across most organisms.

# Cowpea AIR synthetase
AIR synthetase is found in both mitochondria and plastids; the mitochondrial form has 5 more amino acids than the plastid form.   The enzyme is encoded by a single gene in cowpeas despite the fact that it exists in different forms in plastids and mitochondria. This suggests that the different versions may be derived from a single transcript. One study proposes that there is tight transcriptional control of pur5, the gene encoding AIR synthetase.
Abbreviated mental test score

# Overview
The abbreviated mental test score (AMTS) was introduced by Hodkinson in 1972 to rapidly assess elderly patients for the possibility of dementia. Its uses in medicine have become somewhat wider, e.g. to assess for confusion, although it has mainly been validated in the elderly.
The following questions are put to the patient. Each question correctly answered scores one point. A score of less than 6 suggests dementia, although further and more formal tests are necessary to confirm the diagnosis.
An alternative to the AMTS is the 30 point mini-mental state examination (MMSE).
Abdominal distension overview

# Overview
Abdominal distension is most commonly caused by gas or intolerance of certain foods, but sometimes it is a sign of a more serious underlying disease or condition. For this reason, if the abdominal distension is new, different, or does not respond to over-the-counter medications, it is recommended to see a physician.

# Causes
Abdominal distension  can be a sign of many conditions affecting many organ systems.  

# Treatment

## Surgery
Surgery is done if the underlying cause is a bowel obstruction, a hernia or a tumor.
Abscess (patient information)
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# Overview
An abscess is a collection of pus in any part of the body that, in most cases, causes swelling and inflammation around it.

# What are the symptoms of Abscess?
Symptoms of an abscess depend largely on where the abscess forms. Some common symptoms include:
- Pain at the site of  the abscess
- Chills
- Fever
- Decreased function in the affected part of the body
- General discomfort, uneasiness, or ill feeling
- Headache
- Local swelling, hardening of tissue
- Loss of appetite
- Loss of sensation in the affected area
- Nausea and vomiting
- Swelling

# What causes Abscess?
Abscesses occur when an area of tissue becomes infected and the body's immune system tries to fight it. White blood cells move through the walls of the blood vessels into the area of the infection and collect within the damaged tissue. During this process, pus forms. Pus is the buildup of fluid, living and dead white blood cells, dead tissue, and bacteria or other foreign substances. Abscesses can form in almost any part of the body. The skin, under the skin, and the teeth are the most common sites. Abscesses may be caused by bacteria, parasites, and foreign substances.Abscesses in the skin are easy to see. They are red, raised, and painful. Abscesses in other areas of the body may not be obvious, but they may cause significant organ damage. Some specific type of abscesses are:
- Abdominal abscess
- Amebic liver abscess
- Anorectal abscess
- Bartholin's abscess
- Brain abscess
- Epidural abscess
- Peritonsillar abscess
- Pyogenic liver abscess
- Skin abscess
- Spinal cord abscess
- Subcutaneous abscess
- Tooth abscess

# Who is at highest risk?
People with recent history of infection are at increased risk for abscess.

# When to seek urgent medical care?
Call your health care provider if you think that you may have any type of abscess.

# Diagnosis
Often, a sample of fluid will be taken from the abscess and tested to see what organism is causing the problem.

# Treatment options
Treatment varies, but often surgery, antibiotics, or both are needed.

# Where to find medical care for Abscess?
Directions to Hospitals Treating Abscess

# What to expect (Outlook/Prognosis)?
The prognosis depends on site of infection, type of organisms causing it and the patient profile(age, immunity status, comorbidities)

# Possible complications
It can spread to other parts of body through blood(septicemia)

# Sources
Sakati-Nyhan-Tisdale syndrome

# Overview
Sakati-Nyhan-Tisdale Syndrome, also called acrocephalopolysyndactyly type III, is a rare genetic disorder that has been associated with abnormalities in the bones of the legs, congenital heart defects and craniofacial defects. The syndrome belongs to a group of rare genetic disorders known as acrocephalopolysyndactyly  or ACPS, for short.

# Eponym
The disease was named after a female Syrian pediatrician named Nadia Awni Sakati and her two American counterparts, William Leo Nyhan  and W.K. Tisdale, who were working alongside with her in the pediatrics department at University of California, San Diego.
It was characterized in 1971.

# Presentation
The syndrome was first reported in an eight-year old boy, but very few cases have been reported since then. The syndrome is detected by multiple abnormalities noted at birth involving the head, limbs, heart, ears, and skin. The syndrome is characterized by premature closure of the fibrous joints between certain bones of the skull in a process known as craniosynostosis. As documented in the first case of the syndrome, the victim tends to suffer from cyanosis, and other respiratory and breathing infections, all before the age of one. Body development subsequently slows down, but some problems can be fixed under proper guidance from other individuals, such as learning to walk with special crutches by five years of age. Craniofacial problems are present, but have no effect on the patient's intelligence and mental growth.
Most problems resulting from the syndrome are physical. It causes Acrocephaly, making the head appear pointed, and webbing or syndactyly of certain toes or fingers.

# Causes
Although no cause has been officially confirmed, researchers speculate the disease might result from a genetic mutation that sporadically occurs for unknown reasons.
Advanced sleep phase syndrome

# Overview
Advanced sleep phase syndrome (ASPS) is a sleep disorder in which patients feel very sleepy early in the evening (e.g. 18:00-19:00) and wake up very early in the night (e.g. midnight, 1:00, etc.). It is the opposite of delayed sleep phase syndrome. ASPS is frequently encountered in the elderly and in post-menopausal women. It can be treated pharmacologically, with evening bright lights, or behaviorally with chronotherapy or free-running sleep.

# Familial Advanced Sleep Phase Syndrome (FASPS)
In 1999, Louis Ptaceks research group at the University of California, San Francisco reported findings of a human circadian rhythm disorder showing a familial tendency. The disorder was characterized by a life-long pattern of sleep onset around 7:30pm and offset around 4:30am. Among three lineages, 29 people were identified as affected with this familial advanced sleep-phase syndrome (FASPS), and 46 were considered unaffected. The pedigrees demonstrated FASPS to be a highly penetrant, autosomal dominant trait.
Two years after reporting the finding of FASPS, Ptaceks group published results of genetic sequencing analysis on a family with FASPS. To narrow their search they took a cue from research on Per mutations in Drosophila and mouse models, which produced short-day mutants and were predicted to produce a phase advance in humans. With this guidance they quickly found what they were looking for. Sequencing of the hPer2 gene revealed a serine-to-glycine point mutation in the CK1 binding domain of the hPER2 protein.
In 2005, Ptaceks lab reported discovery of a different mutation causing FASPS. This time the CK1 was implicated, demonstrating an A-to-G missense mutation that resulted in a threonine-to-alanine alteration in the protein. The evidence for both of these reported causes of FASPS is strengthened by the absence of said mutations in all tested control subjects.

# Related Chapters
- Circadian rhythm sleep disorder
- Delayed sleep phase syndrome
- Non-24-hour sleep-wake syndrome