Persius/hicric huggingface dataset:
Lysinuric protein intolerance
Lysinuric protein intolerance (LPI), also named hyperdibasic aminoaciduria type 2 or familial protein intolerance, is an autosomal recessive disorder of diamino acid transport. About 100 patients have been reported, almost half of them of Finnish origin.

# Etiology
In LPI, urinary  excretion of cationic amino acids (ornithine, arginine and lysine) is increased and these amino acids are poorly absorbed from the intestine. Therefore, their plasma concentrations are low and their body pools become depleted. Deficiency of arginine and ornithine restricts the function of the urea cycle and leads to hyperammonemia after protein-rich meals. Deficiency of lysine may play a major role in the skeletal and immunological abnormalities observed in LPI patients.

# Diagnostics
The diagnosis is based on the biochemical findings (increased concentrations of lysine, arginine and ornithine in urine and low concentrations of these amino acids in plasma, elevation of urinary orotic acid excretion after protein-rich meals, and inappropriately high concentrations of serum ferritin and lactate dehydrogenase isoenzymes) and the screening of known mutations of the causative gene from a DNA sample.

# Symptoms
Infants with LPI are usually symptom-free when breastfed because of the low protein concentration in human milk, but develop vomiting and diarrhea after weaning. The patients show failure to thrive, poor appetite, growth retardation, enlarged liver and spleen, prominent osteoporosis, delayed bone age and spontaneous protein aversion. Forced feeding of protein may lead to convulsions and coma. Mental development is normal if prolonged episode of hyperammonemia can be avoided. Some patients develop severe pulmonary and renal complications. High levels of plasma glutamine and glycine are observed.

# Treatment and prognosis
Treatment of LPI consists of protein-restricted diet and supplementation with oral citrulline. Citrulline is a neutral amino acid that improves the function of the urea cycle and allows sufficient protein intake without hyperammonemia. Under proper dietary control and supplementation, the majority of the LPI patients are able to have a nearly normal life.
Divalproex sodium description

# Description
Divalproex sodium is a stable co-ordination compound comprised of sodium valproate and valproic acid in a 1:1 molar relationship and formed during the partial neutralization of valproic acid with 0.5 equivalent of sodium hydroxide. Chemically it is designated as sodium hydrogen bis(2-propylpentanoate). Divalproex sodium has the following structure:
Divalproex sodium occurs as a white powder with a characteristic odor.
Depakote tablets are for oral administration. Depakote tablets are supplied in three dosage strengths containing divalproex sodium equivalent to 125 mg, 250 mg, or 500 mg of valproic acid.

### Inactive Ingredients
Depakote tablets: cellulosic polymers, diacetylated monoglycerides, povidone, pregelatinized starch (contains corn starch), silica gel, talc, titanium dioxide, and vanillin.
In addition, individual tablets contain:
125 mg tablets: FD&C Blue No. 1 and FD&C Red No. 40.
250 mg tablets: FD&C Yellow No. 6 and iron oxide.
500 mg tablets: D&C Red No. 30, FD&C Blue No. 2, and iron oxide.
Dorsal interossei of the foot

# Overview
The dorsal interossei, four in number, are situated between the metatarsal bones.
They are bipenniform muscles, each arising by two heads from the adjacent sides of the metatarsal bones between which it is placed; their tendons are inserted into the bases of the first phalanges, and into the aponeurosis of the tendons of the Extensor digitorum longus.
In the angular interval left between the heads of each of the three lateral muscles, one of the perforating arteries passes to the dorsum of the foot; through the space between the heads of the first muscle the deep plantar branch of the dorsalis pedis artery enters the sole of the foot.
The first is inserted into the medial side of the second toe; the other three are inserted into the lateral sides of the second, third, and fourth toes.
Posterior interosseous artery
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The posterior interosseous artery (dorsal interosseous artery) is an artery of the forearm.
It passes backward between the oblique cord and the upper border of the interosseous membrane. It appears between the contiguous borders of the supinator and the abductor pollicis longus, and runs down the back of the forearm between the superficial and deep layers of muscles, to both of which it distributes branches.
Where it lies upon the abductor pollicis longus and the extensor pollicis brevis, it is accompanied by the dorsal interosseous nerve.
At the lower part of the forearm it anastomoses with the termination of the volar interosseous artery, and with the dorsal carpal network.
It gives off, near its origin, the interosseous recurrent artery, which ascends to the interval between the lateral epicondyle and olecranon, on or through the fibers of the Supinator, but beneath the anconeus, and anastomoses with the radial collateral branch of the profunda brachii, the posterior ulnar recurrent and the inferior ulnar collateral.

# Additional images
- Left elbow-joint, showing anterior and ulnar collateral ligaments.
- Cross-section through the middle of the forearm.
Dorsal nucleus of vagus nerve

# Overview
The dorsal nucleus of the vagus nerve (or posterior motor nucleus of vagus) is a cranial nerve nucleus for the vagus nerve that arises from the floor of the fourth ventricle.

# Additional images
- Section of the medulla oblongata at about the middle of the olive.
- The cranial nerve nuclei schematically represented; dorsal view. Motor nuclei in red; sensory in blue.
- Primary terminal nuclei of the afferent (sensory) cranial nerves schematically represented; lateral view.
Epidermolysis bullosa simplex

# Overview
Epidermolysis bullosa simplex (EBS) is a disorder resulting from mutations in the genes encoding keratin 5 or keratin 14.
Blister formation of EBS is within the basal keratinocyte of the epidermis. Sometimes EBS is called epidermolytic.

# Subtypes
There are four subtypes of EBS:
- EBS - Weber-Cockayne (EBS-WC)
- EBS - Koebner (EBS-K)
- EBS - Meara (EBS-DM)
- EBS - Mottled pigmentation (EBS-MP)

## Weber-Cockayne
Weber-Cockayne is the mildest form of EBS, leading to blistering of the hands and feet since these are most susceptible to frequent abrasion. The presence of heat and humidity, either through climate or physical activity, accelerates the formation of blisters. Typically, the blisters formed are tense and painful, and make walking difficult. Carefully lancing, draining and bandaging the blisters can provide relief and prevent them from expanding.

## Koebner
Koebner results in generalised blisters.

## Dowling-Meara
Dowling-Meara (EBS-DM) is the most severe form of EBS, leading to clusteres of blisters and spherical keratin aggregates. It results from a missense mutation in KRT5 (E477K) or one of two missense mutations in KRT14 (R125C and R125H)

## Mottled pigmentation
Mottled pigmentation (EBS-MP) is caused by one missense mutation in KRT5 (I161S) or by missense mutations in the plectin gene.

# Diagnosis

## Physical Examination

### Skin
- Epidermolysis bullosa simplex. Adapted from Dermatology Atlas.
- Epidermolysis bullosa simplex. Adapted from Dermatology Atlas.
- Epidermolysis bullosa simplex. Adapted from Dermatology Atlas.
- Epidermolysis bullosa simplex. Adapted from Dermatology Atlas.
- Epidermolysis bullosa simplex. Adapted from Dermatology Atlas.
Ecthyma (patient information)
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# Overview
Ecthyma is a skin infection similar to impetigo. It is often called "deep impetigo" because it occurs deep inside the skin.

# What are the symptoms of Ecthyma?
The main symptom of ecthyma is a small blister with a red border that may be filled with pus. The blister is similar to that seen in persons with impetigo, but the infection spreads much deeper into the skin.
After the blister goes away, a crusty ulcer appears.

# What causes Ecthyma?
Ecthyma is most often caused by the bacteria streptococcus. Sometimes, staphylococcus bacteria causes this skin infection.

# Who is at highest risk?
The infection may start in skin that has been injured due to a scratch or insect bite. It often develops on the legs.

# Diagnosis
Your doctor can usually diagnose this condition simply by looking at your skin. In rare cases, the fluid inside the blister may be sent to a lab for closer examination or a skin biopsy may be done.

# When to seek urgent medical care?
Make an appointment with your health care provider if you have symptoms of ecthyma.

# Treatment options
Your doctor will usually prescribe antibiotics by mouth (oral antibiotics). Very early cases may be treated with topical medications. More advanced forms may need antibiotics given through a vein (intravenous antibiotics).
Placing a warm wet cloth over the area can help remove ulcer crusts. Your doctor may recommend antiseptic soap or peroxide washes to speed recovery.

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

# What to expect (Outlook/Prognosis)?
Unlike impetigo, ecthyma can sometimes result in scarring.

# Possible complications
- Spread of infection to other parts of the body
- Permanent skin damage with scarring

# Prevention of Ecthyma
Carefully clean the skin after an injury (such as a bite or scratch). Avoid scratching or digging at scabs and sores.

# Sources
Editing the Table of Contents

# Overview
Sometimes you will want to remove the Table of Contents on a page. Type this text
__NOTOC__
to accomplish this.
More Table of Contents (TOC) commands are found in the table below:

# Table of contents

# More magic

# Behavior switches
A behavior switch controls the layout or behavior of the page and can often be used to specify desired omissions and inclusions in the content.
Electron capture dissociation
In mass spectrometry, electron capture dissociation (ECD) is a method of fragmenting gas phase ions for tandem mass spectrometric analysis (structural elucidation). ECD involves the direct introduction of low energy electrons to trapped gas phase ions.

# Principles
Electron capture dissociation typically involves a multiply protonated molecule M interacting with a free electron to form an odd-electron ion
Liberation of the electric potential energy results in fragmentation of the product ion.
ECD produces significantly different types of fragment ions than other fragmentation methods such as collision-induced dissociation and infrared multiphoton dissociation. These other methods introduce internal vibrational energy in some way or another while ECD does not. The unique (and complementary) fragments observed and the ability to fragment whole macromolecules effectively has been promising. The low efficiencies and other experimental difficulties have prevented wide spread use. ECD is primarily used in Fourier transform ion cyclotron resonance mass spectrometry.
ECD is a recently introduced technique and is still being investigated. The mechanism of ECD is still under debate but appears not to necessarily break the weakest bond and is therefore thought to be a fast process (nonergodic) where energy is not free to relax intramolecularly. Suggestions have been made that radical reactions initiated by the electron may be responsible for the action of ECD.
In a similar technique called electron transfer dissociation the electrons are transferred by collision between the analyte cations and anions.
Epidemiology and demographics

# Overview
The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually. The prevalence of delusional disorders is approximately 24 to 30 cases per 100, 000 individuals annually.

# Epidemiology and Demographics
Delusional disorder accounts for approximately 1-2% of admissions to inpatient mental health facilities. The incidence of first admissions for delusional disorder is approximately 0.001-0.003%. The lifetime morbid risk of delusional disorder has been estimated to range from 0.05 to 0.1 percent. According to DSM-5, the estimated lifetime prevalence of delusional disorder is 0.2 percent, which is far lower than the estimated lifetime prevalence for other major psychotic disorders such as schizophrenia and bipolar I disorder with lifetime prevalence of 0.3 to 0.87 percent and  0.24 to 0.6 percent respectively. Approximate rates of delusional disorder reported in samples of patients receiving mental health treatment have ranged from 0.5 to 1.2 percent. As the majority of people with delusional disorder do not regard it as an illness or receive treatment, studies likely underestimate the prevalence of the disorder. Delusional disorders are uncommon in psychiatric practice, though this may be an underestimation due to the fact that those afflicted lack insight and thus avoid psychiatric assessment.

# Incidence
The incidence of delusional disorders is approximately 0.7 to 3.0 cases per 100, 000 individuals annually.

# Prevalence
The prevalence of delusional disorders is approximately 24 to 30 cases per 100, 000 individuals annually.

# Gender
Females are more commonly affected with delusional disorder than males.

# Age
Delusional disorder commonly affects individuals in middle to late adult life. First admissions to hospital for delusional disorder occur between age 33 and 55 years of age.
Erythropoietic protoporphyria
Erythropoietic protoporphyria (EPP) is a relatively mild form of porphyria, although very painful, which arises from a deficiency in the enzyme ferrochelatase, leading to abnormally high levels of protoporphyrin in the tissue. The severity varies significantly from individual to individual.
Both autosomal dominant and autosomal recessive inheritance have been reported with this disorder.

# History
Erythropoietic protoporphyria was first identified in 1960 by Magnus et al at the St John's Institute of Dermatology in London.

# Symptoms and presentation
A common symptom is painful photosensitivity, manifesting itself as a burning sensation on the surface of the skin. This usually first presents in childhood, and most often affects the face and the upper surfaces of the hands and feet. Prolonged exposure to the sun can lead to edema and blistering. After many years, chronically sun-exposed skin may become thick and wrinkled. In a small percentage of cases, protoporphyrin accumulates to toxic levels in the liver, leading to liver failure.

# Treatment and prognosis
There is no cure for this disorder; however, symptoms can usually be managed by the simple expedient of limiting sun exposure. Protective clothing is also very helpful; however, since the photosensitivity results from light in the visible spectrum, most sunscreens (with the exception of light-reflecting substances such as zinc oxide) are of little use. Some individuals can decrease their sun sensitivity with daily doses of beta carotene; others gradually build a protective layer of melanin by regularly exposing themselves for short times to ultraviolet radiation.  The most severe cases are sometimes treated with liver transplants.  People with EPP are also at increased risk to develop gallstones.
Ethionamide adverse reactions

# Adverse Reactions

## Gastrointestinal
The most common side effects of ethionamide are gastrointestinal disturbances including nausea, vomiting, diarrhea, abdominal pain, excessive salivation, metallic taste, stomatitis, anorexia and weight loss. Adverse gastrointestinal effects appear to be dose related, with approximately 50% of patients unable to tolerate 1 gm as a single dose. Gastrointestinal effects may be minimized by decreasing dosage, by changing the time of drug administration, or by the concurrent administration of an antiemetic agent.

## Nervous System
Psychotic disturbances (including mental depression), drowsiness, dizziness, restlessness, headache, and postural hypotension have been reported with ethionamide. Rare reports of peripheral neuritis, optic neuritis, diplopia, blurred vision, and a pellagra-like syndrome also have been reported. Concurrent administration of pyridoxine has been recommended to prevent or relieve neurotoxic effects.

## Hepatic
Transient increases in serum bilirubin, SGOT, SGPT. Hepatitis (with or without jaundice).

## Other
Hypersensitivity reactions including rash, photosensitivity, thrombocytopenia and purpura have been reported rarely. Hypoglycemia, hypothyroidism, gynecomastia, impotence, and acne also have occurred. The management of patients with diabetes mellitus may become more difficult in those receiving ethionamide.
Ethylenediamine dihydroiodide
Ethylenediamine dihydroiodide (EDDI) is a water-soluble salt of ethylenediamine and hydrogen iodide.  It is a colorless to light yellow crystalline powder. Its chemical formula is C2H6N2.2HI. It is nonflammable, but iodine may be released during a fire.
EDDI is used as a pet food additive and cattle feed additive with high bioavailability.  It is used to prevent iodine deficiency.  The United States Food and Drug Administration suggests a limit of intake to 50 mg/head/day.  Although EDDI is generally recognized as safe (GRAS) only as a nutrient source of iodine, administration of EDDI also has preventative effects on foot rot in cattle.
EDDI may react with sulfates and release free iodine.  Other iodine supplements in animal feed are calcium iodate (most stable) and potassium iodide (most water-soluble, least stable).
Extensor carpi ulnaris muscle
Extensor carpi ulnaris is a muscle located in the human forearm that acts to extend and adduct the wrist.
Being an extensor muscle, extensor carpi ulnaris is on the posterior side of the forearm.

# Origin and insertion
It originates from the lateral epicondyle of the humerus and the posterior border of the ulna, and crosses the forearm to the ulnar (medial) side to insert at the base of the 5th metacarpal.

# Action
The Extensor carpi ulnaris extends the wrist, but when acting alone inclines the hand toward the ulnar side; by its continued action it extends the elbow-joint.
The muscle is a minor extensor of the carpus in carnivores, but has become a flexor in ungulates. In this case it is described as ulnaris lateralis.

# Additional images
- Bones of left forearm. Posterior aspect.
- Bones of the left hand. Dorsal surface.
- Cross-section through the middle of the forearm.
- Posterior surface of the forearm. Deep muscles.
- Transverse section across distal ends of radius and ulna.
- Transverse section across the wrist and digits.
- The mucous sheaths of the tendons on the back of the wrist.
Hereditary spastic paraplegia

# Overview
Hereditary spastic paraplegia (HSP), also called familial spastic paraparesis (FSP), refers to a group of inherited disorders that are characterized by progressive weakness and stiffness of the legs. Adolph Strumpell (a German neurologist) was the first MD to study this disease in a German family (1880), and Maurice Lorrain (a French MD) published a study about the disease in 1888.

# Symptoms
Though the primary feature of HSP is severe, progressive, lower extremity spasticity, in more complicated forms it can be accompanied by other neurological symptoms. These include optic neuropathy, retinopathy (diseases of the retina), dementia, ataxia (lack of muscle control), icthyosis (a skin disorder resulting in dry, rough, scaly skin), mental retardation, peripheral neuropathy, and deafness.

# Diagnosis
Diagnosis is primarily by neurological examination and testing to exclude other disorders. Specialized genetic testing and diagnosis are available at some medical centers.

# Treatment
There are no specific treatments to prevent, slow, or reverse HSP. Symptomatic treatments used for other forms of chronic paraplegia are sometimes helpful. Regular physical therapy is important for improving muscle strength and preserving range of motion.

# Prognosis
The prognosis for individuals with HSP varies. Some cases are seriously disabling while others are less disabling and are compatible with a productive and full life. The majority of individuals with HSP have a normal life expectancy.

# Research
The National Institute of Neurological Disorders and Stroke supports research on genetic disorders such as HSP. Genes that are responsible for several forms of HSP have already been identified, and many more will likely be identified in the future. Understanding how these genes cause HSP will lead to ways to prevent, treat, and cure HSP.
Famciclovir adverse reactions

# Adverse Reactions
Acute renal failure is discussed in greater detail in other sections of the label .
The most common adverse events reported in at least 1 indication by >10% of adult patients treated with FAMVIR are headache and nausea.

## Clinical Trials Experience in Adult Patients
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared with rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Immunocompetent patients: The safety of FAMVIR has been evaluated in active- and placebo-controlled clinical studies involving 816 FAMVIR-treated patients with herpes zoster (FAMVIR, 250 mg three times daily to 750 mg three times daily); 163 FAMVIR-treated patients with recurrent genital herpes (FAMVIR, 1000 mg twice daily); 1,197 patients with recurrent genital herpes treated with FAMVIR as suppressive therapy (125 mg once daily to 250 mg three times daily) of which 570 patients received FAMVIR (open-labeled and/or double-blind) for at least 10 months; and 447 FAMVIR-treated patients with herpes labialis (FAMVIR, 1500 mg once daily or 750 mg twice daily). Table 2 lists selected adverse events.

## Postmarketing Experience
The adverse events listed below have been reported during postapproval use of FAMVIR. Because these events are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure:
Blood and lymphatic system disorders: Thrombocytopenia
Hepatobiliary disorders: Abnormal liver function tests, cholestatic jaundice
Nervous system disorders: Dizziness, somnolence
Psychiatric disorders: Confusion (including delirium, disorientation, and confusional state occurring predominantly in the elderly), hallucinations
Skin and subcutaneous tissue disorders: Urticaria, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, angioedema (e.g., face, eyelid, periorbital, and pharyngeal edema), leukocytoclastic vasculitis
Cardiac disorders: Palpitations