Persius/hicric huggingface dataset:
Primary progressive aphasia

# Overview
Primary progressive aphasia (PPA) is a gradually worsening disorder of speech with an insidious onset. It was first described by Marsel Mesulam in 1982.
There is considerable controversy over the nosology of this disorder. Clinical and pathological overlap have led it to being considered as part of the frontotemporal lobar degeneration (FTLD) spectrum of disorders. In the classical Mesulam criteria for PPA there are 2 variants: a non-fluent type (progressive non-fluent aphasia or PNFA) and a fluent aphasia. However, recent work has suggested that the underlying cognitive impairment in patients with progressive fluent aphasias is loss of semantic knowledge (semantic dementia or SD).  In the consensus criteria for FTLD described by Neary et al in 1989, PNFA and SD are the two classifications used.
The San Francisco group have recently suggested that there is a third variant of PPA (so-called logopaenic PPA - Gorno-Tempini et al, 2004). However, there are limited descriptions of this disorder in the medical literature and early reports suggest that it is an atypical form of Alzheimer's disease rather than a disease falling into the frontotemporal lobar degeneration spectrum.
There are no known risk factors for the progressive aphasias. However, one observational study has recently suggested that vasectomy could be a risk factor for PPA in men. These results have yet to be replicated elsewhere.
Metabolic acidosis overview

# Overview
In medicine, metabolic acidosis is an acid-base imbalance in which the blood pH is low (less than 7.35) due to increased production of H+ by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney. Its causes are diverse, and its consequences can be serious, including diarrhea, coma and death. Together with respiratory acidosis, it is one of the two general types of acidosis, the other being respiratory acidosis.

# Treatment

## Medical Therapy
A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention however, is not effective in case of lactic acidosis.
If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.
Methylchloroisothiazolinone
Methylchloroisothiazolinone (5-chloro-2-methyl-4-isothiazolinon-3-one) is a preservative with antibacterial and antifungal effects within the group of isothiazolinones. It is effective against gram-positive and gram-negative bacteria, yeast and fungi.
It is found in many water-based personal care products and cosmetics. It is also used in glue production, detergents, paints, fuels and other industrial processes. Methylchloroisothiazolinone is known by the registered tradename Kathon CG when used in combination with methylisothiazolinone.
It can be used in combination with alcohols and other long-chain organics in compounds such as methylchloroisothiazolinone ethylparaben benzalkonium chloride or methylchloroisothiazolinone 2-bromo-2-nitropropane-1,3-diol benzalkonium chloride.
It was first used in cosmetics in the 1970s. In high concentrations it can cause chemical burns and it is a skin and membrane irritant and so it was largely removed from most cosmetic products except for those with only short duration skin contact such as rinse-offs. Its inclusion in certain forms makes it more acceptable to sensitive users, so it can be found in cosmetic creams and lotions which require skin contact. In the US accepted concentrations are 15 ppm in rinse-offs and 8 ppm in other cosmetics.

# Safety concerns
Like a number of other common cosmetics ingredients, methylchloroisothiazolinone has been considered to be a carcinogen.
Methylchloroisothiazolinone is an allergen.
Methylmalonyl CoA epimerase
Methylmalonyl CoA epimerase (EC 5.1.99.1, methylmalonyl-CoA racemase, methylmalonyl coenzyme A racemase, DL-methylmalonyl-CoA racemase, 2-methyl-3-oxopropanoyl-CoA 2-epimerase ) is an enzyme involved in fatty acid catabolism that is encoded in human by the "MCEE" gene located on chromosome 2. It is routinely and incorrectly labeled as "methylmalonyl-CoA racemase". It is not a racemase because the CoA moiety has 5 other stereocenters.

# Structure
The "MCEE" gene is located in the 2p13 region and contains 4 exons, and encodes for a protein that is approximately 18 kDa in size and located to the mitochondrial matrix. Several natural variants in amino acid sequences exist. The structure of the MCEE protein has been resolved by X-ray crystallography  at 1.8-angstrom resolution.

# Function
The MCEE gene encodes an enzyme that interconverts D- and L- methylmalonyl-CoA during the degradation of branched-chain amino acids, odd chain-length fatty acids, and other metabolites. In biochemistry terms, it catalyzes the reaction that converts (S)-methylmalonyl-CoA to the (R) form. This enzyme catalyses the following chemical reaction
Methylmalonyl CoA epimerase plays an important role in the catabolism of fatty acids with odd-length carbon chains.  In the catabolism of even-chain saturated fatty acids, the -oxidation pathway breaks down fatty acyl-CoA molecules in repeated sequences of four reactions to yield one acetyl CoA per repeated sequence.  This means that, for each round of -oxidation, the fatty acyl-Co-A is shortened by two carbons.  If the fatty acid began with an even number of carbons, this process could break down an entire saturated fatty acid into acetyl-CoA units.  If the fatty acid began with an odd number of carbons, however, -oxidation would break the fatty acyl-CoA down until the three carbon propionyl-CoA is formed.  In order to convert this to the metabolically useful succinyl-CoA, three reactions are needed.  The propionyl-CoA is first carboxylated to (S)-methylmalonyl-CoA by the enzyme Propionyl-CoA carboxylase.  Methylmalonyl CoA epimerase then catalyzes the rearrangement of (S)-methylmalonyl-CoA to the (R) form in a reaction that uses a vitamin B12 cofactor and a resonance-stabilized carbanion intermediate.  The (R)-methylmalonyl-CoA is then converted to succinyl-CoA in a reaction catalyzed by methylmalonyl-CoA mutase.
Acting as a general base, the enzyme abstracts a proton from the -carbon of (R)-methylmalonyl-CoA.  This results in the formation of a carbanion intermediate in which the -carbon is stabilized by resonance.  The enzyme then acts as a general acid to protonate the -carbon, resulting in the formation of (S)-methylmalonyl-CoA.

# Clinical significance
Mutations in the MCEE gene causes methymalonyl-Coa epimerase deficiency (MCEED), a rare autosomal recessive inborn error of metabolism in amino acid metabolisms involving branched-chain amino acids valine, leucine, and isoleucine. Patients with MCEED may present with life-threatening neonatal metabolic acidosis, hyperammonemia, feeding difficulties, and coma.
Pseudo-Hurler polydystrophy
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# Overview
Pseudo-Hurler polydystrophy, also referred to as mucolipidosis III (ML III), is lysosomal storage disease closely related to I-cell disease (ML II). Symptoms of ML III are often not noticed until the child is 3-5 years of age.

# Pathophysiology
As in ML II, ML III results from genetic defects in GlcNAc phosphotransferase (N-acetylglucosamine-1-phosphotransferase). However, ML III produces less severe symptoms and progresses more slowly, probably because the defect in GlcNAc phosphotranspherase lies in its protein recognition domain. Therefore, the catalytic domain retains some of its activity, resulting in a smaller accumulation of carbohydrates, lipids, and proteins in the inclusion bodies.

# Presentation
Patients with ML III are generally of normal intelligence (trait) or have only mild mental retardation. These patients usually have skeletal abnormalities, coarse facial features, short height, and corneal clouding. Some individuals with ML III survive until their fourth or fifth decade of life.
Mupirocin adverse reactions

# Adverse Reactions
In 2 randomized, double-blind, double-dummy trials, 339 patients were treated with topical BACTROBAN CREAM plus oral placebo. Adverse events thought to be possibly or probably drug-related occurred in 28 (8.3%) patients. The incidence of those events that were reported in at least 1% of patients enrolled in these trials were: Headache (1.7%), rash, and nausea (1.1% each).
Other adverse events thought to be possibly or probably drug-related which occurred in less than 1% of patients were: Abdominal pain, burning at application site, cellulitis, dermatitis, dizziness, pruritus, secondary wound infection, and ulcerative stomatitis.
In a supportive study in the treatment of secondarily infected eczema, 82 patients were treated with BACTROBAN CREAM. The incidence of adverse events thought to be possibly or probably drug-related was as follows: Nausea (4.9%), headache, and burning at application site (3.6% each), pruritus (2.4%) and 1 report each of abdominal pain, bleeding secondary to eczema, pain secondary to eczema, hives, dry skin, and rash.
Neutralisation (immunology)
Assistant Editor-in-Chief: Soumya Sachdeva
Neutralisation (or neutralization) in the immunological sense refers to the ability of antibodies to block the site(s) on bacteria or viruses that they use to enter their target cell.
An antibody produced in response to a bacterial exotoxin or a toxoid that neutralizes the exotoxin is called an antitoxin
In neutralization reactions, the harmful effects of a bacterial exotoxin or virus are eliminated by a specific antibody.
In a virus neutralization test, the presence of antibodies against a virus can be detected by the antibodies ability to prevent cytopathic effects of viruses in cell cultures.
Antibodies against certain viruses can be detected by their ability to interfere with viral hemagglutination in viral hemagglutination inhibition tests.
neutralisation is an act or aprocess of neutralising.
Nocturnal Penile Tumescence
Nocturnal penile tumescence (NPT) is the spontaneous occurrence of a penile erection during sleep. All men without erectile dysfunction experience this phenomenon, usually several times during the night. It typically happens during REM sleep and it is not uncommon for an erection to be present when a man wakes up  such an erection is colloquially referred to as morning wood in North America, and as morning glory in the United Kingdom (though in some areas of the U.K. the adjective piss-proud is often used instead).
The existence and predictability of nocturnal tumescence is used by sexual health practitioners to ascertain whether a given case of erectile dysfunction (E.D.) is psychological or physiological in origin. A patient presenting with E.D. is fitted with an elastic device to wear around his penis during sleep; the device detects changes in girth and relays the information to a computer for later analysis. If nocturnal tumescence is detected, then the E.D. is presumed to be due to a psychosomatic illness such as sexual anxiety; if not, then it is presumed to be due to a physiological cause.
The cause of NPT is not known certainly. Bancroft (2005) hypothesizes that the noradrenergic neurons of the locus ceruleus are inhibitory to penile erection, and that the cessation of their discharge that occurs during REM sleep may allow testosterone-related excitatory actions to manifest as NPT.
Orthorhombic crystal system
In crystallography, the orthorhombic crystal system is one of the 7 lattice point groups. Orthorhombic lattices result from stretching a cubic lattice along two of its lattice vectors by two different factors, resulting in a rectangular prism with a rectangular base (a by b) and height (c), such that a = b = c. All three bases intersect at 90 angles. The three lattice vectors remain mutually orthogonal.
There are four orthorhombic Bravais lattices: simple orthorhombic, base-centered orthorhombic, body-centered orthorhombic, and face-centered orthorhombic.
The point groups (or crystal classes) that fall under this crystal system are listed below, followed by their representations in International {Hermann-Mauguin) notation and Schoenflies notation, and mineral examples.
Panton-Valentine leukocidin
Panton-Valentine leukocidin (PVL) is a cytotoxinone of the -pore forming toxins. Presence of PVL is associated with extremely high virulence in species of Staphylococcus aureus. It is nearly always found in isolates of community-acquired S. aureus infections. PVL is produced from the genetic material of a bacteriophage which infects Staphylococcus aureus, making it more virulent.

# History
It was initially discovered by Van deVelde in 1894 due to its ability to lyse leukocytes. It was named after Panton and Valentine when they associated it with soft tissue infections in 1932.

# Mechanism of action

# Clinical effects
PVL causes leukocyte destruction and necrotizing pneumonia, an aggressive condition that often kills patients within 72 hours.  It has played a role in a number of outbreaks of fatal bacterial infections.  PVL may increase the expression of staphylococcal protein A, a key pro-inflammatory factor for pneumonia.

# Epidemiology
Community-acquired Methicillin-resistant Staphylococcus aureus (CA-MRSA) is particularly difficult to treat when it carries PVL.  Genetic analysis shows that PVL CA-MRSA has emerged several times, on different continents, rather than being the worldwide spread of a single clone.
Parthenocissus quinquefolia
Virginia creeper or five-leaved ivy (Parthenocissus quinquefolia) is a woody vine native to eastern and central North America, in southeastern Canada, the eastern and central United States, eastern Mexico, and Guatemala, west as far as Manitoba, South Dakota, Utah and Texas.
It is a prolific climber, reaching heights of 20 to 30 m in the wild, it climbs smooth surfaces using small forked tendrils tipped with small strongly adhesive pads 5 mm in size. The leaves are palmately compound, comprised of five leaflets (rarely three leaflets, particularly on younger vines) joined from a central point on the leafstalk, and range from 3 to 20 cm (rarely 30 cm) across. The leaflets have a toothed margin, which makes it easy to distinguish from poison-ivy, which has three leaflets with smooth edges.
The flowers are small and greenish, produced in clusters in late spring, and mature in late summer or early fall into small hard purplish-black berries 5 to 7 mm diameter. These berries contain oxalic acid, which is poisonous to humans and other mammals, and may be fatal if eaten. However, accidental poisoning is uncommon, likely because of the bad taste of the berries. Despite being poisonous to mammals, they provide an important winter food source for birds.

# Cultivation and uses
Virginia creeper is grown as an ornamental plant, because of its deep red to burgundy fall foliage. It is frequently seen covering telephone poles or trees. The creeper may kill vegetation it covers by shading its support and thus limiting the supporting plants' ability to photosynthesize.
Virginia creeper can be used as a shading vine for buildings on masonry walls.  Because the vine, like its relative Boston ivy, adheres to the surface by disks rather than penetrating roots, it will not harm the masonry but will keep a building cooler by shading the wall surface during the summer, saving money on air conditioning. As with ivy, trying to rip the plant from the wall will damage the surface; but if the plant is first killed, such as by severing the vine from the root, the adhesive pads will eventually deteriorate and release their grip.
Native Americans used the plant as an herbal remedy for diarrhea, difficult urination, swelling, and lockjaw.
Also known as "Engelman Ivy" in Canada.
Perforated eardrum overview

# Overview
Rupture or perforation (hole) of the eardrum can occur in infection, trauma (e.g. by trying to clean the ear with sharp instruments), explosion or loud noise. Flying with a severe cold can also cause perforation due to changes in air pressure and blocked eustachian tubes resulting from the cold. This is especially true on landing.
Perforation of the eardrum leads to conductive hearing loss.
The perforation may heal in a few weeks, or up to a few months. Some perforations require intervention - this may use a paper patch to promote healing (simple procedure in the office of an ear, nose and throat specialist), or surgery (tympanoplasty).
Hearing is usually recovered fully, but chronic infection over a long period may lead to permanent hearing loss.

# Treatment

## Surgery
Surgical repair of the eardrum tympanoplasty may be needed if the eardrum does not heal on its own.
Perforating cutaneous nerve
The perforating cutaneous nerve is a cutaneous nerve that supplies skin over the gluteus maximus muscle.

# Structure
The perforating cutaneous nerve arises from the sacral plexus.  It pierces the lower part of the sacrotuberous ligament, and winds around the inferior border of the gluteus maximus.  It is an inferior clunial (buttocks) nerve; it supplies the skin covering the medial and lower parts of gluteus maximus.
The perforating cutaneous nerve may arise from the pudendal nerve.  It is absent in approximately one third of people; its place may be taken by a branch from the posterior cutaneous nerve of thigh or by a branch from the third and fourth, or fourth and fifth, sacral nerves.
Total peripheral resistance
Total peripheral resistance refers to the cumulative resistance of the thousands of arterioles in the body, or the lungs, respectively. It is approximately equal to the resistance of the arterioles, since the arterioles are the chief resistance vessels in the body.
Peripheral resistance occurs when arterioles are unable to completely relieve pressure in the arteries. When the heart contracts, blood enters the arteries faster than it can leave, and the arteries stretch from the pressure. Although the vessels return to their normal state during diastole, the heart will contract again before all the blood has completely flowed into the arterioles. This inhibits the arterioles' ability to fully relieve the pressure in the arteries, causing peripheral resistance.
Total Peripheral Resistance = Mean Arterial Pressure / Cardiac Output
The total peripheral resistance of healthy lung arterioles is typically about 15 to 20 percent that of the body, so pulmonary artery mean blood pressures are typically about 15-20% of aortic mean blood pressures.
As a consequence of the arteries being forced to work against peripheral resistance, there is substantial blood pressure even during diastole. Arterioles are sometimes referred to as resistance vessels because of their peripheral resistance.
Plantar metatarsal arteries
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The plantar metatarsal arteries (digital branches) are four in number, and run forward between the metatarsal bones and in contact with the Interossei.
Each divides into a pair of plantar digital arteries which supply the adjacent sides of the toes.
Near their points of division each sends upward an anterior perforating branch to join the corresponding dorsal metatarsal artery.
The first plantar metatarsal artery (arteria princeps hallucis) springs from the junction between the lateral plantar and deep plantar arteries and sends a digital branch to the medial side of the first toe.
The digital branch for the lateral side of the fifth toe arise from the lateral plantar artery near the base of the fifth metatarsal bone.
Polymorphous light eruption

# Overview
Polymorphous light eruption (PLE), or polymorphic light eruption, is a skin complaint caused by sunlight.  Symptoms include skin irritations, which may be itchy or painful, and are sometimes confused with hives.  These irritations appear upon exposure to sunlightsometimes as little as 15 minutes of exposure to the sun can bring onset of the conditionand may last from 1 to 7 days.  Generally, PLE resolves without treatment; also, PLE irritations generally leave no scar.  The cases of this condition are most common between the spring and autumn months in the northern hemisphere.
Typically, 10-20% of the population are affected.  It is more common in females than in males. The condition can affect all ethnic groups and research suggests that 20% of patients have a family history of the complaint.  Those suffering from PMLE usually do so by age 30.
The cause of PLE is not yet understood. It is thought to be due to a type IV delayed-type hypersensitivity reaction.

# Diagnosis

## Physical Examination

### Skin
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.
- Polymorphic light eruption. With permission from Dermatology Atlas.

# Experimental treatments
As of 2008 a company in Australia named Clinuvel Pharmaceuticals Limited is performing clinical trials with a melanocyte-stimulating hormone named melanotan (which they refer to as CUV1647) for polymorphous light eruption.
Post-viral fatigue syndrome
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# Overview
Post-viral fatigue syndrome (PVFS) is a condition that presents a fatigue-like state resulting from a viral infection. The term is not widely used, but the state of prolonged or severe fatigue after illness is not uncommon. Some persons will experience fatigue and related symptoms for months or years following a severe viral infection.

# Classification
In the WHO's ICD10, PVFS is a group header within 'other disorders of the brain', a neurological category G93.3. It is furthermore explicitly excluded from neurotic disorders. Listed under PVFS is Benign Myalgic encephalomyelitis (ME); several alternative diagnoses to ME such as Chronic fatigue syndrome (CFS) and Neuromyasthenia are included in the alphabetic list of the ICD10.
Post-viral syndromes may also include: post-polio syndrome, late Lyme disease, and possibly chronic mononucleosis or other severe chronic viral infections.
Some researchers claim that post-viral fatigue syndrome is a biological state of weakness or activation of, or damage to the immune system, and that it is common to many post-viral syndromes. It is hoped that immune system research, especially that connected to HIV, may lead to better understanding of, and treatments for, other post-viral syndromes.