Persius/hicric huggingface dataset:
Mycobacterium arupense
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Mycobacterium arupense is a rapidly growing mycobacterium first isolated from soil and human sputum samples in Spain.  Etymology: arupense, pertaining to the ARUP Institute for Clinical and Experimental Pathology, where the type strain was characterized.

# Description
Microscopy
- Gram-positive, nonmotile and acid-fast rods (1-3m x 0.5-0.7m), mostly strong acid-fast.
Colony characteristics
- Colonies are eugonic, rough and nonpigmented.
Physiology
- Colonies occur within 5 days at 30C (optimum temperature, no growth at 45C) on Lowenstein-Jensen medium and on Middlebrook 7H10 agar.
- No growth on MacConkey agar without crystal violet.
- The type strain is resistant to D-cycloserine, streptomycin, isoniazid (0.1 and 1 mg/l), rifampin, and thiacetazone and is susceptible to isoniazid (10 mg/l), kanamycin, and capreomycin.

# Pathogenesis
- Not associated with disease.

# Type Strain
- First isolated from water samples, from soil and human sputum samples, Spain.
- Strain AR30097 = ATCC BAA-1242 = DSM 44942.
Mycobacterium bolletii
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Mycobacterium bolletii
Type strain: strain BD = CCUG 50184 = CIP 108541.
Etymology: N.L. gen. n. bolletii, of Bollet, to honour Claude Bollet, a famous clinical microbiologist and taxonomist.
Mycobacterium branderi
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Mycobacterium branderi is a slowly growing, nonchromogenic Mycobacterium first isolated from patients in Finland.  Etymology: of Brander, referring to Eljas Brander, the former head of the Tuberculosis Laboratory of the National Public Health Institute, Finland, who collected the strains.

# Description
Microscopy
- Acid-fast delicate slender rods that are often slightly curved, 1.2 to 3 um long.
Colony characteristics
- Colonies are nonchromogenic and produce smooth, often umbonate, off-white to grayish colonies on Middlebrook 7H11 agar.
Physiology
- Slowly growing, reaching full colony size after 2 to 3 weeks.
- Growth is equally good at 37C and 45C and is only slightly delayed at 25C.
- The type strain is negative for Tween 80 hydrolysis, catalase, urease, and nitrate reductase activities and niacin.
- Strongly positive for arylsulfatase activity in 14-day tests and moderately to weakly positive for nicotinamidase and pyrazinamidase activities.
- In susceptibility tests the type strain was resistant to isoniazid, rifampin, pyrazinamide, and cycloserine but susceptible to ethambutol, streptomycin, ethionamide, and capreomycin.
Differential characteristics
- Differentiation by 16S rRNA sequencing
- Distinguishing of M. branderi from M. celatum by pigment production
- Differentiation of M. branderi from M. xenopi on the basis of good growth of M. branderi at room temperature, the lack of pigment production by M. branderi
- Differentiation of M. branderi and M. cookii: M. cookii is scotochromogenic and does not grow at 37C.

# Pathogenesis
- The first strains of M. branderi were isolated from samples obtained from nine patients, some of whom had cavitary mycobacteriosis of the lungs that was resistant to available drugs. In most cases, repeat samples obtained from each patient were positive for acid-fast bacilli as determined by microscopy, and the only cultivable species was M. branderi.  M. branderi has to be considered a potential human pathogen.

# Type Strain
- Strain 52157 = ATCC 51789 = CIP 104592 = DSM 44624 = JCM 12687.
Mycobacterium chelonae

# Overview
Mycobacterium chelonae is a species of the phylum actinobacteria (Gram-positive bacteria with high guanine and cytosine content, one of the dominant phyla of all bacteria), belonging to the genus mycobacterium.

# Causes
- Mycobacterium chelonae is a rapidly growing mycobacterium, that is found all throughout the environment including sewage and tap water.
- It can occasionally cause opportunistic infections of humans. It is grouped in Runyon group IV.
- Type strain: strain CM 6388 = ATCC 35752 = CCUG 47445 = CIP 104535 = DSM 43804 = JCM 6388 = NCTC 946.

# Epidemiology
- On average, 2 cases of nonpulmonary M. chelonae infection are reported in South Australia each year.

# Treatment

## Antimicrobial Regimen
- 1.  Localized infections 
- Preferred regimen: Clarithromycin 500 mg PO BID
- Alternative regimen: Azithromycin
- 2. Disseminated or extensive disease
- 2.1 monotherapy
- Preferred regimen: Clarithromycin 500 mg PO BID
- 2.2 multidrug therapy
- Preferred regimen: Clarithromycin 500 mg PO BID AND Tobramycin 5 mg IV/kg/day PO OR Imipenem 0.5-1 g IV q6h OR Linezolid 600 mg IV/PO BID for 4-8 weeks
- Alternative regimen: Moxifloxacin 400 mg PO qd AND Linezolid 600 mg PO BID
- Note (1): During initial treatment, multidrug therapy may prevent development of acquired resistance
- Note (2): Total treatment duration is 6 months
- 3. Keratitis (LASIK-related)
- Preferred regimen: Clarithromycin 500 mg PO BID AND topicals (Tobramycin 0.3%, 2 gtts q4h AND Gatifloxacin 0.3%, 1 gtt q4h OR Moxifloxacin 0.5%, 1 gtt q4h
Mycobacterium chimaera
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Mycobacterium chimaera
Type strain: strain FI-01069 = CCUG 50989 = CIP 107892 = DSM 44623.
Etymology: L. fem. n. chimaera, the chimaera, the mythological being made up of parts of three different animals, referring to the apparent mix of genetic features characterizing the strains.
Mycobacterium gordonae
Mycobacterium gordonae

# Description
Gram-positive, nonmotile and moderate to long acid-fast rods.
- Commonly found in tap water and soil. Casual resident in human sputum and gastric lavage specimens.
Colony characteristics
- Smooth, with yellow or orange scotochromogenic colonies.  Even though they are scotochromogenic pigment is intensified by growing in continuous light.
Physiology
- Growth on Lowenstein-Jensen medium and Middlebrook 7H10 agar within 7 or more days at 37C (optimal 25C).
- Does not grow in the presence of ethambutol (1mg/l), isoniazid (10mg/l) and sodium chloride (5%).
Differential characteristics
- A commercial hybridisation assay (AccuProbe) to identify M. gordonae exists.
- Intraspecies variability in 16S rDNA sequences

# Pathogenesis
- Rarely if ever implicated in disease processes unless patients are immunocompromised.
- Biosafety level 1

# Type Strain
Strain ATCC 14470 = CCUG 21801 = CCUG 21811 = CIP 104529 = DSM 44160 = JCM 6382 = NCTC 10267.

# Treatment

## Antimicrobial regimen
- M. gordonae 
- Preferred regimen: Ethambutol OR Rifabutin OR Clarithromycin OR Linezolid OR Fluoroquinolones
Myxedematous psychosis
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Myxedema psychosis, more colloquially known as myxedema madness, is a relatively uncommon consequence of hypothyroidism, particularly Hashimoto's thyroiditis. A chronically under-active thyroid can lead to slowly progressive dementia, delirium, and in extreme cases to hallucinations, coma, or psychosis, particularly in the elderly.
Treatment is via the standard treatment for hypothyroidism with thyroxine replacement.
Oral T4, or in especially acute cases liothyronine, a sodium salt of T3. Hormone replacement in these patients usually reverses the psychotic symptoms, but may not help with cognitive deficits caused by changes in metabolic activity in the CNS.
The "myxedema" part of the name simply refers to the pitting edema common to hypothyroidism.
N-Nitroso-N-Methylurea

# Overview
N-Nitroso-N-methylurea (CAS No.684-93-5), also known as MNU, is a highly potent carcinogen, mutagen, and teratogen.  MNU is an alkylating agent, and exhibits its toxicity by transferring its methyl group to nucleobases in nucleic acids.
Acute exposure to MNU in humans can result in skin and eye irritation, headache, nausea, and vomiting.  MNU is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals (IARC 1972, 1978, 1987).  Various cancers induced in animal models include: squamous cell carcinomas of the forestomach, sarcomas and gliomas of the brain, adenocarcinomas of the pancreas, leukemia, and lymphomas.  However, the actual potential for human exposure is quite limited, as the chemical is not produced or used in large quantities 
MNU is teratogenic and embryotoxic, resulting in craniofacial (cleft palate) and skeletal defects, increased fetal resorption, and fetal growth retardation.  Exposure to MNU during pre-implantation, post-implantation, organogenesis, or by paternal exposure can result in these effects.
N-Nitroso-N-methylurea

# Overview
N-Nitroso-N-methylurea (NMU) is a highly reliable carcinogen, mutagen, and teratogen.  NMU is an alkylating agent, and exhibits its toxicity by transferring its methyl group to nucleobases in nucleic acids, which can lead to AT:GC transition mutations.
NMU is the traditional precursor in the synthesis of diazomethane. However, since it is unstable at temperatures beyond 20 C and shock-sensitive to a degree, for this purpose it has become obsolete and replaced by other (N-methyl)nitrosamides. Most chemical supply houses have stopped carrying it.
Acute exposure to NMU in humans can result in skin and eye irritation, headache, nausea, and vomiting.  NMU is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals (IARC 1972, 1978, 1987).  Various cancers induced in animal models include: squamous cell carcinomas of the forestomach, sarcomas and gliomas of the brain, adenocarcinomas of the pancreas, leukemia, and lymphomas.  However, the actual potential for human exposure is quite limited, as the chemical is not produced or used in large quantities 
NMU is teratogenic and embryotoxic, resulting in craniofacial (cleft palate) and skeletal defects, increased fetal resorption, and fetal growth retardation.  Exposure to NMU during pre-implantation, post-implantation, organogenesis, or by paternal exposure can result in these effects.
NHS Primary Care Trust

# Overview
NHS Primary Care Trusts (PCTs) are English statutory bodies, part of the National Health Service,  responsible for delivering health care and health improvements to their local area.  They grew out of committees or Primary Care Groups of the former Health Authorities (see article Strategic Health Authority).  Collectively PCTs are responsible for spending around 80% of the total NHS budget.
PCTs have their own budgets and set their own priorities, within the overriding priorities and budgets set by the relevant Strategic Health Authority they belong to, and Department of Health.  They directly provide a range of community health services; they provide funding for general practitioners and medical prescriptions; they also commission hospital and mental health services from appropriate NHS trusts or from the private sector.  (This activity makes them the analog of "payors" in the United States).  Present government directives envisage that at least 15% of services will eventually be commissioned from the private or voluntary sectors. The direct services presently provided by PCTs will also eventually be commissioned on an 'arm's length' basis.
PCTs are managed by a team of Executive Directors headed by a Chief Executive. These directors are members of the Trust's Board, together with non-executive directors appointed after open advertisement. The Chairman of the Trust is a non-executive director. Other board members may include representatives from the Trust's Professional Executive Committee (PEC) (elected from local GPs, community nurses, pharmacists, dentists etc.) From October 2006, the Chair of the Audit Committee of PCTs will also be appointed specifically on an open advertisement basis, rather than being selected by the Board from amongst the non-executive directors.
The finance and much of the agenda of PCTs is effectively determined by directives from the Strategic Health Authority (SHA) or the Department of Health.
In 2005 the Government announced that the number of Strategic Health Authorities and Primary Care Trusts would be reduced, the latter by about 50%. The result is that, as of 1st October 2006, there are 152 PCTs (reduced from 303) in England, with an average population of just under 330,000 per trust. Only the London PCTs have remained with their former boundaries. After these changes, about 70% of PCTs are co-terminous with local authorities having social service responsibilities, which it is hoped will facilitate joint planning. It is also hoped that the mergers will release about 259m in annual savings for the NHS.

# Lists
- For listing of PCTs as at November 22, 2005 see List of Primary Care Trusts in England
- For listing of PCT mergers from October 1, 2006 see NHS Connecting for Health website
Number needed to treat

# Overview
The number needed to treat (NNT) is an epidemiological measure that indicates how many patients would require treatment with a form of medication to reduce the expected number of cases of a defined endpoint by one.  It is defined as the inverse of the absolute risk reduction.

# Historical Perspective
The number needed to treat was described in 1988.

# Calculation of NNT
Consider a hypothetical drug which reduces the risk of colon cancer by 50%. Even without the drug, colon cancer is fairly rare, maybe 1 in 3,000 in every 5 year period. The NNT for a 5-year treatment with the drug is therefore 6,000: by treating 6,000 people with the drug, one can expect to reduce the number of colon cancer cases from 2 to 1.
In general, NNT is always computed with respect to two treatments A and B, with A typically a drug and B a placebo (in our example above, A is a 5-year treatment with the hypothetical drug, and B is no treatment). A defined endpoint has to be specified (in our example: the appearance of colon cancer in the 5 year period). If the probabilities pA and pB of this endpoint under treatments A and B, respectively, are known, then the NNT is computed as 1/(pB-pA).
The NNT is an important measure in pharmacoeconomics. If a clinical endpoint is devastating enough (e.g. death, heart attack), drugs with a high NNT may still be indicated in particular situations. If the endpoint is minor, health insurers may decline to reimburse drugs with a high NNT.

# Worked Example

# Variations

## Number Needed to Screen
In  screening, the number needed to screen (NNS) is the number of patients who must be screened for one patient to benefit.  Number need to screen is smaller than number needed to invite.

## Number Needed to Invite
In  screening, the number needed to invite (NNI) is the number of patients who must be invited for screening for one patient to benefit.  NNI is the number needed to screen divided by the rate of acceptance of screening.
Nabumetone precautions

# List of precautions
Renal Effects
Hepatic Function
Fluid Retention and Edema
Photosensitivity

## Renal Effects
As a class, NSAIDs have been associated with renal papillary necrosis and
-ther abnormal renal pathology during long-term administration to animals.
A second form of renal toxicity often associated with NSAIDs is seen in patients with
conditions leading to a reduction in renal blood flow or blood volume, where renal prostaglandins have
a supportive role in the maintenance of renal perfusion. In these patients, administration of an NSAID
results in a dose-dependent decrease in prostaglandin synthesis and, secondarily, in a reduction of renal
blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction
are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics, and the
elderly. Discontinuation of NSAID therapy is typically followed by recovery to the pretreatment state.

## Hepatic Function
As with other NSAIDs, borderline elevations of 1 or more liver function
tests may occur in up to 15% of patients. These abnormalities may progress, may remain essentially
unchanged, or may return to normal with continued therapy. The ALT (SGPT) test is probably the
most sensitive indicator of liver dysfunction. Meaningful (3 times the upper limit of normal) elevations
-f ALT (SGPT) or AST (SGOT) have occurred in controlled clinical trials of RELAFEN in less than
1% of patients. A patient with symptoms and/or signs suggesting liver dysfunction, or in whom an
abnormal liver test has occurred, should be evaluated for evidence of the development of a more severe
hepatic reaction while on therapy with RELAFEN. Severe hepatic reactions, including jaundice and
fatal hepatitis, have been reported with RELAFEN and other NSAIDs. Although such reactions are
rare, if abnormal liver tests persist or worsen, if clinical signs and symptoms consistent with liver
disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), RELAFEN should
be discontinued.

## Fluid Retention and Edema
Fluid retention and edema have been observed in some
patients taking RELAFEN; therefore, as with other NSAIDs, RELAFEN should be used cautiously in patients with a history of congestive heart failure, hypertension, or other conditions predisposing to
fluid retention

## Photosensitivity
Based on ultraviolet (U.V.) light photosensitivity testing, RELAFEN may
be associated with more reactions to sun exposure than might be expected based on skin tanning types.
Adapted from the FDA Package Insert.
Pachyonychia congenita
Synonyms and keywords: Pachyonychia; thickened nails; nail thickness increased; pachyonychia congenita syndrome

# Overview
Pachyonychia congenita is an autosomal dominant skin disorder.

# Pathophysiology
The condition is caused by genetic mutations in one of four genes that encode keratin proteins specific to the epithelial tissues affected in the two forms of the disorder.  Pachyonychia congenita type 1 (PC1) is caused by mutations in keratin 6A (protein name K6A; gene name KRT6A) or keratin 16 (protein K16; gene KRT16). The PC2 form is due to mutations in the genes encoding keratin 6B (protein name K6B; gene name KRT6B) or keratin 17 (protein K17; gene KRT17).  Three of the genes causing PC were identified in 1995 with the fourth gene following in 1998.

## Genetics
- Pachyonychia congenita has an autosomal dominant pattern of inheritance.
Pachyonychia congenita follows an autosomal dominant pattern of inheritance, which means the defective gene is located on an autosome, and only one copy of the gene is required to inherit the disorder from a parent who has the disorder.
On average, 50% of the offspring of an affected person will inherit the disorder, regardless of gender.
Occasionally, however, a solitary case can emerge in a family with no prior history of the disorder due to the occurrence of a new mutation (often referred to as a sporadic or spontaneous mutation).

# Causes

## Causes in Alphabetical Order
- Jackson-Lawler congenital pachyonychia
- Jadassohn-Lewandowsky syndrome
- Olmsted syndrome
- Tyrosinaemia type 2

# Diagnosis

## Symptoms
Common symptoms include:
- Excess keratin in nail beds and thickening of the nails
- Hyperkeratosis on hands and feet
- Oral lesions that look like thick white plaques
Naratriptan overdosage

# Overdosage
A patient who was mildly hypertensive experienced a significant increase in blood pressure after administration of a 10 mg dose starting at 30 minutes (baseline value of 150/98 to 204/144 mmHg 225 minutes). This event resolved after treatment with antihypertensive therapy. Oral administration of 25 mg of naratriptan in 1 healthy young male subject increased blood pressure from 120/67 mmHg pretreatment up to 191/113 mmHg at approximately 6 hours postdose and resulted in adverse events including lightheadedness, tension in the neck, tiredness, and loss of coordination. Blood pressure returned to near baseline by 8 hours after dosing without any pharmacological intervention.
Another subject experienced asymptomatic ischemic ECG changes likely due to coronary artery vasospasm approximately 2 hours following a 7.5 mg oral dose.
The elimination half-life of naratriptan is about 6 hours (see CLINICAL PHARMACOLOGY), and therefore monitoring of patients after overdose with naratriptan tablets should continue for at least 24 hours or while symptoms or signs persist. There is no specific antidote to naratriptan. Standard supportive treatment should be applied as required. If the patient presents with chest pain or other symptoms consistent with angina pectoris, ECG monitoring should be performed for evidence of ischemia. It is unknown what effect hemodialysis or peritoneal dialysis has on the serum concentrations of naratriptan.
National Hotel disease
National Hotel Disease was an outbreak of virulent dysentery that afflicted guests staying at Washington D.C.'s National Hotel on the eve of James Buchanan's inauguration as president of the United States in February of 1857.  The National Hotel, at the time, was Washington's largest and was quite popular with Southerners.
Buchanan himself became sick, as did several of his closest friends and associates.  This led conspiracy theorists at the time to suggest that National Hotel Disease was actually poison slipped into the hotel's food supply by abolitionists bitter over the election of the pro-slavery Buchanan over Republican John C. Fremont.  Alternative theories suggested that in fact pro-slavery partisans had been responsible as Vice President John C. Breckinridge, a pro-slavery Southerner, would assume Buchanan's duties were he to die. However, the more likely explanation is that the disease was caused by unsanitary conditions present in the nation's capital.  In fact, the frigid winter that year had caused the hotel plumbing to freeze, leading to a sewage backup that overflowed into and contaminated the hotel's kitchen.
Whatever strain or strains of bacteria were involved must have been particularly virulent, because many of the guests remained sick for months or even years after, and several died from the disease. Buchanan himself was bed-ridden for the first six weeks of his presidency and among the people who ultimately died of the illness were Mississippi congressman John Quitman and Pennsylvania congressman John Gallagher Montgomery .  Massachusetts congressman Jonathan Edwards Field and New Hampshire Senator John Parker Hale also became sick from the disease and lived with the effects for several years.