Persius/hicric huggingface dataset:
Metronidazole adverse reactions

# Adverse Reactions
The following reactions have been reported during treatment with metronidazole:

## Central Nervous System
The most serious adverse reactions reported in patients treated with metronidazole have been convulsive seizures, encephalopathy, aseptic meningitis, optic and peripheral neuropathy, the latter characterized mainly by numbness or paresthesia of an extremity. Since persistent peripheral neuropathy has been reported in some patients receiving prolonged administration of metronidazole, patients should be specifically warned about these reactions and should be told to stop the drug and report immediately to their physicians if any neurologic symptoms occur. In addition, patients have reported headache, syncope, dizziness, vertigo, incoordination, ataxia, confusion, dysarthria, irritability, depression, weakness, and insomnia (see Warnings).

## Gastrointestinal
The most common adverse reactions reported have been referable to the gastrointestinal tract, particularly nausea, sometimes accompanied by headache, anorexia, and occasionally vomiting; diarrhea; epigastric distress; abdominal cramping; and constipation.

## Mouth
A sharp, unpleasant metallic taste is not unusual. Furry tongue, glossitis, and stomatitis have occurred; these may be associated with a sudden overgrowth of Candida which may occur during therapy.

## Dermatologic
Erythematous rash and pruritus.

## Hematopoietic
Reversible neutropenia (leukopenia); rarely, reversible thrombocytopenia.

## Cardiovascular
Flattening of the T-wave may be seen in electrocardiographic tracings.

## Hypersensitivity
Urticaria, erythematous rash, Stevens-Johnson Syndrome, toxic epidermal necrolysis, flushing, nasal congestion, dryness of the mouth (or vagina or vulva), and fever.

## Renal
Dysuria, cystitis, polyuria, incontinence, and a sense of pelvic pressure. Instances of darkened urine have been reported by approximately one patient in 100,000. Although the pigment which is probably responsible for this phenomenon has not been positively identified, it is almost certainly a metabolite of metronidazole and seems to have no clinical significance.

## Other
Proliferation of Candida in the vagina, dyspareunia, decrease of libido, proctitis, and fleeting joint pains sometimes resembling "serum sickness." Rare cases of pancreatitis, which generally abated on withdrawal of the drug, have been reported.
Patients with Crohn's disease are known to have an increased incidence of gastrointestinal and certain extraintestinal cancers. There have been some reports in the medical literature of breast and colon cancer in Crohn's disease patients who have been treated with metronidazole at high doses for extended periods of time. A cause and effect relationship has not been established. Crohn's disease is not an approved indication for FLAGYL 375 capsules.
Metronidazole contraindications

# Contraindications

## Hypersensitivity
FLAGYL 375 capsules are contraindicated in patients with a prior history of hypersensitivity to metronidazole or other nitroimidazole derivatives.
In patients with trichomoniasis, FLAGYL 375 capsules are contraindicated during the first trimester of pregnancy (see Precautions).

## Psychotic Reaction with Disulfiram
Use of oral metronidazole is associated with psychotic reactions in alcoholic patients who were using disulfiram concurrently. Do not administer metronidazole to patients who have taken disulfiram within the last two weeks (see Precautions, Drug Interactions).

## Interaction with Alcohol
Use of oral metronidazole is associated with a disulfiram-like reaction to alcohol, including abdominal cramps, nausea, vomiting, headaches, and flushing. Discontinue consumption of alcohol or products containing propylene glycol during and for at least three days after therapy with metronidazole (see Precautions, Drug Interactions).
Metronidazole drug interactions

# Drug Interactions

## Disulfiram
Psychotic reactions have been reported in alcoholic patients who are using metronidazole and disulfiram concurrently. Metronidazole should not be given to patients who have taken disulfiram within the last 2 weeks (see Contraindications).

## Alcoholic Beverages
Abdominal cramps, nausea, vomiting, headaches, and flushing may occur if alcoholic beverages or products containing propylene glycol are consumed during or following metronidazole therapy (see CONTRAINDICATIONS).

## Warfarin and other Oral Anticoagulants
Metronidazole has been reported to potentiate the anticoagulant effect of warfarin and other oral coumarin anticoagulants, resulting in a prolongation of prothrombin time. When FLAGYL 375 capsules is prescribed for patients on this type of anticoagulant therapy prothrombin time and INR should be carefully monitored.

## Lithium
In patients stabilized on relatively high doses of lithium, short-term metronidazole therapy has been associated with elevation of serum lithium and, in a few cases, signs of lithium toxicity. Serum lithium and serum creatinine levels should be obtained several days after beginning metronidazole to detect any increase that may precede clinical symptoms of lithium intoxication.

## Busulfan
Metronidazole has been reported to increase plasma concentrations of busulfan, which can result in an increased risk for serious busulfan toxicity. Metronidazole should not be administered concomitantly with busulfan unless the benefit outweighs the risk. If no therapeutic alternatives to metronidazole are available, and concomitant administration with busulfan is medically needed, frequent monitoring of busulfan plasma concentration should be performed and the busulfan dose should be adjusted accordingly.

## Drugs that Inhibit CYP450 Enzymes
The simultaneous administration of drugs that decrease microsomal liver enzyme activity, such as cimetidine, may prolong the half-life and decrease plasma clearance of metronidazole.

## Drugs that Induce CYP450 Enzymes
The simultaneous administration of drugs that induce microsomal liver enzymes, such as phenytoin or phenobarbital, may accelerate the elimination of metronidazole, resulting in reduced plasma levels; impaired clearance ofphenytoin has also been reported.

## Drug/Laboratory Test Interactions
Metronidazole may interfere with certain types of determinations of serum chemistry values, such as aspartate aminotransferase (AST, SGOT), alanine aminotransferase (ALT, SGPT), lactate dehydrogenase (LDH), triglycerides, and glucose hexokinase. Values of zero may be observed. All of the assays in which interference has been reported involve enzymatic coupling of the assay to oxidation-reduction of nicotinamide adenine dinucleotide (NAD+  NADH). Interference is due to the similarity in absorbance peaks of NADH (340 nm) and metronidazole (322 nm) at pH 7.
Mirrored self-misidentification

# Overview
Mirrored self-misidentification is the delusional belief that one's reflection in a mirror is some other person (often believed to be someone who is following them around). Often people who suffer from this delusion are not delusional about anything else. It is considered to be a monothematic delusion and sometimes also labeled as a delusional misidentification syndrome. This disorder is often found within the context of dementia and can also be caused by the organic disfunction resulting from traumatic brain injury, stroke, or neurological illness.

# Causes
Like other monothematic delusions, mirrored self-misidentification is currently thought to be initially caused by a neurological defect, typically in the right hemisphere, which affects one's experience. Current research points toward two potential disfunctions that may lead to this disorder:
- Patients who have impaired face perception and thus can no longer recognize themselves (similar to Capgras delusion)
- Patients who have lost the ability to interact appropriately with mirrors.
Misuse of Drugs Act (Singapore)
The Misuse of Drugs Act is a national drug control law classifying substances into three categories, Classes A, B, and C. Section 44 provides that "The Minister may, by an order published in the Gazette" add, remove, or transfer drugs among the classes. The statute's penal provisions are draconian by most nations' standards, providing for long terms of imprisonment, caning, and capital punishment. The law creates a presumption of trafficking for certain threshold amounts, e.g. 30 grams of cannabis. It also creates a presumption that a person possesses drugs if he possesses the keys to a premises containing the drugs, and that "Any person found in or escaping from any place or premises which is proved or presumed to be used for the purpose of smoking or administering a controlled drug shall, until the contrary is proved, be presumed to have been smoking or administering a controlled drug in that place or premises." Thus, it is dangerous to even be in the company of drug users. The law also allows officers to search premises and individuals, without a search warrant, if he "reasonably suspects that there is to be found a controlled drug or article liable to seizure". Moreover, Section 31 allows officers to demand urinalysis of suspected drug offenders.

# Amount of controlled drugs that would qualify as drug trafficking
Section 17 of the Misuse of Drugs Act lists the amount of controlled drugs beyond which, the person who carries them shall be presumed to possess them for the purpose of drug trafficking unless proven otherwise:
- Opium: 100 grammes
- Morphine: 3 grammes
- Diamorphine (Heroin): 2 grammes
- Cannabis: 15 grammes
- Cannabis mixture: 30 grammes
- Cannabis resin: 10 grammes
- Cocaine: 3 grammes
- Methamphetamine: 25 grammes
- 10 grammes of any or any combination of the following:
N, -dimethyl-3,4-(methylenedioxy)phenethylamine
-methyl-3,4-(methylenedioxy)phenethylamine
N-ethyl--methyl-3,4-(methylenedioxy)phenethylamine
- N, -dimethyl-3,4-(methylenedioxy)phenethylamine
- -methyl-3,4-(methylenedioxy)phenethylamine
- N-ethyl--methyl-3,4-(methylenedioxy)phenethylamine
It should be noted that, unless authorized by the government, the possession, consumption, manufacturing, import, export, or trafficking of these and other controlled drugs in any amount are illegal.
Mitochondrial calcium uniporter
The mitochondrial calcium uniporter (MCU) is a transmembrane protein that allows the passage of calcium ions from a cell's cytosol into mitochondria. Its activity is regulated by MICU1 and MICU2, which together with the MCU make up the mitochondrial calcium uniporter complex.
The MCU is one of the primary sources of mitochondria uptake of calcium, and flow is dependent on membrane potential of the inner mitochondrial membrane and the concentration of calcium in the cytosol relative to the concentration in the mitochondria. Balancing calcium concentration is necessary to increase the cell's energy supply and regulate cell death. Calcium is balanced through the MCU in conjunction with the sodium-calcium exchanger.
The MCU has a very low affinity for calcium, so the cytosolic calcium concentration needs to be approximately 5-10 uM for significant transport of calcium into the mitochondria. Mitochondria are closely associated with the endoplasmic reticulum (ER), at contact sites, which contains stores of cellular calcium ions for calcium signaling. The presence of 1,4,5-triphosphate (IP3) triggers the release of calcium from these intracellular stores, which creates microdomains of high calcium concentration between the ER and the mitochondria, creating the conditions for the MCU to take up calcium.
Ruthenium red and Ru360 are typical reagents used to experimentally block the MCU to study its properties and role in mitochondrial signaling.
Motor vehicle accident overview
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# Overview
A traffic collision,  occurs when a vehicle collides with another vehicle, pedestrian, animal, road debris, or other stationary obstruction, such as a tree or utility pole. Traffic collisions may result in injury, death, vehicle damage and property damage. A number of factors contribute to the risk of collision including; vehicle design, speed of operation, road design, road environment, driver skill and/or impairment and driver behaviour. Worldwide, motor vehicle collisions lead to death and disability as well as financial costs to both society and the individuals involved.

# Classification
Traffic collisions can be classified by general type. Types of collision include head-on, road departure, rear-end, side collisions, and rollovers.
Mycobacterium avium hominissuis
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"Mycobacterium avium hominissuis"
Suggested name for Mycobacterium avium avium isolates from humans and pigs.
Based on differences in IS1245 RFLP, 16S-23S rDNA ITS and growth temperature, Mijs et al. 2002 propose to reserve the designation Mycobacterium avium subsp. avium for bird-type isolates. These authors suggest, but not formally propose, the designation "Mycobacterium avium subsp. hominissuis" for the isolates from humans and pigs.
Mycobacterium frederiksbergense
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Mycobacterium frederiksbergense
Etymology: frederiksbergense, of Frederiksberg, Denmark, referring to the place of isolation.

# Type Strain
First isolated in Frederiksberg, Denmark.
Strain FAn9 = CIP 107205 = DSM 44346 = NRRL B-24126.
N-acetylglucosamine-6-sulfatase
N-acetylglucosamine-6-sulfatase also known as glucosamine (N-acetyl)-6-sulfatase is an enzyme that in humans is encoded by the GNS gene. This enzyme is deficient in Sanfilippo Syndrome type IIId. This enzyme catalyses the following chemical reaction:

# Function
N-acetylglucosamine-6-sulfatase is a lysosomal enzyme found in all cells. It is involved in the catabolism of heparin, heparan sulphate, and keratan sulphate.

# Clinical significance
Deficiency of this enzyme results in the accumulation of undergraded substrate and the lysosomal storage disorder mucopolysaccharidosis type IIID (Sanfilippo D syndrome). Mucopolysaccharidosis type IIID is the least common of the four subtypes of Sanfilippo syndrome.

# Nomenclature
The systematic name of this enzyme is "N-acetyl-D-glucosamine-6-sulfate 6-sulfohydrolase".  Other accepted names include:
- N-acetylglucosamine-6-sulfatase,
- glucosamine (N-acetyl)-6-sulfatase,
- 2-acetamido-2-deoxy-D-glucose 6-sulfate sulfatase,
- N-acetylglucosamine 6-sulfate sulfatase,
- O,N-disulfate O-sulfohydrolase,
- acetylglucosamine 6-sulfatase,
- chondroitinsulfatase, and
- glucosamine-6-sulfatase.
New England Journal of Medicine
The New England Journal of Medicine (New Engl J Med or NEJM) is a English-language peer-reviewed medical journal published by the Massachusetts Medical Society.  It is one of the most popular and widely-read peer-reviewed general medical journals in the world.  It is also the oldest continuously published medical journal in the world.
It was founded by Dr. John Collins Warren in 1812 as a quarterly called The New England Journal of Medicine and Surgery. In 1828, it became a weekly, and was renamed The Boston Medical and Surgical Journal; one hundred years later, it took on its present name.
It publishes editorials, papers on original research, widely-cited review articles, correspondences, case reports, and has a special section called "Images in Clinical Medicine".
Authors have included Oliver Wendell Holmes, Sr., Hans Zinsser, and Lewis Thomas. One of its early editors, Jerome V. C. Smith, resigned in 1857 to assume his duties as mayor of the City of Boston.
The website for the George Polk Awards noted that its 1977 award to the New England Journal of Medicine "provided the first significant mainstream visibility for a publication that would achieve enormous attention and prestige in the ensuing decades"
The journal usually has the highest impact factor of the journals of clinical medicine (including the Journal of the American Medical Association, and The Lancet); in 2006, the impact factor was 51, according to Journal Citation Reports, the first research journal to break 50.

# Open access policy
NEJM provides delayed free online access to its research articles (it does so six months after publication, and maintains that access dating back to 1993). This delay does not apply to readers from the least developed countries, for whom the content is available at no charge for personal use.
NEJM also has two podcast features, one with interviews of doctors and researchers that are publishing in the journal, and another summarizing the content of each issue. Other offerings include Continuing Medical Education, Videos in Clinical Medicine (showing videos of medical procedures), and the weekly Image Challenge.
- Walter Prentice Bowers, 19211937
- Robert Nason Nye, 19371947
- Joseph Garland, 19471967
- Franz J. Ingelfinger, 19671977
- Arnold S. Relman, 19771991
- Jerome P. Kassirer, 19911999
- Marcia Angell, 19992000
- Jeffrey M. Drazen, 2000-

# Other leading medical journals
- JAMA
- Nature Medicine
- The Lancet
- British Medical Journal
- Annals of Internal Medicine
- Archives of Internal Medicine
- Journal Watch, sibling publication to NEJM
- The Medical Letter on Drugs and Therapeutics
- Canadian Medical Association Journal
Naftifine clinical pharmacology

# Clinical Pharmacology
Naftifine Hydrochloride is a synthetic allylamine derivative. The following in vitro data are available but their clinical significance is unknown. Naftifine hydrochloride has been shown to exhibit fungicidal activity in vitro against a broad spectrum of organisms, including Trichophyton rubrum, Trichophyton mentagrophytes, Trichophyton tonsurans, Epidermophyton floccosum, Microsporum canis, Microsporum audouini, and microsporum gypseum, and fungistatic activity against Candida species, including Candida albicans. Naftin Cream and Gel, 1% have only been shown to be clinically effective against the disease entities listed in the INDICATIONS AND USAGE section.
Although the exact mechanism of action against fungi is not known, naftifine hydrochloride appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2, 3-epoxidase. This inhibition of enzyme activity results in decreased amounts of sterols, especially ergosterol, and a corresponding accumulation of squalene in the cells.

### Pharmacokinetics
In vitro and in vivo bioavailability studies have demonstrated that naftifine penetrates the stratum corneum in sufficient concentration to inhibit the growth of dermatophytes.
Following a single topical application of 1% of naftifine cream to the skin of healthy subjects, systemic absorption of naftifine was approximately 6% of the applied dose. Following single topical applications of 3H- labeled naftifine gel 1% to the skin of healthy subjects, up to 4.2% of the applied dose was absorbed. Naftifine and/or its metabolites are excreted via the urine and feces with a half-life of approximately two to three days.
National Neuroscience Institute
The National Neuroscience Institute (NNI; Chinese: ) is a medical institute located in Singapore specialising in the neurosciences.  It is a national referral centre.  There are over 20 subspecialties that are served.

# Subspecialties and conditions related to the neurosciences
Epilepsy, headache, neuromuscular disorders, paediatric neurology, Parkinson's Disease, sleep disorders, stroke, and neuro-rehabilitation are among some of the problems treated at the institute. 

# Location
The institute is located within Tan Tock Seng Hospital (TTSH) and Singapore General Hospital (SGH).  TTSH is located near the Novena MRT.  SGH is located near the Outram Park MRT station.
The institute was founded on 28 March 1989 and commenced operations 1 April 1989.  Associate Professor Lee Wei Ling, daughter of the Minister Mentor, is a director in the institute.
Non-24-hour sleep-wake syndrome

# Overview
Non-24-hour sleep-wake syndrome, also termed circadian rhythm sleep disorder, free-running type, circadian arrhythmia, non-24-hour circadian rhythm disorder or hypernychthemeral syndrome, is a circadian rhythm sleep disorder. The International Classification of Sleep Disorders defines the disorder as, "a chronic steady pattern comprising one- to two-hour daily delays in sleep onset and wake times in an individual living in society."
In people with this disorder, the person's body essentially insists that the day is longer than 24 hours. This tends to not allow socially accepted sleeping patterns, and makes it difficult for the sufferer to sleep at "normal" times. Most cases that have been reported in the medical literature have occurred in blind patients.
Left untreated, non-24-hour sleep-wake syndrome causes a person's sleep-wake cycle to change every day, the degree determined by how much over 24 hours the cycle lasts. The cycle may go around the clock, eventually returning to "normal" for one or two days before going "off" again.  This is known as "Free-running".
People with the disorder often have a hard time "resetting" their internal clocks to socially accepted sleep-wake patterns. They may have an especially hard time adjusting to changes in "regular" sleep-wake cycles, such as vacations, stress, evening activities, time changes like daylight saving time, travel to different time zones, illness, medications (especially stimulants or sedatives), changes in daylight hours in different seasons, and growth spurts, which are typically known to cause fatigue.
Common treatments for non-24-hour sleep-wake syndrome are similar to those for delayed sleep phase syndrome. They include light therapy with a full spectrum lamp givingusually10000 lux, chronotherapy, acupuncture, vitamin B12 supplements, and melatonin supplements. It often takes several treatments before any progress is noticed, and for many the treatments may only be marginally effective or not effective at all. In addition, the treatment is not a cure, and the condition can only be managed.
Treatment with melatonin taken 30 minutes to two hours before the desired bedtime may be helpful in righting a pattern "gone awry". Too high a dose of melatonin may have the unintended effect of disturbing the sleep or even causing nightmares, and uncontrollable yawning the next day. Bright light therapy combined with the use of melatonin may be the most effective treatment. The timing of both is tricky and a lot of determination and experimentation is usually necessary.