Persius/hicric huggingface dataset:
Vytorin contraindications

# Contraindications
VYTORIN is contraindicated in the following conditions:
- Concomitant administration of strong CYP3A4 inhibitors (e.g., itraconazole, ketoconazole, posaconazole, voriconazole, HIV protease inhibitors, boceprevir, telaprevir, erythromycin, clarithromycin, telithromycin and nefazodone) .
- Concomitant administration of gemfibrozil, cyclosporine, or danazol .
- Hypersensitivity to any component of this medication .
- Active liver disease or unexplained persistent elevations in hepatic transaminase levels .
- Women who are pregnant or may become pregnant. Serum cholesterol and triglycerides increase during normal pregnancy, and cholesterol or cholesterol derivatives are essential for fetal development. *Because HMG-CoA reductase inhibitors (statins), such as simvastatin, decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, VYTORIN may cause fetal harm when administered to a pregnant woman. Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. There are no adequate and well-controlled studies of VYTORIN use during pregnancy; however, in rare reports congenital anomalies were observed following intrauterine exposure to statins. In rat and rabbit animal reproduction studies, simvastatin revealed no evidence of teratogenicity. VYTORIN should be administered to women of childbearing age only when such patients are highly unlikely to conceive. If the patient becomes pregnant while taking this drug, VYTORIN should be discontinued immediately and the patient should be apprised of the potential hazard to the fetus .
- Nursing mothers. It is not known whether simvastatin is excreted into human milk; however, a small amount of another drug in this class does pass into breast milk. Because statins have the potential for serious adverse reactions in nursing infants, women who require VYTORIN treatment should not breast-feed their infants .
Fusobacterium necrophorum

# Overview
Fusobacterium necrophorum is a species of bacteria responsible for Lemierre's syndrome and other medical problems. It is an obligate anaerobe and is a common inhabitant of the alimentary tract within humans and animals.

# Biology
F. necrophorum is a rod-shaped species of Gram-negative bacteria. It is an obligate anaerobe and is a common inhabitant of the alimentary tract within humans and animals.

# Pathogenicity
F. necrophorum is responsible for 10% of acute sore throats, 21% of recurrent sore throats and 23% of peritonsillar abscesses with the remainder being caused by Group A streptococci or viruses. Other complications from F. necrophorum include meningitis, complicated by thrombosis of the internal jugular vein, thrombosis of the cerebral veins, and infection of the urogenital and the gastrointestinal tracts.
Although this infection is rare, researchers agree that this diagnosis should be considered in a septicaemic patient with thrombosis in an unusual site, and underlying malignancy should be excluded in cases of confirmed F. necrophorum occurring at sites caudal to the head.

## Treatment
F. necrophorum infection (also called F-throat) usually responds to treatment with penicillin or metronidazole, but penicillin treatment for persistent pharyngitis appears anecdotally to have a higher relapse rate, although the reasons are unclear.

## Infection in animals
This bacterium has been found to be associated with the foot disease thrush in horses. Thrush is a common fungal infection that occurs on the hoof of a horse, specifically in the region of the frog. F. necrophorum occurs naturally in the animal's environment, especially in wet, muddy, or unsanitary conditions, such as an unclean stall.  Horses with deep clefts, or narrow or contracted heels are more at-risk to develop thrush.
F. necrophorum is also a cause for lameness in sheep. Its infection is commonly called scald. It can last for several years on land used by either sheep or cattle, and is found on most land of this type throughout the world. Due to its survival length in these areas, it is unrealistic to try to remove it. Sheep most often get scald due to breakage or weakness of the skin surrounding the hoof. This can occur due to strong footbaths, sandy soils, mild frostbite, or prolongened waterlogging of a field, and  results in denaturing of the skin between the cleats.

# Treatment

## Antimicrobial regimen
- Fusobacterium necrophorum treatment
- 1. In adults
- Preferred regimen: Combination therapy of Metronidazole 500 mg IV q8h AND Ceftriaxone 2 gm IV q24h
- 2. In children
- Preferred regimen: Combination therapy of Metronidazole 1015 IV mg/kg q8h AND Ceftriaxone 80100 mg/kg q12h
- Alternative regimen (1): Imipenem
- Alternative regimen (2): Ampicillin-Sulbactam
- Alternative regimen (3): antipseudomonal penicillins
- Alternative regimen (4): Clindamycin
- Note: More frequent dosing of ceftriaxone is needed in cases of CNS infection.
Glucocorticoid resistance
Synonyms and keywords: Cortisol resistance; glucocorticoid insensitivity; steroid hormone resistance; glucocorticoid receptor, steroid hormone insensitivity; overexpression of human glucocorticoid receptor beta, generalized partial end-organ insensitivity to physiologic glucocorticoid concentrations; elevations in circulating cortisol; mineralocorticoid excess; androgen excess
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# Overview
Patients can be both resistant and hypersensitive to glucocorticoids.
In glucocorticoid resistance, the target tissue is unable to respond to glucocorticoids. The lack of responsiveness can be
- Generalized or tissue-specific
- Transient or permanent
- Partial or complete
- Compensated or noncompensated.
The presence of complete glucocorticoid resistance is fatal.  Absence of functional glucocorticoid receptors (GRs) in GR -/- knockout mice is associated with death within hours.

# Acknowledgements
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
Fanconi syndrome overview

# Overview
Fanconi syndrome is a disorder in which the  proximal tubular function of the kidney is impaired, resulting in decreased reabsorption of electrolytes and nutrients back into the bloodstream. Compounds involved include glucose, amino acids, uric acid, phosphate, and bicarbonate.
The reduced reabsorption of bicarbonate results in type 2 or proximal renal tubular acidosis, which may in some cases exist on its own, or more usually in combination with the Fanconi syndrome.
In many cases, the disease is developed in the context of  multi-system genetic diseases(e.g Cystinosis, Galactosemia). And in many others, high exposure to toxic substances(e.g heavy metals, drugs) is discovered as the main risk factor. The disease can also develop as a consequence of other acquired diseases(e.g multiple myeloma, PNH).
Patients mainly present with dehydration, growth failure, rickets(children) and osteomalacia(adults).
It is named after Guido Fanconi, a Swiss pediatrician; this may be a misnomer since Fanconi himself never identified it as a syndrome.
It should not be confused with Fanconi anemia, a separate disease.
Fetal genital development
Fetal genital development refers to the sequence of events which leads to the develoment of the genitals and their adnexa.

# Sequence
A few weeks after fertilization, the initial appearance of the human fetal genitalia is basically feminine: a pair of "urogenital folds" with a small protuberance in the middle, and the urethra behind the protuberance.
In typical fetal development, the presence of the SRY gene causes the fetal gonads to become testes; the absence of it allows the gonads to continue to develop into ovaries. Thereafter, the development of the internal reproductive organs and the external genitalia is determined by hormones produced by fetal gonads (ovaries or testes) and the cells' response to them.
If the fetus has testes, and if the testes produce testosterone, and if the cells of the genitals respond to the testosterone, the outer urogenital folds swell and fuse in the midline to produce the scrotum; the protuberance grows larger and straighter to form the penis; the inner urogenital swellings swell, wrap around the penis, and fuse in the midline to form the penile urethra.
If testosterone is not present, normal female development continues, with the development of a perineal urethra and the formation of a uterus, clitoris and vagina.
The Mullerian ducts, which are paired ducts of the embryo which empty into the cloaca, and which develop into the upper vagina, cervix, uterus and oviducts; in the male they disappear except for the vestigial vagina masculina and the appendix testis.
Although female development is usually considered the "default" configuration in the absence of induction, recent evidence has indicated that Wnt4 plays a role in the development of female anatomy.

# Homologies
Because of their common origin in fetal anatomy, a number of male and female anatomical features are said to be homologous; for example, the clitoris and penis are homologous with one another, as are Skene's glands in females and the prostate gland in males.

# Intersexuality
Most of the time, the result of fetal genital development follows the stereotypical male or stereotypical female development path. However, in a small but significant minority of cases, the path of development follows an intermediate or other pathway, leading to what are called "ambiguous genitalia", one condition of those known as intersexuality.
See congenital anomalies of the genitalia for a list of congenital disorders caused by problems with fetal genital development.
Schotten-Baumann reaction
The Schotten-Baumann-reaction is a method to synthesise amides from amines and acid chlorides:
Sometimes the name for this reaction is also used to indicate the reaction between an acid chloride and a alcohol to form an ester. The reaction was first described in 1883 by German chemists Carl Schotten and Eugen Baumann  .

# Reaction mechanism
In the first step an acid chloride reacts with an amine so that an amide is formed, together with a proton and a chloride ion. Addition of a base is required to absorb this acidic proton, or the reaction will not proceed. Often, a watery solution of a base is slowly added to the reaction mixture.
The name "Schotten-Baumann reaction conditions" is often used to indicate the use of a two-phase solvent system, consisting of water and an organic solvent. The base within the water phase neutralizes the acid, generated in the reaction, while the starting materials and product remain in the organic phase, often dichloromethane or diethylether.

# Applications
The Schotten-Baumann-reaction (or -reaction conditions)are widely used today in organic chemistry. Examples include:
- synthesis of N-vanillylnonanamide, also known as synthetic capsaicine
- synthesis of benzamide from benzoyl chloride and a fenethylamine
- acylation of a benzylamine with acetyl chloride (acetic acid anhydride is an alternative)
- In the Fischer peptide synthesis (Hermann Emil Fischer, 1903)  an -chloro acid chloride is condensed with the ester of an amino acid. The ester is then hydrolyzed and the acid converted to the acid chloride enabling the extension of the peptide chain by another unit. In a final step the chloride atom is replaced by an amino group completing the Peptide synthesis.
Fitz-Hugh-Curtis syndrome
Fitz-Hugh-Curtis syndrome is a rare complication of pelvic inflammatory disease (PID) named after the two physicians, Fitz-Hugh and Curtis who first reported this condition in 1934 and 1930 respectively.
Fitz-Hugh-Curtis syndrome is usually caused by gonorrhoea (acute gonococcal perihepatitis) or chlamydia bacteria, which cause a thinning of cervical mucous and allow bacteria from the vagina into the uterus and oviducts, causing infection and inflammation.  Occasionally, this inflammation can affect Glisson's capsule, a thin layer of connective tissue surrounding the liver.
The signs are an acute onset, upper right-quadrant abdominal pain and tenderness aggravated by breathing, coughing or movement, and referred to the right shoulder following an episode of PID. Laparoscopy may reveal "violin string" adhesions.
Treatment involves diagnosing and treating the underlying cause correctly. The adhesions can be cut laparoscopically.
Flunitrazepam indications

# Overview
Flunitrazepam/Rohypnol is a prescription drug - the only sedative that has been used in many date rapes in the US. Rohypnol's medical use is a preoperation anesthetic or strong sleeping pill, but stronger doses can bring on amnesia. It takes effect very quickly - sometimes as quick as 10 minutes after taken - and reaches its peak eight hours later when it can render a patient totally unconscious. 
Rohypnol comes as a pill that can diissolve in liquids. Some are round , small and white. Newer pills are oval and green-grey in colour. When slipped into a drink , a dye in these new pills makes clear liquids turn blue and the dark drinks turn cloudy. But this colour change might br hard to see in a dark drink, or in a dark room.Also the pills with no dye are available. these pills may be grounded up into a powder.

# Desired effects
There are few effects of Rohypnol which are desired and for which purpose it is used. Desired effects include disinhibition, amnesia and muscle relaxation, but individual effects vary. The amnesia is anterograde, that is, it involves memory loss for events that occur after the medication is taken.
Flunitrazepam precautions

# Overview
Flunitrazepam/Rohypnol is a prescription drug - the only sedative that has been used in many date rapes in the US. Rohypnol's medical use is a preoperation anesthetic or strong sleeping pill, but stronger doses can bring on amnesia. It takes effect very quickly - sometimes as quick as 10 minutes after taken - and reaches its peak eight hours later when it can render a patient totally unconscious. 
Rohypnol comes as a pill that can diissolve in liquids. Some are round , small and white. Newer pills are oval and green-grey in colour. When slipped into a drink , a dye in these new pills makes clear liquids turn blue and the dark drinks turn cloudy. But this colour change might br hard to see in a dark drink, or in a dark room.Also the pills with no dye are available. these pills may be grounded up into a powder.

# Warning/precautions
Flunitrazepam should be used with caution in patients with respiratory disease, muscle weakness, history of drug or alcohol abuse, marked personality disorder; avoid regular use during pregnancy (risk of neonatal withdrawl symptoms); use only if clear indication such as seizure control (high doses during late pregnancy or labour may cause neonatal hypothermia, hypotonia and respiratory depression); breast-feeding (present in milk, avoid if possible); reduce dose in elderly and debilitated, and in hepatic (avoid if severe) and renal impairment (start with small doses if severe); avoid prolong use (abrupt withdrawl thereafter); porphyria. It should not be used alone to treat depression (or anxiety associated with depression) or psychosis
Fosamprenavir description

# Description
LEXIVA (fosamprenavir calcium) is a prodrug of amprenavir, an inhibitor of HIV protease. The chemical name of fosamprenavir calcium is (3S)-tetrahydrofuran-3-yl (1S,2R)-3-amino]-1-benzyl-2-(phosphonooxy) propylcarbamate monocalcium salt. Fosamprenavir calcium is a single stereoisomer with the (3S)(1S,2R) configuration. It has a molecular formula of C25H34CaN3O9PS and a molecular weight of 623.7. It has the following structural formula:
Fosamprenavir calcium is a white to cream-colored solid with a solubility of approximately 0.31 mg per mL in water at 25C.
LEXIVA Tablets are available for oral administration in a strength of 700 mg of fosamprenavir as fosamprenavir calcium (equivalent to approximately 600 mg of amprenavir). Each 700 mg tablet contains the inactive ingredients colloidal silicon dioxide, croscarmellose sodium, magnesium stearate, microcrystalline cellulose, and povidone K30. The tablet film-coating contains the inactive ingredients hypromellose, iron oxide red, titanium dioxide, and triacetin.
LEXIVA Oral Suspension is available in a strength of 50 mg per mL of fosamprenavir as fosamprenavir calcium equivalent to approximately 43 mg of amprenavir. LEXIVA Oral Suspension is a white to off-white suspension with a grape-bubblegum-peppermint flavor. Each one milliliter (1 mL) contains the inactive ingredients artificial grape-bubblegum flavor, calcium chloride dihydrate, hypromellose, methylparaben, natural peppermint flavor, polysorbate 80, propylene glycol, propylparaben, purified water, and sucralose.
Frenulum labiorum pudendi
In female human anatomy, the frenulum labiorum pudendi (aka. the fourchette) is a frenulum where the labia minora meet at the back. Above it is the vulval vestibule.
The area where the labia minora meet posteriorly is called the posterior commissure of the labia minora.

# Pathology
The fourchette may be torn during delivery due to the sudden stretching of the vulval orifice.  To prevent this tearing in a haphazard manner, obstetricians and, less frequently, midwives may perform an episiotomy, which is a deliberate cut made in the perineum starting from the fourchette downwards. Episiotomies may result in reduced sexual sensation following recovery as the fourchette is a part of the clitoris and contains sensory nerve endings which are severed in the procedure.
The fourchette may also be torn in acts of sex wherein forced entry occurs such as rape. When the fourchette gets torn the bleeding which ensues sometimes requires surgical suturing for containment.

# Etymology
"Fourchette" is French for "little fork", and the word is also used as a technical term for a type of dessert fork. (See frenulum for details on the eytmology of that word.)
Treacher Collins syndrome
Synonyms and keywords: Franceschetti-Zwahlen-Klein syndrome; FranceschettiKlein syndrome; Mandibulofacial dysostosis

# Overview
Treacher Collins syndromeis a rare genetic disorder characterized by craniofacial deformities. Treacher Collins syndrome is found in 1 in 10,000 births.  The typical physical features include downward slanting eyes, a small lower jaw, and malformed or absent ears.
This condition is a result of a defect of the first arch during development.

# Eponym
It is named after Edward Treacher Collins (18621932), the English surgeon and ophthalmologist who described its essential traits in 1900.

# Cause
One known cause of this syndrome is a mutation in the TCOF1 gene, at chromosome 5-q32-q33.1. The protein coded by this gene is called treacle and has been hypothesised to assist in protein sorting during particular stages in embryonic development, particularly that of the structures of the head and face. The disorder is inherited in an autosomal-dominant pattern.

# Symptoms
The symptoms of this disorder vary greatly, ranging from almost unnoticeable to severe. Most affected individuals have underdeveloped facial bones, which result in a sunken appearance in the middle of the face, a prominent nose, and a very small jaw and chin (micrognathia). Some people with this condition are also born with an opening in the roof of the mouth, called a cleft palate. In severe cases, underdevelopment of the facial bones may restrict an affected infant's airway, causing potentially life-threatening respiratory problems.
People with Treacher Collins syndrome often have eyes that slant downward, sparse eyelashes, and a notch in the lower eyelids called a coloboma. People with Treacher Collins Syndrome may also need a feeding tube because some cases are so severe people can't swallow . This condition is also characterized by absent, small, or unusually formed ears (pinnae), called microtia. Defects in the middle ear (which contains three small bones that transmit sound) cause hearing loss in about half of cases. People with Treacher Collins syndrome usually have normal intelligence.

# Trivia
Treacher Collins Syndrome was featured in the 2006 Nip/Tuck episode Blu Mondae.
Juliana Wetmore was born with this syndrome. She is featured in TLC's "Born Without A Face.", in which she is missing 30%-40% of bones in her face.
Fructose 1,6-bisphosphate

# Overview
Fructose 1,6-phosphate is fructose sugar phosphorylated on carbons 1 and 6 (ie. is a fructosephosphate). The -D-form of this compound is very common in cells.  The vast majority of glucose and fructose entering a cell will become converted to fructose 1,6-phosphate at some point.

# Fructose 1,6-phosphate in glycolysis
Fructose 1,6-phosphate lies within the glycolysis metabolic pathway and is produced by phosphorylation of fructose 6-phosphate. It is in turn broken down into two compounds; glyceraldehyde 3-phosphate and glycerone phosphate. It is allosteric activator of pyruvate kinase.
The numbering of the carbon atoms indicates the fate of the carbons according to their position in fructose 6-phosphate.

# Fructose 1,6-phosphate isomerism
Fructose 1,6-phosphate has only one biologically active isomer, the -D-form. There are many other isomers, analogous to those of fructose.
Glycophosphatidylinositol
Glycosylphosphatidylinositol (GPI anchor ) is a glycolipid that can be attached to the C-terminus of a protein during posttranslational modification. It is composed of a hydrophobic phosphatidylinositol group linked through a carbohydrate containing linker (glucosamine and mannose glycosidically bound to the inositol residue) to the C-terminal amino acid of a mature protein. The two fatty acids within the hydrophobic phosphatidyl-inositol group anchor the protein to the cell membrane.
Glypiated proteins contain a signal peptide, thus directing them into the endoplasmic reticulum (ER). The C-terminus is composed of hydrophobic amino acids which stay inserted in the ER membrane. The hydrophobic end is then cleaved off and replaced by the GPI-anchor. As the protein processes through the secretory pathway, it is transferred via vesicles to the Golgi apparatus and finally to the extracellular space where it remains attached to the exterior leaflet of the cell membrane. Since the glypiation is the sole means of attachment of such proteins to the membrane, cleavage of the group by phospholipases will result in controlled release of the protein from the membrane. The latter mechanism is used in vitro, i.e. the membrane proteins released from the membranes in the enzymatic assay are glypiated protein.
Phospholipase C (PLC) is an enzyme that is known to cleave the phospho-glycerol bond found in GPI-anchored proteins. Treatment with PLC will cause release of GPI-linked proteins from the outer cell membrane.  The T-cell marker Thy-1, acetylcholinesterase, as well as both intestinal and placental alkaline phosphatase are known to be GPI-linked and are released by treatment with PLC.  GPI-linked proteins are thought to be preferentially located in lipid rafts, suggesting a high level of organization within microdomains plasma membrane.
Defects of GPI anchors occur in the rare disease paroxysmal nocturnal hemoglobinuria.