Persius/hicric huggingface dataset:
Popliteal pterygium syndrome
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Popliteal pterygium syndrome (PPS) is an inherited condition affecting the face, limbs, and genitalia.  The syndrome goes by a number of names including the popliteal web syndrome and, more inclusively, the facio-genito-popliteal syndrome.  The term PPS was coined by Gorlin et al. in 1968 on the basis of the most unusual anomaly, the popliteal pterygium (a web behind the knee). 

# Clinical Features
Clinical expressions of PPS are highly variable, but include the following:
- Limb findings: an extensive web running from behind the knee down to the heel (90%), malformed toenails, and webbed toes.
- Facial findings: cleft palate with or without cleft lip (75%), pits in the lower lip (40%), and fibrous bands in the mouth known as syngnathia (25%).
- Genital findings (50%): hypoplasia of the labia majora, malformation of the scrotum, and cryptorchidism.

# Epidemiology
The diagnosis of PPS has been made in several ethnic groups, including Caucasian, Japanese, and sub-Saharan African.  Males and females are equally likely to suffer from the syndrome.  Since the disorder is very rare, its incidence rate is difficult to estimate, but is less than 1 in 10,000.

# Genetics
The genetic locus for PPS was localized to chromosome 1 in 1999.
The disorder is inherited in an autosomal dominant manner and is due to mutation of the IRF6 gene.  Most reported cases are sporadic; advanced parental age is found in a number of these cases, suggesting new mutations.
The term PPS has also been used for two rare autosomal recessively inherited conditions: Lethal PPS and PPS with Ectodermal Dysplasia.  Although both conditions feature a cleft lip/palate, syngnathia, and popliteal pterygium, they are clinically distinguishable from the autosomal dominant case.  Lethal PPS is differentiated by microcephaly, corneal aplasia, ectropion, bony fusions, hypoplastic nose, and absent thumbs, while PPS with Ectodermal Dysplasia is differentiated by woolly hair, brittle nails, ectodermal anomalies, and fissure of the sacral vertebrae.

# Relationship to Van der Woude syndrome
Van der Woude syndrome (VDWS) and popliteal pterygium syndrome (PPS) are allelic variants of the same condition; that is, they are caused by different mutations of the same gene.  PPS includes all the features of VDWS, plus popliteal pterygium, syngnathia, distinct toe/nail abnormality, syndactyly, and genito-urinary malformations.
Factor Xa inhibitor antidote
Synonyms and keywords: Factor Xa inhibitor antidote, factor Xa inhibitor reversal agent, FXa inhibitor antidote, Factor 10a inhibitor antidote

# Overview
Direct Factor Xa inhibitors include Rivaroxaban, Betrixaban, Apixaban and Edoxaban.  These agents bind directly to a serine residue of Factor Xa and inhibit the ability of Factor Xa to bind to the active site. They work by steric hinderance. They bind reversibly. Thus there is an equilibrium where these inhibitor molecules are binding and falling off of the Factor Xa molecule.  Indirect inhibitors like fondaparinux and enoxaperin require antithrombin 3 (AT3) in addition.

# Mechanism of Action
This is a "decoy" mechanism whereby the antidote binds to the Factor Xa inhibitor and soaks it up so it doesnt bind and inhibit the Factor Xa. The binding to the Factor Xa inhibitor is reversible. The avidity of the binding is about the same as the avidity with which the Factor Xa inhibitor binds to the Factor Xa molecule. The antidote soaks up or binds all of the Factor Xa inhibitor by binding to it. As a Factor Xa inhibitor falls off of the Factor Xa molecule, it gets soaked up or bound to the antidote. The antidote does not appear to be procoagulant or anticoagulant.
Multiple endocrine neoplasia
Synonyms and keywords: MEN syndromes; Familial endocrine adenomatosis; Multiple endocrine adenomatosis; Multiple endocrine neoplasia syndrome; MEN; MEN-Multiple endocrine neoplasia syndrome; Multiple endocrine neoplasms

# Overview
Multiple endocrine neoplasia (MEN) encompasses several distinct syndromes featuring tumors of endocrine glands, each with its own characteristic pattern. Multiple endocrine neoplasia may be classified according to tumor characteristics into 3 subtypes: multiple endocrine neoplasia type 1, multiple endocrine neoplasia type 2 and multiple endocrine neoplasia type 4.

# Classification
- The following flowchart depicts the classification of multiple endocrine neoplasia.

# Comparison
- The following diagram compares the various types of multiple endocrine neoplasia.
- The following table compares the various types of multiple endocrine neoplasia.
 of patients with MEN1 and gastrinoma
Fosfomycin adverse reactions

# Clinical Trials:
In clinical studies, drug related adverse events which were reported in greater than 1% of the fosfomycin-treated study population are listed below:
In clinical trials, the most frequently reported adverse events occurring in > 1 % of the study population regardless of drug relationship were:
diarrhea 10.4%, headache 10.3%, vaginitis 7.6%, nausea 5.2%, rhinitis 4.5%, back pain 3.0%, dysmenorrheal 2.6%, pharyngitis 2.5%, dizziness 2.3%, abdominal pain 2.2%, pain 2.2%, dyspepsia 1.8%, asthenia 1.7%, and rash 1.4%.
The following adverse events occurred in clinical trials at a rate of less than 1%, regardless of drug relationship:
abnormal stools, anorexia, constipation, dry mouth, dysuria, ear disorder, fever, flatulence, flu syndrome, hematuria, infection, insomnia, lymphadenopathy, menstrual disorder, migraine, myalgia, nervousness, paresthesia, pruritus, SGPT increased, skin disorder, somnolence, and vomiting.
One patient developed unilateral optic neuritis, an event considered possibly related to MONUROL therapy.

# Post-marketing Experience:
Serious adverse events from the marketing experience with MONUROL outside of the United States have been rarely reported and include: angioedema, aplastic anemia, asthma (exacerbation), cholestatic jaundice, hepatic necrosis, and toxic megacolon.
Although causality has not been established, during post marketing surveillance, the following events have occurred in patients prescribed Monurol: anaphylaxis and hearing loss.

# Laboratory Changes:
Significant laboratory changes reported in U.S. clinical trials of MONUROL without regard to drug relationship include: increased eosinophil count, increased or decreased WBC count, increased bilirubin, increased SGPT, increased SGOT, increased alkaline phosphatase, decreased hematocrit, decreased hemoglobin, increased and decreased platelet count. The changes were generally transient and were not clinically significant.
Frequency of sexual activity
The frequency of sexual activity of humans is determined by several parameters, and varies greatly from person to person, and within a person's lifetime.
The frequency of sexual intercourse might range from zero (sexual abstinence) for some to 15 or 20 times a week. It is generally recognized that postmenopausal women experience declines in frequency of sexual intercourse.. The average frequency of sexual intercourse for married couples is 2 to 3 times a week.
Sexual frequency often falls off in relationships when the initial period of limerence ends, and a common belief is that frequency of sexual intercourse often falls after marriage.  However, recent evidence shows that 43% of married couples have sex a few times a month, as compared with 36% of cohabiting couples.
Functional residual capacity
Functional Residual Capacity (FRC) is the volume of air present in the lungs at the end of passive expiration. At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles.
FRC is the sum of Expiratory Reserve Volume (ERV) and Residual Volume (RV) and measures approximately 2400 ml in a 70 kg, average-sized male. It can be estimated through spirometry, but in order to measure it more precisely, one would need to perform a test that directly measures RV such as nitrogen washout, helium dilution or body plethysmography.
A lowered or elevated FRC is often an indication of some form of respiratory disease. For instance, in emphysema, the lungs are more compliant and therefore are more susceptible to the outward recoil forces of the chest wall. Emphysema patients often have noticeably broader chests because they are breathing at larger volumes.
General transcription factor
General transcription factors  (GTF's) are protein transcription factors which have been shown to be important in the transcription of class II genes to mRNA templates. Many of them are involved in the formation of a preinitiation complex, which, together with RNA polymerase II, bind to and read the single-stranded DNA gene template.

# Functions
GTF's are intimately involved in the process of gene regulation, and most are required for life. Tata binding protein, (TBP) is a GTF that binds to the TATAA  box (T=Thymine, A=Adenine) the motif of nucleic acids that is directly upstream from the coding region in all genes. TBP is responsible for the recruitment of the RNA Pol II holoenzyme, the final event in transcription initiation.  These proteins are ubiquitous and interact with the core promoter region of DNA, which contains the transcription start site(s) of all class II genes.
Not all GTFs play a role in transcriptional initiation; some are required for the second general step in transcription, elongation. For example, members of the FACT complex, Spt16/Pob3, facilitate the rapid movement of RNA Pol II over the encoding region of genes. This is accomplished by moving the histone octamer out of the way of an active polymerase and thereby decondensing the chromatin.

# Types
The most common general transcription factors are:
- TFIIA (see also TFIIA; TFIIA is not a real basal transcription factor.)
- TFIIB (see also TFIIB)
- TFIID (see also TFIID)
- TFIIE (see also TFIIE)
- TFIIF (see also TFIIF)
- TFIIH (see also TFIIH)
- Spt16
- TBP (also known as Spt15)
Note: Basal transcription in test tubes has been achieved using only highly-purified recombinant TFIIB and TFIIF.
Genital candidiasis overview

# Overview
Candidiasis is a common fungal infection that occurs when there is overgrowth of the fungus called Candida. Candida is always present in the body in small amounts. However, when an imbalance occurs, such as when the normal acidity of the vagina changes or when hormonal balance changes, Candida can multiply. When that happens, symptoms of candidiasis appear.

# Pathophysiology
Candida albicans and C. glabrata. Less commonly, C.tropicalis, C. parapsilosis, and C. krusei. Rarely, other Candida species.

# Epidemiology and Demographics
It is the fourth most common cause of nosocomial bloodstream infections. Incidence is 8 cases per 100,000 in the general population. Mortality rate is almost 50% with bloodstream and disseminated infection.

# Risk Factors
Invasive disease occurs in critically ill patients in intensive-care units, in persons with severe granulocytopenia, and in hematopoietic stem cell and organ transplant recipients. Genital candidiasis can be associated with HIV infection. Vulvo-vaginal candidiasis is often associated with pregnancy, diabetes mellitus, and antibiotic therapy.

# Treatment

## Medical Therapy
Antifungal drugs which are taken orally, applied directly to the affected area, or used vaginally are the drugs of choice for vaginal yeast infections. Although these drugs usually work to cure the infection (80%-90% success rate), infections that do not respond to treatment are becoming more common, especially in HIV-infected women receiving long-term antifungal therapy. Prolonged and frequent use of these treatments can lessen their effectiveness.
Gentamicin adverse reactions

# Adverse Reactions

### Nephrotoxicity
Adverse renal effects, as demonstrated by the presence of casts, cells or protein in the urine or by rising BUN, NPN, serum creatinine or oliguria, have been reported.  They occur more frequently in patients with a history of renal impairment (especially if dialysis is required) and in patients treated for longer periods or with larger doses than recommended.

### Neurotoxicity
Serious adverse effects on both vestibular and auditory branches of the eighth nerve have been reported, primarily in patients with renal impairment (especially if hemodialysis is required) and in patients on high doses and/or prolonged therapy.  Symptoms include dizziness, vertigo, tinnitus, roaring in the ears and also hearing loss, which, as with the other aminoglycosides, may be irreversible.  Hearing loss is usually manifested initially by diminution of high-tone acuity.  Other factors which may increase the risk of toxicity include excessive dosage, dehydration and previous exposure to other ototoxic drugs.
Peripheral neuropathy or encephalopathy, including numbness, skin tingling, muscle twitching, convulsions and a myasthenia gravis-like syndrome have been reported.
NOTE: The risk of toxic reactions is low in patients with normal renal function who did not receive gentamicin sulfate at higher doses or for longer periods of time than recommended.
Other reported adverse reactions possibly related to gentamicin include: respiratory depression, lethargy, confusion, depression, visual disturbances, decreased appetite, weight loss and hypotension and hypertension; rash, itching, urticaria, generalized burning, laryngeal edema, anaphylactoid reactions, fever and headache; nausea, vomiting, increased salivation and stomatitis; purpura, pseudotumor cerebri, acute organic brain syndrome, pulmonary fibrosis, alopecia, joint pain, transient hepatomegaly and splenomegaly.
Laboratory abnormalities possibly related to gentamicin include: increased levels of serum transaminase (SGOT, SGPT), serum LDH and bilirubin; decreased serum calcium, magnesium, sodium and potassium; anemia, leukopenia, granulocytopenia, transient agranulocytosis, eosinophilia, increased and decreased reticulocyte counts and thrombocytopenia.  While clinical laboratory test abnormalities may be isolated findings, they may also be associated with clinically related signs and symptoms.  For example, tetany and muscle weakness may be associated with hypomagnesemia, hypocalcemia and hypokalemia.
While the local tolerance of gentamicin sulfate is generally excellent, there has been an occasional report of pain at the injection site.  Subcutaneous atrophy or fat necrosis suggesting local irritation has been reported rarely.
Glomerular basement membrane
The glomerular basement membrane is the basal laminal portion of the glomerulus which performs the actual filtration though the filtration slits between the podocytes , separating the blood on the inside from the filtrate on the outside. It is a fusion of the endothelial cell and podocyte basal laminas. 

# Layers
The GBM contains three layers: 

# Pathology
- Goodpasture's syndrome is also known as "anti-glomerular basement membrane disease". Capillaries become inflamed as a result of damage to the basement membrane by antibodies.
- Nephrotic syndrome is a change in the structure of the glomerular filtration mechanism usually in the glomerular basement membrane. Some symptoms include proteinuria, hypoalbuminaemia, oedema, and hyperlipidemia.
- Diabetic glomerulosclerosis is a thickening of the basement membrane, which can become up to 4-5 times thicker than normal. Can be caused by insulin deficiency or resultant hyperglycemia.
Glutathione S-transferase A1
Glutathione S-transferase A1 is an enzyme that in humans is encoded by the GSTA1 gene.
Cytosolic and membrane-bound forms of glutathione S-transferase are encoded by two distinct supergene families. These enzymes function in the detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins and products of oxidative stress, by conjugation with glutathione. The genes encoding these enzymes are known to be highly polymorphic. These genetic variations can change an individual's susceptibility to carcinogens and toxins as well as affect the toxicity and efficacy of some drugs. At present, eight distinct classes of the soluble cytoplasmic mammalian glutathione S-transferases have been identified: alpha, kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes a glutathione S-transferase belonging to the alpha class. The alpha class genes, located in a cluster mapped to chromosome 6, are the most abundantly expressed glutathione S-transferases in liver (hepatocytes) and kidney (proximal tubules). In addition to metabolizing bilirubin and certain anti-cancer drugs in the liver, the alpha class of these enzymes exhibit glutathione peroxidase activity, thereby protecting the cells from reactive oxygen species and the products of peroxidation.

# Release of GST-A1 as an indication of cellular necrosis
Increases in serum and urinary GST-A1 have been found in association with hepatocyte and renal proximal tubular necrosis respectively and have potential for monitoring injury to these tissues.
Guidewire general techniques

# Overview
The ability to cross an atherosclerotic lesion with a coronary guidewire depends upon both the performance characteristics of the giudewire and the skill of the operating physician.  This chapter discusses the technique of crossing an atherosclerotic lesion with a coronary guidewire.

# Workhorse Guidewire
It is a good general practice to use the same coronary guidewire for the majority of cases.  In doing so, the operator becomes very familiar with the behavior characteristics of the wire, and becomes very sensitive to any changes in the behavior of the wire. In general, a flexible wire with a floppy tip that does not have a hydrophilic coating is a good choice as a workhorse guidewire.  90% of lesions should be able to be crossed with this workhorse guidewire.

# Preparing the Guidewire
- For the majority of lesions, create a curve at the tip of the guidewire which is roughly the length of the diameter of the vessel proximal to the lesion.
- If you are attempting to cross a total occlusion the tip of the guidewire should be left straighter or with a minimal bend.

# Strategies If the Guidewire Fails to Cross the Lesion
- Adjust the guide so that it is more coaxial with the lumen of the artery
- Use a balloon, transit, ultrafuse or twin pass catheter to direct the wire in a more favorable direction
- Modify the bend at the tip of the wire. In tortuous segments, a more proximal secondary bend approximating shape the artery may be required
- Change the wire

# Safety Tips In Advancing The Coronary Guidewire
- Avoid bending or buckling the wire.  Buckling or bending of the wire can be a sign of a subintimal position.
- Never push a wire if you feel undue resistance.
- A ventricular premature beat could be a suggestion that the wire is too dital or has perforated the artery. Check the position of the wire in the presence of PVCs.
- If the patient goes into sustained ventricular tachycardia, check the position of the wire but do not lose wire position if at all possible.
- Be vigilant for coronary perforation when hydrophilic wires are used.
- Once you cross with the hydrophilic wire consider switching out for a non-hydrophilic wire.
- If there is a suspicion of a perforation, then an emergent Echo should be performed immediately while the patient is on the table.
HAZMAT Class 9 Miscellaneous

# Overview
The miscellaneous hazardous materials category encompasses all hazardous materials that do not fit one of the definitions listed in Class 1 through Class 8.

# Divisions
The miscellaneous hazardous material is a material that presents a hazard during transportation but which does not meet the definition of any other hazard class. This class includes:
- Any material which has an anesthetic, noxious or other similar property which could cause extreme annoyance or discomfort to a flight crew member so as to prevent the correct performance of assigned duties; or
- Any material that meets the definition in 49 CFR 171.8 for an elevated temperature material, a hazardous substance, a hazardous waste, or a marine pollutant.

# Placards

# Compatibility Table

# Packing Groups
The packing group of a Class 9 material is as indicated in Column 5 of the 49CFR 172.101 Table.
Pediculosis capitis overview

# Overview
The head louse (Pediculus humanus capitis) is one of the many varieties of sucking lice specialized to live on different areas of various animals.
As the name implies, head lice are specialized to live among the hair present on the human head and are exquisitely adapted to living mainly on the scalp and neck hairs of their human host. Lice present on other body parts covered by hair are not head lice but are either pubic lice (Pthirus pubis) or body lice (Pediculus humanus humanus).

# Pathophysiology
The main mode of transmission is contact with a person who is already infested (i.e., head-to-head contact).  Contact is common during play (sports activities, playgrounds, at camp, and slumber parties) at school and at home.

# Causes
Pediculus humanus capitis, the head louse, is an insect of the order Anoplura and is an ectoparasite whose only host are humans.  The louse feeds on blood several times daily and resides close to the scalp to maintain its body temperature.

# Epidemiology and Demographics
In the United States, infestation with head lice (Pediculus humanus capitis) is most common among preschool- and elementary school-age children and their household members and caretakers. Head lice are not known to transmit disease; however, secondary bacterial infection of the skin resulting from scratching can occur with any lice infestation.

# Diagnosis

## History and Symptoms
Pediculosis capitiss can be asymptomatic, particularly with a first infestation or when an infestation is light. Itching ("pruritus") is the most common symptom of Pediculosis capitis and is caused by an allergic reaction to louse bites. It may take 4-6 weeks for itching to appear the first time a person has head lice.

## Physical Examination
An infestation is diagnosed by looking closely through the hair and scalp for nits, nymphs, or adults. Finding a nymph or adult may be difficult; there are usually few of them and they can move quickly from searching fingers. If crawling lice are not seen, finding nits within a 1/4 inch of the scalp confirms that a person is infested and should be treated.

## Other Diagnostic Studies
The condition is diagnosed by the presence of lice or eggs in the hair, which is facilitated by using a magnifying glass or running a comb through the child's hair. In questionable cases, a child can be referred to a health professional. However, the condition is overdiagnosed, with extinct infestations being mistaken for active ones. As a result, lice-killing treatments are more often used on noninfested than infested children. The use of a louse comb is the most effective way to detect living lice.

# Treatment

## Secondary Prevention
Examination of the childs head at regular intervals using a louse comb allows the diagnosis of louse infestation at an early stage.