Persius/hicric huggingface dataset:
Geneva score calculator

# Geneva Score Calculator
- The Geneva score is a clinical prediction rule used to determine the pre-test probability of pulmonary embolism based on the patient's risk factors and clinical findings.
- The Geneva score has shown to be as accurate as the Wells score, but it is less reliant on the physicians clinical judgement.
- The Geneva score has been revised and simplified from its original version, but it has been shown to have the same diagnostic utility as the original score.

## Calculation of the Original Geneva Score for PE
This handy calculator computes the pre-test probability of pulmonary embolism using original Geneva criteria.
Check all boxes that apply to your patient:
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 3;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 4;}
if(document.forms.checked == 1){score += 3;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
document.forms.value = score;
if(score <=4){document.forms.value = "Low probability of PE (~10%)";}
if(score >= 5 && score <= 8){document.forms.value = "Moderate probability of PE (~38%)";} 
if(score >= 9){document.forms.value = "High probability of PE (~81%)";}

## Interpretation of the Original Geneva Score for PE
Shown below is the interpretation of the Geneva score:
- Score  4 points: Low probability of PE (~10%)
- Score 5 to 8 points: Moderate probability of PE (~38%)
- Score  9 points: High probability of PE (~81%)
Gentamicin microbiology

# Microbiology
In vitro tests have demonstrated that gentamicin is a bactericidal antibiotic which acts by inhibiting normal protein synthesis in susceptible microorganisms.  It is active against a wide variety of pathogenic bacteria including Escherichia coli, Proteus species, (indole-positive and indole-negative), Pseudomonas aeruginosa, species of the Klebsiella-Enterobacter-Serratia group, Citrobacter species and Staphylococcus species (including penicillin and methicillin-resistant strains).  Gentamicin is also active in vitro against species of Salmonella and Shigella. The following bacteria are usually resistant to aminoglycosides: Streptococcus pneumoniae, most species of streptococci, particularly group D and anaerobic organisms, such as Bacteroides species or Clostridium species.
In vitro studies have shown that an aminoglycoside combined with an antibiotic that interferes with cell wall synthesis may act synergistically against some group D streptococcal strains.  The combination of gentamicin and penicillin G has a synergistic bactericidal effect against virtually all strains of Streptococcus faecalis and its varieties (S. faecalis var. liquifaciens, S. faecalis var. zymogenes), S. faecium and S. durans.  An enhanced killing effect against many of these strains has also been shown in vitro with combinations of gentamicin and ampicillin, carbenicillin, nafcillin or oxacillin.
The combined effect of gentamicin and carbenicillin is synergistic for many strains of Pseudomonas aeruginosa.  In vitro synergism against other gram-negative organisms has been shown with combinations of gentamicin and cephalosporins.
Gentamicin may be active against clinical isolates of bacteria resistant to other aminoglycosides.  Bacteria resistant to one aminoglycoside may be resistant to one or more other aminoglycosides.  Bacterial resistance to gentamicin is generally developed slowly.

### Susceptibility Testing
If the disc method of susceptibility testing used is that described by Bauer et al. (Am J Clin Path 45:493,1966; Federal Register 37:20525-20529,1972), a disc containing 10 mcg of gentamicin should give a zone of inhibition of 15 mm or more to indicate susceptibility of the infecting organism.  A zone of 12 mm or less indicates that the infecting organism is likely to be resistant.
Zones of greater than 12 mm and less than 15 mm indicate intermediate susceptibility.  In certain conditions it may be desirable to do additional susceptibility testing by the tube or agar dilution method; gentamicin substance is available for this purpose.
Geothermal desalination
Geothermal desalination is an proven process under development for the production of fresh water using heat energy.  Claimed benefits of this method of desalination are that it requires less maintenance than reverse osmosis membranes and that the primary energy input is from geothermal heat, which is a low-environmental-impact source of energy.
Around 1995, several entrepreneurs came together with an idea to use geothermal water directly as a source for desalination. About 1998 several individuals began working with evaporation/condensation air loop desalination about 1998. The experiment was moderately successful and a proof of concept, proving that geothermal waters could be used as process water to produce potable water in 2001. In 2003 Professor Ronald A. Newcomb, formerly working on the process with Autek LLC, now at San Diego State University International Consortium for Advanced Technologies and Security or ICATS began to work to enhance the process of using geothermal energy for the purpose of desalination. The University explains that the device is owned by World Wide Assets LLC and Strident Ltd.  and that geothermal energy is a primary energy source.
In 2005 some testing was done in a fifth prototype of a device referred to as a delta t device a closed air loop, atmospheric pressure, evaporation condensation loop geothermally powered desalination device. The device used filtered sea water from Scripps Institute of Oceanography and reduced the salt concentration from 35,000 ppm to 51 ppm.
A total of five prototypes and three modifications demonstrated that, with process water approaching 210 degrees Fahrenheit (100 degrees Celsius) and a chill source about 35 F (2 C), a full-size device would produce about one-half acre foot (600 m3) of water per day. Salt concentration in the wastewater would only be about 10% above the level of the original water, thus, from, say, 35,000 to about 38,000 parts per million, well within the ability of osmoregulators to adjust.
SDSU ICATS continues to develop different devices for the same purpose with the goal of making desalination an environmentally friendly process.
Giant axonal neuropathy
Giant axonal neuropathy is a rare inherited condition that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function.
Giant axonal neuropathy generally appears in infancy or early childhood, and slowly progresses as more cells become involved. Signs of giant axonal neuropathy usually begin in the peripheral nervous system, which controls the arms, legs and many other areas of the body. Most individuals with this disorder first have problems with walking. Later they may lose sensation, coordination, strength, and reflexes in their limbs. Hearing or vision problems may also occur. Extremely kinky hair is characteristic of giant axonal neuropathy, appearing in almost all affected people. As the disorder progresses, central nervous system becomes involved. This may cause a gradual decline in mental function, loss of control of body movement, and seizures.
Giant axonal neuropathy is caused by mutations in the GAN gene, which provides instructions for making a protein called gigaxonin. Some GAN mutations affect the shape of the protein, changing how it binds to others in organizing the structure of the neuron. Other mutations result in the absence of any functional gigaxonin protein.
Neurons affected by a mutated GAN gene accumulate excess neurofilaments in the axon, the long extension from the nerve cell that transmits its signal to other nerve cells and to muscles. These distended or giant axons do not transmit signals properly and eventually deteriorate, resulting in problems with movement and other nervous system functions. The disease is inherited in an autosomal recessive pattern which means both parents must have mutated GAN genes.
This article incorporates public domain text from The U.S. National Library of Medicine
Giant platelet disorder

# Overview
Giant platelet disorders are rare disorders featuring abnormally large platelets, thrombocytopenia and a tendency to bleeding. Giant platelet disorder occurs for inherited diseases like Bernard-Soulier syndrome, gray platelet syndrome and May-Hegglin anomaly.

# Classification
Giant platelet disorders can be further categorized:
- caused by auto-immune disorders, i.e. Immune Thrombocytopenic Purpura (ITP) , characterized by low platelet count, but high MPV (Mean-Platelet Volume).
- Caused by glycoprotein abnormalities: Bernard-Soulier syndrome, Velocardiofacial syndrome
- Caused by calpain defect: Montreal platelet syndrome
- Caused by alpha granules defect: Gray platelet syndrome
- Characterized by  abnormal neutrophil inclusions: May-Hegglin anomaly, Sebastian syndrome
- With systemic manifestations: Hereditary macrothrombocytopenia with hearing loss, Epstein syndrome, Fechtner syndrome
- With no specific abnormalities: Mediterranean macrothrombocytopenia
- Harris platelet syndrome

# Signs and symptoms
Glucuronosyltransferase

# Overview
Uridine 5'-diphospho-glucuronosyltransferase (UDP-glucuronosyltransferase, UGT) is a glycosyltransferase (EC 2.4.1.17) that catalyzes the glucuronidation reaction.
Alternative names:
- glucuronyltransferase

# Function
This reaction involves the addition of sugars to lipids and other apolar xenobiotics and is an important step in the body's elimination of foreign substances (such as drugs and medications) as well as endogenous substances (including endogenous toxins).  UGT is present in humans, other animals, plants, and bacteria.
The glucuronidation reaction consists of the transfer of the glucuronosyl group from uridine 5'-diphospho-glucuronic acid (UDPGA) to substrate molecules that contain oxygen, nitrogen, sulfur or carboxyl functional groups.  
The resulting glucuronide more polar (e.g. hydrophilic) and is more easily excreted than the substrate molecule.  The product solubility in blood is increased allowing it to be eliminated from the body by the kidneys.

# Diseases
A deficiency in the bilirubin specific form of glucuronosyltransferase is thought to be the cause of Gilbert's syndrome, which is characterized by hyperbilirubinemia.
It is also associated with Crigler-Najjar syndrome, a more serious disorder where the enzyme's activity is either completely absent (Crigler-Najjar syndrome type I) or less than 10% of normal (type II).

# Genes
- B3GAT1, B3GAT2, B3GAT3
- UGT1A1, UGT1A3, UGT1A4, UGT1A5, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10
- UGT2A1, UGT2A2, UGT2A3, UGT2B4, UGT2B7, UGT2B10, UGT2B11, UGT2B15, UGT2B17, UGT2B28
Triphenylmethyl radical
The triphenylmethyl radical is a persistent radical and the first ever radical described in organic chemistry. It can be prepared by homolysis of triphenylmethylchloride 1 (scheme 1) by a metal like silver or zinc in benzene or diethyl ether. The radical 2 forms a chemical equilibrium with the quinoid type dimer 3. In benzene the concentration of the radical is 2% .
Solutions containing the radical are yellow and when the temperature of the solution is increased the yellow color becomes more intense as the equilibrium is shifted in favor of the radical following Le Chatelier's principle. Conversely when the solution is cooled it becomes less yellow.
When exposed to air the radical rapidly oxidizes to the peroxide (Scheme 2) and the color of the solution changes from yellow to colorless. Likewise, the radical reacts with iodine to triphenylmethyliodide.
The radical was discovered by Moses Gomberg in 1900.  He tried to prepare hexaphenylethane from triphenylmethylchloride and zinc in benzene in a Wurtz reaction and found that the product, based on its behaviour towards iodine and oxygen, was far more reactive than anticipated.
The correct quinoid structure for the dimer was suggested as early as 1904 but this structure was soon after abandoned by the scientific community in favor of hexaphenylethane which is structure 4 in scheme 1 . It subsequently took until 1968 for its rediscovery when researchers at the Vrije Universiteit Amsterdam published proton NMR data . In hindsight the substituted ethane molecule does not make sense at all because it is simply too sterically overcrowded.

# Miscellany
- Gomberg concluded his 1900 article with the sentence "This work will be continued and I wish to reserve the field for myself."  He ended his 1902 article by writing, "It is my intention to extend this study to other oxygen compounds, as well as to nitrogen derivatives, and I beg to reserve this field for further work." It is true that nineteenth-century chemists did not intrude on each other's research; to his dismay, Gomberg found out that this was not the case in the twentieth century.
Gordon Hamilton-Fairley

# Overview
Gordon Hamilton-Fairley (1930-1975), was one of the world's leading cancer specialists. Born and raised in Australia, he moved to the United Kingdom where he studied and worked.  He was killed by the Provisional Irish Republican Army.

# His life
The son of an eminent research worker in tropical diseases (Sir Neil Hamilton Fairley), Gordon Fairley grew up in Australia. He studied at Magdalen College, Oxford, and St Bartholomew's Hospital, London.
Trained in hematology as Leverhulme Research Scholar at the Royal College of Physicians, he continued his research with an emphasis on immunohematology.
In 1968 he became director of the Clinical Research Unit at the Institute of Cancer Research. In 1970 he became director of the Medical Oncology Research Unit. In 1972 he became Imperial Cancer Fund Professor of Oncology.
He was killed by a Provisional Irish Republican Army car bomb in London on 22 October 1975. The bomb was intended for Sir Hugh Fraser, his wife Lady Antonia Fraser and their guest Caroline Kennedy, who lived nearby but Dr. Hamilton-Fairley accidentally set it off when he spotted the suspicious package under their car while walking his dog.
Great American Smokeout
The Great American Smokeout is an annual event in the United States to encourage Americans (of whom 45.8 million smoke) to quit tobacco smoking. It was first held in 1977, and is sponsored by the American Cancer Society. Its spokesman is Smokey Robinson. The event challenges people not to smoke cigarettes for 24 hours, hoping it will last forever.
It is held on the third Thursday in November, one week before Thanksgiving. In  2007 the 31st Great American Smokeout will be held on November 15.
The event evolved from a series of events.
- In 1971, in Randolph, Massachusetts, Arthur P. Mullaney suggested people give up cigarettes for a day and donate the money to a local high school.
- In 1974, a "Don't Smoke Day" (or "D-Day") was promoted by Lynn R. Smith of the Monticello Times in Monticello, Minnesota.
Great Plague of Seville
The Great Plague (1647-1652) was a massive outbreak of disease in Spain that killed 60,000 people, up to 25% of Sevilla's population.
Unlike the plague of 1596-1602 which initially struck northern and central Spain and Andalucia, the Great Plague, which may have gotten its start in Algeria, struck eastern Spain first. Valencia was the first city to be hit, losing an estimated 30,000 people. The disease chewed through Andalucia in addition to sweeping the north into Catalonia and Aragon. The coast of Malaga lost upwards of 50,000 people. In Sevilla quarantine measures were evaded, ignored, unproposed and/or unenforced. The result was horrific, if unsurprising. The city of Sevilla and its rural districts were thought to have lost 150,000 people -- a full quarter of its total population of 600,000. Sevilla, and indeed the economy of Andalucia, would never recover from so complete a devastation. Altogether Spain was thought to have lost 500,000 people, out of a population of slightly fewer than 10,000,000, or nearly 5% of its entire population. In perspective, it would be akin to a nation with a population of 300 million to losing upwards of 15 million men, women and children. This was the greatest -- but not the only -- plague of 17th century Spain.
Not quite twenty-five years later Spain found itself once again in the grips of a furious plague. For nine years (1676-1685), ebbing and flowing like a great wave, it ravaged all Spain. It struck with especial virulence in the areas of Andalucia and Valencia. The poor harvest of 1682-83 brought with it famine conditions which weakened the exhausted population still further. This last plague of the 17th century, plus the famine that followed in its wake, is estimated to have claimed an additional 250,000 Spanish lives.
Three great plagues ravaged Spain in the 17th century. They were:
- The Plague of 1596-1602
- The Plague of 1646-1652 
- The Plague of 1676-1685
Factoring in normal births, deaths, plus immigration, historians reckon the total cost in human lives due to these plagues throughout Spain, throughout the entire 17th century, to be a minimum of nearly 1.25 million. As a result, the population numbers Spain scarcely budged between the years 1596 and 1696.
The disease is generally believed to have been bubonic plague, an infection by the bacterium Yersinia pestis, transmitted via a rat vector. Other symptom patterns of the bubonic plague, such as septicemic plague and pneumonic plague were also present.
Greater occipital nerve
The greater occipital nerve is a spinal nerve arising from the dorsal primary rami of cervical spinal nerve 2, between the first and second cervical vertebrae, along with the lesser occipital nerve.
It innervates the scalp at the top of the head, over the ear and over the parotid glands.

# Clinical relevance
Disorder of this nerve is one of the causes of cervicogenic headaches, referred to as occipital neuralgias.

# Additional images
- The nerves of the scalp, face, and side of neck.
Griffonia simplicifolia
Griffonia simplicifolia (syn. Bandeiraea simplicifolia Benth.) is a woody climbing shrub native to West Africa and Central Africa.  It grows to about 3 m, and bears greenish flowers followed by black pods.
The seeds of the plant are used as a herbal supplement for their 5-Hydroxytryptophan content.
Botanical synonyms for the plant also include Schotia simplicifolia (Vahl ex DC) Baill.
Growth hormone receptor
Growth hormone receptor is a protein that in humans is encoded by the GHR gene. GHR orthologs  have been identified in most mammals.

# Function
This gene encodes a protein that is a transmembrane receptor for growth hormone. Binding of growth hormone to the receptor leads to reorientation of a pre-assembled receptor dimer dimerization (the receptor may however also exist as monomers on the cell surface ) and the activation of an intra- and intercellular signal transduction pathway leading to growth. A common alternate allele of this gene, called GHRd3, lacks exon three and has been well characterized. Mutations in this gene have been associated with Laron syndrome, also known as the growth hormone insensitivity syndrome (GHIS), a disorder characterized by short stature (proportional dwarfism). Other splice variants, including one encoding a soluble form of the protein (GHRtr), have been observed but have not been thoroughly characterized. Laron mice (that is mice genetically engineered to carry defective Ghr), have a dramatic reduction in body mass (only reaching 50% of the weight of normal siblings), and also show a ~40% increase in lifespan.

# Interactions
Growth hormone receptor has been shown to interact with SGTA, PTPN11, Janus kinase 2, Suppressor of cytokine signaling 1 and CISH.

# Evolution
The GHR gene is used in animals as a nuclear DNA phylogenetic marker. The exon 10 has first been experienced to explore the phylogeny of the major groups of Rodentia.
GHR has also proven useful at lower taxonomic levels, e.g., in octodontoid, arvicoline, muroid, murine, and peromyscine  rodents, in arctoid  and felid  carnivores, and in dermopterans.
Note that the GHR intron 9 has also been used to investigate the mustelid  and hyaenid  carnivores phylogenetics.

# Antagonists
Growth hormone receptor antagonists such as pegvisomant (trade name Somavert) are used in the treatment of acromegaly. They are used if the tumor of the pituitary gland causing the acromegaly cannot be controlled with surgery or radiation, and the use of somatostatin analogues is unsuccessful. Pegvisomant is delivered as a powder that is mixed with water and injected under the skin.
Guide to medical syntax

# Overview
Many words that are used interchangeably in common language take on different meanings when used in the context of medicine.  This guide serves to highlight words that are commonly found on WikiDoc to be used incorrectly and to provide more appropriate alternatives.  Like all aspects of WikiDoc, this page should be updated as more examples are found.

# Words Mistakenly Interchanged

## Incidence vs. Prevalence
Both incidence and prevalence are often used to mean the same thing in common language.  In medicine, however, they have two distinct meanings. The definition of each term, as well as an example of each, is provided below.

## Trial vs. Study
Use of the word trial versus study / analysis:  Results of randomized observations can be referred to as a trial.  Results of non-randomized observations should be referred to as studies or analyses.

# Words to Find and Replace

# General Instructions
- If English is not your first language, have a native writer review your content after it is created.
- Do not end sentences with the word "with" or adverbs.
- Minimize the use a conversational tone with words ending in "ing" (passive tense).