Persius/hicric huggingface dataset:
Radioactive dentin abrasion

# Overview
A procedure for the measurement of either tooth enamel or dentin abrasion by the use of human teeth made radioactive by mild neutron irradiation.
Abrasive is the term for a dentifrice cleaning agent which, in concert with the brushing action of the toothbrush, cleans teeth by dislodging food particles and plaque. Several abrasives or cleaning agents are currently marketed in various toothpastes, including dicalcium
phosphate, hydrated silica and sodium bicarbonate or baking soda.
Radioactive dentin abrasion method of measurement  of dentifrice abrassivenes toward  human teeth was described in 1958 by researchers R. J. GRABENSTETTER, R. W. BROGE, F. L. JACKSON, AND A. W. RADIKE in their article THE MEASUREMENT OF THE ABRASION OF HUMAN TEETH BY DENTIFRICE ABRASIVES: A TEST UTILIZING RADIOACTIVE TEETH.
The procedure is more precise and faster than former methods dependent upon the measurement of the depth of a groove cut into tooth structure. (The former methods was first studied by W. D. Miller in 1907). The results are obtained directly in terms of the amount of human tooth structure worn away by a toothbrush and dentifrice abrasive slurry operating at a known, constant brush pressure and a constant stroke speed. The coefficient of variation of the test is 6-7 when 8 replications are carried out, and 10-15 when only duplicates are run as in the usual routine testing. This is one half to one fourth of the variation involved in the depth-of-cut method and results can be obtained with an expenditure of one half to one third of the time of the former method.
The procedure was later adopted by ADA for measuring of Relative Dentin Abrasion Index,
de:Radioactive Dentin Abrasion
Rebound tenderness overview

# Overview
Rebound tenderness is one of the most important signs of peritonitis when evaluating an acute abdomen.  In recent years the value of rebound tenderness has been questioned, since it may not add any diagnostic value beyond the observation that the patient has severe tenderness.

# Pathophysiology
Rebound tenderness is thought to be due to stretching of the peritoneum.

# Epidemiology and Demographics
Children, the immunocompromised, and the elderly are less likely to show peritoneal signs and may have atypical presentations.

# Diagnosis

## Physical Examination
Rebound tenderness is a clinical sign that a doctor may detect in physical examination of a patient's abdomen. It refers to pain upon removal of pressure rather than application of pressure to the abdomen.  (The latter is referred to simply as abdominal tenderness.) To elicit the sign, gentle pressure is placed on the abdomen and then the hand is lifted suddenly. A sudden increase in abdominal pain occurs when the examiner's hand is lifted. The other physical examination findings to distinguish rebound tenderness are abdominal tenderness and guarding.

# Treatment

## Medical Therapy
Blood volume should be immediately replaced with saline and/or blood transfusion for those patients that are hemodynamically unstable and bowel rest for diverticulitis or bowel obstruction (possible colon resection).

## Surgery
Indications for surgery when elicited would be as a result of life threatening emergencies such as; early sepsis or evidence of hemorrhage, which would require immediate surgical intervention, ruptured aneurysm, ectopic pregnancy, bowel perforation or other pathologies require definite surgical repair.
Refreshable Braille display
A refreshable Braille display or Braille terminal is an electro-mechanical device for displaying Braille characters, usually by means of raising dots through holes in a flat surface. Blind computer users who cannot use a normal computer monitor use it to read text output. Speech synthesizers are also commonly used for the same task, and a blind user may switch between the two systems or use both at the same time depending on circumstances.
Because of the complexity of producing a reliable display that will cope with daily wear and tear, these displays are expensive. Usually, only 40 or 80 Braille cells are displayed. Models with 18-40 cells exist in some notetaker devices.
On some models the position of the cursor is represented by vibrating the dots, and some models have a switch associated with each cell to move the cursor to that cell directly.
The mechanism which raises the dots uses the piezo effect of some crystals, where they expand when a voltage is applied to them. Such a crystal is connected to a lever, which in turn raises the dot. There has to be a crystal for each dot of the display, i.e eight per character.
The software that controls the display is called a screen reader. It gathers the content of the screen from the operating system, converts it into braille characters and sends it to the display. Screen readers for graphical operating systems are especially complex, because graphical elements like windows or slidebars have to be interpreted and described in text form. Modern operating systems usually have an Application Programming Interface to help screen readers obtain this information, such as MSAA for Microsoft Windows or AT-SPI for GNOME.
A new development, called the rotating-wheel Braille display, was developed in 2000 by the National Institute of Standards and Technology (NIST) and although a second rotating display was designed by the Leuven University in Belgium both wheels are still in the process of commercialization. Braille dots are put on the edge of a spinning wheel, which allows the user to read continuously with a stationary finger while the wheel spins at a selected speed. The Braille dots are set in a simple scanning-style fashion as the dots on the wheel spins past a stationary actuator that sets the Braille characters. As a result, manufacturing complexity is greatly reduced and rotating-wheel Braille displays will be much less expensive than traditional Braille displays.

# History
The base of a refreshable braille display is a pure braille terminal. There the input is performed by two sets of three keys plus a space bar (as in the Perkins Brailler), while output is via a refreshable braille display consisting of a row of electromechanical character cells, each of which can raise or lower a combination of six round-tipped pins. Other variants exist that use a conventional QWERTY keyboard for input and braille pins for output, as well as input-only and output-only devices. In 1951, David Abraham, a woodworking teacher at Perkins, created a portable braille terminal.
Relatively compact subspace
In mathematics, a relatively compact subspace (or relatively compact subset) Y of a topological space X is a subset whose closure is compact.
Since closed subsets of compact spaces are compact, every set in a compact space is relatively compact. In the case of a metric topology, or more generally when sequences may be used to test for compactness, the criterion for relative compactness becomes that any sequence in Y has a subsequence convergent in X. This condition is also called pre-compact or relatively bounded.
Some major theorems characterise relatively compact subsets, in particular in function spaces. An example is the Arzela-Ascoli theorem. Other cases of interest relate to uniform integrability, and the concept of normal family in complex analysis. Mahler's compactness theorem in the geometry of numbers characterises relatively compact subsets in certain non-compact homogeneous spaces (specifically spaces of lattices).
The definition of almost periodic function F is at a conceptual level to do with the translates of F being a relatively compact set. This needs to be made precise in terms of the topology used, in a particular theory.
de:Relative Kompaktheit
Retinal homeobox protein Rx
Retinal homeobox protein Rx also known as retina and anterior neural fold homeobox is a protein that in humans is encoded by the RAX gene. The RAX gene is located on chromosome 18 in humans, mice, and rats.

# Function
This gene encodes a homeobox-containing transcription factor that functions in eye development. The gene is expressed early in the eye primordia, and is required for retinal cell fate determination and also regulates stem cell proliferation.
Towards the end of late gastrulation a single eye field has formed and splits into bilateral fields via action by the signaling molecule, sonic hedgehog (Shh) secreted from the forebrain. Rax and Six-3 (also a transcription factor) maintain the forebrain's ability to secrete Shh by inhibiting activity of the signaling molecule Wnt.
Rax (Retina and Anterior Neural Fold Homeobox) is a gene in the OAR (Otx, Arx,& Rax) subgroup of the paired-like homeodomain family of transcription factors. Discovered in 1997, the Rax gene is known to contribute to the development of the retina, hypothalamus, pineal gland and pituitary gland.

# Clinical significance
Mutations in this gene have been reported in patients with defects in ocular development, including microphthalmia, anophthalmia, and coloboma.
Mutations to the Rax gene cause malformation of the retinal field, including anophthalmia and micropthalmai.
Individuals who have a mutation in the RAX gene fail to develop ocular structures, referred to as anophthalmia. RAX mutant individuals can also have micropthalmia, where one or both of the eyes is smaller than normal.

# Animal studies
Xenopus tropicalis rax mutant frogs are eyeless where the future retinal tissue instead has diencephalon and telencephalon features. Also, RAX knockout mice have no eyes and abnormal forebrain formation.
Retinoic acid receptor beta
Retinoic acid receptor beta (RAR-beta), also known as NR1B2 (nuclear receptor subfamily 1, group B, member 2) is a nuclear receptor that in humans is encoded by the RARB gene.

# Function
This gene encodes retinoic acid receptor beta, a member of the thyroid-steroid hormone receptor superfamily of nuclear transcriptional regulators. This receptor localizes to the cytoplasm and to subnuclear compartments. It binds retinoic acid, the biologically active form of vitamin A which mediates cellular signalling in embryonic morphogenesis, cell growth and differentiation. It is thought that this protein limits growth of many cell types by regulating gene expression. The gene was first identified in a hepatocellular carcinoma where it flanks a hepatitis B virus integration site. The gene expresses at least two transcript variants; one additional transcript has been described, but its full length nature has not been determined.

# Interactions
Retinoic acid receptor beta has been shown to interact with NR4A2.
Retroaortic left renal vein

# Overview
- Seen in 2-3% of individuals (less common than circumaortic left renal vein, seen in 5-7%)
- Retroaortic left renal vein derived from the renal collar (circumaortic renal venous ring) at an embryonic stage and completed by the regression and disappearance of the ventral (preaortic) limb and the persistence of the dorsal (postaortic) limb at a later stage
- Drainage of lumbar veins may also be anomalous in these cases, although by variable anatomy
- In some cases, the retroaortic left renal vein exits the renal hilum posterior to the left renal artery (anomalous)
- The retroaortic vein may receive flow from lumbar veins and may run caudad and enter the inferior vena cava in the lower lumbar region, or it may subdivide before entering the inferior vena cava.  

# Diagnosis

## Multi Sliced CT
Images shown below are courtesy of RadsWiki and copylefted
Ribavirin contraindications

# Contraindications
REBETOL combination therapy is contraindicated in:
- women who are pregnant. REBETOL may cause fetal harm when administered to a pregnant woman. REBETOL is contraindicated in women who are or may become pregnant. If REBETOL is used during pregnancy, or if the patient becomes pregnant while taking REBETOL, the patient should be apprised of the potential hazard to her fetus 
- men whose female partners are pregnant
- patients with known hypersensitivity reactions such as Stevens-Johnson syndrome, toxic, epidermal necrolysis, and erythema multiforme to ribavirin or any component of the product
- patients with autoimmune hepatitis
- patients with hemoglobinopathies (e.g., thalassemia major, sickle-cell anemia)
- patients with creatinine clearance less than 50 mL/min. 
- Coadministration of REBETOL and didanosine is contraindicated because exposure to the active metabolite of didanosine (dideoxyadenosine 5'-triphosphate) is increased. Fatal hepatic failure, as well as peripheral neuropathy, pancreatitis, and symptomatic hyperlactatemia/lactic acidosis have been reported in patients receiving didanosine in combination with ribavirin .
Rifaximin drug interactions

# Drug Interactions
In vitro studies have shown that rifaximin did not inhibit cytochrome P450 isoenzymes 1A2, 2A6, 2B6, 2C9, 2C19, 2D6, 2E1 and CYP3A4 at concentrations ranging from 2 to 200 ng/mL . Rifaximin is not expected to inhibit these enzymes in clinical use.
An in vitro study has suggested that rifaximin induces CYP3A4 .  However, in patients with normal liver function, rifaximin at the recommended dosing regimen is not expected to induce CYP3A4.  It is unknown whether rifaximin can have a significant effect on the pharmacokinetics of concomitant CYP3A4 substrates in patients with reduced liver function who have elevated rifaximin concentrations.
An in vitro study suggested that rifaximin is a substrate of P-glycoprotein.  It is unknown whether concomitant drugs that inhibit P-glycoprotein can increase the systemic exposure of rifaximin .
Right gastro-omental artery

# Overview
The right gastro-omental artery (or right gastroepiploic artery)  runs from right to left along the greater curvature of the stomach, between the layers of the greater omentum, anastomosing with the left gastroepiploic branch of the splenic artery.
Except at the pylorus where it is in contact with the stomach, it lies about a finger's breadth from the greater curvature.

# Branches
This vessel gives off numerous branches:
- "gastric branches": ascend to supply both surfaces of the stomach.
- "omental branches": descend to supply the greater omentum and anastomose with branches of the middle colic.
Ritonavir contraindications

# Contraindications
- When co-administering NORVIR with other protease inhibitors, see the full prescribing information for that protease inhibitor including contraindication information.
- NORVIR is contraindicated in patients with known hypersensitivity (e.g., toxic epidermal necrolysis (TEN) or Stevens-Johnson syndrome) to ritonavir or any of its ingredients.
- Co-administration of NORVIR with several classes of drugs (including sedative hypnotics, antiarrhythmics, or ergot alkaloid preparations) is contraindicated and may result in potentially serious and/or life-threatening adverse events due to possible effects of NORVIR on the hepatic metabolism of these drugs (see Table 1). Voriconazole and St. Johns Wort are exceptions in that co-administration of NORVIR and voriconazole results in a significant decrease in plasma concentrations of voriconazole, and co-administration of NORVIR with St. Johns Wort may result in decreased ritonavir plasma concentrations.
Ritonavir drug interactions

# DRUG INTERACTIONS
See also Contraindications , Warnings and Precautions , and Clinical Pharmacology
When co-administering NORVIR with other protease inhibitors (atazanavir, darunavir, fosamprenavir, saquinavir, and tipranavir), see the full prescribing information for that protease inhibitor including important information for drug interactions.

## Potential for NORVIR to Affect Other Drugs
Ritonavir has been found to be an inhibitor of cytochrome P450 3A (CYP3A) and may increase plasma concentrations of agents that are primarily metabolized by CYP3A. Agents that are extensively metabolized by CYP3A and have high first pass metabolism appear to be the most susceptible to large increases in AUC (greater than 3-fold) when co-administered with ritonavir. Thus, co-administration of NORVIR with drugs highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events is contraindicated. Co-administration with other CYP3A substrates may require a dose adjustment or additional monitoring as shown in Table 4.
Ritonavir also inhibits CYP2D6 to a lesser extent. Co-administration of substrates of CYP2D6 with ritonavir could result in increases (up to 2-fold) in the AUC of the other agent, possibly requiring a proportional dosage reduction. Ritonavir also appears to induce CYP3A, CYP1A2, CYP2C9, CYP2C19, and CYP2B6 as well as other enzymes, including glucuronosyl transferase.

## Established and Other Potentially Significant Drug Interactions
Table 4 provides a list of established or potentially clinically significant drug interactions. Alteration in dose or regimen may be recommended based on drug interaction studies or predicted interaction .
SLE resident survival guide

# Overview

# Causes
- Genetic predisposition:
HLA class polymorphism
Complement genes
Female sexual gene due to high levels of estrogen and prolactin
- HLA class polymorphism
- Complement genes
- Female sexual gene due to high levels of estrogen and prolactin
- Auto-immune disease
- Infections
Parvovirus B19
Epstein-Barr virus (EBV)
Trypanosomiasis
Mycobacterial infections
- Parvovirus B19
- Epstein-Barr virus (EBV)
- Trypanosomiasis
- Mycobacterial infections
- Exposure to ultraviolet (UV) light
Can exacerbate or induce systemic manifestations of SLE
- Can exacerbate or induce systemic manifestations of SLE
- Drug-induced lupus

# FIRE

# Diagnosis

## Diagnostic criteria:
In 2012, Systemic Lupus International Collaboration Criteria (SLICC) developed a new criteria for SLE diagnosis. SLICC criteria for the classification of systemic lupus erythematosus was developed based on the old ACR criteria for the classification of systemic lupus erythematosus to address a more sensitive diagnostic criteria and also to cover weaknesses of the previous ACR criteria.
Based on SLICC criteria, diagnosis of SLE is defined as:
- Meeting at least 4 of 17 criteria, including at least 1 of the 11 clinical criteria and one of the six immunologic criteria
OR
- Biopsy-proven nephritis compatible with SLE in the presence of antinuclear antibodies (ANA) or anti-double-stranded DNA (dsDNA) antibodies
A criterion is considered positive if one or more of the observations listed in the definition for the criterion are present in the patient. A criterion should only be counted once, regardless of the number of observations in the definition that the patient presents with.

## Complete diagnostic approach:

# Treatment

# Do's

# Don'ts
STD resident survival guide
Synonyms and keywords:

# Overview
Sexually Transmitted Diseases (STDs) are infections that are passed usually through sexual contact. STDs are also termed as Sexually Transmitted Infections (STIs) or venereal disease. A person usually contracts STD through unprotected vaginal, anal, or oral sex. Usage of condoms usually reduces chances of getting STDs greatly. It can also be transmitted through breast-feeding and sharing needles.   STDs could be caused by bacterias, viruses or parasites. Bacterial and parasitic infections can be treated by antibiotics but there is no cure for a viral STD. For viral disease, medications are given to keep the symptoms and disease under control.

# Causes

## Life Threatening Causes
STDs can cause serious life threatening complications. This is because many STDs are often asymptomatic and there for goes undetected. Because many STDs go undetected for a long time, major health consequences such as cancers, infertility, neurologic changes and other chronic diseases follow years after the initial infection. Viral causes of STDs especially result in life long infection for which there is currently no curative treatment.
- Cancers caused by STDs: There are several sexually transmitted pathogens that cause cancer. Some strains of Human Papilloma Virus (HPV) are considered to be the cause of cancer of the cervix, vulva, vagina, penis, and anus. Epstein-Barr Virus (EBV) transmitted by intimate contact including kissing and sexual intercourse. Hepatitis B virus contracted by sexual intercourse or by intravenous drug use,
- Reproductive health problems
- Deaths associated with STDs

## Common Causes
- Common cause 1
- Common cause 2
- Common cause 3
- Common cause 4
- Common cause 5

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of ] according the the  guidelines.

# Treatment
Shown below is an algorithm summarizing the treatment of ] according the the  guidelines.

# Do's
- The content in this section is in bullet points.

# Don'ts
- The content in this section is in bullet points.
Sandbox:Laboratory findings

# Overview
- An elevated/reduced concentration of serum/blood/urinary/CSF/other  is diagnostic of .
- Laboratory findings consistent with the diagnosis of  include , , and .
-  is usually normal among patients with .
- Some patients with  may have elevated/reduced concentration of , which is usually suggestive of .
OR
- There are no diagnostic laboratory findings associated with .

# Laboratory Findings
- There are no diagnostic laboratory findings associated with .
OR
- An elevated/reduced concentration of serum/blood/urinary/CSF/other  is diagnostic of .
-  is usually normal among patients with .
- Laboratory findings consistent with the diagnosis of  include
- Some patients with  may have elevated/reduced concentration of , which is usually suggestive of .
Sandbox:Otitis media causes

# Overview
For each ear, an eustachian tube runs from the middle ear to the back of the throat. This tube drains fluid that is normally made in the middle ear. If the eustachian tube becomes blocked, fluid can build up. When this happens, germs such as bacteria and viruses can multiply and cause an infection. Ear infections are common in infants and children, in part because the eustachian tubes become easily clogged. Ear infections may also occur in adults, although they are less common than in children.

# Causes
Streptococcus pneumoniae and nontypable Haemophilus influenzae are the most common bacterial causes of otitis media. Tubal dysfunction leads to the ineffective clearing of bacteria from the middle ear.  In older adolescents and young adults, the most common cause of ear infections during their childhoods was Haemophilus influenzae.  The role of the anti-H. influenzae vaccine that children are regularly given in changing patterns of ear infections is unclear, as this vaccine is active only against strains of serotype b, which rarely cause otitis media.
As well as being caused by Streptococcus pneumoniae and Haemophilus influenzae  it can also be caused by the common cold. Colds indirectly cause many cases of otitis media by damaging the normal defenses of the epithelial cells in the upper respiratory tract.
Another common culprit of otitis media includes Moraxella catarrhalis, a gram-negative, aerobic, oxidase positive diplococcus. Less commonly otitis media can be caused by Mycobacterium tuberculosis.
Anything that causes the eustachian tubes to become swollen or blocked causes more fluids to build up in the middle ear behind the eardrum. These causes include:
- Allergies
- Colds and sinus infections
- Excess mucus and saliva produced during teething
- Infected or overgrown adenoids
- Tobacco smoke or other irritants
Ear infections are also more likely if a child spends a lot of time drinking from a sippy cup or bottle while lying on his or her back. Contrary to popular opinion, getting water in the ears will not cause an acute ear infection, unless the eardrum has a hole from a previous episode. Ear infections occur most often in the winter. You cannot catch an ear infection from someone else, but a cold may spread among children and cause some of them to get ear infections.
Drug Side effect
- Cidofovir
- Moxifloxacin ophthalmic
- Secukinumab