Persius/hicric huggingface dataset:
Superficial branch of ulnar nerve
The superficial branch of the ulnar nerve supplies the palmaris brevis and the skin on the ulnar side of the hand, and divides into a proper palmar digital nerve for the ulnar side of the little finger, and a common palmar digital nerve which gives a communicating twig to the median nerve and divides into two proper digital nerves for the adjoining sides of the little and ring fingers.
The proper digital branches are distributed to the fingers in the same manner as those of the median nerve.

# Additional images
- Diagram of segmental distribution of the cutaneous nerves of the right upper extremity. Anterior view.
TIMI myocardial perfusion grade 1

# Overview
Dye slowly enters, but fails to exit the microvasculature. There is ground glass appearance (blush) or opacification of the myocardium in the distribution of the artery that fails to clear from the microvasculature, and dye staining is present on the next injection (approximately 30 seconds between injections).
Dye staining does not include arterial or venular stains. The TMPG should not be given a grade of 1 solely because either of the former are present, but only if myocardial or arteriole stains are present.

# Example
Shown below are a static image and an animated image depicting TIMI perfusion grade 1.

# Additional Examples
TIMI myocardial perfusion grade 2

# Overview
Delayed entry and exit from the microvasculature. There is the ground glass appearance (blush) or opacification of the myocardium in the distribution of the artery that is strongly persistent during the washout phase (i.e. dye is strongly persistent after 3 cardiac cycles and either does not or minimally diminishes in intensity during washout).
The 3 cardiac cycles are determined from the point when dye touches either none or only one of the arterial borders (TIMI Frame 0). Strongly persistent blush at its maximum intensity is as intense/bright or more intense/bright as the fully-opacified surrounding collaterals.
- Intensity Range: 2 - 3

# Example
Shown below are a static image and an animated image depicting TIMI perfusion grade 2.

# Additional Examples
Telbivudine indications and usage

# Indications and Usage

## Chronic Hepatitis B
Tyzeka is indicated for the treatment of chronic hepatitis B in adult patients with evidence of viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease.
The following points should be considered when initiating therapy with Tyzeka:
- This indication is based on virologic, serologic, biochemical and histologic responses in nucleoside treatment naive adult patients with HBeAg positive and HBeAg negative chronic hepatitis B with compensated liver disease .
- For HBeAg-positive patients, Tyzeka should only be initiated in patients with HBV DNA less than 9 log10 copies per mL and ALT greater than or equal to 2x Upper Limit of Normal (ULN) prior to treatment.
- For HBeAg-negative patients, Tyzeka should only be initiated in patients with HBV DNA less than 7 log10 copies per mL prior to treatment.
- On-treatment response should guide continued therapy .
- Tyzeka has not been evaluated in patients co-infected with HIV, HCV, or HDV.
- Tyzeka has not been evaluated in liver transplant recipients or in patients with decompensated liver disease.
- Tyzeka has not been studied in well-controlled trials for the treatment of patients with established nucleoside analog reverse transcriptase inhibitor-resistant hepatitis B virus infection, but is expected to be cross-resistant to lamivudine .
- The safety and efficacy of Tyzeka have not been evaluated in Black/African American or Hispanic patients .
Tenecteplase detailed information

# Overview
Tenecteplase is an enzyme used as a thrombolytic drug.
Tenecteplase is a tissue plasminogen activator (tPA) produced by recombinant DNA technology using an established mammalian cell line (Chinese Hamster Ovary cells). Tenecteplase is a 527 amino acid glycoprotein developed by introducing the following modifications to the complementary DNA (cDNA) for natural human tPA: a substitution of threonine 103 with asparagine, and a substitution of asparagine 117 with glutamine, both within the kringle 1 domain, and a tetra-alanine substitution at amino acids 296299 in the protease domain.
Tenecteplase is a recombinant fibrin-specific plasminogen activator that is derived from native t-PA by modifications at three sites of the protein structure. It binds to the fibrin component of the thrombus (blood clot) and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase has a higher fibrin specificity and greater resistance to inactivation by its endogenous inhibitor (PAI-1) compared to native  t-PA.
Tenecteplase is indicated in thrombolytic treatment of the acute phase of myocardial infarction (AMI) for reduction of mortality associated with AMI. Treatment should be initiated as soon as possible after the onset of AMI symptoms.
Terconazole clinical pharmacology

# Clinical Pharmacology
Following intravaginal administration of terconazole in humans, absorption ranged from 58% in three hysterectomized subjects and 1216% in two non-hysterectomized subjects with tubal ligations.
Following daily intravaginal administration of 0.8% terconazole 40 mg (0.8% cream  5 g) for seven days to normal humans, plasma concentrations were low and gradually rose to a daily peak (mean of 5.9 ng/mL or 0.006 mcg/mL) at 6.6 hours.
Results from similar studies in patients with vulvovaginal candidiasis indicate that the slow rate of absorption, the lack of accumulation, and the mean peak plasma concentration of terconazole was not different from that observed in healthy women. The absorption characteristics of terconazole 0.8% in pregnant or non-pregnant patients with vulvovaginal candidiasis were also similar to those found in normal volunteers.
Following oral (30 mg) administration of 14C-labelled terconazole, the harmonic half-life of elimination from the blood for the parent terconazole was 6.9 hours (range 4.011.3). Terconazole is extensively metabolized; the plasma AUC for terconazole compared to the AUC for total radioactivity was 0.6%. Total radioactivity was eliminated from the blood with a harmonic half-life of 52.2 hours (range 4460). Excretion of radioactivity was both by renal (3256%) and fecal (4752%) routes.
In vitro, terconazole is highly protein bound (94.9%) and the degree of binding is independent of drug concentration.
Photosensitivity reactions were observed in some normal volunteers following repeated dermal application of terconazole 2.0% and 0.8% creams under conditions of filtered artificial ultraviolet light.
Photosensitivity reactions have not been observed in U.S. and foreign clinical trials in patients who were treated with terconazole suppositories or vaginal cream (0.4% and 0.8%).
Tigecycline indications and usage

# Indications And Usage
TYGACIL is a tetracycline-class antibacterial drug indicated for the treatment of infections caused by susceptible isolates of the designated microorganisms in the conditions listed below for patients 18 years of age and older:

## Complicated Skin and Skin Structure Infections
Complicated skin and skin structure infections caused by Escherichia coli, Enterococcus faecalis (vancomycin-susceptible isolates), Staphylococcus aureus (methicillin-susceptible and -resistant isolates), Streptococcus agalactiae, Streptococcus anginosus grp. (includes S. anginosus, S. intermedius, and S. constellatus),Streptococcus pyogenes, Enterobacter cloacae, Klebsiella pneumoniae, and Bacteroides fragilis.

## Complicated Intra-abdominal Infections
Complicated intra-abdominal infections caused by Citrobacter freundii, Enterobacter cloacae, Escherichia coli, Klebsiella oxytoca, Klebsiella pneumoniae, Enterococcus faecalis (vancomycin-susceptible isolates), Staphylococcus aureus (methicillin-susceptible and -resistant isolates), Streptococcus anginosus grp. (includesS. anginosus, S. intermedius, and S. constellatus), Bacteroides fragilis, Bacteroides thetaiotaomicron, Bacteroides uniformis, Bacteroides vulgatus, Clostridium perfringens, and Peptostreptococcus micros.

## Community-Acquired Bacterial Pneumonia
Community-acquired bacterial pneumonia caused by Streptococcus pneumoniae (penicillin-susceptible isolates), including cases with concurrent bacteremia, Haemophilus influenzae (beta-lactamase negative isolates), and Legionella pneumophila.

## Limitations of Use
TYGACIL is not indicated for the treatment of diabetic foot infections. A clinical trial failed to demonstrate non-inferiority of TYGACIL for treatment of diabetic foot infections.
TYGACIL is not indicated for the treatment of hospital-acquired or ventilator-associated pneumonia. In a comparative clinical trial, greater mortality and decreased efficacy were reported in TYGACIL-treated patients .
To reduce the development of drug-resistant bacteria and maintain the effectiveness of TYGACIL and other antibacterial drugs, TYGACIL should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Appropriate specimens for bacteriological examination should be obtained in order to isolate and identify the causative organisms and to determine their susceptibility to tigecycline. TYGACIL may be initiated as empiric monotherapy before results of these tests are known.
Tolterodine (patient information)
Tolterodine is an antimuscarinic drug that is used to treat urinary incontinence.  It is sold under the trade name Detrol.

# Pharmacology
Tolterodine acts on M2 and M3 subtypes of muscarinic receptors whereas most antimuscarinic treatments for overactive bladder only act on M3 receptors making them more selective.
Tolterodine, although it acts on two types of receptors, has fewer side effects than other antimuscarinics eg. oxybutynin (which is selective for M3 only) as tolterodine targets the bladder more than other areas of the body. This means that less drug needs to be given daily (due to efficient targeting of the bladder) and so there are fewer side effects.

# Side effects
Known Side Effects:
- Hyposalivation (Dry mouth)
- Decreased gastric motility (Upset stomach)
- Headache
- Constipation
- Dry eyes
- Sleepiness
Reports of Patients Experiences Since Detrol Became Available:
The following reactions have been reported in patients who have taken Detrol since it has become available:
- Allergic reactions including swelling
- Rapid heartbeat or abnormal heartbeat
- Accumulation of fluid in the arms and legs
- Hallucinations
Topiramate nonclinical toxicology
For patient information about topiramate, click here.

# Nonclinical Toxicology

## Carcinogenesis
An increase in urinary bladder tumors was observed in mice given topiramate (20, 75, and 300 mg/kg) in the diet for 21 months. The elevated bladder tumor incidence, which was statistically significant in males and females receiving 300 mg/kg, was primarily due to the increased occurrence of a smooth muscle tumor considered histomorphologically unique to mice. Plasma exposures in mice receiving 300 mg/kg were approximately 0.5 to 1 times steady-state exposures measured in patients receiving topiramate monotherapy at the recommended human dose (RHD) of 400 mg, and 1.5 to 2 times steady-state topiramate exposures in patients receiving 400 mg of topiramate plus phenytoin. The relevance of this finding to human carcinogenic risk is uncertain. No evidence of carcinogenicity was seen in rats following oral administration of topiramate for 2 years at doses up to 120 mg/kg (approximately 3 times the RHD on a mg/m2 basis).

## Mutagenesis
Topiramate did not demonstrate genotoxic potential when tested in a battery of in vitro and in vivo assays. Topiramate was not mutagenic in the Ames test or the in vitro mouse lymphoma assay; it did not increase unscheduled DNA synthesis in rat hepatocytes in vitro; and it did not increase chromosomal aberrations in human lymphocytes in vitro or in rat bone marrow in vivo.

## Impairment of Fertility
No adverse effects on male or female fertility were observed in rats at doses up to 100 mg/kg (2.5 times the RHD on a mg/m2 basis).
Translocase of the outer membrane
The translocase of the outer membrane (TOM) is a protein found in the outer mitochondrial membrane of the mitochondria. Its function is allow movement of proteins through this barrier and into the intermembrane space of the mitochondrion. Most of the proteins needed for mitochondrial function are encoded by the nucleus of the cell. The outer membrane of the mitochondrion is impermeable to large molecules greater than 5000 Daltons. The TOM works in conjunction with the translocase of the inner membrane (TIM) to translocate proteins into the mitochondrion. Many of the proteins in the TOM complex, such as TOMM22, were first identified in Neurospora crassa and Saccharomyces cerevisiae.

# Protein targeting to the mitochondrion
Proteins destined for the mitochondrion have several characteristics. For example, HSP90 aids the delivery of the mitochondrial protein to the mitochondrion in an ATP-dependent process. The N-terminal end of the protein encodes a mitochondrial targeting sequence of 10-80 amino acids which can form amphipathic helices. Further, not all mitochondrial proteins have defined N-terminal targeting sequences. Some have "internal" sequences which lack consistent patterns.

# Members of the complex
The translocase of the outer membrane (TOM) forms a complex made of Tom70, Tom22, and Tom20, along with Tom40, Tom7, Tom6, and Tom5. Tom40 is the core element of the translocase complex and Tom40 complexes with Tom22 with a mass of approximately 350k Daltons. It forms the  central protein-conducting channel with a diameter of approximately 2.5 nm. The human Tom22 is approximately 15.5k Daltons and complexes with Tom20. It N-terminal end of Tom22 extends into the cytosol and is involved in preprotein binding.
Traumatic aortic rupture overview

# Overview
Traumatic aortic rupture is a condition in which the aorta, the largest artery in the body, is torn or ruptured as the result of trauma.

# Epidemiology and Demographics
Traumatic aortic rupture is a common killer of victims of automotive accidents and other traumas, with up to 18% of deaths that occur in automobile collisions being related to the injury.

# Natural History, Complications and Prognosis
The condition is frequently fatal due to the massive bleeding that results from the rupture.  Since the aorta branches directly from the heart to supply blood to the rest of the body, the pressure within it is very great, and blood may be pumped out of a tear in the blood vessel very rapidly. This can quickly result in hemorrhagic shock and death. Death occurs immediately after traumatic rupture of the thoracic aorta 75% to 90% of the time since bleeding is so severe, and 80 to 85% of patients die before arriving at a hospital.  Though there is a concern that a small, stable tear in the aorta could enlarge and cause complete rupture of the aorta and heavy bleeding, this may be less common than previously believed as long as the patient's blood pressure does not get too high. Patients who survive to hospital admission generally have a partial tear with pseudoaneurysm formation.

# Diagnosis

## Chest X Ray
Though not completely reliable, chest X-rays are sometime used to diagnose the condition.

## Other Imaging Findings
The preferred method of diagnosis is aortography.

## Other Diagnostic Studies
If a chest tube drains a large amount of bright red arterial blood, or if there is sustained drainage of over 200mls, then aortic rupture should be suspected and the patient should undergo thoracotomy.

# Treatment

## Medical Therapy
Since a high blood pressure could exacerbate the tear in the aorta or even separate it completely from the heart, which would almost inevitably kill the patient, hospital staff take measures to keep a patient's blood pressure low.  Such measures include giving pain medication, administration of beta blockers, keeping the patient calm, and avoiding procedures that could cause gagging or vomiting.

## Surgery
Traumatic aortic rupture is treated with surgery.  However, morbidity and mortality rates for surgical repair of the aorta for this condition are among the highest of any cardiovascular surgery. For example, surgery is associated with a high rate of paraplegia, because the spinal cord is very sensitive to ischemia (lack of blood supply), and the nerve tissue can be damaged or killed by the interruption of the blood supply during surgery.
US Preventive Services Task Force
According to the Agency for Healthcare Research Quality, US Preventive Services Task Force is "an independent panel of experts in primary care and prevention that systematically reviews the evidence of effectiveness and develops recommendations for clinical preventive services." The task force, a panel of experts, is funded and appointed by the government of the United States.

# Methods
The methods of evidence synthesis used by the Task Force have been described in detail. In 2007, their methods were revised.

# History
From 1984 to 1989, the task force's stated purpose was to "develop recommendations for primary care clinicians on the appropriate content of periodic health examinations."
Ventilator-associated lung injury
Synonyms and keywords: VALI

# Overview
Ventilator-associated lung injury is lung injury thought to be due to artifical (mechanical) ventilation.

# Pathophysiology
VALI is thought to be caused by multiple factors.
The human lung normally ventilates by using negative pressure in the thorax. Once positive pressure is applied, some degree of VALI is likely to occur. VALI is also caused by use of increased  tidal volumes.VALI is also thought  to occur more frequently in patients with diseased or inflammed interstitial tissue of lungs.
One major causative factor is the over stretching of the airways and alveoli. During mechanical ventilation, the flow of gas into the lung will take the path of least resistance. Areas of the lung that are collapsed (atelectasis) or filled with secretions will be under inflated, while those areas that are relatively normal will be over inflated. These areas will become over distended and injured. This may be reduced by using smaller tidal volumes.
During positive pressure ventilation, atelectatic regions will inflate, however the alveoli will be unstable and will collapse during the expiratory phase of the breath. This repeated alveolar collapse and expansion (RACE) is thought to cause VALI. By opening the lung and keeping the lung open RACE (and VALI) is reduced.

# Treatment

## Prevention
High frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury.
Vancomycin-resistant enterococcus
Vancomycin-resistant enterococcus (VRE) is the name given to a group of bacterial species of the genus Enterococcus that is resistant to the antibiotic vancomycin. Enterococci are enteric and can be found in the digestive and urinary tracts of some humans. VRE was discovered in 1985 and are particularly dangerous to immunocompromised individuals. VRE spp. have an enhanced ability to pass resistant genes to other bacteria. While infection of healthy individuals is uncommon, it is possible that they could be colonized with newly-resistant bacteria.
There are six different types of vancomycin resistance shown by enterococci: Van-A, Van-B, Van-C, Van-D, Van-E and Van-F. Of these, only Van-A, Van-B and Van-C have been seen in general clinical practice so far. The significance is that Van-A VRE is resistant to both vancomycin and teicoplanin, Van-B VRE is resistant to vancomycin but sensitive to teicoplanin, and Van-C is only partly resistant to vancomycin, and sensitive to teicoplanin.
VRE can be carried by healthy people who have come into contact with the bacteria. The most likely place where such contact can occur is in a hospital (nosocomial infections), although it is thought that a significant percentage of intensively-farmed chicken also carries VRE.,
In 2005, Lactobacillus rhamnosus GG (LGG), a strain of L. rhamnosus, was used successfully for the first time to treat gastrointestinal carriage of VRE in renal patients.
Vitamin D deficiency risk factors

# Overview
Important risk factors for vitamin D deficiency that can not be changed are non-western ethnicity, older age and colder seasons. Sedentary lifestyle and less sun exposure play a significant role in increasing vitamin D deficiency.

# Risk Factors
The risk factors of vitamin D deficiency can be categorized into three main groups; non-modifiable risk factors, modifiable risk factors, and also factors that are related to mothers' conditions.

## Non-modifiable risk factors
- Age
- Ethnicity: non-western ethnicity like African, Asian, Turkish, and Moroccan children are at greater risks than children of western ethnic background.
- Dark skin color
- Season: late fall, winter, and spring
- Geography: higher latitude, lower altitude, cloudy weather

## Modifiable risk factors
- Life style including sedentary behavior, high child television watching, and less outdoor activities
- Less sun exposure including use of sunscreen or clothing
- Obesity
- Being underweight
- Less milk drinking
- Not taking vitamin D supplements
- Exclusive breastfeeding

## Maternal risk factors
- Lower maternal age
- Lower household income
- Multiparity
- Higher maternal BMI
Weissenbacher-Zweymuller syndrome

# Overview
Weissenbacher-Zweymuller syndrome is an autosomal recessive genetic disorder, linked to mutations (955 gly -> glu) in the COL11A2 gene (located on chromosomal position 6p21.3), which codes for the 2 strand of collagen type XI. 
It is a collagenopathy, types II and XI disorder.

# Presentation
It causes facial abnormalities, skeletal malformation and occasionally neural tube defects; the skeletal disfigurements resolve to a degree in the course of development.
Mutations in different parts of the gene may lead to deafness or Stickler syndrome type III (eye problems: myopia, retinal detachment and skeletal abnormalities).

# Eponym
It was first characterized in 1964 by G. Weissenbacher and Ernst Zweymuller.