Persius/hicric huggingface dataset:
Synovial chondromatosis
Synovial chondromatosis is a disease affecting the synovium, a thin flexible membrane around a joint.

# Symptoms
Patients usually complain of pain in one joint, which persists or months, or even years, does not ease with exercise, steroid injection or heat treatment, shows nothing on X-ray, but shows a definite restriction of movement.
There are 3 defined stages to this disease:
In the early stages of the disease it is often confused with tendinitis and/or arthritis. Once it reaches transitional the loose bodies become apparent with X-ray in greater than 70% of cases, with MRI often showing where xray fails.
In the disease, the thin flexible membrane of the synovium gradually forms blisters which calcify and enlarge. These nodules eventually break free and float around the joint space becoming larger  these add to the discomfort and stiffness of the joint.
The disease is rare and little known and currently no know cure. The affected tissue will show up as a semi-solid mass in an NMR scan, final diagnosis is usually confirmed by taking a biopsy.
People suffering from this disease are nearly always (but not exclusively) male, and usually in their forties. The disease generally affects only one of the larger weight bearing joints (hip, ankle, knee)  although the elbow, and wrist can also be affected.
For the first time a website has been set up for sufferers and their families to discuss their condition as there is currently little known about the condition and its treatment options. 

# Treatment
Treatment is frequently by means of removal of the loose bodies and of a partial or full Synovectomy (removal of the synovium)
Full synovectomy is a moderately major operation and involves completely exposing the joint and removing the affected tissue. Partial synovectomy is normally done arthroscopically. Synovectomies are normally carried out by shaving the lining of the knee but there are other ways of achieveing this by either freezing the synovium or by the use of radiation treatment.
The need for further procedures is greater than 25% although normally the frequency of the required removal of loose bodies is reduced by the previous synovectomy. There have been documented cases of malignant transformation however this is rare.
Whilst the condition can be described as a benign growth it seldom affects more than one joint, and does not usually affect surrounding tissue.
Thymine-DNA glycosylase
G/T mismatch-specific thymine DNA glycosylase is an enzyme that in humans is encoded by the TDG gene. Several bacterial proteins have strong sequence homology with this protein.

# Function
The protein encoded by this gene belongs to the TDG/mug DNA glycosylase family. Thymine-DNA glycosylase (TDG) removes thymine moieties from G/T mismatches by hydrolyzing the carbon-nitrogen bond between the sugar-phosphate backbone of DNA and the mispaired thymine. With lower activity, this enzyme also removes thymine from C/T and T/T mispairings. TDG can also remove uracil and 5-bromouracil from mispairings with guanine. TDG knockout mouse models showed no increase in mispairing frequency suggesting that other enzymes, like the functional homologue MBD4, may provide functional redundancy.  This gene may have a pseudogene in the p arm of chromosome 12.
Additionally, in 2011, the human thymine DNA glycosylase (hTDG) was reported to efficiently excises 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC), the key oxidation products of 5-methylcytosine in genomic DNA. Later on, the crystal structure of the hTDG catalytic domain in complex with duplex DNA containing 5caC was published, which supports the role of TDG in mammalian 5-methylcytosine demethylation.

# Interactions
Thymine-DNA glycosylase has been shown to interact with:
- CREB-binding protein,
- Estrogen receptor alpha,
- Promyelocytic leukemia protein,
- SUMO3, and
- Small ubiquitin-related modifier 1.

# Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles.
-  The interactive pathway map can be edited at WikiPathways: "FluoropyrimidineActivity_WP1601"..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
Tel Aviv Medical Center
The Tel Aviv Sourasky Medical Center is the main hospital serving the metropolitan area of Tel Aviv, Israel. It is the third-largest hospital complex in Israel.
Founded in 1963 as a one-building facility, The Tel Aviv Medical Center is now spread-out over an area of 150,000 square meters and incorporates three hospitals: the Ichilov General Hospital and Ida Sourasky Rehabilitation Center, the Lis Maternity Hospital, and the Dana Childrens' Hospital. The Tel Aviv Medical Center also serves as an instructional and research center affiliated with the Sackler Medical School and the Sheinborn Nursing School of Tel Aviv University.
The main building of the Ichilov Hospital was built with the donations of Ted Arison and Shari Arison.
On November 4, 1995 after being shot, Prime Minister of Israel Yitzhak Rabin was driven to Ichilov Hospital where he later died on the operating table.
Telavancin how supplied

# HOW SUPPLIED/STORAGE AND HANDLING
- Cartons of 10 individually packaged 250 mg single-dose vials (NDC 0469-3525-30)
- Cartons of 10 individually packaged 750 mg single-dose vials (NDC 0469-3575-50)
Store original packages at refrigerated temperatures of 2 to 8C (35 to 46 F). Excursions to ambient temperatures (up to 25 C (77 F)) are acceptable. Avoid excessive heat.
Telbivudine description

# Description
Tyzeka is the trade name for telbivudine, a synthetic thymidine nucleoside analogue with activity against hepatitis B virus (HBV). The chemical name for telbivudine is 1-((2S,4R,5S)-4-hydroxy-5-hydroxymethyltetrahydrofuran-2-y1)-5-methyl-1H-pyrimidine-2,4-dione, or 1-(2-deoxy--L-ribofuranosyl)-5-methyluracil. Telbivudine is the unmodified -L enantiomer of the naturally occurring nucleoside, thymidine. Its molecular formula is C10H14N2O5, which corresponds to a molecular weight of 242.23. Telbivudine has the following structural formula:
Telbivudine is a white to slightly yellowish powder. Telbivudine is sparingly soluble in water (greater than 20 mg per mL), and very slightly soluble in absolute ethanol (0.7 mg per mL) and n-octanol (0.1 mg per mL).
Tyzeka film-coated tablets are available for oral administration in 600 mg strength. Tyzeka 600 mg film-coated tablets contain the following inactive ingredients: colloidal silicon dioxide, magnesium stearate, microcrystalline cellulose, povidone, and sodium starch glycolate. The tablet coating contains titanium dioxide, polyethylene glycol, talc, and hypromellose.
Tyzeka oral solution is available for oral administration in 100 mg per 5 mL strength. Tyzeka oral solution contains the following inactive ingredients: citric acid anhydrous, benzoic acid, passion fruit flavor, sodium saccharin, sodium hydroxide, and purified water. A 600 mg dose (30 mL) of Tyzeka oral solution contains approximately 47 mg of sodium.
Tellurium tetrafluoride
Tellurium tetrafluoride, TeF4, is a stable, white, hygroscopic crystalline solid and is one of two fluorides of tellurium.  The other binary fluoride is tellurium hexafluoride. The widely reported Te2F10 has been shown to be F5TeOTeF5  There are other tellurium compounds that contain fluorine, but only the two mentioned contain solely tellurium and fluorine. Tellurium difluoride, TeF2, and ditellurium fluoride, Te2F are not known.

# Preparation
Tellurium tetrafluoride can be prepared by the following reaction:
TeO2 + 2SF4  TeF4 + 2SOF2
It is also prepared by reacting nitryl fluoride with tellurium or from the elements at 0 C or by reacting selenium tetrafluoride with tellurium dioxide at 80 C.
Fluorine in nitrogen can react with TeCl2 or TeBr2 to form TeF4.  PbF2 will also fluorinate tellurium to TeF4.

# Reactivity
Tellurium tetrafluoride will react with water or silica and forms tellurium oxides.  Copper, silver, gold or nickel will react with tellurium tetrafluoride at 185 C.  It does not react with platinum.  It is soluble in SbF5 and will precipitate out the complex TeF4SbF5.

# Properties
Tellurium tetrafluoride melts at 130 C and decomposes to tellurium hexafluoride at 194 C.  In the solid phase it consists of infinite chains of TeF3F2/2 in an octahedral geometry. A lone pair of electrons occupies the sixth position.
Terbinafine description

# Description
Terbinafine tablets, USP contain the synthetic allylamine antifungal compound terbinafine hydrochloride USP.
Chemically, terbinafine hydrochloride is (E)-N-(6,6-dimethyl-2-hepten-4-ynyl)-N-methyl-1-naphthalenemethanamine hydrochloride. The molecular formula C21H26ClN with a molecular weight of 327.90, and the following structural formula:
Terbinafine hydrochloride USP is a white to off-white fine crystalline powder. It is freely soluble in methanol and methylene chloride, soluble in ethanol, and slightly soluble in water.
Each tablet contains:
Active Ingredient: Terbinafine hydrochloride USP (equivalent to 250 mg of terbinafine)
Inactive Ingredients:  Microcrystalline cellulose, sodium starch glycolate, colloidal silicon dioxide, hypromellose, and magnesium stearate.
Terconazole description

# Description
TERAZOL 7 (terconazole) Vaginal Cream 0.4% is a white to off-white, water washable cream for intravaginal administration containing 0.4% of the antifungal agent terconazole, cis-1-methoxy]phenyl]-4-isopropylpiperazine, compounded in a cream base consisting of butylated hydroxyanisole, cetyl alcohol, isopropyl myristate, polysorbate 60, polysorbate 80, propylene glycol, stearyl alcohol, and purified water.
TERAZOL 3 (terconazole) Vaginal Cream 0.8% is a white to off-white, water washable cream for intravaginal administration containing 0.8% of the antifungal agent terconazole, cis-1-methoxy]phenyl]-4-isopropylpiperazine, compounded in a cream base consisting of butylated hydroxyanisole, cetyl alcohol, isopropyl myristate, polysorbate 60, polysorbate 80, propylene glycol, stearyl alcohol, and purified water.
TERAZOL 3 (terconazole) Vaginal Suppositories are white to off-white suppositories for intravaginal administration containing 80 mg of the antifungal agent terconazole, cis-1-methoxy]phenyl]-4-isopropylpiperazine, in triglycerides derived from coconut and/or palm kernel oil (a base of hydrogenated vegetable oils) and butylated hydroxyanisole.
The structural formula of terconazole is as follows:
Terminalia schimperiana
Terminalia schimperiana is a species of Terminalia, native to tropical Africa from Guinea and Sierra Leone east to Uganda and Ethiopia.
It is a broadleaved small tree that can reach up to 714 m, variably deciduous in the dry season to semi-evergreen, depending on the climate. The leaves are alternate, simple, elliptic to obovate, entire, 915 cm long and 38 cm broad, green above with pale undersides. The flowers are tiny and form pale spikes at the base of the leaves. The fruit is a samara with a single wing 69 cm long, that turns brown with age.
It can be found in open forest habitats with more than 1300 mm of rainfall per year. as well as closed forest. When it is found in closed forest, it typically is part of the forest canopy. It may be the dominant large tree species where it is found. Fire and debarking by elephants can damage the trees.

# Uses
In parts of West Africa, T. schimperiana is used as a medicinal plant.  The bark is applied to wounds, and the twigs may be chewed to promote oral hygiene.  In laboratory experiments, extracts of the plant were effective as antibiotics against Staphylococcus. The plant extracts also have antifungal properties.
The Specials Laboratory
Specials Laboratory started back in 1999 with 3 people and now has around 135 employees based across three MHRA-licensed sites.
In recent years, Specials Laboratory have launched a number of services to assist hospitals across the UK. They provide hospitals with a space and time saving Over Labelling service, which involves the bespoke design and labelling of products.
Specials Laboratory offer a service to manufacture Investigational Medicinal Products (IMPs), in order to meet the supply needs of hospital-based clinical trials. Specials Laboratory has three sites and each are licensed to offer a IMP manufacturing service for non-sterile medicines for use in small clinical studies. This GMP manufacturing service supports clinical trial pharmacists and technicians, University medical schools and research doctors carrying out such trials and requiring an outsourced manufacturing partner.
Thiamine-triphosphatase
Thiamine-triphosphatase is an enzyme involved in thiamine metabolism. It catalyzes the chemical reaction
This enzyme belongs to the family of acid anhydride hydrolases, specifically those acting on phosphorus-containing anhydrides. Its systematic name is thiamine triphosphate phosphohydrolase.

# Structural studies
As of late 2007, only one structure has been solved for this class of enzymes, with the PDB accession code 2JMU.
Thomas Graham (chemist)
Thomas Graham FRS (December 21, 1805  September 16, 1869) was born in Glasgow, Scotland. Graham's father was a successful  textile manufacturer, and wanted his son to enter into the Church of Scotland. Instead, defying his father's wishes, Graham became a student at the University of Glasgow in 1819.  There he developed a strong interest in chemistry, and left the University after receiving his M.A. in 1826.  He later became a professor of chemistry at numerous colleges, including the Royal College of Science and Technology and the University of London.
Graham also founded the Chemical Society of London in 1841.
His final postition was as the Master of the Mint, where he stayed for 15 years until his death.  He was the last person to hold that position.

# Scientific work
Thomas Graham is best known for two things:
1. His studies on the diffusion of gases resulted in "Graham's Law", which states that the rate of effusion of a gas is inversely proportional to the square root of its molar mass.
2. His discovery of dialysis, which is used in many medical facilities today, was the result of Graham's study of colloids.  This work resulted in Graham's ability to separate colloids and crystalloids using a so-called "dialyzer", the precursor of today's dialysis machine. This study initiated the scientific field known as colloid chemistry, of which Graham is credited as the founder.

# Honours, activities, and recognition
- Fellow of the Royal Society (1836)
- First President of the Chemical Society of London (1841)
- Royal Medal of the Royal Society (1837 and 1863)
- Copley Medal of the Royal Society (1862)
- Prix Jecker of the Paris Academy of Sciences (1862)
- (Unofficial Honour) Statue of Graham in Glasgow ("given" in 1872)
- The University of Strathclyde, where Graham worked at one of its precursor institutions, has named the building housing the chemistry department after him.
- The headquarters of the Royal Society of Chemistry in Cambridge, UK is the Thomas Graham House.
Thrifty gene hypothesis
The thrifty gene hypothesis is a hypothesis proposed in 1962 by geneticist James Neel to explain the tendency of certain ethnic groups, such as American Indian (see New World Syndrome), to tend towards obesity and diabetes. It postulates that certain genes in humans have evolved to maximize metabolic efficiency, lipid storage and food searching behaviour, and that in times of abundance these genes predispose their carriers to diseases caused by excess nutritional intake, such as obesity.
In the past, this genotype would have been advantageous for puberty or child-bearing women during periods of famine. However, with the advent of high fat, high carbohydrate, and low fiber diets, and relative inactivity this genotype is no longer advantageous because it is too efficient. This has led to obesity and related health problems.
It follows from the theory that ethnic groups with a history of food scarcity will have undergone a relatively high evolutionary pressure and hence may harbor more thrifty genes than other populations.
It is often cited alongside the thrifty phenotype hypothesis (or Barker hypothesis) as an explanation for progressive prevalence of obesity in the Western world.
The fundamental basis of the thrifty gene hypothesis has recently been challenged in papers by Speakman.  who suggests that famines have occurred too infrequently and involve insufficient mortality to favour selection of thrifty genes. He suggests that instead release from predation around 2 million years ago may have allowed the regulation system in humans to drift - generating the pattern we observe today of a distribution of body weights: with some people obese but many others quite thin.
Thrombopoietin receptor
The thrombopoietin receptor also known as the myeloproliferative leukemia protein or CD110 (Cluster of Differentiation 110) is a protein that in humans is encoded by the MPL (myeloproliferative leukemia virus) oncogene.

# Discovery
In 1990 an oncogene, v-mpl, was identified from the murine myeloproliferative leukemia virus that was capable of immortalizing bone marrow hematopoietic cells from different lineages. In 1992 the human homologue, named, c-mpl, was cloned. Sequence data revealed that c-mpl encoded a protein that was homologous with members of the hematopoietic receptor superfamily. Presence of anti-sense oligodeoxynucleotides of c-mpl inhibited megakaryocyte colony formation.

# Function
The ligand for c-mpl, thrombopoietin, was cloned in 1994. Thrombopoietin was shown to be the major regulator of megakaryocytopoiesis and platelet formation.
The protein encoded by the c-mpl gene, CD110, is a 635 amino acid transmembrane domain, with two extracellular cytokine receptor domains and two intracellular cytokine receptor box motifs . TPO-R deficient mice were severely thrombocytopenic, emphasizing the important role of CD110 and thrombopoietin in megakaryocyte and platelet formation. Upon binding of thrombopoietin, CD110 is dimerized and the JAK family of non-receptor tyrosine kinases, as well as the STAT family, the MAPK family, the adaptor protein Shc and the receptors themselves become tyrosine phosphorylated.

# Interactions
Myeloproliferative leukemia virus oncogene has been shown to interact with:
- ATXN2L
- JAK2
- thrombopoietin

# Clinical relevance
Inactivating mutations in this gene have been shown to cause familial aplastic anemia.
Specific mutations to this gene are associated with myelofibrosis and essential thrombocythemia. In essential thrombocythemia, mutations occur at position 505 or 515 in the protein. In myelofibrosis, a mutation occurs at position 515. 
These mutations lead to the production of thrombopoietin receptors that are permanently activated, which results in the overproduction of abnormal megakaryocytes.
Tinidazole how supplied

# How Supplied/Storage and Handling
Tindamax 250 mg tablets are pink, round, scored tablets, with TM debossed on one side and 250 on the other, supplied in bottles with child-resistant caps as:
Tindamax 500 mg tablets are pink, oval, scored tablets, with TM debossed on one side and 500 on the other, supplied in bottles with child-resistant caps as:
Professional Samples:
Storage: Store at controlled room temperature 20-25 C (68-77 F); excursions permitted to 15-30 C (59-86 F) . Protect contents from light.
Tinidazole microbiology

# Microbiology

## Mechanism of Action
Tinidazole is an antiprotozoal, antibacterial agent. The nitro- group of tinidazole is reduced by cell extracts of Trichomonas. The free nitro- radical generated as a result of this reduction may be responsible for the antiprotozoal activity. Chemically reduced tinidazole was shown to release nitrites and cause damage to purified bacterial DNA in vitro. Additionally, the drug caused DNA base changes in bacterial cells and DNA strand breakage in mammalian cells. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known.
Antibacterial: Culture and sensitivity testing of bacteria are not routinely performed to establish the diagnosis of bacterial vaginosis. The standard methodology for the susceptibility testing of potential bacterial pathogens, Gardnerella vaginalis, Mobiluncus spp. or Mycoplasma hominis, has not been defined. The following in vitro data are available, but their clinical significance is unknown. Tinidazole is active in vitro against most strains of the following organisms that have been reported to be associated with bacterial vaginosis:
- Bacteroides spp.
- Gardnerella vaginalis
- Prevotella spp.
Tinidazole does not appear to have activity against most strains of vaginal lactobacilli.
Antiprotozoal: Tinidazole demonstrates activity both in vitro and in clinical infections against the following protozoa:Trichomonas vaginalis; Giardia duodenalis (also termed G. lamblia); and Entamoeba histolytica.
For protozoal parasites, standardized susceptibility tests do not exist for use in clinical microbiology laboratories.

### Drug Resistance
The development of resistance to tinidazole by G. duodenalis, E. histolytica, or bacteria associated with bacterial vaginosis has not been examined.

### Cross-resistance
Approximately 38% of T. vaginalis isolates exhibiting reduced susceptibility to metronidazole also show reduced susceptibility to tinidazole in vitro. The clinical significance of such an effect is not known.
Tipranavir how supplied

# How Supplied/Storage And Handling
APTIVUS capsules 250 mg are pink, oblong soft gelatin capsules imprinted in black with "TPV 250". They are packaged in HDPE unit-of-use bottles with a child resistant closure and 120 capsules. (NDC 0597-0003-02)
APTIVUS oral solution is a clear yellow viscous buttermint-butter toffee flavored liquid containing 100 mg tipranavir in each mL. The solution is supplied in a unit-of-use amber glass bottle providing 95 mL of solution with a child resistant closure. 
A 5 mL plastic oral dispensing syringe is also provided. (NDC 0597-0002-01).

# Storage
APTIVUS capsules should be stored in a refrigerator 2-8C (36-46F) prior to opening the bottle. After opening the bottle, the capsules may be stored at 25C (77F); excursions permitted to 15-30C (59-86F) and must be used within 60 days after first opening the bottle.
APTIVUS oral solution should be stored at 25C (77F); excursions permitted to 15-30C (59-86F). Do not refrigerate or freeze. The solution must be used within 60 days after first opening the bottle.
Store in a safe place out of the reach of children.