Persius/hicric huggingface dataset:
Thermo Fisher Scientific

# Overview
Thermo Fisher Scientific is a large life sciences supply company that was created in 2006 by the merger of Thermo Electron and Fisher Scientific.

# Predecessors and merger
Thermo Electron was founded in 1956 by George Hatsopoulos, an  MIT PhD in mechanical engineering.   It focused on providing analytical and laboratory products and services, and had revenues of over $2 billion in 2004. 
Fisher Scientific was founded in 1902 by Chester G. Fisher.  It focused on providing laboratory equipment, chemicals, supplies and services used in healthcare, scientific research, safety, and education.
On May 14, 2006, Thermo Electron and Fisher Scientific announced that they would merge in a tax-free, stock-for-stock exchange; the merged company was named Thermo Fisher Scientific.  On November 9, 2006, the companies announced that the merger had been completed.  However, the Federal Trade Commission ruled that this acquisition was anticompetitive with regard to centrifugal evaporators, requiring Fisher to divest Genevac.  In April 2007, Genevac was sold to Riverlake Equity Partners LP  and the merger closed with FTC approval.
Currently, the company's products are sold under the brand names of both Thermo Scientific and Fisher Scientific.  According to company figures, 46% of its sales are in life sciences, 20% in healthcare, and 34% in industrial/environmental and safety.

# Products
Thiabendazole overdosage

# Overdosage
Overdosage may be associated with transient disturbances of vision and psychic alterations.
There is no specific antidote in the event of overdosage. Therefore, symptomatic and supportive measures should be employed. Emesis should be induced or gastric lavage performed carefully.
The oral LD50 of MINTEZOL is 3.6 g/kg, 3.1 g/kg and 3.8 g/kg in the mouse, rat, and rabbit, respectively.
Thoraco-abdominal nerves
The anterior divisions of the seventh, eighth, ninth, tenth, and eleventh thoracic  intercostal nerves are continued anteriorly from the intercostal spaces into the abdominal wall; hence they are named thoraco-abdominal nerves (or thoracicoabdominal intercostal nerves).
They have the same arrangement as the upper ones as far as the anterior ends of the intercostal spaces, where they pass behind the costal cartilages, and between the Obliquus internus and Transversus abdominis, to the sheath of the Rectus abdominis, which they perforate.
They supply the Rectus abdominis and end as the anterior cutaneous branches of the abdomen; they supply the skin of the front of the abdomen.
The lower intercostal nerves supply the Intercostales and abdominal muscles; the last three send branches to the Serratus posterior inferior. About the middle of their course they give off lateral cutaneous branches.
These pierce the Intercostales externi and the Obliquus externus abdominis, in the same line as the lateral cutaneous branches of the upper thoracic nerves, and divide into anterior and posterior branches, which are distributed to the skin of the abdomen and back; the anterior branches supply the digitations of the Obliquus externus abdominis, and extend downward and forward nearly as far as the margin of the Rectus abdominis; the posterior branches pass backward to supply the skin over the Latissimus dorsi.
Thyroid hormone receptor
The thyroid hormone receptor (TR) is a type of nuclear receptor that is activated by binding thyroid hormone.

# Function
Among the most important functions of thyroid hormone receptors are regulation of metabolism and heart rate.   In addition, they play critical roles in the development of organisms.

# Mechanism of action
Thyroid hormone receptors regulate gene expression by binding to hormone response elements (HREs) in DNA either as monomers, heterodimers with retinoid X receptor (RXR; which in turn is activated by binding to 9-cis-retinoic acid) or as homodimers.  However TR/RXR heterodimers are the most transcriptionally active form of TR.
In the absence of hormone, TR in complex with corepressor proteins bind to HREs in a transcriptionally inactive state.  Binding of thyroid hormone results in a conformational change in TR which displaces corepressor from the receptor/DNA complex and recruitment of coactivator proteins.  The DNA/TR/coactivator complex then recruits RNA polymerase that transcribes downstream DNA into messenger RNA and eventually protein that results in a change in cell function.

# Isoforms
There are three forms of the thyroid hormone receptor designated alpha-1, beta-1 and beta-2 that are able to bind thyroid hormone. 
There are two TR- receptor splice variants encoded by the THRA gene and two TR- isoform splice variants encoded by the THRB gene:
- TR-1 (widely expressed and especially high expression in cardiac and skeletal muscles)
- TR-2 (homologous with viral oncogene c-erb-A, also widely expressed but unable to bind hormone)
- TR-1 (predominately expressed in brain, liver and kidney)
- TR-2 (expression primarily limited to the hypothalamus and pituitary)

# Disease linkage
Certain mutations in the thyroid hormone receptor are associated with thyroid hormone resistance.
Ticagrelor NICE guidance
The NICE guidance regarding the utilzation of Ticagrelor is as follows:
"1.1 Ticagrelor in combination with aspirin is recommended as a treatment option in adults with acute coronary syndromes (ACS) that is, people with:
ST-segment-elevation myocardial infarction (STEMI) - defined as ST elevation or new left bundle branch block on electrocardiogram - that cardiologists intend to treat with primary percutaneous coronary intervention (PCI) or
non-ST-segment-elevation myocardial infarction (NSTEMI) or
unstable angina - defined as ST or T wave changes on electrocardiogram suggestive of ischaemia and one risk factor for cardiovascular disease (see section 1.2)- in hospitalised patients. After treatment is initiated it should only be continued if the diagnosis is confirmed by a cardiologist.
1.2 For the purposes of this guidance risk factors for cardiovascular disease are: age 60 years or older; previous myocardial infarction; previous coronary artery bypass grafting (CABG); coronary artery disease with stenosis of 50% or more in at least two vessels; previous ischaemic stroke; previous transient ischaemic attack; previous carotid stenosis of at least 50%; previous cerebral revascularisation; diabetes mellitus; peripheral arterial disease; or chronic renal dysfunction, defined as a creatinine clearance of less than 60 ml per minute per 1.73 m2 of body-surface area."

# Sources
Tight junction protein 2
Tight junction protein ZO-2 is a protein that in humans is encoded by the TJP2 gene.
Tight junction proteins (TJPs) belong to a family of membrane-associated guanylate kinase (MAGUK) homologs that are involved in the organization of epithelial and endothelial intercellular junctions. TJPs bind to the cytoplasmic C termini of junctional transmembrane proteins and link them to the actin cytoskeleton .

# Interactions
Tight junction protein 2 has been shown to interact with tight junction protein 1, band 4.1, occludin and USP53.
Transmarginal inhibition
Transmarginal inhibition, or TMI, is an organism's response to overwhelming stimuli.

# Research
Ivan Pavlov enumerated details of TMI on his work of conditioning animals to pain.  He found that organisms responded had different levels of tolerance.  He commented "that the most basic inherited difference among people was how soon they reached this shutdown point and that the quick-to-shut-down have a fundamentally different type of nervous system."
Patients who have reached this shutdown point often become socially dysfunctional or develop one of several personality disorders.  Often patients who dissociate during and after the experience, will more easily dissociate or shut down during stressful or painful experiences, and may experience post traumatic stress disorder for the remainder of their lives.
There are three stages passed through for state of TMI to be reached. The first, equivalent phase, is when the response matches the stimuli, which is considered the normal baseline behavior. The paradoxical phase occurs when small stimuli receive major response and a major stimuli elicit small responses.  Finally, the ultra-paradoxical stage where negative stimulation results in positive responses and vice versa.  Additional research on these phases was done by William Sargant in his work on shell-shocked servicemen.
An organism can progress through these stages by increased stimulation, random negative stimulation, reversing positive and negative stimulation, or physically debilitating the organism.
As observed by Pavlov, tolerance of stimulation varies greatly between individuals. Highly sensitive persons may be overstimulated by the loud volumes in a movie theater or the background confusion of a large social gathering. Other individuals will find those same stimulations as ideal stimulation levels, or even understimulating.

# Use in mental conditioning
The sudden conversion methods of mental conditioning rely heavily on TMI. Of the ten elements of control (environment control, physical fatigue, mental fatigue, tension or uncertainty, confession, superstimulation, crisis, euphoria, proselytization, and restimulation), six can be seen as stimulation toward TMI. Organizations that practice sudden conversion, such as military boot camps, prisons, and extreme psychiatric treatments, often have individuals enter TMI states which may result in permanent psychological damage.
Transmembrane protein 44
Transmembrane protein 44 is a protein that in humans is encoded by the TMEM44 gene.

# Gene
mRNA sequence of the TMEM44 gene is 1483 base pairs long, with 13 exons.

# Locus
TMEM44 gene is located at the end of the long arm of chromosome 3 in humans (Homo sapiens).

# Protein
TMEM44 is 428 amino acids in length. The molecular weight of the protein is 47.1kDa, and its formula is  C2086H3315N585O611S22, with a total of 6619 atoms. TMEM44 is predicted to be integrated in the plasma membrane of the endoplasmic reticulum.

## Expression
There is a overall low level expression of TMEM44 protein throughout the developmental stages of an organism.

## Transcripts
There are 12 isoforms of TMEM44 including isoform a, isoform b, isoform c, isoform d, isoform X1, isoform X2, isoform X3, isoform X4, isoform X5, isoform X6, isoform X7, isoform X8.

## Transmembrane Region Allocation
There are seven predicted transmembrane domains in TMEM44 protein.

## Interacting Proteins
GSK3B (Glycogen synthase kinase 3 beta) is a protein predicted to physically interact with TMEM44.

## Post-Translational Modification
TMEM44 is predicted to undergo threonine, tyrosine and serine phosphorylations.

## Orthologs
TMEM44 orthologs includes groups such as amphibians, birds, fish, mammals.

## Paralogs
Predicted paralogous proteins of TMEM44 are C9IZ85, F8WCY1, F8WE47, H7C3X7, J3KQW3, Q6PL43, and Q96I73.
Transmembrane protein 53
Transmembrane protein 53, or TMEM53, is a protein that is encoded on chromosome 1 in humans.  It has no paralogs but is predicted to have many orthologs across eukaryotes.

# Properties and Structure

## General Properties
- DUF829 makes up 87% of TMEM53's length
- Contains a transmembrane domain but lacks a signal peptide
- Molecular weight 31.6 kilodaltons
- Isoelectric point 8.56
- Leucine-rich (14.4% of amino acids are leucines)
- Predicted to be localized to the nucleus 

## Secondary Structure
The secondary structure of TMEM53 is predicted to consist of alternating pairs of alpha helices and beta sheets.

## Alternative Splicing
TMEM53 has 3 exons. Twelve alternative splice forms have been identified using 26 alternative exons.  The following table includes the predicted post-translational modifications for each isoform.

# Function
The function of TMEM53 is not fully understood.  It contains a domain of unknown function, DUF829, which is approximately 240 amino acids long.  This domain has not been found in proteins other than TMEM53 and its orthologs.

## Expression
Based on human and mouse EST profiles and a human tissue GEO profile, TMEM53 appears to be expressed ubiquitously at low levels in both normal and cancerous tissues.
More specific expression patterns have also been observed:
- Expressed in mice at higher levels in dorsal root ganglia than in the spinal cord
- Expressed at lower levels in brain tissue with Huntington's disease than in normal brain tissue
- Expressed at very low levels in the mouse brain, with the areas of highest detectable expression being the hypothalamus, pons, midbrain, and amygdala

## Homology
Transmembrane protein 53 has no paralogs.  It does, however, have orthologs extending throughout eukaryotes, from primates to amoeba.  The following table presents a selection of orthologs found using searches in BLAST and BLAT.  It is not a comprehensive list, but rather a small selection meant to display the diversity of species in which orthologs are found.
Based on ClustalW multiple sequence alignments of 38 orthologs, including the ones above, 11 amino acids are completely conserved throughout all species with this protein.

## Predicted Post-Translational Modification
Using bioinformatic analysis tools like MyHits Motif Scan and various tools at ExPASy and comparing to multiple sequence alignments, highly conserved potential sites of post-translational modification were identified.  The following is not a comprehensive list of predicted modification sites; it includes only the ones that use highly conserved amino acids.
- CK2 phosphorylation sites 140-143, 217-220
- Tyrosine phosphorylation sites 209-216, 263
- PKC phosphorylation site 19-21 conserved in mammals
- N-myristoylation site 27-32 conserved in mammals
- N-myristoylation site 153-158 conserved in vertebrates
T216, the tyrosine for a tyrosine phosphorylation site, and S217, the serine for a predicted CK2 phosphorylation site, are completely conserved throughout the protein's evolutionary history.  This suggests high likelihood that these sites are real and important for the protein's function.
Transverse facial artery
The transverse facial artery is an artery that branches from the superficial temporal artery and runs across the face.

# Structure
The transverse facial artery is given off from the superficial temporal artery before that vessel leaves the parotid gland; running forward through the substance of the gland, it passes transversely across the side of the face, between the parotid duct and the lower border of the zygomatic arch, and divides into numerous branches, which supply the parotid gland and duct, the masseter muscle, and the integument, and anastomose with the facial artery, the masseteric artery, the buccinator artery, and the infraorbital artery.
This vessel rests on the masseter, and is accompanied by one or two branches of the facial nerve.
Tris(2-chloroethyl)amine

# Overview
Tris(2-chloroethyl)ethylamine is the organic compound with the formula N(CH2CH2Cl)3.  Often abbreviated HN3, it is a  powerful blister agent  and a so-called nitrogen mustard gas (it is not a gas) used for chemical warfare.  HN-3 was the last of the nitrogen mustard agents developed. It was designed as a military agent and is the only one of the nitrogen mustards that is still used for military purposes. It is the principal representative of the nitrogen mustards because its vesicant properties are almost equal to those of HD.

## Mode of action
Nitrogen mustards react via an initial cyclization to the corresponding iminium salt. The rate of this reaction is pH dependent because the protonated amine cannot cyclize.

## Applications
HN-3 has found some applications in chemotherapy, e.g. for Hodgkin's disease, but it is mainly of interest for its military uses and is the only one of these agents that remains anywhere as a military agent. These agents are more immediately toxic than the sulfur mustards.

# Safety
Like other chemical warfare agents, tris92-chloroethyl)amine is highly toxic.
Turner Memorial Hospital
Turner Memorial Hospital is a UK National Health Service  hospital in Keith, Morayshire, Scotland. It is administered by the NHS Grampian region.
Community Hospital with 22 beds providing for GP Acute, Palliative Care, Rehabillitation and assessment. Also 24 hour minor injury unit.
On 28 April 1877 a meeting was called by Mr William Longmore to consider a proposal to build a cottage hospital for the parish of Keith.  By January 1879 the committee had raised 2,185 and decided to start building the hospital, to be called "The Turner Memorial Hospital" in memory of the late Dr Robert Turner. Many changes and expansions have occurred following the original opening in 1880. The most notable dates have been the addition of the two Kynoch Wards in 1893, and the extensions and renovations completed in 1926 and 1992.
Type II hypersensitivity
In type II hypersensitivity (or cytotoxic hypersensitivity) the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells which act as antigen presenting cells, this causes a B cell response where antibodies are produced against the foreign antigen.
An example here is the reaction to penicillin where the drug can bind to red blood cells causing them to be recognised as different, B cell proliferation will take place and antibodies to the drug are produced.  IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day.
Another form of type 2 hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcRIII)), which in turn kill these tagged cells.

# Some examples
- Autoimmune hemolytic anemia
- Goodpasture's syndrome
- Pemphigus
- Pernicious anemia (if autoimmune)
- Immune thrombocytopenia
- Transfusion reactions
- Graves disease
- Myasthenia gravis
- Rheumatic fever
- Hemolytic disease of the newborn (erythroblastosis fetalis)
- Acute transplant rejection
Uterine rupture overview

# Overview
Uterine rupture is a potentially catastrophic event during childbirth by which the integrity of the myometrial wall is breached. In an incomplete rupture the peritoneum is still intact. With a complete rupture the contents of the uterus may spill into the peritoneal cavity or the broad ligament. A uterine rupture is a life-threatening event for mother and baby.

# Causes
A uterine rupture typically occurs during early labor, but may already develop during late pregnancy.

# Risk Factors
A uterine scar from a previous cesarean section is the most common risk factor. Other forms of uterine surgery that result in full-thickness incisions (such as a myomectomy), dysfunctional labor, labor augmentation by oxytocin or prostaglandins, and high parity may also set the stage for uterine rupture.  In 2006, an extremely rare case of uterine rupture in a first pregnancy with no risk factors was reported.

# Diagnosis

## History and Symptoms
Symptoms of a rupture may be initially quite subtle. An old cesarean scar may undergo dehiscence, but with further labor, the paturient may experience abdominal pain and vaginal bleeding.

## Physical Examination
Often a deterioration of the fetal heart rate is a leading sign. Intraabdominal bleeding, of course, can lead to hypovolemic shock and death.

# Treatment

## Surgery
Emergency exploratory laparotomy with cesarean delivery accompanied by fluid and blood transfusion are indicated for the management of uterine rupture. Depending on the nature of the rupture and the condition of the patient the uterus may be either repaired or needs to be removed (cesarean hysterectomy).
Vaccinia Immune Globulin

# Overview
Vaccinia immune globulin (VIG) is made from the pooled blood of individuals who have been inoculated with the smallpox vaccine. The antibodies these individuals developed in response to the smallpox vaccine are removed and purified. This results in VIG. It can be administered intravenously. It is used to treat individuals who have developed progressive vaccinia after smallpox vaccination. It was also used along with cidofovirinfor the 2003 Midwest monkeypox outbreak as concomitant therapy to reduce the serious side effects of smallpox vaccine.

# Adverse effects of smallpox vaccine
For a small percentage of the population, the smallpox vaccine either doesn't "take" or it produces adverse events. These include postvaccinial central nervous system disease, progressive vaccinia, eczema vaccinatum, accidental implantations, generalized vaccinia, and the common erythematous and/or urticarial rashes. 

# Development of immune globulin
In the late 1940s,  Dr. Henry Kempe suggested that the solution to the complications of the smallpox vaccine was to provide antibodies in the form of gamma globulin.  Kempe noted that for some infants, the smallpox vaccine failed to "take." Kempe believed this failure might be due to the high levels of maternal antibodies to vaccinia in the infants' blood. It appeared to Kempe, that the presence of the antibodies blocked viral replication and therefore a transfusion of antibodies from people who were immune due to vaccination, would help those in whom vaccination had failed.
Valacyclovir description

# Description
VALTREX (valacyclovir hydrochloride) is the hydrochloride salt of the Lvalyl ester of the antiviral drug acyclovir.
VALTREX Caplets are for oral administration. Each caplet contains valacyclovir hydrochloride equivalent to 500 mg or 1 gram valacyclovir and the inactive ingredients carnauba wax, colloidal silicon dioxide, crospovidone, FD&C Blue No. 2 Lake, hypromellose, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, povidone, and titanium dioxide. The blue, filmcoated caplets are printed with edible white ink.
The chemical name of valacyclovir hydrochloride is L-valine, 2-ethyl ester, monohydrochloride. It has the following structural formula:
Valacyclovir hydrochloride is a white to offwhite powder with the molecular formula C13H20N6O4HCl and a molecular weight of 360.80. The maximum solubility in water at 25C is 174 mg/mL. The pkas for valacyclovir hydrochloride are 1.90, 7.47, and 9.43.