Persius/hicric huggingface dataset:
TAGteam gene transcriptions
The "heptamer consensus sequence CAGGTAG (i.e., the TAGteam) is overrepresented in regulatory regions of the earliest expressed zygotic genes ."

# Human genes

# Consensus sequences
The "heptamer consensus sequence  CAGGTAG".

# TAGteam samplings
Copying the consensus TAGteam: CAGGTAG and putting the sequence in "F" finds one location between ZNF497 and A1BG or no locations between ZSCAN22 and A1BG as can be found by the computer programs.
For the Basic programs testing consensus sequence CAGGTAG (starting with SuccessablesTAG.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:
- negative strand, negative direction, looking for CAGGTAG, 0.
- positive strand, negative direction, looking for CAGGTAG, 0.
- positive strand, positive direction, looking for CAGGTAG, 0.
- negative strand, positive direction, looking for CAGGTAG, 1, CAGGTAG at 4035.
- complement, negative strand, negative direction, looking for GTCCATC, 0.
- complement, positive strand, negative direction, looking for GTCCATC, 0.
- complement, positive strand, positive direction, looking for GTCCATC, 1, GTCCATC at 4035.
- complement, negative strand, positive direction, looking for GTCCATC, 0.
- inverse complement, negative strand, negative direction, looking for CTACCTG, 0.
- inverse complement, positive strand, negative direction, looking for CTACCTG, 0.
- inverse complement, positive strand, positive direction, looking for CTACCTG, 0.
- inverse complement, negative strand, positive direction, looking for CTACCTG, 1, CTACCTG at 1198.
- inverse negative strand, negative direction, looking for GATGGAC, 0.
- inverse positive strand, negative direction, looking for GATGGAC, 0.
- inverse positive strand, positive direction, looking for GATGGAC, 1, GATGGAC at 1198.
- inverse negative strand, positive direction, looking for GATGGAC, 0.

## TAG positive direction (4050-1) distal promoters
- Negative strand, positive direction: CAGGTAG at 4035.
- Negative strand, positive direction: CTACCTG at 1198.

# TAGteam random dataset samplings
- TAGr0: 0.
- TAGr1: 0.
- TAGr2: 0.
- TAGr3: 0.
- TAGr4: 0.
- TAGr5: 0.
- TAGr6: 0.
- TAGr7: 0.
- TAGr8: 1, CAGGTAG at 2738.
- TAGr9: 0.
- TAGr0ci: 0.
- TAGr1ci: 0.
- TAGr2ci: 0.
- TAGr3ci: 0.
- TAGr4ci: 0.
- TAGr5ci: 0.
- TAGr6ci: 0.
- TAGr7ci: 0.
- TAGr8ci: 1, CTACCTG at 2372.
- TAGr9ci: 0.

## TAGr arbitrary negative direction (evens) (2811-2596) proximal promoters
- TAGr8: CAGGTAG at 2738.

## TAGr arbitrary negative direction (evens) (2596-1) distal promoters
- TAGr8ci: CTACCTG at 2372.

## TAGr alternate positive direction (evens) (4050-1) distal promoters
- TAGr8: CAGGTAG at 2738.
- TAGr8ci: CTACCTG at 2372.

# TAGteam analysis and results
The "heptamer consensus sequence  CAGGTAG".
Comparison:
The occurrences of real TAGteams are greater than the randoms. This suggests that the real TAGteams are likely active or activable.

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Total iron-binding capacity
Total iron-binding capacity is a medical laboratory test. The test measures the extent to which iron-binding sites in the serum can be saturated. Because the iron-binding sites in the serum are almost entirely dependent on circulating transferrin, this is really an indirect measurement of the amount of transferrin in the blood.
Taken together with serum iron and percent transferrin saturation clinicians usually perform this test when they are concerned about anemia, iron deficiency or iron deficiency anemia. However, because the liver produces transferrin, liver function must be considered when performing this test. It can also be an indirect test of liver function, but is rarely used for this purpose.
The liver produces more transferrin in response to iron deficiency, so the percent transferrin saturation (i.e., the result of the formula of serum iron/TIBC x 100) can also be a useful indicator.
In simple iron deficiency anemia, the serum iron is low, the transferrin is high, and therefore the percent transferrin saturation is very low.
On the other hand, in anemia of chronic disease, the body holds iron out of the serum but also produces less transferrin (presumably as part of a response to keep iron away from pathogens that require it for their metabolism). In this case, serum iron is low but the TIBC (that is, the transferrin) is low. So the percent transferrin saturation is normal.
In women who are pregnant or are using hormonal contraception, the liver increases the production of transferrin. This produces a higher TIBC and a lower percent transferrin saturation even with normal iron.
These examples demonstrate that to properly understand a value for TIBC, one also must know the serum iron, the percent transferrin saturation, and the individual clinical situation.
To do the test, labs use serum from blood drawn from a vein.

# Usual values
- Serum iron: Male 65-177 g/dL (11.6-31.3 mol/L)
- Serum iron: Female 50-170 g/dL  (9.0-30.4 mol/L)
- TIBC: 240-450 mg/dL  (44.8-71.6 mol/L)
- Transferrin saturation: Male 20-50%
- Transferrin saturation: Female 15-50%
g/dL = micrograms per deciliter; mol/L = micromoles per litre.
Laboratories often use different units and "normal" may vary by population and the lab techniques used. Look at the individual laboratory reference values to interpret a specific test (for instance, your own).
Tenofovir drug interactions

# Drug Interactions
This section describes clinically relevant drug interactions with VIREAD. Drug interactions trials are described elsewhere in the labeling.

## Didanosine
Coadministration of VIREAD and didanosine should be undertaken with caution and patients receiving this combination should be monitored closely for didanosine-associated adverse reactions. Didanosine should be discontinued in patients who develop didanosine-associated adverse reactions.
When administered with VIREAD, Cmax and AUC of didanosine increased significantly. The mechanism of this interaction is unknown. Higher didanosine concentrations could potentiate didanosine-associated adverse reactions, including pancreatitis and neuropathy. Suppression of CD4+ cell counts has been observed in patients receiving VIREAD with didanosine 400 mg daily.
In patients weighing greater than 60 kg, the didanosine dose should be reduced to 250 mg once daily when it is coadministered with VIREAD. In patients weighing less than 60 kg, the didanosine dose should be reduced to 200 mg once daily when it is coadministered with VIREAD. When coadministered, VIREAD and didanosine EC may be taken under fasted conditions or with a light meal (less than 400 kcal, 20% fat). For additional information on coadministration of VIREAD and didanosine, please refer to the full prescribing information for didanosine.

## HIV-1 Protease Inhibitors
VIREAD decreases the AUC and Cmin of atazanavir . When coadministered with VIREAD, it is recommended that atazanavir 300 mg is given with ritonavir 100 mg. VIREAD should not be coadministered with atazanavir without ritonavir.
Lopinavir/ritonavir, atazanavir coadministered with ritonavir, and darunavir coadministered with ritonavir have been shown to increase tenofovir concentrations . Tenofovir disoproxil fumarate is a substrate of P-glycoprotein (Pgp) and breast cancer resistance protein (BCRP) transporters. When tenofovir disoproxil fumarate is co-administered with an inhibitor of these transporters, an increase in absorption may be observed. Patients receiving VIREAD concomitantly with lopinavir/ritonavir, ritonavir-boosted atazanavir, or ritonavir-boosted darunavir should be monitored for VIREAD-associated adverse reactions. VIREAD should be discontinued in patients who develop VIREAD-associated adverse reactions.

## Drugs Affecting Renal Function
Since tenofovir is primarily eliminated by the kidneys , coadministration of VIREAD with drugs that reduce renal function or compete for active tubular secretion may increase serum concentrations of tenofovir and/or increase the concentrations of other renally eliminated drugs. Some examples include, but are not limited to cidofovir, acyclovir, valacyclovir, ganciclovir, valganciclovir, aminoglycosides (e.g., gentamicin), and high-dose or multiple NSAIDs.
In the treatment of chronic hepatitis B, VIREAD should not be administered in combination with HEPSERA (adefovir dipivoxil).
Testicular torsion overview
Steven C. Campbell, M.D., Ph.D.

# Overview
In testicular torsion the spermatic cord that provides the blood supply to a testicle is twisted, cutting off the blood supply, often causing orchalgia. Prolonged testicular torsion will result in the death of the testicle and surrounding tissues.
It is also believed that torsion occurring during fetal development can lead to the so-called neonatal torsion or vanishing testis, and is one of the causes of an infant being born with monorchism.

# Causes
Some men may be predisposed to testicular torsion as a result of inadequate connective tissue within the scrotum. However, the condition can result from trauma to the scrotum, particularly if significant swelling occurs. It may also occur after strenuous exercise or may not have an obvious cause.

# Epidemiology and Demographics
While torsion is more frequent among adolescents, it should be considered in all cases where there is testicular pain. Torsion occurs more frequently in patients who do not have evidence of inflammation or infection.

# Diagnosis

## Laboratory Findings
Urinalysis (analyzing chemical composition of urine) can be used to rule out bacterial infections.

# Treatment

## Primary Prevention
Use precautions to avoid trauma to the scrotum. Many cases are not preventable.
Tetrarhodium dodecacarbonyl
Tetrarhodium dodecacarbonyl is the chemical compound with the formula Rh4(CO)12.  This dark-red crystalline solid is the smallest stable binary rhodium carbonyl.  It is used as a catalyst in organic synthesis.

# Structure, synthesis, reactions
The structure of Rh4(CO)12 is described by a tetrahedral array of four Rh atoms with nine terminal CO ligands and three bridging CO ligands.  The structure can be expressed as Rh4(CO)9(-CO)3.
It is prepared by treatment of an aqueous solution of  rhodium trichloride with activated copper metal under an atmosphere of CO.
Alternatively, the compound can be prepared by treatment of a methanolic solution of RhCl3(H2O)3 with CO to afford H, followed by carbonylation in the presence of sodium citrate.
The cluster undergoes thermal substitution with phosphorus ligands:

# Related metal carbonyls
Because of their relevance to hydroformylation catalysis, the metal carbonyls has been systematically  studied to a high degree. The instability of Rh2(CO)8 has been a source of curiosity.  The analogous binary carbonyl of cobalt, Co2(CO)8, is well known.  Solutions of Rh5(CO)12 under high pressures of CO do convert to the dirhodium compound:
The relative instability of Rh2(CO)8 conforms with a general trend: Ru(CO)5 loses CO spontaneously to give Ru3(CO)12.
Thalamocortical dysrhythmia
Thalamocortical Dysrhythmia (TCD) is a theoretical framework in which neuroscientists try to explain the positive and negative symptoms induced by neurological disorders like Parkinson's Disease, neurogenic pain, Tinnitus, Epilepsy as well as neuropsychiatric disorders like Depression.
In TCD the intricate dynamics between thalamus and cerebral cortex are disrupted by changes in the behaviour of neurons in the thalamus.
TCD can be treated with neurosurgical methods like the central lateral thalamotomy, which due to its invasiveness is only used on patients that have proven resistant to conventional therapies.

# Background
At the base of the theory lies diminished excitatory or increased inhibitory input at the thalamic level. This leads to a switch of the thalamocortical neurons from tonic to burst firing and subsequently entrains thalamic and cortical areas with pathological oscillations at around 5Hz.

# Evidence
Evidence for TCD comes from Electroencephalography (EEG) recordings on the scalp as well as local field potential (LFP) recordings in the patients' thalamus during surgery. Analysing the power spectra reveals increased coherence as well as increased bicoherence in the power spectra in the theta band compared to healthy controls. This indicates a close coupling of cortex and thalamus in the generation of the pathological theta rhythmicity.

# Therapy
While it is not clear how this happens in detail, surgical intervention by means of lesioning small parts of the central lateral thalamic areas has proven successful as a therapy for Parkinson's Disease as well as neurogenic pain.
The WikiDoc Manual of Style

# Overview
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# Avoid the passive tense, use the present or past tense
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# Avoid the words "causes" and "predicts"
Biology is largely phenomenology and it is hard to verify causal pathways.
Do not use the phrase  ___"causes" ____  unless a causal pathway is firmly established.
Instead use the phrase  ___ was associated with ___.
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# Table to translate conversational / casual styel to WikiDoc / Scientific style
Thoracic independent volume
A term coined by Dr. Gerald Gause of the University of Florida College of Pharmacy, Thoracic Independent Volume is the volume of the thoracic cavity without the lungs.  Another way of looking at it is TIV is the volume at which the thoracic cavity's elastic forces are at equilibrium independent of the lung's inward elastic forces.
This volume is approximately 70% of Total Lung Capacity, or 4060 mL in a typical healthy male of 70 kg.  At any volume lower than TIV, the thoracic cavity wants to expand. At any volume higher, it wants to contract.
When taking into account the inward elastic forces of the lungs; above TIV, the forces work congruously (inward recoil of the lung, inward recoil of the thoracic cavity), below TIV, the forces work opposite (inward recoil of the lung, outward recoil of the thoracic cavity).

# See Also
Tobramycin clinical studies

# Clinical Studies
Two identically designed, double-blind, randomized, placebo-controlled, parallel group, 24-week clinical studies (Study 1 and Study 2) at a total of 69 cystic fibrosis centers in the United States were conducted in cystic fibrosis patients with P. aeruginosa. Subjects who were less than 6 years of age, had a baseline creatinine of >2 mg/dL, or had Burkholderia cepacia isolated from sputum were excluded. All subjects had baseline FEV1 % predicted between 25% and 75%. In these clinical studies, 258 patients received TOBI therapy on an outpatient basis (see Table 2) using a hand-held PARI LC PLUSTM Reusable Nebulizer with a DeVilbiss Pulmo-Aide compressor.
All patients received either TOBI or placebo (saline with 1.25 mg quinine for flavoring) in addition to standard treatment recommended for cystic fibrosis patients, which included oral and parenteral anti-pseudomonal therapy, 2-agonists, cromolyn, inhaled steroids, and airway clearance techniques. In addition, approximately 77% of patients were concurrently treated with dornase alfa (PULMOZYME, Genentech).
In each study, TOBI-treated patients experienced significant improvement in pulmonary function. Improvement was demonstrated in the TOBI group in Study 1 by an average increase in FEV1 % predicted of about 11% relative to baseline (Week 0) during 24 weeks compared to no average change in placebo patients. In Study 2, TOBI-treated patients had an average increase of about 7% compared to an average decrease of about 1% in placebo patients. Figure 1 shows the average relative change in FEV1% predicted over 24 weeks for both studies.
In each study, TOBI therapy resulted in a significant reduction in the number of P. aeruginosa colony forming units (CFUs) in sputum during the on-drug periods. Sputum bacterial density returned to baseline during the off-drug periods. Reductions in sputum bacterial density were smaller in each successive cycle. (see Figure 2).
Patients treated with TOBI were hospitalized for an average of 5.1 days compared to 8.1 days for placebo patients. Patients treated with TOBI required an average of 9.6 days of parenteral anti-pseudomonal antibiotic treatment compared to 14.1 days for placebo patients. During the 6 months of treatment, 40% of TOBI patients and 53% of placebo patients were treated with parenteral anti-pseudomonal antibiotics.
The relationship between in-vitro susceptibility test results and clinical outcome with TOBI therapy is not clear. However, 4 TOBI patients who began the clinical trial with P. aeruginosa isolates having MIC values 128 g/mL did not experience an improvement in FEV1 or a decrease in sputum bacterial density.
Treatment with TOBI did not affect the susceptibility of the majority of P. aeruginosa isolates during the 6-month studies. However, some P. aeruginosa isolates did exhibit increased tobramycin MICs. The percentage of patients with P. aeruginosa isolates with tobramycin MICs 16 g/mL was 13% at the beginning, and 23% at the end of 6 months of the TOBI regimen.
Transcortical motor aphasia

# Overview
Transcortical Motor Aphasia (TMA) results from an injury to the anterior superior frontal lobe. The injury is typically caused by a cerebrovascular accident (CVA), commonly referred to as a stroke. The area of insult is sometimes referred to as a watershed region, a region surrounding Broca's area. The insult typically involves the left hemisphere as most people (regardless of handedness) are left hemisphere dominant for language (nearly 100% of right-handers, about 85% of left-handers).
Characteristics: TMA is a less common impairment than Broca's aphasia. People with TMA generally have good comprehension since Wernicke's area is usually not affected. People with TMA experience non-fluent (halting and effortful) speech due to frontal lobe damage and their utterances are typically only one or two words long. People with TMA retain the ability to repeat words, phrases or sentences. Repetition is preserved since the arcuate fasciculus (the neural pathway that connects Wernickes and Brocas areas via the parietal lobe) is intact. Preserved repetition is a defining quality of all transcortical aphasias. People who suffer from transcortical motor aphasia, however, may experience delays in initiation when they try to repeat words due to damage in the frontal lobe.
People who suffer from TMA also have severely impaired writing ability. As writing is a secondary modality (learned through formal instruction in grade school) it is always more severely affected than a primary modality like speaking.
Transferability (chemistry)
This page is about transferability in chemistry. Transferability in economics also exists.
Transferability, in chemistry, is the assumption that a chemical property that is associated with an atom or a functional group in a molecule will have a similar (but not identical) value in a variety of different circumstances. Examples of transferable properties include:
- Electronegativity
- Nucleophilicity
- Chemical shifts in NMR spectroscopy
- Characteristic frequencies in Infrared spectroscopy
Transferable properties are distinguished from conserved properties, which are assumed to always have the same value whatever the chemical situation, e.g. relative atomic mass.
Transversus thoracis muscle
The tranversus thoracis lies internal to the thoracic cage, anteriorly.  It is a thin plane of muscular and tendinous fibers, situated upon the inner surface of the front wall of the chest. It is in the same layer as the subcostal muscles.
It arises on either side from the lower third of the posterior surface of the body of the sternum, from the posterior surface of the xiphoid process, and from the sternal ends of the costal cartilages of the lower three or four true ribs.
Its fibers diverge upward and lateralward, to be inserted by slips into the lower borders and inner surfaces of the costal cartilages of the second, third, fourth, fifth, and sixth ribs.
The lowest fibers of this muscle are horizontal in their direction, and are continuous with those of the Transversus abdominis; the intermediate fibers are oblique, while the highest are almost vertical.
This muscle varies in its attachments, not only in different subjects, but on opposite sides of the same subject.

# Nerve supply
It is supplied by ventral rami of intercostal nerves.

# Function
It is almost completely without function, but it separates the thoracic cage from the parietal pleura.
Contraction of this muscle aids in exertional expiration by decreasing the transverse diameter of the thoracic cage.

# Additional images
- Transverse section of thorax, showing relations of pulmonary artery.
- Diagram of the course and branches of a typical intercostal nerve.
Tyrosine-protein kinase CSK
Tyrosine-protein kinase CSK also known as C-terminal Src kinase is an enzyme that, in humans, is encoded by the CSK gene. This enzyme phosphorylates tyrosine residues located in the C-terminal end of Src-family kinases (SFKs) including SRC, HCK, FYN, LCK, LYN and YES1.

# Function
This Non-receptor tyrosine-protein kinase plays an important role in the regulation of cell growth, differentiation, migration and immune response. CSK acts by suppressing the activity of the Src family of protein kinases by phosphorylation of Src family members at a conserved C-terminal tail site in Src. Upon phosphorylation by other kinases, Src-family members engage in intramolecular interactions between the phosphotyrosine tail and the SH2 domain that result in an inactive conformation. To inhibit SFKs, CSK is then recruited to the plasma membrane via binding to transmembrane proteins or adapter proteins located near the plasma membrane and ultimately suppresses signaling through various surface receptors, including T-cell receptor (TCR) and B-cell receptor (BCR) by phosphorylating and maintaining inactive several effector molecules.

# Role in development and regulation
Tyrosine-protein kinase CSK is involved in the following developmental, metabolic, and signal transduction cascades:
Adherens junction organization, blood coagulation, brain development, cell differentiation, cell migration, cellular response to peptide hormone stimulus, central nervous system development, epidermal growth factor receptor signaling pathway, innate immune response, epithelium morphogenesis, regulation of bone resorption, negative regulation of cell proliferation, negative regulation of ERK1 and ERK2 cascade, negative regulation of Golgi to plasma membrane protein transport, negative regulation of interleukin-6 production, negative regulation of kinase activity, negative regulation of low-density lipoprotein particle clearance, negative regulation of phagocytosis, dendrocyte differentiation, peptidyl-tyrosine autophosphorylation, platelet activation, positive regulation of MAP kinase activity, regulation of cell proliferation, regulation of cytokine production, regulation of Fc receptor mediated stimulatory signaling pathway, T cell costimulation, T cell receptor signaling pathway.

# Expression and subcellular location
CSK is expressed in the lungs and macrophages as well as several other tissues. Tyrosine-Kinase CSK is mainly present in the cytoplasm, but also found in lipid rafts making cell-cell junction.

# Mutations
- Y184F  Abolishes phosphorylation.
- Y304F  Decreases activity by two-thirds and alters conformation.
- S364A  Strong decrease of phosphorylation by PRKACA (the catalytic subunit of protein kinase A).

# Clinical significance
Csk's interaction with a phosphatase ("Lyp", gene product of PTPN22) is possibly associated with the increased autoimmune diseases associated with PTPN22 mutations.