Persius/hicric huggingface dataset:
Sympathomimetic amine

# Overview
Sympathomimetic drugs are substances that mimic the effects of the hormone epinephrine (adrenaline) and the hormone/neurotransmitter norepinephrine (noradrenaline). They all raise blood pressure and are all weak bases.

# Mechanisms of Action

## Norepinephrine Transporter Blockade
Classical sympathomimetic drugs are amphetamines (including MDMA), ephedrine and cocaine, which act by blocking and reversing norepinephrine transporter (NET) activity. NET is a transport protein expressed on the surface of some cells that clears noradrenaline and adrenaline from the extracellular space and into cells, terminating the signaling effects.

## Adrenergic Receptor Agonism
Direct stimulation of the - and -adrenergic receptors can produce sympathomimetic effects. Albuterol is a very commonly used direct-acting 2-agonist.

## Inhibition of Epinephrine and Norepinephrine Metabolism
Inhibition of norepinephrine metabolism can produce sympathomimetic effects. Norepinephrine is mainly metabolized by the enzyme monoamine oxidase, the monoamine oxidase inhibitor (MAOI) drugs can induce such effects.

# Cross-reactivity
Substances like cocaine also affect dopamine, and some substances like MDMA affect serotonin.
Norepinephrine is synthesized by the body into epinephrine, causing central nervous system stimulation. Thus, all sympathimimetic amines fall into the larger group of stimulants (see psychoactive drug chart). Many of these stimulants have therepeutic use and abuse potential, can induce tolerance, and possibly physical dependence.
Synonyms and keywords

# Synonyms
Synonyms are different words with identical or very similar meanings. Words that are synonyms are said to be synonymous, and the state of being a synonym is called synonymy.
The word comes from Ancient Greek syn ("with") and onoma ("name").
For example, the words car and automobile are synonyms. Similarly, if we talk about a long time or an extended time, long and extended become synonyms.

# Keywords
Keyword or index term or descriptor in Information Retrieval is a term that captures the essence of the topic of a document. It is used as keyword to retrieve documents in an information system, for instance a catalog or a search engine.  A popular form of keywords on the web are tags which are directly visible and can be assigned by non-experts also. Index terms can consist of a word, phrase, or alphanumerical term. They are created by analyzing the document either manually with subject indexing or automatically with automatic indexing or more sophisticated methods of keyword extraction. Index terms can either come from a controlled vocabulary or be freely assigned.
Keywords are stored in a search index. Common words like articles (a, an, the) and conjunctions (and, or, but) are not treated as keywords because it is inefficient to do so. Almost every English-language site on the Internet has the article "the", and so it makes no sense to search for it. The most popular search engine, Google removed stop words such as "the" and "a" from its indexes for several years, but then re-introduced them, making certain types of precise search possible again.
The term "descriptor" was coined by Calvin Mooers in 1948.
Systemic inflammation

# Overview
Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system.
It can contribute to the development or progression of certain conditions.

# Mechanisms Inducing SI
Release of pro-inflammatory cytokines and activation of the innate immune system may be the result of either external (biological or chemical agents) or internal (genetic mutations/variations) factors.

# Lack of Control by Tolerogenic Dendritic Cells and T-regulatory Cells
While SI may be induced by multiple external factors, research suggests that a lack of control by tolerogenic dendritic cells and T-regulatory cells (Treg) is possibly the primary risk factor for the development of SI.  In functioning immune responses, T-helper and T-cytotoxic cells are activated by presentation of antigens by antigen-presenting cells (APCs).  Chief among these are dendritic cells (DCs).  When a DC presents an antigen to a Treg cell, a signal is then sent to the nucleus of the DC, resulting in the production of Indoleamine 2,3- Dioxygenase (IDO). IDO inhibits T cell responses by depleting tryptophan and producing kynurenine, which is toxic to the cell.
Individuals susceptible to developing chronic systemic inflammation appear to lack proper functioning of Treg cells and TDCs.  In these individuals, a lack of control of inflammatory processes results in multiple chemical and food intolerances, autoimmune diseases and many other symptoms and diseases.
Systolic heart murmur

# Overview
Systolic heart murmurs are heart murmurs heard during systole.  They can be classified by when the murmur begins and ends, between S1 and S2.  Many involve stenosis of the semilunar valves or regurgitation of the atrioventricular valves.

# Types
- Mid-systolic ejection murmurs are due to blood flow through the semilunar valves. They occur at the start of blood ejection  which starts after S1  and ends with the cessation of the blood flow  which is before S2. Therefore, the onset of a midsystolic ejection murmur is separated from S1 by the isovolumic contraction phase; the cessation of the murmur and the S2 interval is the aortic or pulmonary hangout time. The resultant configuration of this murmur is a crescendo-decrescendo murmur. Causes of midsystolic ejection murmurs include outflow obstruction, increased flow through normal semilunar valves, dilation of aortic root or pulmonary trunk, or structural changes in the semilunar valves without obstruction.
- Late systolic murmurs starts after S1 and, if left sided, extends up to S2, usually in a crescendo manner. Causes include mitral valve prolapse, tricuspid valve prolapse and papillary muscle dysfunction.
- Holosystolic (pansystolic) murmurs start at S1 and extends up to S2. They are usually due to regurgitation in cases such as mitral regurgitation, tricuspid regurgitation, or ventricular septal defect (VSD).

# Individual murmurs

## Mid-systolic ejection

## Late systolic

## Holosystolic (pansystolic)

# 2008 and Incorporated 2006 ACC/AHA Guidelines for the Management of Patients with Valvular Heart Disease (DO NOT EDIT) 

## Echocardiography in Systolic Heart Murmur (DO NOT EDIT) 

# Sources
- 2008 and incorporated 2006 ACC/AHA Guidelines incorporated into the 2006 guidelines for the management of patients with valvular heart disease
TANK-binding kinase 1
Serine/threonine-protein kinase TBK1 is an enzyme that in humans is encoded by the TBK1 gene.
The NF-kappa-B (NFKB) complex of proteins is inhibited by I-kappa-B (IKB) proteins, which inactivate NFKB by trapping it in the cytoplasm. Phosphorylation of serine residues on the IKB proteins by IKB kinases marks them for destruction via the ubiquitination pathway, thereby allowing activation and nuclear translocation of the NFKB complex. The protein encoded by this gene is similar to IKB kinases and can mediate NFKB activation in response to certain growth factors. For example, the protein can form a complex with the IKB protein TANK and TRAF2 and release the NFKB inhibition caused by TANK.

# Interactions
TANK-binding kinase 1 has been shown to interact with:
- NCK1,
- TANK,
- TRAF2 and
- TBKBP1 aka SINTBAD
Transcriptional factors activated upon TBK1 activation include IRF3, IRF7  and ZEB1.

# Clinical significance
Inhibition of IB kinase (IKK) and  IKK-related kinases, IKBKE (IKK) and TANK-binding kinase 1 (TBK1), has been investigated as a therapeutic option for the treatment of inflammatory diseases and cancer.
TAVR Critical pathway

# Overview
Patients with severe AS should be evaluated by a multidisciplinary Heart Valve Team when intervention is considered. It is important to have a pathway to schedule the appropriate patient for this procedure.

# Heart valve team
Patients with severe AS should be evaluated by a multidisciplinary Heart Valve Team when intervention is considered.
Team members include:
- Cardiology Valve Expert
- Cardiovascular Imaging Expert(s)
- Interventional Cardiologist
- Cardio-Thoracic Surgeon
- Cardiovascular Anesthesiologist
- Valve Clinic Care Coordinators
Their specific tasks are:
- Review the patient's medical condition and the severity of the valve abnormality
- Determine which interventions are indicated, technically feasible, and reasonable
- Discuss benefits and risks of these interventions with the patient and family, keeping in mind their values and preferences.

# Critical pathway
Abbreviations:
CV: Cardiovascular, AVR: aortic valve replacement, AS: aortic stenosis, MR: Mitral regurgitation, AR: Aortic regurgitation, PAP: Pulmonary artery pressure, RV: right ventricle, CTA: CT angiography, PA: Pulmonary artery, TEE: Trans Esophageal Echocardiography, TTE: Trans Thoracic Echocardiography

## Care Providing Team

## Clinical Evaluation

## Cardio-vascular Imaging
TCM model of the body
The model of the body in traditional Chinese medicine has the following elements:
- the Fundamental Substances;
- Qi, Blood, Jing (Essence), Shen (Mind) that nourish and protect the Zang-Fu organs;
- and the meridians (jing-luo) which connect and unify the body.
Every diagnosis is a "Pattern of disharmony" that affects one or more organs, such as "Spleen Qi Deficiency" or "Liver Fire Blazing" or "Invasion of the Stomach by Cold", and every treatment is centered on correcting the disharmony.
The traditional Chinese model is concerned with function. Thus, the TCM Spleen is not a specific piece of flesh, but an aspect of function related to transformation and transportation within the body, and of the mental functions of thinking and studying. Indeed, the  San Jiao or Triple Burner has no anatomical correspondent at all, and is said to be completely a functional entity.
Tachykinin receptor 2
Substance-K receptor is a protein that in humans is encoded by the TACR2 gene.

# Function
This gene belongs to a family of genes that function as receptors for tachykinins.  Receptor affinities are specified by variations in the 5'-end of the sequence.  The receptors belonging to this family are characterized by interactions with G proteins and 7 hydrophobic transmembrane regions.  This gene encodes the receptor for the tachykinin neuropeptide substance K, also referred to as neurokinin A.

# Selective Ligands
Several selective ligands for NK2 are now available, and although most of the compounds developed so far are peptides, one small-molecule antagonist Saredutant is currently in clinical trials as an anxiolytic and antidepressant.

## Agonists
- GR-64349 - potent and selective agonist, EC50 3.7nM, 7-amino acid polypeptide chain. CAS# 137593-52-3

## Antagonists
- Ibodutant
- Saredutant
- GR-159,897
- MEN-10376 - potent and selective antagonist, 7-amino acid polypeptide chain. CAS# 135306-85-3
Tachykinin receptor 3
Tachykinin receptor 3, also known as TACR3, is a protein which in humans is encoded by the TACR3 gene.

# Function
This gene belongs to a family of genes that function as receptors for tachykinins.  Receptor affinities are specified by variations in the 5'-end of the sequence.  The receptors belonging to this family are characterized by interactions with G proteins and 7 hydrophobic transmembrane regions.  This gene encodes the receptor for the tachykinin neurokinin 3, also referred to as neurokinin B.

# Selective ligands
A number of selective ligands are available for NK3. NK3 receptor antagonists are being investigated as treatments for various indications.

## Agonists
- Neurokinin B  endogenous peptide ligand, also interacts with other neurokinin receptors but has highest affinity for NK3
- Senktide  7-amino acid polypeptide, NK3 selective, CAS# 106128-89-6

## Antagonists
- Fezolinetant (ESN-364)
- Osanetant (SR-142,801)
- Pavinetant (MLE-4901, AZD-4901, AZD-2624)
- Talnetant (SB-223,412)
- SB-222,200  potent and selective antagonist, Ki = 4.4 nM, 3-Methyl-2-phenyl-N--4-quinolinecarboxamide, CAS# 174635-69-9
- SB-218,795  more selective than SB-222,200, Ki = 13 nM, (R)--methyl ester benzeneacetic acid, CAS# 174635-53-1
Tamm-Horsfall protein
Uromodulin, also known as UMOD, Tamm-Horsfall protein (THP), or Tamm-Horsfall mucoprotein, is a human gene.
This gene encodes uromodulin, the most abundant protein in normal urine. Its excretion in urine follows proteolytic cleavage of the ectodomain of its glycosyl phosphatidylinosital-anchored counterpart that is situated on the luminal cell surface of the loop of Henle. Uromodulin may act as a constitutive inhibitor of calcium crystallization in renal fluids. Excretion of uromodulin in urine may provide defense against urinary tract infections caused by uropathogenic bacteria. Defects in this gene are associated with the autosomal dominant renal disorders medullary cystic kidney disease-2 (MCKD2) and familial juvenile hyperuricemic nephropathy (FJHN). These disorders are characterized by juvenile onset of hyperuricemia, gout, and progressive renal failure. While several transcript variants may exist for this gene, the full-length natures of only two have been described to date. These two represent the major variants of this gene and encode the same isoform.
THP is a GPI-anchored glycoprotein which is not derived from blood plasma, but is produced by the thick ascending limb of the loop of Henle of mammalian kidney. While the monomeric molecule has a MW of approx. 68 kD, it is physiologically present in a highly agrregated state in urine.  When this protein is concentrated at low pH, it forms gel. Tamm-Horsfall protein is the most abundant protein in mammalian urine. It is the matrix of urinary casts derived from the secretion of renal tubular cells.
Uropontin, nephrocalcin and uromodulin are the 3 known urinary glycoproteins that affect the formation of calcium-containing kidney stones or calculus.
The protein was first purified by Tamm and Horsfall from the urine of healthy individuals (Tamms I & Horsfall FL, 1950). It was later detected in the urine of all mammals studied.
The function of THP is not well understood. Studies using THP deficient mice revealed that THP may have a role in regulatory physiology and actually participates in transporter function.  A role in bacterial binding and sequestration is suggested by studies showing that E.coli expressing MS (mannose-sensitive) pili or fimbriae can be trapped by Tamm-Horsfall protein via its mannose-containing side chains.  Tamm-Horsfall protein is part of the matrix in renal calculi but a role in kidney stone formation remains debatable.  Antibodies to Tamm-Horsfall protein have been seen in various forms of nephritis (eg, Balkan nephropathy), however, it remains unclear whether there is any (patho-)physiologic relevance to these findings.
Tar (tobacco residue)
Tar is the common name for the resinous partially combusted particulate matter produced by the burning of tobacco, cannabis, and other plant material in the act of smoking. Tar is purportedly the most destructive component in habitual tobacco smoking, accumulating in the smoker's lungs over time and damaging them through various biochemical and mechanical processes.
Tar includes the majority of mutagenic and carcinogenic agents in tobacco smoke (IARC, 1986). Polycyclic aromatic hydrocarbons (PAH), for example, are genotoxic via epoxidation.
There is a common misconception that the tar in cigarettes is equivalent to the tar used on roads. As a result of this, cigarette companies in the United States, when prompted to give tar/nicotine ratings for cigarettes, usually use "tar", in quotation marks, to indicate that it is not the road surface component. Tar is occasionally referred to as an acronym for total aerosol residue
although it's possible this is a backronym.
The European Union currently limits the tar yield of cigarettes to 10mg.
Taussig-Bing syndrome

# Overview
Taussig-Bing syndrome is a cyanotic congenital heart defect (CHD) in which the patient has both double outlet right ventricle (DORV) and subpulmonic ventricular septal defect (VSD).
In DORV, instead of the normal situation where blood from the left ventricle (LV) flows out to the aorta and blood from the right ventricle (RV) flows out to the pulmonary artery, both aorta and pulmonary artery are connected to the RV, and the only path for blood from the LV is across the VSD.  When the VSD is subpulmonic (sitting just below the pulmonary artery), the LV blood then flows preferentially to the pulmonary artery.  Then the RV blood, by default, flows mainly to the aorta.
The clinical manifestations of a Taussig-Bing anomaly, therefore, are much like those of dextro-Transposition of the great arteries (but the surgical repair is different).
Telaprevir overdosage

# Overdosage
The highest documented dose administered is 1875 mg every 8 hours for 4 days in healthy subjects with INCIVEK alone. In that trial, the following common adverse events were reported more frequently with the 1875 mg q8h regimen compared to the 750 mg q8h regimen: nausea, headache, diarrhea, decreased appetite, dysgeusia, and vomiting.
No specific antidote is available for overdose with INCIVEK. Treatment of overdose with INCIVEK consists of general supportive measures including monitoring of vital signs and observation of the clinical status of the patient. In the event of an overdose, it is reasonable to employ the standard supportive measures, such as removing unabsorbed material from the gastrointestinal tract, employing clinical monitoring (including obtaining an electrocardiogram), and instituting supportive therapy if required.
It is not known whether telaprevir is dialyzable by peritoneal or hemodialysis.
Telluride (chemistry)
The telluride ion is Te2.  It is the final stable member of the series of dianions O2, S2,  and Se2.
Tellurides also describe a class of compounds formally derived from Te2; i.e., their electronic structure is reasonably well approximated by considering the tellurium atom as having an octet configuration.  Using this approach, Ag2Te is derived from Ag+.
Examples:
- hydrogen telluride, H2Te
- sodium telluride, Na2Te
See category for a list.

# Discussion
In aqueous solution, Te2 exists only at high pH. In neutral conditions, hydrogen telluride ion, HTe, is prevalent. In acid conditions, hydrogen telluride, H2Te, forms.
Tenofovir description

# Description
VIREAD is the brand name for tenofovir disoproxil fumarate (a prodrug of tenofovir) which is a fumaric acid salt of bis-isopropoxycarbonyloxymethyl ester derivative of tenofovir. In vivo tenofovir disoproxil fumarate is converted to tenofovir, an acyclic nucleoside phosphonate (nucleotide) analog of adenosine 5'-monophosphate. Tenofovir exhibits activity against HIV-1 reverse transcriptase.
The chemical name of tenofovir disoproxil fumarate is 9-methoxy]phosphinyl]methoxy]propyl]adenine fumarate (1:1). It has a molecular formula of C19H30N5O10P - C4H4O4 and a molecular weight of 635.52. It has the following structural formula:
Tenofovir disoproxil fumarate is a white to off-white crystalline powder with a solubility of 13.4 mg/mL in distilled water at 25 C. It has an octanol/phosphate buffer (pH 6.5) partition coefficient (log p) of 1.25 at 25 C.
VIREAD is available as tablets or as an oral powder.
VIREAD tablets are for oral administration in strengths of 150, 200, 250, and 300 mg of tenofovir disoproxil fumarate, which are equivalent to 123, 163, 204 and 245 mg of tenofovir disoproxil, respectively. Each tablet contains the following inactive ingredients: croscarmellose sodium, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and pregelatinized starch. The 300 mg tablets are coated with Opadry II Y3010671A, which contains FD&C blue #2 aluminum lake, hypromellose 2910, lactose monohydrate, titanium dioxide, and triacetin. The 150, 200, and 250 mg tablets are coated with Opadry II 32K-18425, which contains hypromellose 2910, lactose monohydrate, titanium dioxide, and triacetin.
VIREAD oral powder is available for oral administration as white, taste-masked, coated granules containing 40 mg of tenofovir disoproxil fumarate per gram of oral powder, which is equivalent to 33 mg of tenofovir disoproxil. The oral powder contains the following inactive ingredients: mannitol, hydroxypropyl cellulose, ethylcellulose, and silicon dioxide.
Tetany (medical sign)
Tetany is a medical sign, the involuntary contraction of muscles, caused by diseases and other conditions that increase the action potential frequency. The muscle cramps caused by the disease tetanus are due to a blocking of the inhibition to the neurons that supply muscles and are not classified as tetany.

# Mechanism
When the membrane potential is upset, for instance by low levels of ions (such as calcium) in the blood (hypocalcaemia), neurons will depolarize too easily. In the case of hypocalcaemia, calcium ions are drawn away from their association with the voltage-gated sodium channels thus sensitising them. The upset to membrane potential is therefore caused by an influx of sodium to the cell, not directly by the hypocalcaemia. As a result, too many action potentials are sent to muscles causing spasm.

# Causes
The usual cause of tetany is lack of calcium, but excess of phosphate (high phosphate-to-calcium ratio) can also trigger the spasms.  Milk-and-alkali tetany is an example of this imbalance.
Underfunction of the parathyroid gland can lead to tetany.
Low levels of carbon dioxide causes tetany by altering the albumin binding of calcium such that the ionised (physiologically influencing) fraction of calcium is reduced; the most common reason for low carbon dioxide levels is hyperventilation.

# Diagnosis
The nineteenth-century clinician Professor Armand Trousseau devised the trick of occluding the brachial artery by squeezing to trigger the cramps in the fingers (Trousseau sign).
Topiramate overdosage
For patient information about topiramate, click here.

# Drug Abuse and Dependence

### Controlled Substance
Topiramate is not a controlled substance.

## Abuse
The abuse and dependence potential of topiramate has not been evaluated in human studies.

## Dependence
Topiramate has not been systematically studied in animals or humans for its potential for tolerance or physical dependence.

# Overdosage
Overdoses of topiramate have been reported. Signs and symptoms included convulsions, drowsiness, speech disturbance, blurred vision, diplopia, mentation impaired, lethargy, abnormal coordination, stupor, hypotension, abdominal pain, agitation, dizziness, and depression. The clinical consequences were not severe in most cases, but deaths have been reported after poly-drug overdoses involving topiramate.
Topiramate overdose has resulted in severe metabolic acidosis .
A patient who ingested a dose between 96 and 110 g topiramate was admitted to a hospital with a coma lasting 20 to 24 hours followed by full recovery after 3 to 4 days.
In acute topiramate overdose, if the ingestion is recent, the stomach should be emptied immediately by lavage or by induction of emesis. Activated charcoal has been shown to adsorb topiramate in vitro. Treatment should be appropriately supportive. Hemodialysis is an effective means of removing topiramate from the body.
Symptoms of overdose may include but are not limited to:
- Seizures
- Dizziness, drowsiness, tiredness
- Agitation
- Depression
- Speech problems
- Blurred vision, double vision
- Troubled thinking
- Loss of coordination
- Inability to respond to things around you
- Loss of consciousness
- Confusion and coma
- Fainting
- Upset stomach and stomach pain
- Loss of appetite and vomiting
- Excessive hunger
- Shortness of breath; fast, shallow breathing
- Pounding or irregular heartbeat
- Muscle weakness
- Bone pain
A specific antidote is not available. Treatment is entirely symptomatic.