Persius/hicric huggingface dataset:
Suprascapular artery
The suprascapular artery (or transverse scapular artery) is a branch of the thyrocervical trunk.  At first, it passes downward and laterally across the scalenus anterior and phrenic nerve, being covered by the sternocleidomastoid muscle; it then crosses the subclavian artery and the brachial plexus, running behind and parallel with the clavicle and subclavius muscle and beneath the inferior belly of the omohyoid to the superior border of the scapula. It passes over the superior transverse scapular ligament (unlike the suprascapular nerve, which passes below the ligament). (This can be remembered with the mnemonic, "Army over Navy"
The artery then enters the supraspinatous fossa of the scapula.  It travels close to the bone, running between the scapula and the supraspinatus muscle, to which it supplies branches.
It then descends behind the neck of the scapula, through the great scapular notch and under cover of the inferior transverse ligament, to reach the infraspinatous fossa, where it anastomoses with the scapular circumflex artery and the descending branch of the transverse cervical artery.
Besides distributing branches to the sternocleidomastoid, subclavius, and neighboring muscles, it gives off a suprasternal branch, which crosses over the sternal end of the clavicle to the skin of the upper part of the chest; and an acromial branch, which pierces the trapezius and supplies the skin over the acromion, anastomosing with the thoracoacromial artery.
As the artery passes over the superior transverse scapular ligament, it sends a branch into the subscapular fossa, where it ramifies beneath the subscapularis, and anastomoses with the subscapular artery and with the descending branch of the transverse cervical artery.
It also sends articular branches to the acromioclavicular joint and the shoulder joint, and a nutrient artery to the clavicle.

# Additional images
- Superficial dissection of the right side of the neck, showing the carotid and subclavian arteries.
Supratrochlear nerve

# Overview
The supratrochlear nerve is a branch of the frontal nerve, which itself comes from the ophthalmic division of the trigeminal (or fifth) cranial nerve. 
It is smaller than the nearby supraorbital nerve. It passes above the pulley of the Superior oblique muscle, and gives off a descending filament that joins the infratrochlear branch of the nasociliary nerve.
The supratrochlear nerve then exits the orbit between the pulley of the superior oblique and the supraorbital foramen, curves up on to the forehead close to the bone, and ascends beneath the Corrugator supercilii and Frontalis muscles. It then divides into branches which pierce these muscles and supplies the following areas:
- skin of the lower part of the forehead, close to the midline
- conjunctiva
- skin of the upper eyelid.

# Etymology
Supratrochlear means "above the trochlea".  The term trochlea means "pulley" in Latin.  Specifically, the trochlea referred to is a loop inside the orbit of the eye, through which the tendon of the superior oblique muscle passes.
Surfactant protein A
Surfactant protein A is an innate immune system collectin. It is water-soluble and has collagen-like domains similar to SP-D. It is part of the innate immune system and is used to opsonize bacterial cells in the alveoli marking them for phagocytosis by alveolar macrophages. SP-A may also play a role in negative feedback limiting the secretion of pulmonary surfactant. SP-A is not required for pulmonary surfactant to function but does confer immune effects to the organism.

# During Parturition
The role of Surfactant protein A (or SP-A) in childbirth is indicated in studies with mice. Mice which gestate for 19 days typically show signs of SP-A in amniotic fluid at around 16 days. If SP-A is injected into the uterus at 15 days, mice typically deliver early. Inversely, an SP-A inhibitor injection causes notable delays in birth.
The presence of Surfactant Protein A seemed to trigger an inflammatory response in the uterus of the mice, but later studies found an anti-inflammatory response in humans. In fact, the level of SP-A in a human uterus typically decreases during labor.

# Immune Functions
Research on SP-A has been done mainly in rodents including mice and rats. This research has shown that mice deficient in SP-A are more susceptible to infections from group B Streptoccoal organisms, Pseudomonas aeruginosa, and likely other organisms. The immune functions of SP-A are time, temperature, and concentration dependant.

# Location
SP-A is found in the pulmonary surfactant in lungs. SP-A and SP-D are also present in extrapulmonary tissues.
Sympathetic ganglion
Sympathetic ganglia are the ganglia of the sympathetic nervous system. They deliver information to the body about stress and impending danger, and are responsible for the familiar fight-or-flight response. They contain approximately 2000030000 nerve cell bodies and are located close to and either side of the spinal cord in long chains.

# Anatomy

## Sympathetic chain ganglia
The bilaterally symmetric sympathetic chain ganglia, also called the paravertebral ganglia, are located just anterior and lateral to the spinal cord. The chain extends from the upper neck down to the coccyx, forming the unpaired coccygeal ganglion. Preganglionic nerves from the spinal cord synapse at one of the chain ganglia and the postganglionic fiber extends to an effector, typically a visceral organ in the thoracic cavity.

## Collateral ganglia
Neurons of the collateral ganglia, also called the prevertebral ganglia, receive input from the splanchnic nerves and innervate organs of the abdominal and pelvic region. These include the celiac ganglia, superior mesenteric ganglia, and inferior mesenteric ganglia.

# Additional images
- The thoracic aorta, viewed from the left side.
- Scheme showing structure of a typical spinal nerve.
- Transverse section of human embryo eight and a half to nine weeks old.
Sympathomimetic drug
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
The mechanisms of sympathomimetic drugs are to act as catecholamine synthesis precursors, norepinephrine transporter blockade, adrenergic receptor agonism, inhibition of epinephrine and norepinephrine metabolism and/or cholinergic inhibition.

## Synthesis precursor
Synthesis precursors of catecholamines stimulate the catecholamine synthesis. One example is levodopa.

## 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.

## Cholinergic inhibition
Sympathomimetic drugs may also work by inhibiting the opposite system, i.e. the parasympathetic system. It does so by inhibiting the effects of acetylcholine, e.g. by inhibiting synaptic vesicle release, antagonize acetylcholine receptors,
- synaptic vesicle release inhibitors:
botulinum toxin
- botulinum toxin
- ACh receptor inhibitors
atropine (all muscarinic)
scopolamine (M1 receptors)
tubocurarine (Muscle type nicotinic)
- atropine (all muscarinic)
- scopolamine (M1 receptors)
- tubocurarine (Muscle type nicotinic)

# 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 sympathomimetic 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.
Systolic dysfunction

# Overview
Left ventricular systolic dysfunction is the condition where the left ventricle can only manage to eject less than 40% (occasionally less than 35%) of the blood in it, with each contraction. The term is used when the echocardiogram shows this but the patient isnt in overt heart failure.

# Diagnosis

# Treatment

## Non-pharmacologic treatment
- Exercise
- Dietary changes
- Operative therapy: Surgery for underlying valvular heart diseases

## Pharmacotherapy
For patients with systolic dysfunction (EF < 40%) who have no contraindications:
- ACE (angiotensin-converting enzyme) inhibitors for all patients.
- Beta blockers for all patients except those who are hemodynamically unstable, or those who have rest dyspnea with signs of congestion.
- Aldosterone antagonist (low dose) for patients with rest dyspnea or with a history of rest dyspnea or for symptomatic patients who have suffered a recent myocardial infarction.
- Isorbide dinitrates-hydralazine combination for symptomatic heart failure patients who are African-American.
- ARBs (angiotensin receptor blockers) as a substitute for patients intolerant of ACE inhibitors.
- Digoxin only for patients who remain symptomatic despite diuretics, ACE inhibitors and beta blockers or for those in atrial fibrillation.
- Diuretics for symptomatic patients to maintain appropriate fluid balance.

## Device based therapy
- Implantable defibrillators considered for prophylaxis against sudden cardiac death in patients with EF  35%.
- Bi-ventricular pacemakers considered for patients requiring defibrillators who have symptomatic HF and QRS durations  120 msec.

# ACC / AHA Guidelines- Recommendations for Cardiac Resynchronization Therapy in Patients With Severe Systolic Heart Failure (DO NOT EDIT) 

# Related Chapters
- Heart failure
- Diastolic dysfunction

# Guideline Resource
- The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities 

# Additional Readings
- Shekelle P, Rich M, Morton S, et al. Pharmacologic Management of Heart Failure and Left Ventricular Systolic Dysfunction: Effect in Female, Black, and Diabetic Patients, and Cost-Effectiveness. Evidence Report/Technology Assessment No. 82 (Prepared by the Southern California-RAND Evidence-based Practice Center under Contract No 290-97-0001). AHRQ Publication No. 03-E045. Rockville, MD: Agency for Healthcare Research and Quality. July 2003
- McAlister FA, Ezekowitz J, Dryden DM, Hooton N, Vandermeer B, Friesen C, Spooner C, Rowe BH. Cardiac Resynchronization Therapy and Implantable Cardiac Defibrillators in Left Ventricular Systolic Dysfunction. Evidence Report/Technology Assessment No. 152 (Prepared by the University of Alberta Evidence-based Practice Center under Contract No. 290-02-0023). AHRQ Publication No. 07-E009. Rockville, MD: Agency for Healthcare Research and Quality. June 2007.
Tetrahydrogestrinone

# Overview
Tetrahydrogestrinone (often referred to as THG) is an anabolic steroid. It has affinity to the androgen receptor and the progesterone receptor, but not to the estrogen receptor. The drug 
has been considered a "designer drug", closely related to the banned anabolic steroids gestrinone and trenbolone, and was banned by the Food and Drug Administration (FDA) at the end of 2003.
It was created by Patrick Arnold.
Anecdotal sources and some unpublished SAR studies report that the potency of the drug is outstanding, surpassing, on a milligram per milligram basis, every known synthesized or commercial available anabolic steroid. It was the drug of choice for safe and "invisible" world record breaking in athletics.
The drug was again made public when the United States Anti-Doping Agency was contacted by an anonymous athletics coach, later identified as Trevor Graham, who claimed that several top athletes were using THG and provided the USADA with a syringe containing THG, which the USADA then used to develop a test for the substance.
The USADA identified the Bay Area Laboratory Co-operative (BALCO), an American nutritional supplement company, as the source of THG. The company manufactured the drug through palladium-charcoal catalyzed hydrogenation from gestrinone, a substance used in gynecology for treatment of endometriosis.
THG had been distributed to several leading athletes, including many during the BALCO scandal.
Thyrotropin receptor
The thyrotropin receptor (or TSH receptor) is a receptor (and associated protein) that responds to thyroid-stimulating hormone (also known as "thyrotropin") and stimulates the production of thyroxine (T4) and triiodothyronine (T3).  The TSH receptor is a member of the G protein-coupled receptor superfamily of integral membrane proteins and is coupled to the Gs protein.
It is primarily found on the surface of the thyroid epithelial cells, but also found on adipose tissue and fibroblasts. The latter explains the reason of the myxedema finding during Graves disease.

# Function
Upon binding circulating TSH, a G-protein signal cascade activates adenylyl cyclase and intracellular levels of cAMP rise. cAMP activates all functional aspects of the thyroid cell, including iodine pumping; thyroglobulin synthesis, iodination, endocytosis, and proteolysis; thyroid peroxidase activity; and hormone release.
Tenofovir overdosage

# Overdosage
Limited clinical experience at doses higher than the therapeutic dose of VIREAD 300 mg is available. In Study 901, 600 mg tenofovir disoproxil fumarate was administered to 8 subjects orally for 28 days. No severe adverse reactions were reported. The effects of higher doses are not known.
If overdose occurs the patient must be monitored for evidence of toxicity, and standard supportive treatment applied as necessary.
Tenofovir is efficiently removed by hemodialysis with an extraction coefficient of approximately 54%. Following a single 300 mg dose of VIREAD, a four-hour hemodialysis session removed approximately 10% of the administered tenofovir dose.
Therapeutic metaphor
Therapeutic metaphor is a type of conceptual metaphor presented as a story or other parallel to an entire aspect of a situation, related by a psychotherapist to a patient. The purpose of this is to highlight to a person, in an effective way, some aspects and lessons that otherwise they might not be able to perceive as clearly in their current situation, or to suggest new outlooks on it. Thus a therapist, told about the untimely death of a loved one, might respond by describing two roses in a garden, one of which is dug up.
In his book, Guru: Metaphors from a psychotherapist, Sheldon Kopp states: "Generally, a metaphor is defined as a way of speaking in which one thing is expressed in terms of another, whereby this bringing together throws new light on the character of what is being described." (p.17)
Two influential figures in modern use of metaphor are: George Lakoff, one of America's foremost linguists, and Milton Erickson, the so-called "father of modern hypnotherapy". Both have emphasized strongly the crucial place that metaphor holds in human communication and experience. The use of therapeutic metaphor is discussed within neuro-linguistic programming circles.
Erickson, in particular, viewed much of human communication as metaphor, and metaphors that he used are often studied by  hypnotherapists and others insofar as they communicate on so many levels simultaneously.
Therapeutic nihilism
Therapeutic nihilism is a contention that curing people, or societies, of their ills by treatment is impossible.
In medicine, it was connected to the idea that many "cures" do more harm than good, and that one should instead encourage the body to heal itself. This position was popular, among other places, in France in the 1820s and 1830s, but has mostly faded away in the modern era due to the development of provably effective medicines such as antibiotics, starting with the release of sulfonamide in 1936. A variant of the belief is still held by people who believe in homeopathy and other forms of alternative medicine.
In relation to society, it was the idea that nothing can be done to cure society of the problems facing it.  It was never mainstream thought and did not grow beyond its origins in early 20th century Germany.  It had no main proponent save for the novelist Joseph Conrad whose writings reflect the theory.
The component of therapeutic nihilism that holds that nothing can cure human ills has analogs in modern Christian science.
Thomas Huckle Weller

# Overview
Thomas Huckle Weller (born June 15, 1915) is an American virologist.  He, John Franklin Enders and  Frederick Chapman Robbins were awarded a Nobel Prize in Physiology or Medicine in 1954 for showing how to cultivate poliomyelitis viruses in the test tube.
Weller was born and grew up in Ann Arbor, Michigan, and then went to the University of Michigan, where his father Carl Vernon Weller was a professor in the Department of Pathology. At Michigan, he studied medical zoology received a B.S. and an M.S., with his masters thesis on fish parasites.  In 1936, Weller entered Harvard Medical School, and in 1939 began working under John Franklin Enders, with whom he would later (along with Frederick Chapman Robbins) share the Nobel Prize. It was Enders who got Weller involved in researching viruses and tissue-culture techniques for determining infectious disease causes.  Weller received his MD in 1940, and went to work at Children's Hospital in Boston. In 1942, in the middle of World War II, he entered the Army Medical Corps and was stationed at the Antilles Medical Laboratory in Puerto Rico, earning the rank of Major and heading up the facility's Departments of Bacteriology, Virology and Parasitology. After the war, he returned to Children's Hospital in Boston, and it was there in 1947, he rejoined J.F. Enders in the newly created Research Division of Infectious Diseases. After several leading positions, he was appointed in 1954 the In July 1954, he was appointed Tropical Public Health Department Head the Harvard School of Public Health. Weller also served, from 1953-1959, as Director of the Commission on Parasitic Diseases of the American Armed Forces Epidemiological Board.
In addition to his research on polio, for which he won the Nobel Prize, Weller has also contributed to treating schistosomiasis, and Coxsackie viruses. He was also the first to isolate the viruses responsible for herpes and for varicella.
In 1945, Weller married Kathleen Fahey. They had two sons and two daughters together.

# Further reading
- Ligon BL. 2002. Thomas Huckle Weller MD: Nobel Laureate and research pioneer in poliomyelitis, varicella-zoster virus, cytomegalovirus, rubella, and other infectious diseases. Seminars in Pediatric Infectious Diseases 13:55-63 PMID 12118846
Thorpe-Ingold effect
The Thorpe-Ingold effect or gem-dimethyl effect, or angle compression is an effect observed in organic chemistry where increasing the size of two substituents on a tetrahedral center leads to enhanced reactions between parts of the other two substituents. The effect was first reported by Beesley, Thorpe and Ingold in 1916 as part of a study of cyclization reactions.
A common application of this effect is addition of a quaternary carbon (e.g., a gem-dimethyl group) in an alkyl chain to increase the reaction rate and/or equilibrium constant of cyclization reactions. An example is this is an olefin metathesis reaction:
One proposed explanation for this effect is that the increased size of the substituents increases the angle between them. As a result, the angle between the other two substituents decreases. By moving them closer together, reactions between them are accelerated.
Thunderclap headache

# Overview
A thunderclap headache is a sudden and severe headache. Since it is sometimes a sign of a medical emergency, one should "seek immediate medical attention for any headache that comes on suddenly and severely." The name "thunderclap" signifies the intensity and acuity of such headaches.

# Causes
In 25% of cases, a thunderclap headache is an indication of aneurysmal subarachnoid hemorrhage (SAH), which often leads to death or severe disability.

# Diagnosis

## History and Symptoms
Headaches which accompany SAH are "frequently described as being the worst headache of one's life, although other clinical presentations are possible."

## CT
Diagnosis is made via a process of exclusion with accompanying negative computed tomography and lumbar puncture results.
Tinospora cordifolia
Tinospora cordifolia, also called Guduchi is an herbaceous vine of the family Menispermaceae  indigenous to the tropical areas of India, Myanmar and Sri Lanka.
Synonyms: Guduchi , amrita (Sanskrit), giloe , gulancha (Bengali), giloya (Hindi), gado , galo (Gujarati), duyutige , teppatige (Telugu), heartleaf moonseed (English)
According to the 1911 British Pharmaceutical Codex, "Tinospora or Gulancha consists of the dried stem of Tinospora cordifolia, Miers (N.O. Menispermaceae), a climbing shrub indigenous to tropical India. The stems are collected in the hot season and dried. The drug occurs in straight or twisted cylindrical pieces and in slices, averaging about 2 centimetres in diameter, some pieces being much smaller. Externally, they are covered with a thin, papery, brown cork, bearing the raised scars of numerous lenticels. The cork readily exfoliates and discloses a greenish cortex longitudinally wrinkled and marked with lenticels. The fracture is fibrous and the transverse section exhibits a yellowish wood with radially arranged wedge-shaped wood bundles, containing large vessels, separated by narrower medullary rays. The odour is not characteristic, but the taste is bitter."

# Constituents
The active adaptogenic constituents are diterpene compounds including tinosporone, tinosporic acid, cordifolisides A to E, syringen, the yellow alkaloid, berberine, Giloin, crude Giloininand, a glucosidal bitter principle as well as polysaccharides, including arabinogalactan polysaccharide (TSP).

# Ethnobotanical Uses
According to the 1918 United States Dispensatory edited by Joseph Remington, Horatio Wood et. al.:
Tinospora. Br. Add. 1900."The dried stem of Tinospora cordifolia Miers (Fam. Menispermaceae), collected in the hot season." Br. Add., 1900. Tinospora has long been used in India as a medicine and in the preparation of a starch known as gilae-ka-sat or as palo. It is said to be a tonic, antiperiodic, and a diuretic. Fluckiger obtained from it traces of an alkaloid and a bitter glucoside. The Br. Add., 1900, recognized an infusion (Infusum Tinosporae Br. Add., 1900, two ounces to the pint), dose one-half to one fluidounce (15-30 mils); a tincture (Tinctura Tinosporae Br. Add., 1900, four ounces to the pint), dose, one-half to one fluidrachm (1.8-3.75 mils); and a concentrated solution