Persius/hicric huggingface dataset:
Ansa cervicalis
The ansa cervicalis (or ansa hypoglossi in older literature) is a loop of nerves that are part of the cervical plexus.
Branches from the ansa cervicalis innervate all but one of the infrahyoid muscles, including the sternohyoid muscle, the sternothyroid muscle, and the omohyoid muscle.  The thyrohyoid muscle is innervated by C1 only.

# Roots
Two roots make up the ansa cervicalis.
- The superior root (descendens hypoglossi) of the ansa cervicalis is formed by a branch of spinal nerve C1.  These nerve fibers travel in the hypoglossal nerve before leaving to form the superior root.  The superior root goes around the occipital artery and then descends in the carotid sheath.  It sends off branches to the superior belly of the omohyoid muscle, and the upper parts of the sternothyroid and sternohyoid muscles and is then joined by the inferior root.
- The inferior root (descendens cervicalis) is formed by fibers from spinal nerves C2 and C3. The inferior root gives off branches to the inferior belly of the omohyoid muscle, and the lower parts of the sternothyroid and sternohyoid muscles.

# Additional Images
- Plan of the cervical plexus.
- The right brachial plexus with its short branches, viewed from in front.
- Cervical plexus
Antiaromaticity
Antiaromatic or pseudoaromatic molecules are cyclic systems containing alternating single and double bonds,  where the pi electron energy of antiaromatic compounds is higher than that of its open-chain counterpart.  Therefore antiaromatic compounds are unstable and highly reactive; often antiaromatic compounds distort themselves out of planarity to resolve this instability. Antiaromatic compounds usually fail the Huckel's rule of aromaticity.
Examples of antiaromatic systems are cyclobutadiene (A), the cyclopentadienyl cation (B) and the cyclopropenyl anion (C).  Cyclooctatetraene is a 4n system but neither aromatic or antiaromatic because the molecules escapes a planar geometry.
By adding or removing an electron pair via a redox reaction, a  system can become aromatic and therefore more stable than the original non- or anti-aromatic compound, for instance the cyclooctatetraenide dianion. 
The IUPAC criteria for antiaromaticity are as follows:
- The molecule must have 4n  electrons where n is any integer.
- The molecule must be cyclic.
- The molecule must have a conjugated pi electron system.
- The molecule must be planar.
However, most chemists agree on the definition based on empirical (or simulated) energetic observations.
It is observed that the energy difference between aromatic and antiaromatic compounds diminishes with increasing size . For instance the 12-pi system diphenylene is an antiaromatic compound but stable and even commercially available. The low energy penalty for antiaromaticity is also demonstrated in certain pyrazine - dihydropyrazine pairs:
The compound on the left is a 14 pi-electron aromatic compound (NICS value -26.1 ppm) which can be reduced in a strongly exothermic reaction to the 16 pi-electron antiaromatic compound (NICS +27.7 ppm) on the right . The dihydropyrazine slowly converts back to the pyrazine under the action of oxygen. It shows that other electronic factors can overpower aromaticity.
Antiaromaticity is also observed in a chemical equilibrium between these two porphyrin derivatives :
A regular porphyrin is an 18 electron aromatic compound (not counting two non-contributing double bonds) but on substituting a pyrrole ring by a meta-phenylene ring aromaticity is lost due to lack of conjugation. In this system the phenylene group is also a phenol and structure A is found to interconvert with 20 electron antiaromat B via phenol-keto tautomerism. Antiaromaticity is evident from NMR spectroscopy with the inner NH protons  shifting downfield by 10 ppm to 21 ppm. The NICS values compare +0.7 for A (non-aromatic) and +5 (antiaromatic) for B and other in silico experimentation predicts that B is actually more stable than A.
Antigenic drift
Antigenic drift is the process of random accumulation of mutations in viral genes recognized by the immune system.  Such accumulation may significantly change the antigens of the virus, and may help it evade the immune system.  This process may lead to a loss of immunity, or in vaccine mismatch when one of the strains selected for the vaccine doesn't optimally match the circulating strains.  Antigenic drift may also allow a virus to jump to a new host species.

# Antigenic drift in Influenza Viruses
In the influenza virus, the two relevant genes are the surface proteins, hemagglutinin and neuraminidase.  The hemagglutinin is responsible for entry into host epithelial cells while the neuraminidase is involved in the process of new virions budding out of host cells.  The host immune response to viral infection is largely determined by the immune system's recognition of these influenza antigens.  Vaccine mismatch is a potentially serious problem.  Antigenic Drift is continuous process of genetic change among flu strains.
As in all RNA viruses, mutations in influenza occur frequently because the virus' RNA polymerase has no proofreading mechanism, providing a strong source of mutations.  Mutations in the surface proteins allow the virus to elude some host immunity, and the numbers and locations of these mutations that confer the greatest amount of immune escape has been an important topic of study for over a decade.
Antigenic drift has been responsible for heavier-than-normal flu seasons in the past, like the outbreak of influenza A Fujian (H3N2) in the 2003 - 2004 flu season. All influenza viruses experience some form of antigenic drift, but it is most pronounced in the influenza A virus.
Antigenic drift should not be confused with antigenic shift, which refers to a more abrupt change in the antigenes.
As well, it is different from random genetic drift which is a very different but important process in population genetics.
Ascending aorta

# Overview
The ascending aorta is about 5 cm. in length. It commences at the upper part of the base of the left ventricle, on a level with the lower border of the third costal cartilage behind the left half of the sternum; it passes obliquely upward, forward, and to the right, in the direction of the hearts axis, as high as the upper border of the second right costal cartilage, describing a slight curve in its course, and being situated, about 6 cm. behind the posterior surface of the sternum.
At its origin it presents, opposite the segments of the aortic valve, three small dilatations called the aortic sinuses.
At the union of the ascending aorta with the aortic arch the caliber of the vessel is increased, owing to a bulging of its right wall.
This dilatation is termed the bulb of the aorta, and on transverse section presents a somewhat oval figure.
The ascending aorta is contained within the pericardium, and is enclosed in a tube of the serous pericardium, common to it and the pulmonary artery.

# Relations
The ascending aorta is covered at its commencement by the trunk of the pulmonary artery and the right auricula, and, higher up, is separated from the sternum by the pericardium, the right pleura, the anterior margin of the right lung, some loose areolar tissue, and the remains of the thymus; posteriorly, it rests upon the left atrium and right pulmonary artery.
On the right side, it is in relation with the superior vena cava and right atrium, the former lying partly behind it; on the left side, with the pulmonary artery.

# Branches
The only branches of the ascending aorta are the two coronary arteries which supply the heart; they arise near the commencement of the aorta immediately above the attached margins of the semilunar valves.

# Additional images
- Front view of heart and lungs.
Apical membrane

# Overview
The apical membrane of a polarized cell is the part of the plasma membrane that forms its lumenal surface, distinct from the basolateral membrane. This is particularly evident in epithelial cells, but also describes other polarized cells, such as neurons.
Tight junctions that join epithelial cells near their apical surface prevent the migration of proteins to the apical membrane. The basal and lateral surfaces thus remain roughly equivalent to one another, yet distinct from the apical surface.
Referring to the tip (apex) of a cell, an organ or other body structure. For example, epithelial cells have their apical surface exposed to the body exterior, or (depending on their location) an internal open space like the intestinal lumen.
Chloral hydrate

# Overview
Chloral hydrate, also known as trichloroacetaldehyde monohydrate, 2,2,2-trichloro-1,1-ethanediol, and under the tradenames Aquachloral, Novo-Chlorhydrate, Somnos, Noctec, and Somnote, is a sedative and hypnotic drug as well as a chemical reagent and precursor. Its chemical formula is C2H3Cl3O2.
It was discovered through the chlorination of ethanol in 1832 by Justus von Liebig in Gieen. It was widely abused and misprescribed in the late 19th century.  Chloral hydrate is soluble in both water and alcohol, readily forming concentrated solutions.  A solution of chloral hydrate in alcohol called "knockout drops" was used to prepare a Mickey Finn.
It is a minor side-product of the chlorination of water, concentrations rarely exceeding 5 micrograms per litre (g/l).

# Uses
It is used for the short-term treatment of insomnia and as a sedative before minor medical or dental treatment. It has been largely displaced by the development of benzodiazepines. It was also formerly used in veterinary medicine as a general anesthetic.  Today, it is commonly used as an ingredient in the veterinary anesthetic Equithesin.
In therapeutic doses for insomnia it is effective within sixty minutes, it is metabolized within 4 minutes into trichloroethanol by erythrocytes and plasma esterases and many hours later into trichloroacetic acid. Higher doses can depress respiration and blood pressure. An overdose is marked by confusion, convulsions, nausea and vomiting, severe drowsiness, slow and irregular breathing, cardiac arrhythmia and weakness. It may also cause liver damage. It is moderately addictive. Chronic use can cause dependency and withdrawal symptoms. It can potentiate various anticoagulants and is weakly mutagenic in vitro and in vivo.
The corresponding anhydrous aldehyde, chloral, is used as an intermediate in insecticide and herbicide manufacture (including DDT, dichlorvos, and naled).  Chloral reacts rapidly with water to form chloral hydrate.
Chloral hydrate is now illegal in the United States without a prescription. Chloral hydrate is a schedule IV controlled substance in the United States. Its properties sometimes lead to its use as a date rape drug.
Arachnoid mater

# Overview
The arachnoid mater is one of the three meninges, the membranes that cover the brain and spinal cord.  It is interposed between the two other meninges, the more superficial dura mater and the deeper pia mater, and is separated from the pia mater by the subarachnoid space.
The delicate, spiderweb-like (therefore the name) arachnoid layer, attached to the inside of the dura, surrounds the brain and spinal cord but does not line the brain down into its sulci (folds). Cerebrospinal fluid flows under this membrane in the subarachnoid space, which is full of the delicate fibres of the arachnoid extending down to attach to the pia mater.
The portions covering the brain and spinal cord are called arachnoidea encephali and  arachnoidea spinalis, respectively.
The arachnoid and pia mater are sometimes considered as a single structure, the leptomeninx, or the plural version, leptomeninges. (Lepto- from the root meaning thin in Greek). Similarly, the dura in this situation is called the pachymeninx.

# Historical Perspective
Arachnoid is from a Greek root, and means cob web like. The mater designation (meaning mother in Latin) is borrowed from the dura mater and pia mater, which were Latin translations of Arabic terms. While mater does not technically belong with the arachnoid layer, it has nevertheless been adopted by it for uniformity with the other meninges, and arachnoid mater is currently the Terminologia Anatomica international standard.

# Images
- Meninges of the CNS
- Diagrammatic section of scalp.

# Related Chapters
- Arachnoid cyst
Archaeogenetics

# Overview
Archaeogenetics, a term coined by Colin Renfrew, refers to the application of the techniques of molecular population genetics to the study of the human past. This can involve:
- the analysis of DNA recovered from archaeological remains, i.e. ancient DNA;
- the analysis of DNA from modern populations (including humans and domestic plant and animal species) in order to study human past and the genetic legacy of human interaction with the biosphere; and
- the application of statistical methods developed by molecular geneticists to archaeological data.
The topic has its origins in the study of human blood groups and the realisation that this classical genetic marker provides information about the relationships between linguistic and ethnic groupings. Early work in this field included that of Ludwik and Hanka Hirszfeld, William Boyd and Arthur Mourant. From the 1960s onwards, Luca Cavalli-Sforza used classical genetic markers to examine the prehistoric population of Europe, culminating in the publication of The History and Geography of Human Genes in 1994.
Since then, the genetic history of all of our major domestic plants (e.g., wheat, rice, maize) and animals (e.g., cattle, goats, pigs, horses) has been analysed. Models for the timing and biogeography of their domestication and subsequent husbandry have been put forward, mainly based on mitochondrial DNA variation, though other markers are currently being analysed to supplement the genetic narrative (e.g., the Y chromosome for describing the history of the male lineage).
Greater burdock

# Overview
Greater burdock, Edible burdock, or Lappa Burdock is a biennial plant of the Arctium (burdock) genus in the Asteraceae family, cultivated in gardens for its root used as a vegetable.

# Description
Greater Burdock is rather tall, reaching as much as 2 metres. It has large, alternating, cordiform leaves that have a long petiole petiole and are pubescent on the underside.
The flowers are purple and grouped in globular capitula, united in clusters. They appear in mid-summer.
The capitula are surrounded by an involucre made out of many bracts, each curving to form a hook, allowing them to be carried long distances on the fur of animals. The fruits are achenes; they are long, compressed, with short pappuses.
The fleshy tap-root can grow up to 1m long.

# Origin and distribution
This species is native to the temperate regions of the old world, from Scandinavia to the Mediterranean, and from the British Isles through Russia, and the Middle East to China and Japan, including India. It is naturalized almost everywhere and is usually found in disturbed areas, especially in soil rich in nitrogen. It is commonly cultivated in Japan where it gives its name to a particular construction technique, burdock piling.

# Cultivation
It prefers a fresh, worked soil, rich in humus, and should be positioned in full sunlight. Burdock is very reactive to nitrogen fertilizer. Propagation is achieved through direct sowing the seeds midsummer. The harvest occurs three to four months after the seeding until late autumn, when the roots become too fibrous.

# Use in traditional medicine
Folk herbalists consider dried burdock to be a diuretic, diaphoretic, and a blood purifying agent.  The seeds of greater burdock are used in traditional Chinese medicine, under the name niupangzi
Metal acetylide
A metal acetylide is an alkyne that has had a proton (hydrogen) removed from the terminal end by a metal such as sodium or an organolithium. So, for example, the alkyne CH3CCH could be deprotonated to form the acetylide ion CH3CC.  Once it has been deprotonated it becomes a strong nucleophile. Some acetylides, eg. silver acetylide or copper acetylide, are explosives.
Acetylide ions are very useful in organic chemistry reactions in combining carbon chains, particularly addition and substitution reactions. One type of reaction displayed by acetylides are addition reactions with ketones to form tertiary alcohols. In the reaction in scheme 1 the alkyne proton of ethyl propiolate is deprotonated by n-butyllithium at -78C to form lithium ethyl propiolate to which cyclopentanone is added forming a lithium alkoxide. Acetic acid is added to remove lithium and liberate the free alcohol.
Coupling reactions of alkynes like the Sonogashira coupling, the Cadiot-Chodkiewicz coupling, the Glaser coupling and the Eglinton coupling often have metal acetylides as intermediates.
Several modifications of the reaction with carbonyls are known:
- In the Arens-van Dorp Synthesis the compound ethoxyacetylene  is converted to a Grignard reagent and reacted with a ketone, the reaction product is a propargyl alcohol .
- In the Isler modification ethoxyacetylene is replaced by beta-chlorovinyl ether and lithium amide.
- In the Favorskii-Babayan synthesis ketones and acetylenic compounds react in presence of alkali .
Formation of acetylides poses a risk in handling of gaseous acetylene in presence of metals such as mercury, silver or copper, or alloys with their high content (brass, bronze, silver solder).
Arrestin beta 1
Arrestin, beta 1, also known as ARRB1, is a protein which in humans is encoded by the ARRB1 gene.

# Function
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals.  Arrestin beta 1 is a cytosolic protein and acts as a cofactor in the beta-adrenergic receptor kinase (BARK) mediated desensitization of beta-adrenergic receptors.  Besides the central nervous system, it is expressed at high levels in  peripheral blood leukocytes, and thus the BARK/beta-arrestin system is believed to play a major role in regulating receptor-mediated immune functions.  Alternatively spliced transcripts encoding different isoforms of arrestin beta 1 have been described, however, their exact functions are not known.
Beta-arrestin might also play a role as scaffold protein in the GPCR pathways.

# Interactions
Arrestin beta 1 has been shown to interact with
- Arf6,
- PTHLH,
- DVL2
- Mdm2,
- OPRD1,
- PSCD2, and
- RALGDS.
Arrestin beta 2
Beta-arrestin-2, also known as arrestin beta-2, is an intracellular protein that in humans is encoded by the ARRB2 gene.
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals, as well as having signalling roles in their own right. Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high levels in the central nervous system and may play a role in the regulation of synaptic receptors. Besides the brain, a cDNA for arrestin beta 2 was isolated from thyroid gland, and thus it may also be involved in hormone-specific desensitization of TSH receptors. Multiple alternatively spliced transcript variants have been found for this gene, but the full-length nature of some variants has not been defined.
The protein may interact with the agonist DOI in 5-HT2A receptor signaling.

# Interactions
Arrestin beta 2 has been shown to interact with
- AP2B1,
- PSCD2,
- Mdm2, and
- RALGDS.
Arthus reaction

# Overview
In immunology, the Arthus reaction is a type of local type III hypersensitivity reaction.  Type III hypersensitivity reactions are immune complex mediated, and involve the deposition of an antigen/antibody complex mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli.
The Arthus reaction was discovered by Arthus in 1903.
Arthus repeatedly injected horse
serum subcutaneously into rabbits.  After four injections,
he found that there was edema and that the serum was absorbed slowly.  Further injections eventually led to gangrene.
The Arthus reaction involves the in situ formation of antigen/antibody complexes after the intradermal injection of an antigen.  If the animal/patient was previously sensitized (has circulating antibody), an Arthus reaction occurs.  This manifests as local vasculitis due to deposition of immune complexes in dermal blood vessels.  Activation of complement and recruitment of PMNs ensue resulting in an inflammatory response.
Arthus reactions have been infrequently reported after vaccination against
diphtheria and tetanus.  To quote from the CDC:
Arthus reactions (type III hypersensitivity reactions) are
rarely reported after vaccination and can occur after tetanus
toxoidcontaining or diphtheria toxoidcontaining vaccines.  An Arthus
reaction is a local vasculitis associated with deposition of
immune complexes and activation of complement. Immune
complexes form in the setting of high local concentration of
vaccine antigens and high circulating antibody concentration.  Arthus reactions are characterized by
severe pain, swelling, induration, edema, hemorrhage, and
-ccasionally by necrosis. These symptoms and signs usually
-ccur 412 hours after vaccination.....ACIP has recommended that
persons who experienced an Arthus reaction after a dose of
tetanus toxoidcontaining vaccine should not receive Td more
frequently than every 10 years, even for tetanus prophylaxis as
part of wound management.
Artificial bone

# Overview
Artificial bone refers to bone-like material created in a laboratory that can be used in bone grafts, to replace human bone that was lost due to severe fractures, disease, etc. 
Bones are rigid organs that serve various functions in the human body (or generally in vertebrates), including mechanical support, protection of soft organs, blood production (from bone marrow), etc. Bone is a very complex tissue: strong, elastic, and self-repairing.
Damaged bone can be replaced with bone from other parts of the body (autografts), from cadavers (allograft), or with various ceramics or metallic alloys. The use of autografts limits how much bone is available, while the other options can result in rejection by the human body.
There has been much research towards creating artificial bone. Richard J. Lagow, at the University of Texas at Austin, developed a way of creating a  strong bone-like porous structure from bone powder, which, when introduced in the body, can allow the growth of blood vessels, and which can be  gradually replaced by natural bone. Research at the Lawrence Berkeley National Laboratory has resulted in a metal-ceramic composite that has, like bone, a fine microstructure, and which may help create artificial bone. 
A team of British scientists have developed "injectable bone", a soft substance which hardens in the body. They won the Medical Futures Innovation Award for their discovery, and it is planned to test this material in clinical trials.
Arylsulfatase A
Arylsulfatase A (or cerebroside-sulfatase) is an enzyme that breaks down sulfatides, namely cerebroside 3-sulfate into cerebroside and sulfate. In humans, arylsulfatase A is encoded by the ARSA gene.

# Pathology
A deficiency is associated with metachromatic leukodystrophy, an autosomal recessive disease.

# Biochemistry

## Enzyme regulation
Arylsulfatase A is inhibited by phosphate, which forms a covalent bond with the active site 3-oxoalanine.
Arylsulfatase E
Arylsulfatase E, also known as ARSE, is an enzyme that, in humans, is encoded by the ARSE gene.

# Function
Arylsulfatase E is a member of the  arylsulfatase subfamily of sulfatase enzymes that catalyze the hydrolysis of sulfate esters. It is glycosylated postranslationally and localized to the golgi apparatus. Sulfatases are essential for the correct composition of bone and cartilage matrix.

# Clinical significance
Deficiencies in ARSE are associated with X-linked recessive chondrodysplasia punctata, a disease characterized by abnormalities in cartilage and bone development.