Persius/hicric huggingface dataset:
Adrenodoxin reductase
Adrenodoxin reductase (Enzyme Nomenclature name: adrenodoxin-NADP+ reductase, EC 1.18.1.6), was first isolated from bovine adrenal cortex where it functions as the first enzyme in the mitochondrial P450 systems that catalyze essential steps in steroid hormone biosynthesis.
Examination of complete genome sequences revealed that adrenodoxin reductase gene is present in most metazoans and prokaryotes.
The name of the enzyme was coined based on its function to reduce a  (2 iron, 2 sulfur) electron-transfer protein that was named adrenodoxin. Later, in some studies, the enzyme was also referred to as a "ferredoxin reductase" assuming a homology to plant ferredoxin reductase. In the human gene nomenclature, the standard name is ferredoxin reductase and the symbol is FDXR, with ADXR specified as a synonym.
The assignment of the name "ferredoxin reductase" has been criticized as a misnomer because determination of the structure of adrenodoxin reductase revealed that it is completely different from that of plant ferredoxin reductase and there is no homology between these two enzymes.

# Function
Adrenodoxin reductase is a flavoprotein as it carries a FAD type coenzyme. The enzyme functions as the first electron transfer protein of mitochondrial P450 systems such as P450scc. The FAD coenzyme receives two electrons from NADPH and transfers them one at a time to the electron transfer protein adrenodoxin. Adrenodoxin functions as a mobile shuttle that transfers electrons between ADXR and mitochondrial P450s.
It catalyzes the following reaction:

# Gene structure
The cDNA for adrenodoxin reductase was first cloned in 1987. In both bovine and human genomes there is only a single copy of the gene.

# Sites of expression
ADXR gene is expressed in all tissues that have mitochondrial P450s. The highest levels of the enzyme are found in the adrenal cortex, granulosa cells of the ovary and leydig cells of the testis that specialize in steroid hormone synthesis. Immmunofluorescent staining shows that enzyme is localized in mitochondria.
The enzyme is also expressed in the liver, the kidney and the placenta.

# Enzyme structure
Adrenodoxin reductase has two domains that bind NADPH and FAD separately. The FAD and NADP binding sites of the enzyme were predicted by sequence analysis of the enzyme. 
While the FAD-binding site has a consensus sequence (Gly-x-Gly-x-x-Gly) that is similar to other Rossmann folds in FAD and NAD binding sites, the NADPH binding site consensus sequence differs from the FAD-binding site by the substitution of an alanine instead of the last Gly (Gly-x-Gly-x-x-Ala). The location of these FAD and NADP binding sites were confirmed by the crystal structure of the enzyme.
Agaricus subrufescens
Agaricus subrufescens (formerly known as Agaricus blazei) is a species of mushroom, sometimes known as himematsutake and by a number of other names. This Agaricus is a choice edible, with a somewhat sweet taste and fragrance of almonds. The almond flavor is due to the presence of benzaldehyde, benzyl alcohol, benzonitrile, and methyl benzoate (Chen and Wu 1987). This mushroom is also well known for its purported medicinal properties.

# History
Agaricus subrufescens was first described by the American botanist Charles Horton Peck in 1893. During the late 19th and early 20th century, it was cultivated for the table in the eastern United States (Kerrigan 2005).
It was discovered again in Brazil during the 1970s, and thought to be a new species, Agaricus blazei. It was soon marketed for its purported medicinal properties under various names, including:
- ABM (for Agaricus blazei mushroom)
- Cogumelo do Sol (mushroom of the sun)
- Cogumelo de Deus (mushroom of God)
- Cogumelo de Vida (mushroom of life)
- Himematsutake
- Royal Sun Agaricus
- Mandelpilz
- Almond Mushroom
In 2002, Didukh and Wasser rejected the name A. blazei and called the Brazilian fungi Agaricus brasiliensis; this was rejected when Kerrigan (2005) performed genetic and interfertility testing on several fungal strains.  Samples of the Brazilian strains called A. blazei and A. braziliensis proved to be genetically similar to, and interfertile with, the North American population of Agaricus subrufescens.  These tests also found European samples called A. rufotegulis to be of the same species.  Because Agaricus subrufescensis the oldest name, it is traditionally considered the scientifically, historically correct name.

# Commercial use
Because of its high beta glucan content  higher than both Reishi and Shiitake mushrooms  Agaricus subrufescens is used in oncological therapy, mainly in Japan and California. It has been commercially cultivated in Asia and South America since 1993.   Because of this valuable polysaccharide, and lack of supply, Agaricus blazei used to be relatively expensive, until it was successfully artificiallly cultivated in mushroom farms.  China(Maucua) and Brazil are major exporters.
Agaricus blazei mushroom specifically assists in the production of interferon and interleukin, which are potent in fighting off cancer cell metastasis, especially cancer of the uterus. It also reduces blood glucose, blood pressure, cholesterol levels and the effects of arteriosclerosis.
ABM is known to contain three different beta-glucans  beta-(1-3)-D-glucan, beta-(1-4)-a -D-glucan, and beta-(1-6)-D-glucan.
Airborne transmission
Bacteria and viruses showing the ability to be transmitted through aerosols are considered to be airborne. Viruses such as Human Influenza viruses are transmissible through aerosols.

# Theory behind Airborne Transmission
Before the theory is explained, a phenomenon will first be presented. Everyone has felt a cool ocean breeze on their face before, but did they know that the ocean breeze contains more ocean bacteria in its few aerosolized water particles than in 1m3 of ocean water?
When air moves rapidly above a water surface, some particles aerosolize and are carried in the air. It might seem by chance that some particles and not others are carried, but this is not the case and the phenomenon of surface tension plays a role.
Water forms fairly strong bonds with itself due to hydrogen bonding. However, when something gets in the way of water molecules, and disturbs the lattice that they form, water can no longer make strong bonds with each other and water molecules can be separated more easily. In the case of the ocean breeze, when wind passes above ocean water, it picks up portions of water with the weakest bonds, which are most easily aerosolized. Bacteria have surface proteins that are charged and attract water molecules, they act as particles that disturb the lattice of water molecules, so places on the surface where bacteria reside have weakened water molecule bonds and so become aerosolized.
This brings us to the requirements for an airborne virus or bacterium. There must be charged proteins present on the surface that will lower surface tension of water allowing aerosolization of the particles.
Alveolar lung disease
Synonyms and keywords: Airspace disease

# Overview
Alveolar lung disease is a general term that described edema and exudates in the airspaces of the lung (the acini and alveoli).

# Causes
Alveolar lung disease may be divided into acute or chronic. Causes of acute alveolar lung disease include pulmonary edema (cardiogenic or neurogenic), pneumonia (bacterial or viral), pulmonary embolism, systemic lupus erythemosus, pulmonary hemorrhae (e.g., Goodpasture syndrome), idiopathic pulmonary hemosiderosis, and Wegner granulomatosis.
Chronic alveolar lung disease can be caused by pulmonary alveolar proteinosis, alveolar cell carcinoma, mineral oil pneumonia, sarcoidosis (alveolar form), lymphoma, tuberculosis, metastases, desquamative interstitial pneumonia

# Diagnosis

## Imaging

### Chest X Ray
Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered around the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.
When the nodules are centered around the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.
These findings appear soon after the onset of symptoms and change rapidly thereafter.
A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.
Alfred Lebbeus Loomis
Alfred Lebbeus Loomis (1831-95) was an American physician who served as president of the Association of American Physicians.
He was born at Bennington, Vermont.  He graduated from Union College in 1851, studied medicine at the College of Physicians and Surgeons, New York, and graduated in 1852.  At this time the science of auscultation and percussion was developing very rapidly;  and this circumstance led him to adopt diseases of the lungs and heart as his specialty.  He was appointed visiting physician to Bellevue Hospital in 1859, and became lecturer on physical diagnosis at the College of Physicians and Surgeons in 1862.
Shortly after this his health broke down completely, and he spent six months in the Adirondacks.  The benefit derived from his residence there led to the establishment, years later, of the sanatorium at Saranac, and also, at Liberty, Sullivan Co., N. Y., of a Hospital for Consumptives.  In 1866 he became professor of the theory and practice of medicine at the University of the City of New York, the medical department of which later became University and Bellevue Hospital Medical College.  Professor Loomis was appointed visiting physician to Mount Sinai Hospital in 1874;
He was president of the New York Academy of Medicine in 1889-90 and again in 1891-92; and in 1893 served as president of the Association of American Physicians.  He published Lessons in Physical Diagnosis (1868; 11th edition, revised and enlarged, 1899);  Lectures on Fevers (1877);  A Text-Book of Practical Medicine (1884).  He was, in addition, editor of An American System of Medicine (1894).

# Term
- Loomis' mixture  a diarrhea mixture containing oil of sassafras I, tincture of opium 12, tincture of rhubarb 8, tincture of gambir 40, compound tincture of lavender to make 100.  Dose, 30 minims (2cc).  The American Illustrated Medical Dictionary (1938)

# External References
Association of American Physicians
- Template:NIE
Allergic inflammation
Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases.  Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction.  While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease .
The early phase of the allergic reaction typically occurs within minutes, or even seconds, following allergen exposure and is also commonly referred to as the immediate allergic reaction or as a Type I allergic reaction .  The reaction is caused by the release of histamine and mast cell granule proteins by a process called degranulation, as well as the production of leukotrienes, prostaglandins and cytokines, by mast cells following the cross-linking of allergen specific IgE molecules bound to mast cell FcRI receptors .  These mediators affect nerve cells causing itching , smooth muscle cells causing contraction (leading to the airway narrowing seen in allergic asthma) , goblet cells causing mucus production , and endothelial cells causing vasodilatation and edema .
The late phase reaction is also sometimes called the Type IV allergic reaction or delayed type hypersensitivity and may take as long as 6  12 hours to fully develop following an encounter with allergen .  The products of the early phase reaction include chemokines and molecules that act on endothelial cells and cause them to express Intercellular adhesion molecule (such as vascular cell adhesion molecule and selectins), which together result in the recruitment and activation of leukocytes from the blood into the site of the allergic reaction .  Typically, the infiltrating cells observed in allergic reactions contain a high proportion of lymphocytes, and especially, of eosinophils.  The recruited eosinophils will degranulate releasing a number of cytotoxic molecules (including Major Basic Protein and eosinophil peroxidase) as well as produce a number of cytokines such as IL-5 .  The recruited T-cells are typically of the Th2 variety and the cytokines they produce lead to further recruitment of mast cells and eosinophils, and in plasma cell isotype switching to IgE which will bind to the mast cell FcRI receptors and prime the individual for further allergic responses.
Allopatric speciation
Allopatric speciation, also known as geographic speciation, is the phenomenon whereby biological populations are physically isolated by an extrinsic barrier and evolve intrinsic (genetic) reproductive isolation, such that if the barrier breaks down, individuals of the populations can no longer interbreed.  Evolutionary biologists agree that allopatry is a common method by which new species arise. (The word is derived from the ancient Greek allos, "other" + Greek patra, "fatherland".) By contrast, the frequency of other types of speciation, such as sympatric speciation, parapatric speciation, and heteropatric speciation, is debated.
Evolution of reproductive isolation is generally thought to be an incidental by-product of genetic divergence of other traits, particularly adaptive changes that evolve through natural selection in response to different environmental conditions in separate geographic areas.  Ernst Mayr, an evolutionary biologist and famous proponent of allopatric speciation, hypothesized that adaptive genetic changes that accumulate between allopatric populations cause negative epistasis in hybrids, resulting in sterility or inviability.
Allopatric speciation may occur when a species is subdivided into two large populations (dichopatric or vicariant speciation), or when a small number of individuals colonize a novel habitat on the periphery of a species' geographic range (peripatric speciation).  Because natural selection is a powerful evolutionary force in large populations, adaptive evolution likely causes the genetic changes that results in reproductive isolation in vicariant speciation. In peripatric speciation, however, the genetic changes that are thought to occur within the peripheral isolate are more controversial.
Proponents of peripatric speciation contend that small population size in the peripheral isolate (sometimes referred to as a "splinter population") allows genetic drift, which can be a more powerful force than natural selection in small populations, to deconstruct complex genotypes, allowing the creation of novel gene combinations. Both forms need not be mutually exclusive; in practice, passive isolation or fragmentation as well as active dispersal seem to play a role in many cases of speciation.
A famous example of allopatric speciation is that of Charles Darwin's Galapagos Finches, another one involves the Asian Elephant.
Allylic rearrangement
A allylic rearrangement or allylic shift is an organic reaction in which the double bond in an allyl chemical compound shifts to the next carbon atom. It is encountered in nucleophilic substitution.
In reaction conditions that favor a SN1 reaction mechanism the intermediate is a carbocation for which several resonance structures are possible. This explains the product distribution (or product spread) after recombination with nucleophile Y. This type of process is called an SN1' substitution.
Alternatively, it is possible for nucleophile to attack directly at the allylic position, displacing the leaving group in a single step, in a process referred to as SN2' substitution.  This is likely in cases when the allyl compound is unhindered, and a strong nucleophile is used.  The products will be similar to those seen with SN1' substitution.  Thus reaction of 1-chloro-2-butene with sodium hydroxide gives a mixture of 2-buten-1-ol and 1-buten-3-ol:
Nevertheless, the product in which the OH group is on the primary atom is minor. In the substitution of 1-chloro-3-methyl-2-butene, the tertiary 2-methyl-3-buten-2-ol is produced in a yield of 85%, while that for the primary 3-methyl-2-buten-1-ol is 15%.
In one reaction mechanism the nucleophile attacks not directly at the electrophilic site but in a conjugate addition over the double bond:

## Scope
The synthetic utility can be extended to substitutions over butadiene bonds:
In the first step of this macrocyclization the thiol group in one end of 1,5-pentanedithiol reacts with the butadiene tail in 1 to the enone 2 in  an allylic shift with a sulfone leaving group which reacts further with the other end in a conjugate addition reaction.
In one study the allylic shift was applied twice in a ring system:
In this reaction sequence a Jacobson epoxidation adds an epoxy group to a diene which serves as the leaving group in reaction with the pyrazole nucleophile. The second nucleophile is methylmagnesium bromide expulsing the pyrazole group.
An SN2' reaction should explain the outcome of the reaction of an aziridine carrying a methylene bromide group with methyllithium :
In this reaction one equivalent of acetylene is lost.
Examples of allylic shifts:
- Ferrier rearrangement
- Meyer-Schuster rearrangement

# SN2' reduction
In one adaptation called a SN2' reduction a formal organic reduction on an allyl group containing a good leaving group is accompanied by a rearrangement. One example of such reaction is found as part of a Taxol total synthesis (ring C):
The hydride is lithium aluminium hydride and the leaving group a phosphonium salt. The product contains a new exocyclic double bond. Only when the cyclohexane ring is properly substituted will the proton add in a trans position with respect to the adjacent methyl group. A conceptually related reaction is the Whiting reaction forming dienes.

# Electrophilic allyl shifts
Allyl shifts can also take place with electrophiles. In the example below the carbonyl group in benzaldehyde is activated by diboronic acid prior to reaction with the allyl alcohol (see: Prins reaction):
Alpha 2-macroglobulin
Alpha-2 macroglobulin (abbreviated 2M or A2M) is a large plasma protein found in the blood. It is produced by the liver, and is a major component of the alpha-2 band in protein electrophoresis.

# Structure
Alpha-2 macroglobulin is compose of four identical subunits bound together by -S-S- bonds.

# Function
Alpha-2 macroglobulin is able to inactivate an enormous variety of proteinases (including serine-, cysteine-, aspartic- and metalloproteinases).
Alpha-2 macroglobulin has in its structure a 35 aminoacid "bait" region.  Proteinases binding and cleaving the bait region become bound to 2M. The proteinase-2M complex is recognised by macrophage receptors and cleared from the system.
It functions as an inhibitor of coagulation:

# Disease
Alpha-2 macroglobulin levels are increased in nephrotic syndrome, a condition wherein the kidneys start to leak out some of the smaller blood proteins. Because of its size, 2-macroglobulin is retained in the bloodstream. Increased production of all proteins means 2-macroglobulin concentration increases. This increase has little adverse effect on the health, but is used as a diagnostic clue. Longstanding chronic renal failure can lead to amyloid by alpha-2 macroglobulin (see main article: amyloid).
A common variant (29.5%) (polymorphism) of 2-macroglobulin leads to increased risk of Alzheimer's disease, although the mechanism is unknown.
-2 macroglobulin binds to and removes the active forms of the gelatinase (MMP-2 and MMP-9) from the circulation via scavenger receptors on the phagocytes.
Alveolar gas equation

# Overview
The alveolar pO2 is not routinely measured but is calculated from blood gas measurements by the Alveolar gas equation:
p_AO_2 = p_IO_2 - p_ACO_2/R + F \, 
where:
- R is the Respiratory quotient (normally about 0.8)
- pAO2 is the Alveolar pO2
- pIO2 is the Inspired pO2, equal to about 150 mm Hg (0.21 x 713 mmHg at sea level).  The given pressure at sea level is due to atmospheric pressure (760 mmHg) minus the partial pressure of water vapor (47 mmHg), as alveolar gas is completely saturated with water.  The mole fraction of oxygen is about 0.21 in dry atmospheric gas.
- pACO2 is the Alveolar pCO2 (assumed to be equal to the measured arterial pCO2)
- F is a correction factor (usually less than 2 mmHg)
Amantadine overdosage

# Overdosage
Deaths have been reported from overdose with amantadine hydrochloride. The lowest reported acute lethal dose was 1 gram. Because some patients have attempted suicide by overdosing with amantadine, prescriptions should be written for the smallest quantity consistent with good patient management.
Acute toxicity may be attributable to the anticholinergic effects of amantadine. Drug overdose has resulted in cardiac, respiratory, renal or central nervous system toxicity. Cardiac dysfunction includes arrhythmia, tachycardia and hypertension. Pulmonary edema and respiratory distress (including adult respiratory distress syndrome-ARDS) have been reported; renal dysfunction including increased BUN, decreased creatinine clearance and renal insufficiency can occur. Central nervous system effects that have been reported includeinsomnia, anxiety, agitation, aggressive behavior, hypertonia, hyperkinesia, ataxia, gait abnormality, tremor, confusion, disorientation, depersonalization, fear, delirium, hallucinations, psychotic reactions, lethargy, somnolence and coma. Seizures may be exacerbated in patients with prior history of seizure disorders. Hyperthermia has also been observed in cases where a drug overdose has occurred.
There is no specific antidote for an overdose of amantadine hydrochloride. However, slowly administered intravenous physostigmine in 1 and 2 mg doses in an adult 2 at 1- to 2-hour intervals and 0.5 mg doses in a child 3 at 5- to 10-minute intervals up to a maximum of 2 mg/hour have been reported to be effective in the control of central nervous system toxicity caused by amantadine hydrochloride. For acute overdosing, general supportive measures should be employed along with immediate gastric lavage or induction of emesis. Fluids should be forced, and if necessary, given intravenously. The pH of the urine has been reported to influence the excretion rate of amantadine hydrochloride. Since the excretion rate of amantadine hydrochloride increases rapidly when the urine is acidic, the administration of urine acidifying drugs may increase the elimination of the drug from the body. The blood pressure, pulse, respiration and temperature should be monitored. The patient should be observed for hyperactivity and convulsions; if required, sedation, and anticonvulsant therapy should be administered. The patient should be observed for the possible development of arrhythmias and hypotension; if required, appropriate antiarrhythmic and antihypotensive therapy should be given. Electrocardiographic monitoring may be required after ingestion, since malignant tachyarrhythmias can appear after overdose.
Care should be exercised when administering adrenergic agents, such as isoproterenol, to patients with an amantadine hydrochloride overdose, since the dopaminergic activity of amantadine hydrochloride has been reported to induce malignant arrhythmias.
The blood electrolytes, urine pH and urinary output should be monitored. If there is no record of recent voiding, catheterization should be done.