Persius/hicric huggingface dataset:
Flamingo (protein)
Flamingo is a member of the adhesion-GPCR family of proteins. Flamingo has sequence homology to cadherins and G protein-coupled receptors (GPCR). Flamingo was originally identified as a Drosophila protein involved in planar cell polarity. Mammals have three flamingo homologs, CELSR1, CELSR2, CELSR3. In mice all three have distinct expression patterns in the brain.

# Adhesion G protein coupled receptors
The adhesion-GPCR family has over thirty members in the human genome. The adhesion GPCRs are seven transmembrane helix proteins that have long N-terminal domains. For example, flamingo has EGF-like, Laminin G-like and Cadherin-like sequences in its N-terminal extracellular domain.

# Axon fascicles
Mice that lack CELSR3 have altered bundeling of axons to form fascicles.

# Function in dendrite morphology
In Drosophila, flamingo mutants were found to have abnormal dendrite branching, outgrowth and routing. Kimura et al proposed that flamingo regulates dendrite branch elongation and prevents the dendritic trees of adjacent Drosophila sensory neurons from having overlap of dendritic arbors.
A study of mammalian flamingo homolog CELSR2 found that it is involved in the regulation of dendrite growth. RNAi was used to alter CELSR2 expression in cortical and cerebral brain slice cultures. The dendrites of pyramidal neurons in cortical cultures and Purkinje neurons in cerebellar cultures were simplified when CELSR2 expression was reduced.

# Vertebrate planar cell polarity
CELSR1 was shown to be required for the normal polarized position of kinocilia to one side of  hair cells of the mouse inner ear.
Flight nurse badge
Assistant Editor-In-Chief: Michelle Lew

# Overview
The Flight Nurse Badge is a Military badges of the United States of the United States armed forces which is issued by the United States Air Force and United States Navy.  The badge has existed since World War II, when the decoration was first created as the United States Army Air Forces Flight Nurse Badge.
The Flight Nurse Badge is issued in two different versions, one for the Navy and the other for the Air Force.  To be awarded the Flight Nurse Badge, a service member must be a commissioned officer and a Registered Nurse and must also complete training normally befitting the award of the Aircrew Badge.  Upon completion of prerequisite training, a service member must complete advanced studies in Aerospace Medicine and be qualified as a military flight nurse.  The Flight Nurse Badge is then presented after a probationary period of in-flight instruction and observation.
The Air Force version of the Flight Nurse Badge is issued in three degrees: Basic, Senior, and Master.  The Basic Flight Nurse Badge is awarded upon completion of all training and qualification as a flight nurse.  The Senior and Master versions of the Flight Nurse Badge are awarded based on years of service in the Air Force and number of flight hours obtained.  The different degrees of the Flight Nurse Badge are denoted by a star (Senior level) or a star with wreath (Master level) centered above the decoration.
The United States Navy issues the Flight Nurse Badge in a single degree.  None of the other military branches maintains an equivalent to the Flight Nurse Badge.  The decoration is similar to the flight surgeon badge.
Immunofluorescence

# Overview
Immunofluorescence is the labeling of antibodies or antigens with fluorescent dyes.  This technique is often used to visualize subcellular distribution of biomolecules of interest.  Immunofluorescent labelled tissue sections are studied using a fluorescence microscope or by confocal microscopy.
Most commonly, immunofluorescence employs two sets of antibodies: a primary antibody is used against the antigen of interest; a subsequent, secondary, dye-coupled antibody is introduced that recognizes the primary antibody. In this fashion the researcher may create several primary antibodies that recognize various antigens, but, because they all share a common constant region, may be recognized by a single dye-coupled antibody. Typically this is done by using antibodies made in different species. For example, a researcher might create antibodies in a goat that recognize several antigens, and then employ dye-coupled rabbit antibodies that recognize the goat antibody constant region (denoted rabbit anti-goat). This allows re-use of the difficult-to-make dye-coupled antibodies in multiple experiments.
In some cases, it is advantageous to use primary antibodies directly labelled with a fluorophore. This direct labelling decreases the number of steps in the staining procedure and, more importantly, often avoids cross-reactivity and high background problems. Fluorescent labelling can be performed in less than one hour with readily available labeling kits.
As with most fluorescence techniques, a significant problem with immunofluorescence is photobleaching. Loss of activity caused by photobleaching can be controlled by reducing the intensity or time-span of light exposure, by increasing the concentration of fluorophores, or by employing more robust fluorophores that are less prone to bleaching (e.g. Alexa Fluors or DyLight Fluors).
Many uses of immunofluorescence have been outmoded by the development of recombinant proteins containing fluorescent protein domains, e.g. green fluorescent protein (GFP). Use of such "tagged" proteins allows much better localization and less disruption of protein function.
Food fortification
Food fortification is the public health policy of adding Micronutrients (essential trace elements and vitamins) to foodstuffs to ensure that minimum dietary requirements are met.
Simple diets based on staple foods with little variation are often deficient in certain nutrients, either because they are not present in sufficient amounts in the soil of a region, or because of the inherent inadequacy of the diet.  Addition of micronutrients to staples and condiments can prevent large-scale deficiency diseases in these cases.
The fortification of foodstuffs with iron is considered an unethical form of mass medication by many doctors.  While it may benefit some, others already have excessive iron stores  iron overload (hyperferremia)  a condition affecting most males over 35, and far more common and more serious than hypoferremia.  Anemia is not lack of iron, but lack of iron-containing hemoglobin in the blood; some anemias are actually iron-loading.  A far safer anti-anemia supplementation would be vitamin C, which increases the absorption of iron.  Iron has been identified as exacerbating many conditions, including acute myocardial infarct and vitamin tablets without iron are now available for men.

# Examples of fortified foods
Iodised salt has been used in the United States since before World War II.
Folic acid is added to flour in many industrialized countries, and has prevented a significant number of neural tube defects in infants. 
It is, however, not uniform in its application, with more intake of folic acid through fortified flour among those who were already receiving high amounts through their diet.
A wide range of iron compounds, including ferrous sulfate, ferrous fumarate and even elemental iron powder are added to food (usually cereal flours, but also table salt, milk and condiments) in a number of countries to prevent iron deficiency anemia.  Although iron intake is often sufficient in developing countries, the bioavailability of the dietary iron is low, due to such factors as polyphenols and phytic acid binding the iron and preventing its absorption.  Major challenges in iron fortification are to avoid undesirable changes in the appearance and taste of the food, and to target the population segment that needs the fortification the most.
Niacin has been added to bread in the USA since 1938 (when voluntary addition started), a programme which substantially reduced the incidence of pellagra.
Vitamin D is added to a few foods (especially margarine).
Fluoride salts are added to water and toothpastes to prevent tooth decay.  Water fluoridation is a controversial topic.
Calcium is frequently added to fruit juices, carbonated beverages and rice.
"Golden rice" is a variety of rice which has been genetically modified to increase its beta carotene content.
Fourth nerve palsy

# Overview
Fourth nerve palsy is a condition caused by weakness or paralysis of the superior oblique muscle. When present at birth, it is known as congenital fourth nerve palsy.

# Causes
- Brown's syndrome: Restriction of superior oblique movement is found in Brown's syndrome, leading to difficulty elevating the eye in the adducted position
- Congenital fourth nerve palsy
- Head trauma: Superior oblique palsy is a common complication of closed head trauma
- Superior oblique myokymia is an uncommon neurological condition caused by vascular compression of the trochlear nerve resulting in repeated, brief, involuntary episodes of movement of the eye.
Fusarium venenatum
Fusarium venenatum is a fungus, more precisely a mold, from which a mycoprotein can be derived.
It is used in the manufacture of Quorn, a meat substitute marketed to vegetarians.
In 2003 the Center for Science in the Public Interest issued the claim that the mycoprotein used in Quorn can be gastrotoxic, causing severe vomiting, stomach cramps, and diarrhea in susceptible individuals.
The manufacturer of Quorn disputes the figure, claiming that only 0.0007% (1 in 146,000) suffers adverse reactions.
Leslie Bonci, a spokeswoman for the American Dietetic Association, has described the CSPI's claims as "overblown".
GABA transporter 1
GABA transporter 1 (GAT1) also known as sodium- and chloride-dependent GABA transporter 1 is a protein that in humans is encoded by the SLC6A1 gene.

# Function
GAT1 is a gamma-aminobutyric acid (GABA) transporter, which removes GABA from the synaptic cleft. GABA Transporter 1 uses energy from the dissipation of a Na+ gradient, aided by the presence of a Cl gradient, to translocate GABA across CNS neuronal membranes. The stoichiometry for GABA Transporter 1 is 2 Na+: 1 Cl: 1 GABA.

# Diseases
Research recorded in The American Journal of Psychiatry has shown that schizophrenia patients have GABA synthesis and expression altered, leading to the conclusion that GABA Transporter-1, which adds and removes GABA from the synaptic cleft, plays a role in the development of neurological disorders such as Schizophrenia.

# Interactions
SLC6A1 has been shown to interact with STX1A.
GM1 gangliosidoses

# Overview
The GM1 gangliosidoses are caused by a deficiency of beta-galactosidase, with resulting abnormal storage of acidic lipid materials in cells of the central and peripheral nervous systems, but particularly in the nerve cells.
GM1 has three forms:  early infantile, late infantile, and adult.

# Early infantile GM1
Symptoms of early infantile GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver and spleen enlargement, coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.
About half of affected patients develop cherry-red spots in the eye.
Children may be deaf and blind by age 1 and often die by age 3 from cardiac complications or pneumonia.

# Late infantile GM1
Onset of late infantile GM1 is typically between ages 1 and 3 years.
Neurological symptoms include ataxia, seizures, dementia, and difficulties with speech.

# Adult GM1
Onset of adult GM1 is between ages 3 and 30.
Symptoms include muscle atrophy, neurological complications that are less severe and progress at a slower rate than in other forms of the disorder, corneal clouding in some patients, and dystonia (sustained muscle contractions that cause twisting and repetitive movements or abnormal postures).
Angiokeratomas may develop on the lower part of the trunk of the body.
Most patients have a normal size liver and spleen.
GM2 gangliosidoses
The GM2 gangliosidoses cause the body to store excess acidic fatty materials in tissues and cells, most notably in nerve cells.  These disorders result from a deficiency of the enzyme beta-hexosaminidase.  The GM2 disorders include:

# Tay-Sachs disease
Tay-Sachs disease (also known as GM2 variant B). Tay-Sachs and its variant forms are caused by a deficiency in the enzyme beta-hexosaminidase A.  The incidence is particularly high among Eastern European and Ashkenazi Jewish populations, as well as certain French Canadians and Louisianan Cajuns.  Affected children appear to develop normally for the first few months of life. Symptoms begin by 6 months of age and include progressive loss of mental ability, dementia, decreased eye contact, increased startle reflex to noise, progressive loss of hearing leading to deafness, difficulty in swallowing, blindness, cherry-red spots in the retinas, and some paralysis. Seizures may begin in the childs second year.  Children may eventually need a feeding tube and they often die by age 4 from recurring infection. No specific treatment is available.  Anticonvulsant medications may initially control seizures.  Other supportive treatment includes proper nutrition and hydration and techniques to keep the airway open. A much rarer form of the disorder, which occurs in patients in their twenties and early thirties, is characterized by unsteadiness of gait and progressive neurological deterioration.

# Sandhoff disease
Sandhoff disease (variant AB). This is a severe form of Tay-Sachs disease. Onset usually occurs at the age of 6 months and is not limited to any ethnic group.  Neurological symptoms may include progressive deterioration of the central nervous system, motor weakness, early blindness, marked startle response to sound, spasticity, myoclonus (shock-like contractions of a muscle), seizures, macrocephaly (an abnormally enlarged head), and cherry-red spots in the eye. Other symptoms may include frequent respiratory infections, murmurs of the heart, doll-like facial features, and an enlarged liver and spleen. There is no specific treatment for Sandhoff disease.  As with Tay-Sachs disease, supportive treatment includes keeping the airway open and proper nutrition and hydration. Anticonvulsant medications may initially control seizures. Children generally die by age 3 from respiratory infections.
GNAS complex locus
GNAS complex locus, also known as GNAS, is a protein which in humans is encoded by the GNAS gene. It is the stimulatory G-protein alpha subunit (Gs-), a key component of many signal transduction pathways.

# Gene
This gene locus has a highly complex imprinted expression pattern. It gives rise to maternally, paternally, and biallelically expressed transcripts that are derived from four alternative promoters and 5' exons. Some transcripts contains a differentially methylated region (DMR) at their 5' exons, and this DMR is commonly found in imprinted genes and correlates with transcript expression. An antisense transcript exists, and this antisense transcript and one of the transcripts are paternally expressed, produce noncoding RNAs, and may regulate imprinting in this region. In addition, one of the transcripts contains a second overlapping open reading frame, which encodes a structurally unrelated protein, called ALEX.
The GNAS locus is imprinted and encodes 5 main transcripts:
- Gs-
- XLAS
- NESP55
- A/B transcript
- antisense GNAS transcript

# Protein
Alternative splicing of downstream exons is also observed, which results in different forms of the stimulatory G-protein alpha subunit (Gs-), a key element of the classical signal transduction pathway linking receptor-ligand interactions with the activation of adenylyl cyclase and a variety of cellular responses. Multiple transcript variants have been found for this gene, but the full-length nature and/or biological validity of some variants have not been determined.

# Clinical significance
Mutations are associated with:
- Albright hereditary osteodystrophy
- pseudohypoparathyroidism type Ia
- pseudohypoparathyroidism type Ib
- pseudopseudohypoparathyroidism
- McCune-Albright syndrome
- Myxoma
Mutations in this gene also result in progressive osseus heteroplasia, polyostotic fibrous dysplasia of bone, and some pituitary tumors.

# Interactions
GNAS complex locus has been shown to interact with RIC8A.
Galea aponeurotica
The galea aponeurotica (epicranial aponeurosis) covers the upper part of the cranium; behind, it is attached, in the interval between its union with the Occipitales, to the external occipital protuberance and highest nuchal lines of the occipital bone; in front, it forms a short and narrow prolongation between its union with the Frontales.
On either side it gives origin to the Auriculares anterior and superior; in this situation it loses its aponeurotic character, and is continued over the temporal fascia to the zygomatic arch as a layer of laminated areolar tissue.
It is closely connected to the integument by the firm, dense, fibro-fatty layer which forms the superficial fascia of the scalp: it is attached to the pericranium by loose cellular tissue, which allows the aponeurosis, carrying with it the integument to move through a considerable distance.
Galega officinalis
Galega officinalis (also known as Goat's Rue, French Lilac, Italian Fitch or Professor-weed) is a plant from the Galega genus of the Faboideae. Its name derives from gale (milk) and ega (to bring on), as Galega has been used as a galactologue in small domestic animals (hence the name "Goat's rue"). Galega bicolor is a synonym. It is a hardy perennial that blooms in the summer months.
Other Galega species are Galega orientalis.
Galega is used as a food plant by the larva of Coleophora vicinella, a species of moth.

# Medical use
Galega officinalis has been known since the Middle Ages for relieving the symptoms of diabetes mellitus. Upon analysis, it turned out to contain guanidine, a substance that decreases blood sugar by decreasing insulin resistance.
Chemical derivatives from the biguanide class of medication include metformin (Glucophage, commonly prescribed for diabetics) and the older, withdrawn agent phenformin.

# Sources
- Witters LA. The blooming of the French lilac. J Clin Invest 2001;108:11051107. DOI 10.1172/JCI200114178.
Gardner's syndrome
Gardner's syndrome is a genetic disorder characterized by the presence of multiple polyps in the colon together with tumors outside the colon. The extracolonic tumors may include osteomas of the skull, thyroid cancer, epidermoid cysts, fibromas and sebaceous cysts. The countless polyps in the colon predispose to the development of colon cancer.

# Inheritance
Gardner's syndrome is inherited in an autosomal dominant manner. Typically, one parent has Gardner's syndrome. Each of their children, male and female alike, are at 50% risk of inheriting the gene for Gardner's syndrome and manifesting it.

# Diagnosis
Gardner's syndrome can be identified based on oral findings, including multiple impacted and supernumerary teeth, multiple jaw osteomas which give a "cotton-wool" appearance to the jaws, as well as multiple odontomas, congenital
hypertrophy of the retinal pigment epithelium (CHRPE), in addition to multiple adenomatous polyps of the colon.

# Eponym
The syndrome is named for Eldon J. Gardner (1909-1989), a college teacher of genetics, who first described it in 1951. Gardner had been introduced to a large Utah family with the syndrome by a premedical student in his course in genetics.

# Genetics
Gardner's syndrome is now known to be caused by mutation in the APC gene located in chromosome 5q21 (band q21 on chromosome 5). This is the same gene as is mutant in  familial adenomatous polyposis (FAP), a more common disease that also predisposes to colon cancer.
New genetic and molecular information has caused some genetic disorders to be split into multiple entities while other genetic disorders merge into one condition. After existing for most of the second half of the 20th century, Gardner's syndrome has vanished as a separate entity. It has been merged into familial adenomatous polyposis (FAP) and is now considered simply a phenotypic variant of FAP.

# DIfferentiating Gardner's syndrome from other diseases
Gastric chief cell

# Overview
A  gastric chief cell (or peptic cell, or gastric zymogenic cell) is a cell in the stomach that releases pepsinogen, gastric lipase and rennin. The cell stains basophilic upon H&E prep due to the large proportion of rough endoplasmic reticulum in it's cytoplasm.
It works in conjunction with the parietal cell which releases gastric acid, converting the pepsinogen into pepsin.

# Nomenclature
The terms "chief cell" and "zymogenic cell" are often used without the word "gastric" to name this type of cell. However those terms can also be used to describe other cell types (for example, parathyroid chief cells).
Gastric distension
Gastric Distention is bloating of the stomach when air is pumped into it. This may be done when someone is performing cardiopulmonary resuscitation and blowing air into the mouth of someone who is not breathing spontaneously.
It may also occur when more advanced medical procedures are performed by emergency or hospital personnel, and air leaks past the opening of the lungs and into the stomach.
Gastric distention is potentially dangerous since it can cause the contents of the stomach to come up the esophagus (gullet) and spill back down into the lungs.  This can cause drowning, by filling the lungs with fluid, if there has been enough material in the stomach, or, with less material, can cause stomach acids to damage the lungs and create a condition known as "aspiration pneumonia".
CPR standards issued by the American Heart Association suggest that people suffering gastric distention be turned on their sides and the stomach be compressed gently to push out the air bloating the stomach.  By turning the individual on their side into what is known as the recovery position, the stomach contents will often continue past the opening of the lungs and drain out the mouth, thus sparing the victim lung damage or the internal drowning which can be caused by large volumes of stomach material getting into the lungs.
Gastrocolic reflex

# Overview
The gastrocolic reflex or gastrocolic response is one of a number of physiological reflexes controlling the motility, or peristalsis, of the gastrointestinal tract.  It involves an increase in motility of the colon in response to stretch in the stomach and byproducts of digestion in the small intestine.  The small intestine also shows a similar motility response.
The reflex was demonstrated by myoelectric recordings in the colons of animals and humans, which showed an increase in electrical activity within as little as 15 minutes after eating.  The recordings also demonstrated that the gastrocolic reflex is uneven in its distribution throughout the colon.  The sigmoid colon is more greatly affected than the right side of the colon in terms of a phasic response; however, the tonic response across the colon is uncertain.  A number of neuropeptides have been proposed as mediators of the gastrocolic reflex.  These include serotonin, neurotensin, cholecystokinin (CCK), and gastrin.
Clinically, the gastrocolic reflex has been implicated in pathogenesis of irritable bowel syndrome.  Also, the serotonin (5HT3) antagonist ondansetron decreases the tonic response to stretch.