Persius/hicric huggingface dataset:
Enteric coating

# Overview
An enteric coating is a barrier applied to oral medication that controls the location in the digestive system where it is absorbed. Enteric refers to the small intestine, therefore enteric coatings prevent release of medication before it reaches the small intestine.
Most enteric coatings work by presenting a surface that is stable at the highly acidic pH found in the stomach, but breaks down rapidly at a less acidic (relatively more basic) pH. For example, they will not dissolve in the acidic juices of the stomach (pH ~3), but they will in the higher pH (above pH 5.5) environment present in the small intestine.
Drugs such as aspirin, which have an irritant effect on the stomach, can be coated with a substance that will only dissolve in the small intestine. Similarly, certain groups of Azoles (Esomeprazole, omeprazole, pantoprazole and all grouped azoles) are acid-unstable. For such types of drugs, enteric coating added to the formulation tends to avoid the stomach's acidic exposure, delivering them instead to a basic pH environment (intestine's pH 5.5 and above) where they do not degrade, and give their desired action.
Recently, some companies have begun to utilize enteric coatings on fish oil (omega 3 fatty acids) supplements. The coating prevents the fish oil capsules from being digested in the stomach, which has been known to cause "fish burps".
Epicanthal fold

# Overview
An epicanthal fold, epicanthic fold, or epicanthus is a skin fold of the upper eyelid (from the nose to the inner side of the eyebrow) covering the inner corner (medial canthus) of the eye.                
The epicanthal fold is present in people of East Asian descent including Mongols, Turks, Chinese, Koreans,  Japanese, Vietnamese and other ethnic groups of East Asian and Southeast Asian origin such as Indonesians, Malaysians, Inuit, Indians and Khoisans in Africa and Madagascar. Epicanthal folds may also be seen in young children of any race before the bridge of the nose begins to elevate.
The term "epicanthal fold" refers to a visually categorized feature; however the underlying physiological reason and purpose for its presence in any given individual may be entirely different.

# In children
All humans initially develop epicanthal folds in the womb. Some children lose them by birth, but epicanthal folds may also be seen in young children of any ethnicity before the bridge of the nose begins to elevate. They may persist where birth is pre-term, and sometimes also where the mother is alcoholic.
Epicanthal folds can cause a child's eyes to appear crossed, a scenario known as pseudostrabismus.

# Causes (Pathological)
In many persons of caucasian background and other groups who do not commonly possess the trait, the presence of the epicanthal fold can be a symptom of fetal alcohol syndrome, chromosomal disorders such as Down syndrome (Trisomy 21),, Cri du Chat syndrome, or pre-term birth.

# Inherited
There are numerous populations, across the world, that lack an epicanthic fold. However, the epicanthic fold is common in people of many, though not all groups of East Asian and Southeast Asian descent. It is found in significant numbers amongst Native Americans, the Khoisan of Southern Africa, many Central Asians and some people of Sami origin. It also present on people of Tibetan descent, especially Tibetans and North-East Burmese people. Due to classic genetics children of a parent with a pronounced epicanthal fold and one without an epicanthal fold will have varying degrees of epicanthal folds as a result.
In Asian ethnicities, the presence of an epicanthic fold is associated with a less prominent upper eyelid crease, commonly termed "single eyelids" as opposed to "double eyelids". The two features are distinct; a person may have both epicanthal fold and upper eyelid crease, one and not the other, or neither.

# Treatment
The procedure of reducing or removing epicanthal folds is epicanthoplasty. It is now an extremely rare procedure. Asian blepharoplasty, however, is a popular form of cosmetic surgery in East Asia.
Epichlorohydrin

# Overview
Epichlorohydrin is reactive organic compound.  It is an epoxide and an organochloride.  It is a colorless liquid with a pungent, garlic-like odor that is insoluble in water, but miscible with most polar organic solvents.  Epichlorohydrin is a highly reactive compound and will polymerize upon treatment with acid or strong base.
Epichlorohydrin is manufactured from propylene through the intermediacy of allyl chloride.  A major industrial use of epichlorohydrin has been in the production of glycerin, though this application has become less attractive as the price of glycerine has fallen. Indeed, at least three companies have announced plans to convert glycerine to epicholorohydrin. "Epi" is also used as a building block in the manufacture of plastics, epoxy resins, phenoxy resins and other polymers.   It used as a solvent for cellulose, resins and paints and it has found use as an insect fumigant.
Epichlorohydrin is a precursor to glycidyl nitrate, an energetic binder used in explosive and propellant compositions. The epichlorohydrin is reacted with an alkali nitrate, such as sodium nitrate, producing gylcydyl nitrate and alkali chloride.
Epichlorohydrin is flammable, toxic and carcinogenic.
Epidermoid cyst

# Overview
An epidermoid cyst is a benign cyst, developed out of ectodermal tissue. Histologically, it is made of a thin layer of squamous epithelium.
It's very common for women and can be found on the major or minor labia.

# Terminology
The more general term for an Epidermal Inclusion Cyst (which strictly means implantation of epidermal elements into the dermis), Epidermoid cyst includes cysts originating from the infundibular portion of the hair follicle.
The majority of Epidermal Inclusion Cysts do in fact originate from the infundibular portion of the hair follicle thus explaining the interchangeable, yet technically incorrect, use of these two terms.

# Causes
These cysts are caused by a bacterium and form into a pimple-like shape.

# Presentation
It's very common for women and can be found on the major or minor labia.  For some individuals, it doesn't even irritate. For others, it can hurt and when touched, it can release pus. If any of this occurs, its best to discuss it with a doctor.
In contrast to pilar cysts, epidermoid cysts usually present on parts of the body with relatively little hair.
Although they are not malignant, it is possible for malignant tumors to arise from them.

# Diagnosis
MRT isointens, FLAIR hyperintens.

## Physical Examination

### Skin
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.
- Epidermoid cyst. Adapted from Dermatology Atlas.

# Treatment
Cysts can be removed by excision.
Epididymal cyst

# Overview
- Epididymal cysts are less common than spermatoceles and are indistinguishable from the latter at US.
- Epididymal cysts contain clear serous fluid and may arise throughout the epididymis (spermatoceles almost always arise in the epididymal head).
- An increased incidence of epididymal cysts has been reported in boys who are exposed in utero to diethylstilbestrol.
- Although epididymal head cysts cannot be differentiated from spermatoceles, they usually are not clinically relevant.
Patient #1
Patient #2: Ultrasound images demonstrate a large epididymal cyst
- Large epididymal cyst
- Large epididymal cyst
- Large epididymal cyst
Epitestosterone
Epitestosterone is a natural steroid, an inactive epimer of the hormone testosterone. Structurally, it differs from testosterone only in the configuration at the OH-bearing carbon, C17.  Epitestosterone is believed to form in a similar way to testosterone; a 1993 study found that around 50% of epitestosterone production in human males can be ascribed to the testis, although the exact pathway of its formation is still the subject of research. It has been shown to accumulate in mammary cyst fluid and in the prostate. Epitestosterone levels are typically highest in young males; however, by adulthood, most healthy males exhibit a testosterone to epitestosterone ratio (T/E ratio) of about 1:1.

# Epitestosterone and testosterone
It has been shown that exogenous administration of testosterone does not affect levels of epitestosterone in the body. As a result, tests to determine the ratio of testosterone to epitestosterone in urine are used to find athletes who are doping. Most persons have a ratio of about 1:1 testosterone to epitestosterone (T/E ratio) in their urine. However, it is not uncommon to find T/E ratios of up to 4:1 and even T/E ratios of 10:1 can be normal for some individuals. T/E tests are most common because a person may naturally have high levels of testosterone, but even so T/E ratios tend to stay close to 1:1.
Epitestosterone has not been shown to enhance athletic performance, although administration of epistestosterone can be used to mask a high level of testosterone if the standard T/E ratio test is used. As such, epitestosterone is banned by many sporting authorities as a masking agent for testosterone.
In 1996 the US athlete Mary Decker failed a T/E test with a T/E ratio of greater than 6, the limit in force at the time. She took the case to arbitration, arguing that birth control pills can cause false positives for the test, but the arbitration panel ruled against her.
On September 20, 2007 Floyd Landis was stripped of his title as winner of the Tour de France, and was subjected to a two year ban from professional racing after a second test showing an elevated T/E ratio. Test results from Floyd Landis' "A" test sample indicated that while the ratio was 11:1, his testosterone level was in the normal range and the problem was actually a deficient level of epitestosterone.  Landis won the 17th stage of the tour; however, tests taken immediately after the stage victory showed a T/E ratio of 11:1, more than double the 4:1 imposed limit (recently lowered from prior limits of 8:1 and 6:1).  Landis had emphatically denied the charge, pointing out the scientific data that testosterone cannot enhance athletic performance unless taken over an extended period of time with regular doses.
Erbin (protein)
Erbb2 interacting protein (ERBB2IP) also known as Erbin is a protein which in humans is encoded by the ERBB2IP gene. Discovered in 1997, Erbin is a 200kDa protein containing a PDZ domain.

# Function
This gene is a member of the leucine-rich repeat and PDZ domain (LAP) family. The encoded protein contains 17 leucine-rich repeats and one PDZ domain. It binds to the unphosphorylated form of the ERBB2 protein and regulates ERBB2 function and localization. It has also been shown to affect the Ras signaling pathway by disrupting Ras-Raf interaction. Alternate transcriptional splice variants encoding different isoforms have been found for this gene, but only two of them have been characterized to date.

# Clinical significance
Erbin's C-terminal PDZ domain is able to bind to ErbB2, a protein tyrosine kinase which is often associated with poor prognosis in epidermal oncogenesis.   Erbin's N-terminal region has been shown to disrupt Ras to Raf binding and may be, through this action, a tumor suppressing protein.

# Interactions
Erbin (protein) has been shown to interact with:
- Dystonin,
- HER2/neu,
- ITGB4,
- Mothers against decapentaplegic homolog 3  and
- PKP4.
Ericsson method
The Ericsson Method is a child conception idea that is reputed to help determine a baby's sex, developed and patented by Dr. Ronald Ericsson.  The method has been in use since the mid 1970s.  Dr. Ericsson maintains that the method is up to 85 percent effective, but some experts question the effectiveness of the method.
Experiments with the Ericsson method have determined that the method does not create X- or Y-enriched sperm samples.  Nevertheless some studies have suggested that, at least with parents seeking girls, a 71 percent success rate can be obtained.
The Ericsson method is based on the belief that X-sperm swim slower than Y-sperm.  Sperm are placed in a test tube atop a "column" of increasingly thicker layers of albumin, and allowed to swim down into the solution. After a certain time period has elapsed, the sperm can be separated into the faster and slower swimmers.  If the couple desires a male baby the faster swimmers are artificially inseminated, and if the couple desires a female baby the same procedure is enacted with the slower swimmers.
Espin (protein)
Espin, also known as autosomal recessive deafness type 36 protein or ectoplasmic specialization protein, is a protein that in humans is encoded by the ESPN gene. Espin is a microfilament binding protein.

# Function
Espin is a multifunctional actin-bundling protein. It plays a major role in regulating the organization, dimensions, dynamics, and signaling capacities of the actin filament-rich, microvillus-type specializations that mediate sensory transduction in various mechanosensory and chemosensory cells.

# Clinical significance
Mutations in this gene are associated with autosomal recessive neurosensory deafness, autosomal dominant sensorineural deafness without vestibular involvement, and DFNB36.
Exoribonuclease
An exoribonuclease is an exonuclease ribonuclease, which are enzymes that degrade RNA by removing terminal nucleotides from either the 5' end or 3' end of the RNA molecule. Enzymes that remove nucleotides from the 5' end are called 5'-3' exoribonucleases and enzymes that remove nucleotides from the 3' end are called 3'-5' exoribonucleases.
Exoribonucleases can use either water to cleave the nucleotide-nucleotide bond (which is called hydrolytic activity) or inorganic phosphate (which is called phosphorolytic activity). Hydrolytic exoribonucleases are classified under EC number 3.1 and phosphorolytic exoribonucleases under EC number 2.7.7. As the phosphorolytic enzymes use inorganic phosphate to cleave bonds they release nucleotide disphosphates), whereas the hydrolytic enzymes (which use water) release nucleotide monosphosphates).
Exoribonucleases exist in all kingdoms of life, the eubacteria, archaebacteria and eukaryotes. Exoribonucleases are involved in the degradation of many different RNA species, including messenger RNA, transfer RNA and ribosomal RNA. Exoribonucleases can be single proteins (like RNase D or RNase PH) but also can be complexes of multiple proteins, like the exosome complex (in which four of the major exoribonuclease families are represented).

# Major families
Mucolytic agent

# Overview
A mucolytic agent is any agent which dissolves thick mucus usually used to help relieve respiratory difficulties. (hydrolyzing glycosaminoglycans: tending to break down/lower the viscosity of mucin-containing body secretions/components).  The viscosity of mucous secretions in the lungs is dependent upon the concentrations of mucoprotein, the presence of disulfide bonds between these macromolecules and DNA.
Mucolytics:
N-acetylcysteine: an aerosolized mucolytic agent often used as adjunctive therapy for pulmonary complications of cystic fibrosis (CF) in combination with vigorous chest physiotherapy.  N-acetylcysteine acts to split the sulfide bonds in the macromolecules thereby decreasing viscosity, allowing for removal by normal chest physiology. The action of N-acetylcysteine is pH dependent. Mucolytic action is significant at ranges of pH 7-9.(1)
Natural Mucolytics:
- Mugwort
- Bromelain
- Papain
- Clerodendrum
Non-Mucolytics:
- Guaifenesin: increases volume and decreases viscosity of respiratory tract secretions.  (Robitussin)
EXPECTORANTS should not be confused with a mucolytic. Expectorants increase mucous production.

# Indications
- cough
- cystic fibrosis
- COPD
- asthma
- bronchitis
- bronchiectasis
- emphysema
Eye development

# Overview
The eye develops from the neural tube, the epidermis, and the periocular mesenchyme, which receives contributions from both the neural crest and mesoderm lineages.

# Sequential inductions
This development is an example of sequential inductions where the organ is formed from three different tissues.
First, there is an outpocketing of the neural tube called optic vesicles. The optic vesicles come into contact with the epidermis and induce the epidermis. The epidermis thickens to form the lens placode.
The lens differientiates and invaginates until it pinches off from the epidermis. The lens acts as an inducer back to the optic vesicle to transform it into the optic cup and back to the epidermis to transform it into the cornea.
The optic cup then delaminates into two layers: The neural retina and the retinal pigment epithelium.
The periocular mesenchyme migrates in during the formation of the optic cup and is critical for the induction of the retinal pigment epithelium and the optic nerve. The mesenchyme contributes to the cornea, iris , ciliary body, sclera and blood vessels of the eye.

# Responsivity of head epidermis
Only the epidermis in the head is competent to respond to the signal from the optic vesicles. Both the optic vesicle and the head epidermis are required for eye development. The competence of the head epidermis to respond to the optic vesicle signals comes from the expression of Pax6 in the epidermis. Pax6 is necessary and sufficient for eye induction. This competenece is acquired gradually during gastrulation and neurulation from interactions with the endoderm, mesoderm, and neural plate.

# Regulation and inhibition
Sonic hedgehog reduces the expression of Pax6. When Shh is inhibited during development, the domain of expression for Pax6 is expanded and the eyes fail to separate causing cyclopia. Overexpression of Shh causes a loss of eye structures.
Eyring equation
The Eyring equation also known as EyringPolanyi equation in chemical kinetics relates the reaction rate to temperature. It was developed almost simultaneously in 1935 by Henry Eyring, M.G. Evans and Michael Polanyi. This equation follows from the transition state theory (aka, activated-complex theory) and contrary to the empirical Arrhenius equation this model is theoretical and based on statistical thermodynamics.
The general form of the EyringPolanyi equation somewhat resembles the Arrhenius equation:
\ k = \frac{k_\mathrm{B}T}{h}\mathrm{e}^{-\frac{\Delta G^\Dagger}{RT}}
where G is the Gibbs energy of activation, kB is Boltzmann's constant, and h is Planck's constant.
It can be rewritten as:
 k = \left(\frac{k_\mathrm{B}T}{h}\right) \mathrm{exp}\left(\frac{\Delta S^\ddagger}{R}\right) \mathrm{exp}\left(-\frac{\Delta H^\ddagger}{RT}\right)
To find the linear form of the Eyring-Polanyi equation:
 \ln \frac{k}{T} = \frac{-\Delta H^\ddagger}{R} \cdot \frac{1}{T} + \ln \frac{k_\mathrm{B}}{h} + \frac{\Delta S^\ddagger}{R} 
where:
- \ k  = reaction rate constant
- \ T  = absolute temperature
- \ \Delta H^\ddagger   = enthalpy of activation
- \ R   = gas constant
- \ k_\mathrm{B}   = Boltzmann constant
- \ h  = Planck's constant
- \ \Delta S^\ddagger  = entropy of activation
A certain chemical reaction is performed at different temperatures and the reaction rate is determined. The plot of \ \ln(k/T)  versus \ 1/T  gives a straight line with slope \  -\Delta H^\ddagger / R   from which the enthalpy of activation can be derived and with intercept \  \ln(k_\mathrm{B}/h) + \Delta S^\ddagger / R  from which the entropy of activation is derived.
Muenke syndrome
Muenke Syndrome, also known as FGFR3-related craniosynostosis, is a human specific condition characterized by the premature closure of certain bones of the skull during development, which affects the shape of the head and face. Muenke syndrome occurs in about 1 in 30,000 newborns. This condition accounts for an estimated 8 percent of all cases of craniosynostosis.

# Symptoms
Many people with this disorder have a premature fusion of skull bones along the coronal suture. Other parts of the skull may be malformed as well. This will usually cause an abnormally shaped head, wide-set eyes, and flattened cheekbones in these patients. About 5 percent of affected individuals have an enlarged head (macrocephaly).There may also be associated hearing loss in 10 - 30% of cases and it is important for affected individuals to have hearing tests to check on the possibility of a problem.
Most people with this condition have normal intellect, but developmental delay and learning disabilities are possible. The signs and symptoms of Muenke syndrome vary among affected people, and some findings overlap with those seen in other craniosynostosis syndromes. Between 6 percent and 7 percent of people with the gene mutation associated with Muenke syndrome do not have any of the characteristic features of the disorder.

# Genetics
Muenke Syndrome is inherited in an autosomal dominant pattern. In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family.
A single mutation in the FGFR3 gene cause this syndrome. The FGFR3 gene provides instructions for making a protein that is involved in the development and maintenance of bone and brain tissue. This mutation causes the FGFR3 protein to be overly active, which interferes with normal bone growth and allows the bones of the skull to fuse before they should.