Persius/hicric huggingface dataset:
Genetic carrier
A genetic carrier (or just carrier), is a person or other organism that has inherited a genetic trait or mutation, but who does not display that trait or show symptoms of the disease.  They are, however, able to pass the gene onto their offspring, who may then express the gene.  This phenomenon is a direct result of the recessive nature of many genes.
For example, the daughters of Queen Victoria, the princesses Alice and Beatrix, were carriers of the X-linked hemophilia gene (more precisely, an abnormal allele of a gene necessary to produce one of the blood clotting factors).  Both had children who continued to pass the gene to succeeding generations of the royal houses of Spain and Russia, into which they married.  Males who carried the altered gene had hemophilia, while females simply passed it to about half of their children.
Up to 1 in 25 individuals of Northern European ancestry may be considered carriers of mutations that could lead to Cystic Fibrosis.  The disease appears only when two of these carriers have children (25% of whom will be affected by the disease).  However, it is also thought that carriers may be more resistant to diarrhea during typhoid fever or cholera, and are therefore not truly asymptomatic.  This resistance leads to increased survival of the carriers, thereby increasing the frequency of the altered genes in the population.
{WH}}
Germinal center
Germinal centres (GC) are an important part of the humoral immune response. They develop dynamically after the activation of B-cells by T-dependent antigen. 
Histologically, the GCs describe microscopically distinguishable parts in lymphoid tissues.

# Process
1. Activated B-cells migrate into the follicular system and begin monoclonal expansion in the environment of follicular dendritic cells (FDC).
2. After three days of expansion the B cells mutate their 
antibody-encoding DNA and thus generate a diversity of clones in the 
germinal centre. This also involves deletions, insertions and  
recombination of the V, D, J genes.
3. Upon some unidentified stimulus 
from the FDC, the B cells start to expose their antibody to their 
surface and in this stage are referred to as centrocytes. The 
centrocytes are in a state of activated apoptosis and compete for 
survival signals from FDCs that present the 
antigen. This rescue process is believed to be dependent on the affinity
-f the antibody to the antigen.
4. The functional B-cells have then to interact with helper T cells to get final differentiation signals. This also involves isotype switching for example from IgM to IgG.
The interaction with T cells is believed to 
prevent the generation of autoreactive antibodies.
5. The B cells become either a plasma cell 
spreading antibodies or a memory B cell that will be activated in 
subsequent contacts with the same antigen. They may also restart the 
whole process of proliferation, mutation and selection according to the 
recycling hypothesis.

# Morphology at different stages
The morphology of GCs is very specific and shows properties which are characteristic for different stages of the reaction.
- In an early state of the reaction a network of FDCs is fully filled with proliferating B cells.
- Later at day 4 of the reaction GCs show a separation of two zones, the dark and the light zone. The former still contains dominantly proliferating cells while the latter one is the area of B cells selection.
- These zones dissolve after 10 days of GC development which ends after about 3 weeks.
Gestational age
Gestational age is usually considered to be the age of an embryo or fetus (or newborn infant) from the first day of the woman's last menstrual period (LMP).  This standard system of counting the progression of pregnancy starts approximately two weeks before fertilization takes place; it does not in itself constitute the  beginning of pregnancy.   There is some controversy over the beginning of pregnancy, and alternative counting systems have been suggested.
The gestational age should not be confused with the fertilization age (also called conceptional age or developmental age) of an embryo or fetus; the fertilization age is always counted from fertilization, and the gestational age is usually greater by about two weeks.
A full-term human pregnancy is considered to be 40 weeks (280 days), though pregnancy lengths between 38 and 42 weeks are considered normal. A fetus born prior to the 37th week of gestation is considered premature and faces increased risk of morbidity and mortality.
The events of prenatal development usually occur at known gestational ages. The gestational timing of a toxin exposure or infection can be used to predict the potential consequences to the fetus.
Calculations of gestational age from LMP are sometimes incorrect due to normal varation from the average ovulation date.  The gestational age of an individual infant can be more accurately estimated from:
- The mother's knowledge of the date of sexual intercourse.
- The mother's knowledge of fertility signs related to ovulation. The needed observations are normally made by mothers who use fertility awareness methods to get pregnant.
- Examination of the newborn infant. In the twentieth century, doctors (especially pediatricians) were trained to recognize the physical changes occurring to the fetus in the latter half of pregnancy so that a maturational age could be estimated.
- An obstetric ultrasound ("dating scan", in the UK routinely offered around 12 weeks) during the pregnancy, whereby sizes of certain fetal body parts are measured.
The fertilization age of children conceived by in vitro fertilization is known to the hour.
Gibson's murmur
Gibson's murmur is a continuous murmur that heard in patent ductus arteriosus.
PDA is an abnormal connection between the aorta and the pulmonary artery, which normally should be closed in infancy. Since aortic pressure is higher than pulmonary pressure, a continuous murmur occurs, which is often described as a machinery murmur or Gibson's murmur. 
The maximum intensity of the murmur usually occurs at S2. The duration of the murmur depends upon the pressure difference between aorta and pulmonary artery.

# Pathophysiology
In patients with pulmonary hypertension, pulmonary artery diastolic pressure increases; when it approaches systemic level, the diastolic portion of the continuous murmur becomes shorter and ultimately absent 
In patients with more severe pulmonary hypertension, pulmonary artery systolic pressure can equalize with aortic systolic pressure and the systolic component of the murmur may also be absent (silent ductus).

# Differential Diagnosis
Cyanosis due to the reversal of the shunt and signs of pulmonary hypertension with or without evidence of right sided heart failure are the only physical findings that are recognizable at the bedside in these circumstances.
Gingival fibers

# Overview
The gingival fibers are the connective tissue fibers that attach a tooth to the gingival tissue.  They are primarily composed to type I collagen, although type III fibers are also involved.
These fibers, unlike the fibers of the periodontal ligament, in general, attach the tooth to the gingival tissue, rather than from the tooth to the alveolar bone.

# Functions of the gingival fibers
The gingival fibers accomplish the following tasks:
- They hold the marginal gingiva against the tooth
- They provide the marginal gingiva with enough rigidity to withstand the forces of mastication without distorting
- They serve to stabilize the marginal gingiva by uniting it with both the tissue of the more rigid attached gingiva as well as the cementum layer of the tooth.

# Gingival fibers and periodontitis
In theory, gingival fibers are the protectors against periodontitis, as once they are breached, they cannot be regenerated.  When destroyed, the gingival sulcus (labelled G in the diagram) increases in depth apically, allowing more debris and bacteria to remain in intimate contacts with the delicate sulcular and junctional epithelia for longer periods of time.

# Types of gingival fibers
There are three groups within which gingival fibers are arranged:
- gingivodental group - there are three types of fibers within this group:
fibers that extend towards the crest of the gingiva
fibers that extend laterally to the outer surface of the gingiva and
fibers that extend outward, past the height of the alveolar crest, and then downward along the cortex of the alveolar bone.
- fibers that extend towards the crest of the gingiva
- fibers that extend laterally to the outer surface of the gingiva and
- fibers that extend outward, past the height of the alveolar crest, and then downward along the cortex of the alveolar bone.
- circular group - these fibers are unique in that they exist entirely within the gingiva and do not contact the tooth
- transseptal group - these fibers have traditionally been described as spanning the interproximal tissue between adjacent teeth, into which they are embedded.  However, two other types of fibers have been described in this group:
semicicular fibers - fibers that run through the facial and lingual gingiva around each tooth, attaching to the interproximal surfaces of the same tooth.
transgingival fibers - fibers that run between two non-adjacent teeth and are embedded in the cementum of their proximal surfaces, passing around the tooth in the middle of the two teeth attached with these fibers.
- semicicular fibers - fibers that run through the facial and lingual gingiva around each tooth, attaching to the interproximal surfaces of the same tooth.
- transgingival fibers - fibers that run between two non-adjacent teeth and are embedded in the cementum of their proximal surfaces, passing around the tooth in the middle of the two teeth attached with these fibers.
Glucoglycinuria
Glucoglycinuria belongs to a group of inherited metabolic disorders which have in common elevations of serum Lysine levels. Enzyme deficiencies of alpha-aminoadipic semialdehyde dehydrogenase and the saccharopine dehydrogenases have been associated with hyperlysinemia.
Clinical manifestations include mental retardation, recurrent emesis, hypotonia, lethargy, diarrhea, and developmental delay. All disorders in this group are;
- Glucoglycinuria
- Glycinemia (with methylmalonic acidemia)
- Hyperglycinemia
- Hyperlysinemia
- Pipecolic acidemia
- Saccharopinuria
- Other disturbances of metabolism of glycine, threonine, serine, glutamine, and lysine
Glucose paradox
Glucose paradox is a theory formulated by biochemist Dr. J. D. McGarry and his research associates. It is a theory that demonstrates the importance of lactic acid in carbohydrate metabolism. The paradox is that the large amount of glycogen (10%) in the liver cannot be explained by its relatively minimal glucose absorption.
After the digestion of carbohydrates and their entering into the circulatory system in the form of glucose (blood sugar), some glucose rather than going directly to the liver and being converted into glycogen, will be absorbed directly into the muscle tissue and convert into lactic acid in the anaerobic energy system. This is true especially in situations of energy depletion and exercise.
The lactic acid is then taken to and converted by the liver into the building blocks for liver glycogen. Much of the body's liver glycogen is produced indirectly from lactic acid rather than directly from glucose in the blood.
Glucuronidation

# Overview
Glucuronide: a glycoside that yields glucuronic acid upon hydrolysis.
Glucaronic acid: an acid, C6H10O7, formed by the oxidation of glucose, found combined with other products of metabolism in the blood and urine.
Glucuronidase (beta-glucuronidase): an enzyme that hydrolyzes a glucuronide, destroying glucuronidation, especially that which occurs widely (as in liver and spleen) and hydrolyzes the beta form of a glucuronide
Glucuronidation plays many roles in the body, not just that of binding estrogen, thus one may have low or normal levels of glucaronic acid along with low, normal or high levels of estrogen. The healthy body employs many different detoxification pathways, in the liver and elsewhere, of which glucuronidation is one. Glucuronidation removes several toxic and potentially toxic chemicals from our system, such as polycyclic aromatic hydrocarbons, steroid hormones, some nitrosamines, heterocyclic amines, some fungal toxins, and aromatic amines. It also removes "used" hormones, such as estrogen and T4, that are produced naturally by the body. This, glucuronidation represents a major means of converting most drugs, steroids, and many toxic and endogenous substances to metabolites that can then be excreted into the urine or bile.
The liver, spleen, and gut may be damaged or otherwise impaired by several means:
- Liver disease or disorder, such as hepatitis
- Drugs or toxic exposure disrupts phase 1 or phase 2 function
- Accidental ingestion of toxic substances (such as plants, poisons, drug overdose, mercury)
- Intentional ingestion of substances which overload detox pathways (such as nicotine, acetaminophen, NSAIDs, xenobiotics, therapeutic glycosides, etc.
Many of these toxic and otherwise therapeutic substances (xenobiotics, drugs) disrupt the glucuronidation by impairing it, stopping it, or causing the binds to be rupture, separating the bound molecules from its inert transport. The toxins that are thus not removed by normal binding and excretion may settle elsewhere in the body, causing tumors and other signs of toxicity.
Glucuronidase is an enzyme that inhibits the glucuronidation process, breaking apart the bound toxins. Calcium D-glucarate (a calcium salt that is found in some plants, such as apples, grapefruit, broccoli and alfalfa) suppresses that enzyme, restoring this particular detoxification pathway. A benefical fungus, Saccharomyces boulardii, helps reduce some of the gut organisms that produce glucuronidase.
For more information related to glucuronidation, please see the 2002 Update in my Estrogen Dominance article.
Acetaminophen Users:
Acetaminophen also affects the glutathione detoxification pathway in the liver, so those taking acetaminophen products should also take a glutathione supplement.
Glycerol kinase
Glycerol kinase, encoded by the gene GK, is a phosphotransferase enzyme involved in triglycerides and glycerophospholipids synthesis.
Glycerol kinase catalyzes the transfer of a phosphate from ATP to glycerol thus forming glycerol 3-phosphate:
Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation.  This glycerol is instead shuttled to the liver via the blood where it is:
- phosphorylated by glycerol kinase to glycerol 3-phosphate
- Converted from glycerol 3-phosphate to dihydroxyacetone phosphate (DHAP) via glycerol 3-phosphate dehydrogenase. DHAP can participate in glycolysis or gluconeogenesis.

# Enzyme regulation
This protein may use the morpheein model of allosteric regulation.

# Structure
Glycerol Kinase (alternative name, ATP:glycerol 3-phosphotransferase or Glycerokinase) adopts a ribonuclease H-like fold consisting of an alpha-beta 2-layer sandwich of CATH family 3.30.420.40. As of  March 2010, there were 20 structures of this protein in the PDB, most of which are homodimeric.
Protein isoform
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: 
There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us  to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
A protein isoform is a version of a protein with only small differences to another isoform of the same protein. Different forms of a protein may be produced from different but related genes, or may arise from the same gene by alternative splicing. A large number of isoforms are caused by single nucleotide polymorphisms, small genetic differences between alleles of the same gene.
The discovery of isoforms explains the apparently small number of coding genes revealed in the human genome project: the ability to create catalytically different proteins from the same gene increases the diversity of the proteome. Isoforms are readily described and discovered by microarray studies and cDNA libraries.

# Theoretical isoforms
A protein isoform, or "protein variant", is a member of a set of highly similar proteins that originate from a single gene or gene family and are the result of genetic differences.
Many human genes possess confirmed alternative splicing isoforms. It has been estimated that ~100,000 expressed sequence tags (ESTs) can be identified in humans. Isoforms at the protein level can manifest in the deletion of whole domains or shorter loops, usually located on the surface of the protein.
Def. any "of several different forms of the same protein, arising from either single nucleotide polymorphisms, differential splicing of mRNA, or post-translational modifications (e.g. sulfation, glycosylation, etc.)" is called an isoform, or protein isoform.
Def. a "different sequence of a gene (locus)" is called a variant.

# Glycoforms
A glycoform is an isoform where different ways of a glycoprotein have different polysaccharides attached to them, by either posttranslational or cotranslational modifications.

# Examples
- Creatine kinase, the presence of which in the blood can be used as an aid in the diagnosis of myocardial infarction, exists in 3 isoforms.
- Hyaluronan synthase, the enzyme responsible for the production of hyaluronan, has three isoforms in mammalian cells.
Gnathostomiasis
Gnathostomiasis is the human infection by the nematode (roundworm) Gnathostoma spinigerum and/or Gnathostoma hispidum, which infects vertebrate animals. Specifically, the disease is due to migrating immature worms.

# Symptoms
Migration in the subcutaneous tissues (under the skin) causes intermittent, migratory, painful, pruritic swellings (cutaneous larva migrans). Migration to other tissues (visceral larva migrans), can result in cough, hematuria, ocular (eye) involvement, meningitis, encephalitis and eosinophilia.

# Laboratory Diagnosis
Diagnosis of gnathostomiasis is possible (with microscopy) after removal of the worm.

# Treatment
Surgical removal or treatment with Albendazole or Ivermectin is recommended.
Goodsall's rule

# Overview
Goodsall's rule relates the external opening of an anal fistula to its internal opening.
Goodsall's Rule states that the external opening situated behind the transverse anal line will open into the anal canal in the midline posteriorly. An anterior opening is usually associated with a radial tract.
Fistulas can be described as anterior or posterior relating to a line drawn in the coronal plane across the anus, the so called transverse anal line. Anterior fistulas will have a direct track into the anal canal. Posterior fistulas will have a curved track with their internal opening lying in the posterior midline of the anal canal. An exception to the rule are anterior fistulas lying more than 3 cm. from the anus, which may open in the anterior midline of the anal canal.
The investigation of choice for anal fistulas is magnetic resonance imaging (MRI).
Granulosa cells
A granulosa cell is a somatic cell found closely associated with the developing female gamete (called an oocyte or egg) in the ovary of mammals.

# Anatomy and function
Granulosa cells form a single flattened layer around the mammalian oocyte in the primary ovarian follicle and later in follicle development (folliculogenesis) they advance to form a multilayered cumulus oophorus surrounding the oocyte in the preovulatory or Graafian follicle.
The major functions of granulosa cells include the production of steroids, as well as a myriad of growth factors thought to interact with the oocyte during its development.
Also FSH stimulates granulosa cells to convert androgens (coming from the thecal cells) to estradiol by aromatase.  However, after ovulation the granulosa cells produce progesterone that may maintain a potential pregnancy and produce a thick cervical mucus which inhibits sperm entry into the uterus

# Embryology of ovarian granulosa cells
In the development of the urinary and reproductive organs, the oogonia become invaginated in the gonadal ridge.
In the 1970s, evidence emerged that the first cells to make contact with the oogonia were of mesonephric origin. It was suggested that mesonephric cells already closely associated with the oogonia proliferated throughout development to form the granulosa cell layer.
Recently this hypothesis has been challenged with some thorough histology. Sawyer et al. hypothesised that in sheep most of the granulosa cells develop from cells of the mesothelium (i.e., epithelial cells from the presumptive surface epithelium of the ovary). 
The embryological origin of granulosa cells remains controversial.

# Additional images
- Oocyte granulosa cells
Group 3 element
The Group 3 elements are chemical elements comprising the third vertical column of the periodic table.
IUPAC has not recommended a specific format for the periodic table, so different conventions are permitted and are often used for group 3. The following d-block transition metals are always considered members of group 3:
- scandium (Sc)
- yttrium (Y)
When defining the remainder of group 3, four different conventions may be encountered. (See group number of lanthanides and actinides):
- Some tables  include lanthanum (La) and actinium (Ac), (the beginnings of the lanthanide and actinide series of elements, respectively) as the remaining members of group 3. In their most commonly encountered tripositive ion forms, these elements do not possess any partially filled f orbitals, thus resulting in more d-block-like behavior.
- Some tables  include lutetium (Lu) and lawrencium (Lr) as the remaining members of group 3. These elements terminate the lanthanide and actinide series, respectively. Since the f-shell is nominally full in the ground state electron configuration for both of these metals, they behave most like d-block metals out of all the lanthanides and actinides, and thus exhibit the most similarities in properties with Sc and Y. For Lr, this behavior is expected, but it has not been observed because sufficient quantities are not available. (Also see Periodic table (wide) and Periodic table (extended).)
Some tables  refer to all lanthanides and actinides by a marker in group 3. A third and fourth alternative are suggested by this arrangement:
- The third alternative is to regard all 30 lanthanide and actinide elements as included in Group 3. Lanthanides, as electropositive trivalent metals, all have a closely related chemistry, and all show many similarities to Sc and Y.
- The fourth alternative is to include none of the lanthanides and actinides in group 3.  The lanthanides possess additional properties characteristic of their partially-filled f orbitals which are not common to Sc and Y. Furthermore, the actinides show a much wider variety of chemistry (for instance, in range of oxidation states) within their series than the lanthanides, and comparisons to Sc and Y are even less useful.

# Occurrence
Scandium, yttrium, and the lanthanides (except promethium) tend to occur together in the Earth's crust, and are relatively abundant compared with most d-block metals, but often harder to extract from their ores.

# Biological chemistry
Group 3 elements are generally hard metals with low aqueous solubility, and have low availability to the biosphere. No group 3 has any documented biological role in living organisms. The radioactivity of the actinides generally makes them highly toxic to living cells.

# Notes