Persius/hicric huggingface dataset:
Endothelial protein C receptor
Endothelial protein C receptor (EPCR) also known as activated protein C receptor (APC receptor) is a protein that in humans is encoded by the PROCR gene. PROCR has also recently been designated CD201 (cluster of differentiation 201).
The protein encoded by this gene is a receptor for protein C that enhances its activation. Protein C is an anti-coagulant serine protease activated by the blood coagulation pathway.

# Structure
EPCR protein is an N-glycosylated type I membrane protein that enhances the activation of protein C. It belongs to the MHC class I/CD1 family of proteins, that is characterized by having a deep groove, that in other proteins in the family (but not in EPCR) is usually used for antigen binding.
Like the CD1 series, EPCR has a lipid in the corresponding groove. The bound lipid in EPCR is usually phosphatidylcholine, but it may be phosphatidylethanolamine, and it contributes to protein C binding, though probably not through direct contact 

# Clinical significance
Mutations in this gene have been associated with venous thromboembolism and myocardial infarction, as well as with late fetal loss during pregnancy.
The protein is also involved in Plasmodium falciparum malaria as subtypes of the Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family use EPCR of the host as a receptor.
Electron transfer dissociation
Electron transfer dissociation (ETD) is a method to fragment ions in a mass spectrometer. Similar to electron capture dissociation, ETD induces fragmentation of cations  (e.g. peptides or proteins) by transferring electrons to them.

# ETD fragmentation
ETD does not use free electrons but employs radical anions (e.g. anthracene or azobenzene) for this purpose:
ETD cleaves randomly along the peptide backbone (so called c and z ions) while side chains and modifications such as phosphorylation are left intact. The technique only works well for higher charge state ions (z>2), however relative to collision-induced dissociation (CID), ETD is advantageous for the fragmentation of longer peptides or even entire proteins. This makes the technique important for top-down proteomics.
Pacemaker mediated tachycardia
Synonyms and keywords: PMT, endless loop tachycardia,

# Overview
Pacemaker mediated tachycardia is a condition in which an artificial implanted pacemaker stimulates the the ventricles (the lower chambers of the heart) to beat at rates that are inappropriately fast.

# Pathophysiology
Pacemaker mediated tachycardia is a form of AV nodal reentrant tachycardia.  In PMT, the artificial pacemaker forms the anterograde (atrium to ventricle) limb of the circuit and the atrioventricular (AV) node forms the retrograde limb (ventricle to atrium) of the circuit.

# Causes
- The rate response setting of the pacemaker is set too sensitive
- Tracking of noise in the atrium as can occur with electromagnetic interference
- The electrical activity or myopotentials from the chest wall muscles may stimulate the pacer
- The electrocautery device in the operating room may generate electromechanical signals that may be oversensed by the pacemaker

# Differential Diagnosis
Disorders from which pacemaker mediated tachycardia must be differentiated include:
- Tracking an atrial tachyarrhythmia by the dual chamber pacemaker
- Runaway pacemaker syndrome in which the pacemaker fires at a rate of nearly 2000 bpm
- Sensor induced tachycardia in which case the pacemaker fires at a rate of nearly 160-180 bpm in response to electrocautery, noise, vibration, limb movement or other stimuli.

# Diagnosis

## Symptoms
The majority of patients are asymptomatic.  Some patients may complain of the following:
- Chest pain
- Lightheadedness
- Palpitations
- Rapid heart rate
- Syncope

## Physical Examination

### Vital Signs
- A tachycardia at a regular rate of 120 to 130 beats per minute is present
- Hypotension may be present if tachycardia mediated heart failure is present

### Neck
- Cannon a waves may be present

### Chest
- The pacemaker is present

## Electrocardiogram
There is a ventricular-paced rhythm at or near the upper rate limit at approximately 120-130 beats per minute.  given the mechanical nature of the trigger, the EKG is absolutely regular.
Shown below is a rhythm strip demonstrating pacemaker mediated tachycardia:

# Treatment
The pacemaker can be turned off by placing a magnet over it.  The treatment of PMT typically involves reprogramming the pacemaker.
Limb-girdle muscular dystrophy
Limb-girdle muscular dystrophy or Erb's muscular dystrophy is an autosomal class of muscular dystrophy that is similar but distinct from Duchenne muscular dystrophy and Becker's muscular dystrophy. Limb-girdle muscular dystrophy encompasses a large number of rare disorders.

# Presentation
The term "limb-girdle" is used to describe these disorders because the muscles most severely affected are generally those of the hips and shoulders -- the limb girdle muscles.
Common symptoms of limb-girdle muscular dystrophy are muscle weakness, myoglobinuria, pain, myotonia, cardiomyopathy, elevated serum CK, and rippling muscles.
The muscle weakness is generally symmetric, proximal, and slowly progressive.
Generally pain is not present with LGMD, and mental function is not affected.
LGMD can begin in childhood, adolescence, young adulthood or even later. The age of onset is usually between 10 and 30. Both genders are affected equally. When limb-girdle muscular dystrophy begins in childhood the progression appears to be faster and the disease more disabling. When the disorder begins in adolescence or adulthood the disease is generally not as severe and progresses more slowly.

## AHA Scientific Statement: Management of Cardiac Involvement Associated With Neuromuscular Diseases

### Cardiac Evaluation in Limb-girdle muscular dystrophies (LGMD)

# Prognosis
The distal muscles are affected late in LGMD, if at all. Over time (usually many years), the person with LGMD loses muscle bulk and strength. Eventually, s/he may need a power wheelchair or scooter, especially for long distances.
While LGMD isn't a fatal disease, it may eventually weaken the heart and lung muscles, leading to illness or death due to secondary disorders.

# Genetics
LGMD is typically an inherited disorder, though it may be inherited as a dominant, recessive, or X-linked genetic defect.  The result of the defect is that the muscles cannot properly form the proteins needed for normal muscle function.  Several different proteins can be affected, and the specific protein that is absent or defective identifies the specific type of muscular dystrophy.

# Treatment
Treatment for LGMD is primarily supportive.  Exercise and physical therapy are advised to maintain as much muscle strength and joint flexibility as possible. Calipers may be used to maintain mobility and quality of life.  Careful attention to lung and heart health is also required. IVIg may increase strength in some forms and prevent progression in others, possibly through the prevention of fibrosis and inflammation without the secondary weakening caused by corticosteroids.

# List of limb-girdle muscular dystrophies
The "LGMD1" family is autosomal dominant, and the "LGMD2" family is autosomal recessive.
External orifice of the uterus
The external orifice of the uterus (or ostium of uterus, or external os) is a small, depressed, somewhat circular aperture on the rounded extremity of the vaginal portion of the cervix. Through this aperture, the cervical cavity communicates with that of the vagina.
The external orifice is bounded by two lips, an anterior and a posterior. The anterior is shorter and thicker, though it projects lower than the posterior because of the slope of the cervix. Normally, both lips are in contact with the posterior vaginal wall.
Prior to pregnancy, the external orifice has a rounded shape when viewed through the vaginal canal (as through a speculum). Following parturition, the orifice takes on an appearance more like a transverse slit or is "H-shaped".

# Additional images
- Vessels of the uterus and its appendages, rear view.
- Median sagittal section of female pelvis.
Extracellular matrix protein 1
Extracellular matrix protein 1 is a protein that in humans is encoded by the ECM1 gene.
This gene encodes an extracellular protein containing motifs with a cysteine pattern characteristic of the cysteine pattern of the ligand-binding "double-loop" domains of the albumin protein family. This gene maps outside the epidermal differentiation complex (EDC), a cluster of three gene families involved in epidermal differentiation. Alternatively spliced transcript variants encoding distinct isoforms have been described.

# Diseases
ECM1 is implicated in breast cancer, thyroid cancer, hepatocellular carcinoma, and other cancers, and also in ulcerative colitis  Germline mutations in ECM-1 cause the genetic disease lipoid proteinosis. Autoimmune attack on ECM-1 is responsible for lichen sclerosus.(see the Atlas of Genetics and Cytogenetics in Oncology and Haematology,).
Facioscapulo-humeral dystrophy
Synonyms and related keywords: Facio-Scapulo-Humeral Dystrophy, FSH, FMD, FSHD, Muscular Dystrophy, Facioscapulohumeral, Muscular Dystrophy, Landouzy Dejerine
Facioscapulohumeral muscular dystrophy (FSHD), also known as Landouzy-Dejerine muscular dystrophy, is a neuromuscular disorder.
- Facial weakness is the initial manifestation with inability to smile, whistle, etc.
- Shoulder muscles are weak with scapular winging during arm abduction.
- Biceps / triceps are involved with sparing of the deltoids.
- 20% progress to involve the pelvic girdle.
- Labile hypertension, ocular involvement (Coats disease) and deafness can occur.
Facioscapulohumeral muscular dystrophy is usually inherited as an autosomal dominant trait. However, in up to approximately 30 percent of affected individuals, there is no apparent family history of the disorder.
Facultative anaerobic organism

# Overview
A facultative  anaerobic organism is an organism, usually a bacterium, that makes ATP by aerobic respiration if oxygen is present but is also capable of switching to fermentation.  In contrast, obligate anaerobes die in presence of oxygen.
Some examples of Facultative anaerobic bacteria are the Staphylococci (Gram positive), Escherichia coli (Gram negative), Corynebacterium (Gram positive), and Listeria (Gram positive).  Organisms in the Kingdom Fungi can also be facultative anaerobic, such as yeasts.
Factors influencing the switch are the concentrations of oxygen and fermentable material in the environment.  In brewer's yeast, the Pasteur shift is the observed cessation of oxygen consumption when fermentable sugar is supplied. In a growing culture, the energy "economics" disfavors respiration due to the "overhead cost" of producing the apparatus, as long as sufficient fermentable substrate is available, even though the energy output per mole of fermented material is far less than from respiration's complete oxidation of the same substrate.
Gut-associated lymphoid tissue

# Overview
The digestive tract's immune system is often referred to as gut-associated lymphoid tissue (GALT) and works to protect the body from invasion. GALT is an example of mucosa-associated lymphoid tissue.

# Function
About 70% of the body's immune system is found in the digestive tract. The GALT is made up of several types of lymphoid tissue that produce and store immune cells that carry out attacks and defend against pathogens.
New research indicates that GALT may continue to be a major site of HIV activity, even if drug treatment has reduced HIV count in the peripheral blood.

# Components
Lymphoid tissue in the gut is comprised of the following :
- Tonsils (Waldeyer's ring)
- Adenoids (Pharyngeal tonsils)
- Peyer's patches
- Lymphoid aggregates in the appendix and large intestine
- Lymphoid tissue accumulating with age in the stomach
- Small lymphoid aggregates in the oesophagus
- Diffusely distributed lymphoid cells and plasma cells in the lamina propria of the gut

# Additional images
- Lymphatics of colon.
- Section of the human esophagus.
- Transverse section of human vermiform process. X 20.
- Section of mucous membrane of human rectum.  X 60.
GM2-gangliosidosis, AB variant
GM2-gangliosidosis, AB variant is a rare inherited disorder that causes progressive destruction of nerve cells in the brain and spinal cord. It has a similar pathology to Sandhoff disease and Tay-Sachs disease.
Signs and symptoms of the AB variant begin in infancy. Infants with this disorder typically appear normal until the age of 3 to 6 months, when development slows and muscles used for movement weaken. Affected infants lose motor skills such as turning over, sitting, and crawling. As the disease progresses, infants develop seizures, vision and hearing loss, mental retardation, and paralysis. An eye abnormality called a cherry-red spot, which can be identified with an eye examination, is characteristic of this disorder. Children with the AB variant usually live only into early childhood.
Mutations in the GM2A gene cause GM2-gangliosidosis, AB variant. The GM2A gene provides instructions for making a protein called the GM2 activator. This protein is required for the normal function of beta-hexosaminidase A, a critical enzyme in the nervous system that breaks down a fatty substance called GM2 ganglioside. If mutations disrupt the activity of the GM2 activator, beta-hexosaminidase A cannot perform its normal function. As a result, GM2 ganglioside can accumulate to toxic levels in the brain and spinal cord. Progressive damage caused by the buildup of GM2 ganglioside leads to the destruction of nerve cells, which causes the severe medical problems characteristic of the AB variant. This condition is inherited in an autosomal recessive pattern.
Gamete intrafallopian transfer
Gamete intrafallopian transfer (GIFT) is a tool of assisted reproductive technology against infertility. Eggs are removed from a woman's ovaries, and placed in one of the Fallopian tubes, along with the man's sperm. The technique, which was pioneered by endocrinologist Ricardo Asch, allows fertilization to take place inside the woman's body.
Many specialists in infertility would look at GIFT as a procedure that is outdated (2004) as pregnancy rates in IVF tend to be equal or better and do not require laparoscopy.

# Method
It takes, on average, four to six weeks to complete a cycle of GIFT. First, the woman must take a fertility drug to stimulate egg production in the ovaries. The doctor will monitor the growth of the ovarian follicles, and once they are mature, the woman will be injected with Human chorionic gonadotropin (hCG). The eggs will be harvested approximately 36 hours later, mixed with the man's sperm, and placed back into the woman's Fallopian tubes using a laparoscope.

# Indications
A woman must have at least one normal fallopian tube in order for GIFT to be suitable. It is used in instances where the fertility problem relates to sperm dysfunction, and where the couple has idiopathic (unknown cause) infertility. Some patients may prefer the procedure to IVF for ethical reasons, since the fertilization takes place inside the body.

# Success rate
As with most fertility procedures, success depends on the couple's age and the woman's egg quality. It is estimated that approximately 25-30% of GIFT cycles result in pregnancy , with a third of those being multiple pregnancies.

# See Also
- Zygote intrafallopian transfer
Gastric inhibitory polypeptide
Gastric inhibitory polypeptide (GIP) or gastroinhibitory peptide, also known as the glucose-dependent insulinotropic peptide, is an inhibiting hormone of the secretin family of hormones.  While it is weak inhibitor of gastric acid secretion, its main role is to stimulate insulin secretion.
GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins.

# Synthesis and transport
GIP is derived from a 153-amino acid proprotein encoded by the GIP gene and circulates as a biologically active 42-amino acid peptide. It is synthesized by K cells, which are found in the mucosa of the duodenum and the jejunum of the gastrointestinal tract.
Like all endocrine hormones, it is transported by blood.
Gastric inhibitory polypeptide receptors are seven-transmembrane proteins found on beta-cells in the pancreas.

# Functions
It has traditionally been named gastrointestinal inhibitory peptide or gastric inhibitory peptide and was found to decrease the secretion of stomach acid  to protect the small intestine from acid damage, reduce the rate at which food is transferred through the stomach, and inhibit the GI motility and secretion of acid. However, this is incorrect, as it was discovered that these effects are achieved only with higher-than-normal physiological level, and that these results naturally occur in the body through a similar hormone, secretin.
It is now believed that the function of GIP is to induce insulin secretion, which is stimulated primarily by hyperosmolarity of glucose in the duodenum. After this discovery, some researchers prefer the new name of glucose-dependent insulinotropic peptide, while retaining the acronym "GIP."  The amount of insulin secreted is greater when glucose is administered orally than intravenously.
In addition to its role as an incretin GIP is known to inhibit apoptosis of the pancreatic beta cells and to promote their proliferation. It also stimulates glucagon secretion and fat accumulation. GIP receptors are expressed in many organs and tissues including the central nervous system enabling GIP to influence hippocampal memory formation and regulation of appetite and satiety.
GIP recently appeared as a major player in bone remodeling. Researchers at Universities of Angers and Ulster evidenced that genetic ablation of the GIP receptor in mice resulted in profound alterations of bone microarchitecture through modification of the adipokine network. Furthermore, the deficiency in GIP receptors has also been associated in mice with a dramatic decrease in bone quality and a subsequent increase in fracture risk. However, the results obtained by these groups are far from conclusive because their animal models give discordant answers and  these works should be analysed very carefully.

# Pathology
It has been found that Type 2 diabetics are not responsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics. In research involving knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.
Gatifloxacin adverse reactions
Clinical Studies Experience
Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.
In clinical studies with ZYMAXID, the most frequently reported adverse reactions occurring in  1% of patients in the gatifloxacin study population (N=717) were: worsening of the conjunctivitis, eye irritation, dysgeusia, and eye pain.
Additional adverse events reported with other formulations of gatifloxacin ophthalmic solution include chemosis, conjunctival hemorrhage, dry eye, eye discharge, eyelid edema, headache, increased lacrimation, keratitis, papillary conjunctivitis, and reduced visual acuity.
Glipizide detailed information
Glipizide is an oral medium-to-long acting anti-diabetic drug from the sulfonylurea class. It is classified as a second generation Sulfonylurea, which means that it undergoes enterohepatic circulation. The structure on the R2 group is a much larger cyclo or aromatic group compared to the 1st generation sulfonylureas. This leads to a once a day dosing that is much less than the first generation, about 100 fold.
Mechanism of action is produced by blocking potassium channels in the Beta cells of the Islets of Langerhans. By partially blocking the potassium channels, you will increase the time the cell spends in the Calcium release stage of cell signaling leading to an increase in calcium. The increase in Calcium will initiate more Insulin release from each Beta cell.
Originally available in 1984, it is marketed by Pfizer under the brand name Glucotrol in the USA, where Pfizer sells Glucotrol in doses of 5 and 10 milligrams and Glucotrol XL (an extended release form of glipizide) in doses of 2.5, 5, and 10 milligrams. Other companies sell generic forms of glipizide, most commonly extended release tablets of 5 and 10 milligrams.
Glutathione S-transferase Mu 1
Glutathione S-transferase Mu 1 (gene name GSTM1) is a human Glutathione S-transferase.

# Function
Cytosolic and membrane-bound forms of glutathione S-transferase are encoded by two distinct supergene families. At present, eight distinct classes of the soluble cytoplasmic mammalian glutathione S-transferases have been identified: alpha, kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes a cytoplasmic glutathione S-transferase that belongs to the mu class. The mu class of enzymes functions in the detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins, and products of oxidative stress, by conjugation with glutathione.
The genes encoding the mu class of enzymes are organized in a gene cluster on chromosome 1p13.3, and are known to be highly polymorphic. These genetic variations can change an individual's susceptibility to carcinogens and toxins, as well as affect the toxicity and efficacy of certain drugs. Null mutations of this class mu gene have been linked with an increase in a number of cancers, likely due to an increased susceptibility to environmental toxins and carcinogens. Multiple protein isoforms are encoded by transcript variants of this gene.
Griseofulvin adverse reactions

# Adverse Reactions
When adverse reactions occur, they are most commonly of the hypersensitivity type such as skin rashes, urticaria and rarely, angioneurotic edema or erythema multiforme-like drug reaction, and may necessitate withdrawal of therapy and appropriate countermeasures. Paresthesias of the hands and feet have been reported rarely after extended therapy. Other side effects reported occasionally are oral thrush, nausea, vomiting, epigastric distress, diarrhea, headache, fatigue, dizziness, insomnia, mental confusion and impairment of performance of routine activities.
Proteinuria and leukopenia have been reported rarely. Administration of the drug should be discontinued if granulocytopenia occurs.
When rare, serious reactions occur with griseofulvin, they are usually associated with high dosages, long periods of therapy, or both.
Healthy Mothers Healthy Babies
The National Healthy Mothers, Healthy Babies Coalition is an American non-profit organization founded in 1981 by the American College of Obstetricians and Gynecologists (ACOG), the March of Dimes, the National Congress of Parents and Teachers and the United States Public Health Service.
The coalition has 90 member organizations, including one for 21 U.S. states, which do outreach, education, and advocacy. The coalition's goal is reducing infant mortality, premature birth, and postpartum depression as well as other health issues facing mothers and infants.

# Fish controversy
In October 2007, HHMB published a story claiming that pregnant and new mothers should consume more seafood. This recommendation conflicted with official public health advice, due to the amount of mercury found in seafood posing a risk to fetal and newborn brain development.
It was discovered that HMHB received a $70,000 donation from the National Fisheries Institute, an industry group formed to promote eating seafood, prior to releasing this recommendation. 

# Footnotes
-  Something Fishy About Mothers and Fish Story