Persius/hicric huggingface dataset:
Bombesin-like receptor 3
The bombesin receptor subtype 3 also known as BRS-3 or BB3 is a protein which in humans is encoded by the BRS3 gene.

# Function
Mammalian bombesin-like peptides are widely distributed in the central nervous system as well as in the gastrointestinal tract, where they modulate smooth-muscle contraction, exocrine and endocrine processes, metabolism, and behavior. They bind to G protein-coupled receptors on the cell surface to elicit their effects. Bombesin-like peptide receptors include gastrin-releasing peptide receptor, neuromedin B receptor, and bombesin-like receptor-3 (BRS3; this article).
BB3 is a G protein-coupled receptor.  BB3 only interacts with known naturally occurring bombesin-related peptides with low affinity and therefore, as it has no natural high-affinity ligand, is classified as an orphan receptor.
Bond dissociation energy
In chemistry, bond dissociation energy, D0 or BDE,  is one measure of the bond strength in a chemical bond.  It is defined as the standard enthalpy change when a bond is cleaved by homolysis, with reactants and products of the homolysis reaction at 0K (absolute zero). For instance, the bond dissociation energy for one of the C-H bonds in ethane (C2H6) is defined by the process:
CH3CH2-H  CH3CH2 + H
D0 = H = 101.1 kcal/mol (423.0 kJ/mol)
The bond dissociation energy is sometimes also called the bond dissociation enthalpy (or bond enthalpy), but these terms are not strictly correct, as they refer to the above reaction enthalpy at standard conditions, and may differ from D0 by more than 3 kcal/mol (12 kJ/mol).
The bond dissociation energy is usually different from the bond energy, which is calculated from the sum of the bond dissociation energies of all bonds in a molecule. 
For example, an O-H bond of a water molecule (H-O-H) has 493.4 kJ/mol of bond dissociation energy, and 424.4 kJ/mol is needed to cleave the remaining O-H bond. The bond energy of the O-H bonds in water is 458.9 kJ/mol, which is the average of the values.
In the same way for removing successive hydrogen atoms from methane the bond dissociating energies are 104 kcal/mol (435 kJ/mol) for D(CH3-H), 106 kcal/mol (444 kJ/mol) for D(CH2-H), 106 kcal/mol (444 kJ/mol) for D(CH-H) and finally 81 kcal/mol (339 kJ/mol) for D(C-H). The bond energy is thus 99 kcal/mol or 414 kJ/mol (the average of the bond dissociation energies).
Note that  following dissociation, if new bonds are formed at lower enthalpy, then there is a net loss of energy, and thus an overall exothermic process.
Heterolytic bond dissociation energy is involved in chemical bond breaking by heterolysis rather than homolysis.
Bothnia retina dystrophy
Synonyms and keywords: Vasterbotten dystrophy

# Overview
Bothnia retina dystrophy is inherited as an autosomal recessive disease with characteristic features of night blindness, retinitis punctata albescens, macular degeneration and abnormal electroretinography (ERG).

# Pathogenesis
Bothnia retina dystrophy molecular basis caused by mutations in the cellular retinaldehyde-binding protein-1 gene (RLBP1).

# Diagnosis

## Symptoms
Bothnia retina dystrophy is characterised by night blindness from early childhood, retinitis punctata albescens and macular degeneration starting in late childhood to early teens, allelic to retinitis punctata albescens, fundus albipunctatus, autosomal recessive retinitis pigmentosa, newfoundland rod-cone dystrophy.
Brain stimulation reward
James Olds was the first to discover that rats will perform arbitrary operant responses to obtain electrical stimulation of some brain regions (e.g. the lateral hypothalamus).  The phenomenon is called brain stimulation reward (BSR), and also refers to the reward produced by injections of certain drugs of abuse (e.g. amphetamine or morphine) directly into the brain.
This behaviour is found in all vertebrates tested and animals will work to stimulate different neural sites depending on their current state. For example, stimulation at one site is chosen when rats are hungry and at another when rats are thirsty. Thus BSR can act like a specific natural reward, activating the same neurons that are activated in natural circumstances. For example, hunger increases BSR in the lateral hypothalamus and orbitofrontal cortex, and the same neurons are activated by the sight, taste or smell of food when the organism is hungry. The implication is that BSR taps into the natural reward system of the brain.
An interesting finding that has resulted from BSR experiments, is that reward, in itself, does not produce satiety. BSR experiments have also been helpful in understanding the way that the brain is organised to govern behavior, especially with regard to addictive behavior. BSR is not found in brain areas involved in early sensory processing areas (e.g. visual areas up to and including the inferior temporal cortex), so it can be deduced that reward is only represented at certain stages of the pathways that lead from sensory input to motor output (e.g. orbitofrontal cortex).
Brief reactive psychosis

# Overview
Brief reactive psychosis is the psychiatric term for psychosis which can be triggered by an extremely stressful event in the life of a patient.  This 'stressful life event' can take many forms, including (but not limited to) the death of a loved one, professional loss such as unexpected redundancy or otherwise becoming unemployed, or serious adverse changes in the patient's personal life, such as the breakdown of their family through divorce, etc.
It must be stressed that this is by no means an exhaustive list of stressful life events, because the events which trigger brief reactive psychosis tend, due to the individualistic nature of human psychology, to be extremely personalized.
The condition usually spontaneously resolves itself within two weeks, and the main goal of treatment is to prevent the patient from harming either themself or others.
Bulimia nervosa overview

# Overview
Bulimia is an eating disorder in which an individual purges after they eat large quantities of food in a short period of time. Bulimia is linked with many mental disorders, one of the most prominent of which is depression. Those with this disorder fear gaining weight as a result of the binge eating episodes they go on, so they resort to extreme ways to counteract that such as forcing themselves to vomit.

# Historical Perspective
Bulimia is a Greek term that translates to "ravenous hunger". Gerald Russell became the first person to publish a description of bulimia nervosa in 1979.

# Pathophysiology
Bulimia is related to deep psychological issues and feelings of lack of control. They may feel a loss of control during a binge, and consume great quantities of food (over 20,000 calories). There are higher rates of eating disorders in groups involved in activities that emphasize thinness and body type, such as gymnastics, dance and cheerleading, figure skating.

# Classification
Bulimia nervosa may be classified in to two types on the basis of purging behavior into purging and non-purging types.

# Causes

# Screening

# Differential Diagnosis

# Epidemiology and Demographics
Very few studies regarding bulimia nervosa have been conducted on the general population, and thus, very little data is available. Bulimia nervosa is more prominent in females than in males. 0.1% to  1.4% of males are affected whereas 0.3% to 9.4% of females are affected.

# Risk Factors
The risk for Bulimia nervosa may be increased due to possible genetic predisposition, hormonal imbalances, and poor body image and self esteem.

# Natural History, Complications and Prognosis
Bulimia typically tends to start in late teens or early 20s. Bulimics go through cycles of over-eating and purging, that may be severe and devastating to the body. This cycle may be repeated several times a week or, in serious cases, several times a day. Bulimics may appear underweight, normal weight or overweight. Bulimia may cause several complications including malnutrition, dehydration, electrolyte imbalance, and vitamin and mineral deficiencies. The Eating Disorders Association of UK estimates it at 10%. An 18% mortality rate has been suggested for anorexia.

# Diagnosis

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Primary Prevention

## Secondary Prevention

## Cost-effectiveness of Therapy

## Future or Investigational Therapies
Butoconazole description

# Description
GYNAZOLE - 1 Butoconazole Nitrate Vaginal Cream USP, 2% contains butoconazole nitrate 2%, an imidazole derivative with antifungal activity. Its chemical name is ()-1-butyl] imidazole mononitrate, and it has the following chemical structure:
Butoconazole nitrate is a white to off-white crystalline powder with a molecular weight of 474.79. It is sparingly soluble in methanol; slightly soluble in chloroform, methylene chloride, acetone, and ethanol; very slightly soluble in ethyl acetate; and practically insoluble in water. It melts at about 159C with decomposition.
GYNAZOLE - 1 Butoconazole Nitrate Vaginal Cream USP, 2% contains 2% butoconazole nitrate in a cream of edentate disodium, glyceryl monoisostearate, methylparaben, mineral oil, polyglyceryl-3 oleate, propylene glycol, propylparaben, colloidal silicon dioxide, sorbitol solution, purified water, and microcrystalline wax.
Butylated hydroxyanisole
Butylated hydroxyanisole (BHA) is a mixture of two isomeric organic compounds, 2-tert-butyl-4-hydroxyanisole and 3-tert-butyl-4-hydroxyanisole.  It is prepared from 4-methoxyphenol and isobutylene. It is a waxy solid that exhibits antioxidant properties.
Like butylated hydroxytoluene (BHT), the conjugated aromatic ring of BHA is able to stabilize free radicals, sequestering them. By acting as free radical scavengers, further free radical reactions are prevented.
The National Institutes of Health considers BHA reasonably anticipated to be a human carcinogen.
Butylated hydroxytoluene
Butylated hydroxytoluene (BHT) is the organic compound with the formula MeC6H2(CMe3)2OH (Me = methyl). This lipophilic (fat-soluble) phenol is primarily used as an antioxidant food additive (E number E321) as well as in cosmetics, pharmaceuticals, jet fuels, rubber, petroleum products, and embalming fluid.

# Chemistry
BHT is produced by alkylation reaction of p-cresol with isobutylene.  The species behaves as a synthetic analogue of vitamin E, primarily acting as a terminating agent" that suppressed autoxidation, a process whereby unsaturated (usually) organic compounds are attacked by atmospheric oxygen.  BHT stops this autocatalytic reaction by converting peroxy radicals to hydroperoxides.  It effects this function by donating a hydrogen atom:
where R is alkyl or aryl, and where ArOH is BHT or related phenolic antioxidants.  One can see that each BHT consumes two peroxy radicals.
In the chemical industry it is added to tetrahydrofuran and diethyl ether in order to inhibit the formation of dangerous organic peroxides.

# Use in foods
BHT was patented in 1947 and received approval of the Food and Drug Administration for use as a food additive and preservative in 1954. BHT reacts with free radicals, slowing the rate of autoxidation in food, preventing changes in the food's color, odor, and taste.

# Controversy
Concerns have been raised about the use of BHT in food products.  The compound has been banned for use in food in Japan (1958), Romania, Sweden, and Australia.  The US has barred it from infant foods.  Some food industries have voluntarily eliminated it from their products.  However, BHT is also marketed as a health food supplement in capsule form.
CDGSH iron sulfur domain
The CDGSH iron sulfur domain are a group of iron-sulfur (Fe-S) clusters and a unique 39 amino acid CDGSH domain .
The CDGSH iron sulfur domain 1 protein (also referred to as mitoNEET) is an integral membrane protein located in the outer mitochondrial membrane and whose function may be to transport iron into the mitochondria.  Iron in turn is essential for the function of several mitochondrial enzymes.
The antidiabetic drug pioglitazone, in addition to binding to the nuclear receptor PPAR, also has been shown to bind mitoNEET with approximately equal affinity.
Calcium-sensing receptor
The calcium-sensing receptor (CaSR) is a Class C G-protein coupled receptor which senses extracellular levels of calcium ion.  It is primarily expressed in the parathyroid gland and the renal tubules of the kidney. In the parathyroid gland, the calcium-sensing receptor controls calcium homeostasis by regulating the release of parathyroid hormone (PTH). In the kidney it has an inhibitory effect on the reabsorption of calcium, potassium, sodium, and water depending on which segment of the tubule is being activated.

# Signal transduction
The release of PTH is inhibited in response to elevations in plasma calcium concentrations and activation of the calcium receptor. Increased calcium binding on the extracellular side gives a conformational change in the receptor, which, on the intracellular side, initiates the phospholipase C pathway, presumably through a Gq type of G protein, which ultimately increases intracellular concentration of calcium, which inhibits vesicle fusion and exocytosis of parathyroid hormone. It also inhibits (not stimulates, as some sources state) the cAMP dependent pathway.

# Pathology
Mutations that inactivate a CaSR gene cause familial hypocalciuric hypercalcemia (FHH) (also known as familial benign hypercalcemia because it is generally asymptomatic and does not require treatment), when present in heterozygotes. Patients who are homozygous for CaSR inactivating mutations have more severe hypercalcemia. Other mutations that activate CaSR are the cause of autosomal dominant hypocalcemia or Type 5 Bartter syndrome. An alternatively spliced transcript variant encoding 1088 aa has been found for this gene, but its full-length nature has not been defined.

# Therapeutic application
The drugs cinacalcet and etelcalcetide are allosteric modifiers of the calcium-sensing receptor. They are classified as a calcimimetics, binding to the calcium-sensing receptor and decreasing parathyroid hormone release.
Calcilytic drugs, which block CaSR, produce increased bone density in animal studies and have been researched for the treatment of osteoporosis. Unfortunately clinical trial results in humans have proved disappointing, with sustained changes in bone density not observed despite the drug being well tolerated. More recent research has shown the CaSR receptor to be involved in numerous other conditions including Alzheimer's disease, asthma and some forms of cancer, and calcilytic drugs are being researched as potential treatments for these. Recently it has been shown that biomimetic bone like apatite inhibits formation of bone through endochondral ossification pathway via hyperstimulation of extracellular calcium sensing receptor.

# Interactions
Calcium-sensing receptor has been shown to interact with filamin.
Captopril challenge test
In medicine, the captopril challenge test, also CCT, is a non-invasive test used to help diagnose renal artery stenosis.
The CCT, in adults, has a high sensitivity, but a low  specificity. A better test for diagnosing renal artery stenosis is subtraction renal angiography.

# How it is done
The CCT is performed by measuring the renin prior to and following the administration of captopril, an angiotensin converting enzyme inhibitor.  A CCT is considered positive if the renin levels increase substaintially or the baseline renin level is abnormally high.

# Use of the CCT in children
The CCT has not been found to be very useful in children.
Carcinoembryonic antigen

# Overview
- Carcinoembryonic antigen (CEA) is a protein-polysaccharide complex
- Located in colon carcinomas, fetal intestine, liver and pancreas
- Reference range: < 3 ug/l 
Carcinoembryonic antigen (CEA) is a glycoprotein involved in cell adhesion. It is normally produced during fetal development, but the production of CEA stops before birth. Therefore, it is not usually present in the blood of healthy adults, although levels are raised in heavy smokers.

# Pathophysiology
CEA and related genes make up the CEA family belonging to the immunoglobulin superfamily. In humans, the carcinoembryonic antigen family consists of 29 genes, 18 of which are normally expressed. 

# Historical perspective
CEA was first identified in 1965 by Phil Gold and Samuel O. Freedman in human colon cancer tissue extracts. It was found that serum from individuals with colorectal, gastric, pancreatic, lung and breast carcinomas had higher levels of CEA than healthy individuals.

# Diagnosis
CEA measurement is mainly used as a tumor marker to identify recurrences after surgical resection. Elevated CEA levels should return to normal after surgical resection, as elevation of CEA during follow up is an indicator of recurrence of tumour.

# Differential Diagnosis
In alphabetical order.  

### Increased
- Alcoholic Cirrhosis
- Breast Cancer
- Bronchial carcinoma
- Cervical Cancer
- Cholangiocarcinoma
- Cirrhosis
- Colorectal tumors
- Emphysema
- Gastric carcinoma
- Inflammatory Bowel Disease
- Inflammatory liver diseases
- Medullar thyroid carcinoma
- Mesothelioma
- Neuroendocrine tumors
- Ovarian Cancer
- Pancreatic Cancer
- Pancreatitis
- Recurrence of cancer
- Smoking
- Stomach cancer
- Thyroid cancer
- Tumor recurrence
- Ulcerative colitis
Casein kinase 2, alpha 1
Casein kinase II subunit alpha is an enzyme that in humans is encoded by the CSNK2A1 gene.
Casein kinase II is a serine/threonine protein kinase that phosphorylates acidic proteins such as casein.  The kinase exists as a tetramer and is composed of an alpha, an alpha-prime, and two beta subunits. The alpha subunits contain the catalytic activity while the beta subunits undergo autophosphorylation. The protein encoded by this gene represents the alpha subunit. While this gene is found on chromosome 20, a related transcribed pseudogene is found on chromosome 11. Three transcript variants encoding two different proteins have been found for this gene.

# Interactions
Casein kinase 2, alpha 1 has been shown to interact with:
- APC,
- ATF1,
- ATF2,
- C-Fos,
- C-jun,
- CDC25B,
- CHEK1,
- CREBBP,
- CSNK2B,
- DDIT3,
- FGF1,
- FGF2,
- HNRPA2B1
- MAPK14,
- PIN1,
- PLEKHO1,
- PTEN,
- RELA,
- TAF1,  and
- UBTF.
Caspofungin how supplied

# How Supplied/Storage and Handling

## How Supplied
CANCIDAS 50 mg is a white to off-white powder/cake for infusion in a vial with a red aluminum band and a plastic cap.
NDC 0006-3822-10 supplied as one single-use vial.
CANCIDAS 70 mg is a white to off-white powder/cake for infusion in a vial with a yellow/orange aluminum band and a plastic cap.
NDC 0006-3823-10 supplied as one single-use vial.

## Storage and Handling
Vials
The lyophilized vials should be stored refrigerated at 2 to 8C (36 to 46F).
Reconstituted Concentrate
Reconstituted CANCIDAS in the vial may be stored at 25C (77F) for one hour prior to the preparation of the patient infusion solution.
Diluted Product
The final patient infusion solution in the IV bag or bottle can be stored at 25C (77F) for 24 hours or at 2 to 8C (36 to 46F) for 48 hours.
Castro-Stephens coupling
The Castro-Stephens Coupling is a cross coupling reaction between a Copper(I) acetylide and an aryl halide forming a disubstituted alkyne and a copper(I) halide.
The reaction was discovered in 1963 by chemists Casto and Stephens   and is used as a tool in the organic synthesis of organic compounds. The reaction has similarities with the much older Rosenmund-von Braun synthesis (1916) between aryl halides and copper(I) cyanide and was itself modified in 1973 with as the Sonogashira coupling by adding a palladium catalyst and preparing the organocopper compound in situ.
A typical reaction is the coupling of iodobenzene with the copper acetylide of phenylacetylene in refluxing pyridine to diphenylacetylene:
Cation channels of sperm
The cation channels of sperm also known as Catsper channels or CatSper, are ion channels that are related to the two-pore channels and distantly related to TRP channels. The four members of this family form voltage-gated Ca2+ channels that seem to be specific to sperm. As sperm encounter the more alkaline environment of the female reproductive tract, CatSper channels become activated by the altered ion concentration. These channels are required for proper fertilization. The study of these channels has been slow because they do not traffic to the cell membrane in many heterologous systems.
There are several factors that can activate the CatSper calcium channel, depending on species. In the mouse, channel is activated by progesterone released by the oocyte. The human CatSper channel is pH-sensitive, and requires a high-pH environment.  CatSper plays a key role in mediating hyperactive motility  prior to fertilization, sperm become entrapped within the fingerlike projections of the microvilli of the oviduct. In order for the sperm to fertilize the oocyte, CatSper must be present in order to initiate hyperactive motility, allowing the sperm to escape the microvilli and reach the oocyte for fertilization. 
Of the four members of the Catsper family, Catsper1 is found in the primary piece of sperm. Catsper1 plays an important role in evoked Ca2+ entry and regulation of hyperactivation in sperm. Catsper2 is localized in the sperm tail and is responsible for regulation of hyperactivation. Catsper3 and Catsper4 are found in both, the testes and sperm and play an important role in the motility of hyperactivated sperm. Although Catsper seems to play an important role in sperm function, Catspers1-4 null mice have been found to have normal testicular histology, sperm counts and morphology, which is indicative of normal progression of spermatogenesis.
Cefoperazone description
CEFOBID (sterile cefoperazone), formerly known as sterile cefoperazone sodium, contains cefoperazone as cefoperazone sodium. It is a semisynthetic, broad-spectrum cephalosporin antibiotic. Chemically, cefoperazone sodium is sodium (6R,7R)-7-methyl]-8-oxo-5-thia-1-azabicyclooct-2-ene-2-carboxylate. Its molecular formula is C25H26N9NaO8S2 with a molecular weight of 667.65. The structural formula is given below:
CEFOBID (sterile cefoperazone) contains 34 mg sodium (1.5 mEq) per gram. CEFOBID is a white powder which is freely soluble in water. The pH of a 25% (w/v) freshly reconstituted solution varies between 4.56.5 and the solution ranges from colorless to straw yellow depending on the concentration.
CEFOBID (sterile cefoperazone) in crystalline form is supplied in vials containing 1 g or 2 g cefoperazone as cefoperazone sodium for intravenous or intramuscular administration.