Persius/hicric huggingface dataset:
Beta-binomial model

# Overview
In empirical Bayes methods, the Beta-binomial model is an analytic model where the likelihood function L(x|\theta) is specifed by a binomial distribution
and the conjugate prior \pi(\theta|\alpha,\beta) is a Beta distribution

## Derivation of the posterior and the marginal
It is convenient to reparameterize the distributions so that the expected mean of the prior is a single parameter: Let
where
so that
The posterior distribution \rho(\theta|x) is also a beta distribution
while the marginal distribution m(x|\mu, M) is given by
\frac{\Gamma (x+M\mu)\Gamma(n-x+M(1-\mu)) }{\Gamma(n+M)} 

## Moment estimates
Because the marginal is a complex, non-linear function of Gamma and Digamma functions, it is quite difficult to obtain a marginal maximum likelihood estimate (MMLE) for the mean and variance.  Instead, we use the method of iterated expectations to find the expected value of the marginal moments.
Let us write our model as a two-stage compund sampling model (for each event i out of ni possible events):
We can find iterated moment estimates for the mean and variance using the moments for the distributions in the two-stage model:
We now seek a point estimate \tilde{\theta} as a weighted average of the sample estimate \hat{\theta_{i}} and an estimate for \hat{\mu}. The sample estimate \hat{\theta_{i}} is given by
Therefore we need point estimates for  \mu and M.   The estimated mean \hat{\mu}  is given as a weighted average
The hyperparameter M is obtained using the moment estimates for the variance of the two-stage model:
We can now solve for \hat{M}:
Given our point estimates for the prior, we may now plug in these values to find a point estimate for the posterior

## Shrinkage factors
We may write the posterior estimate as a weighted average:
where  \hat{B_{i}} is called the Shrinkage Factor.

## Example

## Maximum likelihood estimation

## Improved estimates: James-Stein estimator
Betahydroxyfentanyl
-hydroxyfentanyl is an opioid analgesic that is an analogue of fentanyl.
-hydroxyfentanyl was sold briefly on the black market in the early 1980s, before the introduction of the Federal Analog Act which for the first time attempted to control entire families of drugs based on their structural similarity rather than scheduling each drug individually as they appeared. 
-hydroxyfentanyl has similar effects to fentanyl. Side effects of fentanyl analogues are similar to those of fentanyl itself, which include itching, nausea and potentially serious respiratory depression which can be life-threatening.
Binasal hemianopsia

# Overview
Binasal hemianopsia (or Binasal hemianopia) is the medical description of a type of partial blindness where vision is missing in the inner half of both the right and left visual field. It is associated with certain lesions of the eye and of the central nervous system, such as congenital hydrocephalus.

# Etymology
The absence of vision in half of a visual field is described as hemianopsia.
The visual field of each eye can be divided in two vertically, with the outer half being described as temporal, and the inner half being described as nasal.
"Binasal hemianopsia" can be broken down as follows:
- bi-: involves both left and right visual fields
- nasal: involves the nasal visual field
- hemi-: involves half of each visual field
- anopsia: blindness

# Causes
In binasal hemianopsia, vision is missing in the inner (nasal or medial) half of both the right and left visual fields. Information from the nasal visual field falls on the temporal (lateral) retina. Those lateral retinal nerve fibers do not cross in the optic chiasm. Calcification of the internal carotid arteries can impinge the uncrossed, lateral retinal fibers leading to loss of vision in the nasal field.
Note: Clinical testing of visual fields (by confrontation) can produce false +ive result (particularly in inferior nasal quadrants).
Biological membrane
A biological membrane or biomembrane is an enclosing or separating tissue which acts as a barrier within or around a cell.  It is, almost invariably, a lipid bilayer, composed of a double layer of lipid-class molecules, specifically phospholipids, with occasional proteins intertwined, some of which function as channels.

# Function
Such membranes typically define enclosed spaces or compartments in which cells may maintain a chemical or biochemical environment that differs from the outside.  For example, the membrane around peroxisomes shields the rest of the cell from peroxides, and the plasma membrane separates a cell from its surrounding medium.  Most organelles are defined by such membranes, and are called membrane-bound organelles.
Probably the most important feature of a biomembrane is that it is a selectively permeable structure. This means that the size, charge and other chemical properties of the atoms and molecules attempting to cross it will determine whether they succeed to do so. Selective permeability is essential for effective separation of a cell or organelle from its surroundings. Biological membranes also have certain mechanical or elastic properties.
If a particle is too large or otherwise unable to cross the membrane by itself, but is still needed by a cell, it could either go through one of the protein channels, or be taken in by means of endocytosis.

# Types of biological membranes
- Cell membrane
- Mucous membrane
- S-layer
Blantyre Coma Scale
The Blantyre Coma Scale is a modification of the Pediatric Glasgow Coma Scale, designed to assess malarial coma in children.
It was designed by Drs Terrie Taylor and Malcolm Molyneux in 1987, and named for the Malawian city of Blantyre, Malawi|Blantyre]], site of the Blantyre Malaria Project.

# Using the scale
The score assigned by the Blantyre Coma Scale is a number from 0 to 5. The score is determined by adding the results from three groups: Motor response, verbal response, and eye movement.
The minimum score is 0 which indicates poor results while the maximum is 5 indicating good results. All scores under 5 are considered abnormal.

## Eye movement
- Watches or follows
- Fails to watch or follow

## Best motor response
- Localizes painful stimulus
- Withdraws limb from painful stimulus
- No response or inappropriate response

## Best verbal response
- Cries appropriately with pain, or, if verbal, speaks
- Moan or abnormal cry with pain
- No vocal response to pain
Bleb (cell biology)

# Overview
In cell biology, a bleb is an irregular bulge in the plasma membrane of a cell caused by localized decoupling of the cytoskeleton from the plasma membrane (recently reviewed in ).  Blebbing is the term used to describe the formation of blebs.

# Physiological Functions
During apoptosis (programmed cell death), the cell's cytoskeleton breaks up and causes the membrane to bulge outward (reviewed in ). These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic bodies. Phagocytic cells eventually consume these fragments and the components are recycled (see figure).
Blebbing also has important functions in other cellular processes, including cell locomotion, cell division, and physical or chemical stresses.  The types of blebs vary greatly, including variations in bleb growth rates, size, contents, and actin content.

# Pharmacology
A chemical known as blebbistatin (Sigma Aldrich) was recently shown to inhibit the formation of blebs.  This agent was discovered in a screen for small molecule inhibitors of nonmuscle myosin IIA and was shown to lower the affinity of myosin with actin , thus altering the contractile forces that impinge on the cytoskeleton-membrane interface.
Bleomycin hydrolase
Bleomycin hydrolase is an enzyme that in humans is encoded by the BLMH gene.
Bleomycin hydrolase (BMH) is a cytoplasmic cysteine peptidase that is highly conserved through evolution. Its biological function is hydrolysis of the reactive electrophile homocysteine thiolactone. Another of its activities is metabolic inactivation of the glycopeptide bleomycin (BLM), an essential component of combination chemotherapy regimens for cancer. The protein contains the signature active site residues of the cysteine protease papain superfamily.

# Interactions
BLMH has been shown to interact with RPL29, RPL11, UBE2I and Amyloid precursor protein.
Blood-borne disease

# Overview
A blood-borne disease is one that can be spread by contamination by blood.  The most common examples are HIV, hepatitis B, hepatitis C and viral haemorrhagic fevers.
Diseases that are not usually transmitted directly by blood contact, but rather by insect or other vector, are more usefully classified as vector-borne disease, even though the causative agent can be found in blood. Vector-borne diseases include West Nile virus and malaria.
Many blood-borne diseases can also be transmitted by other means.
Since it is difficult to determine what pathogens any given blood contains, and some blood-borne diseases are lethal, standard medical practice regards all blood (and any body fluid) as potentially infective. Blood and Body Fluid precautions are a type of infection control practice that seeks to minimize this sort of disease transmission.
Blood for blood transfusion is screened for many blood-borne diseases.
Needle exchanges are an attempt to reduce the spread of blood-borne diseases in intravenous drug users.

# Related Chapters
- Blood test
- Needlestick injury
Boomerang dysplasia
Boomerang dysplasia is a lethal form of osteochondrodysplasia known for a characteristic congenital feature in which the long bones of the arms and legs are malformed into the shape of a boomerang. Death usually occurs in early infancy due to complications arising from overwhelming systemic bone malformations.
Osteochondrodysplasias are skeletal disorders that cause malformations of both bone and cartilage.

# Presentation
Prenatal and neonatal diagnosis of boomerang dysplasia includes the presentation of several prominant features found in other osteochondrodysplasias, though the "boomerang" malformation seen in the long bones is the delineating factor.
Featured symptoms of boomerang dysplasia include: dwarfism (a lethal type of infantile dwarfism caused by systemic bone deformities), underossification (lack of bone tissue formation) in the limbs, spine and ilium (pelvis); proliferation of multinucleated giant-cell chondrocytes (cells that produce cartilage and play a role in skeletal development - chondrocytes of this type are rarely found in osteochondrodysplasias), brachydactyly (shortened fingers) and micromelia (a severely under-developed bone in any limb).
The characteristic "boomerang" malformation presents intermittently among random absences of long bones throughout the skeleton, in affected individuals. For example, one individual may have an absent radius and fibula, with the "boomerang" formation found in both ulnas and tibias. Another patient may present "boomerang" femora, and an absent tibia.

# Inheritance
Early journal reports of boomerang dysplasia suggested X-linked recessive inheritance, based on observation and family history. It was later discovered, however, that the disorder is actually caused by a sporadic genetic mutation fitting an autosomal dominant genetic profile.
Autosomal dominant inheritance indicates that the defective gene responsible for such a disorder is located on an autosome, and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder.
Boomerang dysplasia, although an autosomal dominant disorder, is not inherited due to the fact that those afflicted do not live beyond infancy. They cannot pass the gene to the next generation.

# Pathophysiology
Mutations in the Filamin B (FLNB) gene cause boomerang dysplasia. FLNB is a cytoplasmic protein that regulates intracellular communication and signalling by cross-linking the protein actin to allow direct communication between the cell membrane and cytoskeletal network, to control and guide proper skeletal development. Disruptions in this pathway, caused by FLNB mutations, result in the bone and cartilage abnormalities associated with boomerang dysplasia.
Chondrocytes, which also have a role in bone development, are susceptible to these disruptions and either fail to undergo ossification, or ossify incorrectly.
FLNB mutations are involved in a spectrum of lethal bone dysplasias. One such disorder, atelosteogenesis type I, is very similar to boomerang dysplasia, and several symptoms of both often overlap.
Borders of the lung
The anterior border of the lung is thin and sharp, and overlaps the front of the pericardium.
The anterior border of the right lung is almost vertical, and projects into the costomediastinal sinus; that of the left lung presents, below, an angular notch, the cardiac notch, in which the pericardium is exposed.
Opposite this notch the anterior margin of the left lung is situated some little distance lateral to the line of reflection of the corresponding part of the pleura.
The posterior border of the lung is broad and rounded, and is received into the deep concavity on either side of the vertebral column.
It is much longer than the anterior border, and projects, below, into the phrenicocostal sinus.
The inferior border of the lung is thin and sharp where it separates the base from the costal surface and extends into the phrenicocostal sinus; medially where it divides the base from the mediastinal surface it is blunt and rounded.
Bouveret's syndrome
Bouveret's syndrome is a gastric outlet obstruction produced by a gallstone impacted in the distal stomach or proximal duodenum.

# Demographics
Occurs most commonly in elderly women with a mean age of 69 years.

# Symptoms & Signs
The presenting clinical situation is variable and nonspecific but often includes nausea, vomiting, and epigastric pain.
Early diagnosis is important because mortality is historically high at 33%, although it has decreased to 12% in recent years.

# Diagnosis
- Rigler's triad is characteristic findings of imaging studies:
- bowel obstruction
- pneumobilia
- ectopic gallstone

# Treatment
Endoscopy is preferred as a therapeutic option because removal may be performed with mechanical, electrohydraulic, or laser lithotripsy.
Surgery often is not desirable as the patients are often poor surgical candidates secondary to concomitant illnesses and advanced age.
Brace (orthopaedic)
An orthopaedic brace (also orthosis or orthotic) is a device used to:
- immobilize a joint or body segment,
- restrict movement in a given direction,
- assist movement,
- reduce weight-bearing forces, or
- correct the shape of the body.
(adapted from Rehabilitation Medicine, ISBN 0-397-50764-X)
Most often in the U.S., the last purpose listed above is what persons call in common speech a brace, whether it is made from elastic, neoprene, or a stiffer, more restrictive construction such as hard plastic or metal.  An orthotic is most often understood to be a somewhat flexible device, often an insert for shoes, to correct leg length, fallen arches (flat feet), or some other foot problem.
In the UK a brace of this kind is usually referred to as a caliper (sometimes calliper in British spelling). Often the older type of leg brace is meant, constructed of steel side bars and ring, with spurs which fit into a metal tube in the heel of an adapted shoe or boot, and with leather straps and bands around the leg to hold the splint in position. The straps can be secured with velcro but many patients prefer buckles. This type of caliper can either be non-weight relieving or, by slight lengthening, made to relieve weight by raising the heel of the foot away from the heel of the shoe or boot. These splints have to be individually made by an orthotist or appliance maker closely to fit the particular contours of the leg being supported.
Bradykinin receptor
The bradykinin receptor family is a group of G-protein coupled receptors whose principal ligand is the protein bradykinin.
There are two Bradykinin receptors: the B1 receptor and the B2 receptor.

# B1 receptor
Bradykinin receptor B1 (B1) is a G-protein coupled receptor encoded by the BDKRB1 gene in humans. Its principal ligand is bradykinin, a 9 amino acid peptide generated in pathophysiologic conditions such as inflammation, trauma, burns, shock, and allergy. The B1 receptor is one of two G protein-coupled receptors that have been found which bind bradykinin and mediate responses to these pathophysiologic conditions.
B1 protein is synthesized by de novo following tissue injury and receptor binding leads to an increase in the cytosolic calcium ion concentration, ultimately resulting in chronic and acute inflammatory responses.

# B2 receptor
The B2 receptor is a G protein-coupled receptor, coupled to Gq and Gi. Gq stimulates phospholipase C to increase intracellular free calcium and Gi inhibits adenylate cyclase. Furthermore, the receptor stimulates the mitogen-activated protein kinase pathways. It is ubiquitously and constitutively expressed in healthy tissues.
The B2 receptor forms a complex with angiotensin converting enzyme (ACE), and this is thought to play a role in cross-talk between the renin-angiotensin system (RAS) and the kinin-kallikrein system (KKS). The heptapeptide angiotensin (1-7) also potentiates bradykinin action on B2 receptors.
Icatibant is a second generation B2 receptor antagonist which has undergone limited clinical trials in pain and inflammation. FR 173657 is another orally active non-peptide B2 antagonist that has undergone limited trials as analgesic and antiinflammatory drug.
Kallidin also signals through the B2 receptor.
Brian Barratt-Boyes
Sir Brian Gerald Barratt-Boyes, KBE (January 13, 1924 - March 8, 2006) was a pioneering heart surgeon from New Zealand.
Barratt-Boyes went to Victoria University before study medicine at Otago's Medical School, graduating in 1946. He continued his training as a surgeon, initially in New Zealand, and later at the Mayo Clinic (1953-5) and as a Nuffield Fellow in Bristol (1955-6). At Mayo he worked under John W. Kirklin, the two developing a high mutual regard that endured and grew over the years.
In 1956 he was recruited back to Auckland, New Zealand by Sir Douglas Robb, and pioneered the development of cardiopulmonary bypass in that country, the first patient being operated on in 1958. While this task must have been made more difficult by New Zealand's relative remoteness and small population, the Greenlane Hospital surgical team quickly achieved an international reputation for innovative excellence. Indeed he suggested that Auckland's isolation conferred an advantage comparable to that enjoyed by the Mayo Clinic in small-town Rochester, Minnesota, making it less likely that day-to-day interruptions would interfere with the real purpose of their work. Much of the original equipment had to be fashioned or modified locally. Sid Yarrow, an engineer on the team, built an early external pacemaker for intra-operative use. The first permanent unit, from Medtronic, was implanted in 1961.
In 1962 he introduced, independently but simultaneously with Donald Ross in London, the human cadaveric aortic homograft for aortic valve replacement and for many years he worked to perfect valve preparation, emphasizing its inherent physiologic advantages and simplifying its surgical implant technique. He and his team's results became the standard for others to match.
In 1969 he brought the technique of profound hypothermia and circulatory arrest into the limelight as a practical method for dealing with major corrective surgery in neonates with congenital heart disease, in so doing further establishing Greenlane Hospital on the international stage. In recognition of these and other achievements he was knighted in 1971 further confirming a national prominence comparable to that achieved by Rene Favaloro in Argentina and Christiaan Barnard in South Africa. Sir Brian Barratt-Boyes showcased the Greenlane experience at many international meetings as well as in workshops he hosted in Auckland. The 1987 Asian Pacific Congress was a particular success for him for the size of the international contingent it drew and the bright spotlight it shone on Greenlane's history of achievement. In 1985 he and John Kirklin published their authoritative text Cardiac Surgery, a colossal achievement of more than 1,500 pages that quickly became the standard reference for the sub-specialty.
Bromine trifluoride
Bromine trifluoride is a highly toxic and corrosive fluoride of bromine with chemical formula BrF3.  It was discovered by Paul Lebeau in 1906.  It occurs as a colorless, yellow, or gray fuming liquid with an irritating odor. It is soluble in sulfuric acid but may explode on contact with water.

# Synthesis
Bromine trifluoride can be obtained by the reaction of bromine with fluorine at 20 C.
The disproportionation of bromine monofluoride is also a source for bromine trifluoride.

# Structure
Bromine-trifluoride-chemical-structure
Like ClF3 and IF3 the BrF3 molecule is T-shaped. With the two electron pairs the coordination number is 5. The distance from the bromine each axial fluorine is 1.81 A and to the equatorial fluorine is 1.72 A. The angle between an axial fluorine and the equatorial fluorine is slightly smaller than 90  the 86.2 angle observed is due to the replusion generated by the electron pairs being greater than that of the Br-F bonds.
Bronchitis overview

# Overview
Bronchitis is an inflammation of the bronchi (medium and large size airways). Acute bronchitis is a self-limiting disease caused by viruses or bacteria. Chronic bronchitis is a disease by definition and is part of chronic obstructive pulmonary disease (COPD) which is defined as productive cough for at least three months in two consecutive years. Inflammatory response of the bronchial epithelium to infections or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa. Hallmark features of chronic bronchitis pathophysiology include: hyperplasia and hypertrophy of the goblet cells of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction.  
Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia and fibrosis of the lower airway. The consequence of these changes is a limitation of airflow. 
Acute bronchitis affects young children and old people. Its overall incidence is approximately 5% in the U.S. There is no racial or gender predilection for this disease.Although, Chronic bronchitis is common among geriatric patients. It occurs more commonly among Caucasian individuals compared to other races, but equally between males and females.
Age, season of the year and the immunization status are the main determining risk factors for acquiring acute bronchitis. The most potent risk factor in the development of chronic bronchitis is cigarette smoking. Other risk factors are occupational pollutants, such as cadmium, silica, and air pollutants, and genetic factors, such as alpha 1 antitrypsin deficiency
Acute bronchitis is a self limiting lower respiratory tract infection that usually presents with cough that lasts for up to 3 weeks. Chronic bronchitis usually gradually worsens over time and can result in death. The rate of deterioration varies between individuals and depends on the level of airflow obstruction. Prognosis is dependent on early recognition and smoking cessation, which improves the outcome significantly. Cigarette cessation, hand hygiene, vaccination and reduction in occupational exposure are the mainstays to decrease the severity and the risk of bronchitis.

# Classification
Bronchitis is classified in to two major categorize based on symptom chronicity.
- Acute bronchitis
- Chronic bronchitis

# Differential diagnosis