Persius/hicric huggingface dataset:
Bayesian model comparison

# Overview
A common problem in statistical inference is to use data to decide between two or more competing models. Frequentist statistics uses hypothesis tests for this purpose. There are several Bayesian approaches. One approach is through Bayes factors.
The posterior probability of a model given data, Pr(H|D), is given by Bayes' theorem:
The key data-dependent term Pr(D|H) is a likelihood, and is sometimes called the evidence for model H; evaluating it correctly is the key to Bayesian model comparison.
The evidence is usually the normalizing constant or partition function of another inference, namely the inference of the parameters of model H given the data D.
The plausibility of two different models H1 and H2, parametrised by model parameter vectors  \theta_1  and  \theta_2  is assessed by the Bayes factor given by
= \frac{\int \Pr(\theta_2|H_2)\Pr(D|\theta_2,H_2)\,d\theta_2}
{\int \Pr(\theta_1|H_1)\Pr(D|\theta_1,H_1)\,d\theta_1
Thus the Bayesian model comparison does not depend on the parameters used by each model.  Instead, it considers the probability of the model considering all possible parameter values.  Alternatively, the Maximum likelihood estimate could be used for each of the parameters.
An advantage of the use of Bayes factors is that it automatically, and quite naturally, includes a penalty for including too much model structure. It thus guards against overfitting.
Another approach is to treat model comparison as a decision problem, computing the expected value or cost of each model choice.
Another approach is to use Minimum Message Length (MML).
Bellwood General Hospital
Bellwood General Hospital was a hospital in Bellflower, California.  It was closed April 6, 2003.

# History
On February 2, 1982, the hospital was acquired by Paracelsus Healthcare Corporation.  Paracelsus Healthcare Corporation (later renamed to Clarent Hospital Corporation) ceased business operations following an agreement to pay $7.3 million to settle allegations that it defrauded Medicare at two facilities  Orange County Community Hospital ("OCCH") and Bellwood General Hospital.
As part of its bankruptcy, the company sold or closed all of its hospitals with Bellwood General being on the closure list.  Bellwood Health Facility, an OSHPD-Licensed Psychiatric Health Facility, continues to operate adjacent to the original site.
Bipolar disorder overview

# Overview
Bipolar disorder is a psychiatric condition defined as recurrent episodes of significant disturbance in mood.  These disturbances can occur on a spectrum that ranges from debilitating depression to unbridled mania. Individuals suffering from bipolar disorder typically experience fluid states of mania, hypomania or what is referred to as a mixed state in conjunction with depressive episodes.  These clinical states typically alternate with a normal range of moods.  The disorder has been subdivided into bipolar I, bipolar II and cyclothymia, with both bipolar I and bipolar II potentially presenting with rapid cycling.
Previously referred to as bipolar affective disorder, the current term (bipolar disorder) is fairly recent in origin and refers to the cycling between high and low episodes.  This term has also replaced manic-depressive illness coined by Emil Kraepelin (1856-1926) in the late nineteenth century. The current term was designed to be neutral, in order to avoid the stigma that results from conflating "manic" and "depression."
Onset of bipolar disorder symptoms generally occurs during young adulthood. Diagnosis is based on self-reported experiences and observed behavior. Episodes of illness are associated with distress and disruption, as well as increased rates of suicide. 
Studies suggest that genetics, early environment, neurobiology, and psychological and social processes are important contributing factors.  Psychiatric research is focused on the role of neurobiology, but a clear organic cause has not been found. Bipolar disorder is usually treated with a combination of medication, therapy, and counseling. The mainstay of medication are a number of drugs termed 'mood stabilizers', in particular lithium and sodium valproate. These are a group of unrelated medications used to prevent relapses of further episodes. Antipsychotic medications, sometimes called neuroleptics, in particular olanzapine, are used in the treatment of manic episodes and in maintenance. The benefits of using antidepressants during depressive episodes is unclear. In serious cases where there is risk to self and others, generally involving severe manic episodes with dangerous behaviour or depressive episodes with suicidal ideation, involuntary hospitalization may be necessary.
Several studies have identified a significant correlation between creativity and bipolar disorder, though this relationship remains unclear. Bipolar disorder is also thought to correlate with increased ambition and motivation.
Body of lateral ventricle

# Overview
The body of lateral ventricle (cella) of the lateral ventricle extends from the interventricular foramen to the splenium of the corpus callosum.
It is an irregularly curved cavity, triangular on transverse section, with a roof, a floor, and a medial wall.
The roof is formed by the under surface of the corpus callosum; the floor by the following parts, enumerated in their order of position, from before backward: the caudate nucleus of the corpus striatum, the stria terminalis and the terminal vein, the lateral portion of the upper surface of the thalamus, the choroid plexus, and the lateral part of the fornix; the medial wall is the posterior part of the septum pellucidum, which separates it from the opposite ventricle.
Bordetella bronchiseptica
Bordetella bronchiseptica is a bacterium of the genus Bordetella and a causative agent of infectious bronchitis. Closely related to B. pertussisthe obligate human pathogen which causes pertussis or whooping coughB. bronchiseptica can persist in the environment for extended periods.

# Pathogenesis
Unlike B. pertussis or B. parapertussis, humans are not natural carriers of B. bronchiseptica, which typically infects the respiratory tracts of smaller mammals (cats, dogs, rabbits, etc).
While B. bronchiseptica does not express pertussis toxin which is one of the characteristic virulence factors of B. pertussis, it does contain the genes to do so, highlighting the close evolutionary relationship between the two species.,

## Veterinary pathogenesis
In veterinary medicine, B. bronchiseptica leads to a range of pathologies in different hosts. B. bronchiseptica and Pasteurella multocida act synergistically to cause atrophic rhinitis in pigs, a disease resulting in arrested growth and distortion of the turbinates in the nasal terminus (or snout) . B. bronchiseptica is also a causative agent of acute tracheobronchitis in dogs  (see Kennel cough) and in rabbits and guinea pigs B. bronchiseptica leads to a nearly asymptomatic infection known as snuffles .
Breast pain and discharge
Synonyms and key words: Mastalgia
Breast pain is a common symptom in general surgical practice. Breast discharge is rarely normal except for lactating and pregnant women.

# Differential Diagnosis
In alphabetical order.  

## Breast Discharge
- Breast Abscess
- Breast Cancer
- Chronic nipple stimulation
- Cirrhosis (or other hepatic disease)
- Duct ectasia
- Early pregnancy
- Fibroadenosis
- Fibrocystic change
- Galactorrhea
- Hypothalamic and pituitary abnormalities
- Hypothyroidism
- Intraductal papilloma
- Lactation
- Lactorrhoea
- Late pregnancy
- Medications
- Mondor's Disease
- Paget's Disease of the Nipple
- Prolactinoma
- Puberty
- Pseudocyesis
- Retroareolar Abscess
- Sarcoidosis
- Systemic lupus erythematosus
- Tuberculosis

## Breast Pain
- Breast Abscess
- Breast Cancer
- Cyclical mastalgia
- Cyst
- Duct ectasia
- Extramammary causes of pain
- Fat necrosis
- Fibroadenoma
- Fibrocystic changes
- Herpes Zoster
- Intraductal papilloma
- Lactation
- Lipoma
- Mastitis
- Mondor's Disease
- Non-cyclical mastalgia
- Pregnancy
- Phylloides tumor
- Rib secondaries
- Tietze's Disease
- Trauma
- Unilateral or bilateral gynecomastia

# Diagnosis

# History and Symptoms
- Thorough history examination
Family history
Menstrual history
Pregnancy history
- Family history
- Menstrual history
- Pregnancy history

# Physical Examination
- Pattern and duration of pain (and/or discharge)
- Complete breast examination after menstrual flow (at least 7-9 days)

# Laboratory Findings
- Complete blood count (CBC)
- Erythrocyte sedimentation rate (ESR)
- Follicle stimulating hormone (FSH)
- Thyroid stimulating hormone (TSH)
- Liver function tests (LFTs)
- Prolactin levels
- Calcium
- Beta-human chorionic gonadotropin (HCG)
- Luteinizing hormone (LH)

## Chest X Ray
- Chest x-rays may be indicated to rule out secondaries in lungs or ribs.
- Chest x-rays also show pleural effusion in cancer

## Echocardiography or Ultrasound
- Ultrasounds distinguish between a cyst or a solid mass

## Other Imaging Findings
- In patients older than 30 years, a diagnostic mammogram is indicated
- If available, compare with previous mammogram

## Other Diagnostic Studies
- Breast biopsy
- Galactogram
- Ductogram
- Fine needle aspiration
- Cytologic exam (of discharge)

# Treatment
- Avoid caffeine for those patients with fibrocystic changes (decreases pain)
- Routine follow-up
- Warm compress for those patients with mastitis

# Pharmacotherapy
- Medical therapies as a means of pain relief for those patients with fibrocystic changes

## Acute Pharmacotherapies
- Radiation, chemotherapy, hormonal therapy for those patients with breast cancer
- Antibiotics for those patients with a cyst or for those with mastitis (to take care of streptococci and Staphylococcus aureus)

# Surgery and Device Based Therapy
- Aspirations for fibrocystic changes and for cysts
- Surgery may be required for those patients with breast cancer
- For patients with an abscess, incision and drainage are indicated
Broad-spectrum antibiotic
The term broad-spectrum antibiotic refers to an antibiotic with activity against a wide range of disease-causing bacteria. This is in contrast to a narrow-spectrum antibiotic which is effective against only specific families of bacteria. A good example of a commonly used broad-spectrum antibiotic is levofloxacin.

# Uses
Broad-spectrum antibiotics are properly used in the following medical situations:
- Empirically prior to identifying the causative bacteria when there is a wide differential and potentially serious illness would result in delay of treatment.  This occurs, for example, in meningitis, where the patient can become so ill that he/she could die within hours if broad-spectrum antibiotics are not initiated.
- For drug resistant bacteria that do not respond to other, more narrow-spectrum antibiotics.
- In super-infections where there are multiple types of bacteria causing illness, thus warranting either a broad-spectrum antibiotic or combination antibiotic therapy.
There has been a common usage of broad-spectrum agents in treatment of community acquired infections without attempting to culture or otherwise identify the causative bacteria.  Over the years, this practice has contributed to the emergence of more drug resistant strains of bacteria, necessitating the development of newer broad-spectrum antibiotics.
Ideally, the spectrum should be "narrowed down" by identifying the causative agent of an infection, and then replacing the broad-spectrum antibiotic with an appropriate narrower-spectrum antibiotic. This is believed to limit the development of antibiotic resistance, although evidence for this practice is unclear.

# Examples
In medicine, amoxycillin, levofloxacin.
In veterinary medicine, Co-amoxiclav (e.g. Synulox, from Pfizer) (in small animals); penicillin & streptomycin (e.g. Streptacare from Animalcare Ltd) and oxytetracycline (in farm animals); penicillin and potentiated sulphonamides (e.g. Equitrim, Boehringer) (in horses).
Rubinstein-Taybi syndrome
Rubinstein-Taybi syndrome (also known as Broad Thumb-Hallux syndrome) is a condition characterized by short stature, moderate to severe mental retardation, distinctive facial features, and broad thumbs and first toes. Other features of the disorder vary among affected individuals. People with this condition have an increased risk of developing noncancerous and cancerous tumors, leukemia, and lymphoma. This condition is inherited in an autosomal dominant pattern and is uncommon occurring in an estimated 1 in 125,000 births.

# Features of Rubinstein-Taybi syndrome
An isolated case was described in 1957 by Michail and Matsoukas. In 1963 Rubinstein and Taybi described a larger series of cases. Typical features of the disorder include:
- Broad thumbs and broad first toes
- Mental disability
- Small height, bone growth, small head
- Cryptorchidism in males
- Unusual faces - eyes, nose, palate
1 out of 300,000 children are born with RTS

# Genetics
Mutations in the CREBBP gene cause Rubinstein-Taybi syndrome. The CREBBP gene makes a protein that helps control the activity of many other genes. The protein, called CREB binding protein, plays an important role in regulating cell growth and division and is essential for normal fetal development. If one copy of the CREBBP gene is deleted or mutated, cells make only half of the normal amount of CREB binding protein. A reduction in the amount of this protein disrupts normal development before and after birth, leading to the signs and symptoms of Rubinstein-Taybi syndrome.
Mutations in the EP300 gene are responsible for a small percentage of cases of Rubinstein-Taybi syndrome. These mutations result in the loss of one copy of the gene in each cell, which reduces the amount of p300 protein by half. Some mutations lead to the production of a very short, nonfunctional version of the p300 protein, while others prevent one copy of the gene from making any protein at all. Although researchers do not know how a reduction in the amount of p300 protein leads to the specific features of Rubinstein-Taybi syndrome, it is clear that the loss of one copy of the EP300 gene disrupts normal development.
Brodie-Trendelenburg test

# Overview
The Brodie-Trendelenburg test is used to determine the site of valvular incompetence in a patient with varicose veins.

## How to perform?
- Ask the patient to lie down.
- Elevate the leg, and empty the veins by massaging distal to proximal.
- Using a tourniquet, occlude the superficial veins in the upper thigh.
- Ask the patient to stand. If the tourniquet prevents the veins from re-filling rapidly, the site of the incompetent valve must be above this level i.e. at the sapheno-femoral junction. If the veins re-fill, the communication must be lower down.
Observing the same protocol, proceed down the leg until the tourniquet controls re-filling.  As necessary, test:
- above the knee - to assess the mid-thigh perforator
- below the knee - to assess competence between the short saphenous vein and popliteal vein
If re-filling cannot be controlled, the communication is probably by one or more distal perforating veins.
CME Category::Cardiology
Buchnera (proteobacteria)

# Overview
Buchnera aphidicola a member of the Proteobacteria, is the primary  endosymbiont of  aphids (A. pisum). It is believed that Buchnera was once a free living gram negative ancestor similar to a modern Enterobacteriaceae such as Escherichia coli. Buchnera are 3 m in diameter and have some of the key characteristics of their Enterobacteriaceae relatives such as a gram-negative cell wall. However, unlike most other gram-negative bacteria, Buchnera lack the genes to produce lipopolysaccharides (LPS) for their outer membrane. The long association with aphids and the limitation of crossover events due to strictly vertical transmission has seen the deletion of genes required for anaerobic respiration, the synthesis of amino-sugars, fatty acids, phospholipids, and complex carbohydrates.  This has resulted not only in one of the smallest known genomes of any living organism, it is also one of the most genetically stable.
The symbiotic relationship with aphids began between 200 million  and 150 million years ago, and has persisted through maternal transmission and co-speciation. Aphids have developed bacteriocyte cells to house Buchnera. It is estimated that a mature aphid may carry 5.6  106 Buchnera individuals. Buchnera have lost regulatory factors allowing continuous overproduction of tryptophan and other amino acids. Each bacteriocyte contains multiple vesicles, symbiosomes derived from the plasma membrane.
Buchnera was first named by Paul Baumann and his graduate student, and the first molecular characterization of a symbiotic bacterium was carried out by Baumann, using Buchnera. The initial studies on Buchnera later led to studies on symbionts of many groups of insects, pursued by numerous investigators, including Paul and Linda Baumann, Nancy Moran, Serap Aksoy, Roy Gross, who together investigated symbionts of aphids, tsetse flies, ants, leafhoppers, mealybugs, whiteflies, psyllids and others.
Decay accelerating factor
Decay accelerating factor (CD55) is a 70 kDa membrane protein that regulates the complement system on the cell surface. It prevents the assembly of the C3bBb complex (the C3-convertase of the alternative pathway) or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.
This glycoprotein is broadly distributed among hematopoietic and non-hematopoietic cells. It is a determinant for the Cromer blood group system.

# Pathology
DAF is not expressed on paroxysmal nocturnal hemoglobinuria III (markedly abnormal) RBCs; however, this deficiency is not the cause of PNH.
Cyclin-dependent kinase 3
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Cell division protein kinase 3 is an enzyme that in humans is encoded by the CDK3 gene.

# Function
CDK3 complements cdc28 mutants of Saccharomyces cerevisiae suggesting that it may be involved in cell cycle control.  CDK3 can phosphorylate histone H1 and interacts with an unknown type of cyclin.
Cyclin-dependent kinase 4
Cyclin-dependent kinase 4 also known as cell division protein kinase 4 is an enzyme that in humans is encoded by the CDK4 gene. CDK4 is a member of the cyclin-dependent kinase family.

# Function
The protein encoded by this gene is a member of the Ser/Thr protein kinase family. This protein is highly similar to the gene products of S. cerevisiae cdc28 and S. pombe cdc2. It is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression. The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16INK4a. This kinase was shown to be responsible for the phosphorylation of retinoblastoma gene product (Rb). Ser/Thr-kinase component of cyclin D-CDK4 (DC) complexes that phosphorylate and inhibit members of the retinoblastoma (RB) protein family including RB1 and regulate the cell-cycle during G1/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complexes and the subsequent transcription of E2F target genes which are responsible for the progression through the G1phase. Hypophosphorylates RB1 in early G1 phase. Cyclin D-CDK4 complexes are major integrators of various mitogenic and antimitogenic signals. Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex.

# Clinical significance
Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. Multiple polyadenylation sites of this gene have been reported.
It is regulated by Cyclin D.

## Inhibitors
Palbociclib and Ribociclib are US FDA approved  CDK4 and CDK6 inhibitors for the treatment of estrogen receptor positive/ HER2 negative advanced breast cancer.
See also CDK inhibitor for inhibitors of various CDKs.

# Interactions
Cyclin-dependent kinase 4 has been shown to interact with:
- CDC37,
- CDKN1B,
- CDKN2B,
- CDKN2C,
- CEBPA,
- CCND1,
- CCND3,
- DBNL,
- MyoD,
- P16,
- PCNA,  and
- SERTAD1.
Cyclin-dependent kinase 8
Cell division protein kinase 8 is an enzyme that in humans is encoded by the CDK8 gene.

# Function
The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK8 and cyclin C associate with the mediator complex and regulate transcription by several mechanisms. CDK8 binds to and/or phosphorylates several transcription factors, which can have an activating or inhibitory effect on transcription factor function. CDK8 phosphorylates the Notch intracellular domain, SREBP, and STAT1 S727. CDK8 also inhibits transcriptional activation by influencing turnover of subunits in the mediator complex tail module. In addition, CDK8 influences binding of RNA polymerase II to the mediator complex.

# Clinical significance
CDK8 is a colorectal cancer oncogene: the CDK8 gene is amplified in human colorectal tumors, activating -catenin-mediated transcription that drives colon tumorigenesis. However, CDK8 may not be oncogenic in all cell types, and indeed may act as a tumor suppressor in the notch and EGFR signaling pathways. Specifically, CDK8 promotes turnover of the notch intracellular domain, and inhibits EGFR signaling-driven cell fates in C. elegans. Thus, CDK8 may be an oncogene in cancers driven by Wnt/-catenin signaling, but could instead be a tumor suppressor gene in cancers driven by notch or EGFR signaling. In addition, CDK8 promotes transcriptional activation mediated by the tumor suppressor protein p53, indicating that it may have an important role in tumor suppression  Further research is needed to delineate the effects of CDK8 inhibition in different tissues, so for the time being, drugs targeting CDK8 for cancer treatment remain untested in humans.

# As a potential drug target
The natural product cortistatin A is a potent and selective inhibitor of CDK8 and CDK19. Inhibition of CDK8 and CDK19 with cortistatin A suppresses AML cell growth and has anticancer activity in animal models of AML by causing selective and disproportionate up regulation of super-enhancer-associated genes including the cell identity genes CEBPA and IRF8.

# Interactions
Cyclin-dependent kinase 8 has been shown to interact with:
- CCNC
- CREB binding protein
- CRSP3
- MED1
- MED12
- MED14
- MED16
- MED17
- MED21
- MED24
- MED26
- MED6
- Notch proteins
- POLR2A
- SMARCB1
- STAT1
- SREBP