Persius/hicric huggingface dataset:
Bazin disease overview

# Overview
Bazin disease is a skin ulceration on the back of the calves. It was formerly thought to be a reaction to the tuberculum bacillus. It is very rare now.

# Historical Perspective
Bazin disease is named for Pierre-Antoine-Ernest Bazin.

# Pathophysiology
Bazin disease is a type of panniculitis characterized histologically by the presence of granulomas, vasculitis, and necrosis.

# Causes
Bazin disease was formerly thought to be a reaction to tuberculum bacillus, but it is now considered a panniculitis that is not associated with a single defined pathogen. 

# Epidemiology and Demographics
Bazin disease is seen most commonly in adolescent and menopausal women.

# Risk Factors
Bazin disease is initiated or exacerbated by cold weather.

# Diagnosis

## History and Symptoms
50% of patients will have a past or present history of tuberculosis at extracutaneous site. Patients typically presents as one or more recurrent erythrocyanotic nodules or plaques on the calves.

## Physical Examination
Patients typically presents as one or more recurrent erythrocyanotic nodules or plaques on the calves.
Beck Anxiety Inventory
The Beck Anxiety Inventory (BAI), created by Dr. Aaron T. Beck, is a 21-question multiple-choice self-report inventory that is used for measuring the severity of an individual's anxiety.

# BAI
The BAI consists of twenty-one questions about how the subject has been feeling in the last week. Each question has the same set of four possible answer choices, which are arranged in columns and are answered by marking the appropriate one with a cross. These are:
1. Numbness or tingling
- NOT AT ALL
- MILDLY: It did not bother me much.
- MODERATELY: It was very unpleasant, but I could stand it.
- SEVERELY: I could barely stand it.

# Clinical use
Evidence suggests the scale is best at assessing panic symptomatology. It has been used in a variety of different patient groups, including adolescents and elderly patients.
A 1999 review found that it was the third most used research measure of anxiety, behind the State-Trait Anxiety Inventory and the Fear Survey Schedule.
Beckmann rearrangement
The Beckmann rearrangement, named after the German chemist Ernst Otto Beckmann (1853-1923), is an acid-catalyzed rearrangement of an oxime to an amide.  Cyclic oximes yield lactams.
This example reaction starting with cyclohexanone and forming caprolactam is one of the most important applications of the Beckmann rearrangement, as caprolactam is the feedstock in the production of Nylon 6.
The Beckmann solution consists of acetic acid, hydrochloric acid and acetic anhydride, and was widely used to catalyze the rearrangement.  Other acids, such as sulfuric acid or polyphosphoric acid, can also be used.

# Reaction mechanism
The reaction mechanism of the Beckmann rearrangement is generally believed to consist of an alkyl migration with expulsion of the hydroxyl group to form a nitrilium ion followed by hydrolysis. In one study,  the mechanism is established in silico taking into account the presence of solvent molecules and substituents. The rearrangement of acetone oxime in the Beckmann solution involves three acetic acid molecules and one proton (present as an oxonium ion). In the transition state leading to the iminium ion ( - complex), the methyl group migrates to the nitrogen atom in a concerted reaction and the hydroxyl group is expulsed. The oxygen atom in the hydroxyl group is stabilized by the three acetic acid molecules. In the next step the electrophilic carbon atom in the nitrilium ion is attacked by water and the proton is donated back to acetic acid. In the transition state leading to the N-methyl acetimidic acid, the water oxygen atom is coordinated to 4 other atoms. In the third step, an isomerization step protonates the nitrogen atom leading to the amide.
The same computation with a hydroxonium ion and 6 molecules of water has the same result but when the migrating substituent is phenyl in the reaction of acetophenone oxime with protonated acetic acid the mechanism favors the formation of an intermediate three-membered  - complex. This  - complex is again not found in the H3O+(H2O)6.
With the cyclohexanone-oxime, the relief of ring strain results in a third reaction mechanism leading directly to the protonated caprolactam in a single concerted step without the intermediate formation of a  - complex or  - complex.

# Cyanuric chloride assisted Beckmann reaction
The Beckmann reaction is known to be catalyzed by cyanuric chloride and zinc chloride co-catalyst.  For example, cyclododecanone can be smoothly convered to the corresponding lactam, a monomer for the production of nylon 12.
The reaction mechanism for this reaction is based on a catalytic cycle with cyanuric chloride activating the hydroxyl group via a nucleophilic aromatic substitution. The reaction product is dislodged and replaced by new reactant via an intermediate Meisenheimer complex.
Biological engineering

# Overview
Biological Engineering (including biological systems engineering and bioengineering) is a form of  biotechnology that uses broad-based engineering disciplines of product design, sustainability and analysis to improve and focus utilization of biological systems. 
Biological Engineering is a discipline that applies engineering principles to biological systems for the purpose of developing new technologies of services to improve the living standards of societies. It exploits new developments in molecular biology, biochemistry, cell metabolism, microbiology, ecology and engineering principles and applies them in order to understand living systems and to bring solutions to various problems associated with these systems.
Biological Engineering employs knowledge and expertise from a number of pure and applied sciences, such as: mass and heat transfer, kinetics, biocatalysts, biomechanics, bioinformatics, separation, and purification processes, bioreactor design, surface science, fluid mechanics, thermodynamics, and polymer science that constitute the fundamentals of engineering, and couples them with knowledge in  biological sciences  such as  genetics, molecular biology, protein chemistry, cytology, neurobiology, immunology, ecology, and pharmacology, aiming to solve the different problems of the various sectors of modern societies.
Because other engineering disciplines also address living organisms (e.g., prosthetics in mechanical engineering), the term biological engineering can be applied more broadly to include food engineering and biotechnology. Biological Engineering is called Bioengineering by some colleges and Biomedical engineering is called Bioengineering by others, and is a rapidly developing field with fluid categorization. However, the Main Fields of Biological Engineering may be categorised as:
- Bioprocess Engineering; Bioprocess Design, Biocatalysis, Bioseparation Bioinformatics.
- Genetic Engineering; Synthetic Biology, Cell Engineering, Tissue Culture Engineering, Horizontal gene transfer.
- Biomedical Engineering;  Biomedical technology; Biomedical Diagnosis, Biomedical Therapy, Biomechanics, Biomaterials.
- Agricultural engineering; Ecological Engineering.
Biological Engineers are engineers who use the principles of biology and the tools of engineering to create usable tangible products.  In general, biological engineers attempt to 1) mimic biological systems in order to create products or 2) modify and control biological systems so that they can replace, augment, or sustain chemical and mechanical processes.
Biotinidase deficiency

# Overview
Biotinidase deficiency is an inherited disorder in which the body is not able to process the vitamin biotin properly. Biotin, sometimes called vitamin H, is an important water-soluble vitamin that aids in the metabolism of fats, carbohydrates and proteins.  Biotin Deficiency can result in behavioral disorders, lack of coordination, learning disabilities and seizure. Doses of synthetic Biotin can alleviate and sometimes totally arrest such symptoms.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

## Genetics
Mutations in the BTD gene cause biotinidase deficiency. Biotinidase is the enzyme that is made by the BTD gene. Many mutations that cause the enzyme to be nonfunctional or to be made at extremely low levels have been identified. Biotin is a vitamin that is chemically bound to proteins. (Most vitamins are only loosely associated with proteins.) Without biotinidase activity, the vitamin biotin cannot be separated from foods and therefore cannot be used by the body. Another function of the biotinidase enzyme is to recycle biotin from enzymes that are important in metabolism (processing of substances in cells). When biotin is lacking, specific enzymes called carboxylases cannot process proteins, fats, or carbohydrates. Individuals lacking biotinidase activity can still have normal carboxylases if they ingest small amounts of biotin.
This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell must be altered for a person to be affected by the disorder. Most often, the parents of a child with an autosomal recessive disorder are not affected but are carriers of one copy of the altered gene.

# Differentiating Biotinidase deficiency from Other Diseases

# Epidemiology and Demographics
Approximately 1 in 60,000 newborns are affected by profound (less than 10 percent of normal enzyme activity) or partial (10-30 percent of normal enzyme activity) biotinidase deficiency.

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Incontinentia pigmenti

# Overview
Incontinentia Pigmenti (IP) is a genetic disorder that affects the skin, hair, teeth, and nails.  It is also known as Bloch Sulzberger syndrome, Bloch Siemens syndrome, melanoblastosis cutis and naevus pigmentosus systematicus.

# Presentation
The skin lesions evolve through characteristic stages:
- blistering (from birth to about four months of age),
- a wart-like rash (for several months),
- swirling macular hyperpigmentation (from about six months of age into adulthood), followed by
- linear hypopigmentation.
Alopecia, hypodontia, abnormal tooth shape, and dystrophic nails are observed. Some patients have retinal vascular abnormalities predisposing to retinal detachment in early childhood. Cognitive delays/mental retardation are occasionally seen.

# Diagnosis
The diagnosis of IP is established by clinical findings and occasionally by corroborative skin biopsy. Molecular genetic testing of the IKBKG gene (chromosomal locus Xq28) reveals disease-causing mutations in about 80% of probands. Such testing is available clinically. In addition, females with IP have skewed X-chromosome inactivation; testing for this can be used to support the diagnosis.

## Physical Examination

### Skin
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.
- Incontinentia pigmenti. Adapted from Dermatology Atlas.

# Genetics
IP is inherited in an X-linked dominant manner. IP is lethal in most, but not all, males. A female with IP may have inherited the IKBKG mutation from either parent or have a new gene mutation. Parents may either be clinically affected or have germline mosaicism. Affected women have a 50% risk of transmitting the mutant IKBKG allele at conception; however, most affected male conceptuses miscarry. Thus, the expected ratio for liveborn children is 33% unaffected females, 33% affected females, and 33% unaffected males. Genetic counseling and prenatal testing is available.
In females, the cells expressing the mutated IKBKG gene due to lyonization selectively die around the time of birth so the X-inactivation is extremely skewed.

# History
This disorder was first reported by Bruno Bloch, a German dermatologist in 1926 and Marion Sulzberger, an American dermatologist in 1928.
Blood sugar regulation
Blood sugar regulation is the process by which the levels of blood sugar, primarily glucose, are maintained by the body.

# Mechanisms of blood sugar regulation
Blood sugar levels are regulated by negative feedback in order to keep the body in homeostasis.  The levels of glucose in the blood are monitored by the cells in the pancreas's Islets of Langerhans.  If the blood glucose level falls to dangerous levels (as in very heavy exercise or lack of food for extended periods), the Alpha cells of the pancreas release glucagon, a hormone whose effects on liver cells act to increase blood glucose levels. They  convert glycogen storage into glucose (this process is called glycogenolysis).  The glucose is released into the bloodstream, increasing blood sugar levels.
There are also several other causes for an increase in blood sugar levels. Among them are the 'stress' hormones such as adrenaline, several of the steroids, infections, trauma, and of course, the ingestion of food.
When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from beta cells found in the Islets of Langerhans in the pancreas. This hormone, insulin, causes the liver to convert more glucose into glycogen (this process is called glycogenesis), and to force about 2/3 of body cells (primarily muscle and fat tissue cells) to take up glucose from the blood, thus decreasing blood sugar levels. Insulin also provides signals to several other body systems, and is the chief regulatory metabolic control in humans.
Diabetes mellitus type 1 is caused by insufficient or non-existent production of insulin, while type 2 is primarily due to a decreased response to insulin in the tissues of the body (insulin resistance). Both types of diabetes, if untreated, result in too much glucose remaining in the blood (hyperglycemia) and many of the same complications.  Also, too much insulin and/or exercise without enough corresponding food intake in diabetics can result in low blood sugar (hypoglycemia).

# Hormones that influence blood glucose level
Bloom-Richardson grade

# Overview
The Bloom-Richardson grade (BR grade) is a a histologic grade assigned by pathologists to breast cancers. It is the most common type of cancer grade system currently used. It is a semi-quantitative grading method based on three morphologic features of invasive breast cancers. The morphologic features that are used are:
- degree of tumor tubule formation (percentage of cancer composed of tubular structures)
- tumor mitotic activity (rate of cell division)
- nuclear pleomorphism of tumor cells (nuclear grade, change in cell size and uniformity)
Each of these features is assigned a score ranging from 1 to 3. The scores are then added together for a final sum that will range between 3 to 9. This value is then used to grade the tumor as follows :
- 3-5 Grade 1 tumor (well-differentiated).
- 6-7 Grade 2 tumor (moderately-differentiated).
- 8-9 Grade 3 tumor (poorly-differentiated).
Bloom syndrome protein
Bloom syndrome protein is a protein that in humans is encoded by the BLM gene and is not expressed in Bloom syndrome.
The Bloom syndrome gene product is related to the RecQ subset of DExH box-containing DNA helicases and has both DNA-stimulated ATPase and ATP-dependent DNA helicase activities. Mutations causing Bloom syndrome delete or alter helicase motifs and may disable the 3'  5' helicase activity.  The normal protein may act to suppress inappropriate homologous recombination.

# Meiosis
Recombination during meiosis is often initiated by a DNA double-strand break (DSB). During recombination, sections of DNA at the 5' ends of the break are cut away in a process called resection. In the strand invasion step that follows, an overhanging 3' end of the broken DNA molecule then "invades" the DNA of an homologous chromosome that is not broken. After strand invasion, the further sequence of events may follow either of two main pathways leading to a crossover (CO) or a non-crossover (NCO) recombinant (see Genetic recombination and bottom of Figure in this section).
The budding yeast Saccharomyces cerevisiae encodes an ortholog of the Bloom syndrome (BLM) protein that is designated Sgs1 (Small growth suppressor 1).  Sgs1(BLM) is a helicase that functions in homologous recombinational repair of DSBs.  The Sgs1(BLM) helicase appears to be a central regulator of most of the recombination events that occur during S. cerevisiae meiosis.  During normal meiosis Sgs1(BLM) is responsible for directing recombination towards the alternate formation of either early NCOs or Holliday junction joint molecules, the latter being subsequently resolved as COs.
In the plant Arabidopsis thaliana, homologs of the Sgs1(BLM) helicase act as major barriers to meiotic CO formation.  These helicases are thought to displace the invading strand allowing its annealing with the other 3overhang end of the DSB, leading to NCO recombinant formation by a process called synthesis dependent strand annealing (SDSA) (see Genetic recombination and Figure in this section).  It is estimated that only about 4% of DSBs are repaired by CO recombination.  Sequela-Arnaud et al. suggested that CO numbers are restricted because of the long-term costs of CO recombination, that is, the breaking up of favorable genetic combinations of alleles built up by past natural selection.

# Interactions
Bloom syndrome protein has been shown to interact with:
- ATM,
- CHAF1A,
- CHEK1,
- FANCM,
- FEN1,
- H2AFX,
- MLH1
- P53,
- RAD51L3,
- RAD51,
- RPA1,
- TOP3A,
- TP53BP1,
- WRN,  and
- XRCC2.
Boceprevir description

# Description
VICTRELIS (boceprevir) is an inhibitor of the hepatitis C virus (HCV) non-structural protein 3 (NS3) serine protease.
Boceprevir has the following chemical name: (1R,5S)-N--3-carbonyl]amino]-3,3-dimethyl-1-oxobutyl]-6,6-dimethyl-3-azabicyclohexan-2(S)-carboxamide. The molecular formula is C27H45N5O5 and its molecular weight is 519.7. Boceprevir has the following structural formula:
Boceprevir is manufactured as an approximately equal mixture of two diastereomers. Boceprevir is a white to off-white amorphous powder. It is freely soluble in methanol, ethanol and isopropanol and slightly soluble in water.
VICTRELIS 200 mg capsules are available as hard gelatin capsules for oral administration. Each capsule contains 200 mg of boceprevir and the following inactive ingredients: sodium lauryl sulfate, microcrystalline cellulose, lactose monohydrate, croscarmellose sodium, pre-gelatinized starch, and magnesium stearate. The red capsule cap consists of gelatin, titanium dioxide, D&C Yellow #10, FD&C Blue #1, and FD&C Red #40. The yellow capsule body contains gelatin, titanium dioxide, D&C Yellow #10, FD&C Red #40, and FD&C Yellow #6. The capsule is printed with red and yellow ink. The red ink contains shellac and red iron oxide, while the yellow ink consists of shellac, titanium dioxide, povidone and D&C Yellow #10 Aluminum Lake.
Bone fracture overview

# Overview
A bone fracture is a medical condition in which a bone is cracked or broken.  While many fractures are the result of high force impact or stress,  bone fracture can also occur as a result of certain medical conditions that weaken the bones, such as osteoporosis, certain types of cancer or osteogenesis imperfecta.

# Historical Perspective
Any type of bone break is a fracture. The word break is not used in formal orthopedic terminology.

# Risk Factors
Fractures commonly occur because of falls or sports injuries. Additionally, overuse can cause stress fractures, which are very small cracks in the bone. Therefore, those who participate in rigorous physical activities or in high risk activities are more likely to get a fracture. Another common cause of fractures is osteoporosis, which causes weakening of the bones.  People with this condition, especially the elderly, are at higher risk of fractures due to falls since their bones cannot withstand as much stress.

# Diagnosis
A bone fracture can be diagnosed clinically based on the medical history given and the physical examination performed. Imaging by X-ray is often performed to view the bone suspected of being fractured. In situations where x-ray alone is insufficient, a computed tomograph (CT scan) may be performed.

## X Ray
At the hospital, closed fractures are diagnosed by taking an X-ray photograph of the injury.
Boord olefin synthesis
The Boord olefin synthesis is an organic reaction forming alkenes from ethers carrying a halogen atom 2 carbons removed from the oxygen atom (-halo-ethers) catalyzed by a metal such as magnesium or zinc.  The reaction, discovered by Cecil E. Boord in 1930  is a classic named reaction with high yields and broad scope .
The reaction type is an elimination reaction with magnesium forming an intermediate Grignard reagent. The alkoxy group is a poor leaving group and therefore a E1cB elimination reaction mechanism is proposed .The original publication describes the organic synthesis of the compound isoheptene in several steps with the elimination the final one:
In a 1931 publication   the scope is extended to 1,4-dienes with magnesium replaced by zinc (see also: Barbier reaction). In the first part of the reaction the allyl Grignard acts as a nucleophile in nucleophilic aliphatic substitution.
Bosniak classification
The Bosniak classification system was designed to separate cystic renal masses into surgical and nonsurgical categories by analysis of specific CT features.

# Category I
Category I lesions are simple benign cysts showing homogeneity, water content, and a sharp interface with adjacent renal parenchyma, with no wall thickening, calcification, or enhancement.

# Category II
This category consists of cystic lesions with one or two thin ( 1 mm advances the lesion into surgical category III) and hyperdense benign cysts with all the features of category I cysts except for homogeneously high attenuation. A benign category II lesion must be 3 cm or less in diameter, have one quarter of its wall extending outside the kidney so the wall can be assessed, and be nonenhancing after contrast material is administered.

## Category IIF
This category consists of minimally complicated cysts that need follow-up. This is a group not well defined by Bosniak but consists of lesions that do not neatly fall into category II. These lesions have some suspicious features that deserve follow-up to detect any change in character.

# Category III
Category III consists of true indeterminate cystic masses that need surgical evaluation, although many prove to be benign. They may show uniform wall thickening, nodularity, thick or irregular peripheral calcification, or a multilocular nature with multiple enhancing septa. Hyperdense lesions that do not fulfill category II criteria are included in this group.

# Category IV
These are lesions with a nonuniform or enhancing thick wall, enhancing or large nodules in the wall, or clearly solid components in the cystic lesion. Enhancement was considered present when lesion components increased by at least 10 H.