Persius/hicric huggingface dataset:
Barton-McCombie deoxygenation
The Barton-McCombie deoxygenation is an organic reaction in which an hydroxy functional group in an organic compound is replaced by a proton to an alkane . It is named for the British chemists Sir Derek Harold Richard Barton (19181998) and Stuart W. McCombie.
This deoxygenation reaction is a radical substitution. In the related Barton decarboxylation the reactant is a carboxylic acid.

# Mechanism
The reaction mechanism consists of a catalytic radical initiation step and a propagation step.  The alcohol (1) is first converted into a xanthate (2). The other reactant tributyltin hydride 3 is decomposed by AIBN 8 into a tributyltin radical 4. The tributyltin radical abstracts the xanthate group from 2 leaving an alkyl radical 5 and tributyltin xanthate (7). The sulfur tin bond in this compound is very stable and provides the driving force for this reaction. The alkyl radical in turn abstracts a proton from a new molecule of tributyltin hydride generating the desired deoxygenated product (6) and a new radical species ready for propagation.

# Variations

## Alternative hydride sources
Main disadvantage of this reaction is the use of the tin hydride which is toxic, expensive and difficult to remove from the reaction mixture. One alternative is the use of tributyltin anhydride as the radical source and poly(methylhydridesiloxane) (PMHS) as the hydride source . Phenyl chlorothionoformate used as the starting material ultimately generates carbonyl sulfide.

## Trialkyl boranes
An even more convenient proton donor is provided by trialkylborane-water complexes  such as trimethylborane contaminated with small amounts of water.
In this catalytic cycle the reaction is initiated by air oxidation of the trialkylborane 3 by air to the methyl radical 4. This radical reacts with the xanthate 2 to  S-methyl-S-methyl dithiocarbonate 7 and the radical intermediate 5. The CH3B.H2O complex 3 provides a proton for recombining with this radical to the alkane 6 leaving behind diethyl borinic acid and a new methyl radical.
It is found by theoretical calculations that that a O-H homolysis reaction in the borane-water complex is endothermic with an energy similar to that of the homolysis reaction in tributyltin hydride but much lower than the homolysis reaction of pure water.

# Examples
A variation of this reaction was used as one of the steps in the total synthesis of azadirachtin :
Belousov-Zhabotinsky reaction

# Overview
A Belousov-Zhabotinsky reaction, or BZ reaction, is one of a class of reactions that serve as a classical example of non-equilibrium thermodynamics, resulting in the establishment of a nonlinear chemical oscillator. The only common element in these oscillating systems are the inclusion of bromine and an acid. The reactions are theoretically important in that they show that chemical reactions do not have to be dominated by  equilibrium thermodynamic behavior. These reactions are far from equilibrium and remain so for a significant length of time. In this sense, they provide an interesting chemical model of nonequilibrium biological phenomena, and the mathematical model of the BZ reactions themselves are of theoretical interest.
An essential aspect of the BZ reaction is its so called "excitability"- under the influence of stimuli, patterns develop in what would otherwise be a perfectly quiescent medium. Some clock reactions such as Briggs-Rauscher and BZ using the chemical ruthenium bipyridyl as catalyst can be excited into self-organising activity through the influence of light.
The discovery of the phenomenon is credited to Boris Belousov. He noted, sometime in the 1950s (the dates change depending on source, but it ranges from 1951 to 1958), that in a mix of potassium  bromate, cerium(IV) sulfate, propanedioic acid and citric acid in dilute sulfuric acid, the ratio of concentration of the cerium(IV) and cerium(III) ions oscillated, causing the colour of the solution to oscillate between a yellow solution and a clear solution. This is due to the cerium(IV) ions being reduced by propanedioic acid to cerium(III) ions, which are then oxidized back to cerium(IV) ions by bromate(V) ions.
Belousov made two attempts to publish his finding, but was rejected on the grounds that he could not explain his results to the satisfaction of the editors of the journals to which he submitted his results. His work was finally published in a less respectable, non-reviewed journal.
Later, in 1961, a graduate student named A. M. Zhabotinsky rediscovered this reaction sequence; however, the results of these men's work were still not widely disseminated, and was not known in the West until a conference in Prague in 1968.
There are a number of BZ cocktails available in the chemical literature and on the web. A complex of phenanthroline and iron is a common indicator. These reactions, if carried out in petri dishes, result in the formation first of colored spots. These spots grow into a series of expanding concentric rings or perhaps expanding spirals similar to the patterns generated by a cyclic cellular automaton. The colors disappear if the dishes are shaken, and then reappear. The waves continue until the reagents are consumed. The reaction can also be performed in a beaker using a magnetic stirrer.
Andrew Adamatzky, a computer scientist in the University of the West of England reported on liquid logic gates using the BZ reaction.
Benign paroxysmal torticollis

# Overview
Benign paroxysmal torticollis (BPT) is a rare medical disorder affecting infants.

# Symptoms and Characteristics
The defining characteristic of BPT is a tilting of an infants head in recurrent episodes, for varying periods of time. Furthermore, the childs trunk may bend in the same direction as the head, giving the baby an overall curved shape; this complaint is known as tortipelvis. In addition to this, the individual may also, but not necessarily, experience vomiting, pallor, ataxia, agitation, infantile migraine, unsteadiness of gait upon learning to walk, general malaise and nystagmus.
The periods in which the childs head is tilted and other symptoms appear can last anywhere from a few minutes to a few weeks, with a frequency of anywhere from two per year to two per month.

# Causes
The cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.

# Pathophysiology
The mechanism of action of benign paroxysmal torticollis is not yet understood. It has been suggested that unilateral vestibular dysfunction or vascular disturbance in the brain stem may be responsible for the condition.

# Diagnosis
Diagnosis of BPT can be difficult because it is rare.

# Treatment
No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

# Prognosis
Benign paroxysmal torticollis disappears in the early years of life with no medical intervention.
However, some cases of benign paroxysmal torticollis cases can evolve into benign paroxysmal vertigo of childhood, migrainous vertigo or typical migraines.

# History
The condition was first described by CH Snyder in 1969 in an article titled Paroxysmal torticollis in infancy. A possible form of labyrinthitis. in the American Journal of Diseases of Children.
Seyferth-Gilbert homologation
The Seyferth-Gilbert homologation is a the chemical reaction of an aryl ketone 1 (or aldehyde) with dimethyl (diazomethyl)phosphonate 2 and potassium tert-butoxide to give substituted alkynes 3. Dimethyl (diazomethyl)phosphonate 2 is often called the Seyferth-Gilbert reagent.
This reaction is called a homologation because the product has exactly one additional carbon more than the starting material.

# Reaction mechanism
Deprotonation of the Seyferth-Gilbert reagent A give an anion B which reacts with the ketone to form the oxaphosphatane D.  Elimination of dimethylphosphate E gives the vinyl diazo-intermediate Fa and Fb.  The generation of nitrogen gas gives a vinyl carbene G which via a 1,2-migration forms the desired alkyne H.

# Bestmann modification
Dimethyl (diazomethyl)phosphonate can be generated in situ from dimethyl-1-diazo-2-oxopropylphosphonate (also called Bestmann's reagent) by reaction with methanol and potassium carbonate.  Reaction of Bestmann's reagent with aldehydes gives terminal alkynes often in very high yield.
The use of the milder potassium carbonate makes this procedure much more compatible with a wide variety of functional groups.
Bladder sphincter dyssynergia
Steven C. Campbell, M.D., Ph.D.

# Overview
Bladder sphincter dyssynergia or more technically detrusor sphincter dysynergia (DSD) is a consequence of a neurological condition such as spinal injury or multiple sclerosis (MS) where the contraction of the bladder musculature is not coordinated with the relaxation of the sphincter. Instead of the urethra relaxing completely during voiding it dyssynergically contracts causing the flow to be interrupted and the detrusor pressure to rise.
On cystography there is an irregular appearance of the bladder outline due to muscular contraction against the unrelaxed bladder sphincter. People with this condition generally have daytime and night time wetting and often have a history of urinary tract infections. Constipation and encopresis are often associated with this condition.
Strictly DSD can only be diagnosed from an EMG trace or x-ray findings, but the trace in the image shows both the pressure and flow phenomena mentioned.
de:Detrusor-Sphinkter-Dyssynergie
Bone morphogenetic protein 8B
Bone morphogenetic protein 8B is a protein that in humans is encoded by the BMP8B gene.
The protein encoded by this gene is a member of the TGF- superfamily. It has close sequence homology to BMP7 and BMP5 and is believed to play a role in bone and cartilage development. It has been shown to be expressed in the hippocampus of murine embryos.
The bone morphogenetic proteins (BMPs) are a family of secreted signaling molecules that can induce ectopic bone growth. Many BMPs are part of the transforming growth factor-beta (TGFB) superfamily. BMPs were originally identified by an ability of demineralized bone extract to induce endochondral osteogenesis in vivo in an extraskeletal site. Based on its expression early in embryogenesis, the BMP encoded by this gene has a proposed role in early development. In addition, the fact that this BMP is closely related to BMP5 and BMP7 has led to speculation of possible bone inductive activity.
Bowlegs (patient information)
For the WikiDoc page for this topic, click here

# Overview
Bowlegs is a condition in which the knees stay wide apart when a person stands with the feet and ankles together. In children under 18 months, it is considered normal.

# What are the symptoms of Bowlegs?
- Knees do not touch when standing with feet together (ankles touching)
- Bowing of legs is same on both side of the body (symmetrical)
- Bowed legs continue beyond age 3

# What causes Bowlegs?
Infants are born bowlegged because of their folded position in the uterus. The infant's bowed legs begin to straighten once the child starts to walk and the legs begin to bear weight (about 12 to 18 months old).
By around age 3, the child can usually stand with the ankles apart and the knees just touching. If the bowed legs are still present, the child is called bowlegged.
Bowlegs may be caused by illnesses such as:
- Blount's disease
- Bone dysplasias (abnormal development)
- Fractures that do not heal correctly
- Lead or fluoride poisoning
- Rickets, which is caused by a vitamin D deficiency

# Diagnosis
A doctor can often diagnose bowlegs by simply looking at the child. The distance between the knees is measured while the child is lying on the back.
Blood tests may be needed to rule out rickets.
X-rays may be needed if:
- The child is 3 years old or older
- The bowing is getting worse
- Bowing is not the same on both sides
- Other test results suggest disease

# When to seek urgent medical care?
Call your health care provider if your child shows persistent or worsening bowed legs after age 3.

# Treatment options
No treatment is recommended for bowlegs unless the condition is extreme. The child should be seen by the health care provider at least every 6 months.
If the condition is severe or the child also has another disease, special shoes, braces, or casts can be tried. It is unclear how well these work.
At times, surgery is performed to correct the deformity in an adolescent with severe bowlegs.

# Where to find medical care for Bowlegs?
Directions to Hospitals Treating Bowlegs

# What to expect (Outlook/Prognosis)?
In many cases the outcome is good, and there is usually no problem walking.

# Possible complications
Bowlegs that does not go away and is not treated may lead to arthritis in the knees or hips over time.

# Prevention of Bowlegs
There is no known way to prevent bowlegs, other than to avoid rickets. Make sure your child has normal exposure to sunlight and appropriate levels of vitamin D in the diet.

# Sources
Sabinas brittle hair syndrome

# Overview
Sabinas brittle hair syndrome, also called Sabinas syndrome or brittle hair-mental deficit syndrome, is a hereditary disease affecting the integumentary system.

# Diagnosis
Symptoms include brittle hair, mild mental retardation and nail dysplasia. The syndrome was first observed in Sabinas, a small community in northern Mexico.
The principal biochemical features of the illness are reduced hair cystine levels, increased copper/zinc ratio, and presence of arginosuccinic acid in the blood and urine.

# Inheritance
File:Autorecessive.svg
Sabinas brittle hair syndrome is transmitted as an autosomal recessive genetic trait.
Bronchial hyperresponsiveness

# Overview
Bronchial hyperresponsiveness (or other combinations with airway or hyperreactivity) is a state characterised by easily triggered bronchospasm (contraction of the bronchioles or small airways).

# Bronchial Hyperresponsiveness
- Bronchial hyperresponsiveness can be assessed with a bronchial challenge test. This most often uses products like metacholine or histamine. These chemicals trigger bronchospasm in normal individuals as well, but people with bronchial hyperresponsiveness have a lower threshold.
- Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people suffering from chronic obstructive pulmonary disease (COPD). In the Lung Heart Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other factors. In asthma it tends to be reversible with bronchodilator therapy, while this is not the case in COPD.
C-C chemokine receptor type 6
Chemokine receptor 6 also known as CCR6 is a  CC chemokine receptor protein which in humans is encoded by the CCR6 gene.  CCR6 has also recently been designated CD196 (cluster of differentiation 196).

# Function
This protein belongs to family A of G protein-coupled receptor superfamily. The gene is preferentially expressed by immature dendritic cells and memory T cells. The ligand of this receptor is macrophage inflammatory protein 3 alpha (MIP-3 alpha). This receptor has been shown to be important for B-lineage maturation and antigen-driven B-cell differentiation, and it may regulate the migration and recruitment of dendritic and T cells during inflammatory and immunological responses. Alternatively spliced transcript variants that encode the same protein have been described for this gene.

# Molecular biology
The gene is located on the long arm of Chromosome 6 (6q27) on the Watson (plus) strand. It is 139,737 bases long and encodes a protein of 374 amino acids (molecular weight 42,494 Da).

# Clinical significance
CCR6 has been associated with Crohn's disease.
Expression of CCR6 was found to be up-regulated in colorectal cancer. Novel research has identified a microRNA that is able to downregulate CCR6 in cancer cell lines.
C-C chemokine receptor type 7
C-C chemokine receptor type 7 is a protein that in humans is encoded by the CCR7 gene. Two ligands have been identified for this receptor: the chemokines (C-C motif) ligand 19 (CCL19/ELC) and (C-C motif) ligand 21 (CCL21).
CCR7 has also recently been designated CD197 (cluster of differentiation 197).

# Function
The protein encoded by this gene is a member of the G protein-coupled receptor family. This receptor was identified as a gene induced by the Epstein-Barr virus (EBV), and is thought to be a mediator of EBV effects on B lymphocytes. This receptor is expressed in various lymphoid tissues and activates B and T lymphocytes. CCR7 has been shown to stimulate dendritic cell maturation. CCR7 is also involved in homing of T cells to various secondary lymphoid organs such as lymph nodes and the spleen as well as trafficking of T cells within the spleen.
Activation of Dendritic cells in peripheral tissues induces CCR7 expression on the cell's surface, which recognize CCL19 and CCL21 produced in the Lymph node and increases dendritic cell expression of co-stimulation molecules (B7), and MHC class I or MHC class II.

# Clinical significance
CCR7 is expressed by various cancer cells, such as nonsmall lung cancer, gastric cancer and oesophageal cancer. Expression of CCR7 by cancer cells is linked with metastasis to lymph nodes.
cGMP-dependent protein kinase
cGMP-dependent protein kinase or Protein Kinase G (PKG) is a serine/threonine-specific protein kinase that is activated by cGMP. It phosphorylates a number of biologically important targets and is implicated in the regulation of smooth muscle relaxation, platelet function, sperm metabolism, cell division, and nucleic acid synthesis.

# Genes and proteins
PKG are serine/threonine kinases that are present in a variety of eukaryotes ranging from the unicellular organism Paramecium to humans. Two PKG genes, coding for PKG type I (PKG-I) and type II (PKG-II), have been identified in mammals. The N-terminus of PKG-I is encoded by two alternatively spliced exons that specify for the PKG-I and PKG-I isoforms. PKG-I is activated at ~10-fold higher cGMP concentrations than PKG-I. The PKG-I and PKG-II are homodimers of two identical subunits (~75 kDa and ~85 kDa, respectively) and share common structural features.
Each subunit is composed of three functional domains:
- (1) an N-terminal domain that mediates homodimerization, suppression of the kinase activity in the absence of cGMP, and interactions with other proteins including protein substrates
- (2) a regulatory domain that contains two non-identical cGMP-binding sites
- (3) a kinase domain that catalyzes the phosphate transfer from ATP to the hydroxyl group of a serine/threonine side chain of the target protein
Binding of cGMP to the regulatory domain induces a conformational change which stops the inhibition of the catalytic core by the N-terminus and allows the phosphorylation of substrate proteins. Whereas PKG-I is predominantly localized in the cytoplasm, PKG-II is anchored to the plasma membrane by N-terminal myristoylation.

# Tissue distribution
In general, PKG-I and PKG-II are expressed in different cell types.
- PKG-I has been detected at high concentrations (above 0.1 mol/L) in all types of smooth muscle cells (SMCs) including vascular SMCs and in platelets. Lower levels are present in vascular endothelium and cardiomyocytes. The enzyme is also expressed in fibroblasts, certain types of renal cells and leukocytes, and in specific regions of the nervous system, for example in the hippocampus, in cerebellar Purkinje cells, and in dorsal root ganglia. Neurons express either the PKG-I or the PKG-I isoform, platelets predominantly I, and both isoforms are present in smooth muscle.
- PKG-II has been detected in renal cells, zona glomerulosa cells of the adrenal cortex, club cells in distal airways, intestinal mucosa, pancreatic ducts, parotid and submandibular glands, chondrocytes, and several brain nuclei, but not in cardiac and vascular myocytes.
Specifically, in smooth muscle tissue, PKG promotes the opening of calcium-activated potassium channels, leading to cell hyperpolarization and relaxation, and blocks agonist activity of phospholipase C, reducing liberation of stored calcium ions by inositol triphosphate.

# Role in cancer
Cancerous colon cells stop producing PKG, which apparently limits beta-catenin thus allowing the VEGF enzyme to solicit angiogenesis.
Congenital muscular dystrophy
Congenital muscular dystrophy (CMD) is the term used to describe muscular dystrophy that is present at birth. CMD describes a number of autosomal recessive diseases of muscle weakness and possible joint deformities, present at birth and slowly progressing. Life expectancies for affected individuals vary, although some forms of CMD do not affect life span at all.
All such known dystrophies are genetically recessive and result from mutations in a variety of different genes, including those encoding the laminin-2 chain, fukutin-related protein, LARGE and fukutin, amongst others.  Currently there is no cure. Physical and occupational therapy, surgery, wheelchairs and other assistive technology may be helpful.

# Classification
A classification for CMDs had been proposed in 2004 by Muntoni and Voit, based on genetic mutation.
- Genes encoding for structural proteins of the basal membrane or extracellular matrix of the skeletal muscle fibres.
Laminin-2deficient CMD (MDC1A)
Ullrich CMD (UCMDs 1, 2 and 3)
Integrin-7 deficiency (ITGA7)
- Laminin-2deficient CMD (MDC1A)
- Ullrich CMD (UCMDs 1, 2 and 3)
- Integrin-7 deficiency (ITGA7)
- Genes encoding for putative or demonstrated glycosyltransferases, that in turn affect the glycosylation of dystroglycan, an external membrane protein of the basal membrane.
Walker-Warburg syndrome
MEB disease
Fukuyama CMD (FCMD)
CMD plus secondary laminin deficiency 1 (MDC1B)
CMD plus secondary laminin deficiency 2 (mutation in fukitin-related protein, MDC1C)
CMD with mental retardation and pachygyria (mutation in LARGE, MDC1D)
- Walker-Warburg syndrome
- MEB disease
- Fukuyama CMD (FCMD)
- CMD plus secondary laminin deficiency 1 (MDC1B)
- CMD plus secondary laminin deficiency 2 (mutation in fukitin-related protein, MDC1C)
- CMD with mental retardation and pachygyria (mutation in LARGE, MDC1D)
- Rigid spine with muscular dystrophy Type 1 (RSMD1): deficiency of selenoprotein-N, an endoplasmic reticulum protein of unknown function.
Cannabis flower essential oil
Cannabis flower essential oil, also known as hemp essential oil, is obtained by steam distillation from the flowers and upper leaves of the Cannabis plant. It should not be confused with Hemp oil which is a vegetable oil that is expeller pressed from the seeds of low-THC varieties of hemp like Anka, Crag, Finola, and USO.
A pale yellow liquid, cannabis flower essential oil is a volatile oil that is a mixture of volatile compounds, including monoterpenes, sesquiterpenes, and other terpenoid-like compounds. It is manufactured primarily in France and Switzerland from both low-THC and high-THC varieties of Cannabis.
This essential oil is used as a scent in perfumes, cosmetics, soaps, and candles. It is also used as a flavoring in foods, primarily candy and beverages. Its use in lollies has created quite a lot of controversy in England, Russia, and the United States.
Cannabis flower essential oil is deliberately manufactured to contain no significant amounts of THC and is therefore not a psychoactive drug.