Persius/hicric huggingface dataset:
Anatomical terms of motion
The movement of body structures is accomplished by the contraction of muscles. Muscles may move parts of the skeleton relatively to each other, or may move parts of internal organs relatively to each other. All such movements are classified by the directions in which the affected structures are moved. In human anatomy, all descriptions of position and movement are based on the assumption that the body is in anatomical position.
The prefix hyper- is sometimes added to emphasize movement beyond the normal position, such as in hyperflexion or hyperextension. Such movements can put significant stress on the joints involved. See: Medical terminology
All motions are considered to be a mixture of or a single contribution by the following types of movement.
Most terms of a motion have clear opposites, and as such, are treated below in pairs.

# General motion

# Special motions of the hands and feet

# Other special motions
Some additional motions without clear opposites are as follows:
- Rotation - A motion that occurs when a part turns on its axis.  The head rotates on the neck, as in shaking the head 'no'.
- Circumduction  - The circular (or, more precisely, conical) movement of a body part, such as a ball-and-socket joint or the eye. It consists of a combination of flexion, extension, adduction, and abduction. "Windmilling" the arms or rotating the hand from the wrist are examples of circumductive movement.
- Opposition - A motion involving a grasping motion of the thumb and fingers.
- Reposition - To release an object by spreading the fingers and thumb.
Angioedema natural history

# Natural History
The stomach attacks in angioedema can last anywhere from 1-5 days on average, and can require hospitalization for aggressive pain management and hydration. Abdominal attacks have also been known to cause a significant increase in the patient's white blood cell count, usually in the vicinity of 13-30,000. As the symptoms begin to diminish, the white count slowly begins to decrease, returning to normal when the attack subsides.

# Complications
Possible complications include:
- Anaphylactic reaction.
- Life-threatening airway blockage (if swelling occurs in the throat).

# Prognosis
Angioedema that does not affect the breathing may be uncomfortable, but is usually harmless and goes away in a few days.
Predicting where and when the next episode of edema will occur is impossible. Most patients have an average of one episode per month, but there are also patients who have weekly episodes or only one or two episodes per year. The triggers can vary and include infections, minor injuries, mechanical irritation, operations or stress. In most cases, edema develops over a period of 12-36 hours and then subsides within 2-5 days.
Anidulafungin microbiology

# Microbiology

## Mechanism of Action
Anidulafungin is a semi-synthetic echinocandin with antifungal activity. Anidulafungin inhibits glucan synthase, an enzyme present in fungal, but not mammalian cells. This results in inhibition of the formation of 1,3--D-glucan, an essential component of the fungal cell wall.

## Activity in vitro
Anidulafungin has been shown to be active against Candida albicans, C. glabrata, C. parapsilosis, and C. tropicalis both in vitro and in clinical infections as described in Indications and Usage. Because of the potential for reduced susceptibility to anidulafungin, it is recommended that susceptibility be determined by a standardized method.
Anidulafungin minimal inhibitory concentrations (MICs) were determined for isolates of Candida spp. obtained during clinical studies using a standardized method. However, no correlation between in vitro activity as determined by this method and clinical outcome was established.

## Drug Resistance
Echinocandin resistance is due to point mutations within the genes (FKS1 and FKS2) encoding for subunits in the glucan synthase enzyme complex. There have been reports of Candida isolates with reduced susceptibility to anidulafungin, suggesting a potential for development of drug resistance. The clinical significance of this observation is not fully understood.
Antithyroglobulin antibody

# Overview
Antithyroglobulin antibody (or Thyroid antithyroglobulin antibody or Thyroglobulin antibody) is a test to measure antibodies to a protein called thyroglobulin, which is found in thyroid cells.

# Complete differential diagnosis
A negative test is normal. A negative tests means no antibodies to thyroglobulin are found in blood. A positive test means antithyroglobulin antibodies are found in blood. This may be due to: 
- Grave's disease
- Hashimoto's thyroiditis
- Hypothyroidism
- Myxedema
- Systemic lupus erythematosus (SLE)
- Thyroid cancer
- Thyrotoxicosis
- Type 1 diabetes
Pregnant women and relatives of those with autoimmune thyroiditis may also test positive for these antibodies.
Artificial urinary bladder
Steven C. Campbell, M.D., Ph.D.

# Overview
An artificial urinary bladder is an artificial urinary bladder organ.
On April 4, 2006, it was announced that a team of biologists at the Wake Forest University School of Medicine, led by Professor Anthony Atala, had created the world's first lab-grown organ, a bladder, and transplanted it into a human. Seven people between the ages four and 19, received transplants. The bladders were grown from a small sample of the patients' own bladder tissue, so there was no risk of transplant rejection. Traditionally, damaged urinary bladders are stitched back together using other tissue from the stomach or intestine. Patients with bladders made of intestinal tissues suffer unpleasant side-effects because intestinal tissues reabsorb chemicals that are meant to be eliminated through the urine.

# Development
On January 30, 1999, scientists announced that a lab-grown bladder had been successfully transplanted into dogs. These artificial bladders worked well for almost a year in the dogs. In 2000, a new procedure for creating artificial bladders for humans was developed. This procedure is called an orthotopic neobladder procedure. This procedure involves shaping a part (usually 35 to 40 inches) of a patient's small intestine to form a new bladder.

# Procedure
First a CT scan of the patient is taken, to determine the shape of the bladder that must be created.
Next a tissue sample is taken from the patient's bladder. These cells are grown (this part of the process usually takes 4 weeks), and then layered onto a biodegradable "scaffold" in the shape that the required bladder is to take. Finally, the transplant procedure takes place. The entire bladder along with the biodegradable scaffold is transplanted. Over time, the biodegradable scaffold will degrade within the patient's body.
Auditory brainstem implant
An Auditory Brain Stem Implant (ABI) is a surgically implanted electronic device that provides a sense of sound to a person who is profoundly deaf, due to sensorineural hearing impairment (due to illness or injury damaging the cochlea or auditory nerve, and so precluding the use of a cochlear implant).
The auditory brain stem implant uses similar technology as the cochlear implant, but instead of electrical stimulation being used to stimulate the cochlea, it is instead used to stimulate the brain stem of the recipient.
Only small numbers of recipients are implanted with an auditory brain stem implant, due to the nature of the surgery required to implant the device (as it requires brain surgery to implant the device) and the reduced effectiveness of the implant (when compared to a cochlear implant - most cochlear implant recipients have hearing comparable to normal hearing, but most auditory brain stem implant recipients only have an awareness of sound).
Bare lymphocyte syndrome 2
The bare lymphocyte syndrome, type II (BLS II) is a rare recessive genetic condition in which a group of genes called major histocompatibility complex class II (MHC class II) are not expressed.  The result is that the immune system is severely compromised and cannot effectively fight infection.  Clinically, this is known as a severe combined immunodeficiency (SCID).
The genetic basis for BLSII is not due to defects in the MHC II genes themselves.  The genetic basis is the result of mutations in genes that code for proteins (transcription factors) that normally regulate the expression of the MHC II genes  .  That is, one of the several proteins that are required to switch on MHC II genes in various cells types (primarily those in the immune system) is absent.  The genes responsible were cloned by the laboratories of Bernard Mach  in Switzerland and Jeremy Boss  at Emory University in Atlanta, Georgia.  Mutation in any one of four genes can lead to BLS II.  The genes' names are: class II trans-activator (CIITA), regulatory factor of the X box 5 (RFX5), RFX-associated protein (RFXAP) and RFX ankyrin repeats (RFXANK; also known as RFXB).
Though BLSII is an attractive candidate for gene therapy , bone marrow transplant is currently the only treatment.
  Review article by Bernard Mach et al.
 Review article by Jeremy Boss et al.
Nijmegen breakage syndrome
Nijmegen breakage syndrome (NBS) (also known as Berlin breakage syndrome and Seemanova syndrome) is a rare syndrome characterised by chromosomal instability, probably as a result of a defect in the Double Holliday junction DNA repair mechanism.
It is characterized by microcephaly, a distinct facial appearance, short stature, immunodeficiency, radiation sensitivity and a strong predisposition to lymphoid malignancy. 
It is caused by a mutation in the NBS1 gene. 
The name derives from the Dutch city Nijmegen where the condition was first described.
Most people with NBS have West Slavic origins. The largest number of them live in Poland.
Beta-1 adrenergic receptor
The beta-1 adrenergic receptor (1 adrenoceptor), also known as ADRB1, is a beta-adrenergic receptor, and also denotes the human gene encoding it. It is a G-protein coupled receptor associated with the Gs heterotrimeric G-protein and is expressed predominantly in cardiac tissue.

# Receptor

## Actions
Actions of the 1 receptor include:
The receptor is also present in the cerebral cortex.

## Agonists
Isoprenaline has higher affinity for 1 than adrenaline, which, in turn, binds with higher affinity than noradrenaline at physiologic concentrations. 
Selective agonists to the beta-1 receptor are:
- Denopamine
- Dobutamine (in cardiogenic shock)
- Xamoterol (cardiac stimulant)

## Antagonists
(Beta blockers)
1-selective antagonists include:
- Acebutolol (in hypertension, angina pectoris and arrhythmias)
- Atenolol (in hypertension, coronary heart disease, arrhythmias and myocardial infarction)
- Betaxolol (in hypertension and glaucoma)
- Bisoprolol (in hypertension, coronary heart disease, arrhythmias, myocardial infarction and ischemic heart diseases)
- Esmolol (in arrhythmias)
- Metoprolol (in hypertension, coronary heart disease, myocardial infarction and heart failure)
- Nebivolol (in hypertension)
- Vortioxetine (antidepressant)

## Mechanism in cardiac myocytes
Gs exerts its effects via two pathways. Firstly, it directly opens L-type calcium channels (LTCC) in the plasma membrane. Secondly, it renders adenylate cyclase activated, resulting in an increase of cAMP, activating protein kinase A (PKA) which in turn phosphorylates several targets, such as phospholamban, LTCC, Troponin I (TnI), and potassium channels. Phospholamban phosphorylates deactivates its function which is normally inhibition of SERCA on the sarcoplasmic reticulum (SR) in cardiac myocytes. Due to this, more calcium enters the SR and is therefore available for the next contraction. LTCC phosphorylatation increases its open probability and therefore allows more calcium to enter the myocyte upon cell depolarisation. Both of these mechanisms increase the available calcium for contraction and therefore increase inotropy. Conversely, TnI phosphorylation results in its facilitated dissociation of calcium from troponin C (TnC) which fastens the muscle relaxation (positive lusitropy). Potassium channel phosphorylates increases its open probability which results in shorter refractory period (because the cell repolarises faster), also increasing lusitropy. Furthermore, in nodal cells such as in the SA node, cAMP directly binds to and opens the HCN channels, increasing their open probability, which increases chronotropy.

# Gene
Specific polymorphisms in the ADRB1 gene have been shown to affect the resting heart rate and can be involved in heart failure.

# Interactions
Beta-1 adrenergic receptor has been shown to interact with DLG4 and GIPC1. Interaction between testosterone and -1 ARs have been shown in anxiolytic behaviors in the basolateral amygdala.
Beta-3 adrenergic receptor
The beta-3 adrenergic receptor (3 adrenoreceptor), also known as ADRB3, is a beta-adrenergic receptor, and also denotes the human gene encoding it.

# Function
Actions of the 3 receptor include
- Enhancement of lipolysis in adipose tissue.
- Thermogenesis in skeletal muscle
It is located mainly in adipose tissue and is involved in the regulation of lipolysis and thermogenesis. Some 3 agonists have demonstrated antistress effects in animal studies, suggesting it also has a role in the central nervous system (CNS). 3 receptors are found in the gallbladder, urinary bladder, and in brown adipose tissue. Their role in gallbladder physiology is unknown, but they are thought to play a role in lipolysis and thermogenesis in brown fat. In the urinary bladder it is thought to cause relaxation of the bladder and prevention of urination.

# Mechanism of action
Beta adrenergic receptors are involved in the epinephrine- and norepinephrine-induced activation of adenylate cyclase through the action of the G proteins of the type Gs.

# Ligands

## Agonists
- Amibegron (SR-58611A)
- CL-316,243
- L-742,791
- L-796,568
- LY-368,842
- Mirabegron (YM-178), approved for treatment of overactive bladder in Japan, United States, UK, Canada, China and India.
- Nebivolol selective beta(1)-blocker and beta(3)-agonist.
- Ro40-2148
- Solabegron (GW-427,353)
- Vibegron (MK-4618)

## Antagonists
- L-748,328
- L-748,337
- SR 59230A was thought to be a selective 3 antagonist but later found to also be an antagonist of the 1 receptor.

# Interactions
Beta-3 adrenergic receptor has been shown to interact with Src.
Beta-methylamino L-alanine
-methylamino L-alanine, or BMAA, is a neurotoxin found in the seeds of the cycad. This non-proteinogenic amino acid (very similar to the non-essential amino acid alanine) is produced by cyanobacteria of the genus Nostoc that live on the plant's roots.

# Neurotoxicity
BMAA is considered a possible cause of the amyotrophic lateral sclerosis/parkinsonismdementia complex (ALS/PDC) that has an extremely high rate of incidence among the Chamorro people of Guam. The Chamorro call the condition lytico-bodig.

## Sources of BMAA
In the 1950s, ALS/PDC prevalence ratios and death rates for Chamorro residents of Guam and Rota were 50100 times that of developed countries, including the United States. No demonstrable heritable or viral factors were found for the disease, and a subsequent decline of ALS/PDC after 1955 on Guam, led to the search for responsible environmental agents. The use of cycad (Cycas circinalis) seeds in food and traditional medicine had decreased as the Chamorro population became more Americanized following World War II.
In addition to eating the seeds directly, BMAA may have found its way into human diets by way of biomagnification. Fruit bats, a Chamorro delicacy, may feed on cycad seeds and concentrate the toxin in their flesh. Three museum specimen bats, collected in Guam in the 1950s, contained hundreds of times more BMAA, gram for gram, than cycad seeds.

## BMAA neurotoxic effects
Degenerative locomotor diseases had been described in animals grazing on cycad species, fueling interest in a possible link between the plant and the etiology of ALS/PDC . Subsequent laboratory investigations discovered the presence of BMAA. BMAA induced severe neurotoxicity in rhesus macaques, including:
- limb muscle atrophy
- nonreactive degeneration of anterior horn cells
- degeneration and partial loss of pyramidal neurons of the motor cortex
- behavioral dysfunction
- conduction deficits in the central motor pathway
- neuropathological changes of motor cortex Betz cells
There are reports that low BMAA concentrations can selectively kill cultured motor neurons from mouse spinal cords. In the motor neurons, BMAA activates AMPA-kainate glutamate receptors and boosted production of oxygen radicals.

# Worldwide concerns
The presence of BMAA in cyanobacteria, among the most populous organisms in the world, has raised concerns that humans worldwide may be exposed to levels of BMAA that could be potentially harmful. Cyanobacteria from soil and water samples collected around the world produce BMAA, giving rise to speculative biomagnification in food chains.
Bile salt-dependent lipase
Bile salt-dependent lipase (or BSDL), also known as carboxyl ester lipase (or CEL) is an enzyme produced by the adult pancreas and aids in the digestion of fats. Bile salt-stimulated lipase (or BSSL) is an equivalent enzyme found within breast milk. BSDL has been found in the pancreatic secretions of all species in which it has been looked for. BSSL, originally discovered in the milk of humans and various other primates, has since been found in the milk of many animals including dogs, cats, rats, and rabbits.

# Enzymatic activity
More than 95% of the fat present in human milk and in infant formulas is in the form of triacylglycerols (TG). 
In adults, TGs are thought to be broken down or hydrolyzed mainly by the colipase-dependent lipase enzyme. In the newborn, CDL activity in the duodenum is lower than in adults.
Both BSDL and BSSL have a broad substrate specificity and, like CDL, are capable of hydrolyzing triacylglycerides (in addition to phospholipids, esters of cholesterol, and lipid-soluble vitamins). In particular, they can hydrolyze esters of the essential fatty acids (n-3 and n-6 PUFAs) and DHA. BSDL production in the newborn pancreas is quite low when compared with production in the mammary gland or adult pancreas.
However, newborn infants absorb lipids relatively well, considering the low level of CDL and BSDL they produce. This observation has led to the suggestion that BSDL produced by lactating mammary gland and present within milk, may compensate for the low levels of other TG-digesting enzymes and aid newborns in lipid absorption.
The importance of BSSL in breast milk for the preterm infant nutrition was suggested at 2007.
It was also directly shown recently.
Bioartificial liver device

# Overview
A bioartificial liver device (BAL) is an artificial extracorporeal supportive device for an individual who is suffering from acute liver failure.

# Use
The purpose of BAL-type devices, currently, is not to permanently replace liver functions, but to serve as a supportive device, either allowing the liver to regenerate properly upon acute liver failure, or to bridge the individual's liver functions until a transplant is possible.

# Function
BALs are essentially bioreactors, with embedded hepatocytes (liver cells) that perform the functions of a normal liver. They process oxygenated blood plasma, which is separated from the other blood constituents.
Several types of BALs are being developed, including hollow fiber systems and flat membrane sheet systems.

## Hollow fiber system
One type of BAL is similar to kidney dialysis systems that employ a hollow fiber cartridge. Hepatocytes are suspended in a gel solution, such as collagen, which is injected into a series of hollow fibers. In the case of collagen, the suspension is then gelled within the fibers, usually by a temperature change. The hepatocytes then contract the gel by their attachment to the collagen matrix, reducing the volume of the suspension and creating a flow space within the fibers. Nutrient media is circulated through the fibers to sustain the cells. During use, a patient's blood is fed into the space surrounding the fibers. The fibers, which are composed of a semi-permeable membrane, facilitate transfer of toxins, nutrients and other chemicals between the blood and the suspended cells. The membrane also keeps immune bodies, such as immunoglobulins, from passing to the cells to 
prevent an immune system rejection. 

# Comparison to liver dialysis
The advantages of using a BAL, over other dialysis-type devices (e.g. liver dialysis), is that metabolic functions (such as lipid and plasma lipoprotein synthesis, regulation of carbohydrate homeostasis, production of serum albumin and clotting factors, etc.), in addition to detoxification, can be replicated without the use of multiple devices. There are currently several BAL devices currently in clinical trials.
A series of studies in 2004 showed that a BAL device reduced mortality by about half in acute liver failure cases . The studies, which covered 171 patients in the U.S. and Europe, compared standard supportive care to the use of a bioreactor device using pig liver cells.

# Related Chapters
- Artificial extracorporeal liver support
- Liver dialysis
- Tissue engineering
Biochemical systems theory
Biochemical systems theory is a mathematical modelling framework for biochemical systems, based on ordinary differential equations (ODE), in which biochemical processes are represented using power-law expansions in the variables of the system. This framework, which became known as Biochemical Systems Theory, is developed since the 1960s by Michael Savageau and other groups for systems analysis of biochemical processes. They regard this as a general theory of metabolic control, which includes both metabolic control analysis and flux-oriented theory as special cases.

# Representation
The dynamics of a specie is represented by a differential equation with the structure:
where Xi represents one of the nd variables of the model (metabolite concentrations, protein concentrations or levels of gene expression). j represents the nf biochemical processes affecting the dynamics of the specie. On the other hand, \muij (stoichiometric coefficient), \gammaj (rate constants) and fik (kinetic orders) are two different kinds of parameters defining the dynamics of the system.
The principal difference of power-law models with respect to other ODE models used in biochemical systems is that the kinetic orders can be non-integer numbers. A kinetic order can have even negative value when inhibition is modelled. In this way, power-law models have a higher flexibility to reproduce the non-linearity of biochemical systems.
Models using power-law expansions have been used during the last 35 years to model and analyse several kinds of biochemical systems including metabolic networks, genetic networks and recently in cell signalling.