Persius/hicric huggingface dataset:
Macrophagic myofasciitis

# Overview
Macrophagic Myofasciitis, or MMF, is a rare muscle disease identified in 1993.  The disease is characterized by microscopic lesions found in muscle biopsies that show infiltration of muscle tissue by PAS-positive macrophages.  
Specific causes of MMF are unknown. Intramuscular injections aluminium-containing vaccines have been implicated. Many of those affected with the disease had previously been treated for malaria with chloroquine or hydroxychloroquine for malaria.
Clinical symptoms include muscle pain, joint pain, muscle weakness, fatigue, fever, and muscle tenderness.  A diagnosis can only be identified with an open muscle biopsy of the vaccinated muscle.
Studies at the University of Paris have shown that MMF lesions result when the aluminum hydroxide adjuvant from a vaccine remains embedded in the tissue and causes a steady immune reaction.
Major intrinsic proteins
Major intrinsic proteins are a large family of transmembrane protein channels that are grouped together on the basis of sequence similarities. Proteins from this family exhibit essentially two distinct types of channel properties: (1) specific water
transport by the aquaporins, and (2) small neutral solutes
transport, such as glycerol by the glycerol facilitators.

# Examples
MIP family includes the following channels:
- Mammalian major intrinsic protein (MIP). MIP is the major component of lens fibre gap junctions.
- Mammalian aquaporins. These proteins form water- specific channels that provide the plasma membranes of red cells and kidney prox imal and collecting tubules with high permeability to water, thereby permitting water to move in the direction of an osmotic gradient.
- Soybean nodulin-26, a major component of the peribacteroid membrane induced during nodulation in legume roots after Rhizobium infection.
- Plants tonoplast intrinsic proteins (TIP). There are various isoforms of TIP : alpha (seed), gamma, Rt (root), and Wsi (water-stress induced). These proteins may allow the diffusion of water, amino acids and/or peptides from the tonoplast interior to the cytoplasm..
- Bacterial glycerol facilitator protein (gene glpF), which facilitates the movement of glycerol across the cytoplasmic membrane.
- Salmonella typhimurium propanediol diffusion fac ilitator (gene pduF).
- Yeast FPS1, a glycerol uptake/efflux facilitator protein.
- Drosophila neurogenic protein 'big brain' (bib). This protein may mediate in tercellular communication; it may functions by allowing the transport of certain molecules(s) and thereby sending a signal for an exodermal cell to become an ep idermoblast instead of a neuroblast.
- Yeast hypothetical protein YFL054c.
- A hypothetical protein from the pepX region of Lactococcus lactis.

# Structure
MIP family proteins are thought to contain 6 TM domains. Sequence analysis suggests that the proteins may have arisen through tandem, intragenic duplication from an ancestral protein that contained 3 TM domains.
Some of the proteins in this group are responsible for the molecular basis of the blood group antigens, surface markers on the outside of the red blood cell membrane. Most of these markers are proteins, but some are carbohydrates a ttached to lipids or proteins. Aquaporin-CHIP (Aquaporin 1) belo ngs to the Colton blood group system and is associated with Co(a/b) antigen.

# Subfamilies
- Aquaporin InterPro: IPR012269

# Human proteins containing this domain
AQP1,
AQP2,
AQP3,
AQP4,
AQP5,
AQP6,
AQP7,
AQP8,
AQP9,
AQP10,
MIP
Malate-aspartate shuttle

# Overview
The malate-aspartate shuttle (sometimes also the malate shuttle) is a biochemical system for translocating electrons produced during glycolysis across the impermeable inner membrane of the mitochondrion for oxidative phosphorylation in eukaryotes. This allows the reduction equivalents of the cofactor NADH produced in the cytosol to reach the electron transport chain in the mitochondria and generate ATP. The shuttle system is required because the inner membrane is impermeable to NADH and its oxidized form NAD+.

# Components
It consists of four protein parts:
- malate dehydrogenase in the mitochondrial matrix and intermembrane space.
- aspartate aminotransferase in the mitochondrial matrix and intermembrane space.
- Malate-alpha-Ketoglutarate antiporter in the inner membrane.
- Glutamate-Aspartate antiporter in the inner membrane.

# Mechanism
The key enzyme in the malate-aspartate shuttle is malate dehydrogenase; in the cytosol, it reacts with oxaloacetate and NADH to produce malate and NAD+. The first of two antiporters in the inner membrane imports malate into the mitochondrial matrix and simultaneously exports alpha-ketoglutarate into the cytosol. In the matrix, the reverse reaction catalyzed by the same enzyme produces NADH and oxaloacetate from the newly imported malate and internal NAD+. A transaminase enzyme in the matrix reacts oxaloacetate and glutamate to form aspartate and alpha-ketoglutarate. A second antiporter exports aspartate from the matrix back to the cytoplasm while simultaneously importing glutamate. Finally, in the cytosol, another transaminase reacts aspartate and alpha-ketoglutarate to re-form glutamate and oxaloacetate.
The net effect of the malate-aspartate shuttle is purely redox: NADH in the cytosol is oxidized to NAD+, and NAD+ in the matrix is reduced to NADH. The NAD+ in the cytosol can then be reduced again by another round of glycolysis, and the NADH in the matrix can be used to pass electrons to the electron transport chain so that ATP can be synthesized.
Since the malate-aspartate shuttle regenerates NADH inside of the mitochondrial matrix it is capable of maximizing the number of ATP produced in glycolysis (2.5/NADH). Compare this to the glycerol 3-phosphate shuttle, which donates electrons to Complex II of the electron transport chain (similar to FADH2), and is only capable of generating 1.5 ATP per NADH generated in glycolysis.
Malignant transformation

# Overview
Malignant transformation is the process by which cells acquire the properties of cancer. This may occur as a primary process in normal tissue, or secondarily as malignant degeneration of a previously existing benign tumor.
There are many causes of primary malignant transformation, or tumorigenesis.  The underlying commonality is genetic mutation either by inheritance or more commonly by acquiring mutations in one's DNA over time.  Although malignant transformation may occur because of changes within the cell, it can be induced by inorganic toxic substances such as cadmium or arsenite and organics such as tobacco-specific nitrosamines. It is also thought that some malignant transformations are due to viruses such as the Epstein-Barr virus, although this is currently restricted to just a few cancer types.  A more common cancer associated with viral infection is cervical cancer, which has been linked to the human papilloma virus.
Malignant transformation of cells in a benign tumor may be detected by pathologic examination of tissues. Often the clincial signs and symptoms are suggestive of a malignant tumor.  The physician, during the medical history examination, can find that there have been changes in size or patient sensation and, upon direct examination, that there has been a change in the lesion itself.
Risk assessments can be done and are known for certain types of benign tumor which are known to undergo malignant transformation. One of the better known examples of this phenomenon is the progression of a nevus to melanoma.

# Related chapters
- Teratoma with malignant transformation
- Richter's transformation in blood cancers
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Masson's trichrome stain
Masson's trichrome is a three-color staining protocol used in histology. The recipes evolved from the original Masson's formulation to different specific applications, but all are suited for distinguishing cells from surrounding connective tissue.
Most recipes produce red keratin and muscle fibers, blue or green collagen and bone, light red or pink cytoplasm, and dark brown to black cell nuclei.
The trichrome is applied by immersion of the fixated sample into Weigert's iron hematoxylin, and then three different solutions, labeled A, B, and C:
- Weigert's hematoxylin is a sequence of three solutions: ferric chloride in diluted hydrochloric acid, hematoxylin in 95% ethanol, and potassium ferricyanide solution alkalized by sodium borate. It is used to stain the nuclei.
- Solution A, also called plasma stain, contains acid fuchsin, Xylidine Ponceau, glacial acetic acid, and distilled water. Other red acid dyes can be used, eg. the Biebrich scarlet in Lillie's trichrome.
- Solution B contains phosphomolybdic acid in distilled water.
- Solution C, also called fibre stain, contains Light Green SF yellowish, or alternatively Fast Green FCF. It is used to stain collagen. If blue is preferred to green, methyl blue, water blue or aniline blue can be substituted.
A common variant is Lillie's trichrome. It is often errorneously called Masson's trichrome. It differs in the dyes used, their concentrations, and the immersion times.
Matrix attachment region
Matrix attachment region (MAR), also known as Scaffold/matrix attachment regions (S/MARs), are sequences in the DNA of eukaryotic chromosomes where the nuclear matrix attaches. S/MARs mediate structural organization of the chromatin within the nucleus. These elements constitute anchor points of the DNA for the chromatin scaffold and serve to organize the chromatin into structural domains. Studies on individual genes led to the conclusion that the dynamic and complex organization of the chromatin mediated by S/MAR elements plays an important role in the regulation of gene expression.
Recently, Tetko has found a strong correlation of intragenic S/MARs with spatiotemporal expression of genes in Arabidopsis thaliana. On a genome scale, pronounced tissue- and organ-specific and developmental expression patterns of S/MAR-containing genes have been detected. Notably, transcription factor genes contain a significant higher portion of S/MARs. The pronounced difference in expression characteristics of S/MAR-containing genes emphasizes their functional importance and the importance of structural chromosomal characteristics for gene regulation in plants as well as within other eukaryotes.

# Notes
-  See Tetko, Igor V., Georg Haberer, Stephen Rudd, Blake Meyers, Hans-Werner Mewes, and Klaus F. X. Mayer (2006) Spatiotemporal Expression Control Correlates with Intragenic Scaffold Matrix Attachment Regions (S/MARs) in Arabidopsis thaliana.  PLoS Computational Biology 2:136-145.  Online copy.
Matrix population models
Population models are used in population ecology to model the dynamics of wildlife or human populations.  Matrix population models are a specific type of population model that uses matrix algebra.  Matrix algebra, in turn, is simply a form of algebraic shorthand for summarizing a larger number of often repetitious and tedious algebraic computations.
All populations can be modeled by one simple equation:
N(t+1) = N(t) + B - D + I - E,
where:
N(t+1) = abundance at time t+1
N(t) = abundance at time t
B = number of births within the population between Nt and Nt+1
D = number of deaths within the population between Nt and Nt+1
I = number of individuals immigrating into the population between Nt and Nt+1
E = number of individuals emigrating from the population between Nt and Nt+1
This equation is called a BIDE model.  Although BIDE models are conceptually simple, reliable estimates of the 5 variables contained therein (Nt, B, D, I and E) are often difficult to obtain.
Usually a researcher attempts to estimate current abundance, Nt, often using some form of mark and recapture technique.
Estimates of B might be obtained via a ratio of young to adults soon after the breeding season, Ri.
Number of deaths can be obtained by estimating annual survival probability, usually via mark and recapture methods, then multiplying present abundance and survival rate.
Many times immigration and emigration are ignored because they are so difficult to estimate.
For added simplicity it may help to think of time t as the end of the breeding season in year t and to imagine that one is studying a species that has only one discrete breeding season per year.
The BIDE model can then be expressed as:
Nt+1 = Nt_a - Sa + Nt_a - Ri - Si
where:
Nt_a = number of adult females at time t
Nt_i = number of immature females at time t
Sa = annual survival of adult females from time t to time t+1
Si = annual survival of immature females from time t to time t+1
Ri = ratio of surviving young females at the end of the breeding season per breeding female
In matrix notation this model can be expressed as:
Suppose that you are studying a species with a maximum lifespan of 4 years.  The following is an age-based Leslie matrix for this species.  Each row in the first and third matrices corresponds to animals within a given age range (0-1 years, 1-2 years and 2-3 years).  In a Leslie matrix the top row of the middle matrix consists of age-specific fertilities: F1, F2 and F3.  Note, that F1 = SiRi in the matrix above.  Since this species does not live to be 4 years old the matrix does not contain an S3 term.
These models can give rise to interesting cyclical or seemingly chaotic patterns in abundance over time when fertility rates are high.
The terms Fi and Si can be constants or they can be functions of environment, such as habitat or population size.  Randomness can also be incorporated into the environmental component.

# Reference

# Bibliography
- Caswell, H.  2001.  Matrix population models: Construction, analysis and interpretation, 2nd Edition.  Sinauer Associates, Sunderland, Massachusetts.  ISBN 0-87893-096-5.
Medically indigent adult
Medically indigent adults "(MIAs)" in the health care system of the United States are persons who do not have health insurance and who are not eligible for other health care coverage, such as Medicaid, Medicare, or private health insurance.
Government MIA programs at the state or county or municipal level may help MIAs access medical care by paying for all or part of the cost of their medical care.
Such programs are typically of last resort, and are available only to those who meet the "last resort" socioeconomic eligibility standards.
Mental disorder overview

# Overview
Mental disorder or mental illness are terms used to refer to a psychological or physiological pattern that occurs in an individual and is usually associated with distress or disability that is not expected as part of normal development or culture.  The recognition and understanding of mental disorders has changed over time.
Definitions, assessments, and classifications of mental disorders can vary, but guideline criterion listed in the ICD, DSM and other manuals are widely accepted by mental health professionals. Categories of diagnoses in these schemes may include mood disorders, anxiety disorders, psychotic disorders, eating disorders, developmental disorders, personality disorders, and many other categories. In many cases there is no single accepted or consistent cause of mental disorders, although they are widely understood in terms of a diathesis-stress model and biopsychosocial model. Mental disorders have been found to be common, with over a third of people in most countries reporting sufficient criteria at some point in their life. Mental health services may be based in hospitals or in the community.
Mental health professionals diagnose individuals using different methodologies, often relying on case history and interview. Psychotherapy and psychiatric medication are two major treatment options, as well as supportive interventions.
Treatment may be involuntary where legislation allows. Several movements campaign for changes to mental health services and attitudes, including the Consumer/Survivor Movement. There are widespread problems with stigma and discrimination.
Metastatic calcification

# Overview
Metastatic calcification is deposition of calcium salts in otherwise normal tissue, because of elevated levels of calcium and other minerals in blood because of deranged metabolism, synthesis or disposal.
It occurs as opposed to dystrophic calcification where blood levels of calcium are normal.
Metastatic calcification can occur widely throughout the body but principally affects the interstitial tissues of the vasculature, kidneys, lungs, and gastric mucosa.
Dystrophic calcification occurs in necrotic tissue with normal serum calcium levels; metastatic calcification occurs in normal tissue and requires elevated serum calcium levels.

# Pathological Findings
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- This is a gross photograph of the cut section of the patient's lung showing evidence of severe metastatic calcification. The lung tissue has a rough, firm appearance with open airways.
- This low-power photomicrograph of the patient's lung illustrates large, open alveolar spaces. The pleural surface is the curved surface at the top.
- A higher-power photomicrograph shows a blood vessel cut in longitudinal section (1). Several of the alveoli are filled with a pink-staining proteinaceous fluid (2) indicative of pulmonary edema. The alveolar septa and the wall of the blood vessel have a purplish color due to massive deposition of mineral (primarily calcium) in these tissues (3).
- This high-power photomicrograph of a blood vessel shows calcium deposits in the vascular wall (1) and proteinaceous material (2) (from edema) within some of the alveoli. The smooth muscle in the vessel wall has been almost completely replaced by calcium deposits.
- This photomicrograph demonstrates pulmonary alveoli with extensive calcium depositions (1) in the septa and protein accumulations (2) in the alveoli.
Metastatic pulmonary calcification
Plantar metatarsal veins
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The plantar metatarsal veins run backward in the metatarsal spaces and communicate, by means of perforating veins, with the veins on the dorsum of the foot, and unite to form the deep plantar venous arch which lies alongside the plantar arterial arch.
Methamphetamine overdose

# Overdose information
Anxiety disorders
Panic disorder

## Manifestations
Manifestations of acute overdosage with methamphetamine include restlessness, tremor,
hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states,
hyperpyrexia, and rhabdomyolysis. Fatigue and depression usually follow the central
stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension, and
circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and
abdominal cramps. Fatal poisoning usually terminates in convulsions and coma. Return to top

## Treatment
Consult with a Certified Poison Control Center regarding treatment for up to date
guidance and advice. Management of acute methamphetamine intoxication is largely
symptomatic and includes gastric evacuation, administration of activated charcoal, and sedation.
Experience with hemodialysis or peritoneal dialysis is inadequate to permit recommendations in
this regard.
Acidification of urine increases methamphetamine excretion, but is believed to increase
risk of acute renal failure if myoglobinuria is present. Intravenous phentolamine (Regitine) has
been suggested for possible acute, severe hypertension, if this complicates methamphetamine
-verdosage. Usually a gradual drop in blood pressure will result when sufficient sedation has
been achieved. Chlorpromazine has been reported to be useful in decreasing CNS stimulation
and sympathomimetic effects. Return to top
Adapted from the FDA Package Insert.
Methylphenidate overdose

# Overdosage topics
Manifestations
Treatment
Hemodialysis

## Manifestations
Signs and symptoms of acute overdosage, resulting principally from overstimulation of the central nervous system and from excessive sympathomimetic effects, may include the following: vomiting, agitation, tremors, hyperreflexia, muscle twitching, convulsions (may be followed by coma), euphoria, confusion, hallucinations, delirium, sweating, flushing, headache, hyperpyrexia, tachycardia, palpitations, cardiac arrhythmias, hypertension, mydriasis, and dryness of mucous membranes. Return to top

## Treatment
Treatment consists of appropriate supportive measures. The patient must be protected against self-injury and against external stimuli that would aggravate overstimulation already present. Gastric contents may be evacuated by gastric lavage. In the presence of severe intoxication, use a carefully titrated dosage of a short-acting barbiturate before performing gastric lavage.
Other measures to detoxify the gut include administration of activated charcoal and a cathartic.
Intensive care must be provided to maintain adequate circulation and respiratory exchange; external cooling procedures may be required for hyperpyrexia. Return to top

## Hemodialysis
Efficacy of peritoneal dialysis or extracorporeal hemodialysis for Methylphenidate overdosage has not been established. Return to top
Adapted from the FDA Package Insert.
Methysergide description

# Description
Sansert (methysergide maleate) is a partially synthetic compound structurally related to lysergic acid butanolamide, well-known as methylergonovine in obstetrical practice as an oxytocic agent.
Chemically, methysergide maleate is designated as ergoline-8-carboxamide, 9,10-didehydro-N--1,6-dimethyl-, (8)-, (Z)-2-butenedioate (1:1) (salt).
Its structural formula is:
Methylation in the number 1 position of the ring structure enormously enhances the antagonism to serotonin which is present to a much lesser degree in the partially methylated compound (methylergonovine maleate) as well as profoundly altering other pharmacologic properties.
Active Ingredient: methysergide maleate, USP.
Inactive Ingredients: acacia, carnauba wax, colloidal silicon dioxide, FD&C Blue #1, FD&C Yellow #5, gelatin, lactose, malic acid, povidone, sodium benzoate, starch (corn), stearic acid, sucrose, synthetic black iron oxide, talc, and titanium dioxide.
Metronidazole overdosage

# Overdosage
Single oral doses of metronidazole, up to 15 g, have been reported in suicide attempts and accidental overdoses. Symptoms reported include nausea, vomiting, and ataxia.
Oral metronidazole has been studied as a radiation sensitizer in the treatment of malignant tumors. Neurotoxic effects, includingseizures and peripheral neuropathy, have been reported after 5 to 7 days of doses of 6 to 10.4 g every other day.

### Treatment of Overdosage
There is no specific antidote for metronidazole overdose; therefore, management of the patient should consist of symptomatic and supportive therapy.
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