Persius/hicric huggingface dataset:
Taenia infection overview

# Overview
Taenia infection is an infection with the tapeworm parasite found in beef or pork.

# Epidemiology and Demographics
Both species, Taenia saginata (beef tapeworm) and T. solium are worldwide in distribution. Taenia solium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork, and is very rare in Muslim countries.

# Natural History, Complications and Prognosis
With treatment, the taenia infection goes away. Rarely, worms can cause a blockage in the intestine. If pork tapeworm larvae move out of the intestine, they can cause local growths and damage tissues such as the brain, eye, or heart. This condition is called cysticercosis. Infection of the brain can cause seizures and other nervous system problems.

# Diagnosis

## History and Symptoms
Taenia saginata taeniasis produces only mild abdominal symptoms or may not cause any symptoms. However, some people may have abdominal discomfort. The most striking feature consists of the passage (active and passive) of proglottids. Occasionally, appendicitis or cholangitis can result from migrating proglottids. Taenia solium taeniasis is less frequently symptomatic than Taenia saginata taeniasis.  The main symptom is often the passage (passive) of proglottids. The most important feature of  Taenia solium taeniasis is the risk of development of cysticercosis. People often realize they are infected when they pass segments of the worm in their stool, especially if the segments are moving.

# Treatment

## Medical Therapy
Treatment is simple and very effective. Praziquantel is the drug of choice (This drug is approved by the FDA, but considered investigational for this purpose).

## Primary Prevention
In the U.S., laws on feeding practices and the inspection of domestic food animals have largely eliminated tapeworms. Avoiding raw meat and cooking meat well enough (to greater than 140 degrees F for 5 minutes) will prevent taenia infection. Freezing meats to -4 degrees F for 24 hours also kills tapeworm eggs. Good hygiene and hand washing after using the toilet will prevent self-infection in a person who is already infected with tapeworms.
Telithromycin description

# Description
KETEK tablets contain telithromycin, a semisynthetic antibacterial in the ketolide class for oral administration. Chemically, telithromycin is designated as Erythromycin, 3-de-11,12-dideoxy-6-O-methyl-3-oxo-12,11-butyl]imino]]-.
Telithromycin, a ketolide, differs chemically from the macrolide group of antibacterials by the lack of -L-cladinose at position 3 of the erythronolide A ring, resulting in a 3-keto function. It is further characterized by a C11-12 carbamate substituted by an imidazolyl and pyridyl ring through a butyl chain. Its empirical formula is C43H65N5O10 and its molecular weight is 812.03. Telithromycin is a white to off-white crystalline powder. The following represents the chemical structure of telithromycin.
KETEK tablets are available as light-orange, oval, film-coated tablets, each containing 400 mg or 300 mg of telithromycin, and the following inactive ingredients:  croscarmellose sodium, hypromellose,  magnesium stearate, microcrystalline cellulose, polyethylene glycol, povidone, red ferric oxide, talc, titanium dioxide, and yellow ferric oxide.
Testicular microlithiasis

# Overview
Testicular microlithiasis is a rare condition found in 0.5% of men that causes calcium formations on the testicles. It is an asymptomatic, non-progressive disease. This disease is detected by an ultrasound, usually when the patient is being checked for something else, such as testicular cancer. In 80% of cases, both testicles are affected.
Testicular microlithiasis is not a serious condition, however, some studies have shown that it may increase the risk of developing testicular cancer. There is no cure or treatment for testicular microlithiasis, however, patients are regularly monitored via ultrasound to make sure that other conditions do not develop.
This disease has been associated with testicular cancer, cryptorchidism, infertility and intraepithelial germ cell neoplasia. Some sources report that testicular cancer is found in 40% of patients with testicular microlithiasis.

## Ultrasound
- Small nonshadowing hyperechoic foci ranging in diameter from 1 to 3 mm.
- These occur within the testicular parenchyma but may be distributed peripherally or segmentally.
- Testicular microlithiasis usually occurs bilaterally
Patient #1
Patient #2: US images demonstrate testicular microlithiasis
Testis determining factor
Testis-determining factor (TDF) is a general term for the gene (or product thereof) that results in maleness in humans and some other species.
Certain genes cause chemical reactions that result in the development of testes. Embryos are gonadally identical, regardless of genetic sex, until a certain point in development; then the testis-determining factor causes male sex organs to develop, while lack of this factor will cause the embryo to develop as physically female.
The TDF factor is encoded by the SRY gene located in the Y chromosome. It is a DNA binding protein, that enhances other transmission factors, or is a transcription factor itself. Its expression directly or indirectly causes the development of primary sex chords, which will later develop to seminiferous tubules. These chords form in the central part of the undifferentiated-yet gonad, turning it into a testis. The testis then starts secreting testosterone and the Mullerian Inhibiting Substance.
Older texts discuss the role of the HY antigen in the control of testicular development, but this was later disproven.

# Role in disease
The TDF gene has some interesting implications. The genetic recombination of Crossing over can cause the gene to be transferred on to the X chromosome. In this case, the X chromosome will initiate testis development, so regardless of whether the person has a Y chromosome, the person will turn into a boy. Though everything else will be developed as if it were a girl (other sex related alleles), the apparent sex will be male (a syndrome known as XX male syndrome).
Conversely, such a cross-over event also can result in a Y chromosome that is missing its TDF, replaced with the corresponding sequence from the end of the X chromosome. Individuals who inherit this Y chromosome will develop as females, despite having the normal male chromosomal set of one X and one Y. However, the lack of two X-chromosomes gives complications to such females, called Turner syndrome.
de:Hoden-determinierender Faktor
it:TDF (gene)
The heart in lung cancers

# Histopathological Findings
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Heart metastases from bronchogenic carcinoma
- Heart metastases from bronchogenic carcinoma (closer look)
- HEART: Bronchiogenic carcinoma, smoker, right ventricular dilatation
- HEART: Metastatic Carcinoma: Gross natural color horizontal sections of ventricle showing tumor in subepicardial fat which stops abruptly at myocardium which is quite typical interesting case 44yo BF with adenocarcinoma of lung occurring 25 years after successful treatment for Hodgkin's disease
- HEART: Metastatic Carcinoma: Micro low mag H&E. Lung alveolar cell carcinoma shows tumor in pericardial fat and into subepicardial myocardium
- HEART: Metastatic Carcinoma Lung: Gross natural color external view with coronaries sectioned obvious tumor all over epicardium 44yo BF adenocarcinoma giant cell type right lung occurring 25 years after treatment for Hodgkin's disease
- HEART: Pericarditis, Neoplastic: Gross natural color shaggy pericarditis (primer is adenocarcinoma of lung)
The patient has back pain

# ACTION ITEMS*
1. Obatin a history to fully characterize the nature back pain (onset, sti lml'f;,'fa;k;'ask.
2. Obtain a relevant ROS focusing on systemic diseases, cancer, infection, neurologic symptoms and character of the back pain.
2. Perform a focused physical examination
- sign of local tenderness
- range of motion
- sign of radiculopathy
- spurling sign
- straight leg raise
Is sciatica present?
Yes
No
- While this algorithm provides steps to perform a focused history and physical examination, it is no replacement for a detailed history and physical examination.
Theodor Wilhelm Engelmann
Theodor Wilhelm Engelmann (born 1843 in Leipzig  died 1909) was a German botanist, physiologist, microbiologist, university professor, and musician whose 1882 experiment measured the effects of different colors of light on photosynthetic activity and showed that the conversion of light energy to chemical energy took place in the chloroplast.

# Academic history
Englemann studied natural science and medicine first at the University of Jena, from 1861 to 1862, and later at the University of Heidelberg, the University of Gottingen and the University of Leipzig.  In 1867, he received a doctoral degree in medicine at Leipzig.
He later taught physiology at the University of Utrecht, becoming a professor in 1888.  In 1897, he began teaching physiology at the University of Berlin, where he also became the editor of the Archiv fur Anatomie und Physiologie.  He retired in 1908, but continued to serve as editor until his death.

# Scientific investigations
Engleman's major contribution to the field of physiology emerged from a study lasting from 1873 to 1897, in which he observed the contractions of striated muscles.  Focusing on the visible bands of fibers in the muscles, he noted that the volume of the anistropic band increased during contraction, whereas the volume of the isotropic band decreased.  He theorized that it was this interaction between the two bands which allowed for muscle contraction.
He also demonstrated, after experiments with dissected frogs in 1875, that contractions of the heart were caused by the heart muscle itself, not an external nerve stimulus, as was previously believed.
In 1881, he demonstrated that photosynthesis takes place inside the chloroplasts of plants and that the chloroplasts receive more energy from red and blue light than from other colours.  He illuminated a filamenous alga Spirogyra with light passed through a prism, exposing different segments to different wavelengths. Aerobic bacteria, which grow in the presence of oxygen, were used to determine where the alga was releasing the most oxygen and thus photosynthesizing most. They accumulated under red and blue light, showing that only specific parts of the electromagnetic spectrum are used. A year later Engelmann discovered that purple bacteria utilise ultraviolet light in the same way.
Thrombocytopenia overview

# Overview
Thrombocytopenia (or -paenia, or thrombopenia in short) is the presence of relatively few platelets in blood.
Generally speaking, a normal platelet count ranges from 150,000 and 450,000 per mm3. These limits, however, are determined by the 2.5th lower and upper percentile, and a deviation does not necessarily imply any form of disease. The number of platelets in a blood sample also decreases quickly with time and a low platelet count may be caused by a delay between sampling and analysis.

# Historical Perspective

# Classification
Thrombocytopenia can be divided into several categories based on its extent as well as its underlying etiology.
Based on platelet count:
- mild: (100,000 - 150,000 per L),
- moderate (50,000 to 99,000 per L),
- severe (<50,000 per L).
Note that these amounts may not be the same for every condition and one should interpreted them according to the underlying etiology of thrombocytopenia. For example, in idiopathic thrombocytopenia (ITP), a platelet count of <30,000/L represents severe thrombocytopenia and for gestational thrombocytopenia, a platelet count between 80,000 and 150,000/microL is considered as mild thrombocytopenia.
Based on etiology:
To see the full list of conditions that could cause thrombocytopenia, please click here.

# Pathophysiology
Basically, thrombocytopenia is the result of one of these mechanisms or a combination of some of them:
- Reduced production of platelets due to bone marrow dysfunction
- Increased destruction of platelets in the body
- iatrogenic
- entrapment of platelets in spleen
Several conditions, some of which mentioned below, can activate the mechanisms that ultimately lead to thrombocytopenia.

# Causes

# Differentiating  from Other Diseases

# Epidemiology and Demographics
Among people with normal platelet counts:
- The mean platelet count is 266,000/L in women and 237,000/L in men.
- Younger people and those with African-Americans descent have higher platelet counts than the older ones and caucasians, respectively.
- The variation of the platelet count in a given individual over a certain time course is insignificant.
- Platelet counts are slightly higher (by approximately 5000/L) in the fall/winter compared with spring/summer.
- Almost 2.5 percent of the normal population have platelet counts lower than 150,000/L.

# 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
Toxic leukoencephalopathy
Toxic leukoencephalopathy or toxic spongiform leukoencephalopathy is a  condition that is characterized by progressive damage (-pathy), of the white matter (leuko-) of the brain (-encephalo-) due to ingested toxins (toxic).
It is seen in some people who ingest heroin by route of smoking (chasing the dragon). It is currently unknown by what means the smoking of heroin causes the condition.
Toxic leukoencephalopathy affects white matter tracts devoted to higher cerebral function, causing clinical features that range from inattention, forgetfulness, and changes in personality to dementia, coma, and death.
Obvious signs of the condition are difficulty with cognitive function and equilibrioception.
Toxic multinodular goitre

# Overview
Toxic multinodular goitre (also known as toxic nodular goitre, toxic nodular struma) is a form of hyperthyroidism - where there is excess production of thyroid hormones.
It is the second most common cause of hyperthyroidism after Graves disease.

# Symptoms
Symptoms of toxic multinodular goitre are similar to that of hyperthyroidism, including:
- heat intolerance
- hyperkinesis
- tremor
- irritability
- weight loss
- increased appetite
- goitre (swelling of the thyroid gland)
- tachycardia (high heart rate - above 180 bpm at rest)

# Related eponym
Plummer's disease is named after an American physician Henry Stanley Plummer but refers to a single toxic nodule (adenoma) which may present with the background of a suppressed multinodular goitre.

# Footnotes
-  Template:WhoNamedIt2 eponymously named after Template:WhoNamedIt
Transcription factor II A
Transcription factor TFIIA is a nuclear protein involved in the RNA polymerase II-dependent transcription of DNA.  TFIIA is one of several general (basal) transcription factors (GTFs) that are required for all transcription events that use RNA polymerase II.  Other GTFs include TFIID, a complex composed of the TATA binding protein TBP and TBP-associated factors (TAFs), as well as the factors TFIIB, TFIIE, TFIIF, and TFIIH.  Together, these factors are responsible for promoter recognition and the formation of a transcription preinitiation complex (PIC) capable of initiating RNA synthesis from a DNA template.

# Functions
TFIIA interacts with the TBP subunit of TFIID and aids in the binding of TBP to TATA-box containing promoter DNA.  Interaction of TFIIA with TBP facilitates formation of and stabilizes the preinitiation complex.  Interaction of TFIIA with TBP also results in the exclusion of negative (repressive) factors that might otherwise bind to TBP and interfere with PIC formation. TFIIA also acts as a coactivator for some transcriptional activators, assisting with their ability to increase, or activate, transcription. The requirement for TFIIA in vitro transcription systems has been variable, and it can be considered either as a GTF and/or a loosely associated TAF-like coactivator.  Genetic analysis in yeast has shown that TFIIA is essential for viability.

# Structure
TFIIA is a heterodimer with two subunits: one large unprocessed (subunit 1, or alpha/beta; gene name GTF2A1) and one small (subunit 2, or gamma; gene name GTF2A2). It was originally believed to be a heterotrimer of an alpha (p35), a beta (p19) and a gamma subunit (p12). In humans, the sizes of the encoded proteins are approximately 55 kD and 12 kD.  Both genes are present in species ranging from humans to yeast, and their protein products interact to form a complex composed of a beta barrel domain and an alpha helical bundle domain. It is the N-terminal and C-terminal regions of the large subunit that participate in interactions with the small subunit. These regions are separated by another domain whose sequence is always present in large subunits from various species but whose size varies and whose sequence is poorly conserved. A second gene encoding a large TFIIA subunit has been found in some higher eukaryotes.  This gene, ALF/TFIIAtau (gene name GTF2A1LF) is expressed only in oocytes and spermatocytes, suggesting it has a TFIIA-like regulatory role for gene expression only in germ cells.
Transcription factor II F
Transcription factor IIF (TFIIF) is one of several general transcription factors that make up the RNA polymerase II preinitiation complex.
Transcription factor IIF is encoded by the GTF2F1, GTF2F2, and GTF2F2L genes.
TFIIF binds to RNA Polymerase II when the enzyme is already unbound to any other transcription factor, thus avoiding it from contacting DNA outside the promoter. Furthermore, TFIIF stabilizes the RNA polymerase II while it's contacting TBP and TFIIB.
Transmembrane Protein 175
Transmembrane Protein 175, or TMEM175, is a transmembrane protein that is thought to be an endolysosomal potassium channel. It is predicted to have many orthologs across eukaryotes.

# Expression
Based on human and mouse EST profiles and a human tissue GEO profile, TMEM175 appears to be expressed at a relatively high level(75-98%) in normal tissues.  TMEM175 appears to be down regulated in stage three ovarian cancer

# Homology
Transmembrane protein 175 has no paralogs.  It does have orthologs within eukaryotes.  The following table presents some of the orthologs found using searches in BLASTand BLAT.   This list does not contain all of the orthologs for TMEM175.  It is meant to display the diversity of species for which orthologs are found.

# Predicted Post-Translational Modification
Using various tools at ExPASy the following are possible post-translational modifications for TMEM175.
- 5 possible CK2 phosphorylation sites
- 2 possible PKC phosphorylation sites
- N-myristoylation sites around transmembrane regions
The N-myristoylation sites are conserved in vertebrates.
Transmembrane protein 134
Transmembrane protein 134 is a protein encoded by the TMEM134 gene.  TMEM134 does not have any other known aliases.  There are two transmembrane domains and a domain of unknown function (DUF872). Evolutionary, the majority of the organisms that have this gene are primates and mammals, although there are some organisms dating back to Drosphila and C. elegans.  Through current research, there has not been any confirmed function of TMEM134.

# Gene Structure
The gene is composed of 6 exons spanning from 67464348 to 67469277 kilo bases.  It is located on chromosome 11q13.2, which is the minus strand of the chromosome.  The gene does have three isoforms; a, b, and c.

# Protein

## Protein Structure
The protein is encoded by TMEM134 gene and is 195 amino acids in length.  The protein contains two transmembrane domains but does not contain a signal peptide.  This suggests that there is an internal signal peptide upstream of the translated portion of the protein.  The protein is overall considering normal with its amino acid content but does have two regions of high hydrophobicity, which occur during the transmembrane regions of the protein.  This gives the protein an isoelectric point of 6.08. The overall weight of the protein is 21.6 kilodaltons, which is conserved throughout the different orthologs.  The protein also contains a domain of unknown function 872 (DUF872).  Currently there is no thought to the possible function of this domain.

## Regulation and Translation
TMEM134 is regulated by the promoter GXP50275.  There are 870 amino acids in the promoter and 15 transcripts variants of it.  The promoter is well conserved in mammals.  There are some conserved binding regions in the promoter including EGR/nerve factor and Huntington's disease gene regulatory region.

## Location
The final protein is thought to be in the endoplasmic reticulum and the nuclear membrane.  The protein is anchored in two different regions, from 123-145 and 155-177.  The portion of the protein that extends into the cytosol is heavily phosphorylated.  These phosphorylation sites are conserved into bony fishes.

## Post-Translational Modification
The only post-translational modification that occurs is phosphorylation.  There is no glycosylation, sulfination, or sumoylation sites.

## Interactions
TMEM134 has one interaction with another protein, ELAVL1.  This protein binds to AU rich elements in FOS and IL3/interleukin-3 mRNAs.

# Expression
Microarray analysis of GEO profiles were conducted and TMEM134 is shown to be ubiquitously expressed in the majority of human tissues. Even though there is ubiquitous expression in the human tissues, there are other tissues that have higher expression levels, such as the heart, breast tissue, and prostate tissue.

# Homology
As discussed earlier, there is quite a bit of conservation in primates and mammals but there are some distant orthologs of zebrafish and Drosphila, and a homolog of C. elegans.
Transmembrane protein 222
Transmembrane protein 222 is a protein that in humans is encoded by the TMEM222 gene. One notable feature of the protein encoded by this gene is the presence of three predicted transmembrane domains. The TMEM222 protein is predicted to most likely localize to the secretory vesicles.

# Gene Features
TMEM222 has a domain of unknown function (DUF778). Aliases of this gene include DKFZP564D0478, RP11-4K3__A.4, C1orf160, and MGC111002. Accession NM_032125.2, the longest coding sequence (1629 bp), encodes a protein of 208 amino acid residues (23230 Daltons), which is considered the consensus coding sequence (CCDS297.2). There are two isoforms of the protein encoded by this gene. They are similar except the second (Q9H0R3-2) is lacking the first 96 amino acid residues that are present in the first (Q9H0R3-1).

# Gene Expression
ACEVIEW has labeled TMEM222 as highly expressed with 3.8 times more expression than the average gene in the database. There is expression evidence from 166 tissues including brain, lung, colon, kidney, and placenta.

# Homology
Orthologs and distant homologs of the human TMEM222 have been identified throughout Eukaryota especially in plants and animals. No paralogs of this gene have been found in the human genome.

# Distant Homolog
A distant homolog of TMEM222, RTH (RTE1-Homolog), is a homolog of RTE1 (Reversion-to-Ethylene Perception 1), which is known to induce conformational changes in ETR1 (Ethylene receptor 1) that result in negative regulation corresponding with loss of ethylene perception.

# Protein Interactions
Evidence from yeast two-hybrid screening exists for two protein interactions with this gene. One is a serine protease (PRSS23) that has been identified to be involved in mouse ovulation and is excreted into the extracellular matrix. The other protein is an ab-hydrolase (HLA-B associated transcript 5)  that is integral to the membrane, and its corresponding gene is located in the genome near Tumor Necrosis Factor (TNF)-alpha and TNF-beta.