Persius/hicric huggingface dataset:
Upper gastrointestinal series

# Overview
Upper GI series, also upper gastrointestinal (GI) tract radiography, is a radiologic examination of the upper gastrointestinal tract.  It consists of a series of X-ray images of the esophagus, stomach and duodenum. The most common use for this medical testing is to look for signs of ulcers, acid reflux disease, uncontrollable vomiting, or unexplained blood in the stools (hematochezia or positive fecal occult blood).

# Application

## Preparation
When the patient needs to undertake an Upper GI, he or she is asked to take a fast on the previous day, depending on what the doctor wishes for the patient to take or what might be the need for this testing. Normally, the patient must avoid solid food for up to 8 hours prior to the appointment and avoid any type of consumable, including water, 3 hours prior to the testing.

## Process
This is a non-invasive test, consisting of an X-Ray. In the X-ray room, the patient is given two medications to drink that help improve the quality of the resulting X-rays.  The patient may also be administered glucagon, a pancreatic hormone that is injected intravenously. The first drink is very carbonated, made from baking-soda crystals which expands the stomach by causing gas to build in the stomach. The second drink is a contrast agent, typically a thick, chalky liquid containing a barium salt. (This test is sometimes called a barium swallow.) The barium outlines the stomach on the X-rays, helping the doctor find tumors or other abnormal areas.
The patient then has X-rays taken. The doctors usually take a series of pictures with the patient in a number of different positions to capture different poses and views of the digestive system. Normally the patient needs to hold their breath to avoid the pictures from blurring and causing unneeded challenges in diagnosing the illness.
During the test, the doctor may pump air into the stomach to make features such as small tumors easier to see.

## After the test
Patients may feel nauseous immediately after drinking the barium.  This is common and may last up to 72 hours following the test. You may eat as normal after the procedure but it is important to drink a lot of water to allow the barium to pass through the body easier.  Constipation is common but diarrhea will affect some patients. Another common side effect is the bleaching of solid waste matter; this may last up to 48 hours.
Vogt-Koyanagi-Harada syndrome

# Overview
VogtKoyanagiHarada syndrome (VKH syndrome) is an uncommon multisystem disease of presumed autoimmune etiology that is characterized by chronic, bilateral, diffuse, granulomatous uveitis with accompanying dermatologic, neurologic, and auditory involvement.  VKH syndrome is named for ophthalmologists Alfred Vogt from Switzerland and Yoshizo Koyanagi and Einosuke Harada from Japan.

# Pathophysiology
VKH syndrome is an immune-mediated disease. The mechanism of the disease is thought to be T helper cell mediated autoimmune attack of melanocytes in the skin, uvea, central nervous system and inner ear. A new T-cell subset Th17 may play an important role in the initiation and maintenance of inflammatory disease when stimulated by the interleukin IL-23, thus producing IL-17.
There is a higher rate of VKH syndrome in people of Asian, Latin, and Mediterranean descent

# Clinical Presentation
There are 4 stages of VKH syndrome: prodromal, acute uveitic, convalescent, and chronic recurrent.
- The prodromal stage is marked by flu-like symptoms. Patients present with headache, nausea, meningism, dysacusia (discomfort caused by loud noises or a distortion in the quality of the sounds being heard) and tinnitus.
- The acute uveitic stage is heralded by the onset of blurring of vision in both eyes and is marked by bilateral granulomatous anterior uveitis, variable degree of vitritis, thickening of the posterior choroid with elevation of the peripapillary retinal choroidal layer, hyperemia and edema of the optic nerve, and multiple serous retinal detachments.
- The convalescent stage occurs several weeks later and is marked by gradual depigmentation of the choroid, resulting in the classic orange-red discoloration, or sunset glow fundus appearance. Skin changes, including vitiligo, alopecia and poliosis typically appear during this stage.
- The chronic recurrent stage is marked by repeated bouts of uveitis.

# Diagnosis
The diagnosis of VKH syndrome is made by ophthalmologist or optometrist based on clinical presentation. Imaging techniques such as fluorescein angiography are used to confirm diagnosis.

# Treatment
The acute stage of VKH syndrome is exquisitely responsive to early and aggressive treatment with topical, periocular and systemic corticosteroids and cycloplegic agents.
Valproate semisodium overdose

# Overdose Information
Anxiety disorders
Treatment

## General
Overdosage with valproate may result in somnolence, heart block, and deep coma. Fatalities
have been reported; however patients have recovered from valproate levels as high as
2120 g/mL. Return to top

## Treatment
In overdose situations, the fraction of drug not bound to protein is high and hemodialysis
-r tandem hemodialysis plus hemoperfusion may result in significant removal of drug. The
benefit of gastric lavage or emesis will vary with the time since ingestion. General supportive
measures should be applied with particular attention to the maintenance of adequate urinary
-utput.
Naloxone has been reported to reverse the CNS depressant effects of valproate
-verdosage. Because naloxone could theoretically also reverse the antiepileptic effects of
valproate, it should be used with caution in patients with epilepsy. Return to top
Adapted from the FDA Package Insert.
Vancomycin directions for use
Vancomycin Injection, USP in GALAXY plastic container (PL 2040) is for intravenous administration only.
Storage
Store in a freezer capable of maintaining a temperature at or below -20C (-4F).
Thawing of Plastic Containers:
Thaw frozen containers at room temperature (25C/77F) or under refrigeration (5C/41F). DO NOT FORCE THAW BY IMMERSION IN WATER BATHS OR BY MICROWAVE IRRADIATION.
Check for minute leaks by squeezing the bag firmly. If leaks are detected, discard solution because sterility may be impaired.
DO NOT ADD SUPPLEMENTARY MEDICATION.
Visually inspect the container for particulate matter and discoloration. Components of the solution may precipitate in the frozen state and should dissolve with little or no agitation after the solution has reached room temperature. Potency is not affected. If after visual inspection, the solution is discolored or remains cloudy, an insoluble precipitate is noted, or any seals or outlet ports are not intact, the container should be discarded.
The thawed solution in GALAXY plastic container (PL 2040) remains chemically stable for 72 hours at room temperature (25C/77F) or for 30 days when stored under refrigeration (5C/41F).
Do not refreeze thawed antibiotics.
Preparation for Intravenous Administration:
Suspend container from eyelet support.
Remove protector from outlet port at bottom of container.
Attach administration set. Refer to complete directions accompanying set.
Use sterile equipment.
Caution: Do not use plastic containers in series connections. Such use could result in an embolism due to residual air being drawn from the primary container before administration of the fluid from the secondary container is complete.
Rx only.
Venlafaxine contraindications

# Contraindications
Hypersensitivity to venlafaxine hydrochloride or to any excipients in the formulation.
The use of MAOIs intended to treat psychiatric disorders with Effexor XR or within 7 days of stopping treatment with Effexor XR is contraindicated because of an increased risk of serotonin syndrome. The use of Effexor XR within 14 days of stopping an MAOI intended to treat psychiatric disorders is also contraindicated (seeWARNINGS and DOSAGE AND ADMINISTRATION).
Starting Effexor XR in a patient who is being treated with MAOIs such as linezolid or intravenous methylene blue is also contraindicated because of an increased risk of serotonin syndrome (see WARNINGS and DOSAGE AND ADMINISTRATION).
Virginia Mason Medical Center
Virginia Mason Medical Center (VMMC), founded in 1920, is a private, non-profit organization located on Seattle, Washington's First Hill offering a system of integrated health services. Gary S. Kaplan, MD, serves as chairman and CEO, and J. Michael Rona is president, although Rona announced his resignation on April 20, 2007. The medical center includes:
- a large, multi-specialty group practice of more than 480 physicians, offering both primary and specialized care;
- a regional network of neighborhood clinics including sports and occupational medicine facilities;
- an acute care hospital licensed for 336 beds;
- an internationally recognized research institute;
- an active philanthropic foundation;
- Bailey-Boushay House, a nursing residence and day health center for people living with AIDS.
The organization was named after the daughters of its two founders: Dr. Tate Mason's daughter, Virginia Mason, and Dr. John Blackford's daughter, Virginia Mason Blackford.

# Notes
-  "Rona Announces Resignation as Virginia Mason President". Retrieved 2007-04-23..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
Voltage-gated proton channels

# Overview
Voltage-gated proton channels are ion channels that have the unique property of opening with depolarization, but in a strongly pH-sensitive manner. The result is that these channels open only when the electrochemical gradient is outward, such that their opening will only allow protons to leave cells. Their function thus appears to be acid extrusion from cells.
Another important function occurs in phagocytes (e.g. eosinophils, neutrophils, macrophages) during the respiratory burst. When bacteria or other microbes are engulfed by phagocytes, the enzyme NADPH oxidase assembles in the membrane and begins to produce reactive oxygen species (ROS) that help kill bacteria. NADPH oxidase is electrogenic, moving electrons across the membrane, and proton channels open to allow proton flux to balance the electron movement electrically.
References:
1Cherny, V.V., V.S. Markin, and T.E. DeCoursey. 1995. The voltage-activated hydrogen ion conductance in rat alveolar epithelial cells is determined by the pH gradient. J. Gen. Physiol. 105:861-896.
2DeCoursey, T.E. 2003. Voltage-gated proton channels and other proton transfer pathways. Physiol. Rev. 83:475-579.
3Babior, B.M. 1999. NADPH oxidase: an update. Blood. 93:1464-1476.
4Henderson, L.M., J.B. Chappell, and O.T.G. Jones. 1987. The superoxide-generating NADPH oxidase of human neutrophils is electrogenic and associated with an H+ channel. Biochem. J. 246:325-329.
5Murphy, R., and T.E. DeCoursey. 2006. Charge compensation in phagocytes. Biochim. Biophys. Acta: Bioenergetics. 1757:996-1011.
Weizmann Institute of Science
The Weizmann Institute of Science (Template:Lang-he), known as Machon Weizmann is a university and research institute in Rehovot, Israel. It differs from other Israeli universities in that it offers only graduate and post-graduate studies in the sciences.

# History
Founded in 1934 by Chaim Weizmann as the Daniel Sieff Research Institute, it was renamed the Weizmann Institute of Science in his honor on November 2, 1949. Before he became President of the State of Israel, Weizmann pursued his research in organic chemistry at its laboratories. The Weizmann Institute presently has about 2,500 students, staff, and faculty, and awards M.Sc. and Ph.D. degrees in mathematics, computer science, physics, chemistry, biological chemistry and biology, as well as several interdisciplinary programs.

# Youth programs
In addition to its academic programs, the Weizmann Institute runs programs for young people, including science clubs, camps and competitions.  The  Bessie F. Lawrence International Summer Science Institute accepts high school graduates from all over the world for a four-week science-based summer camp.  The Clore Garden of Science, which opened in 1999, is the worlds first completely interactive outdoor science museum.

# Awards
In 1996 and 2002 respectively, two Weizmann Institute researchers - Amir Pnueli and Adi Shamir - won the Turing Award.

# Distinguished faculty
- Haim Harari, theoretical physicist
- Chaim Weizmann, chemist, first President of the State of Israel
- Ephraim Katzir, biophysicist, fourth President of the State of Israel
- Mordehai Milgrom, physicist
- Amir Pnueli, Computer science
- Adi Shamir, cryptographer
- Ada Yonath,  crystallographer
What causes eating disorders?
Eating disorders can have many different origins. For some clients, there is a fear of growing up and assuming adult responsibilities. Others function well externally, but inside are deeply confused. Some are trapped in the role of perfectionism, being the good child. Some clients experienced a major loss during childhood. Others experienced tremendous pain in social interactions. Some clients families suffer from generations of unresolved trauma. Some are enmeshed, without appropriate boundaries.
Once the eating disorder takes hold as a survival strategy, it can take on a life of its own, perpetuating a cycle of anxiety and isolation. As the cycle continues, it takes more of the same behavior to achieve the desired effect  more restriction, more food, more binging and purging, diet pills, laxatives, exercise, etc.
When a client is no longer dependent on the eating disorder , the whole world can feel upside-down, and initially, impossible to manage. This sense of crisis is a key reason Castlewood exists. We provide a safe, well-cushioned container for the distress, along with the support of a caring community, to help clients learn how to stabilize, rebuild and transform their lives.
Core Symptoms
- Weight loss or gain with endocrine or metabolic abnormalities
- Fat phobia/food phobia
- Rituals around body checking, exercise and food
- Purging by fasting, vomiting, diuretics and exercise
- Dissociation, lack of control, food cravings, rituals or addictions
- Body dissatisfaction, body image distortion
- Binge eating, secretive eating, hoarding and stealing food
- Chewing and spitting food as an attempt to control weight
- Taking in excessive amounts of fluid or restricting fluid intake
- Use or abuse of diet pills, herbal supplements or teas
- Increased isolation, spending less and less time with family and friends
- Refusing or avoiding eating with family and friends

# Reference
- Website : CastleWood Treatment Center For Eating Disorders
Xenotropic MuLV-related virus
Xenotropic MuLV-related virus (XMRV) is a newly identified and provisionally named gammaretrovirus which  may be involved in the pathology of familial prostate cancer. 
Its name refers to its similarity to xenotropic murine leukemia viruses, although it does show some substantial differences.
It is though to be linked to prostate cancer by ribonuclease L, part of the cells natural defense against viruses.  When activated, RNase L destroys RNA in an effort to halt viral gene expression.  R462Q is a mutation that results in a decreased level of RNase L function, and this mutations presence in prostate tumors shows a strong correlation with the presence of XMRV.
The virus was discovered in cancerous prostate tissues using a microarray containing samples of genetic material from over 1000 viruses.  The screen revealed the presence of a gammaretrovirus in a substantial number of the homozygous R462Q cells, but very few of the heterozygous or wild type cells.  An expanded screen showed the virus present in 40% of men homozygous for R462Q and only 1.5% of those not, and also demonstrated that each case showed the same virus.  In another study, the viral genome was reconstructed from prostate mRNA and used to infect prostate tissues in vitro.  The researchers were able to show that RNase L deficient lines were more susceptible to infection.  These data do not necessarily show that XMRV causes prostate cancer, but they do show that RNase L deficiency makes prostate tissue more susceptible to the virus.  This in turn suggests the possibility of a link between the virus and the disease.
2-Arachidonyl glyceryl ether

# Overview
2-Arachidonyl glyceryl ether (2-AGE, Noladin ether) is a putative endocannabinoid discovered by Lumir Hanus at the Hebrew University of Jerusalem, Israel. Its isolation from porcine brain and its structural elucidation and synthesis were described in 2001.

# Detection
The presence of noladin in body tissue is disputed. Although a research group from Teikyo University, Kanagawa, Japan could not detect it in the brains of mice, hamsters, guinea-pigs or pigs, two other research groups successfully detected it in animal tissues.

# Pharmacology
Noladin binds with a Ki of 21 nM to the CB1 receptor and 480 nM to the CB2 receptor. It shows agonistic behaviour on both receptors and is a partial agonist for the TRPV1 channel. After binding to CB2 receptors it inhibits adenylate cyclase and stimulates ERK-MAPK and regulates calcium transients.
In comparison to 2-arachidonoyl glycerol noladin is metabolically more stable resulting in a longer half-life time.
It lowers intraocular pressure, increases the uptake of GABA in the globus pallidus of rats and is neuroprotective by binding to and activation of PPAR.
4-aminobutyrate transaminase
In enzymology, 4-aminobutyrate transaminase (EC 2.6.1.19), also called GABA transaminase or 4-aminobutyrate aminotransferase, is an enzyme that catalyzes the chemical reaction:
Thus, the two substrates of this enzyme are 4-aminobutanoate (GABA) and 2-oxoglutarate. The two products are succinate semialdehyde and L-glutamate.
This enzyme belongs to the family of transferases, specifically the transaminases, which transfer nitrogenous groups. The systematic name of this enzyme class is 4-aminobutanoate:2-oxoglutarate aminotransferase. This enzyme participates in 5 metabolic pathways: alanine and aspartate metabolism, glutamate metabolism, beta-alanine metabolism, propanoate metabolism, and butanoate metabolism. It employs one cofactor, pyridoxal phosphate.

# Structural Studies
As of late 2007, 9 structures have been solved for this class of enzymes, with PDB accession codes 1OHV, 1OHW, 1OHY, 1SF2, 1SFF, 1SZK, 1SZS, 1SZU, and 2EO5.

# Inhibitors
- Aminooxyacetic acid
- Gabaculine
- Phenelzine
- Phenylethylidenehydrazine (PEH)
- Rosmarinic acid
- Valproic acid
- Vigabatrin
Alpha-2A adrenergic receptor
The alpha-2A adrenergic receptor (2A adrenoceptor), also known as ADRA2A, is an 2 adrenergic receptor, and also denotes the human gene encoding it.

# Receptor
2 adrenergic receptors include 3 highly homologous subtypes: 2A, 2B, and 2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. Studies in mice revealed that both the 2A and 2C subtypes were required for normal presynaptic control of transmitter release from sympathetic nerves in the heart and from central noradrenergic neurons; the 2A subtype inhibited transmitter release at high stimulation frequencies, whereas the 2C subtype modulated neurotransmission at lower levels of nerve activity.

# Gene
This gene encodes 2A subtype and it contains no introns in either its coding or untranslated sequences.

# Role in central nervous system
Although the pre-synaptic functions of 2A receptors have been a major focus (see above), the majority of 2 receptors in the brain are actually localized post-synaptically to noradrenergic terminals, and therefore aid in the function of norepinephrine. Many post-synaptic 2A receptors have important effects on brain function; for example, 2A receptors are localized on prefrontal cortical neurons where they regulate higher cognitive function.

# Ligands

## Agonists
- Clonidine
- Lofexidine
- Dexmedetomidine
- Guanfacine

## Antagonists
- 1-PP (active metabolite of buspirone and gepirone)
- Asenapine
- BRL-44408
- Clozapine
- Lurasidone
- Mianserin
- Mirtazapine
- Paliperidone
- Risperidone
- Yohimbine
Alpha-2B adrenergic receptor
The alpha-2B adrenergic receptor (2B adrenoceptor), is a G-protein coupled receptor. It is a subtype of the adrenergic receptor family. The human gene encoding this receptor has the symbol ADRA2B.
ADRA2B orthologs have been identified in several mammals.

# Receptor
2-adrenergic receptors include 3 highly homologous subtypes: 2A, 2B, and 2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system.

# Clinical significance
This gene encodes the 2B subtype, which was observed to associate with eIF-2B, a guanine nucleotide exchange protein that functions in regulation of translation. A polymorphic variant of the 2B subtype, which lacks 3 glutamic acids from a glutamic acid repeat element, was identified to have decreased G protein-coupled receptor kinase-mediated phosphorylation and desensitization; this polymorphic form is also associated with reduced basal metabolic rate in obese subjects and may therefore contribute to the pathogenesis of obesity. This gene contains no introns in either its coding or untranslated sequences.
A deletion variant of the 2B adrenergic receptor has been shown to be related to emotional memory in Europeans and Africans. This variant also predisposed people who had it to focus more on negative aspects of a situation. This predisposition remained present in people with the variant gene who took a single dose of the noradrenergic antidepressant reboxetine, but was weakened in people without the variant.

# Evolution
The ADRA2B gene (sometimes referenced as A2AB) is used in animals as a nuclear DNA phylogenetic marker. This intronless gene has first been used to explore the phylogeny of the major groups of mammals, and contributed to reveal that placental orders are distributed into four major clades: Xenarthra, Afrotheria, Laurasiatheria, and Euarchontoglires. Comparative analysis of the primary protein sequence of ADRA2B across placentals also showed the high conservation of residues thought to be involved in agonist binding and in G proteincoupling. However, great variations are observed in the very long, third intracellular loop, with a polyglutamyl domain displaying pervasive length differences.

# Ligands
- ()-Dibromophakellin
- Imiloxan
- Yohimbine