Persius/hicric huggingface dataset:
Phosphatidylcholine transfer protein
Phosphatidylcholine transfer protein (PCTP) also known as StAR-related lipid transfer domain protein 2 (STARD2) is a specific intracellular phospholipid binding protein that can transfer phosphatidylcholine between different membranes in the cytosol.
In humans, phosphatidylcholine transfer protein is encoded by the PCTP gene.

# Function
PCTP transfers phosphatidylcholine molecules between membranes in vitro.  Further studies found that sensitivity to phosphatidylcholine levels causes PCTP to interact with select enzymes, promoting their activation.  PCTP stimulates the acyl-CoA thioesterase activity of thioesterase superfamily member 2 (Them2)/acyl-CoA thioesterase 13 (ACOT13) and the activity of homeodomain transcription factor paired box gene 3 (PAX3).  Protein kinase C phosphorylation promotes localization of PCTP to the mitochondrion where it may activate Them2.

# Structure
This soluble protein is 214 amino acids long.  It is almost entirely composed of a StAR-related transfer domain (START).  X-ray crystallography shows that this domain forms a pocket that can bind a single molecule of phosphatidylcholine.
This protein also founds the StarD2 subfamily of proteins.  This subfamily consists of PCTP, StarD7, StarD10 and collagen type IV alpha-3-binding protein or StarD11, all of which bind phosphatidylcholine except for StarD11 which prefers ceramide.

# Tissue distribution and pathology
PCTP is produced in all tissues in the body at various levels.  The protein is expressed at high levels in tissues engaged in high metabolism, notably including the liver and macrophages.
No human patients with defects in PCTP have been described to date.  Mice lacking PCTP exhibit a resistance to atherosclerosis linked to changes in plasma lipid levels and changes in body weight linked to the level of brown fat use of fatty acids and Them2 activity.  Loss of PCTP in fasting mice alters the sensitivity of the liver to insulin, reducing glucose and free fatty acid levels.
Pineocytoma other diagnostic studies

# Overview
There are no other diagnostic studies associated with .
OR
 may be helpful in the diagnosis of . Findings suggestive of/diagnostic of  include , , and .
OR
Other diagnostic studies for  include , which demonstrates , , and , and , which demonstrates , , and .

# Other Diagnostic Studies
There are no other diagnostic studies associated with .
OR
 may be helpful in the diagnosis of . Findings suggestive of/diagnostic of  include:
OR
Other diagnostic studies for  include:
- , which demonstrates:
- , which demonstrates:

## Other Diagnostic Studies
Stereotactic biopsy
- A direct, visually guided biopsy of the pineal gland mass with open or neuroendoscopic surgery has been preferred due to concerns about injury to the deep cerebral veins.
- An open procedure also allows CSF to be obtained for
Tumor marker studies
Permits direct visualization of the third ventricle for staging purposes
Allows the third ventriculostomy to be performed for CSF diversion if needed.
- Tumor marker studies
- Permits direct visualization of the third ventricle for staging purposes
- Allows the third ventriculostomy to be performed for CSF diversion if needed.
- The diagnostic yield of stereotactic biopsy ranges from 94 to 100 percent.
- If the biopsy is nondiagnostic, equivocal, or suggests a benign tumor such as mature teratoma or meningioma, surgery is recommended to establish a definitive diagnosis or to identify focal areas of malignant disease
Solitary fibrous tumor of the pleura

# Overview
Solitary fibrous tumor of the pleura is mostly asymptomatic. The lesion is usually discovered incidentally on chest radiographs. The tumor may become large, occupying much of the hemithorax. When present, symptoms are usually related to the local mass effect of large lesions or to the associated paraneoplastic phenomena. Paraneoplastic manifestations include hypertrophic osteoarthropathy and hypoglycemia. Surgery is usually curative. Formerly named "benign solitary fibrous tumor of the pleura" but named changed as some of these lesions are malignant.

# Diagnosis

## Chest X-ray
- Typically demonstrate a well-defined solitary peripheral mass,

## CT
- Typically demonstrates well-defined lobular borders, acute angles with the adjacent pleural surfaces, and heterogeneous enhancement after contrast administration.
- Calcification is seen in approximately 25% of cases.

## MRI
- Heterogeneous signal intensity on both T1- and T2-weighted images.
- May show internal flow voids corresponding to the vascular nature of the tumors.
Polyhydramnios (patient information)
For the WikiDoc page for this topic, click here

# Overview
Polyhydramnios is the presence of excessive amniotic fluid surrounding the unborn infant.

# Considerations
- Amniotic fluid is a clear, slightly yellowish liquid that surrounds the unborn baby (fetus) during pregnancy. It is contained in the amniotic sac.
- While in the womb, the baby floats in the amniotic fluid. Amniotic fluid surrounds and cushions the infant throughout development. The amount of amniotic fluid is greatest at around 34 weeks into the pregnancy (gestation).
- The amniotic fluid constantly moves (circulates) as the baby swallows and "inhales" the fluid, and then releases or "exhales" the fluid through urine.
- The amniotic fluid helps:
- The developing baby move in the womb, which allows for proper bone growth
- The lungs to develop properly
- Keep a relatively constant temperature around the baby, protecting from heat loss
- Protect the baby from outside injury by cushioning sudden blows or movements

# What causes Polyhydramnios?
- Polyhydramnios can occur if the fetus does not swallow and absorb amniotic fluid in normal amounts. This can happen due to:
- Gastrointestinal disorders, such as duodenal atresia, esophageal atresia, gastroschisis, and diaphragmatic hernia
- Brain and nervous system (neurological) problems, such as anencephaly and myotonic dystrophy
- A variety of other causes, such as poorly controlled diabetes, achondroplasia, Beckwith-Wiedemann syndrome
- Polyhydramnios may also be related to increased fluid production, which occurs with:
- Certain fetal lung disorders
- Multiple gestation (for example, twins or triplets)
- Hydrops fetalis
- Sometimes, no specific cause for polyhydramnios is found.

# Diagnosis
- This condition is discovered during pregnancy. You may have noticed that your belly is getting large very quickly. You doctor or nurse measures the size of your uterus at every visit.
- If your uterus is growing faster than expected, or it is larger than normal for your baby's gestational age, the doctor or nurse may:
- Have you come back sooner than normal to re-measure
- Perform an ultrasound
- If the health care provider finds a fetal abnormality (birth defect), you may need an amniocentesis to test for a genetic defect.
- Women with polyhydramnios are also more likely to go into labor early. Mild polyhydramnios that shows up in the later part of pregnancy does not often cause serious problems. More severe polyhydramnios may be treated with medications or by having extra fluid removed.
- The baby will be delivered in a hospital with specialists who can provide immediate evaluation and treatment.

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

# Source
Post-micturition convulsion syndrome
Steven C. Campbell, M.D., Ph.D.
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# Overview
Post-micturition convulsion syndrome, also known as piss shivers, pee shivers, peegasm or whiz willies, is a phenomenon in which one feels a shiver running down the spine following urination.  
The shiver can produce a brief twitch, which is a form of myoclonus.
To date, despite years of Internet discussion and theorizing, there is no agreed-on explanation of the phenomenon and no medical research into it. However, it has been mentioned occasionally in columns, and in one internet poll, where about 83% of males and 58% of females reported experiencing it.
Prolactin-releasing peptide receptor
The prolactin-releasing peptide receptor (PrRPR) also known as G-protein coupled receptor 10 (GPR10) is a protein that in humans is encoded by the PRLHR gene.
PrRPR is a G-protein coupled receptor that binds the prolactin-releasing peptide (PRLH).

# Function
PrRPR is a 7-transmembrane domain receptor for prolactin-releasing peptide that is highly expressed in the anterior pituitary.
Protein Z-related protease inhibitor
Protein Z-dependent protease inhibitor is a protein circulating in the blood which inhibits factors Xa and XIa of the coagulation cascade. It is a member of the class of the serine protease inhibitors (serpins). Its name implies that it requires protein Z, another circulating protein, to function properly, but this only applies to its inhibition of factor X.
It is about 72 kDa heavy and 444 amino acids large. It is produced by the liver.

# Role in disease
Water et al. found deficiency of ZPI in 4.4% of a cohort of patients with thrombophilia (a tendency to thrombosis).

# History
Han et al. first described ZPI in 1998. The same group further characterised it in 2000.
Protein arginine methyltransferase 5
Protein arginine N-methyltransferase 5 is an enzyme that in humans is encoded by the PRMT5 gene.  PRMT5 symmetrically dimethylates H2AR3, H4R3, H3R2, and H3R8 in vivo, all of which are linked to a range of transcriptional regulatory events (Cell. Mol. Life Sci. (2015) 72:20412059 DOI 10.1007/s00018-015-1847-9)
PRMT5 is a highly conserved arginine methyltransferase that translocated from the cytoplasm to the nucleus at embryonic day ~E8.5, and during preimplantation development at the ~4-cell stage.

# Model organisms
Model organisms have been used in the study of PRMT5 function. A conditional knockout mouse line, called Prmt5tm2a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program  a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty five tests were carried out on mutant mice and two significant abnormalities were observed. No homozygous mutant embryos were identified during gestation, and therefore none survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice but no further abnormalities were observed.
A conditional allele of Prmt5 in the mouse limb shows that it is essential for maintaining a progenitor population, as conditional mutants have limb defects 

# Interactions
Protein arginine methyltransferase 5 has been shown to interact with:
- CLNS1A,
- Janus kinase 2,
- SNRPD3,
- SUPT5H, and
- WD repeat-containing protein 77.
Raltegravir warnings and precautions

# Warnings And Precautions

## Severe Skin and Hypersensitivity Reactions
Severe, potentially life-threatening, and fatal skin reactions have been reported. These include cases of Stevens-Johnson syndrome and toxic epidermal necrolysis. Hypersensitivity reactions have also been reported and were characterized by rash, constitutional findings, and sometimes, organ dysfunction, including hepatic failure. Discontinue ISENTRESS and other suspect agents immediately if signs or symptoms of severe skin reactions or hypersensitivity reactions develop (including, but not limited to, severe rash or rash accompanied by fever, general malaise, fatigue, muscle or joint aches, blisters, oral lesions, conjunctivitis, facial edema, hepatitis, eosinophilia, angioedema). Clinical status including liver aminotransferases should be monitored and appropriate therapy initiated. Delay in stopping ISENTRESS treatment or other suspect agents after the onset of severe rash may result in a life-threatening reaction.

## Immune Reconstitution Syndrome
Immune reconstitution syndrome has been reported in patients treated with combination antiretroviral therapy, including ISENTRESS. During the initial phase of combination antiretroviral treatment, patients whose immune systems respond may develop an inflammatory response to indolent or residual opportunistic infections (such as Mycobacterium avium infection, cytomegalovirus, Pneumocystis jiroveci pneumonia, tuberculosis), which may necessitate further evaluation and treatment.
Autoimmune disorders (such as Graves' disease, polymyositis, and Guillain-Barre syndrome) have also been reported to occur in the setting of immune reconstitution; however, the time to onset is more variable, and can occur many months after initiation of treatment.

## Phenylketonurics
ISENTRESS Chewable Tablets contain phenylalanine, a component of aspartame. Each 25 mg ISENTRESS Chewable Tablet contains approximately 0.05 mg phenylalanine. Each 100 mg ISENTRESS Chewable Tablet contains approximately 0.10 mg phenylalanine. Phenylalanine can be harmful to patients with phenylketonuria.
Sinoatrial nodal reentry tachycardia
Synonyms and keywords: SA nodal reentrant tachycardia; SANRT; sinus node reentrant tachycardia

# Overview
Sinoatrial nodal reentry tachycardia (SANRT) is caused by a reentry circuit localized to the SA node.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Ischemic heart disease

## Common Causes
- Ischemic heart disease

## Causes by Organ System

## Causes in Alphabetical Order

# Diagnosis

## Electrocardiogram
- SA node reentry tachycardia has a normal activation sequence with normal appearing p-wave that precedes a regular, narrow QRS complex.
- Although it cannot be distinguished on the surface 12 lead EKG from sinus tachycardia, unlike sinus tachycardia, SA node reentry tachycardia does often terminate with vagal maneuvers.
Sandbox: Peripheral Arterial Disease

# 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases (PAD), in collaboration with the European Society for Vascular Surgery (ESVS)

## Changes in Recommendations

## What is new in the 2017 PAD Guidelines

# 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases, in collaboration with the European Society for Vascular Surgery (ESVS)

## Recommendations in Patients with Peripheral Arterial Diseases: Best Medical Therapy

## Recommendations on Antithrombotic Therapy in Patients with Peripheral Arterial Diseases (PADs)

## Lower Extremities Artery Disease

## Antithrombotic Therapy for Peripheral Arterial Diseases (PADs) Patients Requiring Oral Anticoagulant

## Extracranial Carotid and Vertebral Artery Disease

## Recommendations for Imaging of Extracranial Carotid Arteries

## Recommendation on the Use of Embolic Protection Device During Carotid Stenting

## Recommendations for Management of Asymptomatic Carotid Artery Disease

## Recommendations on Revascularization in Patients with Symptomatic Carotid Disease

## Recommendations on the Management of Acute Mesenteric Ischaemia

## Recommendations for Management of Vertebral Artery Stenoses

## Recommendations on the Management of Subclavian Artery Stenosis

## Recommendations on Revascularization in Patients with Symptomatic Carotid Disease

## Recommendations on the Management of Acute Mesenteric Ischaemia

## Recommendations for Management of Chronic Mesenteric Artery Disease

## Recommendations for Diagnostic Strategies for Renal Artery Disease

## Recommendations for Treatment Strategies for Renal Artery Disease

## Clinical Stages of Lower Extremity Artery Disease
Saquinavir dosage and administration

# Dosage And Administration
INVIRASE must be used in combination with ritonavir because ritonavir significantly inhibits saquinavir's metabolism to provide increased plasma saquinavir levels.

## Recommended Dose
- INVIRASE 1000-mg twice daily (5  200-mg capsules or 2  500-mg tablets) in combination with ritonavir 100-mg twice daily.
- Ritonavir should be taken at the same time as INVIRASE.
- INVIRASE and ritonavir should be taken within 2 hours after a meal.
- No additional ritonavir is recommended when INVIRASE is administered with lopinavir/ritonavir 400/100 mg twice daily.
- Pediatric dose recommendations that are both reliably effective and below thresholds of concern for QT and PR interval prolongation could not be determined.

## Administration for Patients Unable to Swallow Capsules
Open the INVIRASE capsules and place the contents into an empty container. Add 15 mL of either sugar syrup or sorbitol syrup (for patients with Type 1 diabetes or glucose intolerance) OR 3 teaspoons of jam to the contents of INVIRASE capsules that are in the container. Stir with a spoon for 30 to 60 seconds. Administer the full amount prepared for each dose. Suspensions should be at room temperature before administering.
Sclerosing encapsulating peritonitis
Contributors:  Cafer Zorkun M.D., PhD.
Synonyms and Related Keywords: Abdominal cocoon, sclerosing peritonitis, encapsulating peritonitis, peritonitis chronica fibrosa incapsulata. 

# Overview
Sclerosing encapsulating peritonitis (SEP) is a rare benign cause of acute or subacute small bowel obstruction. It is characterized by total or partial encasement of the small bowel within a thick fibrocollagenous membrane.

# Etiology
- Sclerosing encapsulating peritonitis can be idiopathic or mainly secondary to chronic ambulatory peritoneal dialysis, peritoneovenous or ventriculoperitoneal shunts, or treatment with practolol.
- Various abdominal disorders such as tuberculosis, sarcoidosis, familial mediterranean fever, gastrointestinal malignancy, protein S deficiency, liver transplantation, fibrogenic foreign material and luteinized ovarian thecomas are the other rare causative factors.

# Differential Diagnosis
Sclerosing encapsulating peritonitis may be confused with congenital peritoneal encapsulation, which is characterized by a thin accessory peritoneal sac surrounding the small bowel. This asymptomtic condition is generally found incidentally during unrelated surgery and does not fit with the clinical or imaging findings in this group of patients.

# Diagnosis
- Radiographs of the abdomen can show air-fluid levels similar to those in patients with any other cause of small-bowel obstruction.
- In the appropriate clinical setting, recognition of the entire dilated small bowel at the center of the abdomen and encased within a thick fibrocollageneous membrane, as though it were in a cocoon, on a CT image is diagnostic of sclerosing encapsulating peritonitis.
- The other imaging findings may include signs of obstruction, fixation of intestinal loops, ascites or localized fluid collections, bowel wall thickening, peritoneal or mural calcification, and reactive adenopathy.

# Diagnostic Findings
Patient #1:
CT and gross pathological images demonstrate sclerosing encapsulating peritonitis. The patient was on long term peritoneal dialysis
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Scombrotoxic fish poisoning overview
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# Overview
Scombrotoxic fish poisoning, also known as scombroid toxicity or scombrotoxic poisoning is a form of food poisoning. It is caused by histamine and histamine-like products of bacterial breakdown of seafood, inhibiting its metabolism. The exact aetiology is complicated as histamine is not generally absorbed via the gut and administration of oral histamine does not replicate the symptoms. Foods notably associated with it are: tuna, mackerel, and bonito.

# Pathophysiology
Scombrotoxic fish poisoning is caused by bacterial spoilage of certain finfish such as tuna, mackerel, bonito, and, rarely, other fish. As bacteria break down fish proteins, byproducts such as histamine and other substances that block histamine breakdown build up in fish.

# Epidemiology and Demographics
Eating spoiled fish that have high levels of histamines can cause human disease.

# Risk Factors
Symptoms may be more severe in patients taking certain medications that slow the breakdown of histamine by their liver, such as isoniazide and doxycycline.

# Diagnosis

## History and Symptoms
The most common symptoms are; rash, diarrhea, flushing, sweating, headache and vomiting.

# Medical Therapy
Treatment is generally unnecessary, but antihistamines or epinephrine may be needed in certain instances.
Sharpless asymmetric dihydroxylation
Sharpless asymmetric dihydroxylation (also called the Sharpless bishydroxylation) is the chemical reaction of an alkene with osmium tetroxide in the presence of a chiral quinine ligand to form a vicinal diol.
It is common practice to perform this reaction using a catalytic amount of osmium tetroxide, which after reaction is regenerated with either potassium ferricyanide or N-methylmorpholine N-oxide. This dramatically reduces the amount of the highly toxic and very expensive osmium tetroxide needed. These four reagents are commercially available premixed ("AD-mix") The mixture containing (DHQ)2-PHAL is called AD-mix-, and the mixture containing (DHQD)2-PHAL is called AD-mix-.
Such chiral diols are important in organic synthesis. The introduction of chirality into nonchiral reactants through usage of a chiral catalysts is an important concept in organic synthesis.  This reaction was developed principally by K. Barry Sharpless building on the already known racemic Upjohn dihydroxylation, for which he was awarded a share of the 2001 Nobel Prize in Chemistry.

# Reaction mechanism
The reaction mechanism of the Sharpless dihdyroxylation begins with the formation of the osmium tetroxide - ligand complex (2).  A -cycloaddition with the alkene (3) gives the cyclic intermediate 4.  Basic hydrolysis liberates the diol (5) and the reduced osmate (6).  Finally, the stoichiometric oxidant regenerates the osmium tetroxide - ligand complex (2).

# Examples
The first step in the synthesis of azasugar 6 is a dihydroxylation reaction of the prochiral diene 1. Azasugars are pharmacologically relevant. The entire reaction sequence takes place in water as a reaction medium and protective groups were not required. Notice the chemoselectivity in the nucleophilic substitution of bromine by the hydroxyl group in step 2.
For another example of this reaction see: Kuwajima Taxol total synthesis