Persius/hicric huggingface dataset:
Drain (surgery)
A surgical drain is a tube used to remove pus, blood or other fluids from a wound.  Drains inserted after surgery do not result in faster wound healing or prevent infection but are sometimes necessary to drain body fluid which may accumulate and in itself become a focus of infection. The routine use of drains for surgical procedures is diminishing. Better radiological investigation and confidence in surgical technique have reduced their necessity.  It is felt now that drains may hinder recovery by acting as an 'anchor' limiting mobility post surgery and the drain itself may allow infection into the wound. In certain situations their use is unavoidable.
Drains may be hooked to wall suction, a portable suction device, or they may be left to drain by gravity.  Accurate recording of the volume of drainage as well as the contents is vital to ensure proper healing and monitor for excessive bleeding.  Depending on the amount of drainage, a patient may have the drain in place 1 day to weeks.  Signs of new infection or copious amounts of drainage should be reported to the health care provider immediately.  Drains will have protective dressings that will need to be changed daily/as needed.

# Types of drains
- Jackson-Pratt drain - This consists of a tube connected to a see through collection bulb.  The bulb has a drainage port which can be opened to remove fluid or air so that the bulb can be squeezed to create suction.  The drain should always stay below the area of the wound.
- Penrose drain
- Wound Vac System - Involves the use of enclosed foam and a suction device attached; this is one of the newer types of wound healing/drain devices which promotes faster tissue granulation, often used for large surgical/trauma/non-healing wounds.
- Redivac drain
- Pigtail drain - has an exterior screw to release the internal "pigtail" before it can be removed
- Davol
- Chest tube
- Wound manager
Duct of Bellini
The duct of Bellini is an anatomical structure of the kidneys, also known as papillary (collecting) duct.
The straight or collecting tubes commence in the radiate part of the renal cortex, where they receive the curved ends of the distal convoluted tubules.
They unite at short intervals with one another, the resulting tubes presenting a considerable increase in caliber, so that a series of comparatively large tubes passes from the bases of the medullary rays into the renal pyramids.
In the medulla the tubes of each pyramid converge to join a central tube, the duct of Bellini, which finally opens on the summit of one of the renal papillae; the contents of the tube are therefore discharged into one of the renal calyces.

# Eponym
So named in honor of its discoverer, Italian anatomist Lorenzo Bellini (1643-1704).
Pancreatic duct

# Overview
The pancreatic duct, or duct of Wirsung, is a duct joining the pancreas to the common bile duct to supply pancreatic juices which aid in digestion provided by the "exocrine pancreas". The pancreatic duct joins the common bile duct just prior to the ampulla of Vater, after which both ducts perforate the medial side of the second portion of the duodenum at the major duodenal papilla.
The duct of Wirsung is named after its discoverer, German anatomist Johann Georg Wirsung (1589-1643).

# Accessory pancreatic duct
Most people have just one pancreatic duct. However, some have an additional "accessory pancreatic duct", called the Duct of Santorini, which connects straight to the duodenum at the minor duodenal papilla. Both these ducts connect to the second part (the vertical one) of the duodenum.
However, the Duct of Santorini, which bypasses the Ampulla of Vater, is non-functional whereas the Duct of Wirsung is functional and carries the digestive enzymes released by the pancreas.

# Clinical significance
Compression, obstruction or inflammation of the pancreatic duct may lead to acute pancreatitis. The most common cause for obstruction is choledocholithiasis, or gallstones in the common bile duct.

# Additional images
- Accessory digestive system.
- Interior of the descending portion of the duodenum, showing bile papilla.
- Pancreas of a human embryo of five weeks.
- Pancreas of a human embryo at end of sixth week.
it:Dotto pancreatico
Dutch standards
Dutch Standards are environmental pollutant reference values used in environmental remediation, investigation and cleanup. 
The reference values for soil are adjusted for the organic matter (humus) content and soil fraction < 0.2 m (lutum - Latin, meaning "mud" or "clay"). The values below are calculated for a 'Standard Soil' with 10% organic matter and 25% lutum.
The reference values for groundwater depend on the depth of the sample, the values below are for 'shallow' groundwater, 0 - 10 m depth.
A case of environmental contamination is defined as 'serious' if >25 m3 soil or >100 m3 groundwater is contaminated above the intervention value.
Meckel syndrome
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Synonyms and keywords: Meckel-Gruber Syndrome; Gruber Syndrome; Dysencephalia Splanchnocystica;

# Overview
Meckel syndrome  is a rare, lethal, ciliopathic, genetic disorder, characterized by renal cystic dysplasia, central nervous system malformations, and hepatic developmental defects.

# Historical Perspective
It is named for Johann Meckel and Georg Gruber.

# Epidemiology and Demographics
While not precisely known, it is estimated that the general rate of incidence, according to Dr. Bergman, for Meckel syndrome is 0.02 per 10,000 births. According to another study done six years later, the incidence rate could vary from 0.07 to 0.7 per 10,000 births.
The frequency of this syndrome is much higher in Finland, where the incidence is as high as 1.1 per 10,000 births. It is estimated that Meckel syndrome accounts for 5% of all neural tube defects there.

# Diagnosis
Dysplastic kidneys are prevalent in 95% to 100% of all identified cases. When this occurs, microscopic cysts develop within the kidney and slowly destroy it, causing it to enlarge to 10 to 20 times its original size. The level of amniotic fluid within the womb may be significantly altered or remain normal, and a normal level of fluid should not be criteria for exclusion of diagnosis.
Occipital encephalocele is present in 60% to 80% of all cases, and post-axial polydactyly is present in 55% to 75% of the total number of identified cases. Bowing or shortening of the limbs are also common.
Finding at least two of the three features of the classical triad, in the presence of normal karyotype, makes the diagnosis solid. Regular ultrasounds and pro-active prenatal care can usually detect symptoms early on in a pregnancy.
EKG in athletes

# Overview
Corrado et al. have published an ESC consensus document on the screening of athletes for competitive sports. Besides a good medical history and examination, a 12 lead EKG is also part of the screening. They have set up special EKG criteria for participants in competitive sports (table 1). If one of the described findings are present on the EKG, the EKG is considered 'positive' and further evaluation is mandatory which can include echocardiography, 24-h ambulatory Holter monitoring, and exercise testing. EKG Features of cardiac diseases detectable at pre-participation screening in young competitive athletes are shown in table 2.       
Prevalence of EKG abnormalities in competitive athletes has been studied by Pellicia et al.. EKG abnormalities in their study increased with age and level of exercise. In young amateur athletes they found EKG abnormalities in about 7%, a number that rised to 40% in "adult elite athletes". Especially RBBB and left ventricular hypertrophy were often seen.
Recently fierce debate has been going on about whether an EKG should be part of the screening of apparently healthy young sporters. In Italy this screening is compulsory by law and this country is a strong advocate of the use of an EKG as part of this screening. However, others have stated that costs are too high for the yield (expressed in dollars per prevented sudden cardiac death) and an EKG is not included in the screening protocol of the American Heart Association.  

# Criteria for a positive EKG

# Cardiac diseases and their EKG features

# Prevalence of EKG abnormalities in athletes
EPH receptor A2
EPH receptor A2 (ephrin type-A receptor 2) is a protein that in humans is encoded by the EPHA2 gene.

# Function
This gene belongs to the ephrin receptor subfamily of the protein-tyrosine kinase family. EPH and EPH-related receptors have been implicated in mediating developmental events, particularly in the nervous system. Receptors in the EPH subfamily typically have a single kinase domain and an extracellular region containing a Cys-rich domain and 2 fibronectin type III repeats. The ephrin receptors are divided into two groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands. This gene encodes a protein that binds ephrin-A ligands.

# Clinical significance
It may be implicated in BRAF mutated melanomas becoming resistant to BRAF-inhibitors and MEK inhibitors. It is also the receptor by which Kaposi sarcoma-associated herpesvirus (KSHV) enters host cells; small molecule inhibitors of EphA2 have shown some ability to block KSHV entry into human cells.

# Interactions
EPH receptor A2 has been shown to interact with:
- ACP1
- Grb2,
- PIK3R1,  and
- SHC1.
EPH receptor A3
EPH receptor A3 (ephrin type-A receptor 3) is a protein that in humans is encoded by the EPHA3 gene.

# Function
This gene belongs to the ephrin receptor subfamily of the protein-tyrosine kinase family. EPH and EPH-related receptors have been implicated in mediating developmental events, particularly in the nervous system. Receptors in the EPH subfamily typically have a single kinase domain and an extracellular region containing a Cys-rich domain and 2 fibronectin type III repeats. The ephrin receptors are divided into 2 groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands. This gene encodes a protein that binds ephrin-A ligands. Two alternatively spliced transcript variants have been described for this gene.

# Interactions
EPH receptor A3 has been shown to interact with EFNB2 and EFNA5.
EPH receptor A4
EPH receptor A4 (ephrin type-A receptor 4) is a protein that in humans is encoded by the EPHA4 gene.
This gene belongs to the ephrin receptor subfamily of the protein-tyrosine kinase family. EPH and EPH-related receptors have been implicated in mediating developmental events, particularly in the nervous system. Receptors in the EPH subfamily typically have a single kinase domain and an extracellular region containing a Cys-rich domain and 2 fibronectin type III repeats. The ephrin receptors are divided into 2 groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands.
In 2012, a publication in Nature Medicine revealed a connection between EPHA4 and the neurodegenerative disease Amyotrophic lateral sclerosis (ALS), where a defective gene allows ALS patients to live considerably longer than patients with an intact gene. This opens up for development of treatment for this currently untreatable disease.
EPH receptor B2
Ephrin type-B receptor 2 is a protein that in humans is encoded by the EPHB2 gene.

# Function
Ephrin receptors and their ligands, the ephrins, mediate numerous developmental processes, particularly in the nervous system. Based on their structures and sequence relationships, ephrins are divided into the ephrin-A (EFNA) class, which are anchored to the membrane by a glycosylphosphatidylinositol linkage, and the ephrin-B (EFNB) class, which are transmembrane proteins. The Eph family of receptors are divided into 2 groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands. Ephrin receptors make up the largest subgroup of the receptor tyrosine kinase (RTK) family. The protein encoded by this gene is a receptor for ephrin-B family members.

# Animal studies
EphB2 is part of the NMDA signaling pathway and restoring expression rescues cognitive function in an animal model of Alzheimer's disease.
A recessive EphB2 gene is responsible for the  crested-feather mutation in pigeons.

# Interactions
EPH receptor B2 has been shown to interact with:
- Abl gene,
- RAS p21 protein activator 1, the  and
- Src.
THE ERASE TRIAL

# Official Title
Regression of Coronary Atherosclerotic Lesions After rHDL Infusions in Acute Coronary Syndrome Patients as Assessed by Intravascular Ultrasound

# Objective
To study the effects of reconstituted HDL on atheromatous plaque volume as assessed by intravascular ultrasound (IVUS).

# Sponsor
CSL Limited

# Timeline
The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT00225719.

# Study Description
The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT00225719.

# Eligibility Criteria

## Inclusion Criteria
- Male or female 30 - 75 years of age
- Recent acute coronary syndrome, defined as unstable angina, non-Q wave myocardial infarction, or ST elevation indicative of myocardial infarction, within the :last 14 days

## Exclusion Criteria
- Patients with > 50% stenosis in left main coronary artery
- Renal insufficiency
- Liver or hepatic disease
- Uncontrolled diabetes mellitus
- Symptomatic heart failure of NYHA class III or IV
- Soybean allergy (component of CSL-111 infusion)
- History of alcohol or drug abuse
- Warfarin or heparin anticoagulation during infusion period

# Outcomes

## Primary Outcomes
Percentage difference in volume of atheroma between follow-up and baseline on IVUS.

## Secondary Outcomes
Absolute change in coronary score, defined as the mean of minimal lumen diameter for all measured lesions on angiography, and change in plaque volume and characterization on IVUS.

# Publications

## Results
After 4 weeks of infusion, plaque volume changes was not significantly different among the placebo and CSL-111 groups combined (p=0.48). There was a significant change in atheroma volume in both groups when compared to baseline volume(-1.62% in placebo (p=0.07) and -3.41% in CSL-111 40 mg/kg (p<0.001), but the change was not significant when comparing different groups to each other (p=0.39).
There was a significant difference in plaque characterization index on IVUS where index showed -0.0097 for CSL-111 vs. 0.0128 for placebo(p=0.01). Similarly, mean differences of angiographic coronary scores were also significnat whereby mean score change was =0.039 mm for CSL-111 vs. -0.071 mm in placebo (p=0.03).
The safety of CSL-111 was well-studied.  Generally, CSL-111 was well tolerated with mild-moderate adverse events only with no varying rates between CSL-111 treatment and placebo groups except in rates of hypotension (13.8% vs. 7.1%, respectively).  Elevation in liver function tests, especially after 24 hours of infusion, were all subclinical events that later normalized with no intervention.  Notably, there was also a self-limited increase in unconjugated bilirubin.

## Conclusion
Short-term CSL-111 infusions showed significant improvement in plaque characterization index and coronary score on angiography, but did not yield significant changes in plaque or atheroma volume.  Clinically, the importance of these findings is still poorly outlined.
Ectodysplasin A
Ectodysplasin A (EDA) is a protein that in humans is encoded by the EDA gene.
Ectodysplasin A is a transmembrane protein of the TNF family which plays an important role in the development of ectodermal tissues such as skin in humans. It is recognized by the ectodysplasin A receptor.

# Function
The protein encoded by this gene is a type II membrane protein that can be cleaved by furin to produce a secreted form. The encoded protein, which belongs to the tumor necrosis factor family, acts as a homotrimer and may be involved in cell-cell signaling during the development of ectodermal organs. Along with c-Met, it has been shown to be involved in the differentiation of anatomical placodes, precursors of scales, feathers and hair follicles in vertebrates. Defects in this gene are a cause of ectodermal dysplasia, anhidrotic, which is also known as X-linked hypohidrotic ectodermal dysplasia. Several transcript variants encoding many different isoforms have been found for this gene.
Edmonton Clinic
The Edmonton Clinic, formerly known as the Health Sciences Ambulatory Learning Centre (HSALC), will be a multidisciplinary health science facility located on the University of Alberta main campus, in Edmonton, Alberta, CA.  It has been referred to as "The Mayo Clinic of the North".
The estimated cost for the 170,000 square metre facility is C$909 million; the target year for completion is 2011.  The joint venture between the University of Alberta and Capital Health will be funded by the Province of Alberta.
Family medicine, diabetes, orthopedics, neurosciences, rehabilitation and dentistry clinics at the University of Alberta will be relocated to the new facility upon completion.  It will surround the new Health Sciences LRT station, and oppose the Walter C. Mackenzie Health Sciences Centre on 114 Street.
Edward Mellanby
Professor  Edward Mellanby (1884 - 1955) discovered vitamin D and the role of the vitamin in preventing rickets in 1919.  He was born in West Hartlepool, the son of a shipyard owner, and educated at Barnard Castle School and Cambridge University.
He was professor of pharmacology at the University of Sheffield, and consultant physician at the Royal Infirmary in that city. He would serve as the secretary of the Medical Research Council from 1933 to 1949. He was a fellow of the Royal Society.
Publications include Nutrition and Disease - the Interaction of Clinical and Experimental Work (Edinburgh and London: Oliver and Boyd, 1934). In the work, he writes extensively on vitamin deficiency.
 Further biographical information.
Electrical load
If an electric circuit has a well-defined output terminal, the circuit connected to this terminal (or its input impedance) is the load.  (The term 'load' may also refer to the power consumed by a circuit; that topic is not discussed here.)
Load affects the performance of circuits that output voltages or currents, such as sensors, voltage sources, and amplifiers.  A household's power outlets provide an easy example: they are a voltage source, outputting 120 V AC for example (in USA), with the household's appliances collectively making up the load.  When a power-hungry appliance switches on, it dramatically reduces the load impedance, causing the output voltage to drop.  This drop is easily observed; for instance, turning on a vacuum cleaner dims the lights.

# A more technical approach
(Two sidenotes on generality, for advanced readers:  This discussion will disregard nonlinearity.  It will also use simple resistances, but they can be readily generalized to impedances for AC analysis.)
When discussing the effect of load on a circuit, it is helpful to disregard the circuit's actual design and consider only the Thevenin equivalent.  (The Norton equivalent works just as well, but this discussion will use the Thevenin form.)  The Thevenin equivalent of a circuit looks like this:
With no load (open-circuited terminals), all of V_S falls across the output; the output voltage is V_S.  However, the circuit will behave differently if a load is added.  We would like to ignore the details of the load circuit, as we did for the power supply, and represent it as simply as possible.  If we use an input resistance to represent the load, the complete circuit looks like this:
Whereas the voltage source by itself was an open circuit, adding the load makes a closed circuit and allows current to flow.  This current places a voltage drop across R_S, so the voltage at the output terminal is no longer V_S.  The output voltage can be determined by the voltage division rule:
Electroblotting
Electroblotting is a method in molecular biology/biochemistry/immunogenetics to transfer proteins or nucleic acids onto a membrane (generally PVDF or nitrocellulose) after gel electrophoresis. The protein or nucleic acid can then be further analyzed using probes such as specific antibodies or stains. This method can be used with all polyacrylamide and agarose gels. An alternative technique for transferring proteins from a gel is capillary blotting.
This technique was patented in 1989 by William J. Littlehales under the title "Electroblotting technique for transferring specimens from a polyacrylamide electrophoresis or like gel onto a membrane."

# Electroblotting Procedure
This technique relies upon current and a transfer buffer solution to drive proteins or nucleic acids onto a membrane. Following electrophoresis a standard tank or semi-dry blotting transfer system is set-up. A stack is put together in the following order from cathode to anode: sponge | three sheets of filter paper soaked in transfer buffer | gel | PVDF or nitrocellulose membrane | three sheets of filter paper soaked in transfer buffer | sponge. It is a necessity that the membrane is located between the gel and the anode, as the current and sample will be moving in that direction. Once the stack is prepared it is placed in the transfer system, and the current is be run for an amount of time and power based upon the materials being used.
Typically the electrophoresis gel is stained with Coomassie Blue following the transfer to ensure that a sufficient quantity of material has been transferred.
Inner cell mass

# Overview
In early embryogenesis of most eutherian mammals, the inner cell mass (abbreviated ICM and also known as the embryoblast or pluriblast (the latter term being applicable to all mammals)) is the mass of cells inside the primordial embryo that will eventually give rise to the definitive structures of the fetus. This structure forms in the earliest steps of development, before implantation into the endometrium of the uterus has occurred. The ICM lies within the blastocoele (more correctly termed "blastocyst cavity", as it is not strictly homologous to the blastocoele of anamniote vertebrates) and is entirely surrounded by the single layer of cells called trophoblast.

# Further development
The ICM differentiates into two types of cells, epiblast and hypoblast.
Only the cells of the epiblast give rise to cells inside the embryo, while hypoblast cells form only extraembryonic tissue (extraembryonic endoderm).  All three germ layers of the definitive embryo, as well as extraembryonic mesoderm, arise from the epiblast.

# Stem cells
It is the source of early stem cells.
It can form all tissues except trophoblast.

# Additional images
- Blastodermic vesicle of Vespertilio murinus.
- Section through embryonic disk of Vespertilio murinus.
Endoglycosidase
An Endoglycosidase is an enzyme that releases oligosaccharides from glycoproteins or glycolipids. Or it merely cleaves polysacharride chains between residues that are not the terminal residue, although releasing oligosaccharides from conjugated protein and lipid molecules is more common.
It breaks the glycosidic bonds between two sugar monomer in the polymer. It is different from exoglycosidase that it does not do so at the terminal residue. Hence, it is used to release long carbohydrates from conjugated molecules. If an exoglycosidase were used, every monomer in the polymer would have to be removed, one by one from the chain, taking a long time. An endoglycosidase cleaves, giving a polymeric product.
PROTEIN-x1-x2-x3-x4-x5-x6-x7-x8-x9-x10-x11-...-xn
A exoglycosidase would remove each carohydrate monomer (x) one by one from the end, starting at xn, whereas and endogylcosidae can cut at any glycosidic bond (-) and may cleave after a signature 'link oligosaccharide' that links certain carbohydrates to certain proteins.
For more information on linkages to proteins see O- and N- linked glycoproteins