Persius/hicric huggingface dataset:
Recruitment status
Recruitment status indicates the current stage of a trial, whether it is planned, ongoing, or completed. Possible values include:
- Not yet recruiting: participants are not yet being recruited or enrolled
- Recruiting: participants are currently being recruited and enrolled
- Enrolling by invitation: participants are being (or will be) selected from a predetermined population
- Active, not recruiting: study is ongoing (i.e., patients are being treated or examined), but enrollment has completed
- Completed: the study has concluded normally; participants are no longer being examined or treated (i.e., last patient's last visit has occurred)
- Suspended: recruiting or enrolling participants has halted prematurely but potentially will resume
- Terminated: recruiting or enrolling participants has halted prematurely and will not resume; participants are no longer being examined or treated
- Withdrawn: study halted prematurely, prior to enrollment of first participant
Refeeding syndrome

# Overview
Refeeding syndrome was first observed in prisoners in the Far East at the end of World War II. Following prolonged starvation, the resumption of food precipitated cardiac failure & death. It is defined as a syndrome of "severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally or parenterally".

# Pathophysiology
In starvation or effective starvation, the body becomes dependent on the breakdown of endogenous fats and proteins. At the same time, due to poor intake, the total body stores of several essential electrolytes are depleted, namely phosphate, potassium and magnesium. Although serum levels are often low, serum levels can sometimes be maintained.
When feeding is resumed, there is a sudden large load of carbohydrate. The insulin that is secreted in response to this drives potassium and phosphate into cells. The serum levels of both electrolytes, often already low to being with, fall precipitously.
Many of the cellular ion pumps which normally maintain intra-cellular electrolyte levels are down-regulated in the starving state. These pumps normally pump phosphate, potassium and magnesium into the cells. In refeeding, the ion transporters are upregulated leading to depletion of serum levels of the above electrolytes..
The ensuing hypophosphatemia, hypokalemia and hypomagnesemia predispose to cardiac arrhythmias. Cardiac failure is sometimes precipitated by fluid retention, another not completely explained phenomenon observed in refeeding syndrome.

# Causes
Refeeding in these patients/circumstances:
- Anorexia nervosa
- Alcoholics
- Diabetic ketoacidosis
- Morbidly obese after massive weight loss
- Chronic gastrointestinal disese
Neurological dysphagia
Post-operatively, e.g. ileus
- Neurological dysphagia
- Post-operatively, e.g. ileus

# Diagnosis

## History and Symptoms
- Fluid retention
- Electrolyte disturbance
- Congestive heart failure and cardiomyopathy due to myonecrosis
- cardiac arrhythmia
- Sudden death
- Delirium - typically developing a week after refeeding, lasting a few days.  May be convulsions.
- Mild rises in liver function tests
Hypophosphatemia is characteristic, with levels typically under 0.65mmol/l but severe cases are under 0.35mmol/l.  Levels can fall within a few hours of refeeding, but the highest risk is seen in the first week.  Hypokalemia, hyponatremia and hypomagnesemia are variable.

# Treatment

## Medical Therapy
- Pre-empt - identify malnourished patients
- Monitor electrolytes and replace as appropriate. Check levels both before and during feeding as serum levels may be normal despite depletion of total body stores; levels only fall as feeding starts
Phosphate
Potassium
Magnesium
- Phosphate
- Potassium
- Magnesium
- Gentle refeeding, starting at 75% of requirements and building up over 3-5 days
- If symptoms of refeeding syndrome, stop feeding (eg stop TPN) or reduce to 50-75% requirements, and supplement phosphate.
Renal compensation

# Overview
Renal compensation is a mechanism by which the kidneys can regulate the plasma pH. It is slower than respiratory compensation, but has a greater ability to restore normal values.

# Renal compensation in acid-base disorders
In respiratory acidosis, the kidney produces and excretes ammonium (NH4+) and monophosphate, generating bicarbonate in the process while clearing acid.
In respiratory alkalosis, less HCO3- is reabsorbed, thus lowering the pH.
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Reticulocyte index

# Overview
- Reticulocytes are newly-produced red blood cells. They are slightly larger than totally mature red blood cells, and have some residual ribosomal RNA. The presence of RNA allows a visible blue stain to bind or, in the case of fluorescent dye, result in a different brightness. This allows them to be detected and counted as a distinct population.
- The Reticulocyte production index (RPI, also called a corrected reticulocyte count) is a calculated value used in the diagnosis of anemia.
- This calculation is necessary because the raw reticulocyte count is misleading in anemic patients.
- The problem arises because the reticulocyte count is not really a count but rather a percentage: it reports the number of reticulocytes as a percentage of the number of red blood cells.
- In anemia, the patient's red blood cells are depleted, creating an erroneously elevated reticulocyte count.
- The idea of the RPI is to assess whether the bone marrow is producing an appropriate response to an anemic state.
- Reticulocyte production should increase in response to any loss of red blood cells.
- It should increase within 2-3 days of a major acute hemorrhage, for instance, and reach its peak in 6-10 days.
- If reticulocyte production is not raised in response to anemia, then the anemia may be due to an acute cause with insufficient time to compensate, or there is a defect with red blood cell production in the bone marrow.
- Marrow defects include nutritional deficiencies (i.e. iron, folate, or B12) or insufficient erythropoietin, the stimulus for  red blood cell production.
- Reticulocyte Production Index is calculated as follows:
- The degree of anemia (done by normalizing hematocrit of 45%)
- Reticulocyte maturation time (RMT)
- The Reticulocyte maturation time is 1.0 days for a hematocrit of 45 % to 2.5 days for a hematocrit of 15 %:
- Reticulocyte production index =  Reticulocytes %  x  (HCT / 45)  x  (1 / RMT)
- The reticulocyte index (RI) should be between 1.0 and 2.0 for a healthy individual.
- RI < 2 with anemia indicates decreased production of reticulocytes and therefore red blood cells.
- RI > 2 with anemia indicates loss of red blood cells (destruction, bleeding, etc) leading to increased compensatory production of reticulocytes to replace the lost red blood cells. Value of 45 is usually used as a normal hematocrit.
So,in a person whose reticulocyte count is 5%, hemoglobin 7.5 g/dL, hematocrit 25%, the RPI would be:
- So,in a person whose reticulocyte count is 5%, hemoglobin 7.5 g/dL, hematocrit 25%, the RPI would be:
5 x / = 5 x (25/45) /2 = 1.4
Rhizoctonia solani
Rhizoctonia solani (teleomorph: Thanatephorus cucumeris) is a plant pathogen with a wide host range and worldwide distribution. It is one cause of the condition known as damping off, which is a cause of death of seedlings in agriculture.

# Identification
Rhizoctonai solani does not produce spores hence it is identified only from mycelial characteristics.  Its hyphal cells are multinucleate. Also, it produces white to deep brown mycelium when grown on artifical medium. The hypae are 4-15 m wide and tend to branch at righat angles.  A septum near each hyphal branch and a slight constriction at the branch are diagnostic.R. solani is subdivided into anastomosis groups (AG) based on hyphal 
fusion between compatible strains.
The teleomorph of R. solani is Thanatephorus cucumeris  It forms club-shaped basidia and four apical 
sterigmata on which oval, hyaline sporidia are borne.
Rice Krispie treat
A Rice Krispie treat is a sweet dessert or snack made from Rice Krispies, melted margarine or butter and melted marshmallows. Sometimes marshmallows and/or cereal that is seasonal is used to make these treats holiday specific. They are often homemade, but one can find them in many stores usually packaged under the Rice Krispies brand.
There are many variations to the treat; adding caramel instead of marshmallows, adding condensed milk to the mixture before adding the rice krispies, using corn syrup and peanut butter, adding mandarin oranges, vanilla and others. One variation is to use chocolate instead of marshmallows which is known as "Chocolate Crackles". Kellogg's has now produced commercial varieties of both the marshmallow and chocolate-based treats under the name of "Rice Krispies Squares".

# History
Rice Krispie treats were invented in 1928 by Mildred Day, who was at the time working for the Kellogg Company, the maker of Rice Krispies.
She used the cereal to develop the snack as a fundraiser for a Camp Fire Girls group.  Mildred Day died in June 1996 at the age of 92.

# Cereal
Kellogg's company came out with a cereal based on this treat, perhaps making the first cereal based on a dessert that was based on a cereal. Kellog's Rice Krispies Treats cereal briefly surged in popularity, and received a 6 out of 7 rating on popular breakfast critic website Mr. Breakfast. Recently this cereal has become harder to find, though a page on the Kellogg's website can help make finding their rarer cereals easy.

# See Also
- Chocolate crackles - variation with cocoa and coconut
- Sachima
Richard A. Warshak

# Background
Richard A. Warshak (b. December 18, 1949) is a clinical and research psychologist and author based in Dallas, Texas and noteworthy as a leading expert on child custody battles and Parental Alienation Syndrome (PAS). In PAS, parents who divorce often work to turn their children against the other spouse, and so many painful repercussions result when the child becomes the pawn of parental conflicts.
Warshak has written two books on child custody issues. In The Custody Revolution (Simon & Schuster, 1992), he advocates for reform of traditional custody policies, especially in relation to the important role that fathers play in their children's lives and the hazards of traditional approaches to custody in which it is always assumed that the child is better off with the mother than the father. In Divorce Poison: Protecting the Parent-Child Bond from a Vindictive Ex (Regan Books, 2002), Warshak focuses on strategies that a parent can use to deal with the animosity of an ex spouse who seeks to poison the mind and feelings of the child through such techniques as brainwashing, badmouthing, false accusations, revisionist history, and character assassination. Warshak's premise is that a "divorce poison" occurs that is psychologically damaging to the child when bitter custody and visitation battles happen, especially on a prolonged basis. Warshak also explores the violence and aggression (both conscious and unconscious) when parents battle it out for revenge and retaliation against each other.
Warshak earned his B.S. from Cornell University and his Ph.D. from the University of Texas Southwestern Medical Center. He is a Clinical Professor of Psychology at the Southwestern Medical Center and is past president of the Dallas Society for Psychoanalytic Psychology. Since 1977, as Director of the Texas Custody Research Project and Co-Principal Investigator of the National Institute of Mental Health Step-family Project, he has studied the impact of divorce and remarriage. His studies in child custody research are often cited in the social science literature and in courtrooms and legislatures, and he has consulted at the White House on custody reform. He is also the author of the widely used Warshak Inventory for Child and Adolescent Assessment (WICAA), which provides an organized format for developmental and family histories.
Rifampin isoniazid

# Overview

## Rifampin
Rifampin was introduced in 1967, as a major addition to the cocktail-drug treatment of tuberculosis and inactive meningitis, along with pyrazinamide, isoniazid, ethambutol and streptomycin ("PIERS"). It requires a prescription in North America. It must be administered regularly daily for several months without break; otherwise, the risk of drug-resistant tuberculosis is greatly increased. In fact, this is the primary reason it is used in tandem with the three aforementioned drugs, particularly isoniazid. This is also the primary motivation behind directly observed therapy for tuberculosis.

## Isoniazid
Isoniazid also known as isonicotinylhydrazine (INH), is an organic compound that is the first-line medication in prevention and treatment of tuberculosis. The compound was first synthesized in the early 20th century, but its activity against tuberculosis was first reported in the early 1950s, and three pharmaceutical companies attempted unsuccessfully to simultaneously patent the drug (the most prominent one being Roche, which launched its version, Rimifon, in 1952). The drug was first tested at Many Farms, a Navajo community, due to the Navajo reservation's dire tuberculosis problem and the fact that the population was naive with respect to streptomycin, the main tuberculosis treatment at the time. With the introduction of isoniazid, a cure for tuberculosis was first considered reasonable.

# Category
Antimycobacterial

# US Brand Names
RIFAMATE

# FDA Package Insert
Description

# Mechanisms of Action

# Rifampin
Rifampin inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA-dependent RNA polymerase.
Crystal structure data and biochemical data indicate that rifampicin binds to RNA polymerase at a site adjacent to the RNA polymerase active center and blocks RNA synthesis by physically preventing extension of RNA products beyond a length of 2-3 nucleotides ("steric-occlusion" mechanism).
Resistance to rifampin arises from mutations that alter residues of the rifampin binding site on RNA polymerase, resulting in decreased affinity for rifampin.  Resistant mutations map to the rpoB gene, encoding RNA polymerase beta subunit.

# Isoniazid
Isoniazid is a prodrug and must be activated by a bacterial catalase-peroxidase enzyme that in M. tuberculosis is called KatG.  KatG couples the isonicotinic acyl with NADH to form isonicotinic acyl-NADH complex. This complex binds tightly to the enoyl-acyl carrier protein reductase known as InhA, thereby blocking the natural enoyl-AcpM substrate and the action of fatty acid synthase. This process inhibits the synthesis of mycolic acid, required for the mycobacterial cell wall. A range of radicals are produced by KatG activation of isoniazid, including nitric oxide, which has also been shown to be important in the action of another antimycobacterial prodrug PA-824.
Isoniazid is bactericidal to rapidly dividing mycobacteria, but is bacteriostatic if the mycobacteria are slow-growing.
Isoniazid inhibits the CYP450 system.
Right colic artery
The Right Colic Artery arises from about the middle of the concavity of the superior mesenteric artery, or from a stem common to it and the ileocolic.
It passes to the right behind the peritoneum, and in front of the right internal spermatic or ovarian vessels, the right ureter and the Psoas major, toward the middle of the ascending colon; sometimes the vessel lies at a higher level, and crosses the descending part of the duodenum and the lower end of the right kidney.
At the colon it divides into a descending branch, which anastomoses with the ileocolic, and an ascending branch, which anastomoses with the middle colic.
These branches form arches, from the convexity of which vessels are distributed to the ascending colon.
Robert M. Anderson
Robert M. Anderson, M.D., is Emeritus Associate Professor of Surgery and retired Associate Dean of the University of Arizona College of Medicine in Tucson, Arizona.
Address: 4625 E. San Carlos Place, Tucson, AZ 85712
Telephone: (520) 323-6599
e-mail: 
Dr Anderson is a Fellow of both the American College of Cardiology and the American College of Surgeons, and a Diplomate of the American Board of Surgeons.
Dr. Anderson has devoted most of his academic career to cardiovascular research and teaching.
Dr Anderson was a pioneer in heart surgery and an inventor of cardiopulmonary bypass equipment. He is the author of more than fifty scientific papers. His mechanical heart patent (U.S. Patent no. 3,518,033, applied for Nov. 28, 1966) entitled Extracorporeal Heart, is based on physiologic factors that his research delineated as essential for mechanical heart replacement. The model presented herein incorporates those factors. The model has proved to be such an effective teaching tool that it is hoped others will reproduce it to introduce their students to cardiovascular physiology.
Originally published in 1993, the printed version of The Gross Physiology of the Cardiovascular System (ISBN 0-9617528-1-5) is currently available at medical school libraries throughout the United States. Although the book appears to be long out-of-print and hard to find, most of the text can be found in his website. The text in this book is a far more powerful explanation of the determinants of cardiac output than the 'stroke rate times stroke volume' equation we all learned in introductory physiology (indeed, it reveals why that particular equation is not particularly helpful in advancing an understanding of how, in fact, the cardiovascular system works; for example, in most normal physiologic states, increasing the stroke rate leads to a reduction in stroke volume, rather than an increase in output).
Dr. Anderson's account is also revelatory about what accounts for the maintenance of blood volume equilibrium between the pulmonary and systemic circuits (rather than being some complicated homeostatic feedback mechanism, it's basically due to the unique characteristics of the heart as a non-sucking pump).
A video of the model, entitled The Determinants of Cardiac Output, is also available on his website, and is available in the library of the University of Arizona College of Medicine (library call number WG 106 VT 2 1980).

# Additional Resources
- The Gross Physiology of the Cardiovascular System
- US Patent Explanation for Innovation of Extracorporeal Heart
Rocuronium bromide

# Overview
Rocuronium (Zemuron, Esmeron) is an aminosteroid non-depolarizing  neuromuscular blocker or muscle relaxant used in modern anaesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.

# Development
It was designed to be a weaker antagonist at the neuromuscular junction than pancuronium; hence its monoquaternary structure and its having an allyl group and a pyrrolidine group attached to the D ring quaternary nitrogen atom.  Introduced in 1994, rocuronium has rapid onset, and intermediate duration of action.  It is marketed under the trade name of Zemuron  in the United States and Esmeron  in most other countries.
There is considered to be a risk of allergic reaction to the drug in some patients (particularly those with asthma), but a similar incidence of allergic reactions has been observed by using other members of the same drug class (non-depolarizing neuromuscular blocking drugs).
The -cyclodextrin derivative sugammadex (trade name Bridion) has been recently introduced as a novel agent to reverse the action of rocuronium.   Sugammadex has been in use since 2009 in many European countries, however it has been turned down for approval twice by the US FDA and is currently unavailable for use in the US due to concerns over allergic reactions and bleeding. 
On July 27, 2012, the State of Virginia replaced pancuronium bromide, one of the three drugs used in execution by lethal injection, with rocuronium.
Rubidium hydroxide
Rubidium Hydroxide (RbOH) is a strong basic chemical and alkali that is formed by one rubidium ion and one hydroxide ion.
Rubidium hydroxide does not appear in nature. However it can be obtained by synthesis from rubidium oxide. In addition, rubidium hydroxide is commercially available in form of an aqueous solution from a few suppliers.
Rubidium hydroxide is highly corrosive, therefore suitable protective clothing, gloves and eye-face protection are required when handling this material.

# Synthesis
Rubidium hydroxide can be synthesized from rubidium oxide by dissolving the oxide into water:
Rubidium hydroxide is also commercially available from a certain number of chemical suppliers in form of 50% or 99% aqueous solution at multiples of 5 g.

# Uses
Rubidium hydroxide is rarely used in industrial processes because potassium hydroxide and sodium hydroxide can perform nearly all the industrial functions of rubidium hydroxide in a less violent and hence safer way.
Rubidium hydroxide is used in scientific research. It is often used sparingly to prevent waste of the expensive element rubidium.
Despite the fact that rubidium hydroxide is rarely used in normal industrial processes, it is notable that the synthesis of nearly all rubidium compounds involves rubidium hydroxide as an intermediate.  Natural rubidium oxide is added to water, and the resulting reaction forms soluble rubidium hydroxide as a product.

# Hazard prevention
Rubidium hydroxide is a corrosive compound that causes immediate burns to the skin on contact. Ultimate care must be carried out when handling this chemical.
In the laboratory, protective clothing, gloves, and eye-face protection made from alkali-resistant materials are to be worn to prevent injury caused by accidental leakage of rubidium hydroxide onto human skin.
Dilution of this strong alkali must be done by adding the hydroxide slowly into the beaker of water.
In addition, chemical experiments on this compound must be performed with caution to prevent the great amount of heat released in an exothermic reaction from causing the solution to boil-over or damage the vessel.
SMK box riboswitch
The SMK box riboswitch is an RNA element that regulates gene expression in bacteria.  The SMK box riboswitch is found in the 5' UTR of the MetK gene in lactic acid bacteria. The structure of this element changes upon binding to S-adenosyl methionine (SAM) to a conformation that blocks the shine-dalgarno sequence and blocks translation of the gene.
There are two other known SAM-binding riboswitches: SAM-I, SAM-II, but these appear to share no similarity in sequence or structure.

# Structure
This riboswitch is composed of a single stem-loop.  In some species there are large insertions of up to 210 nucleotides within this structure.