Persius/hicric huggingface dataset:
Critical temperature
The critical temperature, Tc, of a material is the temperature above which distinct liquid and gas phases do not exist. As the critical temperature is approached, the properties of the gas and liquid phases become the same resulting in only one phase: the supercritical fluid. Above the critical temperature a liquid cannot be formed by an increase in pressure, but with enough pressure a solid may be formed. The critical pressure is the vapor pressure at the critical temperature. On the diagram showing the thermodynamic properties for a given substance, the point at critical temperature and critical pressure is called the critical point of the substance.   The critical molar volume is the volume of one mole of material at the critical temperature and pressure.
Critical properties vary from material to material, just as is the case for the melting point and boiling point.  Critical properties for many pure substances are readily available in the literature.  Obtaining critical properties for mixtures is somewhat more problematic.
Two immiscible liquids, such as oil and water, will also have a critical temperature and pressure at which the two phases will become consolute.

# Table of critical temperature and pressure for selected substances

# Other uses

## Superconductivity
In superconductivity applications, critical temperature refers to the temperature below which a given material becomes superconductive.

## Construction
In construction, critical temperature refers to the temperature above which structural steel loses its strength and is no longer fully capable of loadbearing support. Maintaining structural and important process steel building components below this critical temperature, which varies from country to country but is generally between 500 and 560C, is an important function of passive fire protection.

# Mathematical definition
For pure substances, there is an inflection point in the critical isotherm on a pV diagram.  This means that at the critical point:
This relation can be used to evaluate two parameters for an equation of state in terms of the critical properties.
Sometimes a set of reduced properties are defined in terms of the critical properties, ie.:
The principle of corresponding states indicates that substances at equal reduced pressures and temperatures have equal reduced volumes.  This relationship is approximately true for many substances, but becomes increasingly inaccurate for large values of pr
Cross-sectional data
Cross-sectional data in statistics and econometrics is a type of one-dimensional data set.  Cross-sectional data refers to data collected by observing many subjects (such as individuals, firms or countries/regions) at the same point of time, or without regard to differences in time.  Analysis of cross-sectional data usually consists of comparing the differences among the subjects.
For example, we want to measure current obesity levels in a population. We could draw a sample of 1'000 people randomly from that population, measure their weight and height, and calculate what percentage of that sample is categorized as obese. For example, 30% of our sample were categorized as obese. This cross-sectional sample provides us with a snapshot of that population, at that one point in time. Note that we do not know based on one cross-sectional sample if obesity is increasing or decreasing; we can only describe the current rate.
Cross-sectional data differs from time series data also known as longitudinal data, which follows one subject's changes over the course of time. Another variant, panel data (or time-series cross-sectional (TSCS) data), combines both and looks at multiple subjects and how they change over the course of time. Panel analysis uses panel data to examine changes in variables over time and differences in variables between subjects.
Cumulative incidence

# Overview
Cumulative incidence (sometimes referred to as incidence proportion) is a measure of disease frequency which counts the proportion of a candidate population that becomes diseased/develops disease over a specified period of time. Cumulative incidence measures occurrence of new cases of disease. It involves the transition from one state to another, such as non-disease to diseased state (incidence of disease) or diseased to non-diseased (incidence of cure).

# Types of Cumulative Incidence Calculations
Specific forms of cumulative incidence include:
- Crude mortality rate: number of deaths due to any cause/100,000 population during a specified time period
- Infant mortality rate: number of infant deaths due to any cause/1,000 population during a specified time period
- Morbidity rate: number of illnesses due to any cause/1,000 population during a specified time period
- Live birth rate: number of live births/1,000 population or childbearing women during a specified time period
- Case fatality rate: number of deaths due to disease X/number of people with disease X during a specified time period
- Attack rate: number of new cases of disease/number population at risk at beginning of time period during specified time period

# Calculating Cumulative Incidence
It may also be calculated by the incidence rate multiplied by duration.
Basic equation: Cumulative Incidence = # new (incident) cases/total population at risk
Applied: CI = IRi - ti (where IRi is the incidence rate, ti is the specified time period)
Cysteine dioxygenase
Cysteine dioxygenase (CDO, CAS number: 37256-59-0) is a mammalian non-heme iron enzyme that catalyzes the conversion of L-cysteine to cysteine sulfinic acid (cysteine sulfinate) via the incorporation of two dioxygen-derived oxygens. Large concentrations of cysteine are toxic, and have been implicated in Parkinson's and Alzheimer's. CDO is also a tumor suppressor enzyme, that helps to prevent metastases by oxidizing the protective layer of cysteine that tumors surround themselves with in order to evade chemo- and radiation-generated hydroxyl radicals.
Mechanism The CDO mechanism is not well understood, but has been proposed to involve dioxygen(O2) binding cis to a thiolate to form reactive RS-Fe-superoxide (RS-Fe-O2), Fe-sulfenate (RS-O; a deprotonated sulfenic acid, and high-valent iron-oxo intermediates. A reactive RS-Fe-superoxide (RS-Fe-O2) intermediate is also involved in the mechanism of Isopenicillin N synthase (IPNS), however, rather than form an S-O bond, IPNS catalyzes C-S bond formation via hydrogen atom abstraction.
Cysteine sulfinic acid lies at a branch-point in cysteine catabolism, where it can follow two pathways resulting in the formation of taurine or sulfate. The cysteine sulfinic acid-dependent pathway of taurine metabolism follows the synthesis of hypotaurine (2-aminoethane sulfinate) which is subsequently oxidized to taurine. Also, cysteine sulfinate can undergo transamination to form -sulfinylpyruvate, decomposing to form pyruvate and sulfite.
Dimethylethanolamine

# Overview
Dimethylaminoethanol, also known as DMAE or dimethylethanolamine, is an organic compound. This compound also goes by the names of N,N-dimethyl-2-aminoethanol, beta-dimethylaminoethyl alcohol, beta-hydroxyethyldimethylamine and Deanol. It is a liquid with a color that ranges from clear to pale yellow.

# Industrial Uses
Dimethylaminoethanol is used as a curing agent for polyurethanes and epoxy resins. It is used to the synthesis of dyestuffs, textile auxiliaries, pharmaceuticals, emulsifiers, and corrosion inhibitors. Also it is an additive to paint removers, boiler water, and amino resins.

# Biochemical Precursor
Dimethylaminoethanol is related to choline and is a biochemical precursor to the neurotransmitter acetylcholine, and found naturally in fishes like sardines and anchovies. It is reported to have nootropic effects, although research on this chemical has found both positive and negative potential results.
It is believed that dimethylaminoethanol is methylated to produce choline in the brain. It is known that dimethylaminoethanol is processed by the liver into choline; however, the choline molecule is charged and cannot pass the blood-brain barrier.

## Research
Short term studies have shown an increase in vigilance and alertness, with a positive influence on mood.  Long term studies are equivocal.  Some showed dimethylaminoethanol to increase the lifespan of animals in which it was tested, while others indicate a possible reduction in the average life span of quail. With the uncertainty of whether this could be extrapolated to humans, dimethylaminoethanol supplementation is not generally recommended.  It is possible that dose is a major determining factor in the overall effects of dimethylaminoethanol - a high dose could produce the opposite effects than sought and contribute to life-shortening.
A recent study indicates that synthetic DMAE applied topically may alter the appearance of skin cells. "From our point of view the cells are altered. They stop dividing, they stop secreting, and after 24 hours a certain proportion of them die," said Dr. Francois Marceau of the Centre Hospitalier Universitaire de Quebec.
Marceau, a cell biologist, said he is reluctant to recommend that these products not be used. However, the findings make it clear that more research is needed on how these and similar products work. "I don't want to scare people," he added. "The risk is probably not very big, but in my opinion it hasn't been measured accurately." .
DURACLON description

# Description
Duraclon (clonidine hydrochloride injection) is a centrally-acting analgesic solution for use in continuous epidural infusion devices.
Clonidine Hydrochloride, USP, is an imidazoline derivative and exists as a mesomeric compound. The chemical names are Benzenamine,2,6-dichloro-N-2-imidazolidinylidene monohydrochloride and 2-imidazolidine monohydrochloride. The following is the structural formula:
Duraclon (clonidine hydrochloride injection) is supplied as a clear, colorless, preservative-free, pyrogen-free, aqueous sterile solution (pH 5 to 7) in single-dose, 10 mL vials.
Each mL of the 100 mcg/mL (0.1 mg/mL) concentration contains 100 mcg of Clonidine Hydrochloride, USP and 9 mg Sodium Chloride, USP in Water for Injection, USP. Hydrochloric Acid and/or Sodium Hydroxide may have been added for pH adjustment. Each 10 mL vial contains 1 mg (1000 mcg) of clonidine hydrochloride.
Each mL of the 500 mcg/mL (0.5 mg/mL) concentration contains 500 mcg of Clonidine Hydrochloride, USP and 9 mg Sodium Chloride, USP in Water for Injection, USP. Hydrochloric Acid and/or Sodium Hydroxide may have been added for pH adjustment. Each 10 mL vial contains 5 mg (5000 mcg) of clonidine hydrochloride.
Dapsone how supplied

# How Supplied
- Dapsone Tablets USP, 25 mg are available as round white scored tablets, debossed 25 above and 102 below the score and on the obverse JACOBUS in a Unit of Use carton of 30 tablets (2 x 15). The blisters are light and child-resistant. NDC 49938-102-30.
- Dapsone Tablets USP, 100 mg are available as round white scored tablets, debossed 100 above and 101 below the score and on the obverse JACOBUS in a Unit of Use carton of 30 tablets (2 x 15).The blisters are light and child-resistant. NDC 49938-101-30.
- Dapsone Tablets USP, 25 mg are available as round white scored tablets, debossed 25 above and 102 below the score and on the obverse JACOBUS in a Unit of Use carton of 28 tablets (2 x 14). The blisters are light and child-resistant. NDC 49938-102-28.
- Dapsone Tablets USP, 100 mg are available as round white scored tablets, debossed100" above and 101 below the score and on the obverse JACOBUS in a Unit of Use carton of 28 tablets (2 x 14). The blisters are light and child-resistant. NDC 49938-101-28.
Hand and foot rashes
- The most common etiologies of hand and foot rashes are irritant and dyshidrotic eczema
- Hand and foot rashes look very different, thus a careful examination is required to make a differential

# Diagnosis
- Possible dermatology referral

## History and Symptoms
- Chronic exposure to harmful chemicals or irritants
- Family history (allergy / atopy, psoriasis)
- Presence of small, clear blisters
- Nail examination
- Examine joints

## Laboratory Findings
- Culture of pustules
- Scale scrap (KOH prep)
- Fungal culture of nail

## Other Diagnostic Studies
- Patch test
- Punch biopsy

# Differential Diagnosis of Causes of Hand and foot rashes
- Dyshidrotic Eczcema
- Erythema multiforme
- Irritant or allergic hand Eczema
- Keratoderma
- Pityriasis rubra pilaris
- Psoriasis
- Reiter's Disease
- Scabies
- Secondary Syphilis
- Tinea manus (hand)
- Tinea pedis (foot)
- Varicella
- Meningococcemia 

# Treatment
- Avoid wet-work, harsh soaps, offending agents (irritants)
- Bland heavy emollients
- Topical or systemic phototherapy with psoralen with ultraviolet A phototherapy (PUVA)

# Pharmacotherapy

## Acute Pharmacotherapies
- Topical steroid ointments
- Topical antifungal agents
- Oral antifungals (for onychomycosis)
- Systemic methotrexate
- Cyclosporine
Obstructive uropathy
For patient information page click here

# Overview
Obstructive uropathy is a structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction (obstructive nephropathy).
It is a very broad term, and does not imply a location or etiology.

# Causes
It can be caused by a lesion at any point in the urinary tract.
Causes include urolithiasis and ureteral herniation.

# Diagnosis
Diagnosis is based on results of bladder catheterization, ultrasonography, CT scan, cystourethroscopy, or pyelography, depending on the level of obstruction.

## Symptoms
Symptoms, less likely in chronic obstruction, are pain radiating to the T11 to T12 dermatomes, anuria, nocturia, or polyuria.

# Treatment
Treatment, depending on cause, may require prompt drainage, instrumentation, surgery (eg, endoscopy, lithotripsy), hormonal therapy, or a combination of these modalities.

## Contraindicated medications
- Methscopolamine bromide
Obstructive_uropathy is considered an absolute contraindication to the use of the following medications:
- Glycopyrrolate
Dead-in-bed syndrome
Dead-in-bed syndrome unexpected death in young type 1 diabetic patients "with no history of diabetic complications, and in particular no autonomic dysfunction. They are found in an undisturbed bed, which seems to exclude death during a convulsive attack".
This was first described in a series of 20 patients in 1991.

# Etiology
Proposed causes include:
- Hypoglycemic unawareness or the 'hypoglycemia-unawareness syndrome'
- Hypoglycemia-induced ventricular dysrhythmia due to QT prolongation during hypoglycemia
- Hypoglycemia-induced autonomic dysfunction which may lead to ventricular dysrhythmia due to QT prolongation

# Diagnosis
Diabetic ketoacidosis may be sought during autopsy by vitreous fluid biochemical analyses .

# Prevention
Nocturnal hypoglycemia may be prevented by glucose sensors
Clinical practice guidelines by the American Diabetic Association recommend.
The MiniMed() ParadigmTM Veo system may be the most effective system. However, the cost effectiveness is not certain.
Closed loop systems (artificial pancreases) may be effective according to a systematic review.
Sensors may not completely prevent dead in bed syndrome
Exercise intolerance

# Overview
Exercise Intolerance is a term used to describe a condition where the patient is unable to do physical exercise at the level that would be expected of someone in his or her general physical condition, or experiences unusually severe post-exercise pain, fatigue, or other negative effects. Exercise intolerance is not a disease or syndrome in and of itself, but a symptom.

# Variations
Since there are many possible specific reasons why exercise could be inhibited, this is a rather slippery term.  For instance, the patient may experience unusual breathlessness (dyspnea), muscle pain (myalgia), or increasing muscle weakness while exercising, or may, after exercise, experience severe headache, nausea, or extreme fatigue.  In most cases the specific reason that exercise is not tolerated is of considerable significance when trying to isolate the cause down to a specific disease.

# Causes

## Diseases
Exercise intolerance is primarily found in organic brain diseases, mitochondrial disease and neuromuscular disease.
Many diseases have exercise intolerance as one of the only symptoms, as in the case of some of the less severe metabolic myopathies. Nonspecific fatigue or pain syndromes such as chronic fatigue syndrome, fibromyalgia and Overtraining Syndrome are all collections of symptoms, one of likely to be exercise intolerance.
- Heart block
- Junctional bradycardia

## Other
Exercise intolerance can also be caused by specific health conditions, such as heart conditions or conditions that cause back pain. Several heart conditions, such as a cardiac arrhythmia (abnormal heart rate or rhythm) or an aortic valve insufficiency, if severe enough can cause activity problems such as shortness of breath and/or exercise intolerance. People with acute back pain from an injury or chronic back pain (e.g., from a degenerative condition) may also experience exercise limitations due to muscle spasms or limited range of spinal motion.  Exercise is key for many heart and back patients, and a variety of specific exercise techniques are available for both groups. Some exercise specialists (e.g., physical therapists, athletic trainers) are trained in modifications specific to these patients.

### Hazardous
Certain conditions in particular exist where exercise, particularly rehabilitation, may be contraindicated, including:
- decompensated heart failure
- recent MI
- hypertrophic cardiomyopathy or cardiomyopathy from recent myocarditis
- active or suspected myocarditis or pericarditis
- low left ventricular ejection fraction
- severe aortic stenosis
- unstable ischemia
- unstable arrhythmia
- irregular or resting pulse greater than 100 bpm
- resting systolic blood pressure >200 mm Hg or resting diastolic blood pressure >110 mm Hg
- severe pulmonary hypertension
- suspected or known dissecting aneurysm
- recent systemic or pulmonary embolus
- pneumothorax and haemoptysis
- thrombophlebitis
Other conditions may also preclude exercising under certain conditions. Passive physiotherapy can in some instances be an alternative for some patients unable to safely self-power.
Deep cervical artery
The deep cervical artery (Profunda cervicalis) arises, in most cases, from the costocervical trunk, and is analogous to the posterior branch of an aortic intercostal artery: occasionally it is a separate branch from the subclavian artery.
Passing backward, above the eighth cervical nerve and between the transverse process of the seventh cervical vertebra and the neck of the first rib, it runs up the back of the neck, between the Semispinalis capitis and Semispinalis colli, as high as the axis vertebra, supplying these and adjacent muscles, and anastomosing with the deep division of the descending branch of the occipital, and with branches of the vertebral.
It gives off a spinal twig which enters the canal through the intervertebral foramen between the seventh cervical and first thoracic vertebrae.
Dehydration overview
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# Overview
Dehydration (hypohydration) is the removal of water (hydro in ancient Greek) from an object. Medically, it is a condition in which the body contains an insufficient volume of water for normal functioning.

# Medical therapy
The best treatment for minor dehydration is drinking water and stopping fluid loss. 
Water is preferable to sport drinks and other commercially-sold rehydration fluids, as the balance of electrolytes they provide may not match the replacement requirements of the individual. To stop fluid loss from vomiting and diarrhea, avoid solid foods and drink only clear liquids.
In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (rehydration, through oral rehydration therapy or intravenous therapy). Even in the case of serious lack of fresh water (e.g., at sea or in a desert), drinking seawater or urine does not help, nor does the consumption of alcohol.  It is often thought that the sudden influx of salt into the body from seawater will cause the cells to dehydrate and  the kidneys to overload and shut down but it has been calculated that an average adult can drink up to 0.2 liters of seawater per day before the kidneys start to fail.
When dehydrated, unnecessary sweating should be avoided, as it wastes water.  If there is only dry food, it is better not to eat, as water is necessary for digestion. For severe cases of dehydration where fainting, unconsciousness, or other severely inhibiting symptom is present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids containing a proper balance of replacement electrolytes are given orally or intravenously with continuing assessment of electrolyte status; complete resolution is the norm in all but the most extreme cases.
Dehydroascorbic acid

# Chemistry
Dehydroascorbic acid (DHA) is  an oxidized form of ascorbic acid. It is actively imported into the endoplasmic reticulum of cells and generates the oxidative potential found there. Protein disulfide isomerases are known to reduce DHA back to ascorbic acid, oxidizing their disulfide bonds in the process. Therefore L-dehydroascorbic acid is a vitamin C compound much like L-ascorbic acid. Oxidized forms of esterified ascorbic acids can be numbered at C(5) or C(6) atoms and the (free) chemical radical semi-dehydroascorbate or semidehydro ascorbic acid (SDA) to the group of dehydroascorbic acids.

# Physiological Significance

## General significance
Although there exists a transporter for Vitamin C, it is mainly present in specialized cells, whereas the glucose transporters, most notably GLUT1, ensure in most cells of the body the transport of vitamin C (in its oxidized form, DHA) where it is required as an enzyme cofactor and an intracellular antioxidant, after it is recycled back to ascorbic acid (see Transport to mitochondria).

## Transport to mitochondria
Vitamin C accumulates in mitochondria, where most of the free radicals are produced, by entering through the glucose transporters, GLUT1. It is the oxidized form (dehydroascorbic acid) that is transported by GLUT1, not the reduced form (ascorbic acid). Ascorbic acid protects the mitochondrial genome and membrane.

## Transport to the brain
Vitamin C does not enter the brain. However, the brain is one of the organs which has the greatest concentrations of vitamin C.  It is dehydroascorbate that is transported through the blood-brain barrier via de GLUT1 transporters.  DHA is then converted to vitamin C. Administration of dehydroascorbic acid confers protection from neuronal injury following stroke (ischemic stroke).
The lack of increased intracerebral hemorrhage (ICH) after the delayed administration of DHA after ischemia confers two significant advantages to this agent, which could lead to its utility at clinically relevant time points.  As a well-tolerated agent, it could be given safely in the field before arrival in the hospital and the definitive diagnosis of stroke. Furthermore, its low risk of increasing ICH when administered after stroke obviates the expenditure of valuable time within the therapeutic window by eliminating the prerequisite radiographic imaging studies.  Taken together, a pharmacological strategy to increase cerebral levels of ascorbate in stroke has tremendous potential to represent the timely translation of basic research into a relevant therapy for thromboembolic stroke in humans.