Persius/hicric huggingface dataset:
Dead arm (people)
Dead arm syndrome starts with repetitive motion and forces on the posterior capsule of the shoulder. The posterior capsule is a band of fibrous tissue that interconnects with tendons of the rotator cuff of the shoulder. Four muscles and their tendons make up the rotator cuff. They cover the outside of the shoulder to hold, protect and move the joint.
Overuse can lead to a build up of tissue around the posterior capsule called hypertrophy. The next step is tightness of the posterior capsule called posterior capsular contracture. This type of problem reduces the amount the shoulder can rotate inwardly -- a motion needed by pitchers to throw the ball forward before releasing it.
Over time, with enough force, the player may develop a tear in the labrum. The labrum is a rim of cartilage around the shoulder socket to help hold the head of the humerus (upper arm) in the joint. This condition is called a superior labrum anterior posterior (SLAP) lesion. The final outcome in all these steps is the dead arm phenomenon.
The shoulder is unstable and dislocation may come next. Dead arm syndrome won't go away on its own with rest -- it must be treated. If there's a SLAP lesion, then surgery is needed to repair the problem. If the injury is caught before a SLAP tear, then physical therapy with stretching and exercise can restore it and return the player to the field.
Deductive closure
Peter D. Klein, in the second edition of The Cambridge Dictionary of Philosophy, defines closure as follows:
A set of objects, O, is said to exhibit closure or to be closed under a given operation, R, provided that for every object, x, if x is a member of O and x is R-related to any object, y, then y is a member of O. 
In propositional logic, the set of all propositions exhibits deductive closure: if set O is the set of propositions, and operation R is logical entailment ("\vdash"), then provided that proposition p is a member of O and p is R-related to q (i.e., p \vdash q), q is also a member of O. In the philosophical branch of epistemology, many philosophers have and continue to debate whether particular subsets of propositionsespecially ones ascribing knowledge or justification of a belief to a subjectare closed under deduction.

# Epistemic closure
It is not the case that knowledge is closed under deduction; that is, if person S knows p, and p entails q, then S knows q. (sometimes called the straight principle). A subject may not actually believe  q, for example, regardless of whether he or she is justified or warranted. Thus, one might instead say that knowledge is closed under known deduction: if, while knowing p, S believes q because S knows that p entails q, then S knows q. An even stronger formulation would be as such: If, while knowing various propositions, S believes p because S knows that they entail p, then S knows p. While the principle of epistemic closure is generally regarded as intuitive, philosophers such as Robert Nozick and Fred Dretske have famously argued against it.

# Justificatory closure
In the seminal 1963 paper, "Is Justified True Belief Knowledge?," Edmund Gettier gave an assumption (later called the "principle of deducibility for justification" by Irving Thalberg Jr.) that would serve as a basis for the rest of his piece: "for any proposition P, if S is justified in believing P and P entails Q, and S deduces Q from P and accepts Q as a result of this deduction, then S is justified in believing Q." This was seized upon by Thalberg, who rejected the principle in order to demonstrate that one of Gettier's examples fails to support Gettier's main thesis that justified true belief is not knowledge (in the following quotation, (1) refers to "Jones will get the job," (2) refers to "Jones has ten coins," and (3) is the logical conjunction of (1) and (2)):
Why doesn't Gettier's principle (PDJ) hold in the evidential situation he has described? You multiply your risks of being wrong with you believe a conjunction. he most elementary theory of probability indicates that Smith's prospects of being right on both (1) and (2), namely, of being right on (3), are bound to be less favorable than his prospects of being right on either (1) or (2). In fact, Smith's chances of being right on (3) might not come up to the minimum standard of justification which (1) and (2) barely satisfy, and Smith would be unjustified in accepting (3).
Urinary hesitancy
Synonyms and keywords: hesitancy; delayed urination; difficulty initiating urination; weak urine stream

# Overview
Urinary hesitancy is defined as difficulty in initiating and maintaining a flow of urine.

# Causes

## Common Causes
- Anticholinergics
- Benign prostatic hyperplasia
- Prostatic cancer
- Prostatitis
- Shy bladder syndrome
- Tricyclic antidepressants
- Urinary tract infection
- Urinary tract obstruction

## Causes by Organ System

## Causes in Alphabetical Order

# Epidemiology and Demographics
Urinary hesitancy is observed in both genders at all ages.  It tends to affect elderly males more frequently.

# Diagnosis

## Laboratory Studies
The following diagnostic studies may be of use:
- Catheterization of the bladder to determine residual urine volume and to get urine for culture (a catheterized urine specimen)
- Cystometrography
- Transrectal ultrasound of the prostate (similar to a transvaginal ultrasound)
- Urethral swab for culture
- Urinalysis and culture
- Voiding cystourethrogram

# Treatment
Treatment for urinary hesitancy depends on the cause. Often, medications such as alpha-blockers can relieve the symptoms. If you have a bacterial infection, your health care provider may prescribe antibiotics. You may need surgery to relieve a prostate obstruction (see TURP).
Delta-sarcoglycan
Delta-sarcoglycan is a protein that in humans is encoded by the SGCD gene.

# Function
The protein encoded by this gene is one of the four known components of the sarcoglycan complex, which is a subcomplex of the dystrophin-glycoprotein complex (DGC). DGC forms a link between the F-actin cytoskeleton and the extracellular matrix. This protein is expressed most abundantly in skeletal and cardiac muscle. The mutations in this gene have been associated with autosomal recessive limb-girdle muscular dystrophy and dilated cardiomyopathy. Alternatively spliced transcript variants encoding distinct isoforms have been observed.
In melanocytic cells SGCD gene expression may be regulated by MITF.

# Interactions
SGCD has been shown to interact with FLNC.
Explorer (dental)

# Overview
A  (sickle probe) is an instrument in dentistry commonly used in the dental armamentarium. A sharp point at the end of the explorer is used to enhance tactile sensation.
Until recently, it was advised that dentists use the explorer to determine the presence of tooth decay on tooth enamel. Some dental professionals have questioned this practice. Since enamel is demineralized in the early stages of tooth decay, they argue that the use of an explorer could open a cavity in the enamel where none existed previously. Instead, they argue that fluoride and oral hygiene should be used to remineralize the enamel and prevent it from decaying further. This debate still continues because sometimes decay can be difficult to diagnose without tactile verification. Additionally, radiographs and products designed to identify decay help the dental professional make a final diagnosis of tooth decay.
There are various types of explorers, though the most common one is the No. 23 explorer, which is also known as a "shepherd's hook". Other types include the 3CH (also known as "cowhorn" or "pigtail") and No. 17 explorers, which are useful for the interproximal areas between teeth.
Dialysis adequacy
In nephrology, dialysis adequacy is the measurement of renal dialysis for the purpose of determining dialysis treatment regime and to better understand the pathophysiology of renal dialysis.  It is an area of considerable controversy in nephrology.
In the US, the dominant way of measuring dialysis adequacy in Kt/V and based on the clearance of urea.

# Urea

## Comparing normal to ERSD
The normal clearance of urea is approximately 100 ml/min.  A patient getting a conventional hemodialysis treatment, without remaining residual function, has a urea clearance of 10-15 ml/min.

# p-Cresol

# beta-2 Microglobulin
Diazepam overdose

# Overdosage topics
Manifestations
Management
Flumazenil
- Seizure
Withdrawal

## Manifestations
Manifestations of Diazepam overdosage include somnolence, confusion, coma and diminished reflexes. Respiration, pulse and blood pressure should be monitored, as in all cases of drug overdosage, although, in general, these effects have been minimal following overdosage. Return to top

## Management
General supportive measures should be employed, along with immediate gastric lavage. Intravenous fluids should be administered and an adequate airway maintained. Hypotension may be combated by the use of norepinephrine or metaraminol. Dialysis is of limited value. As with the management of intentional overdosage with any drug, it should be borne in mind that multiple agents may have been ingested. Return to top

## Flumazenil
Flumazenil, a specific benzodiazepine receptor antagonist, is indicated for the complete or partial reversal of the sedative effects of benzodiazepines and may be used in situations when an overdose with a benzodiazepine is known or suspected. Prior to the administration of flumazenil, necessary measures should be instituted to secure airway, ventilation, and intravenous access. Flumazenil is intended as an adjunct to, not as a substitute for, proper management of benzodiazepine overdose. Patients treated with flumazenil should be monitored for re-sedation, respiratory depression, and other residual benzodiazepine effects for an appropriate period after treatment. Return to top

### Seizure
The prescriber should be aware of a risk of seizure in association with flumazenil treatment, particularly in long-term benzodiazepine users and in cyclic antidepressant overdose. Return to top

## Withdrawal
Withdrawal symptoms of the barbiturate type have occurred after the discontinuation of benzodiazepines. Return to top
Adapted from the FDA Package Insert.
Diazolidinyl urea
Diazolidinyl urea (C8H14N4O7) is a preservative. It has a broad spectrum of application, and is effective against bacteria, fungi and yeasts.

# Uses
It is used in many cosmetics, skin care products, shampoos and conditioners, as well as a wide range of products including bubble baths, baby wipes and household detergents.  Diazolidinyl urea is found in the commercially available preservative Germaben.

# Safety
Some people have a contact allergy to diazolidinyl urea causing dermatitis. Such people are often also allergic to imidazolidinyl urea.
Dibrompropamidine

# Overview
Dibrompropamidine is an antiseptic and disinfectant. As dibrompropamidine isethionate, it is used in eyedrops and ointment for the treatment of minor eye and eyelid infections in adults and children. In the UK, such preparations are sold under the brand names Brolene (Aventis Pharma), Golden Eye (Typharm Ltd) and Brulidine (Manx Healthcare).

# Characteristics
A white or almost white, crystalline powder; odourless or almost odourless.
Freely soluble in water ; soluble in glycerol ; sparingly soluble in ethanol (96%); practically insoluble in chloroform, in ether, in liquid paraffin and in fixed oils.
Dibutyltryptamine
Dibutyltryptamine (DBT) is a psychedelic drug belonging to the tryptamine family.  It is found either as its crystalline hydrochloride salt or as an oily or crystalline base. DBT was first made by the chemist Alexander Shulgin and reported in his book TiHKAL. Shulgin did not test DBT himself, but reports a human dosage of "1 mg/kg i.m." being active, but less so than DMT or DET. This suggests that an active dosage of DBT will be in the 100mg range. This compound has been sold as a "research chemical" and has been confirmed to be an active hallucinogen although somewhat weaker than other similar tryptamine derivatives.
There are four symmetrical isomers of DBT which can be made, or ten isomers in total if unsymmetrical substitution is used. Of these only the n-butyl analogue DBT is known to be active in humans; the isobutyl, sec-butyl, and tert-butyl isomers DIBT, DSBT and DTBT have never been tested and only DBT and DIBT were made by Shulgin.
File:DBT isomers.png
The unsymmetrical isomers BIBT, BSBT, BTBT, IBSBT, IBTBT and SBTBT are also possible but have never been made and no predictions have been made about their activity. Shulgin speculates that the s-butyl isomer DSBT may be more potent than the straight chain compound DBT, but that the more highly branched DIBT and DTBT would probably be inactive due to the bulk of the substituent group. As for longer chain compounds than butyl, they have not been made and would probably be inactive. Shulgin mentions that the monohexyl compound NHT is without activity. However the unsymmetrical compounds such as Methylbutyltryptamine show more promise, and a wide range of possible compounds could be made by pairing the various butyl isomers with methyl, ethyl, propyl, isopropyl or allyl groups.

# Reference
-  Template:CiteTiHKAL

# External link
- TiHKAL entry
Dimethylhydrazine
Dimethylhydrazine is the name of two compounds with the formula C2H8N2. These are:
- 1,1-Dimethylhydrazine, where both methyl groups are bonded to the same nitrogen atom. It is commonly used as a rocket fuel.
- 1,2-Dimethylhydrazine, where one methyl group is bonded to each of the two nitrogen atoms. It is a powerful carcinogen, associated with colon cancer in rats.
Diphenylacetylene
Diphenylacetylene is the chemical compound C6H5CCC6H5.  The molecule consists of phenyl groups attached to both ends of an alkyne.  It is a colorless crystalline material that is widely used as a building block in organic and as a ligand organometallic chemistry.

# Preparation
Several preparations for this compound exist:
- one being from benzil which is condensed with hydrazine to give the bis(hydrazone) that in turn suffers oxidation with mercury oxide HgO. 
- The compound is usually prepared from stilbene by bromination dehydrohalogenation sequence, but the product can be contaminated with stilbene, which is difficult to remove.
- One methods starts from iodobenzene and the copper salt of phenylacetylene in the Castro-Stephens coupling

# Interesting derivatives
- Reaction of Ph2C2 with tetraphenyl substituted cyclopentadienone results in the formation of hexaphenylbenzene.
- Reaction of Ph2C2 with benzal chloride in the presence of potassium t-butoxide affords the 3-alkoxycyclopropene which coverts to the cyclopropenium ion.
Disaster response

# Overview
Disaster response is a phase of the disaster management cycle.  Its preceding cycles aim to reduce the need for a disaster response, or to avoid it altogether.

# Organisations
The organisation in the United Kingdom for the provision of communcations disaster response is RAYNET. 
The UK organisation for the provision of disaster response by Off-road vehicles is the 4x4 Response Network.

### Charities
A great deal of assistance in the wake of any disaster comes from various charities, and non-governmental organisations.  See:
- List of articles about charitable foundations
- Charity Guide
- Charity fraud
- Intelligent Giving
Disease mongering
Disease mongering is a term used to describe a perceived attempt by pharmaceutical companies to promote public awareness of relatively minor conditions or diseases with the aim of increasing sales of medication. Examples include male-type baldness and certain social phobias. In discussions specifically about the validity of psychiatry, the term is frequently also used by proponents of the antipsychiatry movement and Scientology based critics to discredit psychiatry, neurobiological disorders, and the medications used for treatment. Examples include ADHD and bipolar disorder.
Proponents of this practice argue that the pharmaceutical industry is only providing the public with information about its options and that actual prescription is a matter to be discussed between patient and doctor. Opponents, however, claim that this approach leads to the unnecessary prescription of drugs, that its motivation is only to profit the drug companies, and that it may actually harm instead of help patients.
A 2006 Newcastle, New South Wales conference, reported in PLoS Medicine, explored the phenomenon further Journalist Moynihan satirised it in a BMJ "news" item that appeared in its April Fool's Day edition 2006, titled "Scientists find new disease: motivational deficiency disorder".
Joint dislocation
Joint dislocation (Latin: luxatio)  occurs when bones in a joint become displaced or misaligned. It is often caused by a sudden impact to the joint. The ligaments always become damaged as a result of a dislocation.
Once a joint is dislocated, it may reduce (return to its proper position) on its own, or it may require physical manipulation. Such manipulation, if improperly attempted, can greatly increase the severity of the injury. However delay in treatment of a dislocation may affect blood supply, ligaments, bone and joint structures, sometimes resulting in permanent disability. As with most medical conditions, expert help should be sought as soon as possible. Once reduction is achieved, the joint may be held in place through a splint (for straight joints like fingers and toes) or a bandage (for complex joints like shoulders). Shoulder injuries can be surgically stabilized, for example using arthroscopic surgery. Dislocations often require immediate medical attention. After a dislocation caution should be exercised and the joint structures stabilized and muscles strengthened. This will help reduce the chances of repetition.
The shoulders, fingers, knees, and wrists are all common places for a dislocation to occur.
Having a dislocation increases the risk of a re-occurrence. Constant dislocations can be treated via surgery or strengthening the structures surrounding the dislocated area, normally through exercise.
Frequent, or spontaneous dislocations may also be symptomatic of a serious medical condition, such as Ehlers-Danlos Syndrome.
A subluxation is a partial dislocation.
Disordered eating

# Overview
Disordered eating is a term that is used by some people to describe a wide variety of irregularities in eating behavior that do not warrant a diagnosis of a specific eating disorder such as anorexia nervosa or bulimia nervosa. People who have this kind of disordered eating patterns may be diagnosed with an eating disorder not otherwise specified. A change in eating patterns can also be caused by other mental disorders (e.g. clinical depression), or by factors that are generally considered to be unrelated to mental disorders (e.g. extreme home-sickness).
Some people think that disordered eating patterns that are not the result of a specific eating disorder are less serious than symptoms of disorders like anorexia nervosa. Others note that individual cases of disordered eating may involve serious problems with food and body image. Additionally, certain types of disordered eating can include symptoms from both classic cases of anorexia and bulimia, making the disordered eating as dangerous as regular eating disorders.
Some counselors are specialized in dealing with disordered eating patterns. The recognition that some people have eating problems that do not fit into the scope of regular specific eating disorders makes it possible for a larger proportion of people who have eating problems to receive help.
Distal axonopathy
Distal axonopathy (aka dying back neuropathy) is a type of peripheral neuropathy that results from some metabolic or toxic derangement of peripheral nervous system (PNS) neurons.
It is the most common response of nerves to metabolic or toxic disturbances, and as such may be caused by metabolic diseases such as diabetes, renal failure, deficiency syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs.
The most common cause of distal axonopathy is diabetes, and the most common distal axonopathy is diabetic neuropathy.
The most distal portions of axons are usually the first to degenerate, and axonal atrophy advances slowly towards the nerve's cell body.
If the noxious stimulus is removed, regeneration is possible, though prognosis decreases depending on the duration and severity of the stimulus.
Those with distal axonopathies usually present with symmetrical stocking-glove sensori-motor disturbances.
Deep tendon reflexes and autonomic nervous system (ANS) functions are also lost or diminished in affected areas.
Dix-Hallpike test
The Dix-Hallpike test (or Nylen-Barany test) is a diagnostic maneuver used to identify benign paroxysmal positional vertigo (BPPV).
The Dix-Hallpike test is performed with the patient sitting upright with the legs extended. Their head is then rotated by approximately 45 degrees. The clinician helps the patient to lie down backwards quickly with the head held in approximately 20 degrees of extension. This extension may either be achieved by having the clinician supporting the head as it hangs off the table or by placing a pillow under their upper back. The patient's eyes are then observed for about 45 seconds as there is a characteristic 5-10 second period of latency prior to the onset of nystagmus. If rotational nystagmus occurs then the test is considered positive for benign positional vertigo. During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the ear closest to the ground.  The direction of the fast phase is defined by the rotation of the top of the eye, either clockwise or counter-clockwise.  Home devices, such as the DizzyFIX, are available to assist in the performance of the Dix-Hallpike Maneuver for patients with a diagnosis of BPPV. 

# There are several key characteristics of a positive test
- 1) Latency of onset (usually 5-10 seconds)
- 2) Torsional (rotational) nystagmus. If no torsional nystagmus occurs but there is upbeating or downbeating nystagmus, a CNS dysfunction is indicated.
- 3) Upbeating or downbeating nystagmus.  Upbeating nystagmus indicates that the vertigo is present in the posterior semicircular canal of the tested side.  Downbeating nystagmus indicates that the vertigo is in the anterior semicircular canal of the tested side.
- 4) Fatigable nystagmus.  Multiple repetition of the test will result in less and less nystagmus.
- 5) Reversal.  Upon sitting after a positive maneuver the direction of nystagmus should reverse for a brief period of time.
To complete the test, the patient is brought back to the seated position, and the eyes are examined again to see if reversal occurs. If the test is negative it makes benign positional vertigo a less likely diagnosis and CNS involvement should be considered. Note that the nystagmus may come in paroxysms and may be delayed by several seconds after the maneuver is performed.