Persius/hicric huggingface dataset:
Diagnostic kinesiology
Diagnostic Kinesiology is another name for applied kinesiology. This is not to be confused with academic kinesiology which is concerned with the study of human movement.  Chiropractors who have taken courses in the applied/diagnostic kinesiology techniques tend to use the word "diagnostic" instead of "applied".

# History
As a diagnostic method, diagnostic kinesiology was developed in 1964 by a Detroit chiropractor named George J. Goodheart.  After several unsuccessful attempts to treat a man with winging of the scapula, he noticed that there were several palpable nodules on the front of the ribcage where the serratus anterior muscle attaches.  After massaging these nodules for a few minutes he noticed that the winging of the scapula was gone.  Thus was born the idea that there could be an immediate return to strength of muscles after a proper therapy was applied.  Dr. Goodheart went on to discover many new techniques to add to his now named technique called "applied kinesiology." Chiropractors began to take post-graduate seminars from Dr. Goodheart and were soon making discoveries of their own. The field of diagnostic kinesiology quickly expanded as doctors formed their own techniques based on Dr. Goodheart's original AK.

# Research Compendia on Diagnostic and Applied Kinesiology
The official compendium from ICAK
Evidence-based decision making in clinical practice requires, first of all, evidence. The other sites listed below offer more of the research evidence from peer-reviewed scientific journals about the methods, clinical efficacy, and neurologic rationales of applied kinesiology.
Diastolic heart murmur

# Overview
Diastolic heart murmurs are heart murmurs heard during diastole.Diastolic murmurs  start at or after S2 and end before or at S1. Many involve stenosis of the atrioventricular valves or regurgitation of the semilunar valves.

# Types
- Early diastolic murmurs start at the same time as S2 with the close of the semilunar (aortic & pulmonary) valves and typically end before S1. Common causes include aortic or pulmonary regurgitation and left anterior descending artery stenosis.
- Mid-diastolic  murmurs start after S2 and end before S1. They are due to turbulent flow across the atrioventricular (mitral & tricuspid) valves during the rapid filling phase from mitral or tricuspid stenosis.
- Late diastolic (presystolic) murmurs start after S2 and extend up to S1 and have a crescendo configuration.  They can be associated with AV valve narrowing. They include mitral stenosis, tricupsid stenosis, myxoma, and complete heart block.

# Individual murmurs

# 2008 and Incorporated 2006 ACC/AHA Guidelines for the Management of Patients with Valvular Heart Disease (DO NOT EDIT) 

## Echocardiography in Diastolic Heart Murmur (DO NOT EDIT) 

# Sources
- 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease
Diathesis-stress model
The diathesis-stress model is a psychological theory that explains behaviour as both a result of biological and genetic factors ("nature"), and life experiences ("nurture"). This theory is often used to describe the pronunciation of mental disorders, like schizophrenia, that are produced by the interaction of a vulnerable hereditary predisposition, with precipitating events in the environment. This theory was originally introduced as a means to explain some of the causes of schizophrenia (Zubin & Spring, 1977).

# Vulnerability / predisposition
In the diathesis-stress model, a non-biological or genetic vulnerability or predisposition (diathesis) interacts with the environment and life events (stressors) to trigger behaviors or psychological disorders.  The greater the underlying vulnerability, the less stress is needed to trigger the behavior/disorder.  Conversely, where there is a smaller genetic contribution greater life stress is required to produce the particular result. Even so, someone with a diathesis towards a disorder does not necessarily mean they will ever develop the disorder. Both the diathesis and the stress are required for this to happen.

# Reformulation
The diathesis-stress model has been reformulated in the last 20 years as the stress-vulnerability-protective factors model, particularly by Dr. Robert P. Liberman and his colleagues in the field of psychiatric rehabilitation.

# Effects
This model has had profound benefits for people with severe and persistent mental illnesses.  It has stimulated research on the common stressors that people with disorders such as schizophrenia experience.  More importantly, it has stimulated research and treatment on how to mitigate this stress, and therefore reduce the expression of the diathesis, by developing protective factors.  Protective factors include rigorous and nuanced psychopharmacology, skill building (especially problem solving and basic communication skills) and the development of support systems for individuals with these illnesses.  Even more importantly, the stress-vulnerability-protective factors model has allowed mental health workers, family members, and clients to create a sophisticated personal profile of what happens when the person is doing poorly (the diathesis), what hurts (the stressors), and what helps (the protective factors).  This has resulted in more humane, effective, efficient, and empowering treatment interventions.
Didanosine description

# Description
VIDEX is a brand name for didanosine, USP, a synthetic purine nucleoside analogue active against HIV-1.
Didanosine is available as VIDEX, a Pediatric Powder for Oral Solution  and as VIDEX EC Delayed-Release Capsules, containing enteric-coated beadlets.
The chemical name for didanosine is 2,3-dideoxyinosine. The structural formula is:
Didanosine is a white crystalline powder with the molecular formula C10H12N4O3 and a molecular weight of 236.2. The aqueous solubility of didanosine at 25 C and pH of approximately 6 is 27.3 mg/mL. Didanosine is unstable in acidic solutions. For example, at pH less than 3 and 37 C, 10% of didanosine decomposes to hypoxanthine in less than 2 minutes.
Eosinophilic fasciitis
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Synonyms and keywords: EF; Schulman syndrome

# Overview
Eosinophilic fasciitis (pronounced Template:IPA), or EF, is a form of fasciitis. It is distinguished from scleroderma primarily because the affected area is the fascia, not the dermis as in scleroderma. Also, unlike scleroderma, Raynaud's phenomenon and telangiectasia are not observed.
It was first described in 1975, and it is not yet known whether it is actually a distinct condition or just a different presentation. However, it remains used for diagnostic purposes.
It is more common in men than in women. Several cases have been reported after strenuous exercise.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
The cause of eosinophilic fasciitis is unknown. Fewer than 300 cases have been reported in the past 35 years.
People with this condition have a buildup of eosinophils, a type of white blood cell, in the affected fascia and muscles. Eosinophils are related to allergic reactions, but their exact function is unknown.

# Differentiating Eosinophilic Fasciitis from other Diseases
Eosinophilic fasciitis must be differentiated from other diseases that cause skin thickening and edema such as:
- Scleredema
- Scleroderma
- Scleromyxedema
- Chronic graft-versus-host disease
- Drug induced scleroderma
- Scleroderma overlap syndromes
- Diabetic cheiroarthropathy
- Myxedema
- Nephrogenic systemic fibrosis
For more information on differentiating eosinophilic fasciitis, click here.

# Epidemiology and Demographic

## Age

## Gender

## Race

# Risk Factors
The syndrome affects people of any age, but is more common in people ages 30 to 60.

# Natural History, Complications and Prognosis
In most cases, the condition goes away within 3 to 5 years. However, symptoms may return (recur) or persist. The outlook is much worse if blood diseases occur. Arthritis is a rare complication of eosinophilic fasciitis. Some patients may develop very serious blood disorders or blood-related cancers, such as aplastic anemia or leukemia.

# Diagnosis

## Diagnostic Criteria

## Symptoms
- Bone pain or tenderness
- Carpal tunnel syndrome
- Numbness or tingling in one or both hands
- Pain in one or both hands
- Weakness in one or both hands
- Muscle weakness

## Physical Examination
- Tenderness and swelling of the arms and legs (occasionally including joints)
- Thickened skin with puckered appearance

## Laboratory Findings
Tests that may be done include:
- Gamma globulins (a type of immune system cell)
- Erythrocyte sedimentation rate (ESR)
- MRI
- Muscle biopsy
- Skin biopsy

## Imaging Findings

## Other Diagnostic Findings

# Treatment

## Medical Therapy
Common treatments include corticosteroids such as prednisone, though other medications such as hydroxychloroquine have also been used.

## Surgery

## Prevention

# Related Chapters
- Eosinophilia
PCI in the long lesion

# Overview
A diffuse lesion is defined as a coronary artery lesion of greater than 20 mm in length. It may also be referred to as diffuse disease, extensive lesion or long lesion. Resistance to coronary blood flow in a coronary vessel is not only due to the severity of a focal stenosis, but also to the length of that stenosis. Long lesions that are moderate in nature may therefore cause a significant resistance to flow.

# PCI in The Long Lesion

## Treatment
- A single stent that is very long should be placed to minimize stent overlap which is associated with greater risk of stent thrombosis.
- If a bare metal stent is placed, it should be remembered that the risk of restenosis proportional to the length of the bare metal stent placed in the segment.
- There some data to suggest that glycoprotein IIbIIIa inhibition is of greater use in longer lesions given the greater extent of vessel injury.

## Complications
Long lesions are associated with a greater plaque burden and as such are likewise associated with a greater risk of no reflow. Longer lesions are also associated with an increased risk of side branch occlusion.
Diiodohydroxyquinoline

# Overview
The quinoline derivative diiodohydroxyquinoline (INN) or iodoquinol (USAN), can be used in the treatment of amoebiasis.
It is poorly absorbed from the gastrointestinal tract and is used as a luminal amebicide. It acts by chelation of ferrous ions essential for metabolism.
It was discovered by Adco Co. and introduced as diiodohydroxyquinoline.
Susceptibility of Dientamoeba fragilis has been measured.
Iodoquinol is an amebocide used against Entamoeba histolytica, and it is active against both cysts and trophozoites that are localized in the lumen of the intestine. It is considered the drug of choice for treating asymptomatic or moderate forms of amebiasis. The mechanism of action is unknown. Iodoquinol is used for diseases caused by moderate intestinal amebiasis.
Dipeptidyl peptidase-4
Dipeptidyl peptidase-4 (DPP4), also known as adenosine deaminase complexing protein 2 or CD26 (cluster of differentiation 26) is a protein that, in humans, is encoded by the DPP4 gene. DPP4 is related to FAP, DPP8, and DPP9. The enzyme was discovered in 1966 by Hopsu-Havu and Glenner, and as a result of various studies on chemism, was called dipeptidyl peptidase IV .

# Function
The protein encoded by the DPP4 gene is an enzyme expressed on the surface of most cell types and is associated with immune regulation, signal transduction, and apoptosis. It is a type II transmembrane glycoprotein, but a soluble form, which lacks the intracellular and transmembrane part, is present in blood plasma and various body fluids. DPP-4 is a serine exopeptidase that cleaves X-proline or X-alanine dipeptides from the N-terminus of polypeptides. Peptide bonds involving the cyclic amino acid proline cannot be cleaved by the majority of proteases and an N-terminal X-proline "shields" various biopeptides. Extracellular proline-specific proteases therefore play an important role in the regulation of these biopeptides.
DPP-4 is known to cleave a broad range of substrates including growth factors, chemokines, neuropeptides, and vasoactive peptides. The cleaved substrates loose their biological activity in the majority of cases, but in the case of the chemokine RANTES and neuropeptide Y, DPP-4 mediated cleavage leads to a shift in the receptor subtype binding.
DPP4 plays a major role in glucose metabolism. It is responsible for the degradation of incretins such as GLP-1. Furthermore, it appears to work as a suppressor in the development of some tumors.
DPP-4 also binds the enzyme adenosine deaminase specifically and with high affinity. The significance of this interaction has yet to be established.

# Animal studies
Animal studies suggest its pathogenetic role in development of fibrosis of various organs, such as liver and kidney.

# Clinical significance
CD26/DPPIV plays an important role in tumor biology, and is useful as a marker for various cancers, with its levels either on the cell surface or in the serum increased in some neoplasms and decreased in others.
A class of oral hypoglycemics called dipeptidyl peptidase-4 inhibitors works by inhibiting the action of this enzyme, thereby prolonging incretin effect in vivo.
Middle East respiratory syndrome coronavirus has been found to bind to DPP4.  It is found on the surface of cells in the airways (such as the lungs) and kidneys. Scientists may be able to use this to their advantage by blocking the virus's entry into the cell.
Direct inguinal hernia

# Overview
The direct inguinal hernia, a type of inguinal hernia, enters through a weak point in the fascia of the abdominal wall, and its sac is noted to be medial to the inferior epigastric vessels.  Direct inguinal hernias are the same in men and women.
A direct inguinal hernia protrudes through a weakened area in the transversalis fascia near the medial inguinal fossa within an anatomic region known as the medial or Hesselbach's triangle, an area defined by the edge of the rectus abdominis muscle, the inguinal ligament and the inferior epigastric artery. These hernias and are also capable of exiting via the external ring and moving on to the scrotum.
When a patient suffers a simultaneous direct and indirect hernia on the same side, the result is called a "pantaloon" hernia (because it looks like a pair of pants, with the epigastric vessels in the crotch), and the defects can be repaired separately or together.
Dissociative disorders

# Overview
Dissociative Disorders are defined as conditions that involve disruptions or breakdowns of memory, awareness, identity and/or perception. The hypothesis is that symptoms can result, to the extent of interfering with a person's general functioning, when one or more of these functions is disrupted.
The four dissociative disorders listed in the DSM IV TR are as follows:
- Depersonalization disorder (DSM-IV Codes 300.6) - periods of detachment from self or surrounding which may be experienced as "unreal"  (lacking in control of or "outside of" self) while retaining awareness that this is only a feeling and not a reality.
- Derealization disorder feeling as though one's environment is lacking in spontaneity, emotional colouring and depth.
- Dissociative Amnesia (DSM-IV Codes 300.12) - noticeable impairment of recall resulting from emotional trauma
- Dissociative fugue (DSM-IV Codes 300.13) - physical desertion of familiar surroundings and experience of impaired recall of the past. This may lead to confusion about actual identity and the assumption of a new identity.
- Dissociative identity disorder (DSM-IV Codes 300.14) - the alternation of two or more distinct personality states with impaired recall, among personality states, of important information.
In addition, there's the diagnosis of dissociative disorder not otherwise specified (DSM-IV Codes 300.15) which can be used for forms of pathological dissociation not covered by any of the specified dissociative disorders.
In a 2007 study, only 28.7% of the dissociative participants had received psychiatric treatment previously.
Dk phocomelia syndrome
Phocomelia Syndrome is a birth defect that may occur sporadically or be genetically transmitted in some cases. In other cases it may be caused by toxins (such as certain drugs) taken by a pregnant woman. Major symptoms may include growth and mental deficiencies, defects in the eyes, ears, and nose, and characteristic deficient limb development affecting the arms and possibly the legs.

# Summary
Symmetrical phocomelia-like limb defects similar to those seen in thalidomide embryopathy (hence the synonym SC-pseudothalidomide syndrome), flexion contractures of the joints, facial anomalies, micrognathia, scanty blond hair, cloudy corneae, delayed growth, and occasional mental retardation. SC phocomelia and Roberts syndrome are considered by some as the same entity termed Roberts-SC phocomelia syndrome. The syndrome was first observed in a family with surname beginning with S and another with surname beginning with C.

# Major Features
- Head and neck: Micrognathia is the most common characteristic. Microbrachycephalic skull with wormian bones in the occipital region may occur.
- Ears: Hypoplastic cartilage.
- Eyes: Cloudy corneae.
- Nose: Hypoplastic cartilage.
- Hand and foot: Hand abnormalities may include absence of the thumb, shortening of the first metacarpal bone, hypoplasia of the first digit, fusion of the fourth and fifth metacarpals, clinodactyly of the second and fifth digits, and hypoplasia of the middle phalanges.
- Extremities: Symmetric reduction deformity (upper limbs being more severely affected than the lower ones) and flexion contractures of the joints.
- Skin appendages: Hypotrichosis with scanty silvery blond hair.
- Growth and development: Growth and occasional mental retardation.

# Heredity
The syndrome is familial and is transmitted as an autosomal recessive trait. 
Additional features: Capillary hemangioma of the face, ears, and forehead. 
Historical References Hermann J et al A familial dysmorphogenic syndrome of limb deformities, characteristic facial appearance and associated anomalies: The "pseudothalidomide" or "SC-syndrome". Birth Defects, 1969, 5(3):81-9

# External link
- PHOCOMELIA
Dobrava-Belgrade virus

# OVERVIEW
Dobrava-Belgrade virus (DOBV), also known as Dobrava virus, is an enveloped, single-stranded, negative-sense RNA virus species of Old World Hantavirus. It is one of several species of Hantavirus that is the causative agent of severe Hantavirus hemorrhagic fever with renal syndrome. It was first isolated from yellow-necked mice (Apodemus flavicollis) found in Dobrava Village, Slovenia, Yugoslavia. It was subsequently isolated in striped field mice in Estonia and other parts of Eastern Europe. It has also been found in Germany but the reservoir host there is unknown.

# Reservoir
Dobrava virus and the variants of Dobrava-Belgrade virus have been found in the Yellow-necked mouse (Apodemus flavicollis), the Striped field mouse (Apodemus agrarius) and Black Sea field mouse (Apodemus ponticus).

# Morbidity and Mortality
The fatality rate is 12%, making Dobrava virus the most life-threatening hantavirus disease in Europe. Variant DOBV genotypes have different degrees of pathogenicity.
Dorsal carpal ligament
The extensor indicis proprius (Extensor indicis) is a narrow, elongated muscle, placed medial to, and parallel with, the extensor pollicis longus.

# Origin and insertion
It arises, from the dorsal surface of the body of the ulna below the origin of the Extensor pollicis longus, and from the interosseous membrane.
Its tendon passes under the dorsal carpal ligament in the same compartment as that which transmits the tendons of the Extensor digitorum communis, and opposite the head of the second metacarpal bone, joins the ulnar side of the tendon of the Extensor digitorum communis which belongs to the index finger.

# Action
The Extensor indicis proprius extends the index finger, and by its continued action assists in extending the wrist.

# Additional images
- Bones of left forearm. Posterior aspect.
- Posterior surface of the forearm. Deep muscles.
Posterior surface of the forearm. Deep muscles.
- Transverse section across the wrist and digits.
Dorsal scapular artery
The dorsal scapular artery (or descending scapular artery) is a blood vessel which supplies the latissimus dorsi, levator scapulae, rhomboids, and trapezius.
It most frequently arises from the subclavian artery (the second or third part), but a quarter of the time it arises from the transverse cervical artery.  In that case, the artery is also known as the deep branch of the transverse cervical artery.
It passes beneath the levator scapulae to the medial angle of the scapula, and then descends under the rhomboid muscles along the vertebral border of that bone as far as the inferior angle.
Dubin-Johnson syndrome
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# Overview
Dubin-Johnson syndrome is an autosomal recessive disease which presents shortly after birth with an increase of conjugated bilirubin without elevation of liver enzymes (ALT, AST).

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Dubin-Johnson syndrome from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis
Prognosis is good and there's no need to treat this syndrome.

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
There is a lack of canalicular multi-drug resistant protein which causes dysfunction on bilirubin transfer to bile canaliculi.
An isoform of this protein is localized to the lateral hepatocyte membrane, allowing transport of glucuronide and glutathione conjugates back into the blood.
Analysis of urine pophyrins show a normal level of coproporphirin but the I isomer accounts for 80% ot the total(normally 25%)
Liver will present with dark brown appearance due to pigment accumulation.
Econazole how supplied

# HOW SUPPLIED/STORAGE AND HANDLING
Ecoza topical foam, 1% is white to off-white foam supplied in 70 g (NDC 23710-100-70) aluminum pressurized canister.
Store at controlled room temperature 20C to 25C (68F to 77F) with excursions permitted between 15C and 30C (59F and 86F). Do not refrigerate or freeze.
Ecoza topical foam is flammable. Avoid heat, flame, and smoking during and immediately following application.
Contents under pressure. Do not puncture and/or incinerate the containers.
Do not expose containers to heat and/or store at temperatures above 120F (49C) even when empty.
Do not store in direct sunlight.