Persius/hicric huggingface dataset:
Decreased skin pigmentation

# Overview
Knowing the difference between hypopigmentation and depigmentation is essential to determining the differential diagnosis.
Depigmentation is the complete loss of pigment. Hypopigmentation is a decrease in pigment. They can both indicate the diagnosis whether local or general.

# Differential Diagnosis
In alphabetical order.  
- Albinism
- Chemical leukoderma
- Congenital birthmarks
- Piebaldism
- Pityriasis alba
- Tuberous sclerosis that can result in hypopigmentation
- Vitiligo

# Diagnosis

# History and Symptoms
- Determine degree of hypopigmentation and depigmentation
- Family history of thyroid disease, diabetes and endocrine problems
- Obtain personal history, include:
- allergies
- hay fever
- asthma
- these may help determine the diagnosis of atopic dermatitis

## Eyes
- perform eye exam to aid in diagnosis of albinism

## Other
- Wood's lamp exam can be used to emphasize Hypo- and depigmented areas

# Laboratory Findings
- Labs include:
- CBC (in suspected vitiligo patients)
- Thyroid function tests

## Other Diagnostic Studies
- Skin biopsy for vitiligo

# Treatment

## Acute Pharmacotherapies
Vitiligo
- Topical steroids

## Chronic Pharmacotherapies
Vitiligo
- Oral beta-carotene for patients with chronic vitiligo and albanism

## Indications for Surgery
Punch minigrafting from normal skin donors to vitiligo patients can aid in the repopulation of melanocytes

# Primary Prevention
- Sunscreen can protect from further skin issues
Decussation of the pyramids

# Overview
The two pyramids contain the motor fibers that pass from the brain to the medulla oblongata and medulla spinalis, corticobulbar and corticospinal fibers.
When these pyramidal fibers are traced downward, it is found that some two-thirds or more of them leave the pyramids in successive bundles, and decussate in the anterior median fissure of the medulla oblongata, forming what is termed the pyramidal decussation.
Having crossed the middle line, they pass down in the posterior part of the lateral funiculus as the lateral cerebrospinal fasciculus.

# Additional images
- Diagrams of the medulla spinalis.
- Medulla oblongata and pons. Anterior surface.
- Decussation of pyramids. Scheme showing passage of various fasciculi from medulla spinalis to medulla oblongata.
- Section of the medulla oblongata through the lower part of the decussation of the pyramids
- Section of the medulla oblongata at the level of the decussation of the pyramids.
- Superficial dissection of brain-stem. Ventral view.
- The motor tract.
Deglycyrrhizinated licorice
Deglycyrrhizinated Licorice, also known as De-glycyrrhizinated licorice, or commonly referred to by the acronym DGL, is typically used as an herbal supplement in the treatment of gastric and duodenal ulcers. It is made from licorice from which the glycyrrhizin has been removed
The usual dosage is 760 mg, chewed, 20 minutes before a meal. Studies of DGL in humans and animals against placebos showed that DGL significantly reduced the size of gastric ulcers and hastened healing, with 44% of the subjects obtaining complete healing, as opposed to 6% of the control group. DGL has also been found to be an effective treatment for duodenal ulcers. In another study a group of 40 patients who had duodenal ulcers for 412 years were treated with 3 grams of DGL a day for 8 weeks, or 4.5 grams a day for 12 weeks, with all subjects showing vast improvement, with the higher dosage being the most significant. An additional study shows that DGL's therapeutic effect is equal to the effect of cimetidine.
There have been no known cases of overdose, and very little reported side effects (nausea and diarrhea sometimes reported).
There are no known drug interactions with drugs used to treat ulcers.
In Europe, South Africa, and Canada, DGL is marketed in a medicinal preparation called Caved-S. In the U.S., DGL is marketed as a herbal supplement.
DGL has also been reported to help treat aphthous ulcers (canker sores).

# Footnotes
-  Canker Sores: The Full Story
Delayed open access journal

# Overview
Delayed open access journals are journals in which the free availability of the content is available, but only after several months, with the immediate availability being limited to subscribers.  By its nature, it applies only to electronic versions of journals. 
This variation on open access does not meet the standards for a true open access journal, and such journals are not included in the lists of open access journals, such as DOAJ. Nonetheless, it does provide useful access for many purposes.  The term "delayed open access" can, in principle, be used for other material as well.
The purpose of this delay is to permit access to the general public, while still providing incentive to researchers -- and especially research libraries -- to continue their subscriptions. The assumptions behind this model are:
- researchers will want the most recent papers in their subject immediately after publication, and will therefore pay the necessary subscription cost, generally several hundred or several thousand dollars.
- students and others in smaller non-research institutions do not generally need to see the article as quickly, for they will be using it for a term paper or similar project, not for true research.
- the libraries serving such colleges will usually have discontinued such journals (or never subscribed to them) because of their cost. The publisher will thus lose no revenue.
- the marginal cost of distributing an electronic journal to additional users is very small; almost all of the expense is preparing the publication and its electronic version in the first place, and the publishers will therefore spend little additional money, while familiarizing undergraduates with their publications.
The difficulties with this model are
- it does not serve all academic readers. Those at small colleges also want to keep up with the current literature. In particular those there should be encouraged to be researchers in spite of the difficulties for not being in a major centre, and they would be further harmed by delayed access to the literature
- it will not serve key segments of the general public. The public readers of biomedical journals in particular are typically people concerned about particular diseases that they or their loved ones have. This segment of the public is interested in the current findings, for they will hear news of them.
- in some subjects the delay necessary to protect publishers would be very long, especially in some of the "softer" subjects.

# Providers
Perhaps the leading platform for these journals is Highwire Press.

# Publishers
Many of the publishers of delayed open access journals are biomedical societies. This has been the case for several years, and it has in mid-2006 been stimulated by the public access requirements of several funding agencies, which accept delays of up to 6 or 12 months. Some commentators are willing to accept it as "almost open access", but most do not.
Descending genicular artery
The descending genicular artery (highest genicular artery) arises from the femoral just before it passes through the opening in the tendon of the Adductor magnus, and immediately divides into a saphenous and a musculo-articular branch.

# Saphenous branch
The saphenous branch pierces the aponeurotic covering of the adductor canal, and accompanies the saphenous nerve to the medial side of the knee.
It passes between the Sartorius and Gracilis, and, piercing the fascia lata, is distributed to the integument of the upper and medial part of the leg, anastomosing with the medial inferior genicular artery.

# Musculo-articular branch
The musculo-articular branch descends in the substance of the Vastus medialis, and in front of the tendon of the Adductor magnus, to the medial side of the knee, where it anastomoses with the medial superior genicular artery and anterior recurrent tibial artery.
A branch from this vessel crosses above the patellar surface of the femur, forming an anastomotic arch with the lateral superior genicular artery, and supplying branches to the knee-joint.
Devil facial tumour disease
Devil facial tumour disease (DFTD) is a transmittable parasitic cancer in the Tasmanian Devil. The first "official case" was described in 1995, in Australia.
In the subsequent decade the disease ravaged Tasmania's wild devils, with estimates of decline ranging from 20% to as much as a 50% of the devil population, across over 65% of the state.
 Affected high-density populations suffer up to 100% mortality in 1218 months. The disease has mainly been concentrated in Tasmania's eastern half.
Visible signs of DFTD begin with lesions and lumps around the mouth. These develop into cancerous tumours that spread from the face to the entire body. The tumours interfere with feeding, and the affected animal may starve to death.

# Characteristics of the cancer
Using cultures of the cancerous tissue to study the condition, researchers have identified the cancer as a neuroendocrine tumor, and all the cancer cells have identical chromosomal rearrangements. A virus was initially thought to be the cause of DFTD, but no evidence of such a virus could be detected in the cancer cells. Environmental toxins have also been suspected.
The cancer cells themselves are an infective agent, with transmission of the disease occurring by biting, feeding on the same material, and aggressive mating. Final confirmation of this came when researcher Anne-Maree Pearse and colleagues 
found an infected animal that had a chromosomal abnormality in its non-tumourous cells that did not appear in its tumour cells, proving that the tumour cells could not have descended from the animal's own cells. Pearse believes that this may prove vital to the survival of the devils. Since June 2005, three females have been found that are partially resistant to DFTD.
Further research from the University of Sydney has shown that the infectious facial cancer may be able to spread because of vanishingly low genetic diversity in devil immune genes (MHC class I and II). The same genes are also found in the tumours, so the devil's immune system does not recognise the tumour cells as foreign.
Tasmanian Devil cells have 14 chromosomes, while the tumour cells contain 13. The DFTD cells have similar karyotype anomalies as cancer cells from canine transmissible venereal tumor, a cancer of dogs that is transmitted between animals by physical contact.

# Preservation response
In response to the impact of DFTD on Tasmanian Devil populations, forty-seven Devils have been shipped to mainland Australian wildlife parks to attempt to preserve the genetic diversity of the species. The Tasman peninsula is being considered as a possible "clean area" with the single narrow access point controlled by physical barriers.  The Tasmanian Department of Primary Industries and Water is experimenting on culling infected animals with some signs of success.
Dewar-Chatt-Duncanson model
The Dewar-Chatt-Duncanson model is a model in organometallic chemistry which explains the type of chemical bonding between an alkene and a metal (pi-complex) in certain organometallic compounds. The model is named after Michael J. S. Dewar  , Joseph Chatt and L. A. Duncanson  .
The pi-acid alkene donates electron density into a metal d-orbital from -symmetry bonding orbital between the carbon atoms (I).  The metal donates electrons back from (a different) filled d-orbital into the empty - antibonding orbital (II).  Both of these effects tend to reduce the carbon-carbon bond order, leading to an elongated C-C distance and a lowering its vibrational frequency.
In Zeise's salt K.H2O the C-C bond length has increased to 134 picometer from 133 pm for ethylene. In the nickel compound Ni(CH2CH2)(PPh3)2 the value is 143 pm.
The interaction also causes carbon atoms to "rehybridise" from sp2 towards sp3, which is indicated by the bending of the hydrogen atoms on the ethylene  back away from the metal. In silico calculations show that 75% of the binding energy is derived from the forward donation and 25% from backdonation . This model is a specific manifestation of the more general pi backbonding model.
Didanosine clinical studies

# Clinical Studies

## Adult Patients
START 2 was a multicenter, randomized, open-label study comparing VIDEX (200 mg twice daily)/stavudine/indinavir to zidovudine/lamivudine/indinavir in 205 treatment-naive patients. Both regimens resulted in a similar magnitude of suppression of HIV-1 RNA levels and increases in CD4 cell counts through 48 weeks.
Study AI454-148 was a randomized, open-label, multicenter study comparing treatment with VIDEX (400 mg once daily) plus stavudine (40 mg twice daily) and nelfinavir (750 mg three times daily) versus zidovudine (300 mg twice daily) plus lamivudine (150 mg twice daily) and nelfinavir (750 mg three times daily) in 756 treatment-naive patients, with a median CD4 cell count of 340 cells/mm3 (range 80 to 1568 cells/mm3) and a median plasma HIV-1 RNA of 4.69 log10 copies/mL (range 2.6 to 5.9 log10 copies/mL) at baseline. Median CD4 cell count increases at 48 weeks were 188 cells/mm3 in both treatment groups. Treatment response and outcomes through 48 weeks are shown in Figure 1 and Table 14.
The efficacy of VIDEX was demonstrated in two randomized, double-blind studies comparing VIDEX, given on a twice-daily schedule, to zidovudine, given three times daily, in 617 (ACTG 116A, conducted 1989-1992) and 913 (ACTG 116B/117, conducted 1989-1991) patients with symptomatic HIV infection or AIDS who were treated for more than one year. In treatment-naive patients (ACTG 116A), the rate of HIV disease progression or death was similar between the treatment groups; mortality rates were 26% for patients receiving VIDEX and 21% for patients receiving zidovudine. Of the patients who had received previous zidovudine treatment (ACTG 116B/117), those treated with VIDEX had a lower rate of HIV disease progression or death (32%) compared to those treated with zidovudine (41%); however, survival rates were similar between the treatment groups.
Studies have demonstrated that the clinical benefit of monotherapy with antiretrovirals, including VIDEX, was time limited.

## Pediatric Patients
Efficacy in pediatric patients was demonstrated in a randomized, double-blind, controlled study (ACTG 152, conducted 1991-1995) involving 831 patients 3 months to 18 years of age treated for more than 1.5 years with zidovudine (180 mg/m2 every 6 hours), VIDEX (120 mg/m2 every 12 hours), or zidovudine (120 mg/m2 every 6 hours) plus VIDEX (90 mg/m2 every 12 hours). Patients treated with VIDEX or VIDEX plus zidovudine had lower rates of HIV-1 disease progression or death compared with those treated with zidovudine alone.
Diglyceride acyltransferase
Diglyceride acyltransferase (or O-acyltransferase), DGAT, catalyzes the formation of triglycerides from diacylglycerol and Acyl-CoA. The reaction catalyzed by DGAT is considered the terminal and only committed step in triglyceride synthesis and to be essential for intestinal absorption (i.e. DGAT1)  and adipose tissue formation (i.e. DGAT2).
The protein is homologous to other membrane-bound O-acyltransferases.

# Isoforms
There are two isozymes of DGAT encoded by the genes DGAT1 and DGAT2. Although both isozymes catalyze similar reactions, they have no sequence homology to each other.
DGAT1 is mainly located in absorptive enterocyte cells that line the intestine and duodenum where it reassembles triglycerides that were decomposed through lipolysis in the process of intestinal absorption. DGAT1 reconstitutes triglycerides in a committed step after which they are packaged together with cholesterol and proteins to form chylomicrons.
DGAT2 is mainly located in fat, liver and skin cells.

# Mutations
In humans, DGAT1 mutations have been linked to congenital diarrheal disorders . The congenital diarrheal disorder presents 2-3 days after birth with projectile vomiting and failure to thrive.  The congenital diarrheal disorder may be treated with total parenteral nutrition avoiding sepsis with most symptoms resolving at 10 to 12 months of age. The congenital diarrheal disorder requires a strict diet with little or no fat (i.e fatty acids, monoglycerides, diglycerides, and triglycerides which break down and combine to form DGAT1 substrates that build up and irritate the intestinal mucosa). The precise cause of diarrhea is unknown, and is speculated to relate to abnormal fat absorption and buildup of DGAT1 substrates in the intestinal mucosa.

# Knockout studies
Mice with genetic disruption of the DGAT1 or DGAT2 genes have been made by the Farese laboratory at UCSF. Surprisingly, DGAT1/ mice are healthy and fertile and have no changes in triglyceride levels. These mice are also lean and resistant to diet-induced obesity, consequently generating interest in DGAT1 inhibitors for the treatment of obesity. However, these mice also fail to lactate, showing a complete lack of milk production due to their inability to produce milk lipid droplets. In contrast, DGAT2/ mice have reduced triglyceride levels but are lipopenic, suffer from skin barrier abnormalities (including the inability to retain moisture), and die shortly after birth.

# Therapeutic application
DGAT1 inhibitors have potential for the treatment of obesity and a number of DGAT-1 inhibitors are in clinical trials for this indication.
However, recent  findings prompt concern for DGAT1 inhibition in humans because of the severe side effects which include nausea, diarrhea, and vomiting following meals containing fat . However it is important to note that these symptoms were observed in case of total loss of function in DGAT due to knockout mutation. Such symptoms are not observed in case of partial inhibition of DGAT activity such as those induced via medication.
Diisopropyl fluorophosphate

# Overview
Diisopropyl fluorophosphate (DFP, diisopropyl phosphorofluoridate) is an oily, colorless or faint yellow liquid with the chemical formula C6H14FO3P. It is used in medicine and as an organophosphate insecticide. It is stable, but undergoes hydrolysis when subjected to moisture, producing hydrofluoric acid. It is a structural analog of sarin.
It is known also under names Demecarium, Difluorophate, Diflupyl, Diflurphate, Dyflos, Dyphlos, Fluoropropyl, Fluropryl, Fluostigmine, Humorsol, isofluorophate, isofluorphate, Neoglaucit, PF-3, PF3, T-1703, TL 466, and others.

# Uses in medicine
Diisopropyl fluorophosphate (closely related to demecarium bromide) has been used in ophthalmology as a miotic agent in treatment of chronic glaucoma, as a miotic in veterinary medicine, and as an experimental agent in neuroscience because of its acetylcholinesterase inhibitory properties and ability to induce delayed peripheral neuropathy. It is known as fluostigmine and Dyflos in such uses.

# Uses as toxin
The marked toxicity of esters of monofluorophosphoric acid was discovered in 1932, when Willy Lange and his PhD student Gerda von Krueger prepared the methyl, ethyl, n-propyl, and n-butyl esters and incidentally experienced their toxic effects. Another homologue of this series of esters, Diisopropyl fluorophosphate, was developed by British scientist Bernard Charles Saunders. On his search for compounds to be used as chemical warfare agents, Saunders was inspired by the report by Lange und Krueger and decided to prepare the new homologue which he labeled PF-3. It was much less deadly than tabun or sarin, however it could be mixed with mustard gas, forming a more potent mixture with significantly lower melting point, resulting in an agent suitable for use in cold weather. In military research, due to its physical and chemical similarities and comparatively low toxicity, it is used as a simulant of G-agents (GA, GB, GD, GF).
Diisopropyl fluorophosphate is a very potent neurotoxin. Its LD50 for rats is 1.3 mg/kg. It combines with the amino acid serine at the active site of the enzyme acetylcholinesterase, an enzyme that deactivates the neurotransmitter acetylcholine. Neurotransmitters are needed to continue the passage of nerve impulses from one neuron to another across the synapse. Once the impulse has been transmitted, acetylcholinesterase functions to deactivate the acetylcholine almost immediately by breaking it down. If the enzyme is inhibited, acetylcholine accumulates and nerve impulses cannot be stopped, causing prolonged muscle contraction. Paralysis occurs and death may result since the respiratory muscles are affected.

# Sources
- Brenner, G. M. (2000): Pharmacology. Philadelphia, PA: W.B. Saunders Company. ISBN 0-7216-7757-6
- Meiers, P. (2006): History of the fluorophosphates
Dislocated patella overview

# Overview
Luxating patella is a condition in which the patella, or kneecap, dislocates or moves out of its normal location.  The luxation is usually medial, but can be lateral.

# Causes
It can be caused by some form of blunt trauma, or may be a congenital defect.  In congenital cases, it is usually bilateral.

# Natural History, Complications and Prognosis
Osteoarthritis can develop secondarily.

# Diagnosis

## History and Symptoms
Symptoms can range from none to severe pain.

## Physical Examination
Diagnosis is made through palpation of the knee. The patient can do the patella tracking assessment by making a single leg squat and standing, or, lying on his or her back with knee extended from flexed position. A patella that slips medially on early flexion is called the J sign, and indicates imbalance between the VMO and lateral structures.

## X Ray
X-rays are necessary in some cases.

# Treatment

## Medical Therapy
Supplements like glucosamine and NSAIDs can be used to keep the knee strong.

## Surgery
Grades III and IV, as well as most grade II cases, require surgery to correct, if the patient has difficulty walking. The surgery involves a sulcoplasty, a deepening of the trochlear sulcus that the patella sits in.
Doctor-patient relationship
The doctor-patient relationship is considered to be essential in modern medicine and forms one of the foundations of contemporary medical ethics. Universities teach medical students from the beginning, even before they set foot in hospitals, to maintain a professional rapport with patients, uphold patients dignity, and respect their privacy.
The relationship is beyond the concept of physician-patient privilege which is a legal covenant.  Rather, the clinician and patient are in a partnership and both parties can openly discuss choices and ask questions in a trusting manner.  This ideology stems from trying to maintain the most objective outlook by both parties  patient and clinician  in formulating and exercising optimal treatment plans.  In fact, many health care professionals and patients claim that this trust and relationship is therapeutic in its own right. Unfortunately, we are increasingly seeing these boundaries crossed, which can compromise patient care and potentially lead to fatal consequences.
With increasing access to computers and published online medical articles, the internet has contributed to expanding patient knowledge of their own health, conditions, and treatment options.  However, doctors are fearful of misleading information and being inundated by electronic communications for which they are not paid.