Persius/hicric huggingface dataset:
Prednisone how supplied

# How supplied
1 mg white, scored tablets
2.5 mg white, scored tablets
5 mg white, scored tablets
10 mg white, scored tablets
20 mg white, scored tablets
50 mg white, scored tablets
5 mg per 5 mL oral solution
5 mg per mL IntensolTM
Storage and dispense(tablets)
Storage and dispense(oral solution)
 Storage and dispense(intensolTM)

## 1 mg white, scored tablets
(identified 54 092).
NDC 0054-8739-25: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-4741-25: Bottles of 100 tablets.
NDC 0054-4741-31: Bottles of 1000 tablets.   Return to top

## 2.5 mg white, scored tablets
(Identified 54 339)
NDC 0054-8740-25: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-4742-25: Bottles of 100 tablets.   Return to top

## 5 mg white, scored tablets
(Identified 54 612).
NDC 0054-8724-25: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-4728-25: Bottles of 100 tablets.
NDC 0054-4728-31: Bottles of 1000 tablets.  Return to top

## 10 mg white, scored tablets
(Identified 54 899).
NDC 0054-0017-20: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-0017-25: Bottles of 100 tablets.
NDC 0054-0017-29: Bottles of 500 tablets.   Return to top

## 20 mg white, scored tablets
(Identified 54 760).
NDC 0054-0018-20: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-0018-25: Bottles of 100 tablets.
NDC 0054-0018-29: Bottles of 500 tablets.   Return to top

## 50 mg white, scored tablets
(Identified 54 343).
NDC 0054-0019-20: Unit dose, 10 tablets per strip, 10 strips per shelf pack, 10 shelf packs per shipper.
NDC 0054-0019-25: Bottles of 100 tablets.  Return to top

## 5 mg per 5 mL oral solution
NDC 0054-8722-16: Unit dose Patient CupTM filled to deliver 5 mL (5 mg Prednisone), ten 5 mL Patient CupsTM per shelf pack, 4 shelf packs per shipper.
NDC 0054-3722-50: Bottles of 120 mL.
NDC 0054-3722-63: Bottles of 500 mL.  Return to top

## 5 mg per mL IntensolTM
NDC 0054-3721-44: Bottles of 30 mL with calibrated dropper (graduations of 0.25 mL to 1.0 mL on the dropper).  Return to top

## Storage and dispense(tablets)
Store at 25C (77F), excursions permitted to 15 to 30C. Dispense in a tight container, as defined in the USP/NF.  Return to top

## Storage and dispense(oral solution)
Store at 25C (77F), excursions permitted to 15 to 30C. Dispense in a tight container, as defined in the USP/NF.  Return to top

## Storage and dispense(intensolTM)
Store at 25C (77F), excursions permitted to 15 to 30C. Dispense in a tight, light-resistant container, as defined in the USP/NF. Discard opened bottle after 90 days.  Return to top
Adapted from the FDA Package Insert.
Prednisone side effects

# List of side effects
Fluid and Electrolyte Disturbances
Musculoskeletal
Gastrointestinal
Dermatologic
Neurological
Endocrine
Ophthalmic
Metabolic

## Fluid and Electrolyte Disturbances
- Sodium retention
- Fluid retention
- Congestive heart failure in susceptible patients
- Potassium loss
- Hypokalemic alkalosis
- Hypertension Return to top

## Musculoskeletal
- Muscle weakness
- Steroid myopathy
- Loss of muscle mass
- Osteoporosis
- Vertebral compression fractures
- Aseptic necrosis of femoral and humeral heads  Return to top

## Gastrointestinal
- Peptic ulcer with possible perforation and hemorrhage
- Pancreatitis
- Abdominal distention
- Ulcerative esophagitis Return to top

## Dermatologic
- Impaired wound healing
- Thin fragile skin
- Petechiae and ecchymoses
- Facial erythema
- Increased sweating
- May suppress reactions to skin tests Return to top

## Neurological
- Convulsions
- Increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after treatment
- Vertigo
- Headache  Return to top

## Endocrine
- Menstrual irregularities
- Development of cushingoid state
- Suppression of growth in children
- Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or illness
- Decreased carbohydrate tolerance
- Manifestations of latent diabetes mellitus
- Increased requirements for insulin or oral hypoglycemic agents in diabetics Return to top

## Ophthalmic
- Posterior subcapsular cataracts
- Increased intraocular pressure
- Glaucoma
- Exophthalmos  Return to top

## Metabolic
Negative nitrogen balance due to protein catabolism  Return to top
Adapted from the FDA Package Insert.
Prokineticin receptor 2
Prokineticin receptor 2 (PKR2), is a G protein-coupled receptor encoded by the PROKR2 gene in humans.

# Function
Prokineticins are secreted proteins that can promote angiogenesis and induce strong gastrointestinal smooth muscle contraction. The protein encoded by this gene is an integral membrane protein and G protein-coupled receptor for prokineticins. The encoded protein is similar in sequence to GPR73, another G protein-coupled receptor for prokineticins.
Mutations in the PROKR2 (also known as KAL3) gene have been implicated in hypogonadotropic hypogonadism and gynecomastia.
Proline-rich protein 21
Proline-rich protein 21 (PRR21) is a protein of the family of proline-rich proteins. It is encoded by the PRR21 gene, which is found on human chromosome 2, band 2q37.3. The gene exists in several species, both vertebrates and invertebrates, including humans. However, the protein have few conserved regions among species.

# Structure
PRR21 consists of 389 amino acids or 1170 base pairs, all found within one exon. Like other proline-rich proteins, it contains a repeated sequence of amino acids that contains several proline residues. The tandemly repeated sequence of PRR21 is 28 amino acids long and is repeated in full 11 times, with few variations. A logo displaying the variances of the repeat is shown below. The repeat constitute almost the entire protein, except for the very beginning and a short tail.

## Polymorphism
Many single-nucleotide polymorphisms (SNPs) are predicted for the gene, and several of these cause missense mutations. This allows for personal variances within the population, and contribution to the "uniqueness" of each individual.

## Post-translational modifications
PRR21 has 28 possible phosphorylation sites. These follow the patterns of the repeated sequence. 22 out of 28 phosphorylation sites occur at serines at positions 9 and 24 in the repeat, both of which are highly conserved. Though, these serines can be changed by SNPs. Phosphorylation generally either activates or inactivates a protein. The protein has a no potential GPI-modification sites. PRR21 is not predicted to interact with any other proteins.

# Homology
PRR21 have no paralogs, and few orthologs. The orthologs are poorly conserved, as proline-rich proteins lack the need for specificity. Most important is that they have a loose structure and contain many prolines. The repeats often work as spacers only to make the protein big enough to interact with other proteins. Thus, orthologs often look dissimilar.

# Functions
There is 99.97% likelihood that PRR21 enters the mitochondria. PRR21 may be involved in stress responses that are related to phosphorylation of mitochondrial proteins. The gene is ubiquitously expressed, as nearly all eukaryotic cells contain mitochondria. PRR21 may be a salivary protein, as the tandemly repeated sequence constitute almost the entire protein, which is a common feature of salivary proline-rich proteins.

# Other proline-rich proteins
There are several kinds of proline-rich proteins, which can include either repetitive short sequences or tandemly repeated sequences. They have in common that the repeats, and the repeats only, contain unusual amounts of proline. They have a loose structure, which is caused by several features; the prolines have a shape that causes to chain to turn, and especially prevents alpha helices. Also, the proteins contain many positively charged residues that repel each other. This results in loose proteins that are suitable as binding proteins. These binding interactions can be hydrophobic interactions as proline-rich proteins tend to have exposed hydrophobic regions. The prolines themselves work as additional binding sites for hydrogen bonds by being strong hydrogen acceptors.
Prolymphocytic leukemia
For more information regarding B-cell prolymphocytic leukemia, please click here.
For more information regarding T-cell prolymphocytic leukemia, please click here.

# Overview
Prolymphocytic leukemia is a rare lymphoid leukemia, which account for only about 2% of all mature lymphoid leukemias. Prolymphocytic leukemias present similar to leukemia. Like lymphomas, they originate in the lymphocytes, but do not form solid tumors. Prolymphocytic leukemias are also considered lymphoproliferative disorders, which lymphocytes are produced in large amounts. Prolymphocytic leukemia may be classified according to the type of cell involved: B-cell prolymphocytic leukemia and T-cell prolymphocytic leukemia. Originally, it was thought to be a rare variation of chronic lymphocytic leukemia, but is now considered a distinct disease. It is usually classified as a kind of chronic lymphocytic leukemia. Although these 2 types of prolymphocytic leukemias share some of the same characteristics, the World Health Organization (WHO) classifies them as different types of lymphoid leukemias.

# Classification
For more details about each specific type of prolymphocytic leukemia, please select:

# Differentiating B-Prolymphocytic Leukemia from T-Prolymphocytic Leukemia
In order to distinguish B-prolymphocytic leukemia from T-prolymphocytic leukemia, see the table below.

# Differentiating Prolymphocytic Leukemia from other Leukemias
Proprotein convertase 1
Proprotein convertase 1, also known as prohormone convertase, prohormone convertase 3, or neuroendocrine convertase 1 and often abbreviated as PC1/3 is an enzyme that in humans is encoded by the PCSK1 gene. PCSK1 and PCSK2 differentially cleave proopiomelanocortin and they act together to process proinsulin and proglucagon in pancreatic islets.

# Function
PC1/3 is an enzyme that performs the proteolytic cleavage of prohormones to their intermediate (or sometimes completely cleaved) forms. It is present only in neuroendocrine cells such as brain, pituitary and adrenal, and most often cleaves after a pair of basic residues within prohormones but can occasionally cleave after a single arginine. It binds to a protein known as proSAAS, which also represents its endogenous inhibitor. PC1 is synthesized as a 99 kDa proform quickly converted to an 87 kDa major active form, which itself is nearly completely cleaved to a 66 kDa active form within neuroendocrine cells.
Proprotein convertase 1 is the enzyme largely responsible for the first step in the biosynthesis of insulin.  Following the action of proprotein convertase 1, a carboxypeptidase is required to remove the basic residues from the processing intermediate and generate the bioactive form of insulin.  Another prohormone convertase, proprotein convertase 2 plays a more minor role in the first step of insulin biosynthesis, but a greater role in the first step of glucagon biosynthesis. The knockout of proprotein convertase 1 is not lethal in mice or humans, most likely due to the presence of the second convertase, although mice lacking proprotein convertase 1 activity show a number of defects including slow growth.
Proprotein convertase 1 is a calcium (Ca2+) activated serine endoprotease (meaning that a serine residue is part of the active site that hydrolyzes the peptide bond within the substrate).  It is related to the bacterial enzyme known as subtilisin.  There are nine subtilisin homologs in mammals; in addition to proprotein convertase 1 and 2, other members of this enzyme family include furin, PACE4, PC4, PC5/6, PC7/8, PCSK9, and SKI1/S1P.

# Clinical significance
Variants in the PCSK1 gene may be associated with obesity.
Psilocybe subaeruginosa
Psilocybe subaeruginosa is a psychedelic mushroom which has psilocybin and psilocin as main active compounds.

# Description
- Cap: 1-6 cm, conical to convex, tan brown, hygrophanous, margin striate when moist, uplifting in age, often with a slight umbo.  Bruising bluish where damaged.
- Gills: Crowded, cream color when young, violet brown in age, with adnate to adnexed attachment.
- Spores: Dark violet brown, subellipsoid, 14 x 7 um.
- Stipe: 4.5 to 12 cm long, .2 to .4 cm thick, white to grey, finely striate, equal to slightly enlarged near the base.  With a white cortinate partial veil which soon disappears and often leaves traces in the upper stem.
- Taste: Farinaceous.
- Odor: Farinaceous.
- Microscopic features:

# Distribution and habitat
Grows in clusters in wood chips, piles of leaves and woody debris in urban areas and along trails and roads in deciduous forests and gardens.  Found in Tasmania and Australia where it is common. Also one of the most common Psilocybe sp. mushrooms found in and around Auckland, New Zealand.

# Alkaloid content
Psilocybe subaeruginosa alkaloid content can vary widely however it is roughly twice that of Psilocybe cubensis.  The mature mushrooms are not nearly as strong as newly formed fruit.
Psilocybe villarrealiae
Psilocybe villarrealiae is a psilocybin mushroom which has psilocybin and psilocin as main active compounds.

# Description
- Cap: 2-12 cm diameter, at first subconical to campanulate, expanding to convex, or plane in age, often with wavy margin. The cap color starts out tan to walnut brown and fades to yellow-brown as they age, finally turning black.  Cap surface hygrophanous, fading to tan as it dries.  The cap is sometimes translucent-striate near the margin, often with an umbo. Usually staining blue or black in age.
- Gills: Cream color when young, violet brown in age, with subsinuate or adnate attachment.
- Spores: Dark violet brown, oblong to ellipsoid or subrhomboid, thin walled, 7 x 4 um.
- Stipe: Central, equal, flexuous, and cylindric, 3 to 12 cm long, 3 to 7 mm thick.  Reddish brown fading to grey-yellow and finally dark, ornamented with floccose mycelium especially the bottom half, bruising blue-green in the upper part of the stem.  Partial veil is white and arachnoid, disappearing in age.
- Taste: Farinaceous.
- Odor: Farinaceous.
- Microscopic features:

# Distribution and habitat
Grows solitary or gregariously in groups, often forming cespitose clusters.  Found growing directly from the ground in muddy soil in pine and oak woods and subtropical forests, usually near small creeks and ravines. Known only from Jalisco, Mexico.
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
- Psilocybe villarrealiae
Psilocybe villarrealiae
Pterygomandibular raphe
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: 
There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us  to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

# Overview
The pterygomandibular raphe (pterygomandibular ligament) is a tendinous band of the buccopharyngeal fascia, attached by one extremity to the hamulus of the medial pterygoid plate, and by the other to the posterior end of the mylohyoid line of the mandible.
- Its medial surface is covered by the mucous membrane of the mouth.
- Its lateral surface is separated from the ramus of the mandible by a quantity of adipose tissue.
- Its posterior border gives attachment to the superior pharyngeal constrictor muscle.
- Its anterior border attaches to the posterior edge of the buccinator.
Purple Haze (marijuana)
Contrary to highly popular belief regarding cannabis strains, Purple Haze is simply slang for a number of genetic crossbreeds of a purple strain and original Haze, such as Purple Star x Haze #1, Purple #1 x Haze #1, or Purple Skunk x Haze #1. Purple strains are often misidentified as purple haze due to the high popularity it gained due to the song by Jimi Hendrix. In fact, the term "haze" was not used to identify marijuana until the strain was bred in 1970. Purple Haze does not necessarily mean high quality, and the term is often used by dealers to distinguish their product. In concept, there is no original Purple Haze strain.
Purple haze refers to a specific LSD blotter created by Owsley Stanley. In a High Times Magazine article by Bruce Eisner from January 1977, Eisner reports to have actually interviewed Tim Scully, one of the miscreants involved in creating the LSD. According to Scully, Augustus Owsley Stanley III, began to manufacture LSD in Los Angeles in 1965. It was legal then. Owsley's LSD came in 270 microgram tablets of purple (Purple Haze) and white (White Lightning). LSD became illegal in 1966 and Owsley was arrested in 1967.
Many speculate that the 1967 song of the same name by Jimi Hendrix was named after this blotter paper or after the cannabis strain, but Jimi claims that the title of the song only had to do not with drugs but with a dream he had in which he was walking under the sea. In the dream, he said a purple haze surrounded him, engulfed him and got him lost. It was a traumatic experience, but in his dream his faith in Jesus saved him. While Hendrix claims the song is not drug related, the lyrics seem to vividly portray an intense acid trip.
Purple Haze is also the brand name of a marijuana-flavored lollipop available as a novelty candy at some convenience stores.  The lollipop is flavored with hemp oil, which imparts the taste of marijuana without the high, but the candy has still been criticized by anti-drug advocates in the United States (Basically because of the name).
Purtscher's retinopathy

# Overview
Purtscher's retinopathy is a disease where part of the eye (retina) is damaged.  Usually associated with severe head injuries, it may also occur with other types of trauma, such as long bone fractures, or with several non-traumatic systemic diseases.  However, the exact cause of the disease is not well understood.  There are no treatments specific for Purtscher's retinopathy, and the prognosis varies.  The disease can threaten vision, sometimes causing temporary or permanent blindness.
It is named for the Austrians ophthalmologist, Othmar Purtscher (18521927), who detected it in 1910 and described it fully in 1912.

# History of the disease
Purtscher's retinopathy was first characterized in 1910 and 1912 as a syndrome of sudden blindness after head trauma, with patches of hemorrhage and whitening of the retina in both eyes.  Later, it was discovered to occur after other types of |trauma, such as chest trauma, and is associated with several non-traumatic systemic diseases.  Purtscher's retinopathy may also be associated with acute pancreatitis, vasculitis, embolization of such materials as fat and amniotic fluid, systemic lupus erythematosus, thrombotic thrombocytopenic purpura, and chronic renal failure.  Purtscher's retinopathy may be caused by extensive fractures of the long bones.

# Diagnosis
Where trauma is involved, only afunduscopic examination of the back of the eye (retina) is necessary to make the diagnosis.  Fluoroscein angiography may show a decrease in blood flow to the areas of whiteness in the retina.

# Pathophysiology
Purtscher's retinopathy likely involves complex pathophysiology, with several contributing factors, including complement-mediated aggregates, fat, air, fibrin clots and platelet clumps.  The diseases leads to the formation of cotton wool spots in the retina, a finding observed in several other diseases, and atrophy of the optic nerve.

# Associated diseases
- Severe head, chest, or long bone trauma
- Acute pancreatitis
- Amniotic fluid embolism
- Chronic renal failure
- Dermatomyositis
- Fat embolism syndrome
- Scleroderma
- Systemic lupus erythematosus (SLE)
- Thrombotic thrombocytopenic purpura (TTP)

# Treatment
It may be treated with triamcinolone in some cases.  However, in general, there are no treatments for Purtscher's retinopathy.  If it is caused by a systemic disease or emboli, then those conditions should be treated.

# Prognosis
Purtscher's retinopathy can lead to loss of vision, and recovery of vision may occur very little.  However, vision recovery does occur in some cases, and reports have varied on the long-term prognosis.
Pythagorean expectation
Pythagorean expectation is a formula invented by Bill James to estimate how many games a baseball team "should" have won based on the number of runs they scored and allowed.  Comparing a team's actual and Pythagorean winning percentage can be used to evaluate how "lucky" or "clutch" that team was.  The term is derived from the formula's resemblance to the Pythagorean theorem.
The basic formula is:
where Win% is the winning percentage generated by the formula. The expected number of wins would be the expected winning percentage multiplied by the number of games played.

# Empirical origin
Empirically, this formula correlates fairly well with how baseball teams actually perform, although an exponent of 1.81 is slightly more accurate.  This correlation is one justification for using runs as a unit of measurement for player performance. Efforts have been made to find the ideal exponent for the formula, the most widely known being the Pythagenport formula developed by Clay Davenport of Baseball Prospectus (1.5 log((r + ra)/g) + 0.45) and the less well known but equally effective Pythagenpat formula ((r + ra)/g)0.287), developed by David Smyth. Davenport expressed his support for the latter of the two, saying:
After further review, I (Clay) have come to the conclusion that the so-called Smyth/Patriot method, aka Pythagenpat, is a better fit. In that, X=((rs+ra)/g)^.285, although there is some wiggle room for disagreement in the exponent. Anyway, that equation is simpler, more elegant, and gets the better answer over a wider range of runs scored than Pythagenport, including the mandatory value of 1 at 1 rpg.
These formulas are only necessary when dealing with extreme situations in which the average amount of runs scored per game is either very high or very low. For most situations, simply squaring each variable yields accurate results.
There are, some systematic statistical deviations between actual winning percentage and expected winning percentage, which include bullpen quality and luck.  In addition, the formula tends to regress toward the mean, as teams that win a lot of games tend to be underrepresented by the formula (meaning they "should" have won fewer games), and teams that lose a lot of games tend to be overrepresented (they "should" have won more).

# Theoretical explanation
There is no explanation for the correlation between the formula and actual winning percentage in theory, rather the correlation has just been shown to work empirically. However, Professor Steven J. Miller provided a statistical derivation of the formula: if runs for each team follow a Weibull distribution, then the formula gives the probability of winning.

# Use in basketball
When noted basketball analyst Dean Oliver applied James' pythagorean theory to his own sport, the result was similar, except for the exponents:
Another noted basketball statistician, John Hollinger, uses a similar pythagorean formula except with 16.5 as the exponent.