Persius/hicric huggingface dataset:
Voriconazole how supplied

# How Supplied

### Powder for Solution for Injection
VFEND I.V. for Injection is supplied in a single use vial as a sterile lyophilized powder equivalent to 200 mg VFEND and 3200 mg sulfobutyl ether beta-cyclodextrin sodium (SBECD).
Individually packaged vials of 200 mg VFEND I.V.
(NDC 0049-3190-28)

### Tablets
VFEND 50 mg tablets; white, film-coated, round, debossed with "Pfizer" on one side and "VOR50" on the reverse.
Bottles of 30 (NDC 0049-3170-30)
VFEND 200 mg tablets; white, film-coated, capsule shaped, debossed with "Pfizer" on one side and "VOR200" on the reverse.
Bottles of 30 (NDC 0049-3180-30)

### Powder for Oral Suspension
VFEND for Oral Suspension is supplied in 100 mL high density polyethylene (HDPE) bottles. Each bottle contains 45 g of powder for oral suspension. Following reconstitution, the volume of the suspension is 75 mL, providing a usable volume of 70 mL (40 mg voriconazole/mL). A 5 mL oral dispenser and a press-in bottle adaptor are also provided.
(NDC 0049-3160-44)

# Storage
VFEND I.V. for Injection unreconstituted vials should be stored at 15  30C (59  86F) . VFEND is a single dose unpreserved sterile lyophile. From a microbiological point of view, following reconstitution of the lyophile with Water for Injection, the reconstituted solution should be used immediately. If not used immediately, in-use storage times and conditions prior to use are the responsibility of the user and should not be longer than 24 hours at 2 to 8C (36 to 46F). Chemical and physical in-use stability has been demonstrated for 24 hours at 2 to 8C (36 to 46F). This medicinal product is for single use only and any unused solution should be discarded. Only clear solutions without particles should be used .
VFEND Tablets should be stored at 15  30C (59  86F) .
VFEND Powder for Oral Suspension should be stored at 2  8C (36 46 F) (in a refrigerator) before reconstitution. The shelf-life of the powder for oral suspension is 18 months.
The reconstituted suspension should be stored at 15  30C (59  86F) . Do not refrigerate or freeze. Keep the container tightly closed. The shelf-life of the reconstituted suspension is 14 days. Any remaining suspension should be discarded 14 days after reconstitution.
Waldeyer's tonsillar ring
Waldeyer's tonsillar ring is an anatomical term describing the lymphoid tissue ring located in the pharynx.
It was named after the nineteenth century German anatomist Heinrich Wilhelm Gottfried von Waldeyer-Hartz.
The ring consists of (from superior to inferior):
- Adenoids (also termed pharyngeal tonsils)
- Tubal tonsils
- Palatine tonsils (more commonly termed "the tonsils", less commonly termed "faucial tonsils")
- Lingual tonsils
Wilcoxon signed-rank test

# Overview
The Wilcoxon signed-rank test is a non-parametric alternative to the paired Student's t-test for the case of two related samples or repeated measurements on a single sample. The test is named for Frank Wilcoxon (18921965) who, in a single paper, proposed both it and the rank-sum test for two independent samples (Wilcoxon, 1945).
Like the t-test, the Wilcoxon test involves comparisons of differences between measurements, so it requires that the data are measured at an interval level of measurement.  However it does not require assumptions about the form of the distribution of the measurements.  It should therefore be used whenever the distributional assumptions that underlie the t-test cannot be satisfied.

# Setup
Suppose we collect 2n observations, two observations of each of the n subjects. Let i denote the particular subject that is being referred to and the first observation measured on subject i be denoted by x_i and second observation be y_i.

# Assumptions
- Let Zi = Yi - Xi for i = 1, ... , n. The differences Zi are assumed to be independent.
- Each Zi comes from a continuous population (they must be identical) and is symmetric about a common median .

# Test Procedure
The null hypothesis tested is H0:  = 0. The Wilcoxon signed rank statistic W+ is computed by ordering the absolute values |Z1|, ..., |Zn|, the rank of each ordered |Zi| is given a rank of Ri. Denote i = I(Zi>0) where I(.) is an indicator function. The Wilcoxon signed ranked statistic W+ is defined as,
W^+ = \sum_{i=1}^n \phi_i R_i\,\!
It is often used to test difference scores of data collected before and after an experimental manipulation, in which case the central point would be expected to be zero. Scores exactly equal to the central point are excluded and the absolute values of the deviations from the central point of the remaining scores is ranked such that the smallest deviation has a rank of 1. Tied scores are assigned a mean rank. The sums for the ranks of scores with positive and negative deviations from the central point are then calculated separately. A value S is defined as the smaller of these two rank sums. S is then compared to a table of all possible distributions of ranks to calculate p, the statistical probability of attaining S from a population of scores that is symmetrically distributed around the central point.
As the number of scores, n, used increases, the distribution of all possible ranks S tends towards the normal distribution, so for an n of less than 10 this distribution is often used to calculate p.
The Wilcoxon test was popularised by Siegel (1956) in his influential text book on non-parametric statistics.  Siegel used the symbol T for the value defined here as S.  In consequence, the test is sometimes referred to as the Wilcoxon T test, and the test statistic is reported as a value of T.
World Medical Association
The World Medical Association (WMA), an international organization of physicians, was formally established on September 17, 1947, pursuant to the resolutions of the   First General Assembly of WMA held in Paris, France. In 2007, the WMA had a membership of 84 national medical associations and represents some 9 million physicians. 

# Mission
The goal of the World Medical Association is to serve humanity by endeavoring to achieve the highest international standards in medical education, science, ethics, and health care for all peoples of the world.

# Presidency
Yoram Blachar, an Israeli physician, was elected president of the World Health Association in October 2007. Blachar, 67, has been the chairman of the Israel Medical Association since 1995. Blachar said he would work to bring in African and Arab countries that were not yet members of the organization.
Xbp1p gene transcriptions
Transcription factor for the XhoI site-binding protein 1 protein (Xbp1p) binds to the promoters of CLN1, CYS3, SMF2 induced by stress of starvation to function as a transcriptional repressor.

# Human genes

# Interactions

# Consensus sequences
The upstream activating sequence (UAS) for the Xbp1p is GcCTCGA(G/A)G(C/A)g(a/g).

# Xbp samplings
Copying 5'-GCCTCG-3' in "F" yields none between ZSCAN22 and A1BG and none between ZNF497 and A1BG as can be found by the computer programs.
For the Basic programs testing consensus sequence GcCTCGA(G/A)G(C/A)g(a/g) (starting with SuccessablesAAA.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:
- negative strand, negative direction, looking for GCCTCGA(A/G)G(A/C)G(A/G), 0.
- positive strand, negative direction, looking for GCCTCGA(A/G)G(A/C)G(A/G), 0.
- positive strand, positive direction, looking for GCCTCGA(A/G)G(A/C)G(A/G), 0.
- negative strand, positive direction, looking for GCCTCGA(A/G)G(A/C)G(A/G), 0.
- complement, negative strand, negative direction, looking for CGGAGCT(C/T)C(G/T)C(C/T), 0.
- complement, positive strand, negative direction, looking for CGGAGCT(C/T)C(G/T)C(C/T), 0.
- complement, positive strand, positive direction, looking for CGGAGCT(C/T)C(G/T)C(C/T), 0.
- complement, negative strand, positive direction, looking for CGGAGCT(C/T)C(G/T)C(C/T), 0.
- inverse complement, negative strand, negative direction, looking for (C/T)C(G/T)C(C/T)TCGAGGC, 0.
- inverse complement, positive strand, negative direction, looking for (C/T)C(G/T)C(C/T)TCGAGGC, 0.
- inverse complement, positive strand, positive direction, looking for (C/T)C(G/T)C(C/T)TCGAGGC, 0.
- inverse complement, negative strand, positive direction, looking for (C/T)C(G/T)C(C/T)TCGAGGC, 0.
- inverse negative strand, negative direction, looking for (A/G)G(A/C)G(A/G)AGCTCCG, 0.
- inverse positive strand, negative direction, looking for (A/G)G(A/C)G(A/G)AGCTCCG, 0.
- inverse positive strand, positive direction, looking for (A/G)G(A/C)G(A/G)AGCTCCG, 0.
- inverse negative strand, positive direction, looking for (A/G)G(A/C)G(A/G)AGCTCCG, 0.

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Xenon hexafluoroplatinate
Xenon hexafluoroplatinate is the description of the product obtained from the combination of platinum hexafluoride and xenon in an experiment that proved the chemical reactivity of the noble gases.  Neil Bartlett at the University of British Columbia formulated the product as "Xe+", although subsequent work suggests that Bartlett's product was probably a mixture and did not in fact contain this specific salt.

# Preparation
"Xenon hexafluoroplatinate" is prepared from xenon and platinum hexafluoride (PtF6) as gaseous solutions in SF6. The reactants were combined at 77K and slowly warmed, presumably to allow for a controlled reaction.

# Structure
The structure of "xenon hexafluoroplatinate" is likely not Xe+.  The main problem with this formulation is  "Xe+", which would be a radical and would dimerize or abstract an F atom to give XeF+. Thus, Bartlett discovered that Xe undergoes chemical reactions, but the nature of his initial mustard yellow product is complex.  Further work indicates that Bartlett's product probably contained , , .  The title "compound" is a salt, consisting of an octahedral anionic fluoride complex of platinum and various xenon cations.
It has been proposed that the platinum fluoride forms a negatively charged polymeric network with xenon or xenon fluoride cations held in its instices. A preparation of "XePtF6" in HF solution results in a solid which has been characterized as a n polymeric network associated with XeF+. This result is evidence for such a polymeric structure of xenon hexafluoroplatinate.

# History
In 1962, Neil Bartlett discovered that a mixture of platinum hexafluoride gas and oxygen formed a red solid.  The red solid turned out to be dioxygenyl hexafluoroplatinate, O2+-. Bartlett later surmised that the ionization energies for O2 molecule and Xe were similar. He then asked his colleagues to give him some xenon "so that he could try out some reactions", whereupon he established that xenon indeed reacts with PtF6.  Although, as discussed above, the product was probably highly impure, Bartlett's work was the first proof that compounds could be prepared from a noble gas. His discovery illustrates that the finding of new chemical methods often lead initially to impure products.  Since Bartlett's observation, many well-defined compounds of xenon have been reported including XeF2, XeF4, and XeF6.
Zap1p gene transcriptions
"Zinc homeostasis in yeast is controlled primarily through the regulation of zinc uptake. Transcription of the ZRT1 and ZRT2 zinc transporters increases in zinc-limited cells, and this induction is dependent on the ZAP1 gene.  Expression of ZAP1 itself increases in zinc-limited cells.  (ZREs)  in the promoters of the ZRT1, ZRT2, and ZAP1 genes. A ZRE consensus sequence, 5'-ACCYYNAAGGT-3', was identified and found to be both necessary and sufficient for zinc-responsive transcriptional regulation.  ZREs are DNA binding sites for ZAP1."

# Human genes

# Consensus sequences
The upstream activating sequence (UAS) for Zap1p is 5'-ACC(C/T)(C/T)(A/C/G/T)AAGGT-3' in the promoters of ZRT1 and ZRT2 regarding this zinc-regulated transcription factor .

# Hypotheses
- A1BG has no regulatory elements in either promoter.
- A1BG is not transcribed by a regulatory element.
- No regulatory element participates in the transcription of A1BG.

# ZAP samplings
Copying the apparent consensus sequence for Zap1p (ACCCTCA) and putting it in "F" finds none located between ZSCAN22 and none between ZNF497 and A1BG as can be found by the computer programs.
For the Basic programs (starting with SuccessablesZAP.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are looking for, and found:
- negative strand, negative direction, looking for ACC(C/T)(C/T)NAAGGT, 0.
- positive strand, negative direction, looking for ACC(C/T)(C/T)NAAGGT, 0.
- positive strand, positive direction, looking for ACC(C/T)(C/T)NAAGGT, 0.
- negative strand, positive direction, looking for ACC(C/T)(C/T)NAAGGT, 0.
- complement, negative strand, negative direction, looking for TGG(A/G)(A/G)NTTCCA, 0.
- complement, positive strand, negative direction, looking for TGG(A/G)(A/G)NTTCCA, 0.
- complement, positive strand, positive direction, looking for TGG(A/G)(A/G)NTTCCA, 0.
- complement, negative strand, positive direction, looking for TGG(A/G)(A/G)NTTCCA, 0.
- inverse complement, negative strand, negative direction, looking for ACCTTN(A/G)(A/G)GGT, 0.
- inverse complement, positive strand, negative direction, looking for ACCTTN(A/G)(A/G)GGT, 0.
- inverse complement, positive strand, positive direction, looking for ACCTTN(A/G)(A/G)GGT, 0.
- inverse complement, negative strand, positive direction, looking for ACCTTN(A/G)(A/G)GGT, 0.
- inverse negative strand, negative direction, looking for TGGAAN(C/T)(C/T)CCA, 0.
- inverse positive strand, negative direction, looking for TGGAAN(C/T)(C/T)CCA, 0.
- inverse positive strand, positive direction, looking for TGGAAN(C/T)(C/T)CCA, 0.
- inverse negative strand, positive direction, looking for TGGAAN(C/T)(C/T)CCA, 0.

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Wolf-Hirschhorn syndrome
Synonyms and keywords: deletion 4p; 4p- syndrome; chromosome 4p16.3 deletion syndrome; Pitt-Rogers-Danks syndrome; PRDS; Pitt syndrome; Wittwer syndrome

# Overview
Wolf-Hirschhorn syndrome is a rare disease due to the deletion of the short arm on chromosome 4 which causes severe to profound mental retardation, microcephaly (small head), seizures, poor muscle tone, and cleft lip and/or cleft palate.

# Historical Perspective
Wolf-Hirschhorn syndrome was first described in 1961 by the Americans Herbert L. Cooper and Kurt Hirschhorn, and thereafter gained worldwide attention by publications by the German Ulrich Wolf, and Hirschhorn and their co-workers, specifically their articles in the German scientific magazine 'Humangenetik'. It is a characteristic phenotype resulting from a partial deletion of chromosomal material of the short arm of chromosome 4.

# Pathophysiology
Wolf-Hirshhorn syndrome is caused by a partial deletion of the short arm of chromosome 4, particularly in the region of WHSC1 and WHSC2.  About 87% of cases represent a de novo deletion, while about 13% are inherited from a parent with a chromosome translocation.  In the cases of familial translocation, there is a 2 to 1 excess of maternal transmission.  Of the de novo cases, 80% are paternally derived.  The symptoms and phenotype do not differ based on the size of the deletion.  The critical region for determining the phenotype is at 4p16.3 and can often be detected through genetic testing and fluorescent in situ hybridization (FISH).  Genetic testing and genetic counseling is offered to affected families.

## Associated Conditions
- Heart defects
- Renal anomalies
- Delayed bone age

# Diagnosis

# Symptoms
- Seizures
- Severe to profound mental retardation

# Physical Examination

## General
- Scoliosis

## Head
- Cranial asymmetry
- Hypertelorism
- Low hairline
- Microcephaly (small head)
- Small chin

## Eyes
- Ptosis
- Strabismus

## Ears
- Hearing loss
- Ear tags or pits

## Throat
- Cleft lip
- Cleft palate
- Down-turned fishlik mouth
- Fused teeth
- Short upper lip and Short philtrum

## Neck
- Webbed neck

## Genitourinary
- Hypospadias

## Extremities
- Poor muscle tone
60S ribosomal protein L5
60S ribosomal protein L5 is a protein that in humans is encoded by the RPL5 gene.

# Function
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 60S subunit. The protein belongs to the L18P family of ribosomal proteins. It is located in the cytoplasm. The protein binds 5S rRNA to form a stable complex called the 5S ribonucleoprotein particle (RNP), which is necessary for the transport of nonribosome-associated cytoplasmic 5S rRNA to the nucleolus for assembly into ribosomes. The protein interacts specifically with the beta subunit of casein kinase 2.

# Clinical significance
Variable expression of this gene in colorectal cancers compared to adjacent normal tissues has been observed, although no correlation between the level of expression and the severity of the disease has been found. This gene is co-transcribed with the small nucleolar RNA gene U21, which is located in its fifth intron. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome.

# Interactions
Ribosomal protein L5 has been shown to interact with:
- CSNK2B,
- EIF5A,
- Mdm2, and
- PDCD4.
60S ribosomal protein L6
60S ribosomal protein L6 is a protein that in humans is encoded by the RPL6 gene.
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 60S subunit. The protein belongs to the L6E family of ribosomal proteins. It is located in the cytoplasm. The protein can bind specifically to domain C of the tax-responsive enhancer element of human T-cell leukemia virus type 1, and it has been suggested that the protein may participate in tax-mediated transactivation of transcription. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome. Two alternatively spliced transcript variants encoding the same protein have been found for this gene.

# Interactions
RPL6 has been shown to interact with Basic fibroblast growth factor.
Saethre-Chotzen syndrome

# Overview
Saethre-Chotzen syndrome, also known as acrocephalosyndactyly type 3 (ACS III) and Chotzen syndrome is a very rare congenital syndrome characterised by craniosynostosis (premature closure of one or more of the sutures between the bones of the skull).
It is an autosomal dominant disorder with the error being in the TWIST transcription factor.

# Features
Classic features include:
- synostosis of the coronal sutures of the skull resulting in characteristic faces including ptosis, facial asymmetry and small ears
- syndactyly of the fingers, particularly of the second and third digits
- Intelligence is usually normal.  Some affected individuls may have mild to moderate mental retardation.

# Epidemiology
The incidence of this rare syndrome is estimated at between 1 in 25-50,000 live births.
ADP-specific glucokinase
In enzymology, an ADP-specific glucokinase (EC 2.7.1.147) also known as  ADP-dependent glucokinase is an enzyme that catalyzes the chemical reaction
Thus, the two substrates of this enzyme are ADP and D-glucose, whereas its two products are AMP and D-glucose 6-phosphate.
This enzyme belongs to the family of transferases, to be specific those transferring phosphorus-containing groups (phosphotransferases) with an alcohol group as acceptor.
In humans, the ADP-dependent glucokinase is encoded by the ADPGK gene.

# Structural studies
As of late 2007, only one structure has been solved for this class of enzymes, with the PDB accession code 1GC5.
Antistreptolysin O titer
Antistreptolysin O titre (AS(L)O titre or AS(L)OT) - titre of (serum) antistreptolysin O antibodies; a blood test used to assist in the diagnosis of a streptococcal infection or indicate a past exposure to streptococci.
The ASOT helps direct the antimicrobial treatment and is used to assist in the diagnosis of scarlet fever, rheumatic fever and post infectious glomerulonephritis.
A positive test usually is >200 units/mL, but normal ranges vary from laboratory to laboratory and by age.
The false negatives rate is 20-30%.  If a false negative is suspected then an anti-DNase B titre should be sought. False positives can result from liver disease and tuberculosis.
AV reentrant tachycardia
Synonyms and keywords: AVRT; AV-reciprocating tachycardia; atrioventricular reentrant tachycardia; circus movement tachycardia

# Overview
AVRT results from an anatomically distinct atrioventricular connection. The causes, which usually are congenital or genetic, include: Ebstein anomaly, Lown-Ganong-Levine syndrome, Mahaim fiber tachycardia, Wolff-Parkinson-White syndrome.

# Classification
Two types of tachycardia fall under this category:

## Orthodromic Atrioventricular Reentrant Tachycardia
In orthodromic AVRT, the antegrade conduction (from the atria to the ventricles) occurs through the AV node, whereas the retrograde conduction (from the ventricle to the atrium) occurs through the accessory pathway. In this case, the ECG will reveal narrow QRS and retrograde P wave following the QRS complex.

## Antidromic Atrioventricular Reentrant Tachycardia
In antidromic AVRT, the antegrade conduction (from the atrium to the ventricle) occurs through the accessory pathway, whereas the retrograde conduction (from the ventricles to the atria) occurs through the AV node.  In this case, the ECG will reveal wide QRS similar to those found in ventricular tachycardia.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
AV nodal reentrant tachycardia is usually not life-threatening.

## Common Causes
- Mitral valve prolapse

## Causes by Organ Systems

## Causes in Alphabetical Order
- Ebstein anomaly
- Lown-Ganong-Levine syndrome
- Mahaim fiber tachycardia
- Wolff-Parkinson-White syndrome

# Pathophysiology
Electrical activity of the heart is rerouted through an accessory pathway that connects the atria with the ventricles.

# Diagnosis

## Electrocardiogram

### QRS Atlernans
The appearance of QRS alternans as part of a narrow complex tachycardia suggests the diagnosis of orthodromic atrioventricular (AV) reentrant tachycardia which conducts retrograde over an accessory pathway.

# Video
Below is a video explaining the mechanism of AV re-entrant tachycardia
How to read a guideline?

# Class I
Conditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective.

# Class II
Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.

## Class IIa
Weight of evidence/opinion is in favor of usefulness/efficacy.

## Class IIb
Usefulness/efficacy is less well established by evidence/opinion.

# Class III
Conditions for which there is evidence and/or general agreement that a procedure/treatment is not useful / effective and in some cases may be harmful.

# Level of Evidence A
Data derived from multiple randomized clinical trials or meta-analyses.

# Level of Evidence B
Data derived from a single randomized trial, or non-randomized studies.

# Level of Evidence C
Only consensus opinion of experts,case studies, or standard-of-care.