Persius/hicric huggingface dataset:
Variable rules analysis
In linguistics, variable rules analysis is a set of statistical analysis methods commonly used in sociolinguistics and historical linguistics to describe patterns of variation between alternative forms in language use. It is also sometimes known as Varbrul analysis, after the name of a software package dedicated to carrying out the relevant statistical computations (Varbrul, from "variable rule".) The method goes back to a theoretical approach developed by the sociolinguist William Labov in the late 1960s and early 1970s, and its mathematical implementation was developed by Henrietta Cedergren and David Sankoff in 1974.
A variable rules analysis is designed to provide a quantitative model of a situation where speakers alternate between different forms that have the same meaning and stand in free variation, but in such a way that the probability of choice of either the one or the other form is conditioned by a variety of context factors or social characteristics. Such a situation, where variation is not entirely random but rule-governed, is also known as "structured variation". A variable rules analysis computes a multivariate statistical model, on the basis of observed token counts, such that each determining factor is assigned a numerical factor weight that describes how it influences the probabilities of choice of either form. This is done by means of stepwise logistic regression, using a maximum likelihood algorithm.
Although the necessary computations required for a variable rules analysis can be carried out with the help of mainstream general-purpose statistics software packages such as SPSS, it is more often done by means of a specialised software dedicated to the needs of linguists, called Varbrul. It was originally written by David Sankoff and currently exists in freeware implementations for Mac OS and Microsoft Windows, under the title of Goldvarb. There is also a version known as R-Varb implemented in the statistical language R and therefore available on most platforms.
Variable rules approaches are commonly employed for the analysis of corpus data in sociolinguistic research, especially in studies that aim to investigate how reflexes of linguistic change through time appear in the shape of structured variation patterns within a speech community.
Varicose veins overview

# Overview
Varicose veins are veins that have become enlarged and twisted. The term commonly refers to the veins on the leg, although varicose veins occur elsewhere. Veins have leaflet valves to prevent blood from flowing backwards (retrograde). Leg muscles pump the blood in veins to return it to the heart. When veins become enlarged, the leaflets of the valves no longer meet properly, and the valves don't work. A common cause of valve failure is Deep Vein Thrombosis (DVT), which can cause permanent damage to the valves.  The blood collects in the veins and they enlarge even more. Varicose veins are common in the superficial veins of the legs, which are subject to high pressure when standing.

# Causes
Varicose veins are more common in women than in men, and are linked with heredity. Other related factors are pregnancy, obesity, menopause, aging, prolonged standing, leg injury and abdominal straining. Varicose veins are bulging veins that are larger than spider veins, typically 3 mm or more in diameter. Varicose veins are distinguished from reticular veins (blue veins) and telangiectasias (spider veins) which also involve valvular insufficiency, by the size and location of the veins.

# Natural History, Complications and Prognosis
These often occur in people who are involved in work requiring prolonged periods of standing. The high pressure that builds up during those periods cause the veins to become tortuous and their valves to fail. With time, these varicosities can enlarge and cause swelling as well as pain of legs at the end of the day. Eventually, these can become associated with superficial ulcers which  can bleed and/or get infected. Stagnation of the venous blood in these veins can also lead to formation of blood clots.
Serious complications are rare but severe varicosities can lead to major complications such as thrombophlebitis, venous ulcers & clotting of blood, due to the poor circulation through the affected limb.

# Diagnosis

## Symptoms
Besides cosmetic problems, varicose veins are often tortuous and  painful, especially when standing or walking. They often itch, and scratching them can cause ulcers.

# Treatment

## Medical Therapy
Non-surgical treatments include sclerotherapy, elastic stockings, elevating the legs, and exercise. The traditional surgical treatment has been vein stripping to remove the affected veins. Newer surgical treatments are less invasive (see radiofrequency ablation) and are slowly replacing traditional surgical treatments. Since most of the blood in the legs is returned by the deep veins, and the superficial veins only return about 10%, they can be removed or ablated without serious harm.

## Surgery
Several techniques have been performed for over a century, from the more invasive named "saphenous stripping" up to mini invasives like superficial phlectomies and CHIVA cure.
Venlafaxine description

# Description
Effexor XR is an extended-release capsule for oral administration that contains venlafaxine hydrochloride, a structurally novel antidepressant. It is designated (R/S)-1- cyclohexanol hydrochloride or ()-1--p-methoxybenzyl] cyclohexanol hydrochloride and has the empirical formula of C17H27NO2 HCl. Its molecular weight is 313.87. The structural formula is shown below.
Venlafaxine hydrochloride is a white to off-white crystalline solid with a solubility of 572 mg/mL in water (adjusted to ionic strength of 0.2 M with sodium chloride). Its octanol:water (0.2 M sodium chloride) partition coefficient is 0.43.
Effexor XR is formulated as an extended-release capsule for once-a-day oral administration. Drug release is controlled by diffusion through the coating membrane on the spheroids and is not pH dependent. Capsules contain venlafaxine hydrochloride equivalent to 37.5 mg, 75 mg, or 150 mg venlafaxine. Inactive ingredients consist of cellulose, ethylcellulose, gelatin, hypromellose, iron oxide, and titanium dioxide.
Ventricular parasystole

# Ventricular Parasystole
- An ectopic ventricular pacemaker activates the ventricle concurrently with, but independent of, the impulse of the basic rhythm.
- It is protected from the impulse of the basic rhythm by entrance block.
- Its own impulse is able to depolarize the ventricle.
- Probably due to increased automaticity.
- EKG findings:
varying coupling intervals
With PVCs there is usually fixed coupling
RR intervals of the ectopic beats being mathematically related to each other
The interectopic forum is variable, are multiples of the shorter interval
Although the ectopic focus fires regularly, only those that find the ventricles responsive are manifested electrocardiographically.
The ratio between the intervals is seldom exact whole numbers (3:1) and more often 3:2 etc.
Parasystolic rates vary from 20 to 400 BPM
In most patients the rate varies between 30 to 56 BPM
Parasystolic rates greater than 70 BPM is called parasystolic VT.
the presence of fusion beats
May discharge at the same time that an impulse of the basic rhythm arrives at the ventricles.
The ventricles are then depolarized by the two wavefronts.
Can occur with regular PVCs, but with parasystole more frequently.
- varying coupling intervals
With PVCs there is usually fixed coupling
- With PVCs there is usually fixed coupling
- RR intervals of the ectopic beats being mathematically related to each other
The interectopic forum is variable, are multiples of the shorter interval
Although the ectopic focus fires regularly, only those that find the ventricles responsive are manifested electrocardiographically.
The ratio between the intervals is seldom exact whole numbers (3:1) and more often 3:2 etc.
Parasystolic rates vary from 20 to 400 BPM
In most patients the rate varies between 30 to 56 BPM
Parasystolic rates greater than 70 BPM is called parasystolic VT.
- The interectopic forum is variable, are multiples of the shorter interval
- Although the ectopic focus fires regularly, only those that find the ventricles responsive are manifested electrocardiographically.
- The ratio between the intervals is seldom exact whole numbers (3:1) and more often 3:2 etc.
- Parasystolic rates vary from 20 to 400 BPM
- In most patients the rate varies between 30 to 56 BPM
- Parasystolic rates greater than 70 BPM is called parasystolic VT.
- the presence of fusion beats
May discharge at the same time that an impulse of the basic rhythm arrives at the ventricles.
The ventricles are then depolarized by the two wavefronts.
Can occur with regular PVCs, but with parasystole more frequently.
- May discharge at the same time that an impulse of the basic rhythm arrives at the ventricles.
- The ventricles are then depolarized by the two wavefronts.
- Can occur with regular PVCs, but with parasystole more frequently.
- It is relatively uncommon
Seen in 1 to 1.5/1000 EKGS
Long rhythm strip required to demonstrate variability in coupling interval
- Seen in 1 to 1.5/1000 EKGS
- Long rhythm strip required to demonstrate variability in coupling interval
Ventricular hypertrophy

# Overview
Although ventricular hypertrophy may occur in either the left or right or both ventricles of the heart, left ventricular hypertrophy (LVH) is more commonly encountered.

# Physiology
The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or the rest of the body (left ventricle). Increased ventricular mass is an adaptation by the ventricle(s) of the heart to increased stress, such as chronically increased volume load (preload) or increased pressure load (afterload).
It is a physiological response that enables the heart to adapt to increased stress; however, the response can become pathological and ultimately lead to a deterioration in function. For example, hypertrophy is a normal physiological adaptation to exercise that enables the ventricle to enhance its pumping capacity.  Aerobic training results in the heart being able to pump a larger volume of blood through an increase in the size of the ventricles.  Anaerobic training results in the thickening of the myocardial wall to push blood through arteries compressed by muscular contraction. This type of physiologic hypertrophy is reversible and non-pathological, increasing the heart's ability to circulate blood. Chronic hypertension causes pathological ventricular hypertrophy.  This response enables the heart to maintain a normal stroke volume despite the increase in afterload.  However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
If the precipitating stress is volume overload (as through aerobic exercise, which increases blood return to the heart through the action of the skeletal-muscle pump), the ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e. the sarcomeres lengthen rather than thicken). This results in ventricular dilation while maintaining normal sarcomere lengths - the heart can expand to receive a greater volume of blood. The wall thickness normally increases in proportion to the increase in chamber radius. This type of hypertrophy is termed eccentric hypertrophy.
In the case of chronic pressure overload (as through anaerobic exercise, which increases resistance to blood flow by compressing arteries), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed concentric hypertrophy. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced) which can impair filling and lead to diastolic dysfunction.

# Related Chapters
- Cardiac fibrosis
- Cardiology
- Cardiomegaly
- Cardiovascular disease
- Right ventricular hypertrophy
Vibrio parahaemolyticus

# Overview
Vibrio parahaemolyticus is a curved, rod-shaped, Gram-negative bacterium found in saltwater. V. parahaemolyticus is oxidase positive, facultatively aerobic, and does not form spores. Like other members of the genus Vibrio, this species is motile, with a single, polar flagellum.

# Pathogenesis
While infection can occur via the fecal-oral route, ingestion of bacteria in raw or undercooked seafood, usually oysters, is the predominant cause the acute gastroenteritis caused by V. parahaemolyticus. Wound infections also occur, but are less common than seafood-borne disease. The disease mechanism of V. parahaemolyticus infections has not been fully elucidated. However, most clinical disease results from strains that carry either the thermostable direct hemolysin gene (tdh) or the tdh-related hemolysin gene (trh) or both genes.

# Epidemiology
Outbreaks tend to be concentrated along coastal regions during the summer and early fall when higher water temperatures favor higher levels of bacteria. Seafood most often implicated includes squid, mackerel, tuna, sardines, crab, shrimp, and bivalves like oysters and clams. The incubation period of ~24 hours is followed by explosive, watery diarrhea accompanied by nausea, vomiting, abdominal cramps, and sometimes fever. Vibrio parahaemolyticus symptoms typically resolve with-in 72 hours, but can persist for up to 10 days in immunocompromised individuals. As the vast majority of cases of V. parahaemolyticus food infection are self-limiting, treatment is not typically necessary. In severe cases, fluid and electrolyte replacement is indicated.
Additionally, swimming or working in affected areas can lead to infections of the eyes or ears  and open cuts and wounds. Following Hurricane Katrina, there were 22 vibrio wound infections 3 of which were caused by V. parahaemolyticus and 2 of these lead to death.

# Treatment

## Antimicrobial regimen
- Vibrio parahaemolyticus 
- 1. Mild to Moderate
- Treatment is not necessary in most cases of V. parahaemolyticus infection
- There is no evidence that antibiotic treatment decreases the severity or the length of the illness
- Patients should drink plenty of liquids to replace fluids lost through diarrhea
- 2. Severe or prolonged illnesses
- Preferred regimen: Tetracycline OR Ciprofloxacin
Voriconazole overdosage

# Overdosage
In clinical trials, there were three cases of accidental overdose. All occurred in pediatric patients who received up to five times the recommended intravenous dose of voriconazole. A single adverse event of photophobia of 10 minutes duration was reported.
There is no known antidote to voriconazole.
Voriconazole is hemodialyzed with clearance of 121 mL/min. The intravenous vehicle, SBECD, is hemodialyzed with clearance of 55 mL/min. In an overdose, hemodialysis may assist in the removal of voriconazole and SBECD from the body.
The minimum lethal oral dose in mice and rats was 300 mg/kg (equivalent to 4 and 7 times the recommended maintenance dose (RMD), based on body surface area). At this dose, clinical signs observed in both mice and rats included salivation, mydriasis, titubation (loss of balance while moving), depressed behavior, prostration, partially closed eyes, and dyspnea. Other signs in mice were convulsions, corneal opacification and swollen abdomen.
Voxel-based morphometry
Voxel based morphometry (VBM) is a neuroimaging analysis technique that allows investigation of focal differences in brain volume. 
It can be regarded as a form of so-called statistical parametric mapping. Traditionally, brain volume is measured by drawing regions of interest (ROIs) and calculating the volume enclosed.  However, this is time consuming and can only provide measures of large areas.  Smaller differences in volume may be overlooked.  VBM registers every brain to a template, which gets rid of most of the large differences in brain anatomy among people.  Then the brain images are smoothed so that each voxel represents the average of itself and its neighbors.  Finally, volume is compared across brains at every voxel.
One of the first VBM studies and one that came to attention in main stream media was a study on the hippocampus brain structure of London taxi drivers. The VBM analysis showed the back part of the hippocampus was on average larger in the taxi drivers compared to control subjects while the frontal part was smaller. 
London taxi drivers need good spatial navigational skills 
and scientists have usually associated hippocampus with this particular skill.
WeberChristian disease

# Overview
WeberChristian disease (also known as "Idiopathic Relapsing febrile non-suppurative panniculitis") is a cutaneous condition characterized by recurrent subcutaneous nodules that heal with depression of the overlying skin.
It is type of panniculitis.
It is a rare disease seen in females 30-60 years of age. It is a recurring inflammation of fatty layers of tissue present beneath the skin. Clinical course is characterised by exacerbations and remissions. Lesions are bilaterally symmetrical and are usually seen in the lower legs.

# Eponym
It is named for Frederick Parkes Weber and Henry Asbury Christian.
Y box binding protein 1
Y box binding protein 1 also known as Y-box transcription factor or nuclease-sensitive element-binding protein 1 is a protein that in humans is encoded by the YBX1 gene.

# Clinical significance
YBX1 is a potential drug target in cancer therapy. YB-1 helps the replication of adenovirus type 5, a commonly used vector in gene therapy. Thus, YB-1 can cause an "oncolytic" effect in YB-1 positive cancer cells treated with adenoviruses

# Interactions
Y box binding protein 1 has been shown to interact with:
- ANKRD2,
- CTCF,
- P53,
- PCNA,
- RBBP6,  and
- SFRS9.
Yersinia enterocolitica

# Overview
Yersinia enterocolitica is a species of gram-negative coccobacillus-shaped bacterium, belonging to the family Enterobacteriaceae. Primarily a zoonotic disease (cattle, deer, pigs, and birds), animals which recover frequently become asymptomatic carriers of the disease.

# Pathogenesis

## Acute infections
Acute Y. enterocolitica infections produce severe diarrhea in humans, along with Peyer's patch necrosis, chronic lymphadenopathy, and hepatic or splenic abscesses. Additional symptoms may include entero-colitis, fever, mesenteric adenitis, erythema nodosum and acute terminal ileitis, which may be confused with appendicitis or Crohn's disease. See yersiniosis for further details.

### Treatment
Treatment of Y. enterocolitica infections requires aggressive antibiotic therapy, typically involving a combination of chloramphenicol, ampicillin, and polymyxin.

## Long-term effects
Y. enterocolitica infections are sometimes followed by chronic inflammatory diseases such as arthritis.
Y. enterocolitica seems to be associated with autoimmune Graves-Basedow thyroiditis.
Whilst indirect evidence exists, direct causative evidence is limited,
and Y. enterocolitica is probably not a major cause of this disease, but may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.
It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility.
More recently the role for Y. enterocolitica has been disputed.

# Differential diagnosis
Yersinia enterocolitica infection must be differentiated from other causes of viral, bacterial, and parasitic gastroentritis.
8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field
Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
 It could be as high as 1000 based on patient's immunity system.
The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea
Zidovudine how supplied

# How Supplied
RETROVIR Tablets 300 mg (biconvex, white, round, film-coated) containing 300 mg zidovudine, one side engraved GX CW3 and 300 on the other side.
Bottle of 60 (NDC 49702-214-18).
Store at 15 to 25C (59 to 77F).
RETROVIR Capsules 100 mg (white, opaque cap and body) containing 100 mg zidovudine and printed with Wellcome and unicorn logo on cap and Y9C and 100 on body.
Bottles of 100 (NDC 49702-211-20).
Store at 15 to 25C (59 to 77F) and protect from moisture.
RETROVIR Syrup (colorless to pale yellow, strawberry-flavored) containing 10 mg zidovudine in each mL.
Bottle of 240 mL (NDC 49702-212-48) with child-resistant cap.
Store at 15 to 25C (59 to 77F).
Zidovudine microbiology

# Microbiology

## Antiviral Activity
The antiviral activity of zidovudine against HIV-1 was assessed in a number of cell lines (including monocytes and fresh human peripheral blood lymphocytes). The EC50 and EC90 values for zidovudine were 0.01 to 0.49 M (1 M = 0.27 mcg/mL) and 0.1 to 9 M, respectively. HIV-1 from therapy-naive subjects with no mutations associated with resistance gave median EC50 values of 0.011 M (range: 0.005 to 0.110 M) from Virco (n = 92 baseline samples from COL40263) and 0.0017 M (0.006 to 0.0340 M) from Monogram Biosciences (n = 135 baseline samples from ESS30009). The EC50 values of zidovudine against different HIV-1 clades (A-G) ranged from 0.00018 to 0.02 M, and against HIV-2 isolates from 0.00049 to 0.004 M. In cell culture drug combination studies, zidovudine demonstrates synergistic activity with the nucleoside reverse transcriptase inhibitors abacavir, didanosine, and lamivudine; the non-nucleoside reverse transcriptase inhibitors delavirdine and nevirapine; and the protease inhibitors indinavir, nelfinavir, ritonavir, and saquinavir; and additive activity with interferon alfa. Ribavirin has been found to inhibit the phosphorylation of zidovudine in cell culture.

## Resistance
Genotypic analyses of the isolates selected in cell culture and recovered from zidovudine-treated subjects showed mutations in the HIV-1 RT gene resulting in 6 amino acid substitutions (M41L, D67N, K70R, L210W, T215Y or F, and K219Q) that confer zidovudine resistance. In general, higher levels of resistance were associated with greater number of amino acid substitutions. In some subjects harboring zidovudine-resistant virus at baseline, phenotypic sensitivity to zidovudine was restored by 12 weeks of treatment with lamivudine and zidovudine. Combination therapy with lamivudine plus zidovudine delayed the emergence of substitutions conferring resistance to zidovudine.

## Cross-Resistance
In a study of 167 HIV-1-infected subjects, isolates (n = 2) with multi-drug resistance to didanosine, lamivudine, stavudine, zalcitabine, and zidovudine were recovered from subjects treated for 1 year with zidovudine plus didanosine or zidovudine plus zalcitabine. The pattern of resistance-associated amino acid substitutions with such combination therapies was different (A62V, V75I, F77L, F116Y, Q151M) from the pattern with zidovudine monotherapy, with the Q151M substitution being most commonly associated with multi-drug resistance. The substitution at codon 151 in combination with substitutions at 62, 75, 77, and 116 results in a virus with reduced susceptibility to didanosine, lamivudine, stavudine, zalcitabine, and zidovudine. Thymidine analogue mutations (TAMs) are selected by zidovudine and confer cross-resistance to abacavir, didanosine, stavudine, tenofovir, and zalcitabine.
Zinc finger protein 165
Zinc finger protein 165 is a protein that in humans is encoded by the ZNF165 gene.

# Function
This gene encodes a member of the Kruppel family of zinc finger proteins. Members of this DNA-binding protein family act as transcriptional regulators. This gene is located within a cluster of zinc finger family members. The encoded protein may play a role in spermatogenesis.

# Interactions
Zinc finger protein 165 has been shown to interact with Ewing sarcoma breakpoint region 1 and DVL2.