Persius/hicric huggingface dataset:
Sleep paralysis (patient information)
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Phone:617-632-7753; Associate Editor-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S.

# Overview
Isolated sleep paralysis is a type of paralysis that occurs with a sleep disorder. Sleep paralysis is the inability to perform voluntary muscle movements during sleep.

# What are the symptoms of Sleep paralysis?
- People with isolated sleep paralysis have episodes that last from a few seconds to 1 or 2 minutes in which they are unable to move or speak.
- These spells end on their own or when the person is touched or moved.
- Rarely, the person may have dream-like sensations or hallucinations, which may be scary to them.

# What causes Sleep paralysis?
- Isolated sleep paralysis is more likely to happen during the first two hours of sleep. Not getting enough sleep or sleeping on the back may cause more frequent episodes.
- Though this condition may occur with narcolepsy, many people who do not have narcolepsy have isolated sleep paralysis. It is common in adults and is also seen in children.
- Most people with isolated sleep paralysis do not have any mental health problems. However, these episodes seem to occur more often in people with:
- Anxiety disorders
- Bipolar illness
- Depression
- Post traumatic stress disorder
- Rarely, it runs in families.

# Diagnosis
If you do not have other symptoms of narcolepsy, there is usually no need to perform polysomnography.

# Where to find medical care for Sleep paralysis?
Directions to Hospitals Treating Sleep paralysis

# Source
SmartLipo Liposuction and Fat Removal
SmartLipo liposuction and fat removal is a smart new way to achieve beautifully contoured aesthetic results with the least degree of discomfort and surgery-associated complications. Provided the patients have no contraindications such as pregnancy or a delivery within the past three months, a major systemic illness, hernia, Crohns disease, or allergy to epinephrine or lidocaine, they can undergo SmartLipo.
Unwanted fat can be eliminated and loose or inelastic skin tightened in the following areas:
- Chin
- Back
- Upper arms
- Neck
- Knees
- Hips
- Saddle bags
- Male breasts
- Mons pubis
- Abdomen
Dual Platform Laser MPX for Dual Action
SmartLipo scores over Lipo Lite and Cool Lipo in terms of its dual platform laser MPX , one wavelength of which is for fat liquefaction and the other, for skin tightening. The SmartLipo plastic surgeon can thus shift from one blend to another, depending on the quality of skin and kind of body the patient has. Neither of the other two methods has such a feature. SmartLipo can be carried out in the plastic surgeons office with the patient put under local anesthesia, which is safer than general anesthesia.
SmartSense and Thermister
Using the smart and novel handpiece delivery solution called SmartSense, the plastic surgeon performing the SmartLipo   procedure can ensure precision, safety, control, and consistency of results. The degree of heat energy that the patient receives to melt the fat would thus depend on how the surgeon does the procedure, not on a machine setting that has been decided in advance. Thermister is yet another wonderful feature of SmartLipo MPX and of SmartLipo.
Less Pain, Quick Recovery
Results from the SmartLipo liposuction and fat removal procedure would be noticeable in about 6 months or less time. The results would be permanent if they are kept up with exercise and a good diet. With the coming of SmartLipo, it is goodbye to painful plastic surgery procedures, and lengthy time spans for recovery.
Subjective Units of Disturbance Scale
A SUDS or a Subjective Units of Disturbance Scale is a scale of 0 to 10 for measuring the subjective intensity of disturbance or distress currently experienced by an individual. The individual self assesses where they are on the scale. The SUDS may be used as a benchmark for a professional or observer to evaluate the progress of treatment.
The SUD-level was developed by Joseph Wolpe in 1969.  It has been used in EMDR, Trauma-Focused Therapy (TFT), EFT, and for research purposes.

# Basis
There is no hard and fast rule by which a patient can self assign a SUDS rating to his or her disturbance or distress, hence the name subjective.
Some guidelines are:
- The intensity recorded must be as it is experienced now.
- Constriction or congestion or tensing of body parts indicates a higher SUDS than that reported.

# The scale
Here is one version of the scale:
10 = Feels unbearably bad, beside yourself, out of control as in a nervous breakdown, overwhelmed, at the end of your rope.  You may feel so upset that you don't want to talk because you can't imagine how anyone could possibly understand your agitation.
9 = Feeling desperate.  What most people call a 10 is actually a 9.  Feeling extremely freaked out to the point that it almost feels unbearable and you are getting scared of what you might do.  Feeling very, very bad, losing control of your emotions.
8 = Freaking out.  The beginning of alienation.
7 = Starting to freak out, on the edge of some definitely bad feelings.  You can maintain control with difficulty.
6 = Feeling bad to the point that you begin to think something ought to be done about the way you feel.
5 = Moderately upset, uncomfortable.  Unpleasant feelings are still manageable with some effort.
4 = Somewhat upset to the point that you cannot easily ignore an unpleasant thought.  You can handle it OK but don't feel good.
3 = Mildly upset.  Worried, bothered to the point that you notice it.
2 = A little bit upset, but not noticeable unless you took care to pay attention to your feelings and then realize, "yes" there is something bothering me.
1 = No acute distress and feeling basically good.  If you took special effort you might feel something unpleasant but not much.
0 = Peace, serenity, total relief.  No more bad feelings of any kind about any particular issue.
nl:Subjective Units of Disturbance-schaal
Supraventricular tachycardia overview

# Overview
A supraventricular tachycardia (SVT) is a tachycardia or rapid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node.  These rhythms, by definition, are either initiated or maintained by the atria or the AV node.  This is in contrast to ventricular tachycardias, which are rapid rhythms that originate from the ventricles of the heart, that is, below the atria or AV node.  The term SVT encompasses a large number of arrhythmias arising from the atria and the AV node, and the term SVT is often incorrectly applied only to the subgroup of AV nodal re-entrant tachycardias.

# Overview

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Supraventricular Tachycardia from Ventricular Tachycardia
Most supraventricular tachycardias have a narrow QRS complex on the EKG.  It is not infrequent, however, for aberrant conduction to be be present, sometimes as a result of the more rapid rate of conduction.  This widening of the QRS complex yields supraventricular tachycardia with aberrant conduction (SVTAC) which produces a wide-complex tachycardia that may mimic ventricular tachycardia (VT).  In the clinical setting, it is important to determine whether a wide-complex tachycardia is an SVT or a ventricular tachycardia, since they are treated differently.  Ventricular tachycardia has to be treated appropriately, since it can quickly degenerate to ventricular fibrillation and death. A number of different algorithms have been devised to determine whether a wide complex tachycardia is supraventricular or ventricular in origin. In general, a history of structural heart disease, ischemic heart disease or congestive heart failure increases the likelihood that the tachycardia is ventricular in origin.

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis
Supraventricular tachycardias may start and stop abruptly.  Patients may develop syncope.  The prognosis of an SVT is generally good in absence of underlying heart disease.

# Diagnosis

## Diagnostic Study of Choice

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Electrocardiogram
The best method to diagnose supraventricular tachycardia is through electrocardiography. Presentation on EKG will vary depending on the subtype. In general, QRS complexes tend to be tall and narrow, P waves are absent, and rate is greater than 100 beats per minute.  Asystole may occur due to tachycardia-mediated suppression of the sinus node when the rhythm is in AVNRT.

## X-ray

## Echocardiography and Ultrasound

## CT scan

## MRI

## Other Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Interventions

## Surgery

## Primary Prevention

## Secondary Prevention
TCCACCATA element gene transcriptions
"Given that AtACBP4pro::GUS (156/67) could drive promoter activity for pollen expression,  EMSAs were carried out to investigate the role of the putative POLLEN1 cis-element, AGAAA (150/146), and its adjacent co-dependent regulatory element TCCACCATA (141/133)."
"POLLEN1 and the TCCACCATA element are co-dependent regulatory elements responsible for pollen-specific activation of tomato LAT52 (Bate and Twell 1998)."

# Human genes

# Consensus sequences
Consensus sequence for the regulatory element appears to be 3'-TCCACCATA-5'.

# Samplings
Copying the consensus regulatory element: 3'-TCCACCATA-5' and putting the sequence in "F" finds no locations for this sequence in any A1BG direction as can be found by the computer programs.
For the Basic programs testing consensus sequence TCCACCATA (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 TCCACCATA, 0.
- positive strand, negative direction, looking for TCCACCATA, 0.
- positive strand, positive direction, looking for TCCACCATA, 0.
- negative strand, positive direction, looking for TCCACCATA, 0.
- complement, negative strand, negative direction, looking for AGGTGGTAT, 0.
- complement, positive strand, negative direction, looking for AGGTGGTAT, 0.
- complement, positive strand, positive direction, looking for AGGTGGTAT, 0.
- complement, negative strand, positive direction, looking for AGGTGGTAT, 0.
- inverse complement, negative strand, negative direction, looking for TATGGTGGA, 0.
- inverse complement, positive strand, negative direction, looking for TATGGTGGA, 0.
- inverse complement, positive strand, positive direction, looking for TATGGTGGA, 0.
- inverse complement, negative strand, positive direction, looking for TATGGTGGA, 0.
- inverse negative strand, negative direction, looking for ATACCACCT, 0.
- inverse positive strand, negative direction, looking for ATACCACCT, 0.
- inverse positive strand, positive direction, looking for ATACCACCT, 0.
- inverse negative strand, positive direction, looking for ATACCACCT, 0.
Vascular endothelial growth inhibitor
Vascular endothelial growth inhibitor (VEGI), also known as TNF-like ligand 1A (TL1A) and TNF superfamily member 15 (TNFSF15), is protein that in humans is encoded by the TNFSF15 gene. VEGI is an anti-angiogenic protein. It belongs to tumor necrosis factor (ligand) superfamily, where it is member 15. It is the sole known ligand for death receptor 3, and it can also be recognized by decoy receptor 3.

# Function
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is abundantly expressed in endothelial cells, but is not expressed in either B or T cells. The expression of this protein is inducible by TNF-alpha and IL-1 alpha. This cytokine is a ligand for receptor TNFRSF25 (death receptor 3) and TNFRSF6B (decoy receptor 3). It can activate both the NF-B and MAPK signalling pathways, and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial cell proliferation, and thus may function as an angiogenesis inhibitor. An additional isoform encoded by an alternatively spliced transcript variant has been reported but the sequence of this transcript has not been determined.

# Clinical relevance
Several TNFSF15 SNPs have been found to be strongly associated with inflammatory bowel disease.
Telbivudine dosage and administration

# Dosage and Administration

## Adults and Adolescents (16 years of age and older)
Due to higher rates of resistance that may develop with longer term treatment among patients with incomplete viral suppression, treatment should only be initiated, if pre-treatment HBV DNA and ALT measurements are known, in the following patient populations:
For HBeAg-positive patients, HBV DNA should be less than 9 log10 copies per mL and ALT should be greater than or equal to 2x ULN prior to treatment with Tyzeka.
For HBeAg-negative patients, HBV DNA should be less than 7 log10 copies per mL prior to treatment with Tyzeka.
HBV DNA levels should be monitored at 24 weeks of treatment to assure complete viral suppression (HBV DNA less than 300 copies per mL). Alternate therapy should be initiated for patients who have detectable HBV DNA after 24 weeks of treatment. Optimal therapy should be guided by further resistance testing.
The recommended dose of Tyzeka for the treatment of chronic hepatitis B is 600 mg once daily, taken orally, with or without food.
Tyzeka oral solution (30 mL) may be considered for patients who have difficulty with swallowing tablets.

## Renal Impairment
Tyzeka may be used for the treatment of chronic hepatitis B in patients with impaired renal function. No adjustment to the recommended dose of Tyzeka is necessary in patients whose creatinine clearance is greater than or equal to 50 mL per min. Adjustment of the total daily dose of Tyzeka oral solution or of the interval for administration of Tyzeka tablets is required in patients with creatinine clearance less than 50 mL per min including those with ESRD on hemodialysis (Table 1).

## Hepatic Impairment
No adjustment to the recommended dose of Tyzeka is necessary in patients with hepatic impairment.

## Duration of Therapy
For patients with incomplete viral suppression (HBV DNA greater than or equal to 300 copies per mL) after 24 weeks of treatment, alternate therapy should be instituted. HBV DNA should be monitored every 6 months to assure continued response. If patients test positive for HBV DNA at any time after their initial response, alternate treatment should be instituted. Optimal therapy should be guided by resistance testing.
The optimal duration of therapy with Tyzeka for patients with chronic hepatitis B is unknown.
Template to add a clinical trial copy

# Complete Title of Study
None reported

# Study Acronym (The trial's abbreviation if there is one)
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# Principal Investigator, Co-investigators, and Collaborating Institutions
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# Overview of Trial
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# Disease State(s) Studied (e.g. acute MI, breast cancer, etc.)
None reported

# Study Phase (e.g. Phase I,II,III,IV) Study Phases are defined here
None reported

# Study Design (e.g. multicenter, randomized, double blind, placebo controlled)
None reported

# Study Arms and How They Were Treated (Intervention) (Explanation here)
None reported

# Primary Pre-Specified Endpoint
None reported

# Secondary Endpoints
None reported

# Inclusion Criteria
None reported

# Exclusion Criteria
None reported

# Outcome: Primary endpoint (Report both relative risk reduction and absolute risk reduction as well as number needed to treat if available)
None reported

# Outcome: Secondary endpoint (Report both relative risk reduction and absolute risk reduction as well as number needed to treat if available)
None reported

# Outcome: Exploratory endpoints (Report both relative risk reduction and absolute risk reduction as well as number needed to treat if available)
None reported

# Outcome: Safety endpoints (Report both relative risk and absolute risk as well as number needed to harm if available)
None reported

# Conclusions of the Investigators (Quote the investigators conclusions here)
None reported

# Commentary, Discussion and Limitations of the Trial (Anyone can add comments)
None reported

# Slides
None reported

# Video Commentary
None reported

# References (How to insert a reference)
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# External sites for further information (How to insert links)
None reported

# Detailed information about the trial

# Ages
__ years to ___ years

# Gender (Indicate whether men, women or both were enrolled)
None reported

# Accepts Healthy Volunteers (Answer yes or no)
None reported

# Enrollment Period (Study start and end date)
None reported

# Recruitment Status (explanation)
None reported

# Enrollment (Total number of patients enrolled)
None reported

# Study Sponsor (e.g. Investigator initiated or company name)
None reported (this may not have yet been ascertained)

# Source of Data (Where is this data on this page coming from: publication, principal investigator, or co-investigator)
None reported
The content of the clinical trial wiki consists of fields that have been suggested by the World Health Organization and wwww.clinicaltrials.gov.
Terconazole dosage and administration

# Dosage and Administration
- TERAZOL 7 (terconazole) Vaginal Cream 0.4%
One full applicator (5 g) of TERAZOL 7 Vaginal Cream (20 mg terconazole) should be administered intravaginally once daily at bedtime for seven consecutive days.
- TERAZOL 3 (terconazole) Vaginal Cream 0.8%
One full applicator (5 g) of TERAZOL 3 Vaginal Cream (40 mg terconazole) should be administered intravaginally once daily at bedtime for three consecutive days.
- TERAZOL 3 (terconazole) Vaginal Suppositories 80 mg
One TERAZOL 3 Vaginal Suppository (80 mg terconazole) should be administered intravaginally once daily at bedtime for three consecutive days.
Before prescribing another course of therapy, the diagnosis should be reconfirmed by smears and/or cultures and other pathogens commonly associated with vulvovaginitis ruled out. The therapeutic effect of these products is not affected by menstruation.
Thick ascending limb of loop of Henle

# Overview
The thick ascending limb of loop of Henle (or distal straight tubule) is a segment of the nephron in the kidney. It can be divided into two parts: that in the renal medulla, and that in the renal cortex.

# Medullary thick ascending limb
The medullary thick ascending limb remains impermeable to water. Sodium, potassium (K+) and chloride (Cl-) ions are reabsorbed by active transport. K+ is passively transported along its concentration gradient through a K+ leak channel in the apical aspect of the cells, back into the lumen of the ascending limb. This K+ "leak" generates a positive electrochemical potential difference in the lumen. The electrical gradient drives more reabsorption of Na+, as well as other cations such as magnesium (Mg2+) and importantly calcium Ca2+.
Loop diuretics block the K+/Na+/2Cl- co-transporter.
Urea which remains in the loop creates a solute potential that prevents water completely osmosing out into the interstitial space. This means that while almost all the ions are reabsorbed, there will still be some water in the urine, and hence, the concentration of the filtrate in the loop is decreased here. (If only ions were present, and a certain amount of ions were reabsorbed, one would expect the same amount of the water to be reabsorbed too, and hence the concentration would remain the same, but this is not true.)
This is also the part of the tubule that generates Tamm-Horsfall protein.  The function of this protein is not well understood, but is responsible for creating urinary casts.

# Cortical thick ascending limb
The difference between the medullary and cortical thick ascending limbs is mainly anatomical. Functionally, they are very similar.
The cortical thick ascending limb drains urine into the distal convoluted tubule.
Topiramate dosage forms and strengths

# Dosage Forms and Strengths
Topiramate tablets are available as debossed, coated, circular tablets in the following strengths and colors:
25 mg white, circular, biconvex, film-coated tablets debossed with E on one side and 22 on the other side.
50 mg light yellow colored, circular, biconvex, film-coated tablets debossed with E on one side and 33 on the other side.
100 mg dark yellow colored, circular, biconvex, beveled edge, film-coated tablets debossed with E on one side and 23 on the other side.
200 mg pink colored, circular, biconvex, beveled edge, film-coated tablets debossed with E on one side and 24 on the other side.
United Nations Drug Control Programme
The United Nations International Drug Control Programme (UNDCP) and the United Nations Centre for International Crime Prevention (CICP) are part of the United Nations Office on Drugs and Crime (UNODC), which was formerly called the United Nations Office for Drug Control & Crime Prevention (ODCCP).
UNDCP cooperates with several governmental and non-governmental organisations as well as with the business community. It is presently drawing up plans for a more concentrated approach to cooperation with the private sector. Its team of experts helps requesting states to become party to and give effect to the United Nations drug control conventions. UNDCP also performs laboratory services, provides training materials and can refer those in need to the appropriate medical advice.
In central, eastern and southeastern Europe, UNDCP operations have focused on developing cross-border cooperation on the basis of harmonised national drug control capacities. An important component of UNDCP activities in the region has been the establishment of a coordination mechanism for international drug control assistance to eastern Europe, the Baltic States, and the Commonwealth of Independent States.
An external evaluation confirmed the need for coordination of technical assistance projects in the foreseeable future owing to the complexity of the needs of recipient countries and the number of donors involved in the target region. The UNDCP coordination mechanism has played a key role in efforts to coordinate strategies for cooperation among donor countries and international organisations in the field of drug control. The framework of the UNDCP coordination mechanism is being increasingly used in the formulation of joint strategies for UNDCP and donors and in the design and execution of technical cooperation projects and programmes. This coordination mechanism is being further developed during 2000-2001.
In the area of demand reduction, a multiphase regional programme designed to train professionals in the treatment of drug abuse has been successfully completed, creating a core cadre of over 600 professionals and sustainable national training programmes. UNDCP has continued to work with the Pompidou Group of the Council of Europe in expanding its city network to encompass states of eastern Europe, with the ILO in implementing a UNDCP-funded workplace prevention programme, and with the Associazione Casa Familia Rosetta in training professionals in the treatment of drug abuse.
Vasodilator-stimulated phosphoprotein
Vasodilator-stimulated phosphoprotein is a protein that in humans is encoded by the VASP gene.

# Function
Vasodilator-stimulated phosphoprotein (VASP) is a member of the Ena-VASP protein family. Ena-VASP family members contain an N-terminal EVH1 domain that binds proteins containing E/DFPPPPXD/E motifs and targets Ena-VASP proteins to focal adhesions cell membranes. In the mid-region of the protein, family members have a proline-rich region that binds SH3 and WW domain-containing proteins. Their C-terminal EVH2 domain mediates tetramerization and binds both G and F actin. VASP is associated with filamentous actin formation and likely plays a widespread role in cell adhesion and motility. VASP may also be involved in the intracellular signaling pathways that regulate integrin-extracellular matrix interactions. VASP is regulated by the cyclic nucleotide-dependent kinases PKA and PKG.

# Interactions
Vasodilator-stimulated phosphoprotein has been shown to interact with Zyxin, Profilin 1, and PFN2.