Persius/hicric huggingface dataset:
Striae (patient information)
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# Overview
Striae are irregular areas of skin that look like bands, stripes, or lines. Striae are seen when a person grows or gains weight rapidly or has certain diseases or conditions.
Striae are commonly called stretch marks.

# What are the symptoms of Striae?
Stretch marks can appear when there is rapid stretching of the skin. They are often associated with the abdominal enlargement of pregnancy. They can be found in children who have become rapidly obese. They may also occur during the rapid growth of puberty in males and females. Striae are most commonly located on the breasts, hips, thighs, buttocks, abdomen, and flank.
Stretch marks appear as parallel streaks of red, thinned, glossy skin that over time become whitish and scarlike in appearance. The stretch marks may be slightly depressed and have a different texture than normal skin.
Striae may also occur as a result of abnormal collagen formation, or a result of medications or chemicals that interfere with collagen formation. They may also be associated with longtime use of cortisone compounds, diabetes, Cushing disease, and post-pregnancy.

# What causes Striae?
- Cushing syndrome
- Ehlers-Danlos syndrome
- Pregnancy
- Puberty
- Obesity
- Overuse of cortisone skin creams

# When to seek urgent medical care?
If striae or stretch marks appear without obvious cause such as pregnancy or rapid weight gain, call your health care provider.

# Treatment options
There is no specific care for stretch marks. Marks often will disappear after the cause of the skin stretching is gone. Creams and ointments that claim to prevent stretch marks during pregnancy are of little value.
Avoiding rapid weight gain helps reduce stretch marks caused by obesity.

# Where to find medical care for Striae?
Directions to Hospitals Treating Striae

# What to expect (Outlook/Prognosis)?
You health care provider will examine you and ask questions about your symptoms, including:
- Is this the first time that you have developed striae?
- When did you first notice the stretchmarks?
- What medicines have you taken?
- Have you used a cortisone skin cream?
- What other symptoms do you have?
If the striae are not caused by normal physical changes, tests may be done.

# Sources
Sulfamethoxazole description

# Description
BACTRIM (sulfamethoxazole and trimethoprim) is a synthetic antibacterial combination product available in DS (double strength) tablets, each containing 800 mg sulfamethoxazole and 160 mg trimethoprim; in tablets, each containing 400 mg sulfamethoxazole and 80 mg trimethoprim for oral administration.
Sulfamethoxazole is N1-(5-methyl-3-isoxazolyl)sulfanilamide; the molecular formula is C10H11N3O3S. It is an almost white, odorless, tasteless compound with a molecular weight of 253.28 and the following structural formula:
Trimethoprim is 2,4-diamino-5-(3,4,5-trimethoxybenzyl)pyrimidine; the molecular formula is C14H18N4O3. It is a white to light yellow, odorless, bitter compound with a molecular weight of 290.3 and the following structural formula:
Inactive ingredients: Docusate sodium 85%, sodium benzoate 15%, sodium starch glycolate, magnesium stearate and pregelatinized starch.
Supraventricular arrhythmias

# Overview

## Supraventricular ectopic beats
- Atrial Premature Complexes
- Wandering Pacemaker
- AV-nodal complexes

## Also read
- Flowchart: Approach to the Narrow Complex Tachycardia Adapted from ESCnarrowQRS.
- Introduction to Arrhythmias
- Mechanisms of Arrhythmias
- Sinus node rhythms and arrhythmias
- Junctional Tachycardias
- Ventricular Arrhythmias

# EKG Examples
This is an electrocardiogram from a woman in her forties who had several operations for congenital heart disease. At the time of the electrocardiogram the patient was taking flecainide and metoprolol .
This patient was being treated for ventricular tachycardia. She was initially treated with amiodarone and then was switched to a combination of flecainide and metoprolol. She was doing well. The underlying congenital heart disease was Tetralogy of Fallot. The electrocardiogram shows a supraventricular rhythm which is probably not sinus as indicated by the negative P waves in the inferior leads. The cardiogram also shows 1 PVC and a right Branch block with a left anterior hemi-block.

## Causes

## Drug Side Effect
- Cyclophosphamide
- interferon alfacon-1
- Ixabepilone
- Rasburicase
Tamsulosin drug interactions

# List of drug interactions
Nifedipine, Atenolol, Enalapril
Warfarin
Digoxin and Theophylline
Furosemide
Cimetidine

## Nifedipine, Atenolol, Enalapril
In three studies in hypertensive subjects (age range 47-79 years) whose blood pressure was
controlled with stable doses of Procardia XL, atenolol, or enalapril for at least three months,
Tamsulosin capsules 0.4 mg for seven days followed by Tamsulosin capsules 0.8 mg for
another seven days (n=8 per study) resulted in no clinically significant effects on blood
pressure and pulse rate compared to placebo (n=4 per study). Therefore, dosage adjustments
are not necessary when Tamsulosin capsules are administered concomitantly with Procardia
XL, atenolol, or enalapril. Return to top

## Warfarin
A definitive drug-drug interaction study between tamsulosin HCl and warfarin was not
conducted. Results from limited in vitro and in vivo studies are inconclusive. Therefore,
caution should be exercised with concomitant administration of warfarin and FLOMAX
capsules. Return to top

## Digoxin and Theophylline
In two studies in healthy volunteers (n=10 per study; age range 19-39 years) receiving
FLOMAX capsules 0.4 mg/day for two days, followed by Tamsulosin capsules 0.8 mg/day for
five to eight days, single intravenous doses of digoxin 0.5 mg or theophylline 5 mg/kg
resulted in no change in the pharmacokinetics of digoxin or theophylline. Therefore, dosage
adjustments are not necessary when a FLOMAX capsule is administered concomitantly with
digoxin or theophylline. Return to top

## Furosemide
The pharmacokinetic and pharmacodynamic interaction between Tamsulosin capsules 0.8
mg/day (steady-state) and furosemide 20 mg intravenously (single dose) was evaluated in ten
healthy volunteers (age range 21-40 years). Tamsulosin capsules had no effect on the
pharmacodynamics (excretion of electrolytes) of furosemide. While furosemide produced an
11% to 12% reduction in tamsulosin HCl Cmax and AUC, these changes are expected to be
clinically insignificant and do not require adjustment of the FLOMAX capsules dosage. Return to top

## Cimetidine
The effects of cimetidine at the highest recommended dose (400 mg every six hours for six
days) on the pharmacokinetics of a single Tamsulosin capsule 0.4 mg dose was investigated in
ten healthy volunteers (age range 21-38 years). Treatment with cimetidine resulted in a
significant decrease (26%) in the clearance of tamsulosin HCl which resulted in a moderate
increase in tamsulosin HCl AUC (44%). Therefore, Tamsulosin capsules should be used with
caution in combination with cimetidine, particularly at doses higher than 0.4 mg. Return to top
Adapted from the FDA Package Insert.
Telaprevir contraindications

# Contraindications
Contraindications to peginterferon alfa and ribavirin also apply to INCIVEK combination treatment.
INCIVEK combination treatment is contraindicated in:
- women who are or may become pregnant. Ribavirin may cause fetal harm when administered to a pregnant woman. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug treatment, the patient should be apprised of the potential hazard to a fetus .
- men whose female partners are pregnant.
INCIVEK is a strong inhibitor of CYP3A. INCIVEK is contraindicated when combined with drugs that are highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events (narrow therapeutic index). INCIVEK is contraindicated when combined with drugs that strongly induce CYP3A and thus may lead to lower exposure and loss of efficacy of INCIVEK. Contraindicated drugs are listed below in Table 3 .
Telaprevir drug interactions

# Drug Interactions

## Potential for INCIVEK to Affect Other Drugs
INCIVEK is a strong inhibitor of CYP3A. Co-administration of INCIVEK with drugs that are primarily metabolized by CYP3A may result in increased plasma concentrations of such drugs, which could increase adverse reactions (see Table 5). INCIVEK is also an inhibitor of P-gp, OATP1B1, and OATP2B1. Co-administration of INCIVEK with drugs that are substrates for P-gp, OATP1B1, and OATP2B1 transport may result in increased plasma concentrations of such drugs, which could increase adverse reactions (see Table 5). If dose adjustments of concomitant medications are made during INCIVEK treatment, they should be re-adjusted after administration of INCIVEK is completed.

## Potential for Other Drugs to Affect INCIVEK
INCIVEK is a substrate of CYP3A and P-gp; therefore, drugs that induce CYP3A and/or P-gp may decrease INCIVEK plasma concentrations and reduce the therapeutic effect of INCIVEK. Co-administration of INCIVEK with drugs that inhibit CYP3A and/or P-gp may increase INCIVEK plasma concentrations.

## Established and Other Potentially Significant Drug Interactions
Table 5 provides effect on concentration of INCIVEK or concomitant drug with INCIVEK. These recommendations are based on either drug interaction trials (indicated with *) or predicted interactions due to the expected magnitude of interaction and potential for serious adverse events or loss of efficacy. Most drug interaction studies have been performed with a dose of 750 mg q8h of INCIVEK. The 1125 mg twice-daily regimen provides similar total daily exposures of telaprevir; thus drug interactions are expected to be similar between the two regimens when evaluated after multiple doses .
In addition to the drugs included in Table 5, the interaction between INCIVEK and the following drugs was evaluated in clinical trials and no dose adjustment is needed for any drug : esomeprazole, raltegravir, or buprenorphine.
Telavancin adverse reactions

# Adverse Reactions
The following serious adverse reactions are discussed elsewhere in the labeling:
- Nephrotoxicity 
- Infusion-related reactions 
- Clostridium difficile-associated diarrhea 
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

## Clinical Trials Experience
The two Phase 3 cSSSI clinical trials (Trial 1 and Trial 2) for VIBATIV included 929 adult patients treated with VIBATIV at 10 mg/kg IV once daily. The mean age of patients treated with VIBATIV was 49 years (range 18-96). There was a slight male predominance (56%) in patients treated with VIBATIV, and patients were predominantly Caucasian (78%).
In the cSSSI clinical trials, <1% (8/929) patients who received VIBATIV died and <1% (8/938) patients treated with vancomycin died. Serious adverse events were reported in 7% (69/929) of patients treated with VIBATIV and most commonly included renal, respiratory, or cardiac events. Serious adverse events were reported in 5% (43/938) of vancomycin-treated patients, and most commonly included cardiac, respiratory, or infectious events. Treatment discontinuations due to adverse events occurred in 8% (72/929) of patients treated with VIBATIV, the most common events being nausea and rash (~1% each). Treatment discontinuations due to adverse events occurred in 6% (53/938) of vancomycin-treated patients, the most common events being rash and pruritus (~1% each).
The most common adverse reactions occurring in 10% of VIBATIV-treated patients observed in the VIBATIV Phase 3 cSSSI trials were taste disturbance, nausea, vomiting, and foamy urine.
Table 4 displays the incidence of treatment-emergent adverse drug reactions reported in >2% of patients treated with VIBATIV possibly related to the drug (including those reactions known to occur with other glycopeptide antibacterial agents).
Terbinafine clinical studies

# Clinical Studies
The efficacy of terbinafine tablets in the treatment of onychomycosis is illustrated by the response of subjects with toenail and/or fingernail infections who participated in 3 U.S./Canadian placebo-controlled clinical trials.
Results of the first toenail trial, as assessed at week 48 (12 weeks of treatment with 36 weeks follow-up after completion of therapy), demonstrated mycological cure, defined as simultaneous occurrence of negative KOH plus negative culture, in 70% of subjects. Fifty-nine percent (59%) of subjects experienced effective treatment (mycological cure plus 0% nail involvement or >5 mm of new unaffected nail growth); 38% of subjects demonstrated mycological cure plus clinical cure (0% nail involvement).
In a second toenail trial of dermatophytic onychomycosis, in which nondermatophytes were also cultured, similar efficacy against the dermatophytes was demonstrated. The pathogenic role of the nondermatophytes cultured in the presence of dermatophytic onychomycosis has not been established. The clinical significance of this association is unknown.
Results of the fingernail trial, as assessed at week 24 (6 weeks of treatment with 18 weeks follow-up after completion of therapy), demonstrated mycological cure in 79% of subjects, effective treatment in 75% of the subjects, and mycological cure plus clinical cure in 59% of the subjects.
The mean time to overall success was approximately 10 months for the first toenail trial and 4 months for the fingernail trial. In the first toenail trial, for subjects evaluated at least 6 months after achieving clinical cure and at least 1 year after completing therapy with terbinafine tablets, the clinical relapse rate was approximately 15%.
The Cancer Council Australia

# Overview
The Cancer Council Australia is a national, not for profit organisation which aims to promote cancer-control policies and to reduce the illness caused by cancer in Australia. It advises various groups, including the government, on cancer-related issues, acts as an advocate for cancer patients and their families, and is a major funding contributor towards cancer research.
The Cancer Council includes eight member organisations, which operate in their individual states and territories:
- The Cancer Council ACT
- The Cancer Council New South Wales
- The Cancer Council Northern Territory
- The Cancer Council South Australia
- The Cancer Council Tasmania
- The Cancer Council Victoria
- The Cancer Council Western Australia
- The Cancer Council Queensland

# Australias Biggest Morning Tea
One of the Council's major fundraisers is "Australias Biggest Morning Tea" that on 26 May 2005 broke the Guinness Book of Records record for the "World's Largest Simultaneous Tea Party" with around 1 million Australians participating and supporting The Cancer Council on the day.

# See Also
- Cancer Institute of New South Wales

# External link
- Official website
Thiopurine methyltransferase
Thiopurine methyltransferase or thiopurine S-methyltransferase (TPMT) is an enzyme that in humans is encoded by the TPMT gene.  A pseudogene for this locus is located on chromosome 18q.

# Function
Thiopurine methyltransferase methylates thiopurine compounds. The methyl donor is S-adenosyl-L-methionine, which is converted to S-adenosyl-L-homocysteine. This enzyme metabolizes thiopurine drugs via S-adenosyl-L-methionine as the S-methyl donor and S-adenosyl-L-homocysteine as a byproduct.

# Clinical significance
Thiopurine drugs such as 6-mercaptopurine are used as chemotherapeutic agents and immunosuppressive drugs. Genetic polymorphisms that affect this enzymatic activity are correlated with variations in sensitivity and toxicity to such drugs within individuals. About 1/300 individual is deficient for the enzyme.

# Pharmacology
TPMT is best known for its role in the metabolism of the thiopurine drugs such as azathioprine, 6-mercaptopurine and 6-thioguanine.  TPMT catalyzes the S-methylation of thiopurine drugs. Defects in the TPMT gene leads to decreased methylation and decreased inactivation of 6MP leading to enhanced bone marrow toxicity which may cause myelosuppression, anemia, bleeding tendency, leukopenia & infection.

# Diagnostic use
Measurement of TPMT activity is encouraged prior to commencing the treatment of patients with thiopurine drugs such as azathioprine, 6-mercaptopurine and 6-thioguanine. Patients with low activity (10% prevalence) or especially absent activity (prevalence 0.3%) are at a heightened risk of drug-induced bone marrow toxicity due to accumulation of the unmetabolised drug. Reuther et al. found that about 5% of all thiopurine therapies will fail due to toxicity. This intolerant group could be anticipated by routine measurement of TPMT activity.  There appears to be a great deal of variation in TPMT mutation, with ethnic differences in mutation types accounting for variable responses to 6MP.
Genetic variants of TPMT have also been associated with cisplatin-induced ototoxicity in children. TPMT is now listed as a pharmacogenomic biomarker for adverse drug reactions to cisplatin by the FDA.
Thymic stromal lymphopoietin
Thymic stromal lymphopoietin (TSLP) is a protein belonging to the cytokine family. It is known to play an important role in the maturation of T cell populations through activation of antigen presenting cells.
TSLP is produced mainly by non-hematopoietic cells such as fibroblasts, epithelial cells and different types of stromal or stromal-like cells. These cells are located in regions where TSLP activity is required.

# Gene ontology
TSLP production has been observed in various species, including humans and mice.  In humans TSLP is encoded by the TSLP gene. Alternative splicing of this gene results in two transcript variants.

# Function
It mainly impacts myeloid cells and induces the release of T cell-attracting chemokines from monocytes and enhances the maturation of myeloid (CD11c+) dendritic cells. TSLP has also been shown to activate the maturation of a specific subset of dendritic cells located within the epidermis, called Langerhans cells. Within the thymus TSLP activation of both myeloid and plasmacytoid (CD123+) dendritic cells results in the production of regulatory T cells.

## Signalling
TSLP signals through a heterodimeric receptor complex composed of the thymic stromal lymphopoietin receptor CRLF2 and the IL-7R alpha chain. After binding STAT5 phosphorylation is induced resulting in the expression of upstream transcription factors.

# Disease
TSLP expression is linked to many disease states including asthma, inflammatory arthritis, atopic dermatitis, eczema, eosinophilic esophagitis and other allergic states. The factors inducing the activation of TSLP release are not clearly defined.

## Asthma
Expression of TSLP is enhanced under asthma-like conditions (aka Airway HyperResponsiveness or AHR model in the mouse), conditioning APCs in order to orient the differentiation of T cells coming into the lungs towards a TH2 profile (T helper 2 pathway). The TH2 cells then release factors promoting an inflammatory reaction following the repeated contact with a specific antigen in the airways.

## Inflammatory arthritis

## Atopic dermatitis
TSLP-activated Langerhans cells of the epidermis induce the production of pro-inflammatory cytokines like TNF-alpha by T cells potentially causing atopic dermatitis.  It is thought that understanding the mechanism of TSLP production and those potential substances that block the production, one may be able to prevent or treat conditions of asthma and/or eczema.
Traditional Tibetan medicine
Tibetan medicine is a centuries-old traditional medical system that employs a complex approach to diagnosis, incorporating techniques such as pulse analysis and urinalysis, and utilizes behavior and dietary modification, medicines composed of natural materials (e.g., herbs and minerals) and physical therapies (e.g. Tibetan acupuncture, moxabustion, etc.) to treat illness.
The Tibetan medical system is based upon a synthesis of the Indian (Ayurveda), Persian (Unani), Greek, indigenous Tibetan, and Chinese medical systems, and it continues to be practiced in Tibet, India, Nepal, Bhutan, Ladakh, Siberia, China and Mongolia, as well as more recently in parts of Europe and North America.  It embraces the traditional Buddhist belief that all illness ultimately results from the "three poisons" of the mind: ignorance, attachment and aversion.
Like other systems of traditional Asian medicine, and in contrast to biomedicine, Tibetan medicine first puts forth a specific definition of health in its theoretical texts.  To have good health, Tibetan medical theory states that it is necessary to maintain balance in the body's three principles of function : rLung (pron. Loong), mKhris-pa (pron. Tree-pa) , and Bad-kan (pron. Pay-gen) .
- Lung is the source of the body's ability to circulate physical substances (e.g. blood), energy (e.g. nervous system impulses), and the non-physical (e.g. thoughts). In embryological development, the mind's expression of materialism is manifested as the system of rLung. There are five distinct subcategories of rLung each with specific locations and functions: Srog-'Dzin rLung, Gyen-rGyu rLung, Khyab-Byed rLung, Me-mNyam rLung, Thur-Sel rLung.
- mKhris-pa is characterized by the quantitative and qualitative characteristics of heat, and is the source of many functions such as thermoregulation, metabolism, liver function and discriminating intellect. In embryological development, the mind's expression of aggression is manifested as the system of mKhris-pa. There are five distinct subcategories of mKhris-pa each with specific locations and functions: 'Ju-Byed mKhris-pa, sGrub-Byed mKhris-pa, mDangs-sGyur mKhris-pa, mThong-Byed mKhris-pa, mDog-Sel mKhris-pa.
- Bad-kan is characterized by the quantitative and qualitative characteristics of cold, and is the source of many functions such as aspects of digestion, the maintenance of our physical structure, joint health and mental stability. In embryological development, the mind's expression of ignorance is manifested as the system of Bad-kan. There are five distinct subcategories of Bad-kan each with specific locations and functions: rTen-Byed Bad-kan, Myag-byed Bad-kan, Myong-Byed Bad-kan, Tsim-Byed Bad-kan, 'Byor-Byed Bad-kan.