Persius/hicric huggingface dataset:
Tetralogy of Fallot surgical indications

# Overview
A complete surgical repair of Tetralogy of Fallot is now generally undertaken between the ages of 1 and 2, preferably at about one year of age.

# Risk Factors for Early Repair
The following list of risk factors is associated with an increased risk of early repair of tetralogy of Fallot: 
- Low birth weight
- Pulmonary artery atresia
- Major associated anomalies
- Multiple previous surgeries
- Absent pulmonary valve syndrome
- Young or old age
- Severe annular hypoplasia
- Small pulmonary arteries
- High peak RVtoleft ventricular pressure ratio
- Multiple VSDs
- Coexisting cardiac anomalies

# Contraindications to Primary Repair of Tetralogy of Fallot
Contraindications to primary repair in Tetralogy of Fallot include the following:
- The presence of an anomalous coronary artery
- Very low birth weight
- Small pulmonary arteries
- Multiple VSDs
- Multiple coexisting intracardiac malformations
Tick-borne disease (patient information)
For the   WikiDoc page for this topic, click here

# Overview
Tick-borne diseases are transmitted by ticks. Hard and soft-bodied female ticks are believed to make a poison that can cause tick paralysis in children.
While most ticks do not carry diseases, some can carry pathogens, including bacteria, virus or parasites, which may cause:
- Colorado tick fever
- Lyme disease
- Rocky Mountain spotted fever
- Tularemia

# What are the symptoms of Tick-borne disease?
Watch for the following symptoms of tick-borne disease in the weeks following a tick bite:
- Rash
- Skin ulcer
- Fever/ chills
- Headache
- Muscle or joint aches
- Weakness
- Swollen lymph nodes
- Flu-like symptoms
- Stiff neck
The symptoms below refer to the problems resulting from the bite itself, not the diseases that a bite may cause. Some of the symptoms may be specific of one kind of tick:
- Rash
- Blisters
- Swelling at bite site
- Severe pain at bite site lasting for several weeks
- Weakness
- Difficulty breathing
- Uncoordinated movement

# What causes Tick-borne disease?
While most ticks do not carry diseases, some ticks may carry bacteria that can cause:
- Lyme disease (most common tick disease in the US)
- Colorado tick fever
- Rocky Mountain spotted fever
- Tularemia

# Who is at highest risk?
People who spend time outdoors and/or have pets that go outdoors are at risk for tick-borne disease, particularly during the warm seasons.

# Diagnosis
Signs and symptoms may be different according to the kind of tick and the transmitted disease. An example of a skin rash, following tick-bite, is the bull's eye rash from Lyme disease.

# Prevention of Tick-borne disease
Avoid wooded or grassy fields, where ticks reside, particularly in warm seasons.

# Treatment options
- Remove the tick carefully not to leave the tick's head stuck in the skin.
- If there is a collection of pus, the area will need to be incised and drained.
- Antibiotic treatment is often justified:
- Doxycycline to treat suspected tick-borne disease, such as Lyme disease
- IV dose of a cephalosporin followed by Keflex 500 mg PO q 6 hours to treat surrounding cellulitis
- Bactrim twice a day is given to cover Methicillin-resistant Staphylococcus aureus (MRSA) in hospital workers

# When to seek urgent medical care?
If you have symptoms of Tick-borne disease contact health care professional. Long-term treatment may be needed if complications develop. Preventive antibiotics are often given to people who live in areas where Lyme disease is common.

# What to expect (Outlook/Prognosis)
Most tick bites are harmless. The outcome will depend on:
- Kind of infection the tick may have transmitted
- Timing until treatment initiation

# Where to find medical care for Tick-borne disease?
Directions to Hospitals Treating Tick-borne disease

# Possible complications
Complications depend on the type of infection transmitted.

# Sources
Transmembrane domain of ABC transporters

# Overview
ABC transporter transmembrane domain is main transmembrane structural unit of ATP-binding cassette transporter which consist of six transmembrane domaines. Many members of the ABC transporter family (Pfam PF00005) have two such regions..

# Human proteins containing this domain
ABCB1;     ABCB10;    ABCB11;    ABCB4;     ABCB5;     ABCB6;     ABCB7;     ABCB8;
ABCB9;     ABCC1;     ABCC10;    ABCC11;    ABCC12;    ABCC13;    ABCC2;     ABCC3;
ABCC4;     ABCC5;     ABCC6;     ABCC8;     ABCC9;     CFTR;      LOC402251; MRP3;
TAP1;      TAP2;      TAPL;      ara;
Tricuspid prolapse (patient information)
For the WikiDoc page for this topic, click here

# Overview
Tricuspid prolapse is a heart problem in which the valve that separates the right upper heart chamber (atrium) and the right lower heart chamber (ventricle) of the heart does not close properly and slips out of place. This prolapse interrupts the normal blood flow.

# What are the symptoms of Tricuspid prolapse?
The symptoms of tricuspid prolapse include:
- Weakness
- Fatigue
- Irregular heart beats (atrial fibrillation)
- Strong pulse in your neck
- Swelling of the liver
- Abdominal pain
- Swelling in your legs

# What causes Tricuspid prolapse?
The tricuspid valve separates the right lower heart chamber (the right ventricle) from the right upper heart chamber (right atrium).
- The most common cause of tricuspid prolapse is swelling of the right ventricle. Such swelling may be a complication of any disorder that causes failure of the right ventricle, such as rheumatic fever, lung diseases such as emphysema.
- Tricuspid prolapse may be found in those with infections, birth defects that cause the valves to be floppy and not function correctly.
- Degenerative process in the valve can also cause the valve to slip out of place and not function properly.

# How to know you have a Tricuspid prolapse?
- The doctor will perform a physical exam and use a stethoscope to listen to your heart and lungs. The doctor may hear a heart murmur ("midsystolic murmur"). The physical exam may reveal swelling of the liver.
- Tests that are done include:
- ECG,
- Chest X-ray,
- Echocardiogram may show swelling of the right side of the heart,
- Transesophageal echocardiography (TEE),
- CT scan of the chest

# Treatment options
- Most of the time, there are no (or few) symptoms, and treatment is not needed.
- Underlying disorders should be identified and treated.
- If you have severe tricuspid valve prolapse, you may need surgery to repair or replace the tricuspid valve.
- In some cases, if the valve can not be repaired, a valve replacement surgery will be performed.
- Patients with tricuspid valve diseases have an increase risk of endocarditis and hence receive antibiotics before dental or invasive procedures.

# Where to find medical care for Tricuspid prolapse
Directions to Hospitals Treating Tricuspid prolapse

# What to expect (Outlook/Prognosis)
Tricupsid valve valve repair or replacement usually provides a cure.

# Possible complications
- Heart failure
- Endocarditis
Valganciclovir hydrochloride description

# Description
Valcyte contains valganciclovir hydrochloride (valganciclovir HCl), a hydrochloride salt of the L-valyl ester of ganciclovir that exists as a mixture of two diastereomers. Ganciclovir is a synthetic guanine derivative active against CMV.
Valcyte is available as a 450 mg tablet for oral administration. Each tablet contains 496.3 mg of valganciclovir HCl (corresponding to 450 mg of valganciclovir), and the inactive ingredients microcrystalline cellulose, povidone K-30, crospovidone and stearic acid. The film-coat applied to the tablets contains Opadry Pink.
Valcyte is also available as a powder for oral solution, which when constituted with water as directed contains 50 mg/mL valganciclovir free base. The inactive ingredients of Valcyte for oral solution are sodium benzoate, fumaric acid, povidone K-30, sodium saccharin, mannitol and tutti-frutti flavoring.
Valganciclovir HCl is a white to off-white crystalline powder with a molecular formula of C14H22N6O5HCl and a molecular weight of 390.83. The chemical name for valganciclovir HCl is L-Valine, 2--3-hydroxypropyl ester, monohydrochloride. Valganciclovir HCl is a polar hydrophilic compound with a solubility of 70 mg/mL in water at 25C at a pH of 7.0 and an n-octanol/water partition coefficient of 0.0095 at pH 7.0. The pKa for valganciclovir HCl is 7.6.
The chemical structure of valganciclovir HCl is:
All doses in this insert are specified in terms of valganciclovir.
Vitamin D deficiency laboratory findings
There is no consensus on the serum 25-hydroxyvitamin D levels, "25(OH)D",  considered "normal". 12 ng per milliliter (50 nmol per liter) ihas been proposed. However, "a common misconception is that the RDA functions as a cut point and that nearly the entire population must have a serum 25(OH)D level above 20 ng per milliliter to achieve good bone health. The reality is that the majority (about 97.5%) of the population has a requirement of 20 ng per milliliter or less. Moreover, by definition of an average requirement, approximately half the population has a requirement of 16 ng per milliliter (the EAR) or less. " (italics added) Previous opinions suggested a value equal or less than 20 ng per milliliter (50 nmol per liter) is in the deficient range., , , 
The definition can be based on the point at which the parathyroid hormone (PTH) levels off as the cutoff point, which may be at 12 ng per milliliter (30  nmol per liter) or is close to 30 ng per milliliter (75  nmol per liter). 
The Institute of Medicine states (page 13):
- Levels over 20 ng/ml: "Practically all persons are sufficient"
- Levels 12-20 ng/ml (<50 nmol/L): "Some, but not all, persons are potentially at risk for inadequacy."
- Levels below 12 ng/m (< 30 nmol/L): "persons are at risk of deficiency."
WikiDoc scholar program use of templates
- WikiDoc has a rich inventory of ready-to-use templates.
- Templates help the editors make sure that the format of a WikiDoc project they are working on, is consistent with the website's original layout.
- To access the template for a single page, click here.
- To access the template for a microchapter, click here.
- To access the template for a Wikipatient page, click here.
11-Hydroxysteroid dehydrogenase type 1
11-Hydroxysteroid dehydrogenase type 1, also known as cortisone reductase, is an NADPH-dependent enzyme highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. In these tissues, HSD11B1 reduces cortisone to the active hormone cortisol that activates glucocorticoid receptors. It belongs to the family of short-chain dehydrogenases.

# Function
The protein encoded by this gene is a microsomal enzyme that catalyzes the conversion of the stress hormone cortisol to the inactive metabolite cortisone. In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol. Too much cortisol can lead to central obesity, and a particular variation in this gene has been associated with obesity and insulin resistance in children. Two transcript variants encoding the same protein have been found for this gene.

# Clinical significance
11-HSD1 is inhibited by carbenoxolone, a drug typically used in the treatment of peptic ulcers. Moreover, 18alpha-glycyrrhizic acid from the root of glycyrrhiza glabra was discovered as an inhibitor.
Salicylate downregulates 11-HSD1 expression in adipose tissue in obese mice and hence may explain why aspirin improves glycemic control in type 2 diabetes. Epigallocatechin gallate from green tea can also potently inhibit this enzyme,  green tea is a complex mixture of various phenolics with contents varying with production and processing, some of the phenolics are known HDAC inhibitors that alter genetic expression.  EGCG as usually consumed in green tea is poorly absorbed into the bloodstream, more research is needed to reach firm conclusions.
Aldo-keto reductase family 1, member A1
Alcohol dehydrogenase  also known as aldehyde reductase or aldo-keto reductase family 1 member A1 is an enzyme that in humans is encoded by the AKR1A1 gene. AKR1A1 belongs to the aldo-keto reductase (AKR) superfamily. It catalyzes the NADPH-dependent reduction of a variety of aromatic and aliphatic aldehydes to their corresponding alcohols and catalyzes the reduction of mevaldate to mevalonic acid and of glyceraldehyde to glycerol. Mutations in the AKR1A1 gene has been found associated with non-Hodgkin's lymphoma.

# Structure

## Gene
The AKR1A1 gene lies on the chromosome location of 1p34.1 and consists of 10 exons.

## Protein
AKR1A1 consists of 325 amino acids and weighs 36573Da. The tertiary structure consists of a beta/alpha-barrel, with the coenzyme-binding site located at the carboxy-terminus end of the strands of the barrel.Alternative splicing of this gene results in two transcript variants encoding the same protein.

# Function
AKR1A1 gene is found highly expressed in kidney and liver, and moderately expressed in cerebrum, small intestine and testis. Small amounts of AKR1A1 are present in lung, prostate and spleen. However, it is not observed in heart or skeletal muscle. AKR1A1 belongs to the AKR superfamily, which are predominantly monomeric, soluble, NADPH-dependent oxidoreductases involved in the reduction of aldehydes and ketones into primary and secondary alcohols. AKR1A1 is shown to demonstrate characteristically high specific activity towards many aromatic and aliphatic aldehydes, and preferentially catalyses the NADPH-dependent reduction of aliphatic aldehydes, aromatic aldehydes and biogenic amines. It is also reported to be involved in the metabolism of 4-hydroxynonenal and play a role in the resistance to oxidative stress.

# Clinical significance
A SNP in intron 5 of AKR1A1 has been found to be significantly associated with increased risk of non-Hodgkin's lymphoma. AKR1A1 could activate procarcinogens, such as polycyclic aromatic hydrocarbon. AKRs have been linked to metabolism of the anthracyclines doxorubicin (DOX) and daunorubicin (DAUN), allelic variants showed significantly reduced metabolic activities, and hence these allelic variants can possibly act as genetic biomarkers for the clinical development of DAUN-induced cardiotoxicity.

# Interactions
4-hydroxynonenal 
polycyclic aromatic hydrocarbon
DAUN
American Society for Clinical Pathology
The American Society for Clinical Pathology is a professional association based in Chicago encompassing 140,000 pathologists and laboratory professionals.
Founded in 1922, the ASCP provides programs in education, certification and advocacy on behalf of patients, pathologists and lab professionals.  In addition, the ASCP publishes numerous textbooks, newsletters and other manuals, and publishes two industry journals: The American Journal of Clinical Pathology and LabMedicine.
The ASCP also promotes National Medical Laboratory Professionals Week (NMLPW) is a time of recognition for medical laboratory personnel and a chance to celebrate their professionalism and be recognized for their efforts.
National Lab Week is held annually during the last full week of April.
Amitriptyline hydrochloride description

# Description
Amitriptyline HCl is 3-(10, 11-dihydro-5H-dibenzo  cycloheptene-5-ylidene)-N,N-dimethyl-1-propanamine hydrochloride. Its molecular formula is C20H23N - HCl, and its structural formula is:
Amitriptyline HCl, a dibenzocycloheptadiene derivative, has a molecular weight of 313.87. It is a white, odorless, crystalline compound which is freely soluble in water.
Each tablet for oral administration contains the following inactive ingredients: colloidal silicon dioxide, corn starch, hydroxypropyl cellulose, hypromellose, magnesium stearate, microcrystalline cellulose, polyethylene glycol, sodium lauryl sulfate, sodium starch glycolate and titanium dioxide. In addition, the following product specific coloring agents are employed:
10 mg - calcium sulfate, talc 
25 mg - FD&C Blue No. 1 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake 
50 mg - FD&C Blue No. 2 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, FD&C Yellow No. 6 Aluminum Lake 
75 mg - FD&C Blue No. 2 Aluminum Lake 
100 mg - D&C Red No. 30 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake 
150 mg - D&C Red No. 30 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
Amphotericin B warnings and precautions

# Warnings
Anaphylaxis has been reported with amphotericin B desoxycholate and other amphotericin B-containing drugs. Anaphylaxis has been reported with ABELCET with an incidence rate of <0.1%. If severe respiratory distress occurs, the infusion should be immediately discontinued. The patient should not receive further infusions of ABELCET.

# Precautions
- General:
As with any amphotericin B-containing product, during the initial dosing of ABELCET, the drug should be administered under close clinical observation by medically trained personnel.
Acute reactions including fever and chills may occur 1 to 2 hours after starting an intravenous infusion of ABELCET. These reactions are usually more common with the first few doses of ABELCET and generally diminish with subsequent doses. Infusion has been rarely associated with hypotension, bronchospasm, arrhythmias, and shock.
- Laboratory Tests:
Serum creatinine should be monitored frequently during ABELCET therapy (see ADVERSE REACTIONS). It is also advisable to regularly monitor liver function, serum electrolytes (particularly magnesium and potassium), and complete blood counts.
Ampicillin Trihydrate adverse reactions

# Adverse Reactions
As with other penicillins, it may be expected that untoward reactions will be essentially limited to sensitivity phenomena. They are more likely to occur in individuals who have previously demonstrated hypersensitivity to penicillin and in those with a history of allergy, asthma, hay fever, or urticaria.
The following adverse reactions have been reported as associated with the use of ampicillin:
- GASTROINTESTINAL: glossitis, stomatitis, nausea, vomiting, enterocolitis, pseudomembranous colitis, and diarrhea. These reactions are usually associated with oral dosage forms of the drugs.
- HYPERSENSITIVITY REACTIONS: An erythematous, mildly pruritic, maculopapular skin rash has been reported fairly frequently . The rash, which usually does not develop within the first week of therapy, may cover the entire body including the soles, palms, and oral mucosa. The eruption usually disappears in three to seven days. Other hypersensitivity reactions that have been reported are: skin rash, pruritus, urticaria, erythema multiforme, and an occasional case of exfoliative dermatitis. Anaphylaxis is the most serious reaction experienced and has usually been associated with the parenteral dosage form of the drug.
NOTE: Urticaria, other skin rashes, and serum sicknesslike reactions may be controlled by antihistamines, and, if necessary, systemic corticosteroids. Whenever such reactions occur, ampicillin should be discontinued unless, in the opinion of the physician, the condition being treated is life-threatening, and amenable only to ampicillin therapy. Serious anaphylactoid reactions require emergency measures (see WARNINGS).
- LIVER: Moderate elevation in serum glutamic oxaloacetic transaminase (SGOT) has been noted, but the significance of this finding is unknown.
- HEMIC AND LYMPHATIC SYSTEMS: Anemia, thrombocytopenia, thrombocytopenic purpura, eosinophilia, leukopenia, and agranulocytosis have been reported during therapy with penicillins. These reactions are usually reversible on discontinuation of therapy and are believed to be hypersensitivity phenomena.
Other adverse reactions that have been reported with the use of ampicillin are laryngeal stridor and high fever. An occasional patient may complain of sore mouth or tongue as with any oral penicillin preparation.
Ampicillin sulbactam directions for use

# Directions for Use
UNASYN sterile powder for intravenous and intramuscular use may be reconstituted with any of the compatible diluents described in this insert. Solutions should be allowed to stand after dissolution to allow any foaming to dissipate in order to permit visual inspection for complete solubilization.
UNASYN concentrations between 3 and 45 mg (2 to 30 mg ampicillin/1 to 15 mg sulbactam/mL) are recommended for intravenous use.
The 15 gram vial may be reconstituted with either 92 mL Sterile Water for Injection or 0.9% Sodium Chloride Injection. The diluent should be added in two separate aliquots in a suitable work area, such as a laminar flow hood. Add 50 mL of solution, shake to dissolve. Then add an additional 42 mL and shake. The solution should be allowed to stand after dissolution to allow any foaming to dissipate in order to permit visual inspection for complete solubilization. The resultant solution will have a final concentration of approximately 100 mg/mL ampicillin and 50 mg/mL sulbactam. The closure may be penetrated only one time after reconstitution, if needed, using a suitable sterile transfer device or dispensing set that allows for measured dispensing of the contents. After reconstitution, use within two hours if stored at room temperature, or within four hours if stored under refrigeration.
If the reconstituted bulk solution is stored for less than one hour at room temperature (20C/68F) prior to further dilution, the use periods indicated in Table 6 apply for the diluted solutions. If the bulk solution is stored for one to two hours at room temperature (20C/68F) and then diluted with Sterile Water for Injection or 0.9% Sodium Chloride Injection to the following concentrations, the use periods indicated in Table 7 apply. Any unused portions of solution that remain after the indicated time periods should be discarded.
While reversible glycogenosis was observed in laboratory animals, this phenomenon was dose- and time-dependent and is not expected to develop at the therapeutic doses and corresponding plasma levels attained during the relatively short periods of combined ampicillin/sulbactam therapy in man.
Anidulafungin dosage and administration

# Dosage and Administration

## Candidemia and other Candida infections (intra-abdominal abscess, and peritonitis)
The recommended dose is a single 200 mg loading dose of ERAXIS on Day 1, followed by 100 mg daily dose thereafter. Duration of treatment should be based on the patient's clinical response. In general, antifungal therapy should continue for at least 14 days after the last positive culture.

## Esophageal Candidiasis
The recommended dose is a single 100 mg loading dose of ERAXIS on Day 1, followed by 50 mg daily dose thereafter. Patients should be treated for a minimum of 14 days and for at least 7 days following resolution of symptoms. Duration of treatment should be based on the patient's clinical response. Because of the risk of relapse of esophageal candidiasis in patients with HIV infections, suppressive antifungal therapy may be considered after a course of treatment.

## Preparation for Administration
ERAXIS for Injection must be reconstituted with sterile Water for Injection and subsequently diluted only with 5% Dextrose Injection, USP or 0.9% Sodium Chloride Injection, USP (normal saline). The compatibility of reconstituted ERAXIS with intravenous substances, additives, or medications other than 5% Dextrose Injection, USP or 0.9% Sodium Chloride Injection, USP (normal saline) has not been established.
Reconstitution 50 mg/vial
Aseptically reconstitute each 50 mg vial with 15 mL of sterile Water for Injection to provide a concentration of 3.33 mg/mL. The reconstituted solution can be stored for up to 24 hours at temperatures up to 25C (77F) prior to dilution into the infusion solution.
Reconstitution 100 mg/vial
Aseptically reconstitute each 100 mg vial with 30 mL of sterile Water for Injection to provide a concentration of 3.33 mg/mL. The reconstituted solution can be stored for up to 24 hours at temperatures up to 25C (77F) prior to dilution into the infusion solution.
Dilution and Infusion
Aseptically transfer the contents of the reconstituted vial(s) into the appropriately sized IV bag (or bottle) containing either 5% Dextrose Injection, USP or 0.9% Sodium Chloride Injection, USP (normal saline). See Table 1 for the dilution and infusion instructions for each dose.