Persius/hicric huggingface dataset:
Streptomycin clinical pharmacology

# Clinical Pharmacology
Following intramuscular injection of 1 g of streptomycin as the sulfate, a peak serum level of 25 to 50 mcg/mL is reached within 1 hour, diminishing slowly to about 50 percent after 5 to 6 hours.
Appreciable concentrations are found in all organ tissues except the brain. Significant amounts have been found in pleural fluid and tuberculous cavities. Streptomycin passes through the placenta with serum levels in the cord blood similar to maternal levels. Small amounts are excreted in milk, saliva, and sweat.
Streptomycin is excreted by glomerular filtration. In patients with normal kidney function, between 29% and 89% of a single 600 mg dose is excreted in the urine within 24 hours. Any reduction of glomerular function results in decreased excretion of the drug and concurrent rise in serum and tissue levels.
Streptomycin indications and usage

# Indications and Usage
Streptomycin is indicated for the treatment of individuals with moderate to severe infections caused by susceptibile strains of microorganisms in the specific conditions listed below:

### Mycobacterium tuberculosis
The Advisory Council for the Elimination of Tuberculosis, the American Thoracic Society, and the Center for Disease Control recommend that either streptomycin or ethambutol be added as a fourth drug in a regimen containing isoniazid (INH), rifampin and pyrazinamide for initial treatment of tuberculosis unless the likelihood of INH or rifampin resistance is very low. The need for a fourth drug should be reassessed when the results of susceptibility testing are known. In the past when the national rate of primary drug resistance to isoniazid was known to be less than 4% and was either stable or declining, therapy with two and three drug regimens was considered adequate. If community rates of INH resistance are currently less than 4%, an initial treatment regimen with less than four drugs may be considered.                                             
Streptomycin is also indicated for therapy of tuberculosis when one or more of the above drugs is contraindicated because of toxicity or intolerance. The management of tuberculosis has become more complex as a consequence of increasing rates of drug resistance and concomitant HIV infection. Additional consultation from experts in the treatment of tuberculosis may be desirable in those settings.

### Non-tuberculosis infections
The use of streptomycin should be limited to the treatment of infections caused by bacteria which have been shown to be susceptible to the antibacterial effects of streptomycin and which are not amenable to therapy with less potentially toxic agents.
- Pasteurella pestis (plague)
- Francisella tularensis (tularemia)
- Brucella
- Calymmatobacterium granulomatis (donovanosis, granuloma inguinale)
- H. ducreyi (chancroid)
- H. influenzae (in respiratory, endocardial, and meningeal infections-concomitantly with another antibacterial agent)
- K. pneumoniae pneumonia (concomitantly with another antibacterial agent)
- E. coli, Proteus, A. aerogenes, K. pneumoniae, and Enterococcus faecalis in urinary tract infections
- Streptococcus viridans, Enterococcus faecalis (in endocardial infections - concomitantly with penicillin)
- Gram-negative bacillary bacteremia (concomitantly with another antibacterial agent)
To reduce the development of drug-resistant bacteria and maintain the effectiveness of streptomycin and other antibacterial drugs, streptomycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Sudden infant death syndrome x ray

# Overview
There are no specific ECG findings associated with sudden infant death syndrome (SIDS). But a chest x-ray is useful in ruling in or out the infection etiology.

# X Ray
- There are no specific ECG findings associated with sudden infant death syndrome (SIDS).
- An x-ray may be helpful in the diagnosis of the following which are associated with SIDS.
Bronchiolitis
Pertussis
Respiratory syncytial virus infection
- Bronchiolitis
- Pertussis
- Respiratory syncytial virus infection
Sulfadiazine clinical pharmacology

# Clinical Pharmacology
The systemic sulfonamides are bacteriostatic agents having a similar spectrum of activity. Sulfonamides competitively inhibit bacterial synthesis of folic acid (pteroylglutamic acid) from aminobenzoic acid. Resistant strains are capable of utilizing folic acid precursors or preformed folic acid.
Sulfonamides exist in the blood in 3 forms - free, conjugated (acetylated and possibly others) and protein bound. The free form is considered to be the therapeutically active one.
Sulfadiazine given orally is readily absorbed from the gastrointestinal tract. After a single 2 g oral dose, a peak of 6.04 mg/100 mL is reached in 4 hours; of this, 4.65 mg/100 mL is free drug.
When a dose of 100 mg/kg of body weight is given initially and followed by 50 mg/kg every 6 hours, blood levels of free sulfadiazine are about 7 mg/100mL. Protein binding is 38% to 48%. Sulfadiazine diffuses into the cerebrospinal fluid; free drug reaches 32% to 65% of blood levels and total drug 40% to 60%.
Sulfadiazine is excreted largely in the urine, where concentrations are 10 to 25 times greater than serum levels. Approximately 10% of a single oral dose is excreted in the first 6 hours, 50% within 24 hours and 60% to 85% in 48 to 72 hours. Of the amount excreted in the urine, 15% to 40% is in the acetyl form.
Sulfadiazine indications and usage

# Indications and Usage
SulfADIAZine tablets USP are indicated in the following conditions:
Chancroid
Trachoma
Inclusion conjunctivitis
Nocardiosis
Urinary tract infections (primarily pyelonephritis, pyelitis and cystitis) in the absence of obstructive uropathy or foreign bodies, when these infections are caused by susceptible strains of the following organisms: Escherichia coli, Klebsiella species, Enterobacter species, Staphylococcus aureus, Proteus mirabilis and P. vulgaris. Sulfadiazine should be used for urinary tract infections only after use of more soluble sulfonamides has been unsuccessful.
Toxoplasmosis encephalitis in patients with and without acquired immunodeficiency syndrome, as adjunctive therapy with pyrimethamine.
Malaria due to chloroquine-resistant strains of Plasmodium falciparum, when used as adjunctive therapy.
Prophylaxis of meningococcal meningitis when sulfonamide-sensitive group A strains are known to prevail in family groups or larger closed populations (the prophylactic usefulness of sulfonamides when group B or C infections are prevalent is not proved and may be harmful in closed population groups).
Meningococcal meningitis, when the organism has been demonstrated to be susceptible.
Acute otitis media due to Haemophilusinfluenzae, when used concomitantly with adequate doses of penicillin.
Prophylaxis against recurrences of rheumatic fever, as an alternative to penicillin.
H. influenzae meningitis, as adjunctive therapy with parental streptomycin.
IMPORTANT NOTES
In vitro sulfonamide susceptibility tests are not always reliable. The test must be carefully coordinated with bacteriologic and clinical response. When the patient is already taking sulfonamides, follow-up cultures should have aminobenzoic acid added to the culture media.
Currently, the increasing frequency of resistant organisms limits the usefulness of antibacterial agents, including the sulfonamides, especially in the treatment of recurrent and complicated urinary tract infections.
Wide variation in blood levels may result with identical doses. Blood levels should be measured in patients receiving sulfonamides for serious infections. Free sulfonamide blood levels of 5 mg to 15 mg per 100 mL may be considered therapeutically effective for most infections and blood levels of 12 mg to 15 mg per 100 mL may be considered optimal for serious infections. Twenty mg per 100 mL should be the maximum total sulfonamide level, since adverse reactions occur more frequently above this level.
Sulfamethoxazole adverse reactions

# Adverse Reactions
The most common adverse effects are gastrointestinal disturbances (nausea, vomiting, anorexia) and allergic skin reactions (such as rash and urticaria). FATALITIES ASSOCIATED WITH THE ADMINISTRATION OF SULFONAMIDES, ALTHOUGH RARE, HAVE OCCURRED DUE TO SEVERE REACTIONS, INCLUDING STEVENS-JOHNSON SYNDROME, TOXIC EPIDERMAL NECROLYSIS, FULMINANT HEPATIC NECROSIS, AGRANULOCYTOSIS, APLASTIC ANEMIA AND OTHER BLOOD DYSCRASIAS (SEE WARNINGS SECTION).
Hematologic: Agranulocytosis, aplastic anemia, thrombocytopenia, leukopenia, neutropenia, hemolytic anemia, megaloblastic anemia, hypoprothrombinemia, methemoglobinemia, eosinophilia.
- Allergic Reactions: Stevens-Johnson syndrome, toxic epidermal necrolysis, anaphylaxis, allergic myocarditis, erythema multiforme, exfoliative dermatitis, angioedema, drug fever, chills, Henoch-Schoenlein purpura, serum sickness-like syndrome, generalized allergic reactions, generalized skin eruptions, photosensitivity, conjunctival and scleral injection, pruritus, urticaria and rash. In addition, periarteritis nodosa and systemic lupus erythematosus have been reported.
Gastrointestinal: Hepatitis (including cholestatic jaundice and hepatic necrosis), elevation of serum transaminase and bilirubin, pseudomembranous enterocolitis, pancreatitis, stomatitis, glossitis, nausea, emesis, abdominal pain, diarrhea, anorexia.
Genitourinary: Renal failure, interstitial nephritis, BUN and serum creatinine elevation, toxic nephrosis with oliguria and anuria, crystalluria and nephrotoxicity in association with cyclosporine.
Metabolic and Nutritional: Hyperkalemia, hyponatremia (see PRECAUTIONS: Electrolyte Abnormalities).
Neurologic: Aseptic meningitis, convulsions, peripheral neuritis, ataxia, vertigo, tinnitus, headache.
Psychiatric: Hallucinations, depression, apathy, nervousness.
Endocrine: The sulfonamides bear certain chemical similarities to some goitrogens, diuretics (acetazolamide and the thiazides) and oral hypoglycemic agents. Cross-sensitivity may exist with these agents. Diuresis and hypoglycemia have occurred rarely in patients receiving sulfonamides.
Musculoskeletal: Arthralgia and myalgia. Isolated cases of rhabdomyolysis have been reported with BACTRIM, mainly in AIDS patients.
Respiratory: Cough, shortness of breath and pulmonary infiltrates (see WARNINGS).
Miscellaneous: Weakness, fatigue, insomnia.
Postmarketing Experience
The following adverse reactions have been identified during post-approval use of trimethoprim-sulfamethoxazole. Because these reactions were reported voluntarily from a population of uncertain size, it is not possible to reliably estimate their frequency or establish a causal relationship to drug exposure:
- Thrombotic thrombocytopenia purpura
- Idiopathic thrombocytopenic purpura
- QT prolongation resulting in ventricular tachycardia and torsade de pointes.
Suppressor of cytokine signaling 1
Suppressor of cytokine signaling 1 is a protein that in humans is encoded by the SOCS1 gene. SOCS1 orthologs  have been identified in several mammals for which complete genome data are available.

# Function
This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signalling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene can be induced by a subset of cytokines, including IL2, IL3 erythropoietin (EPO), GM-CSF, and interferon-gamma (IFN-). The protein encoded by this gene functions downstream of cytokine receptors, and takes part in a negative feedback loop to attenuate cytokine signaling. Knockout studies in mice suggested the role of this gene as a modulator of IFN- action, which is required for normal postnatal growth and survival.
Several recent viral studies have shown that viral genes, such as Tax gene product (Tax), encoded by HTLV-1, could hijack SOCS1 to inhibit host antiviral pathways, as a strategy to evade host immunity.

# Interactions
The suppressor of cytokine signaling 1 has been shown to interact with:
- Tax,
- CD117,
- Colony stimulating factor 1 receptor
- Growth hormone receptor,
- IRS2,
- Janus kinase 2,  and
- TEC.
Syllable stress of Botanical Latin
Syllable stress of botanical names varies with the language spoken by the person using the botanical name.  In English-speaking countries the Botanical Latin places syllable stress for botanical names derived from ancient Greek and Latin broadly according to two systems, either the Reformed academic pronunciation, or the pronunciation developed initially in some large part by British gardeners, horticulturists, naturalists, and botanists of the 19th century.  Generally in Latin each vowel or diphthong  belongs to a single syllable.  Classical Latin diphthongs are ae, au, oe. Diphthongs from Greek can include oi, eu, ei, and ou, and ui also occasionally occurs in botanical Latin.  Syllables end in vowels, unless there are multiple consonants, in which case the consonants are divided between the two syllables, with certain consonants being treated as pairs.  In words of two syllables the stress is on the first syllable. Words that contain three or more syllables have stresses accorded to their syllables by the quality and location of the different vowels in the words. In words of more than two syllables the stress is on the penultimate syllable when the syllable contains a long vowel or diphthong, otherwise the stress is on the antepenultimate syllable.
Whether a vowel is long or short in a classical Latin word is a function of the vowel and its relationship to the consonants that precede or follow it.  . Modern Latin dictionaries and textbooks may contain diacritics called a macron for long vowels or a breve for short vowels.  Botanical Latin does not traditionally include macrons or breves, and they are prohibited (as diacriticals) by Article 60 of the International Code of Botanical Nomenclature. Some books follow the mediaeval tradition to add an acute accent to mark the stressed syllable.

# Rules
To determine the position of the stress of latin terms
- Vowels followed by two consonants are generally long vowels. Thus Po-ten-til-la, as the I is followed by a double L.
- Diphthongs are to be treated as a long vowels, too. Thus Al-thae-a, as AE is a diphthong.
The genetic basis of heart disease

# Overview
The following is a list of genetic disorders and their origins. Besides, most disorders are a code that indicates the type of fertilization and the chromosome involved.
- P - Point mutation, or any insertion/deletion entirely inside one gene
- D - Deletion of a gene or genes
- C - Whole chromosome extra, missing, or both - see chromosomal aberrations
- T - Trinucleotide repeat disorders - gene is extended in length

# Common disorders

# A

# B

# C

# D

# E

# F

# G

# I

# J

# K

# L

# M

# N

# O

# P

# R

# S

# T

# U

# V

# W

# X

# Y
hu:Genetikai betegsegek listaja
nl:Lijst van erfelijke aandoeningen
The heart in urinary system tumors

# Histopathological Findings
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- HEART: Metastatic Carcinoma: Gross natural color horizontal slices ventricles large metastatic renal cell carcinoma
- HEART: Metastatic Carcinoma: Gross natural color close-up of horizontal section ventricles with large hemorrhagic lesions (an excellent photo) in large metastatic renal cell carcinoma
- HEART: Metastatic Carcinoma: Gross fixed tissue, color, large lesions, primer is renal cell carcinoma.
- HEART: Metastatic Carcinoma: Gross fixed tissue, color, an excellent close-up of large hemorrhagic lesions primary is kidney
Title 21 of the United States Code
Title 21 is the portion of the United States Code that governs food and drugs.
It is divided into 25  chapters:
- Template:Usc-title-chap. Adulterated Or Misbranded Foods Or Drugs
- Template:Usc-title-chap. Teas (Repealed)
- Template:Usc-title-chap. Filled Milk
- Template:Usc-title-chap. Animals, Meats, And Meat And Dairy Products
- Template:Usc-title-chap. Viruses, Serums, Toxins, Antitoxins, And Analogous Products
- Template:Usc-title-chap.  Bureau Of Narcotics (Omitted)
- Template:Usc-title-chap. Narcotic Drugs (Repealed Or Transferred)
- Template:Usc-title-chap. Practice Of Pharmacy And Sale Of Poisons In Consular Districts In China
- Template:Usc-title-chap. Narcotic Farms
- Template:Usc-title-chap. Federal Food, Drug, And Cosmetic Act
- Template:Usc-title-chap. Poultry And Poultry Products Inspection
- Template:Usc-title-chap. Manufacture Of Narcotic Drugs (Repealed)
- Template:Usc-title-chap. Meat Inspection
- Template:Usc-title-chap. Drug Abuse Prevention And Control
- Template:Usc-title-chap. Alcohol And Drug Abuse Educational Programs And Activities
- Template:Usc-title-chap. Egg Products Inspection
- Template:Usc-title-chap. Drug Abuse Prevention, Treatment, And Rehabilitation
- Template:Usc-title-chap. National Drug Enforcement Policy (Repealed)
- Template:Usc-title-chap. Presidents Media Commission On Alcohol And Drug Abuse Prevention
- Template:Usc-title-chap. Pesticide Monitoring Improvements
- Template:Usc-title-chap. National Drug Control Program
- Template:Usc-title-chap. Biomaterials Access Assurance
- Template:Usc-title-chap. National Drug Control Policy
- Template:Usc-title-chap. National Youth Anti-Drug Media Campaign
- Template:Usc-title-chap. International Narcotics Trafficking

# Chapter 13
This chapter contains the Controlled Substances Act, a part of the Comprehensive Drug Abuse Prevention and Control Act of 1970.  See Template:Usc-title-chap.
Transforming growth factor, beta 3
Transforming growth factor beta-3 is a protein that in humans is encoded by the TGFB3 gene.
It is a type of protein, known as a cytokine, which is involved in cell differentiation, embryogenesis and development. It belongs to a large family of cytokines called the Transforming growth factor beta superfamily, which includes the TGF- family, Bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), inhibins and activins.
TGF-3 is believed to regulate molecules involved in cellular adhesion and extracellular matrix (ECM) formation during the process of palate development.  Without TGF-3, mammals develop a deformity known as a cleft palate. This is caused by failure of epithelial cells in both sides of the developing palate to fuse.  TGF-3 also plays an essential role in controlling the development of lungs in mammals, by also regulating cell adhesion and ECM formation in this tissue, and controls wound healing by regulating the movements of epidermal and dermal cells in injured skin.

# Interactions
Transforming growth factor, beta 3 has been shown to interact with TGF beta receptor 2.

# Clinical research
After successful phase I/II trials, human recombinant TGF-3 (Avotermin, planned trade name Juvista) failed in Phase III trials.
Transient ischemic attack overview

# Overview
A transient ischemic attack is caused by the temporary disturbance of blood supply to a restricted area of the brain, resulting in brief neurologic dysfunction that usually persists for less than 24 hours.
Discontinuation of the use of the term transient ischemic attack has been proposed.

# Causes
The most common cause of a TIA is an embolus (a small blood clot) that occludes an artery in the brain. This most frequently arises from an atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart due to atrial fibrillation. Other reasons include excessive narrowing of large vessels due to an atherosclerotic plaque and increased blood viscosity due to some blood diseases. TIA is related with other medical conditions like hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.

# Diagnosis

## History and Symptoms
Symptoms vary widely from person to person depending on the area of the brain involved. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax), difficulty speaking (dysarthria), weakness on one side of the body (hemiparesis), numbness usually on one side of the body, and loss of consciousness. If there are neurological symptoms persisting for more than 24 hours, it is classified as a cerebrovascular accident (stroke).

## Electrocardiogram
An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain.

## CT
TIAs do not show brain changes on CT scans. (Most strokes do show changes on such tests).

## MRI
TIAs do not show brain changes on MRI scans. (Most strokes do show changes on such tests).

## Echocardiography
An echocardiogram is useful in detecting thrombus within the heart chambers. Such patients benefit from anticoagulation.

## Ultrasound
If the TIA affects an area supplied by the carotid artery, an ultrasound (TCD) scan may demonstrate carotid stenosis.

# Treatment

## Surgery
For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended.

# Primary Prevention
Prevention of TIAs includes controlling risk factors, such as high blood pressure, diabetes, heart disease, and other associated disorders. Smoking should be stopped.
Transient tachypnea of the newborn

# Overview
Transient tachypnea of the newborn (TTNB, or "Transitory tachypnea of newborn") is a respiratory problem seen in the newborn shortly after delivery. It consists of a period of rapid breathing (more than the for newborns normal 40-60 times a minute). It is likely due to retained lung fluid, and common in 35+ week gestation babies who are delivered by caesarian section without labour. Usually, this condition resolves over 24-48 hours. Treatment is supportive and may include supplemental oxygen and antibiotics. The chest X-Ray shows hyperinflation of the lungs including prominent pulmonary vasular markings, flattening of the diaphragm, and fluid in the horizontal fissure.

# Pathophysiology
- 1. Due to the higher incidence of TTN in newborns delivered by caesarean section, it has been postulated that TTN could result from a delayed absorption of fetal lung fluid from the pulmonary lymphatic system. The increased fluid in the lungs leads to increased airway resistance and reduced lung compliance.
- 2. Pulmonary immaturity has also been proposed as a causative factor. Levels of phosphatidylglycerol (an indicator of lung maturity) was found to be negative in certain newborns.
- 3. Mild surfactant deficiency has also been suggested as a causative factor.

# Diagnosis

## Chest X-ray
- Finds of pulmonary edema: airspace opacities, prominent interstitial markings, prominent and indistinct pulmonary vasculature, pleural effusions, and cardiomegaly.
- Lungs are normal to increased in volume.
Triamcinolone detailed information
Triamcinolone (trade names Kenalog, Aristocort, Nasacort, Tri-Nasal, Triderm, Azmacort, Trilone, Volon A, Tristoject, Fougera;) is a synthetic corticosteroid given orally, by injection, inhalation, or as a topical ointment or cream.

# Uses
They are also used in the post-operative period of certain cosmetic surgery procedures, notably rhinoplasty. Injected into the subcutaneous area, they may help to alleviate stubborn swelling and decrease the presence of scar tissue.
Topical triamcinolone acetonide paste is often prescribed for mouth or gum irritation following dental procedures.
Triamcinolone is occasionally used to treat severe cases of hayfever.

# Forms
Different triamcinolone salts are available, including acetonide, hexacetonide and diacetate.
Triamcinolone acetonide is a more potent type of triamcinolone, being about 8 times as effective as prednisone.