Persius/hicric huggingface dataset:
Telithromycin contraindications

# contraindications
KETEK is contraindicated in patients with myasthenia gravis. Exacerbations of myasthenia gravis have been reported in patients and sometimes occurred within a few hours of the first dose of telithromycin. Reports have included fatal and life-threatening acute respiratory failure with a rapid onset and progression.
KETEK is contraindicated in patients with previous history of hepatitis and/or jaundice associated with the use of KETEK tablets, or any macrolide antibiotic.
KETEK is contraindicated in patients with a history of hypersensitivity to telithromycin and/or any components of KETEK tablets, or any macrolide antibiotic.
Concomitant administration of KETEK with cisapride or pimozide is contraindicated. (See CLINICAL PHARMACOLOGY, Drug-drug Interactions and PRECAUTIONS.)
Concomitant administration of KETEK and colchicine is contraindicated in patients with renal or hepatic impairment. (See WARNINGS, Drug Interactions and PRECAUTIONS, Drug interactions.)
Tenofovir indications and usage

# Indications and Usage

## HIV-1 Infection
VIREAD is indicated in combination with other antiretroviral agents for the treatment of HIV-1 infection in adults and pediatric patients 2 years of age and older.
The following points should be considered when initiating therapy with VIREAD for the treatment of HIV-1 infection:
VIREAD should not be used in combination with ATRIPLA, COMPLERA, STRIBILD, or TRUVADA.

## Chronic Hepatitis B
VIREAD is indicated for the treatment of chronic hepatitis B in adults and pediatric patients 12 years of age and older.
The following points should be considered when initiating therapy with VIREAD for the treatment of HBV infection:
The indication in adults is based on safety and efficacy data from treatment of subjects who were nucleoside-treatment-naive and subjects who were treatment-experienced with documented resistance to lamivudine. Subjects were adults with HBeAg-positive and HBeAg-negative chronic hepatitis B with compensated liver disease .
VIREAD was evaluated in a limited number of subjects with chronic hepatitis B and decompensated liver disease.
The numbers of subjects in clinical trials who had adefovir resistance-associated substitutions at baseline were too small to reach conclusions of efficacy.
The WikiDoc Journal of Medicine
Wiki Doc now supports one of the first open access journals in medicine. We invite you to submit a manuscript.

# What is an Open Access Journal?
An Open Access Journal has the following advantages over traditional print journals and articles:
- It is freely accessible via the Internet
- The readership is global
- Access to the full text of articles is "open" meaning that any readers can read, download, and/or print the open access article at no cost
- There is no subscription fee for the journal
- The author(s) who publish in our Open Access journals retain the copyright of their article.

# Is there Peer-Review? Is the Quality any Good?
Yes, there is peer review and the quality is quite similar to subscription print journals.

# What Kind of Article Can I Submit?
- Original research
- Negative trial results that are often not accepted elsewhere due to publication bias
- Review articles
- Case reports
- Opion/editorial pieces

# Will My Article by Searchable?
Our site is indexed by Google and Google scholar. We will be applying to PubMed to have articles cited there in three to four months.

# Are There Charges?
At this time there are no charges.

# Can I Become Involved as a Reviewer?
Absolutely! Send us an email  to join our peer review community. Please include a copy of your CV.
The heart in cocaine dependence
Cocaine can cause coronary artery spasms which may lead to a myocardial infarction. This effect can happen randomly to any user. The coronary artery spasms can occur on the user's first usage or any other usage after. The coronary spasms cause the ectopic ventricular foci of the heart to become hypoxic and the extreme irritability can trigger life-threatening ventricular arrhythmias.           

# Pathological Findings

## Gross Images
Images courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Heart: Cocaine dependence: Gross, focal scars in myocardium, a woman in twenties with sudden death.
- Heart: Cocaine dependence: Gross, focal scars in myocardium, a woman in twenties with sudden death.
- Heart: Cocaine dependence: Gross, focal scars in myocardium, a woman in twenties with sudden death.

## Microscopic Images
Images courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Heart: Cocaine dependence: Micro low mag H&E scar in myocardium woman in twenties sudden death
- Heart: Cocaine dependence: Micro med mag small artery in myocardium with marked intimal thickening questionable evidence of previous injury due to spasm. Specimen taken from a woman in twenties after sudden death.
- Heart: Cocaine dependence: Micro high mag small artery in myocardium with marked intimal thickening and vacuolated smooth muscle cells in media questionable evidence of previous spasm woman in twenties sudden death
- Heart: Cocaine dependence: Micro low mag scars in myocardium. Specimen taken from a woman in twenties after sudden death.
- Heart: Cocaine dependence: Micro, high mag, H&E, small artery in epicardium with vacuolated medial smooth muscle cells possible evidence of previous spasm. Specimen taken from a woman in twenties after sudden death.
- Heart: Cocaine dependence: Micro, high mag, H&E, small artery in epicardium with vacuolated medial smooth muscle cells possible evidence of previous spasm. Specimen taken from a woman in twenties after sudden death.
- Micro, med mag small, myocardial artery intimal thickening due to vasospasm. Specimen taken from a woman in twenties after sudden death.
Thiabendazole adverse reactions

# Adverse Reactions
- Gastrointestinal: anorexia, nausea, vomiting, diarrhea, epigastric distress, abdominal pain, jaundice, cholestasis, parenchymal liver damage and hepatic failure. (See WARNINGS.)
- Central Nervous System: dizziness, weariness, drowsiness, giddiness, headache, numbness, hyperirritability, convulsions, collapse, confusion, depression, floating sensation, weakness and lack of coordination.
- Special Senses: tinnitus, abnormal sensation in eyes, xanthopsia, blurred vision, reduced vision, drying of mucous membranes (mouth, eyes, etc.), Sicca syndrome. (See WARNINGS.)
- Cardiovascular: hypotension.
- Metabolic: hyperglycemia.
- Hematologic: transient leukopenia.
- Genitourinary: hematuria, enuresis, malodor of the urine, crystalluria.
- Hypersensitivity: pruritus, fever, facial flush, chills, conjunctival injection, angioedema, anaphylaxis, skin rashes (including perianal), erythema multiforme (including Stevens-Johnson syndrome), and lymphadenopathy.
- Miscellaneous: appearance of live Ascaris in the mouth and nose.
Tissue factor pathway inhibitor
Tissue factor pathway inhibitor (or TFPI) is a single-chain polypeptide which can reversibly inhibit Factor Xa (Xa). While Xa is inhibited, the Xa-TFPI complex can subsequently also inhibit the FVIIa-tissue factor complex.
TFPI contributes significantly to the inhibition of Xa in vivo, despite being present at concentrations of only 2.5 nM.

# Genetics
The gene for TFPI is located on chromosome 2q31-q32.1, and has nine exons which span 70 kb. The gene has not been completely sequenced yet. A similar gene, termed TFPI2, has been identified on chromosome 7q22; in addition to TFPI activity, its product also has retinal pigment epithelial cell growth-promoting properties.

# Protein structure
TFPI has a relative molecular mass of 34,000 to 40,000 depending on the degree of proteolysis of the C-terminal region.
TFPI consists of a highly negatively charged amino-terminus, three tandemly linked Kunitz domains, and a highly positively charged carboxy-terminus. With its Kunitz domains, TFPI exhibits significant homology with human inter-alpha-trypsin inhibitor and bovine basic pancreatic trypsin inhibitor.

# Interactions
Tissue factor pathway inhibitor has been shown to interact with Factor X.
Transverse intermuscular septum

# Overview
The deep transverse fascia of the leg (or transverse intermuscular septum) is a transversely placed, intermuscular septum, between the superficial and deep muscles of the back of the leg.
At the sides it is connected to the margins of the tibia and fibula.
Above, where it covers the Popliteus, it is thick and dense, and receives an expansion from the tendon of the Semimembranosus; it is thinner in the middle of the leg; but below, where it covers the tendons passing behind the malleoli, it is thickened and continuous with the laciniate ligament.
Triple-S Management Corporation
Triple-S Management Corporation, more commonly known simply as Triple-S, Triple SSS, or SSS, is a financial holding company located in San Juan, Puerto Rico which offers a wide range of insurance products and services in Puerto Rico through its wholly-owned subsidiaries. Founded on 1959, it has become the largest medical insurance provider in Puerto Rico thanks to its licensed affiliation with the Blue Cross and Blue Shield Association, and is one of the major participants in the Puerto Rico health reform program, which provides free and low-cost medical coverage to impoverished citizens. Its headquarters are located at 1441 Franklin D. Roosevelt Ave., in the San Patricio section of San Juan.
The companys income is derived exclusively from insurance premiums charged to members, and the company holds a substantial market share in Puerto Rico equal to 33%, 8%, and 25% of the medical insurance, property and casualty insurance, and life insurance segments, respectively, based on net insurance premiums. The company provides coverage through its different insurance services to approximately 1.2 million Puerto Ricans, more than 25% of the countrys population. Its rapid growth was aided in part to a total income tax exemption issued in 1979 by the Puerto Rico Treasury Department (Departamento de Hacienda in Spanish), however this was terminated on December 31, 2002 since the exemption was redefined to apply to life insurance companies only.
On January 13, 2006, the companys Board of Directors issued a statement to announce plans to convert the company from a privately-held company into a publicly-traded corporation. Just 18 days later, on January 31, 2006, Triple-S acquired the Great American Assurance Company of Puerto Rico, also known as GA Life Puerto Rico, for $37.5 million and began to merge its operations with its own life insurance subsidiary Seguros de Vida Triple-S, Inc. in order to expand its market share in the life insurance segment.

# Stats
- Has over $1.137 billion in assets (2005)
- Approx. 1,860 employees.

# Subsidiaries
- Triple-S, Inc.  Its main subsidiary, Triple S is dedicated to providing medical insurance to companies, organizations, governments, and individuals through its Commercial Program, as well as participating in the Puerto Rico Health Reform Program.
- Seguros Triple-S, Inc. - A property and casualty insurance company.
- Seguros de Vida Triple-S, Inc. - A life and disability insurance and annuity products company.
- GA Life Puerto Rico  A life insurance company currently being merged with Seguros de Vida Triple-S, Inc.
- Triple-C, Inc.  Serves as a third-party administrator of Triple-S health reform participation.
- Interactive Systems, Inc.  Provides processing services to Triple-S Management Corporation and its subsidiaries.

# Competitors (in Puerto Rico)
- Humana
- Medical One
- Medical Card Systems
- Puerto Rico Life Insurance Cooperative (Cooperativa de Seguro de Vida de Puerto Rico, or COSVI, in Spanish)
Trousseau sign of latent tetany

# Overview
Trousseau sign of latent tetany is a medical sign observed in patients with low calcium. This sign may become positive before other gross manifestations of hypocalcemia such as hyperreflexia and tetany, as such it is generally believed to be more sensitive (94%) than the Chvostek sign (29%) for hypocalcemia.
To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for "hand of the obstetrician") because it supposedly resembles the position of an obstetrician's hand in delivering a baby.
The sign is named after French physician Armand Trousseau who described the phenomenon in 1861. It is distinct from the Trousseau sign of malignancy.
Tuberculous meningitis overview

# Overview
Tuberculous meningitis is Mycobacterium tuberculosis infection of the meninges.  It is the most common form of CNS tuberculosis.

# Causes
Tuberculous meningitis is caused by Mycobacterium tuberculosis, the bacteria that causes tuberculosis. The bacteria spreads to the brain and spine from another site in the body. Tuberculous meningitis is a very rare disorder in the U.S.

# Diagnosis

## History and Symptoms
Fever and headache are the cardinal features. Confusion is a late feature and coma bears a poor prognosis.  Meningism is absent in a fifth of patients with TB meningitis.  Patients may also have focal neurological deficits.

## Laboratory Findings
Diagnosis of TB meningitis is made by analysing CSF  collected by lumbar puncture.  When collecting CSF for suspected TB meningitis, a minimum of 1ml of fluid should be taken (preferably 5 to 10ml).

## CT
Imaging studies such as CT or MRI may show features strongly suggestive of TB meningitis, but cannot diagnose it.

# Treatment

## Medical Therapy
The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months.  Steroids are always used in the first six weeks of treatment (and sometimes for longer).  A few patients may require immunomodulatory agents such as thalidomide. Treatment must be started as soon as there is a reasonable suspicion of the diagnosis.  Treatment must not be delayed while waiting for confirmation of the diagnosis.

## Surgery
Hydrocephalus occurs as a complication in about a third of patients with TB meningitis and will require a ventricular shunt.

## Primary Prevention
The BCG vaccine may help prevent severe forms of tuberculosis, such as meningitis, in very young children who live in areas where the disease is common.
USMLE Step 2 Clinical Knowledge
The USMLE-Step 2-CK ("Clinical Knowledge") is the multiple-choice portion of the second part of the United States Medical Licensure Examination. Assesses clinical knowledge through a traditional, multiple-choice examination. In contrast to the USMLE Step 1, the focus is much more on clinical application of medical knowledge.  The USMLE Step 2 is generally taken during the 4th year of medical school by medical students.

# Format
The exam is a nine-hour single-day computer-based test composed of eight 46-question sets (368 multiple-choice questions in total). Each section is one hour long. The test taker is permitted 45 minutes, in total for the whole day, for the purpose of breaks that can only be taken between sections.  There is a 15 minute tutorial at the beginning of the exam, which the test-taker can choose to skip, and have the time added to the break time.  If the taker finishes any section before the alloted 1 hour time limit, the remainder of the time is added to break time. The test is administered at the Prometric testing sites around the world.
Scoring is reported in 2 digit and 3 digit scores. Student is required to get 75 and 184 scores to pass the exam in 2 digit and 3 digit scores respectively.

# Topics
- infectious and parasitic diseases
- neoplasms
- immunologic disorders
- diseases of the blood and blood-forming organs
- mental disorders
- diseases of the nervous system and special senses
- cardiovascular disorders
- diseases of the respiratory system
- nutritional and digestive disorders
- gynecologic disorders
- renal, urinary, and male reproductive systems
- disorders of pregnancy, childbirth, and the puerperium
- disorders of the skin and subcutaneous tissues
- diseases of the musculoskeletal system and connective tissue
- endocrine and metabolic disorders
- congenital anomalies
- conditions originating in the perinatal period
- symptoms, signs, and ill-defined conditions
- injury and poisoning
Unstable angina pathophysiology

# Overview
Unstable angina occurs when myocardial oxygen demand exceeds myocardial oxygen supply at rest or with minimal exertion. This supply/demand mismatch can be caused by conditions that increase oxygen demand or reduce oxygen supply.

# Pathophysiology
Unstable angina occurs when myocardial oxygen demand exceeds myocardial oxygen supply at rest or with minimal exertion. This supply/demand mismatch can be caused by conditions that increase oxygen demand or reduce oxygen supply:

### Conditions Causing a Decrease in Oxygen Supply
Altered myocardial oxygen supply underlie most cases of unstable angina.
- Anemia
- Anomalous left coronary artery passing between the aorta and pulmonary artery
- Coronary thromboembolism in which there is rupture at the shoulder of a lipid laden, inflamed coronary artery plaque with formation of thrombus and distal embolization is the classic cause of unstable angina. The artery is open, so there is no ST elevation to suggest transmural injury. Embolization may yield subendocardial ischemia which results in ST segment depression.  Histological features of the plaque that correlate with increased clinical severity of unstable angina include hypercellularity, atheroma, thrombus, stellar shaped smooth muscle cells and neovessel formation.
- Coronary artery disease progression with a severe, lipid laden, atherosclerotic stenosis.  Patients with rapid progression of atherosclerotic disease at multiple sites experience unstable angina more frequently.
- Coronary artery dissection
- Dynamic obstruction (e.g., coronary artery spasm or coronary vasoconstriction) of epicardial and/or microvascular vessels. Coronary vasospasm causing unstable angina is a common finding in Taiwanese and Japanese patients.
- Prinzmetal's angina of the large epicardial coronary arteries
- Syndrome X of the small downstream coronary microvasculature
- Hypotension
- Hypoxemia
- Myocardial bridge
- Polycythemia
- Vasculitis of the coronary arteries

### Conditions Causing an Increase in Myocardial Oxygen Demand
Nearly one third of all unstable angina cases result from increased oxygen demand due to excess work load on the myocardium.
- Amphetamine use
- Aortic stenosis
- Arteriovenous shunts
- Cocaine use
- Congestive heart failure
- Fever
- High cardiac output
- Malignant hypertension
- Obstructive cardiomyopathy
- Pheochromocytoma
- Supravalvular aortic stenosis
- Tachyarrhythmias (e.g., atrial fibrillation or atrial flutter)
- Thyrotoxicosis
Vesicular monoamine transporter

# Overview
The vesicular monoamine transporter is a transport protein located within the presynaptic cell.

# Isoforms
It comprises the two isoforms:
- VMAT1
- VMAT2

# Substrates
Substrates for the transporter is mainly noradrenaline, adrenaline and isoprenaline. However, other substrates include dopamine, 5-HT, guanethidine and MPP+.

# Clinicial significance
It can be inhibited by reserpine and tetrabenazine.
VMAT is the main target of methamphetamine. By acting as a competitive antagonist, methamphetamine blocks the presynaptic cell's ability to use VMAT to package the above mentioned neurotransmitters into vesicles. The result is increased neurotransimtter release that is not dependent on the phasic activity of the presynaptic cell.
V and P box gene transcriptions
"REV-ERB and RORa are nuclear receptors rather than bZIP transcription factors like VRI  and PDP1, and they regulate transcription by binding RORE elements rather than V/P-boxes (Bell-Pedersen et al., 2005)."
"A delayed accumulation of PDP1 leads to a replacement of VRI from P/V (PDP1 and VRI) boxes and restimulates clk transcription."
"For VRI to be a direct repressor of Clk, the 8.0 kb Clk genomic fragment should contain binding sites for VRI. The consensus binding site for VRI has not been determined; however, the basic (DNA binding) domain shares >85% homology with that of mammalian E4BP4, and hence, VRI should bind similar DNA sequences as E4BP4 (George and Terracol, 1997). The optimal binding site for E4BP4 has been determined as 5-(A/G): (A/G)T(A/C)A(A/T/C)-3 (Cowell et al., 1992)."

# Consensus sequences
"As VRI accumulates in the nucleus during the mid to late day, it binds VRI/PDP1 binding sites (V/P-boxes) , to repress Clk and cry transcription (Hardin, 2004)."

# Human genes
Gene ID: 54704 is PDP1 pyruvate dehyrogenase phosphatase catalytic subunit 1. "Pyruvate dehydrogenase (E1) is one of the three components (E1, E2, and E3) of the large pyruvate dehydrogenase complex. Pyruvate dehydrogenase kinases catalyze phosphorylation of serine residues of E1 to inactivate the E1 component and inhibit the complex. Pyruvate dehydrogenase phosphatases catalyze the dephosphorylation and activation of the E1 component to reverse the effects of pyruvate dehydrogenase kinases. Pyruvate dehydrogenase phosphatase is a heterodimer consisting of catalytic and regulatory subunits. Two catalytic subunits have been reported; one is predominantly expressed in skeletal muscle and another one is is much more abundant in the liver. The catalytic subunit, encoded by this gene, is the former, and belongs to the protein phosphatase 2C (PP2C) superfamily. Along with the pyruvate dehydrogenase complex and pyruvate dehydrogenase kinases, this enzyme is located in the mitochondrial matrix. Mutation in this gene causes pyruvate dehydrogenase phosphatase deficiency. Multiple alternatively spliced transcript variants encoding different isoforms have been identified."
- NP_001155251.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform 2 (variant 2).
- NP_001155252.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform 2 (variant 3).
- NP_001155253.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform 3 (variant 4).
- NP_060914.2 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform 3 (variant 5).
- XP_016869077.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform X1.
- XP_011515437.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform X2.
- XP_011515438.1 pyruvate dehyrogenase phosphatase catalytic subunit 1 isoform X3.

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Initial content for this page in some instances came from Wikiversity.