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Related Concept Videos

Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Pleiotropy01:33

Pleiotropy

Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
Dysrhythmias III: Characteristics of Dysrhythmias01:29

Dysrhythmias III: Characteristics of Dysrhythmias

Dysrhythmias, also known as arrhythmias, are irregular heart rhythms that result from abnormal electrical activity in the heart, affecting its ability to circulate blood efficiently. Tachyarrhythmias, a subset of dysrhythmias, are characterized by abnormally fast heart rates exceeding 100 beats per minute. Here are some types of tachyarrhythmias with their distinct ECG features:Sinus Tachycardia:Sinus tachycardia presents a regular heart rhythm with an increased rate of 101-180 beats per minute.
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...

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Related Experiment Video

Updated: Jun 29, 2026

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
07:15

Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation

Published on: January 16, 2019

Long QT Syndrome.

Ilan Goldenberg, Wojciech Zareba, Arthur J Moss

    Current Problems in Cardiology
    |October 7, 2008
    PubMed
    Summary
    This summary is machine-generated.

    Hereditary Long QT syndrome (LQTS) is a genetic disorder increasing sudden cardiac death risk. Diagnosis and risk assessment require considering age, gender, QT duration, and genetics for effective management.

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    Last Updated: Jun 29, 2026

    Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
    07:15

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    Published on: January 16, 2019

    A Robust Polymerase Chain Reaction-based Assay for Quantifying Cytosine-guanine-guanine Trinucleotide Repeats in Fragile X Mental Retardation-1 Gene
    08:22

    A Robust Polymerase Chain Reaction-based Assay for Quantifying Cytosine-guanine-guanine Trinucleotide Repeats in Fragile X Mental Retardation-1 Gene

    Published on: September 16, 2019

    Area of Science:

    • Cardiology
    • Genetics
    • Electrophysiology

    Background:

    • Hereditary Long QT syndrome (LQTS) is a genetic channelopathy.
    • LQTS increases the risk of polymorphic ventricular tachyarrhythmias and sudden cardiac death.
    • Affected individuals typically have normal cardiac morphology.

    Purpose of the Study:

    • To review the diagnosis, risk assessment, and management of LQTS.
    • To highlight age- and gender-specific clinical courses.
    • To discuss current and emerging therapeutic strategies.

    Main Methods:

    • Review of accumulating data from recent studies.
    • Analysis of diagnostic criteria including electrocardiographic, clinical, and genetic factors.
    • Evaluation of risk stratification parameters and therapeutic interventions.

    Main Results:

    • LQTS clinical course is time-dependent and age-specific, with gender differences.
    • Risk assessment should integrate age-gender interactions, syncope history, QT duration, and genetics.
    • Beta-blockers are the primary therapy; other interventions include sympathetic denervation and defibrillators.

    Conclusions:

    • Accurate diagnosis and risk stratification are crucial for managing LQTS.
    • Personalized risk assessment considering demographic and clinical factors improves patient outcomes.
    • Genotype-specific therapies show promise for high-risk LQTS patients.