- Left cardiac sympathetic denervation in children with Jervell Lange-Nielsen syndrome and drug refractory torsades - A case series
- Rapid changes of mRNA expressions of cardiac ion channels affected by Torsadogenic drugs influence susceptibility of rat hearts to arrhythmias induced by Beta-Adrenergic stimulation
- Estimating the Probability of Early Afterdepolarizations and Predicting Arrhythmic Risk associated with Long QT Syndrome Type 1 Mutations
- Family long QT syndrome type 2 associated with <em>KCNH2</em> gene mutation: aborted sudden cardiac death
- 4-phenylbutyric acid re-trafficking hERG/G572R channel protein by modulating the endoplasmic reticulum stress-associated chaperones and endoplasmic reticulum-associated degradation gene
- Corrected QT Interval (QTc) Diagnostic App for the Oncological Routine: Development Study
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- ERG K+ channels mediate a major component of action potential repolarization in lymphatic muscle
- Cardiovascular Screening before Sports Participation: Results of 11487 Children
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Calmodulin mutations affecting Gly114 impair binding to the NaV1.5 IQ-domain
- Generation of patient-specific induced pluripotent stem cell lines with Type 2 Long QT Syndrome and the KCNH2 c.379C > T pathogenic variant
- Clinical and Genetic Features of Korean Inherited Arrhythmia Probands
- Total Intravenous Anaesthesia for Laparoscopic Cholecystectomy in a Patient With Congenital Long QT Syndrome: A Case Report
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)
- Using Ribonucleoprotein-based CRISPR/Cas9 to Edit Single Nucleotide on Human Induced Pluripotent Stem Cells to Model Type 3 Long QT Syndrome (SCN5A±)