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Correction: Atrial arrhythmogenicity of KCNJ2 mutations in short QT syndrome: Insights from virtual human atria.

08:00 EDT 13th June 2019 | BioPortfolio

Summary of "Correction: Atrial arrhythmogenicity of KCNJ2 mutations in short QT syndrome: Insights from virtual human atria."

[This corrects the article
DOI:
10.1371/journal.pcbi.1005593.].

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Journal Details

This article was published in the following journal.

Name: PLoS computational biology
ISSN: 1553-7358
Pages: e1007145

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Medical and Biotech [MESH] Definitions

A form of inherited long QT syndrome (or LQT7) that is characterized by a triad of potassium-sensitive periodic paralysis, VENTRICULAR ECTOPIC BEATS, and abnormal features such as short stature, low-set ears, and SCOLIOSIS. It results from mutations of KCNJ2 gene which encodes a channel protein (INWARD RECTIFIER POTASSIUM CHANNELS) that regulates resting membrane potential.

A condition caused by dysfunctions related to the SINOATRIAL NODE including impulse generation (CARDIAC SINUS ARREST) and impulse conduction (SINOATRIAL EXIT BLOCK). It is characterized by persistent BRADYCARDIA, chronic ATRIAL FIBRILLATION, and failure to resume sinus rhythm following CARDIOVERSION. This syndrome can be congenital or acquired, particularly after surgical correction for heart defects.

A form of ventricular pre-excitation characterized by a short PR interval and a normal QRS complex. In this syndrome, the atrial impulse conducts via the James fibers which connect the atrium to BUNDLE OF HIS bypassing the upper ATRIOVENTRICULAR NODE. HEART VENTRICLES are depolarized normally through the His-Purkinje system.

Impaired or delayed impulse conduction between the right and left HEART ATRIA. Advanced interatrial blocks are often associated with arrhythmias (e.g., ATRIAL FLUTTER; and ATRIAL FIBRILLATION), direct conduction block via the Bachmann's bundle and concomitant left atrial enlargement. Syndrome of advanced interatrial block associated with SUPRAVENTRICULAR TACHYCARDIA is referred to as Bayes syndrome.

A multifaceted disorder characterized by short stature, webbed neck, ptosis, skeletal malformations, hypertelorism, hormonal imbalance, CRYPTORCHIDISM, multiple cardiac abnormalities (most commonly including PULMONARY VALVE STENOSIS), and some degree of MENTAL RETARDATION. The phenotype bears similarities to that of TURNER SYNDROME that occurs only in females and has its basis in a 45, X karyotype abnormality. However, Noonan syndrome occurs in both males and females with a normal sex chromosome constitution (46,XX and 46,XY). NS1 is due to mutations at chromosome location 12q24.1, in PTPN11, a gene encoding PROTEIN TYROSINE PHOSPHATASE, NON-RECEPTOR TYPE 11. LEOPARD SYNDROME, a disorder that has clinical features overlapping those of Noonan Syndrome, is also due to mutations in PTPN11. In addition, there is a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS).

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