The original Loday–Quillen–Tsygan Theorem (LQT) is proven by Loday and Quillen [13] and independently by Tsygan [20]. It states that the ordinary Lie homology (here referred as Chevalley–Eilenberg–Lie homology) of the Lie algebra of the infinite matrices gl(A) over an unital associative algebra A is generated by the cyclic homology of A as an exterior algebra. Although Lie algebras have been st...

OBJECTIVE Fast inward Na current (I(Na)) carried by the voltage-gated Na channel (Na(V)1.5) is critical for action potential (AP) propagation and the rapid upstroke of the cardiac AP. In addition, a small fraction of Na(V)1.5 channels remains open throughout the plateau of the AP, and this current is termed as late I(Na). In patients with mutant Na(V)1.5-based congenital long Q-T (LQT) syndrome...

Defects of the SCN5A gene encoding the cardiac sodium channel alpha-subunit are associated with both the long QT-3 (LQT-3) subtype of long-QT syndrome and Brugada syndrome (BrS). One previously described SCN5A mutation (1795insD) in the C terminus results in a clinical phenotype combining QT prolongation and ST segment elevation, indicating a close interrelationship between the two disorders. H...

OBJECTIVE To describe experience of long QT (LQT) molecular autopsy in sudden infant death syndrome (SIDS). DESIGN Descriptive audit from two distinct periods: (1) A prospective, population-based series between 2006 and 2008 ('unselected'). (2) Before and after 2006-2008, with testing guided by a cardiac genetic service ('selected'). LQT genes 1, 2, 3, 5, 6 and 7 were sequenced. Next of kin w...

Ion channel subunits encoded by KCNQ1 and KCNE1 produce the slowly activating K+ current (IKs) that plays a central role in myocardial repolarization. The KCNQ1 alpha-subunit and the KCNE1 beta-subunit assemble with their membrane-spanning segments interacting, resulting in transformation of channel activation kinetics. We recently reported a functional interaction involving C-terminal portions...

Na channel blockers such as flecainide have found renewed usefulness in the diagnosis and treatment of two clinical syndromes arising from inherited mutations in SCN5A, the gene encoding the subunit of the cardiac voltage–gated Na channel. The Brugada syndrome (BrS) and the LQT-3 variant of the Long QT syndrome are caused by disease-linked SCN5A mutations that act to change functional and pharm...