Justus Anumonwo, PhD  A number of cardiac rhythm disturbances have been associated with mutant ion channel proteins, accessory proteins to the ion channels, or the improper interactions between the two proteins. Research in our laboratory focuses on understanding the molecular interactions of cardiac ion channel proteins under normal and patho- physiological conditions. We use a combination of electrophysiological, biochemical and molecular biological techniques to carry out these investigations.

Omer Berenfeld, PhD   Our research focuses on mechanisms of complex wave propagation and fibrillation in the heart using a combination of experimental, clinical, and numerical approaches, with the aim of better understanding acute and chronic atrial fibrillation as well as ventricular fibrillation. We investigate the basic effects of the ionic and structural properties of the heart on the normal and abnormal propagation of its action potential, and particularly the effects on the unique phenomenon of rotor activity. Our research and developments use analysis in the time, phase and frequency domains together with novel opto-electric approaches for mechanistic correlations between the fibrillatory activation patterns and the cardiac substrate. Emphasis is given to technological developments enabling the translation of knowledge derived from animal and computational models into the clinical setting of patients with atrial fibrillation.   

Jimo Borjigin, PhD    We have developed a new method of displaying and analyzing long streams of EKG signals, called the electrocardiomatrix (ECM). This method preserves all features of cardiac electrical signals decipherable from raw EKG data in a compact manner and permits a single-glance view of time-dependent changes of heart rate and the occurrence of cardiac arrhythmias. The ECM method appears to offer superior sensitivity and specificity for cardiac arrhythmia detection compared with manual detection (Li et al., 2015b) as well as automated arrhythmia detection (manuscripts in preparation) and is predicted to improve diagnosis of cardiac diseases.  Currently, we are collaborating with a number of physicians to conduct a small scale clinical trials to test the sensitivity and specificity of ECM approach for cardiac arrhythmia detection at the University of Michigan Hospital. 

Lori Isom, PhD    Variants in ion channel genes can lead to neurological or cardiovascular diseases called channelopathies. Our work focuses on human variants in genes encoding voltage-gated sodium channel α and β subunits that lead to a devastating pediatric epileptic encephalopathy called Dravet syndrome, a disease with a high risk of Sudden Unexpected Death in Epilepsy (SUDEP). We have proposed that SUDEP arises from simultaneous arrhythmias of brain and heart due to the expression of mutant sodium channel genes in both organs.  Our ultimate goals are to discover novel targets for epilepsy therapeutics and to identify biomarkers for SUDEP risk.

David K. Jones, PhD   Ion channel dysfunction causes the cardiac disorder long QT syndrome. Long QT syndrome patients have an elevated risk for sudden cardiac death. Our lab uses patient-derived and gene edited human stem cell-derived cell lines as models of the human heart and brain. Using techniques in electrophysiology, immunocytochemistry, and molecular biology, we seek to understand the impact of ion channel dysfunction on human physiology and its contribution to sudden death.