- Home
- Search Results
- Page 1 of 1
Search for: All records
-
Total Resources1
- Resource Type
-
00010
- Availability
-
10
- Author / Contributor
- Filter by Author / Creator
-
-
Bennett, Eric S. (1)
-
Ednie, Andrew R. (1)
-
Kim, Haedong (1)
-
Yang, Hui (1)
-
#Tyler Phillips, Kenneth E. (0)
-
#Willis, Ciara (0)
-
& Abreu-Ramos, E. D. (0)
-
& Abramson, C. I. (0)
-
& Abreu-Ramos, E. D. (0)
-
& Adams, S.G. (0)
-
& Ahmed, K. (0)
-
& Ahmed, Khadija. (0)
-
& Akcil-Okan, O. (0)
-
& Akuom, D. (0)
-
& Aleven, V. (0)
-
& Andrews-Larson, C. (0)
-
& Archibald, J. (0)
-
& Arnett, N. (0)
-
& Arya, G. (0)
-
& Attari, S. Z. (0)
-
- Filter by Editor
-
-
& Spizer, S. M. (0)
-
& . Spizer, S. (0)
-
& Ahn, J. (0)
-
& Bateiha, S. (0)
-
& Bosch, N. (0)
-
& Brennan K. (0)
-
& Brennan, K. (0)
-
& Chen, B. (0)
-
& Chen, Bodong (0)
-
& Drown, S. (0)
-
& Ferretti, F. (0)
-
& Higgins, A. (0)
-
& J. Peters (0)
-
& Kali, Y. (0)
-
& Ruiz-Arias, P.M. (0)
-
& S. Spitzer (0)
-
& Spitzer, S. (0)
-
& Spitzer, S.M. (0)
-
(submitted - in Review for IEEE ICASSP-2024) (0)
-
- (0)
-
-
Have feedback or suggestions for a way to improve these results?
!
Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher.
Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?
Some links on this page may take you to non-federal websites. Their policies may differ from this site.
-
Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the primary reason for heart transplantation; upward of 70% of DCM cases are considered idiopathic. Our in-vitro experiments showed that reduced hybrid/complex N-glycosylation in mouse cardiomyocytes is linked with DCM. Further, we observed direct effects of reduced N-glycosylation on K v gating. However, it is difficult to rigorously determine the effects of glycosylation on K v activity, because there are multiple K v isoforms in cardiomyocytes contributing to the cardiac excitation. Due to complex functions of K v isoforms, only the sum of K + currents (I Ksum ) can be recorded experimentally and decomposed later using exponential fitting to estimate component currents, such as I Kto , I Kslow , and I Kss . However, such estimation cannot adequately describe glycosylation effects and K v mechanisms. Here, we propose a framework of simulation modeling of K v kinetics in mouse ventricular myocytes and model calibration using the in-vitro data under normal and reduced glycosylation conditions through ablation of the Mgat1 gene (i.e., Mgat1KO). Calibrated models facilitate the prediction of K v characteristics at different voltages that are not directly observed in the in-vitro experiments. A model calibration procedure is developed based on the genetic algorithm. Experimental results show that, in the Mgat1KO group, both I Kto and I Kslow densities are shown to be significantly reduced and the rate of I Kslow inactivation is much slower. The proposed approach has strong potential to couple simulation models with experimental data for gaining a better understanding of glycosylation effects on K v kinetics.more » « less