GPS phase scintillation at high latitudes during geomagnetic storms of 7-17 March 2012, part 2: interhemispheric comparison

During the ascending phase of solar cycle 24, a series of interplanetary coronal mass ejections (ICMEs) in the period 7–17 March 2012 caused geomagnetic storms that strongly affected high-latitude ionosphere in the Northern and Southern Hemisphere. GPS phase scintillation was observed at northern and southern high latitudes by arrays of GPS ionospheric scintillation and TEC monitors (GISTMs) and geodetic-quality GPS receivers sampling at 1 Hz. Mapped as a function of magnetic latitude and magnetic local time (MLT), the scintillation was observed in the ionospheric cusp, the tongue of ionization fragmented into patches, sun-aligned arcs in the polar cap, and nightside auroral oval and subauroral latitudes. Complementing a companion paper (Prikryl et al., 2015a) that focuses on the high latitude ionospheric response to variable solar wind in the North American sector, interhemispheric comparison reveals commonalities as well as differences and asymmetries between the northern and southern high latitudes, as a consequence of the coupling between the solar wind and magnetosphere. The interhemispheric asymmetries are caused by the dawn–dusk component of the interplanetary magnetic field controlling the MLT of the cusp entry of the storm enhanced density plasma into the polar cap and the orientation relative to the noon–midnight meridian of the tongue of ionization

Changes in Intracellular Na+ following Enhancement of Late Na+ Current in Virtual Human Ventricular Myocytes

The slowly inactivating or late Na+ current, INa-L, can contribute to the initiation of both atrial and ventricular rhythm disturbances in the human heart. However, the cellular and molecular mechanisms that underlie these pro-arrhythmic influences are not fully understood. At present, the major working hypothesis is that the Na+ influx corresponding to I(Na-L)significantly increases intracellular Na+, [Na]; and the resulting reduction in the electrochemical driving force for Na+ reduces and (may reverse) Na+/Ca2+ exchange. These changes increase intracellular Ca2+, [Ca2+]; which may further enhance I(Na-L)due to calmodulindependent phosphorylation of the Na+ channels. This paper is based on mathematical simulations using the O'Hara et al (2011) model of baseline or healthy human ventricular action potential waveforms(s) and its [Ca2(+)]; homeostasis mechanisms. Somewhat surprisingly, our results reveal only very small changes (<= 1.5 mM) in [Na] even when INa-L is increased 5-fold and steady-state stimulation rate is approximately 2 times the normal human heart rate (i.e. 2 Hz). Previous work done using well-established models of the rabbit and human ventricular action potential in heart failure settings also reported little or no change in [Na] when I(Na-L)was increased. Based on our simulations, the major short-term effect of markedly augmenting I(Na-L)is a significant prolongation of the action potential and an associated increase in the likelihood of reactivation of the L-type Ca2+ current, Ica-L. Furthermore, this action potential prolongation does not contribute to [Na]; increase.This work was supported by (i) the "VI Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica" from the Ministerio de Economia y Competitividad of Spain (grant number TIN2012-37546-C03-01) and the European Commission (European Regional Development Funds-ERDF-FEDER), (ii) by the Direccion General de Politica Cientifica de la Generalitat Valenciana (grant number GV/2013/119), and by (iii), Programa Prometeo (PROMETEO/2016/088) de la Conselleria d'Educacio Formacio I Ocupacio, Generalitat Valenciana. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.K Cardona; Trénor Gomis, BA.; W Giles (2016). Changes in Intracellular Na+ following Enhancement of Late Na+ Current in Virtual Human Ventricular Myocytes. PLoS ONE. 11(11). https://doi.org/10.1371/journal.pone.0167060S111