https://www.selleckchem.com/products/forskolin.html Thus, proteins secreted during ER stress mediated by ER calcium depletion can enhance cardiac myocyte viability. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a stress-induced ventricular arrhythmia associated with rhythm disturbance and impaired sinoatrial node cell (SANC) automaticity (pauses). Mutations associated with dysfunction of Ca2+-related mechanisms have been shown to be present in CPVT. These dysfunctions include impaired Ca2+ release from the ryanodine receptor (i.e., RyR2R4496C mutation) or binding to calsequestrin 2 (CASQ2). In SANC, Ca2+ signaling directly and indirectly mediates pacemaker function. We address here the following research questions (i) what coupled-clock mechanisms and pathways mediate pacemaker mutations associated with CPVT in basal and in response to β-adrenergic stimulation? (ii) Can different mechanisms lead to the same CPVT-related pacemaker pauses? (iii) Can the mutation-induced deteriorations in SANC function be reversed by drug intervention or gene manipulation? We used a numerical model of mice SANC that includes membrane and intracellular mechanisms and their nges in gene expression, compensate for the impairment in SANC automaticity. These findings suggest new insights for understanding CPVT and its therapeutic approach. The research on the abnormalities of event-related oscillations in Parkinson's disease (PD) was mostly studied with cognitively normal patients. The present study aims to show the adverse effects of cognitive decline in PD patients via the EEG-Brain Oscillations approach by comparing the electrophysiological responses in two modalities, i.e. auditory, and visual in which PD group show deficit. We conducted a study in which we analyzed event-related theta power and phase-locking during auditory and visual oddball paradigm. Cognitively normal PD (PDCN) patients (N = 15), PD with mild cognitive impairment (PDMCI) patients (N = 22), PD demen