Symmetric Aqueous Batteries of Titanium Hexacyanoferrate in Na+, K+, and Mg2+ Media

Symmetric batteries, in which the same active material is used for the positive and the negative electrode, simplifying the manufacture process and reducing the fabrication cost, have attracted extensive interest for large-scale stationary energy storage. In this paper, we propose a symmetric battery based on titanium hexacyanoferrate (TiHCF) with two well-separated redox peaks of Fe3+/Fe2+ and Ti4+/Ti3+ and tested it in aqueous Na-ion/ K-ion/Mg-ion electrolytes. The result shows that all the symmetric batteries exhibit a voltage plateau centered at around 0.6 V, with discharge capacity around 30 mAhg−1 at C/5. Compared to a Mg-ion electrolyte, the TiHCF symmetric batteries in Na-ion and K-ion electrolytes have better stability. The calculated diffusion coefficient of Na+, K+, and Mg2+ are in the same order of magnitude, which indicates that the three-dimensional ionic channels and interstices in the lattice of TiHCF are large enough for an efficient Na+, K+ and Mg2+ insertion and extraction.

Macroscopic currents of ionic channels using Mass Action Law: A mathematical model

In this work it proposes a mathematical model for ion channels based on two concepts, the Hodgkin and Huxley's as well as the Law of Mass Action in addition, we consider the kinetics of channels as a dynamic process of Markov`s chain. With the previous premises, a system of differential equations is proposed that when it is solved, all properties of the macroscopic currents are determined. The activation, deactivation, inactivation, and recovery of the inactivation concepts remain as processes that are part of a chemical reaction. With this system of equations, all the experimental protocols used in electrophysiology to characterize macroscopic currents can be modeled. Another advantage is that the model allows, with the same system of equations, to determine the properties of voltage-dependent channels regardless of the type of ion that pass through in the channel.

Physiological Bases of Electric Stimulation as a New Approach to Glaucoma IOP Control

This Chapter focuses in the electrophysiological bases to support Trans Palpebral Electrical Stimulation TPES as a new alternative to control Intraocular Pressure IOP. Primary open Angle Glaucoma POAG is described in our approach as a dysfunction of the membrane potential of TM cells due to the dysfunction of the Maxi potassium depended Calcium Channels BKCa2+ of the Trabecular Mesh TM. We review through the paper the main contributions about Trabecular mesh dysfunction related with Voltage dependent ionic channels. We also present in this paper new results in controlling intra ocular pressure IOP during one year of trans palpebral Electric stimulation in patients with Primary open-angle glaucoma (POAG).

Modulation of Adaptive Immunity and Viral Infections by Ion Channels

Most cellular functions require of ion homeostasis and ion movement. Among others, ion channels play a crucial role in controlling the homeostasis of anions and cations concentration between the extracellular and intracellular compartments. Calcium (Ca2+) is one of the most relevant ions involved in regulating critical functions of immune cells, allowing the appropriate development of immune cell responses against pathogens and tumor cells. Due to the importance of Ca2+ in inducing the immune response, some viruses have evolved mechanisms to modulate intracellular Ca2+ concentrations and the mobilization of this cation through Ca2+ channels to increase their infectivity and to evade the immune system using different mechanisms. For instance, some viral infections require the influx of Ca2+ through ionic channels as a first step to enter the cell, as well as their replication and budding. Moreover, through the expression of viral proteins on the surface of infected cells, Ca2+ channels function can be altered, enhancing the pathogen evasion of the adaptive immune response. In this article, we review those ion channels and ion transporters that are essential for the function of immune cells. Specifically, cation channels and Ca2+ channels in the context of viral infections and their contribution to the modulation of adaptive immune responses.

MR pathway in retinal health and diseases

In the retina, mineralocorticoid receptor (MR), expressed in vessels, glial and neuronal cells, is mainly activated by glucocorticoids. Under pathological conditions, ocular MR expression and corticoids change, leading in most cases to MR overactivation. Experimental models using MR agonists or antagonists, administered systemically or intraocularly, acutely or chronically and transgenic models, allowed to identify the deleterious consequences of MR pathway overactivation. Among them, oxidative stress, inflammation, deregulation of hydro-ionic channels, alteration of choroidal vasculature, angiogenesis and cell death, are common to major retinal diseases. Specific MR antagonists showed efficacy in models of diabetic retinopathy, ischaemia, retinal and choroidal angiogenesis and in models of glaucoma. It is highly likely that MR antagonists will find a place in the therapeutic arsenal of age-related macular degeneration, diabetic retinopathy, glaucoma and in pachychoroid associated diseases. Their use in humans is still limited by the need of biomarkers of MR activation and specific ocular formulations.

Memristive Hodgkin-Huxley Spiking Neuron Model for Reproducing Neuron Behaviors

The Hodgkin-Huxley (HH) spiking neuron model reproduces the dynamic characteristics of the neuron by mimicking the action potential, ionic channels, and spiking behaviors. The memristor is a nonlinear device with variable resistance. In this paper, the memristor is introduced to the HH spiking model, and the memristive Hodgkin-Huxley spiking neuron model (MHH) is presented. We experimentally compare the HH spiking model and the MHH spiking model by applying different stimuli. First, the individual current pulse is injected into the HH and MHH spiking models. The comparison between action potentials, current densities, and conductances is carried out. Second, the reverse single pulse stimulus and a series of pulse stimuli are applied to the two models. The effects of current density and action time on the production of the action potential are analyzed. Finally, the sinusoidal current stimulus acts on the two models. The various spiking behaviors are realized by adjusting the frequency of the sinusoidal stimulus. We experimentally demonstrate that the MHH spiking model generates more action potential than the HH spiking model and takes a short time to change the memductance. The reverse stimulus cannot activate the action potential in both models. The MHH spiking model performs smoother waveforms and a faster speed to return to the resting potential. The larger the external stimulus, the faster action potential generated, and the more noticeable change in conductances. Meanwhile, the MHH spiking model shows the various spiking patterns of neurons.

Berberine on the Prevention and Management of Cardiometabolic Disease: Clinical Applications and Mechanisms of Action

Berberine is an alkaloid from several medicinal plants originally used to treat diarrhea and dysentery as a traditional Chinese herbal medicine. In recent years, berberine has been discovered to exhibit a wide spectrum of biological activities in the treatment of diverse diseases ranging from cancer and neurological dysfunctions to metabolic disorders and heart diseases. This review article summarizes the clinical practice and laboratory exploration of berberine for the treatment of cardiometabolic and heart diseases, with a focus on the novel insights and recent advances of the underlying mechanisms recognized in the past decade. Berberine was found to display pleiotropic therapeutic effects against dyslipidemia, hyperglycemia, hypertension, arrhythmia, and heart failure. The mechanisms of berberine for the treatment of cardiometabolic disease involve combating inflammation and oxidative stress such as inhibiting proprotein convertase subtilisin/kexin 9 (PCSK9) activation, regulating electrical signals and ionic channels such as targeting human ether-a-go-go related gene (hERG) currents, promoting energy metabolism such as activating adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, modifying gut microbiota to promote transforming of berberine into its intestine-absorbable form, and interacting with non-coding RNAs via targeting multiple signaling pathways such as AMPK, mechanistic target of rapamycin (mTOR), etc. Collectively, berberine appears to be safe and well-tolerated in clinical practice, especially for those who are intolerant to statins. Knowledge from this field may pave the way for future development of more effective pharmaceutical approaches for managing cardiometabolic risk factors and preventing heart diseases.

Effective Accentuation of Voltage-Gated Sodium Current Caused by Apocynin (4′-Hydroxy-3′-methoxyacetophenone), a Known NADPH-Oxidase Inhibitor

Apocynin (aPO, 4′-Hydroxy-3′-methoxyacetophenone) is a cell-permeable, anti-inflammatory phenolic compound that acts as an inhibitor of NADPH-dependent oxidase (NOX). However, the mechanisms through which aPO can interact directly with plasmalemmal ionic channels to perturb the amplitude or gating of ionic currents in excitable cells remain incompletely understood. Herein, we aimed to investigate any modifications of aPO on ionic currents in pituitary GH3 cells or murine HL-1 cardiomyocytes. In whole-cell current recordings, GH3-cell exposure to aPO effectively stimulated the peak and late components of voltage-gated Na+ current (INa) with different potencies. The EC50 value of aPO required for its differential increase in peak or late INa in GH3 cells was estimated to be 13.2 or 2.8 μM, respectively, whereas the KD value required for its retardation in the slow component of current inactivation was 3.4 μM. The current–voltage relation of INa was shifted slightly to more negative potential during cell exposure to aPO (10 μM); however, the steady-state inactivation curve of the current was shifted in a rightward direction in its presence. Recovery of peak INa inactivation was increased in the presence of 10 μM aPO. In continued presence of aPO, further application of rufinamide or ranolazine attenuated aPO-stimulated INa. In methylglyoxal- or superoxide dismutase-treated cells, the stimulatory effect of aPO on peak INa remained effective. By using upright isosceles-triangular ramp pulse of varying duration, the amplitude of persistent INa measured at low or high threshold was enhanced by the aPO presence, along with increased hysteretic strength appearing at low or high threshold. The addition of aPO (10 μM) mildly inhibited the amplitude of erg-mediated K+ current. Likewise, in HL-1 murine cardiomyocytes, the aPO presence increased the peak amplitude of INa as well as decreased the inactivation or deactivation rate of the current, and further addition of ranolazine or esaxerenone attenuated aPO-accentuated INa. Altogether, this study provides a distinctive yet unidentified finding that, despite its effectiveness in suppressing NOX activity, aPO may directly and concertedly perturb the amplitude, gating and voltage-dependent hysteresis of INa in electrically excitable cells. The interaction of aPO with ionic currents may, at least in part, contribute to the underlying mechanisms through which it affects neuroendocrine, endocrine or cardiac function.