While it was recently reported that the conduction band of iron minerals can mediate electron transfer between Fe(II) and different Fe(III) lattice sites during Fe(II)-catalyzed mineral transformation, it is unclear whether such a conduction band mediation pathway occurs in the microbial Fe(II) oxidation system under dark and anoxic subsurface conditions. Here, using cytochrome c (c-Cyts) as a model protein of microbial Fe(II) oxidation, the in vitro kinetics and thermodynamics of c-Cyts reduction by Fe(II) were studied. The results showed that the rates of c-Cyts reduction were greatly enhanced in the presence of the semiconducting mineral hematite (Hem, α-Fe2O3). The electrochemical experiments separating Fe(II) and c-Cyts demonstrated that electrons from Fe(II) to the electrode or from the electrode to c-Cyts could directly penetrate hematite, resulting in enhanced current. Independent photochemical and photoluminescence experiments indicated that c-Cyts could be directly reduced by the conduction band electrons of hematite which were generated under light illumination. In c-Cyts+Fe(II)+Hem, the redox potential of Fe(II)-Hem was shifted from -0.15 to -0.18 V and that of c-Cyts+Hem changed slightly from -0.05 to -0.04 V. For the bulk hematite, Mott-Schottky plots illustrated that the flat band was shifted negatively and positively in the presence of Fe(II) and oxidized c-Cyts, respectively, and the surface electron/charge density was higher in the presence of Fe(II)/c-Cyts. As a consequence, the redox gradients from adsorbed Fe(II) to adsorbed c-Cyts allow electron transfer across the conduction band of hematite and facilitate c-Cyts reduction. This mechanistic study on conduction band-mediating electron transfer could help interpret the role of semiconducting minerals in the microbial Fe(II) oxidation process under dark anoxic conditions.Cardiac electrophysiology models are among the most mature and well-studied mathematical models of biological systems. This maturity is bringing new challenges as models are being used increasingly to make quantitative rather than qualitative predictions. As such, calibrating the parameters within ion current and action potential (AP) models to experimental data sets is a crucial step in constructing a predictive model. see more This review highlights some of the fundamental concepts in cardiac model calibration and is intended to be readily understood by computational and mathematical modelers working in other fields of biology. We discuss the classic and latest approaches to calibration in the electrophysiology field, at both the ion channel and cellular AP scales. We end with a discussion of the many challenges that work to date has raised and the need for reproducible descriptions of the calibration process to enable models to be recalibrated to new data sets and built upon for new studies. This article is categorized under Analytical and Computational Methods > Computational Methods Physiology > Mammalian Physiology in Health and Disease Models of Systems Properties and Processes > Cellular Models. © 2020 The Authors. WIREs Systems Biology and Medicine published by Wiley Periodicals, Inc.Amiodarone is known to induce hepatic injury in some recipients. We applied an untargeted metabolomics approach to identify endogenous metabolites with potential as biomarkers for amiodarone-induced liver injury. Oral amiodarone administration for 1 week in rats resulted in significant elevation of acylcarnitines and phospholipids in the liver. Hepatic short- and medium-chain acylcarnitines were dramatically increased in a dose-dependent manner, while the serum levels of these acylcarnitines did not change substantially. In addition, glucose levels were significantly increased in both the serum and liver. Gene expression profiling showed that the hepatic mRNA levels of Cpt1, Cpt2, and Acat1 were significantly suppressed, whereas those of Acot1, Acly, Acss2, and Acsl3 were increased. These results suggest that hepatic acylcarnitines and glucose levels might be increased due to disruption of mitochondrial function and suppression of glucose metabolism. Perturbation of energy metabolism might be associated with amiodarone-induced hepatotoxicity. © 2020 John Wiley & Sons, Ltd.BACKGROUND One significant challenge of developing a controller for functional electrical stimulation systems is the time-variant nonlinear dynamics of the neuromusculoskeletal system. In the conventional methods, the stimulation intensity is adjusted by a controller; however, the stimulation frequency is always constant. The previous studies have shown that the stimulation frequency is effective in fatigue formation. OBJECTIVES A simultaneous modulation of the stimulation intensity and frequency is proposed to improve the joint controllability and muscle endurance. The presented control method determines pulse width (PW), amplitude, and frequency of the electrical stimulation signal, synchronously. Three different modulations are applied for control of the knee joint to show the superiority of the proposed modulation. METHODS The stimulation intensity is controlled by the PW and pulse amplitude of the electrical signal using an adaptive fuzzy terminal sliding mode controller and a fuzzy logic controller, resrnational Neuromodulation Society.Acute respiratory infections are amongst the leading causes of childhood morbidity and mortality globally. Viruses are the predominant cause of such infections, but mixed etiologies with bacteria has for decades raised the question of the interplay between them in causality and determination of the outcome of such infections. In this review, we examine recent microbiological, biochemical, and immunological advances that contribute to elucidating the mechanisms by which infections by specific viruses enable bacterial infections in the airway, and exacerbate them. We analyze specific domains in which viruses play such facilitating role including enhancement of bacterial adhesion by unmasking cryptic receptors and upregulation of adhesion proteins, disruption of tight junction integrity favoring paracellular transmigration of bacteria and loss of epithelial barrier integrity, increased availability of nutrient, such as mucins and iron, alteration of innate and adaptive immune responses, and disabling defense against bacteria, and lastly, changes in airway microbiome that render the lung more vulnerable to pathogens.