Optical characterization of lead-free Cs2SnI6 double Perovskite Fabricated from degraded and reconstructed CsSnI3 films

Halide perovskites have experienced a huge development in the past years, but they still have two major challenges for their massive implantation: the long-term stability and the use of lead. One of the most obvious lead-free candidates to replace these perovskites is CsSnI3, but due to its poor environmental stability, it has been discarded for the fabrication of stable devices. Nevertheless, ambient degradation of CsSnI3 and ulterior reconstruction produce a relatively stable lead-free Cs2SnI6 double perovskite with interesting optical properties that have not been deeply characterized previously. In this work, the potential use for the optical properties of Cs2SnI6 is studied and compared with that of the most common halide perovskite, CH3NH3PbI3 (MAPbI3). The Cs2SnI6 films stayed in a standard atmosphere for a week without showing any signs of degradation. They also demonstrated better reflective behavior than MAPbI3 and higher absorption in the 650 and 730 nm spectral range, making this material interesting for the development of photodetectors in this region. This study demonstrates that Cs2SnI6 is a promising material for photodevices, as it highlights its main characteristics and optical parameters, giving an original view on the use of the double perovskite, but at the same time emphasizing the need to improve the electrical properties for the development of efficient optoelectronic devices.E.L.-F. wants to express his gratitude to the Ministerio de Educación y Formación Profesional for his doctoral grant (FPU research fellowship FPU17/00612) and his research stay grant (EST18/00399). This work was partially supported by the European Research Council (ERC) via Consolidator Grant (724424-No-LIMIT) and the European Commission via FET Open Grant (862656 - DROP-IT). We acknowledge SCIC from Jaume I University (UJI) for help with XRD and SEM-EDS characterization

Reduced Myofilament Contraction in Human Heart Failure. Insights From Electromechanical Simulations

[EN] Intracellular Ca2+ is the main activator of myofilament contraction and the altered Ca2+ handling observed in failing cells has been established as the leading cause of reduced inotropy in heart failure. Electrophysiological studies usually quantify Ca2+ transients to estimate contractile effects. However, heart failure remodeling of myofilaments also occurs, modifying the correlation between Ca2+ and force. The aim of this study was to analyze myofilament tension generated by action potentials in human heart failure. In a ventricular electromechanical model we investigated cellular contraction force associated with intracellular Ca2+ in heart failure by implementing the characteristic electrophysiological, beta-adrenergic, and mechanical changes. Despite the inotropic myofilament remodeling induced by heartfailure, the maximal active tension in failing cells was one third of the force generated in normal cells. With isoproterenol, beta-adrenergic stimulation increased systolic Ca2+, which enhanced myofilament tension by up to 150%, but failing cells also showed a smaller contraction force compared to normal. We observed that contractility was very sensitive to changes in intracellular Ca2+, confirming that increasing Ca2+ peak would improve contraction in heart failure.This work was partially supported by the "Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020" from the Ministerio de Ciencia e Innovación y Universidades (PID2019-104356RB-C41/AEI/10.13039/501100011033) and by the Dirección general de PolíticaCientífica de la Generalitat Valenciana (PROMETEO/2020/043). MTM is being funded by "Programa de Ayudas de Investigación y Desarrollo (PAID-01-17)" from the Universitat Politècnica de ValènciaMora-Fenoll, MT.; Gutiérrez, S.; Dasi, A.; Gómez García, JF.; Trenor Gomis, BA. (2020). Reduced Myofilament Contraction in Human Heart Failure. Insights From Electromechanical Simulations. IEEE. 1-4. https://doi.org/10.22489/CinC.2020.056S1