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Nowadays, Coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is one of the most important health problems. The dynamics and nature of humoral responses are relevant to determine the efficacy of both, diagnostic tests and developed vaccines. Since the role of IgA in the COVID-19 disease is not fully understood, we have systematically reviewed the scientific literature on antibody IgA immunity to SARS-CoV-2 to determine if IgA could be useful as a diagnostic tool or as a biomarker of severity. We systematically reviewed 736 abstracts and identified 38 manuscripts relevant to include in the meta-analysis. The seroprevalence of IgA in SARS-CoV-2 PCR (+) confirmed patients was 86.47% (CI: 5.27-178.21). Furthermore, we found out that IgA can be produced on the first days of infection (10 days) and IgA is detected until 75 days after symptomatic onset in some studies. We also observe that IgA production is stronger in severe patients compared with mild or asymptomatic patients. Our research noticed a possible association between IgA and protection; however, the possible role of IgA as a biomarker of protection or severity remains unclear.

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Materials that have hysteretic response to an external field are essential in modern information storage and processing technologies. A myriad of magnetization curves of several natural and artificial materials have previously been measured and each has found a particular mechanism that accounts for it. However, a phenomenological model that captures all the hysteresis loops and at the same time provides a simple way to design the magnetic response of a material while remaining minimal is missing. Here, we propose and experimentally demonstrate an elementary method to engineer hysteresis loops in metamaterials built out of dipolar chains. We show that by tuning the interactions of the system and its geometry we can shape the hysteresis loop which allows for the design of the softness of a magnetic material at will. Additionally, this mechanism allows for the control of the number of loops aimed to realize multiple-valued logic technologies. Our findings pave the way for the rational design of hysteretical responses in a variety of physical systems such as dipolar cold atoms, ferroelectrics, or artificial magnetic lattices, among others.

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INTRODUCTION: Calcium (Ca2+) leak during cardiac diastole is chiefly mediated by intracellular Ca2+ channel/Ryanodine Receptors. Increased diastolic Ca2+ leak has been proposed as the mechanism underlying the appearance of hereditary arrhythmias. However, little is known about alterations in diastolic Ca2+ leak and the specific roles played by key intracellular Ca2+-handling proteins in hyperthyroidism, a known arrhythmogenic condition. AIM: We sought to determine whether there were modifications in diastolic Ca2+ leak, based on the recording of Ca2+ sparks and Ca2+ waves; we also investigated changes in the expression and activity of key Ca2+ handling proteins, including ryanodine receptors, Sarco-Endoplasmic Reticulum Ca2+ ATPase pump and calsequestrin in isolated left-ventricular cardiomyocytes isolated from hyperthyroid rats. MATERIALS AND METHODS: Electrocardiography (ECG) recordings were performed in control and hyperthyroid rats. Ca2+ sparks, Ca2+ waves, and electrically-stimulated Ca2+ transients were recorded in Fluo-3-loaded cardiomyocytes from both experimental groups using confocal microscopy. In addition, left-ventricular homogenates and Ryanodine Receptor-enriched membrane fractions were prepared for assessing [3H]-ryanodine binding, hydrolytic ATPase activity of SERCA pump and expression levels of key proteins by Western blot, and cDNA for real-time qPCR. RESULTS AND CONCLUSIONS: Extrasystoles were observed in hearts of hyperthyroid rats by ECG recordings. Arrhythmogenic activity, high incidence of Ca2+ waves, and de novo Ca2+ wavelets -in the absence of sarcoplasmic reticulum Ca2+ overload- were recorded in these cardiomyocytes. The exacerbated diastolic Ca2+ leak and arrhythmogenic activities were related to a diminished expression of calsequestrin along with increased SERCA pump activity, which, in effect, promoted a gain-of-function in RyRs without alterations in SR Ca2+ load, RyR expression or its Ca2+ sensitivity.

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La participación del canal de Ca2+/receptor de rianodina en el acoplamiento excitación-contracción cardiaco se conoce desde finales de los años ochenta, cuando en varios trabajos trascendentales se comunicó por primera vez su purificación y se encontró que correspondía a las estructuras conocidas como «pies¼ localizadas en las cisternas terminales del retículo sarcoplásmico. Adicionalmente a su papel como canal responsable del aumento global y transitorio de Ca2+ que activa a la maquinaria contráctil durante el ciclo cardiaco, el receptor de rianodina también libera Ca2+ durante la fase de relajación, dando lugar a la fuga de Ca2+ en la diástole que en condiciones fisiológicas regula el nivel de Ca2+ luminal, pero cuando se encuentra alterada participa en la generación de arritmias adquiridas o hereditarias. Recientemente, el esfuerzo de diversos grupos de investigación se ha enfocado en el desarrollo de herramientas farmacológicas para controlar la fuga diastólica de Ca2+ que se presenta alterada en algunas enfermedades cardiacas. En esta revisión nos enfocamos en describir la participación del receptor de rianodina cardiaco en la fuga diastólica de Ca2+ así como los diversos enfoques terapéuticos que se han implementado para controlar su actividad exacerbada en la diástole.

The participation of the ionic Ca2+ release channel/ryanodine receptor in cardiac excitation-contraction coupling is well known since the late '80s, when various seminal papers communicated its purification for the first time and its identity with the "foot" structures located at the terminal cisternae of the sarcoplasmic reticulum. In addition to its main role as the Ca2+ channel responsible for the transient Ca2+ increase that activates the contractile machinery of the cardiomyocytes, the ryanodine receptor releases Ca2+ during the relaxation phase of the cardiac cycle, giving rise to a diastolic Ca2+ leak. In normal physiological conditions, diastolic Ca2+ leak regulates the proper level of luminal Ca2+, but in pathological conditions it participates in the generation of both, acquired and hereditary arrhythmias. Very recently, several groups have focused their efforts into the development of pharmacological tools to control the altered diastolic Ca2+ leak via ryanodine receptors. In this review, we focus our interest on describing the participation of cardiac ryanodine receptor in the diastolic Ca2+ leak under physiological or pathological conditions and also on the therapeutic approaches to control its undesired exacerbated activity during diastole.

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The participation of the ionic Ca(2+) release channel/ryanodine receptor in cardiac excitation-contraction coupling is well known since the late '80s, when various seminal papers communicated its purification for the first time and its identity with the "foot" structures located at the terminal cisternae of the sarcoplasmic reticulum. In addition to its main role as the Ca(2+) channel responsible for the transient Ca(2+) increase that activates the contractile machinery of the cardiomyocytes, the ryanodine receptor releases Ca(2+) during the relaxation phase of the cardiac cycle, giving rise to a diastolic Ca(2+) leak. In normal physiological conditions, diastolic Ca(2+) leak regulates the proper level of luminal Ca(2+), but in pathological conditions it participates in the generation of both, acquired and hereditary arrhythmias. Very recently, several groups have focused their efforts into the development of pharmacological tools to control the altered diastolic Ca(2+) leak via ryanodine receptors. In this review, we focus our interest on describing the participation of cardiac ryanodine receptor in the diastolic Ca(2+) leak under physiological or pathological conditions and also on the therapeutic approaches to control its undesired exacerbated activity during diastole.

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