A Systematic Review and Meta-Analysis of Symptoms of Anxiety, Depression, and Insomnia in Spain in the COVID-19 Crisis.

BACKGROUND: General population, frontline healthcare workers (HCWs), and adult students in Spain are at risk of anxiety, depression, and insomnia symptoms during the COVID-19 crisis. A meta-analysis of the individual studies on these symptoms would provide systematic evidence to aid policymakers and researchers in focusing on prevalence, risk, and best interventions. OBJECTIVE: This paper aims to be the first meta-analysis and systematic review to calculate the prevalence of anxiety, depression, and insomnia symptoms in Spain's adult population (general population, frontline healthcare workers (HCWs), and adult students) during the Covid-19 epidemic. METHOD: Random-effect meta-analysis was used to estimate the prevalence of anxiety, depression, and insomnia. RESULTS: The meta-analysis includes 28 studies with 38 individual samples in Spain. The pooled prevalence of anxiety symptoms in 22 studies comprising a sample population of 82,024 was 20% (95% CI: 15-25%), that of depression symptoms in 22 articles with a total sample comprising 82,890 individuals was 22% (95% CI: 18-28%), and that of insomnia symptoms in three articles with a sample population of 745 was 57% (95% CI: 48-66%. CONCLUSIONS: The accumulative evidence reveals that adults in Spain suffered higher prevalence rates of mental symptoms during the COVID-19 crisis, with a significantly higher rate relative to other countries such as China. Our synthesis also reveals a relative lack of studies on frontline and general HCWs in Spain

Mental Health during the COVID-19 Crisis in Africa: A Systematic Review and Meta-Analysis.

We aim to provide a systematic review and meta-analysis of the prevalence rates of mental health symptoms among major African populations during the COVID-19 pandemic. We include articles from PubMed, Embase, Web of Science, PsycINFO, and medRxiv between 1 February 2020 and 6 February 2021, and pooled data using random-effects meta-analyses. We identify 28 studies and 32 independent samples from 12 African countries with a total of 15,071 participants. The pooled prevalence of anxiety was 37% in 27 studies, of depression was 45% in 24 studies, and of insomnia was 28% in 9 studies. The pooled prevalence rates of anxiety, depression, and insomnia in North Africa (44%, 55%, and 31%, respectively) are higher than those in Sub-Saharan Africa (31%, 30%, and 24%, respectively). We find (a) a scarcity of studies in several African countries with a high number of COVID-19 cases; (b) high heterogeneity among the studies; (c) the extent and pattern of prevalence of mental health symptoms in Africa is high and differs from elsewhere-more African adults suffer from depression rather than anxiety and insomnia during COVID 19 compared to adult populations in other countries/regions. Hence, our findings carry crucial implications and impact future research to enable evidence-based medicine in Africa

Mental disorder symptoms during the COVID-19 pandemic in Latin America - a systematic review and meta-analysis.

AIMS: There is a lack of evidence related to the prevalence of mental health symptoms as well as their heterogeneities during the coronavirus disease 2019 (COVID-19) pandemic in Latin America, a large area spanning the equator. The current study aims to provide meta-analytical evidence on mental health symptoms during COVID-19 among frontline healthcare workers, general healthcare workers, the general population and university students in Latin America. METHODS: Bibliographical databases, such as PubMed, Embase, Web of Science, PsycINFO and medRxiv, were systematically searched to identify pertinent studies up to August 13, 2021. Two coders performed the screening using predefined eligibility criteria. Studies were assigned quality scores using the Mixed Methods Appraisal Tool. The double data extraction method was used to minimise data entry errors. RESULTS: A total of 62 studies with 196 950 participants in Latin America were identified. The pooled prevalence of anxiety, depression, distress and insomnia was 35%, 35%, 32% and 35%, respectively. There was a higher prevalence of mental health symptoms in South America compared to Central America (36% v. 28%, p < 0.001), in countries speaking Portuguese (40%) v. Spanish (30%). The pooled prevalence of mental health symptoms in the general population, general healthcare workers, frontline healthcare workers and students in Latin America was 37%, 34%, 33% and 45%, respectively. CONCLUSIONS: The high yet heterogenous level of prevalence of mental health symptoms emphasises the need for appropriate identification of psychological interventions in Latin America

Isogenic Pairs of Wild Type and Mutant Induced Pluripotent Stem Cell (iPSC) Lines from Rett Syndrome Patients as In Vitro Disease Model

Rett syndrome (RTT) is an autism spectrum developmental disorder caused by mutations in the X-linked methyl-CpG binding protein 2 (MECP2) gene. Excellent RTT mouse models have been created to study the disease mechanisms, leading to many important findings with potential therapeutic implications. These include the identification of many MeCP2 target genes, better understanding of the neurobiological consequences of the loss- or mis-function of MeCP2, and drug testing in RTT mice and clinical trials in human RTT patients. However, because of potential differences in the underlying biology between humans and common research animals, there is a need to establish cell culture-based human models for studying disease mechanisms to validate and expand the knowledge acquired in animal models. Taking advantage of the nonrandom pattern of X chromosome inactivation in female induced pluripotent stem cells (iPSC), we have generated isogenic pairs of wild type and mutant iPSC lines from several female RTT patients with common and rare RTT mutations. R294X (arginine 294 to stop codon) is a common mutation carried by 5–6% of RTT patients. iPSCs carrying the R294X mutation has not been studied. We differentiated three R294X iPSC lines and their isogenic wild type control iPSC into neurons with high efficiency and consistency, and observed characteristic RTT pathology in R294X neurons. These isogenic iPSC lines provide unique resources to the RTT research community for studying disease pathology, screening for novel drugs, and testing toxicology

Dispersive, superfluid-like shock waves in nonlinear optics

In most classical fluids, shock waves are strongly dissipative, their energy being quickly lost through viscous damping. But in systems such as cold plasmas, superfluids, and Bose-Einstein condensates, where viscosity is negligible or non-existent, a fundamentally different type of shock wave can emerge whose behaviour is dominated by dispersion rather than dissipation. Dispersive shock waves are difficult to study experimentally, and analytical solutions to the equations that govern them have only been found in one dimension (1D). By exploiting a well-known, but little appreciated, correspondence between the behaviour of superfluids and nonlinear optical materials, we demonstrate an all-optical experimental platform for studying the dynamics of dispersive shock waves. This enables us to observe the propagation and nonlinear response of dispersive shock waves, including the interaction of colliding shock waves, in 1D and 2D. Our system offers a versatile and more accessible means for exploring superfluid-like and related dispersive phenomena.Comment: 21 pages, 6 figures Revised abstrac

Assessment of contractility in intact ventricular cardiomyocytes using the dimensionless ‘Frank–Starling Gain’ index

This paper briefly recapitulates the Frank–Starling law of the heart, reviews approaches to establishing diastolic and systolic force–length behaviour in intact isolated cardiomyocytes, and introduces a dimensionless index called ‘Frank–Starling Gain’, calculated as the ratio of slopes of end-systolic and end-diastolic force–length relations. The benefits and limitations of this index are illustrated on the example of regional differences in Guinea pig intact ventricular cardiomyocyte mechanics. Potential applicability of the Frank–Starling Gain for the comparison of cell contractility changes upon stretch will be discussed in the context of intra- and inter-individual variability of cardiomyocyte properties

Role of MeCP2, DNA methylation, and HDACs in regulating synapse function

Over the past several years there has been intense effort to delineate the role of epigenetic factors, including methyl-CpG-binding protein 2, histone deacetylases, and DNA methyltransferases, in synaptic function. Studies from our group as well as others have shown that these key epigenetic mechanisms are critical regulators of synapse formation, maturation, as well as function. Although most studies have identified selective deficits in excitatory neurotransmission, the latest work has also uncovered deficits in inhibitory neurotransmission as well. Despite the rapid pace of advances, the exact synaptic mechanisms and gene targets that mediate these effects on neurotransmission remain unclear. Nevertheless, these findings not only open new avenues for understanding neuronal circuit abnormalities associated with neurodevelopmental disorders but also elucidate potential targets for addressing the pathophysiology of several intractable neuropsychiatric disorders

Comparative Proteomics Analysis of the Root Apoplasts of Rice Seedlings in Response to Hydrogen Peroxide

-responsive proteins in the apoplast of rice seedling roots. stress. response

Cerebellar gene expression profiles of mouse models for Rett syndrome reveal novel MeCP2 targets

<p>Abstract</p> <p>Background</p> <p>MeCP2, methyl-CpG-binding protein 2, binds to methylated cytosines at CpG dinucleotides, as well as to unmethylated DNA, and affects chromatin condensation. <it>MECP2 </it>mutations in females lead to Rett syndrome, a neurological disorder characterized by developmental stagnation and regression, loss of purposeful hand movements and speech, stereotypic hand movements, deceleration of brain growth, autonomic dysfunction and seizures. Most mutations occur <it>de novo </it>during spermatogenesis. Located at Xq28, <it>MECP2 </it>is subject to X inactivation, and affected females are mosaic. Rare hemizygous males suffer from a severe congenital encephalopathy.</p> <p>Methods</p> <p>To identify the pathways mis-regulated by MeCP2 deficiency, microarray-based global gene expression studies were carried out in cerebellum of <it>Mecp2 </it>mutant mice. We compared transcript levels in mutant/wildtype male sibs of two different MeCP2-deficient mouse models at 2, 4 and 8 weeks of age. Increased transcript levels were evaluated by real-time quantitative RT-PCR. Chromatin immunoprecipitation assays were used to document <it>in vivo </it>MeCP2 binding to promoter regions of candidate target genes.</p> <p>Results</p> <p>Of several hundred genes with altered expression levels in the mutants, twice as many were increased than decreased, and only 27 were differentially expressed at more than one time point. The number of misregulated genes was 30% lower in mice with the exon 3 deletion (<it>Mecp2</it>^tm1.1Jae) than in mice with the larger deletion (<it>Mecp2</it>^tm1.1Bird). Between the mutants, few genes overlapped at each time point. Real-time quantitative RT-PCR assays validated increased transcript levels for four genes: <it>Irak1</it>, interleukin-1 receptor-associated kinase 1; <it>Fxyd1</it>, phospholemman, associated with Na, K-ATPase;<it>Reln</it>, encoding an extracellular signaling molecule essential for neuronal lamination and synaptic plasticity; and <it>Gtl2/Meg3</it>, an imprinted maternally expressed non-translated RNA that serves as a host gene for C/D box snoRNAs and microRNAs. Chromatin immunoprecipitation assays documented <it>in vivo </it>MeCP2 binding to promoter regions of <it>Fxyd1, Reln</it>, and <it>Gtl2</it>.</p> <p>Conclusion</p> <p>Transcriptional profiling of cerebellum failed to detect significant global changes in <it>Mecp2</it>-mutant mice. Increased transcript levels of <it>Irak1, Fxyd1, Reln</it>, and <it>Gtl2 </it>may contribute to the neuronal dysfunction in MeCP2-deficient mice and individuals with Rett syndrome. Our data provide testable hypotheses for future studies of the regulatory or signaling pathways that these genes act on.</p