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The development of small-sized parabolic trough collectors (PTCs) for processing heat production at medium temperatures (100–250 °C) represents an interesting approach to increase the utilization of solar thermal technologies in industrial applications. Thus, the development of simplified models to analyze and predict their performance under different operative and climatic conditions is crucial for evaluating the application potential of this low-cost technology. In this paper, we present a numerical method that by combining three-dimensional finite element simulations (implemented with COMSOL Multiphysics software version 6.1) with a one-dimensional analysis (based on a MATLAB script) allows for the theoretical determination of the power output of a small-PTC with a nonevacuated tubular receiver operating at a medium temperature. The finite element model considers both the nonuniformity of the concentrated solar flux on the receiver tube (evaluated using Monte Carlo ray-tracing analysis) and the establishment of natural convection in the air gap between the glass envelope and absorber tube. The model calculates, for several values of direct normal irradiance (DNI) and inlet temperatures, the thermal power transferred to the heat transfer fluid (HTF) per unit length. The data are fitted using the multiple linear regression method, obtaining a function that is then used in a one-dimensional multi-nodal model to estimate the temperatures and the heat gains along the receiver tube. The outputs of the model are the outlet temperature and the total thermal power transferred to the HTF. In order to validate the developed methodology for the assessment of the heat transfer characteristics in the small-PTC with a nonevacuated receiver, an experiment at the ENEA Trisaia—Solar Thermal Collector Testing Laboratory was carried out. This work compares the theoretical data with those acquired through experimentation, obtaining a good agreement, with maximum differences of 0.2% and 3.6% for the outlet temperatures and the power outputs, respectively.

Background REST (Repressor‐Element 1 [RE1]‐silencing transcription factor) inhibits Na+/Ca2+exchanger‐1 (Ncx1) transcription in neurons through the binding of RE1 site on brain promoter (Br) after stroke. We identified a new putative RE1 site in Ncx1 heart promoter (Ht) sequence (Ht‐RE1) that participates in neuronal Ncx1 transcription. Because REST recruits DNA‐methyltransferase‐1 (DNMT1) and MeCP2 (methyl‐CpG binding protein 2) on different neuronal genes, we investigated the role of this complex in Ncx1 transcriptional regulation after stroke. Methods and Results Luciferase experiments performed in SH‐SY5Y cells demonstrated that Br activity was selectively decreased by REST, whereas Ht activity was reduced by DNMT1, MeCP2, and REST. Notably, site‐direct mutagenesis of Ht‐RE1 prevented REST‐dependent downregulation of Ncx1. Furthermore, in temporoparietal cortex of 8‐week‐old male wild‐type mice (C57BL/6) subjected to transient middle cerebral artery occlusion, DNMT1, MeCP2, and REST binding to Ht promoter was increased, with a consequent DNA promoter hypermethylation. Intracerebroventricular injection of siREST prevented DNMT1/MeCP2 binding to Ht and Ncx1 downregulation, thus causing a reduction in stroke‐induced damage. Consistently, in cortical neurons subjected to oxygen and glucose deprivation plus reoxygenation Ncx1 knockdown counteracted neuronal protection induced by the demethylating agent 5‐azacytidine. For comparisons between 2 experimental groups, Student's t test was used, whereas for more than 2 experimental groups, 1‐way ANOVA was used, followed by Tukey or Newman Keuls. Statistical significance was set at P

Rett syndrome (RTT) is an extremely invalidating, cureless, developmental disorder, and it is considered one of the leading causes of intellectual disability in female individuals. The vast majority of RTT cases are caused by de novo mutations in the X-linked Methyl-CpG binding protein 2 (MECP2) gene, which encodes a multifunctional reader of methylated DNA. MeCP2 is a master epigenetic modulator of gene expression, with a role in the organization of global chromatin architecture. Based on its interaction with multiple molecular partners and the diverse epigenetic scenario, MeCP2 triggers several downstream mechanisms, also influencing the epigenetic context, and thus leading to transcriptional activation or repression. In this frame, it is conceivable that defects in such a multifaceted factor as MeCP2 lead to large-scale alterations of the epigenome, ranging from an unbalanced deposition of epigenetic modifications to a transcriptional alteration of both protein-coding and non-coding genes, with critical consequences on multiple downstream biological processes. In this review, we provide an overview of the current knowledge concerning the transcriptomic and epigenomic alterations found in RTT patients and animal models.

Pericentric heterochromatin (PCH) is a particular form of constitutive heterochromatin that is localized to both sides of centromeres and that forms silent compartments enriched in repressive marks. These genomic regions contain species-specific repetitive satellite DNA that differs in terms of nucleotide sequences and repeat lengths. In spite of this sequence diversity, PCH is involved in many biological phenomena that are conserved among species, including centromere function, the preservation of genome integrity, the suppression of spurious recombination during meiosis, and the organization of genomic silent compartments in the nucleus. PCH organization and maintenance of its repressive state is tightly regulated by a plethora of factors, including enzymes (e.g., DNA methyltransferases, histone deacetylases, and histone methyltransferases), DNA and histone methylation binding factors (e.g., MECP2 and HP1), chromatin remodeling proteins (e.g., ATRX and DAXX), and non-coding RNAs. This evidence helps us to understand how PCH organization is crucial for genome integrity. It then follows that alterations to the molecular signature of PCH might contribute to the onset of many genetic pathologies and to cancer progression. Here, we describe the most recent updates on the molecular mechanisms known to underlie PCH organization and function.

Methyl-CpG binding protein 2 (MeCP2) is a multi-function factor involved in locus-specific transcriptional modulation and the regulation of genome architecture, e.g., pericentric heterochromatin (PCH) organization. MECP2 mutations are responsible for Rett syndrome (RTT), a devastating postnatal neurodevelopmental disorder, the pathogenetic mechanisms of which are still unknown. MeCP2, together with Alpha-thalassemia/mental retardation syndrome X-linked protein (ATRX), accumulates at chromocenters, which are repressive PCH domains. As with MECP2, mutations in ATRX cause ATR-X syndrome which is associated with severe intellectual disability. We exploited two murine embryonic stem cell lines, in which the expression of MeCP2 or ATRX is abolished. Through immunostaining, chromatin immunoprecipitation and western blot, we show that MeCP2 and ATRX are reciprocally dependent both for their expression and targeting to chromocenters. Moreover, ATRX plays a role in the accumulation of members of the heterochromatin protein 1 (HP1) family at PCH and, as MeCP2, modulates their expression. Furthermore, ATRX and HP1 targeting to chromocenters depends on an RNA component. 3D-DNA fluorescence in situ hybridization (FISH) highlighted, for the first time, a contribution of ATRX in MeCP2-mediated chromocenter clustering during neural differentiation. Overall, we provide a detailed dissection of the functional interplay between MeCP2 and ATRX in higher-order PCH organization in neurons. Our findings suggest molecular defects common to RTT and ATR-X syndrome, including an alteration in PCH.