Is something changing? Preliminary results about the impact of the COVID-19 emergency on the Italians attitudes towards the EU.

The COVID-19 outbreak has had a strong impact on several aspects of private and public life all over the country. This article in particular deals with the impact of the pandemic crisis on attitudes towards the European Union. Based on an opinion survey administered after the COVID-19 first wave to a rep-resentative sample of Italians, this article provides preliminary results on whether the health crisis has impacted Italians’ perceptions of EU membership. Findings suggest that one fifth of the respondents changed their minds about the EU in a relatively short time span. Among possible explanations for this shift, party cueing is shown to be the most important factor in transforming public perception of Eu-rope, while the pattern is less clear for the perception of the pandemic risk and the economic outlook

Glucose-6-phosphate tips the balance in modulating apoptosis in cerebellar granule cells

AbstractA metabolic shift from oxidative phosphorylation to glycolysis (i.e. the Warburg effect) occurs in Alzheimer’s disease accompanied by an increase of both activity and level of HK-I. The findings reported here demonstrate that in the early phase of apoptosis VDAC1 activity, but not its protein level, progressively decreases, in concomitance with the physical interaction of HK-I with VDAC1. In the late phase of apoptosis, glucose-6-phosphate accumulation in the cell causes the dissociation of the two proteins, the re-opening of the channel and the recovery of VDAC1 function, resulting in a reawakening of the mitochondrial function, thus inevitably leading to cell death

Bridging tools to better understand environmental performances and raw materials supply of traction batteries in the future EU fleet

Sustainable and smart mobility and associated energy systems are key to decarbonise the EU and develop a clean, resource efficient, circular and carbon-neutral future. To achieve the 2030 and 2050 targets, technological and societal changes are needed. This transition will inevitably change the composition of the future EU fleet, with an increasing share of electric vehicles (xEVs). To assess the potential contribution of lithium-ion traction batteries (LIBs) in decreasing the environmental burdens of EU mobility, several aspects should be included. Even though environmental assessments of batteries along their life-cycle have been already conducted using life-cycle assessment, a single tool does not likely provide a complete overview of such a complex system. Complementary information is provided by material flow analysis and criticality assessment, with emphasis on supply risk. Bridging complementary aspects can better support decision-making, especially when different strategies are simultaneously tackled. The results point out that the future life-cycle GWP of traction LIBs will likely improve, mainly due to more environmental-friendly energy mix and improved recycling. Even though second-use will postpone available materials for recycling, both these end-of-life strategies allow keeping the values of materials in the circular economy, with recycling also contributing to mitigate the supply risk of Lithium and Nickel

A peptide containing residues 26–44 of tau protein impairs mitochondrial oxidative phosphorylation acting at the level of the adenine nucleotide translocator

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Rtg signaling sustains mitochondrial respiratory capacity in hog1-dependent osmoadaptation

Mitochondrial RTG-dependent retrograde signaling, whose regulators have been characterized in Saccharomyces cerevisiae, plays a recognized role under various environmental stresses. Of special significance, the activity of the transcriptional complex Rtg1/3 has been shown to be modu-lated by Hog1, the master regulator of the high osmolarity glycerol pathway, in response to osmotic stress. The present work focuses on the role of RTG signaling in salt-induced osmotic stress and its interaction with HOG1. Wild-type and mutant cells, lacking HOG1 and/or RTG genes, are compared with respect to cell growth features, retrograde signaling activation and mitochondrial function in the presence and in the absence of high osmostress. We show that RTG2, the main upstream regulator of the RTG pathway, contributes to osmoadaptation in an HOG1-dependent manner and that, with RTG3, it is notably involved in a late phase of growth. Our data demonstrate that impairment of RTG signaling causes a decrease in mitochondrial respiratory capacity exclusively under os-mostress. Overall, these results suggest that HOG1 and the RTG pathway may interact sequentially in the stress signaling cascade and that the RTG pathway may play a role in inter-organellar metabolic communication for osmoadaptation

Ternary Quarter Wavelength Coatings for Gravitational Wave Detector Mirrors: Design Optimization via Exhaustive Search

Multimaterial optical coatings are a promising viable option to meet the challenging requirements (in terms of transmittance, absorbance and thermal noise) of next generation gravitational wave detector mirrors. In this paper we focus on ternary coatings consisting of quarter-wavelength thick layers, where a third material (H') is added to the two presently in use, namely Silica (L) and Titania-doped Tantala (H), featuring higher dielectric contrast (against Silica), and lower thermal noise (compared to Titania-doped Tantala), but higher optical losses. We seek the optimal material sequences, featuring minimal thermal (Brownian) noise under prescribed transmittance and absorbance constraints, by exhaustive simulation over all possible configurations, for different values (in a meaningful range) of the optical density and extinction coefficient of the third material. In all cases studied, the optimal designs consist of a stack of (H'|L) doublets topped by a stack of (H|L) doublets, confirming previous heuristic assumptions, and the achievable coating noise power spectral density reduction factor is \sim 0.5. The robustness of the found optimal designs against layer thickness deposition errors and uncertainties and/or fluctuations in the optical losses of the third material is also investigated. Possible margins for further thermal noise reduction by layer thickness optimization, and strategies to implement it, are discussed.Comment: (twocolum style) 13 pages, 8 figures, 4 table (updated version 5) Appearing on Physical Review Researc

NH2-truncated human tau induces deregulated mitophagy in neurons by aberrant recruitment of Parkin and UCHL-1: implications in Alzheimer's disease.

Disarrangement in functions and quality control of mitochondria at synapses are early events in Alzheimer's disease (AD) pathobiology. We reported that a 20-22 kDa NH2-tau fragment mapping between 26 and 230 amino acids of the longest human tau isoform (aka NH2htau): (i) is detectable in cellular and animal AD models, as well in synaptic mitochondria and cerebrospinal fluids (CSF) from human AD subjects; (ii) is neurotoxic in primary hippocampal neurons; (iii) compromises the mitochondrial biology both directly, by inhibiting the ANT-1-dependent ADP/ATP exchange, and indirectly, by impairing their selective autophagic clearance (mitophagy). Here, we show that the extensive Parkin-dependent turnover of mitochondria occurring in NH2htau-expressing post-mitotic neurons plays a pro-death role and that UCHL-1, the cytosolic Ubiquitin-C-terminal hydrolase L1 which directs the physiological remodeling of synapses by controlling ubiquitin homeostasis, critically contributes to mitochondrial and synaptic failure in this in vitro AD model. Pharmacological or genetic suppression of improper mitophagy, either by inhibition of mitochondrial targeting to autophagosomes or by shRNA-mediated silencing of Parkin or UCHL-1 gene expression, restores synaptic and mitochondrial content providing partial but significant protection against the NH2htau-induced neuronal death. Moreover, in mitochondria from human AD synapses, the endogenous NH2htau is stably associated with Parkin and with UCHL-1. Taken together, our studies show a causative link between the excessive mitochondrial turnover and the NH2htau-induced in vitro neuronal death, suggesting that pathogenetic tau truncation may contribute to synaptic deterioration in AD by aberrant recruitment of Parkin and UCHL-1 to mitochondria making them more prone to detrimental autophagic clearance