Does regional development explain international youth mobility? Spatial patterns and global/local determinants of the recent emigration of young Italians

In this essay, we tackle the issue of the international mobility of young Italians in relation to regional disparities. Our intention is to determine if and to what extent a relationship exists between regional development and the international mobility of young people. We analyze the international migration of Italian citizens aged 15-34 who left the country in the period 2010-2017 using several variables that reflect the varying conditions found in different NUTS 3-level regions in terms of economic dynamism, labor-market efficiency, social fragility, educational underdevelopment and spatial peripherality. Ordinary Least Squares (OLS) and Geographically Weighted Regression (GWR) models show that the international mobility of young Italians is very much dependent on local conditions and affected by spatial differences. It is greatest in the most economically dynamic areas of the country, in border regions and in metropolitan areas, with factors relating to spatial proximity and peripherality, imbalances in local labor markets, and paucity of human capital proving particularly significant

Electromagnetic Fields, Oxidative Stress, and Neurodegeneration

Electromagnetic fields (EMFs) originating both from both natural and manmade sources permeate our environment. As people are continuously exposed to EMFs in everyday life, it is a matter of great debate whether they can be harmful to human health. On the basis of two decades of epidemiological studies, an increased risk for childhood leukemia associated with Extremely Low Frequency fields has been consistently assessed, inducing the International Agency for Research on Cancer to insert them in the 2B section of carcinogens in 2001. EMFs interaction with biological systems may cause oxidative stress under certain circumstances. Since free radicals are essential for brain physiological processes and pathological degeneration, research focusing on the possible influence of the EMFs-driven oxidative stress is still in progress, especially in the light of recent studies suggesting that EMFs may contribute to the etiology of neurodegenerative disorders. This review synthesizes the emerging evidences about this topic, highlighting the wide data uncertainty that still characterizes the EMFs effect on oxidative stress modulation, as both pro-oxidant and neuroprotective effects have been documented. Care should be taken to avoid methodological limitations and to determine the patho-physiological relevance of any alteration found in EMFs-exposed biological system

Does regional development explain international youth mobility?

In this essay, we tackle the issue of the international mobility of young Italians in relation to regional disparities. Our intention is to determine if and to what extent a relationship exists between regional development and the international mobility of young people. We analyze the international migration of Italian citizens aged 15-34 who left the country in the period 2010-2017 using several variables that reflect the varying conditions found in different NUTS 3-level regions in terms of economic dynamism, labor-market efficiency, social fragility, educational underdevelopment and spatial peripherality.Ordinary Least Squares (OLS) and Geographically Weighted Regression (GWR) models show that the international mobility of young Italians is very much dependent on local conditions and affected by spatial differences. It is greatest in the most economically dynamic areas of the country, in border regions and in metropolitan areas, with factors relating to spatial proximity and peripherality, imbalances in local labor markets, and paucity of human capital proving particularly significant.Dans cet article, nous abordons la question de la mobilité internationale des jeunes Italiens par rapport aux disparités régionales. Notre intention est de déterminer si et dans quelle mesure une relation existe entre le développement régional et la mobilité internationale des jeunes. Nous analysons la migration internationale des citoyens italiens âgés de 15 à 34 ans qui ont quitté le pays entre 2010 et 2017 en utilisant plusieurs variables reflétant les différents niveaux de dynamisme économique, efficience du marché du travail, fragilité sociale, retard culturel et périphéricité spatiale des zones NUTS 3.Les modèles de moindres carrés ordinaires (OLS) et de régression pondérée géographique (GWR) montrent que la mobilité internationale des jeunes Italiens est un phénomène très dépendant des conditions locales et affecté par les différences spatiales. Elle est intense dans les zones les plus dynamiques du pays, dans les régions transfrontalières et dans les agglomérations métropolitaines. Les facteurs les plus importants sont liés à la proximité spatiale et à la périphéricité, aux déséquilibres des marchés locaux du travail et au retard en termes de dotation en capital humain

Inhibition of c-Myc Oncoprotein Limits the Growth of Human Melanoma Cells by Inducing Cellular Crisis

Abstract Here, we show that inhibition of c-Myc causes a proliferative arrest of M14 melanoma cells through cellular crisis, evident by the increase in size, multiple nuclei, vacuolated cytoplasm, induction of senescence-associated β-galactosidase activity and massive apoptosis. The c-Myc-induced crisis is associated with decreased human telomerase reverse transcriptase expression, telomerase activity, progressive telomere shortening, glutathione (GSH), depletion and, increased production of reactive oxygen species. Treatment of control cells with l-buthionine sulfoximine decreases GSH to levels of c-Myc low expressing cells, but it does not modify the growth kinetic of the cells. Surprisingly, when GSH is increased in the c-Myc low expressing cells by treatment with N-acetyl-l-cysteine, cells escape crisis. To test the hypothesis that both oxidative stress and telomerase dysfunction are involved in the c-Myc-dependent crisis, we directly inhibited telomerase function and glutathione levels. Inactivation of telomerase, by expression of a catalytically inactive, dominant negative form of reverse transcriptase, reduces cellular lifespan by inducing telomere shortening. Treatment of cells with l-buthionine sulfoximine decreases GSH content and accelerates cell crisis. Analysis of telomere status demonstrated that oxidative stress affects c-Myc-induced crisis by increasing telomere dysfunction. Our results demonstrate that inhibition of c-Myc oncoprotein induces cellular crisis through cooperation between telomerase dysfunction and oxidative stress

Modulation of LDL receptor expression and promoter methylation in HepG2 cells treated with a Corylus avellana L. extract

Abstract The aim of our study was to evaluate the impact of an ethanolic extract of C. avellana on the molecular pathway(s) regulating the low-density lipoprotein receptor (LDLR) in HepG2 cells, mainly in terms of epigenetics. We demonstrated that viability, proliferation and cell cycle distribution were not affected up to 72 h of treatment, whereas LDLR expression was stimulated as early as 24 h following administration (

On the reconstruction of planar lattice-convex sets from the covariogram

A finite subset $K$ of $\mathbb{Z}^d$ is said to be lattice-convex if $K$ is the intersection of $\mathbb{Z}^d$ with a convex set. The covariogram $g_K$ of $K\subseteq \mathbb{Z}^d$ is the function associating to each u \in \integer^d the cardinality of $K\cap (K+u)$. Daurat, G\'erard, and Nivat and independently Gardner, Gronchi, and Zong raised the problem on the reconstruction of lattice-convex sets $K$ from $g_K$. We provide a partial positive answer to this problem by showing that for $d=2$ and under mild extra assumptions, $g_K$ determines $K$ up to translations and reflections. As a complement to the theorem on reconstruction we also extend the known counterexamples (i.e., planar lattice-convex sets which are not reconstructible, up to translations and reflections) to an infinite family of counterexamples.Comment: accepted in Discrete and Computational Geometr

Redox activation of ATM enhances GSNOR translation to sustain mitophagy and tolerance to oxidative stress

The denitrosylase S-nitrosoglutathione reductase (GSNOR) has been suggested to sustain mitochondrial removal by autophagy (mitophagy), functionally linking S-nitrosylation to cell senescence and aging. In this study, we provide evidence that GSNOR is induced at the translational level in response to hydrogen peroxide and mitochondrial ROS. The use of selective pharmacological inhibitors and siRNA demonstrates that GSNOR induction is an event downstream of the redox-mediated activation of ATM, which in turn phosphorylates and activates CHK2 and p53 as intermediate players of this signaling cascade. The modulation of ATM/GSNOR axis, or the expression of a redox-insensitive ATM mutant influences cell sensitivity to nitrosative and oxidative stress, impairs mitophagy and affects cell survival. Remarkably, this interplay modulates T-cell activation, supporting the conclusion that GSNOR is a key molecular effector of the antioxidant function of ATM and providing new clues to comprehend the pleiotropic effects of ATM in the context of immune function

Association between air pollution and ventricular arrhythmias in high-risk patients (ARIA study): a multicentre longitudinal study

Summary Background Although the effects of air pollution on mortality have been clearly shown in many epidemiological and observational studies, the pro-arrhythmic effects remain unknown. We aimed to assess the short-term effects of air pollution on ventricular arrhythmias in a population of high-risk patients with implantable cardioverter-defibrillators (ICDs) or cardiac resynchronisation therapy defibrillators (ICD-CRT). Methods In this prospective multicentre study, we assessed 281 patients (median age 71 years) across nine centres in the Veneto region of Italy. Episodes of ventricular tachycardia and ventricular fibrillation that were recorded by the diagnostic device were considered in this analysis. Concentrations of particulate matter of less than 10 μm (PM 10 ) and less than 2·5 μm (PM 2·5 ) in aerodynamic diameter, carbon monoxide, nitrogen dioxide, sulphur dioxide, and ozone were obtained daily from monitoring stations, and the 24 h median value was considered. Each patient was associated with exposure data from the monitoring station that was closest to their residence. Patients were followed up for 1 year and then scheduled to have a closing visit, within 1 more year. This study is registered with ClinicalTrials.gov, number NCT01723761. Findings Participants were enrolled from April 1, 2011, to Sept 30, 2012, and follow-ups (completed on April 5, 2014) ranged from 637 to 1177 days (median 652 days). The incidence of episodes of ventricular tachycardia and ventricular fibrillation correlated significantly with PM 2·5 (p 10 . An analysis of ventricular fibrillation episodes alone showed a significant increase in risk of higher PM 2·5 (p=0·002) and PM 10 values (p=0·0057). None of the gaseous pollutants were significantly linked to the occurrence of ventricular tachycardia or ventricular fibrillation. In a subgroup analysis of patients with or without a previous myocardial infarction, only the first showed a significant association between particulate matter and episodes of ventricular tachycardia or ventricular fibrillation. Interpretation Particulate matter has acute pro-arrhythmic effects in a population of high-risk patients, which increase on exposure to fine particles and in patients who have experienced a previous myocardial infarction. The time sequence of the arrhythmic events suggests there is an underlying neurally mediated mechanism. From a clinical point of view, the results of our study should encourage physicians to also consider environmental risk when addressing the prevention of arrhythmic events, particularly in patients with coronary heart disease, advising them to avoid exposure to high levels of fine particulate matter. Funding There was no funding source for this study

Glutathione influences c-Myc-induced apoptosis in M14 human melanoma cells

The objective of this article is to dissect the mechanisms by which the down-regulation of c-Myc induces programmed cell death in melanoma cells. In stable and doxycycline-inducible M14 melanoma cells, down-regulation of c-Myc induced apoptosis subsequent to a decrease in the intracellular reduced glutathione content and a concomitant accumulation of its oxidized form. This redox alteration was associated with a decrease of the enzyme activities of γ-glutamyl-cysteine synthetase and NADPH-dependent GSSG reductase, as well as a consequent glutathione release in the extracellular medium. Cytochrome c was released into the cytosol at very early stages of apoptosis induction, long before detectable production of reactive oxygen species and activation of caspase-9 and -3. Macroarray analysis revealed that down-regulation of c-Myc produced striking changes in gene expression in the section related to metabolism, where the expression of γ-glutamyl-cysteine synthetase and GSSG reductase was found to be significantly reduced. The addition of N-acetyl-L-cysteine or glutathione ethyl ester inhibited the apoptotic process, thus confirming the key role of glutathione in programmed cell death induced by c-Myc

High Risk of Secondary Infections Following Thrombotic Complications in Patients With COVID-19

Background. This study’s primary aim was to evaluate the impact of thrombotic complications on the development of secondary infections. The secondary aim was to compare the etiology of secondary infections in patients with and without thrombotic complications. Methods. This was a cohort study (NCT04318366) of coronavirus disease 2019 (COVID-19) patients hospitalized at IRCCS San Raffaele Hospital between February 25 and June 30, 2020. Incidence rates (IRs) were calculated by univariable Poisson regression as the number of cases per 1000 person-days of follow-up (PDFU) with 95% confidence intervals. The cumulative incidence functions of secondary infections according to thrombotic complications were compared with Gray’s method accounting for competing risk of death. A multivariable Fine-Gray model was applied to assess factors associated with risk of secondary infections. Results. Overall, 109/904 patients had 176 secondary infections (IR, 10.0; 95% CI, 8.8–11.5; per 1000-PDFU). The IRs of secondary infections among patients with or without thrombotic complications were 15.0 (95% CI, 10.7–21.0) and 9.3 (95% CI, 7.9–11.0) per 1000-PDFU, respectively (P = .017). At multivariable analysis, thrombotic complications were associated with the development of secondary infections (subdistribution hazard ratio, 1.788; 95% CI, 1.018–3.140; P = .043). The etiology of secondary infections was similar in patients with and without thrombotic complications. Conclusions. In patients with COVID-19, thrombotic complications were associated with a high risk of secondary infections