Living lab on sharing and circular economy: The case of Turin

Cities with their innovative capacity are key places to address critical climate, environmental and health challenges. Urban experimentations, such as Living Labs, can represent a starting point to reintroduce resources into the production cycle and reduce environmental impacts, embracing the paradigm of the circular economy (CE). According to recent studies, Living Labs at a city scale could generate significant environmental benefits, improvements in quality of life and positive impacts on citizens' health.1 This paper aims at presenting the case of the Torino Living Lab on Sharing and Circular Economy (LLSC) to point out possible future scenarios of urban sustainable policies. The case study is analysed in five sections: (1) the description of the new permanent laboratory proposed by the City of Turin; (2) the past experiences of Living Labs in Turin; (3) the birth of LLSC and the involvement strategy; (4) the introduction of the eight admitted experimentations. In the light of the results collected, the last paragraph (5) came up with the Strengths, Weaknesses, Opportunities, Treaths (SWOT) analysis in the LLSC. Eventually, it deals with the research question by offering a common ground for global and local policies focused on sustainability and CE

“Crystalline Syndiotactic Polystyrene as Reinforcing Agent of cis-1,4-Polybutadiene Rubber”

ABSTRACT: Syndiotactic polystyrene (sPS), a thermoplastic polymer characterized by high crystallinity, good chemical resistance and high modulus, has been successfully tested as a reinforcing agent for cis-1,4- polybutadiene (PB) rubber. Blends of sPS and PB have been in situ synthesized using a multistep polymerization process catalyzed by monocyclopentadienyl titanium compounds activated with MAO. This procedure assures an intimate mixing of the components and homogeneous dispersion of the sPS particles having dimension from few hundreds of nanometers to micrometers. The analysis of the mechanical properties of the sPS-PB blends obtained using this process showed enhanced Young’s modulus, toughness, σbreak and ε break: these properties were found to be 1 order of magnitude higher than those of PB and comparable to those of PB charged with inorganic filler as carbon black or silica. A multiblock copolymer (sPSB) comprising segments of sPS and PB was successfully in situ synthesized with the sPS and PB homopolymers and found to be an active compatibilizer of these blends producing a novel semicrystalline phase at the interphase between the sPS particles and the PB matrix

Progettazione e sviluppo di un metodo per lo spostamento dei dati in Grid per l'esperimento CDF

Lo scopo di questa tesi eà quello di descrivere il lavoro di progettazione e sviluppo di un metodo per lo spostamento dei dati in Grid per l'esperimento CDF ( Collision Detector at Fermilab). Negli ultimi mesi le necessita di calcolo per l'esperimento CDF sono aumentate notevolmente. Questo ha portato il CDF a muoversi verso un'architettura di calcolo Grid. Uno dei problemi aperti nel passaggio al grid rimane quello della gestione degli output delle simulazioni montecarlo prodotti nei Worker Node. Nella tesi si descrive la fase di progettazione e sviluppo della soluzione adotatta basata sulla tecnologia SAM (Sequential data Access via Metadata)

Regulation of G protein-coupled receptor kinase subtypes by calcium sensor proteins

AbstractG protein-coupled receptor homologous desensitization is intrinsically related to the function of a class of S/T kinases named G protein-coupled receptor kinases (GRK). The GRK family is composed of six cloned members, named GRK1 to 6. Studies from different laboratories have demonstrated that different calcium sensor proteins (CSP) can selectively regulate the activity of GRK subtypes. In the presence of calcium, rhodopsin kinase (GRK1) is inhibited by the photoreceptor-specific CSP recoverin through direct binding. Several other recoverin homologues (including NCS 1, VILIP 1 and hippocalcin) are also able to inhibit GRK1. The ubiquitous calcium-binding protein calmodulin (CaM) can inhibit GRK5 with a high affinity (IC50=40–50 nM). A direct interaction between GRK5 and Ca2+/CaM was documented and this binding does not influence the catalytic activity of the kinase, but rather reduced GRK5 binding to the membrane. These studies suggest that CSP act as functional analogues in mediating the regulation of different GRK subtypes by Ca2+. This mechanism is, however, highly selective with respect to the GRK subtypes: while GRK1, but not GRK2 and GRK5, is regulated by recoverin and other NCS, GRK4, 5 and 6, that belong to the GRK4 subfamily, are potently inhibited by CaM, which had little or no effect on members of other GRK subfamilies

Tracing and tracking epiallele families in complex DNA populations

DNA methylation is a stable epigenetic modification, extremely polymorphic and driven by stochastic and deterministic events. Most of the current techniques used to analyse methylated sequences identify methylated cytosines (mCpGs) at a single-nucleotide level and compute the average methylation of CpGs in the population of molecules. Stable epialleles, i.e. CpG strings with the same DNA sequence containing a discrete linear succession of phased methylated/non-methylated CpGs in the same DNA molecule, cannot be identified due to the heterogeneity of the 5′–3′ ends of the molecules. Moreover, these are diluted by random unstable methylated CpGs and escape detection. We present here MethCoresProfiler, an R-based tool that provides a simple method to extract and identify combinations of methylated phased CpGs shared by all components of epiallele families in complex DNA populations. The methylated cores are stable over time, evolve by acquiring or losing new methyl sites and, ultimately, display high information content and low stochasticity. We have validated this method by identifying and tracing rare epialleles and their families in synthetic or in vivo complex cell populations derived from mouse brain areas and cells during postnatal differentiation

Molecular targets of developmental exposure to bisphenol A in diabesity: a focus on endoderm-derived organs

Several studies associate foetal human exposure to bisphenol A (BPA) to metabolic/endocrine diseases, mainly diabesity. They describe the role of BPA in the disruption of pancreatic beta cell, adipocyte and hepatocyte functions. Indeed, the complexity of the diabesity phenotype is due to the involvement of different endoderm-derived organs, all targets of BPA. Here, we analyse this point delineating a picture of different mechanisms of BPA toxicity in endoderm-derived organs leading to diabesity. Moving from epidemiological data, we summarize the in vivo experimental data of the BPA effects on endoderm-derived organs (thyroid, pancreas, liver, gut, prostate and lung) after prenatal exposure. Mainly, we gather molecular data evidencing harmful effects at low-dose exposure, pointing to the risk to human health. Although the fragmentation of molecular data does not allow a clear conclusion to be drawn, the present work indicates that the developmental exposure to BPA represents a risk for endoderm-derived organs development as it deregulates the gene expression from the earliest developmental stages. A more systematic analysis of BPA impact on the transcriptomes of endoderm-derived organs is still missing. Here, we suggest in vitro toxicogenomics approaches as a tool for the identification of common mechanisms of BPA toxicity leading to the diabesity in organs having the same developmental origin

Human herpesvirus 6 variant A, but not variant B, infects EBV-positive B lymphoid cells, activating the latent EBV genome through a BZLF-1-dependent mechanism

Human herpesvirus 6, a predominantly T lymphotropic virus, has been recently shown to infect some EBV-positive B cell lines, and to induce in them the activation of the EBV lytic cycle. Here we have confirmed and extended such observations, showing that (1) this phenomenon is restricted to the variant A of HHV-6: in fact two isolates belonging to the HHV-6 variant B (BA92 and Z29) were neither able to infect any B cell line, independently of the EBV status, nor to induce the EBV genome expression. The only exception is represented by the P3HR1 cells, in which, however, the infection by the variant B does not determine induction of EBV antigens; (2) the presence of the EBV genome contributes to the susceptibility of the B cell lines to HHV-6 infection, increasing the binding sites and the percentage of infectable cells, as detected by immunoelectron microscopy; and (3) HHV-6 infected T cells, transfected with plasmids bearing the promoter regions of the EBV early genes BZLF1 and BMRF1, show a strong transactivation of these promoters

Centrality of Striatal Cholinergic Transmission in Basal Ganglia Function

Work over the past two decades revealed a previously unexpected role for striatal cholinergic interneurons in the context of basal ganglia function. The recognition that these interneurons are essential in synaptic plasticity and motor learning represents a significant step ahead in deciphering how the striatum processes cortical inputs, and why pathological circumstances cause motor dysfunction. Loss of the reciprocal modulation between dopaminergic inputs and the intrinsic cholinergic innervation within the striatum appears to be the trigger for pathophysiological changes occurring in basal ganglia disorders. Accordingly, there is now compelling evidence showing profound changes in cholinergic markers in these disorders, in particular Parkinson's disease and dystonia. Based on converging experimental and clinical evidence, we provide an overview of the role of striatal cholinergic transmission in physiological and pathological conditions, in the context of the pathogenesis of movement disorders

Models and methods for conditioning the ischemic brain

Abstract Background In the last decades the need to find new neuroprotective targets has addressed the researchers to investigate the endogenous molecular mechanisms that brain activates when exposed to a conditioning stimulus. Indeed, conditioning is an adaptive biological process activated by those interventions able to confer resistance to a deleterious brain event through the exposure to a sub-threshold insult. Specifically, preconditioning and postconditioning are realized when the conditioning stimulus is applied before or after, respectively, the harmul ischemia. Aims and Results The present review will describe the most common methods to induce brain conditioning, with particular regards to surgical, physical exercise, temperature-induced and pharmacological approaches. It has been well recognized that when the subliminal stimulus is delivered after the ischemic insult, the achieved neuroprotection is comparable to that observed in models of ischemic preconditioning. In addition, subjecting the brain to both preconditioning as well as postconditioning did not cause greater protection than each treatment alone. Conclusions The last decades have provided fascinating insights into the mechanisms and potential application of strategies to induce brain conditioning. Since the identification of intrinsic cell‐survival pathways should provide more direct opportunities for translational neuroprotection trials, an accurate examination of the different models of preconditioning and postconditioning is mandatory before starting any new project