Suchergebnisse

La Direttiva 2012/29/UE tutela le vittime di reato e mira ad assicurare loro un più effettivo accesso alla giustizia nel rispetto delle garanzie del giusto processo, del diritto di difesa e del principio del contraddittorio. La Direttiva sottolinea, in particolare, la necessità di proteggere in modo personalizzato e individualizzato tutte le vittime di reato, con speciale riguardo per le persone 'vulnerabili'. Tanto negli ordinamenti nazionali quanto nell'operato delle istituzioni si riscontra, però, un'ancora insufficiente attenzione verso una nutrita categoria di vittime: le vittime della criminalità d'impresa e, in particolare, le vittime di quella che la letteratura internazionale definisce corporate violence. Con la locuzione corporate violence si identificano le condotte penalmente rilevanti, pur riconducibili all'ordinaria attività d'impresa, lesive della salute, dell'integrità fisica o della vita delle persone: illeciti ambientali che determinano danni alla vita, alla incolumità pubblica o individuale; commercializzazione di prodotti difettosi o pericolosi che cagionano pregiudizio alla vita o alla salute dei consumatori (per esempio, prodotti alimentari e farmaceutici); infortuni sul lavoro dovuti a violazione della disciplina sulla sicurezza sul lavoro. Il volume, frutto di un progetto finanziato dall'Unione Europea (www.victimsandcorporations.eu), offre uno studio approfondito della Direttiva 2012/29/EU sotto i profili giuridici e vittimologico-criminologici, analizzando le implicazioni teoriche e pratiche dell'applicazione della Direttiva Vittima in generale e nei casi di corporate violence, con un'attenzione al più ampio quadro delle politiche europee in materia ambientale, farmaceutica e alimentare e delle politiche europee e internazionali in tema di vittime e soggetti vulnerabili. L'opera affronta le principali questioni connesse alla peculiare vulnerabilità delle vittime di corporate violence (squilibri informativi, patologie lungolatenti, incertezza scientifica, ecc.), delineando, anche alla luce delle indicazioni emerse da una articolata ricerca empirica, proposte e indicazioni in ordine alla partecipazione al procedimento penale e al sostegno, all'assistenza e alla protezione delle persone offese. L'opera include anche una serie di raccomandazioni, distillate dai significativi risultati del progetto e rivolte al legislatore e ai policy maker. Il volume è caratterizzato dal taglio interdisciplinare e da una costante lettura sistematica delle fonti normative europee e internazionali, anche alla luce della giurisprudenza della Corte di Giustizia dell'Unione Europea e della Corte Europea dei Diritti dell'Uomo. L'opera si presta a essere strumento utile per studiosi e professionisti. ; The book is the final publication of the EU-funded project "Victims and Corporations. Implementation of Directive 2012/29/EU for victims of corporate crimes and corporate violence" (www.victimsandcorporations.eu). European Union Directive 2012/29/UE introduces a 'system' of minimum standards on the rights, support and protection for victims of crimes, and their participation to criminal proceedings, without prejudice to the rights of the offender. Within the scope of the Directive and its definition of 'victim', though, there is a relevant group of victims who have not yet received enough consideration, and whose access to justice may be at stake. It is the victims of corporate crimes, and particularly of corporate violence, meaning those criminal offences committed by corporations in the course of their legitimate activities, which result in harms to natural persons' health, integrity, or life. Within the vast area of corporate crime, the project and this publication focus on three main strands of victimisation: environmental crime, food safety violations and offences in the pharmaceutical industry with the aim to explore intersections and potential synergies between Directive 2012/29/EU and the existing body of EU legal tools in these three sectors. The publication also includes an overview of the current 'state of the art' with respect to the general issue of victims' rights, support and protection in light of the EU Directive; a comparison with the principles emerging from the ECtHR case law and the broader field of international law; a study of the existing criminological and victimological literature on corporate crime and corporate violence, its harms, and its victims, integrated with the results of the empirical research which was part of the Project; an analytical discussion of said results with respect to the specific issues related to access to justice by victims of corporate violence and to support needs of said victims; a discussion of the possible benefits of integrating a restorative justice approach in dealing with corporate violence crimes. The book is completed with a set of recommendations for national lawmakers and policymakers.

11 p., 6 figures, 1 table and references. ; Thyroid hormones influence brain development through regulation of gene expression mediated by nuclear receptors. Nuclear receptor concentration increases rapidly in the human fetus during the secondtrimester,aperiod of high sensitivity of the brain to thyroidhormones.In the rat, the equivalent period is the last quarter of pregnancy. However, little is known about thyroid hormone action in the fetal brain, and in rodents, most thyroid hormone-regulated genes have been identified during the postnatal period. To identify potential targets of thyroid hormone in the fetal brain,weinduced maternal and fetal hypothyroidism by maternal thyroidectomy followed by antithyroid drug (2-mercapto-1-methylimidazole) treatment. Microarray analysis identified differentially expressed genes in the cerebral cortex of hypothyroid fetuses on d 21 after conception. Gene function analysis revealed genes involved in the biogenesis of the cytoskeleton, neuronal migration and growth,and branching of neurites. Twenty percent of the differentially expressed genes were related to each other centered on the Ca2 and calmodulin-activated kinase (Camk4) pathway.Camk4was regulated directly by T3 in primary cultured neurons from fetal cortex, and the Camk4 protein was also induced by thyroid hormone. No differentially expressed genes were recovered when euthyroid fetuses from hypothyroid mothers were compared with fetuses from normal mothers. Although the resultsdonot rule out a specific contribution from the mother, especially at earlier stages of pregnancy, they indicate that the main regulators of thyroid hormone-dependent, fetal brain gene expression near term are the fetal thyroid hormones. ; This work was supported by Grants BFU2005-01740, SAF2008-01168, and SAF2006-14068 from the Ministry of Science and Innovation, Spain, by the European Union Integrated Project CRESCENDO (LSHM- CT-2005-018652), and by the Center for Biomedical Research on Rare Diseases (CIBERER). D.D. was supported by the I3P program of the Consejo Superior de Investigaciones Científicas, Spain, and by a postdoctoral fellowship from The Japanese Society for the Promotion of Science. D.N. was supported by a predoctoral fellowship of the Spanish Ministry of Science and Innovation. ; Peer reviewed

Si pubblicano in questo volume le relazioni presentate al Convegno Internazionale organizzato dalla Pontificia Università Gregoriana, in occasione del IV centenario della morte di San Roberto Bellarmino. I diciassette contributi rispecchiano l'itinerario delineato dal comitato scientifico del convegno, intento a "Ripensare Bellarmino tra Teologia, Filosofia e Storia". Si parte dalla situazione del Collegio Romano al tempo di Bellarmino e dalla sua formazione a Lovanio dove si è reso famoso per i sermoni lì pronunciati. Di seguito, sono studiate le caratteristiche della esegesi di Bellarmino e la sua predicazione. Ampio spazio è dato poi alla spiritualità e alla teologia bellarminiane. Seguono le relazioni sul confronto di Bellarmino con la Riforma e i suoi autori, sia nel contesto germanico sia in quello inglese. Il volume include, infine, una presentazione della ritrattistica del cardinale e del suo contributo al dibattito sulle immagini sacre e si conclude con alcune relazioni sul processo di beatificazione e di canonizzazione di Roberto Bellarmino e su possibili linee di ricerca per il futuro.

7 figures, 1 table. ; Aims: Peritonitis is one of the most common causes of sepsis, a serious syndrome characterized by a dysregulated systemic inflammatory response. Recent evidence suggests that Granzyme A (GzmA), a serine protease mainly expressed by NK and T cells, could act as a proinflammatory mediator and could play an important role in the pathogenesis of sepsis. This work aims to analyze the role and the therapeutic potential of GzmA in the pathogenesis of peritoneal sepsis. ; Methods: The level of extracellular GzmA as well as GzmA activity were analyzed in serum from healthy volunteers and patients with confirmed peritonitis and were correlated with the Sequential Organ Failure Assessment (SOFA) score. Peritonitis was induced in C57Bl/6 (WT) and GzmA-/- mice by cecal ligation and puncture (CLP). Mice were treated intraperitoneally with antibiotics alone or in combination serpinb6b, a specific GzmA inhibitor, for 5 days. Mouse survival was monitored during 14 days, levels of some proinflammatory cytokines were measured in serum and bacterial load and diversity was analyzed in blood and spleen at different times. ; Results: Clinically, elevated GzmA was observed in serum from patients with abdominal sepsis suggesting that GzmA plays an important role in this pathology. In the CLP model GzmA deficient mice, or WT mice treated with an extracellular GzmA inhibitor, showed increased survival, which correlated with a reduction in proinflammatory markers in both serum and peritoneal lavage fluid. GzmA deficiency did not influence bacterial load in blood and spleen and GzmA did not affect bacterial replication in macrophages in vitro, indicating that GzmA has no role in bacterial control. Analysis of GzmA in lymphoid cells following CLP showed that it was mainly expressed by NK cells. Mechanistically, we found that extracellular active GzmA acts as a proinflammatory mediator in macrophages by inducing the TLR4-dependent expression of IL-6 and TNFα. ; Conclusions: Our findings implicate GzmA as a key regulator of the inflammatory response during abdominal sepsis and provide solid evidences about its therapeutic potential for the treatment of this severe pathology. ; This work was supported by grant SAF2017-83120-C2-1-R and SAF2014-54763-C2-2-R from the Ministry of Science, Innovation and Universities and FEDER (Group B29_17R, Aragon Government). MG and LS were supported by a PhD fellowship (FPI) from the Ministry of Science, Innovation and Universities. IUM was supported by a PhD fellowship from Aragon Government, MA was supported by a post-doctoral fellowship "Juan de la Cierva-formación" from the Ministry of Science, Innovation and Universities. JP was supported by ARAID Foundation. ; Peer reviewed

6 figures, 6 tables.-- Supplementary material available. ; Coronavirus disease 2019 (COVID19), caused by SARS-CoV-2, is a complex disease, with a variety of clinical manifestations ranging from asymptomatic infection or mild cold-like symptoms to more severe cases requiring hospitalization and critical care. The most severe presentations seem to be related with a delayed, deregulated immune response leading to exacerbated inflammation and organ damage with close similarities to sepsis. ; [Methods]: In order to improve the understanding on the relation between host immune response and disease course, we have studied the differences in the cellular (monocytes, CD8+ T and NK cells) and soluble (cytokines, chemokines and immunoregulatory ligands) immune response in blood between Healthy Donors (HD), COVID19 and a group of patients with non-COVID19 respiratory tract infections (NON-COV-RTI). In addition, the immune response profile has been analyzed in COVID19 patients according to disease severity. ; [Results]: In comparison to HDs and patients with NON-COV-RTI, COVID19 patients show a heterogeneous immune response with the presence of both activated and exhausted CD8+ T and NK cells characterised by the expression of the immune checkpoint LAG3 and the presence of the adaptive NK cell subset. An increased frequency of adaptive NK cells and a reduction of NK cells expressing the activating receptors NKp30 and NKp46 correlated with disease severity. Although both activated and exhausted NK cells expressing LAG3 were increased in moderate/severe cases, unsupervised cell clustering analyses revealed a more complex scenario with single NK cells expressing more than one immune checkpoint (PD1, TIM3 and/or LAG3). A general increased level of inflammatory cytokines and chemokines was found in COVID19 patients, some of which like IL18, IL1RA, IL36B and IL31, IL2, IFNα and TNFα, CXCL10, CCL2 and CCL8 were able to differentiate between COVID19 and NON-COV-RTI and correlated with bad prognosis (IL2, TNFα, IL1RA, CCL2, CXCL10 and CXCL9). Notably, we found that soluble NKG2D ligands from the MIC and ULBPs families were increased in COVID19 compared to NON-COV-RTI and correlated with disease severity. ; [Conclusions:] Our results provide a detailed comprehensive analysis of the presence of activated and exhausted CD8+T, NK and monocyte cell subsets as well as extracellular inflammatory factors beyond cytokines/chemokines, specifically associated to COVID19. Importantly, multivariate analysis including clinical, demographical and immunological experimental variables have allowed us to reveal specific immune signatures to i) differentiate COVID19 from other infections and ii) predict disease severity and the risk of death. ; The authors would like to thank the Biobank of the Aragon Health System integrated in the Spanish National Biobanks Network and the Servicios Científico Técnicos de Citometria de Flujo del CIBA for their collaboration. Work in the JP laboratory is funded by the FEDER (Fondo Europeo de Desarrollo Regional, Gobierno de Aragón, Group B29_17R), Health National Institute Carlos III (COV20-00308), Aragón Government (Fondo COVID-19), Fundación Santander-Universidad de Zaragoza (Programa COVID-19), Agencia Estatal de Investigación (SAF2017-83120-C2-1-R; PID2020-113963RBI00), Fundación Inocente, ASPANOA and Carrera de la Mujer de Monzón. EMG is funded by Agencia Estatal de Investigación (SAF2017-83120-C2-1-R and PID2020-113963RB-I00). IUM and SH are supported by a PhD fellowship from Aragon Government, CP by a PhD fellowship from AECC, LS by a PhD fellowship (FPI) from the Ministry of Science, Innovation and Universities. DDM is supported by a postdoctoral fellowship 'Sara Borrell', and MA is supported by a postdoctoral fellowship 'Juan de la Cierva-incorporacion' from the Ministry of Science, Innovation and Universities. EM and BGT are supported by Rio Hortega contract. JP is supported by the ARAID Foundation. ; Peer reviewed