Environmental disclosure and environmentally-oriented management: an exploratory analysis of consistency.

The main objective of this exploratory research is to determine if consistency exists between some aspects of environmental management and environmental disclosure at organizational level for a sample of Italian companies. Addressing this research question the current study contributes to previous literature in three ways. First, an overview of environmental disclosure activity through different reporting channels is provided. Second, an overview of different environmental management aspects is provided. Finally, the relationship between environmental management and environmental disclosure is examined

On Axially Rational Regular Functions and Schur Analysis in the Clifford-Appell Setting

In this paper we start the study of Schur analysis for Cauchy–Fueter regular quaternionic-valued functions, i.e. null solutions of the Cauchy–Fueter operator in . The novelty of the approach developed in this paper is that we consider axially regular functions, i.e. functions spanned by the so-called Clifford-Appell polynomials. This type of functions arises naturally from two well-known extension results in hypercomplex analysis: the Fueter mapping theorem and the generalized Cauchy–Kovalevskaya (GCK) extension. These results allow one to obtain axially regular functions starting from analytic functions of one real or complex variable. Precisely, in the Fueter theorem two operators play a role. The first one is the so-called slice operator, which extends holomorphic functions of one complex variable to slice hyperholomorphic functions of a quaternionic variable. The second operator is the Laplace operator in four real variables, that maps slice hyperholomorphic functions to axially regular functions. On the other hand, the generalized CK-extension gives a characterization of axially regular functions in terms of their restriction to the real line. In this paper we use these two extensions to define two notions of rational function in the regular setting. For our purposes, the notion coming from the generalized CK-extension is the most suitable. Our results allow to consider the Hardy space, Schur multipliers and their relation with realizations in the framework of Clifford-Appell polynomials. We also introduce two notions of regular Blaschke factors, through the Fueter theorem and the generalized CK-extension

Inhibition of nonsense-mediated mRNA decay reduces the tumorigenicity of human fibrosarcoma cells.

Nonsense-mediated mRNA decay (NMD) is a eukaryotic RNA decay pathway with roles in cellular stress responses, differentiation, and viral defense. It functions in both quality control and post-transcriptional regulation of gene expression. NMD has also emerged as a modulator of cancer progression, although available evidence supports both a tumor suppressor and a pro-tumorigenic role, depending on the model. To further investigate the role of NMD in cancer, we knocked out the NMD factor SMG7 in the HT1080 human fibrosarcoma cell line, resulting in suppression of NMD function. We then compared the oncogenic properties of the parental cell line, the SMG7-knockout, and a rescue cell line in which we re-introduced both isoforms of SMG7. We also tested the effect of a drug inhibiting the NMD factor SMG1 to distinguish NMD-dependent effects from putative NMD-independent functions of SMG7. Using cell-based assays and a mouse xenograft tumor model, we showed that suppression of NMD function severely compromises the oncogenic phenotype. Molecular pathway analysis revealed that NMD suppression strongly reduces matrix metalloprotease 9 (MMP9) expression and that MMP9 re-expression partially rescues the oncogenic phenotype. Since MMP9 promotes cancer cell migration and invasion, metastasis and angiogenesis, its downregulation may contribute to the reduced tumorigenicity of NMD-suppressed cells. Collectively, our results highlight the potential value of NMD inhibition as a therapeutic approach

Transcriptome-wide identification of NMD-targeted human mRNAs reveals extensive redundancy between SMG6- and SMG7-mediated degradation pathways

Besides degrading aberrant mRNAs that harbor a premature translation termination codon (PTC), nonsense-mediated mRNA decay (NMD) also targets many seemingly "normal" mRNAs that encode for full-length proteins. To identify a bona fide set of such endogenous NMD targets in human cells, we applied a meta-analysis approach in which we combined transcriptome profiling of knockdowns and rescues of the three NMD factors UPF1, SMG6 and SMG7. We provide evidence that this combinatorial approach identifies NMD-targeted transcripts more reliably than previous attempts that focused on inactivation of single NMD factors. Our data revealed that SMG6 and SMG7 act on essentially the same transcripts, indicating extensive redundancy between the endo- and exonucleolytic decay routes. Besides mRNAs, we also identified as NMD targets many long non-coding RNAs as well as miRNA and snoRNA host genes. The NMD target feature with the most predictive value is an intron in the 3' UTR, followed by the presence of upstream open reading frames (uORFs) and long 3' UTRs. Furthermore, the 3' UTRs of NMD-targeted transcripts tend to have an increased GC content and to be phylogenetically less conserved when compared to 3' UTRs of NMD insensitive transcripts

IL-27, but not IL-35, inhibits neuroinflammation through modulating GM-CSF expression

IL-27 and IL-35 are heterodimeric cytokines, members of the IL-12 family and considered to have immunomodulatory properties. Their role during neuroinflammation had been investigated using mutant mice devoid of either one of their subunits or lacking components of their receptors, yielding conflicting results. We sought to understand the therapeutic potential of IL-27 and IL-35 delivered by gene therapy in neuroinflammation. We constructed lentiviral vectors expressing IL-27 and IL-35 from a single polypeptide chain, and we validated in vitro their biological activity. We injected IL-27 and IL-35-expressing lentiviral vectors into the cerebrospinal fluid (CSF) of mice affected by experimental neuroinflammation (EAE), and performed clinical, neuropathological and immunological analyses. Both cytokines interfere with neuroinflammation, but only IL-27 significantly modulates disease development, both clinically and neuropathologically. IL-27 protects from autoimmune inflammation by inhibiting granulocyte macrophages colony-stimulating factor (GM-CSF) expression in CD4+ T cells and by inducing program death-ligand 1 (PD-L1) expression in both CNS-resident and CNS-infiltrating myeloid cells. We demonstrate here that IL-27 holds therapeutic potential during neuroinflammation and that IL-27 inhibits GM-CSF and induces pd-l1 mRNA in vivo

Algunas reflexiones sobre como construyen los trabajadores sociales sus propios objetos de estudio en los procesos de investigación

En este trabajo nos proponemos socializar algunas de las reflexiones y discusiones sostenidas al interior del Centro de Investigaciones en Campos de Intervención del Trabajo Social (CIeCITS) los cuales a su vez, forman parte de los interrogantes nodales del Proyecto de Investigación y Desarrollo PID 1POL184/UNR. Ambos espacios dirigidos por la Dra. Alicia González Saibene. Estas giran no solo en torno a qué, porqué y para qué se investiga en Trabajo Social, sino en acerca de los modos en que los Trabajadores Sociales lo hacen, es decir, cómo recuperan argumentadamente sus intervenciones al haberlas reconstruido analíticamente, y el modo en que esto aparece en sus decisiones teórico-metodológicas y en las producciones finales de los proyectos PID y las tesis de maestría y doctorado.Eje Teórico-metodológico en Trabajo Social-GT 27: Metodología y Trabajo Social.Facultad de Trabajo Socia

Aggiornamenti e novità sulle conoscenze di Pancratium maritimum (Amaryllidaceae)

Pancratium maritimum L., bulbosa perenne degli ambienti dunali costieri, è un taxon relativamente recente se comparato con le specie del genere a gravitazione mediterranea. Gli studi noti su questa specie hanno analizzato vari aspetti della biologia (riproduttivi, biochimici, filogenetici, genetici, ecc.). Tuttavia, esistono ancora lacune scientifiche, tra cui l’assenza di studi su ampio areale di genetica di conservazione e sugli adattamenti eco-morfofisiologici alle condizioni di stress. Per ampliare le conoscenze su P. maritimum, la Fondazione Nando Peretti nel novembre 2012 ha finanziato un progetto triennale sulla conoscenza e la salvaguardia di questa specie (Progetto 2012-83). In questo contributo si presentano i risultati ottenuti per le diverse linee di ricerca finora affrontate, che vanno dalle analisi ad ampio areale dei popolamenti, usando un approccio sia genetico che GIS, alla caratterizzazione morfologica e eco-fisiologica di varie popolazioni

Minor intron splicing is regulated by FUS and affected by ALS-associated FUS mutants

Fused in sarcoma (FUS) is a ubiquitously expressed RNA-binding protein proposed to function in various RNA metabolic pathways, including transcription regulation, pre-mRNA splicing, RNA transport and microRNA processing. Mutations in the FUS gene were identified in patients with amyotrophic lateral sclerosis (ALS), but the pathomechanisms by which these mutations cause ALS are not known. Here, we show that FUS interacts with the minor spliceosome constituent U11 snRNP, binds preferentially to minor introns and directly regulates their removal. Furthermore, a FUS knockout in neuroblastoma cells strongly disturbs the splicing of minor intron-containing mRNAs, among them mRNAs required for action potential transmission and for functional spinal motor units. Moreover, an ALS-associated FUS mutant that forms cytoplasmic aggregates inhibits splicing of minor introns by trapping U11 and U12 snRNAs in these aggregates. Collectively, our findings suggest a possible pathomechanism for ALS in which mutated FUS inhibits correct splicing of minor introns in mRNAs encoding proteins required for motor neuron survival