The competitive repositioning of automotive firms in Turin: innovation, internationalisation and the role of ICT

Following the increasing competitive pressure and the emergence of new industrial poles within the auto industry, Italian firms have been the protagonists of an intense reorganisation, which is still ongoing. This case-study involves 13 supplier firms, operating in the automotive industry, localised in Turin, that have adopted a series of strategies aimed at improving their international competitiveness. The empirical findings show that there is a particularly strong innovative drive for the interviewed firms to position themselves in activities with greater added value and to undertake internationalisation strategies, from the 'lighter' to the more 'complex' forms, coupled with a use of information and communication technologies epresents a case of excellence.Innovation, Internationalisation, ICT, Automotive Industry

The Natuzzi Group and the Bari-Matera (Italy) upholstered furniture district. A case study of internationalisation in a traditional industry

The case-study focuses on the strategies adopted by the Natuzzi Group, world leader of the upholstered furniture sector, located in the Bari-Matera district (Southern Italy), to face increasing global competition and on their effects. In particular we consider the modes and determinants of productive internationalisation, carried out since 2000 by Natuzzi in China, Brazil and Romania to produce middle-low end products. By improving the competitiveness of the price-sensitive segment, the strategy contributed to the successful expansion of the Group until 2002. However, high range products, manufactured in Italy, record decreasing sales especially on the US market, despite the companys efforts in R&D and marketing and its investments in information technology. Moreover, due to Natuzzi's considerable weight in the district, the Groups performance impacts on the network of subcontracting firms, where a restructuring process is underway, raising questions about the evolution of the district.Internationalisation, Industrial District, Subcontracting

The Culturable Mycobiota of Sediments and Associated Microplastics: From a Harbor to a Marine Protected Area, a Comparative Study

Fungi are an essential component of marine ecosystems, although little is known about their global distribution and underwater diversity, especially in sediments. Microplastics (MPs) are widespread contaminants worldwide and threaten the organisms present in the oceans. In this study, we investigated the fungal abundance and diversity in sediments, as well as the MPs, of three sites with different anthropogenic impacts in the Mediterranean Sea: the harbor of Livorno, the marine protected area "Secche della Meloria"; and an intermediate point, respectively. A total of 1526 isolates were cultured and identified using a polyphasic approach. For many of the fungal species this is the first record in a marine environment. A comparison with the mycobiota associated with the sediments and MPs underlined a "substrate specificity", highlighting the complexity of MP-associated fungal assemblages, potentially leading to altered microbial activities and hence changes in ecosystem functions. A further driving force that acts on the fungal communities associated with sediments and MPs is sampling sites with different anthropogenic impacts

Pharmacological activation of autophagy favors the clearing of intracellular aggregates of misfolded prion protein peptide to prevent neuronal death

According to the "gain-of-toxicity mechanism", neuronal loss during cerebral proteinopathies is caused by accumulation of aggregation-prone conformers of misfolded cellular proteins, although it is still debated which aggregation state actually corresponds to the neurotoxic entity. Autophagy, originally described as a variant of programmed cell death, is now emerging as a crucial mechanism for cell survival in response to a variety of cell stressors, including nutrient deprivation, damage of cytoplasmic organelles, or accumulation of misfolded proteins. Impairment of autophagic flux in neurons often associates with neurodegeneration during cerebral amyloidosis, suggesting a role in clearing neurons from aggregation-prone misfolded proteins. Thus, autophagy may represent a target for innovative therapies. In this work, we show that alterations of autophagy progression occur in neurons following in vitro exposure to the amyloidogenic and neurotoxic prion protein-derived peptide PrP90-231. We report that the increase of autophagic flux represents a strategy adopted by neurons to survive the intracellular accumulation of misfolded PrP90-231. In particular, PrP90-231 internalization in A1 murine mesencephalic neurons occurs in acidic structures, showing electron microscopy hallmarks of autophagosomes and autophagolysosomes. However, these structures do not undergo resolution and accumulate in cytosol, suggesting that, in the presence of PrP90-231, autophagy is activated but its progression is impaired; the inability to clear PrP90-231 via autophagy induces cytotoxicity, causing impairment of lysosomal integrity and cytosolic diffusion of hydrolytic enzymes. Conversely, the induction of autophagy by pharmacological  blockade of mTOR kinase or trophic factor deprivation restored autophagy resolution, reducing intracellular PrP90-231 accumulation and neuronal death. Taken together, these data indicate that PrP90-231 internalization induces an autophagic defensive response in A1 neurons, although incomplete and insufficient to grant survival; the pharmacological enhancement of this process exerts neuroprotection favoring the clearing of the internalized peptide and could represents a promising neuroprotective tool for neurodegenerative proteinopathies

Characterization of Intertidal Macrofaunal Communities of Two Sandy Beaches under Different Anthropogenic Pressures

The macrofauna in the intertidal zone of sandy beaches provides the trophic connectivity between land and sea, by linking microbiome, meiofauna, and megafauna, representing a food source for several terrestrial animals, including shorebirds and mammals. However, the macrozoobenthos in urbanised beaches is subjected to intense disturbances, such as breakwater barriers and tourism, which limit or impede the energy transfer from the marine to the terrestrial habitats. Because the information about diversity and abundance of the macrozoobenthos of the intertidal zone on the Mediterranean sandy coasts is scant, the main objective of this study is to increase the knowledge on the macrofauna living in this habitat and to identify taxa sensitive to cumulative human-induced stresses. To achieve this purpose, the structure and dynamics of macrozoobenthic communities from (1) a highly frequented beach characterized by breakwater barriers and (2) a marine protected area (MPA) in the Adriatic Sea were compared. The hypotheses that macrofauna composition and abundance changed in the two sites and over time were tested. Results highlighted that the macrozoobenthos in the MPA is mainly dominated by juvenile bivalves, which peaked from autumn to winter, and to a lesser extent by ostracods and mysids. Conversely, ostracods and the bivalve Lentidium mediterraneum (O. G. Costa, 1830) are particularly abundant in the highly disturbed beach, while the gastropod Tritia neritea (Linnaeus, 1758) increased only during summer. A possible combined effect of breakwater barriers and intense trampling has been theorized to explain the main differences between the two sites especially in the summer

Amyloid precursor protein and Presenilin1 interact with the adaptor GRB2 and modulate ERK 1,2 signaling.

The amyloid precursor protein (APP) and the presenilins 1 and 2 are genetically linked to the development of familial Alzheimer disease. APP is a single-pass transmembrane protein and precursor of fibrillar and toxic amyloid-beta peptides, which are considered responsible for Alzheimer disease neurodegeneration. Presenilins are multipass membrane proteins, involved in the enzymatic cleavage of APP and other signaling receptors and transducers. The role of APP and presenilins in Alzheimer disease development seems to be related to the formation of amyloid-beta peptides; however, their physiological function, reciprocal interaction, and molecular mechanisms leading to neurodegeneration are unclear. APP and presenilins are also involved in multiple interactions with intracellular proteins, the significance of which is under investigation. Among the different APP-interacting proteins, we focused our interest on the GRB2 adaptor protein, which connects cell surface receptors to intracellular signaling pathways. In this study we provide evidence by co-immunoprecipitation experiments, confocal and electron microscopy, and by fluorescence resonance energy transfer experiments that both APP and presenilin1 interact with GRB2 in vesicular structures at the centrosome of the cell. The final target for these interactions is ERK1,2, which is activated in mitotic centrosomes in a PS1- and APP-dependent manner. These data suggest that both APP and presenilin1 can be part of a common signaling pathway that regulates ERK1,2 and the cell cycle

HDAC Inhibition Improves the Sarcoendoplasmic Reticulum Ca2+-ATPase Activity in Cardiac Myocytes

SERCA2a is the Ca2+ ATPase playing the major contribution in cardiomyocyte (CM) calcium removal. Its activity can be regulated by both modulatory proteins and several post-translational modifications. The aim of the present work was to investigate whether the function of SERCA2 can be modulated by treating CMs with the histone deacetylase (HDAC) inhibitor suberanilohydroxamic acid (SAHA). The incubation with SAHA (2.5 \ub5M, 90 min) of CMs isolated from rat adult hearts resulted in an increase of SERCA2 acetylation level and improved ATPase activity. This was associated with a significant improvement of calcium transient recovery time and cell contractility. Previous reports have identified K464 as an acetylation site in human SERCA2. Mutants were generated where K464 was substituted with glutamine (Q) or arginine (R), mimicking constitutive acetylation or deacetylation, respectively. The K464Q mutation ameliorated ATPase activity and calcium transient recovery time, thus indicating that constitutive K464 acetylation has a positive impact on human SERCA2a (hSERCA2a) function. In conclusion, SAHA induced deacetylation inhibition had a positive impact on CM calcium handling, that, at least in part, was due to improved SERCA2 activity. This observation can provide the basis for the development of novel pharmacological approaches to ameliorate SERCA2 efficiency

Constraints on the χ_(c1) versus χ_(c2) polarizations in proton-proton collisions at √s = 8 TeV

The polarizations of promptly produced χ_(c1) and χ_(c2) mesons are studied using data collected by the CMS experiment at the LHC, in proton-proton collisions at √s=8  TeV. The χ_c states are reconstructed via their radiative decays χ_c → J/ψγ, with the photons being measured through conversions to e⁺e⁻, which allows the two states to be well resolved. The polarizations are measured in the helicity frame, through the analysis of the χ_(c2) to χ_(c1) yield ratio as a function of the polar or azimuthal angle of the positive muon emitted in the J/ψ → μ⁺μ⁻ decay, in three bins of J/ψ transverse momentum. While no differences are seen between the two states in terms of azimuthal decay angle distributions, they are observed to have significantly different polar anisotropies. The measurement favors a scenario where at least one of the two states is strongly polarized along the helicity quantization axis, in agreement with nonrelativistic quantum chromodynamics predictions. This is the first measurement of significantly polarized quarkonia produced at high transverse momentum