L’instabilità dei nuovi lavori: un’analisi dei percorsi lavorativi

This paper starts from the hypothesis that an effective measurement of the area stability and in the labour market cannot be based only on a an indicator of labour mobility (number of job to job transitions) but requires to take into consideration the actual amount of time worked by each individual (level of saturation of working time). The evidence presented confirms our hypothesis showing that, in the Italian case, the increasing instability of work histories (of young people and in the entrance stage) is due to a growing difficulty of working on a continuous basis, as well as to the increasing time required to get a stable job. The evidence presented also shows that being an unstable worker has a negative impact on wages both in the short and in the long run. The exception is represented by those flexible workers which are able to combine high levels of mobility with a full saturation of working time. However, this category represents a rather marginal share of total young people accessing the labour market.Work Histories, Stayers and Movers, Tenure; Unstability, Duration models

Degeneration and regeneration of peripheral nerves: role of thrombin and its receptor PAR-1

The peripheral nervous system has a striking regeneration potential and after damage extensive changes in the differentiation state both of the injured neurons and of the Schwann cells are observed. Schwann cells, in particular, undergo a large scale change in gene expression becoming able to support axonal regeneration. Nerve injury is generally associated to inflammation and activation of the coagulation cascade. Thrombin acts as a polyfunctional signalling molecule exerting its physiological function through soluble target proteins and G-protein-coupled receptors, the protease-activated receptors (PARs) [1]. Recently, we have demonstrated that the activation of the main thrombin receptor, PAR-1, in Schwann cells favours their regenerative potential determining the release of factors which promote axonal regrowth [2]. The pro-regenerative potential of thrombin seems to be exerted in a narrow range of concentrations (pM-nM range). In fact, our preliminary data indicate that high levels of thrombin in the micromolar range slow down Schwann cell proliferation and induce cell death. On the contrary, PAR-1 activating peptides mimic the pro-survival but not the pro-apoptotic effects of thrombin. Controlling thrombin concentration may preserve neuronal health during nerve injury and represent a novel target for pharmacologic therapies

PAR1 activation induces the release by Schwann cells of factors promoting cell survival and neuritogenesis

Protease-activated receptor 1 (PAR1) is a member of a family of four G-protein-coupled receptors which are activated by proteolytic cleavage of their N-terminal extracellular domain. The expression and the role of PAR1 in peripheral nervous system (PNS) is still poorly investigated, although high PAR1 mRNA expression was found in the dorsal root ganglia and in the non-compacted Schwann cell myelin microvilli at the nodes of Ranvier. Schwann cells (SCs) are the principal population of glial cells of the PNS which myelinate axons and play a key role in axonal regeneration and remyelination. Aim of the present study was to determine if the activation of PAR1 affects the neurotrophic properties of SCs. By double immunofluorescence we observed a specific staining for PAR1 in S100ȕ-positive cells of rat sciatic nerve and sciatic teased fibers. Moreover, PAR1 was highly expressed in SC cultures obtained from both neonatal and adult rat sciatic nerves. When PAR1 specific agonists were added to these cultures an increased proliferation rate was observed. Moreover, the conditioned medium obtained from primary SCs treated with PAR1 agonists increased cell survival and neurite outgrowth on PC12 cells respect to controls. By proteomics, western blot and RT-PCR analyses we identified five proteins which are released by SCs following PAR1 stimulation: Macrophage migration inhibitory factor (Mif), Aldose reductase (Akr1b1), Matrix metalloproteinase-2 (Mmp2), Syndecan-4 (Sdc) and Decorin (Dcn). Conversely, a significant decrease in the level of three proteins was observed: Complement C1r subcomponent (C1r) and Complement component 1 Q subcomponent-bindingprotein (C1qbp). When PAR1 expression was silenced by siRNA the observed pro-survival and neurotrophic properties of SCs appear to be reduced respect to controls. References PAR1 activation affects the neurotrophic properties of Schwann cells. Pompili E1, Fabrizi C2, Somma F2, Correani V3, Maras B3, Schininà ME3, Ciraci V2, Artico M4, Fornai F5, Fumagalli L2. 2017 Jan 4;79:23-33. doi: 10.1016/j.mcn.2017.01.001.Schwann cells (SCs) regulate a wide variety of axonal functions in the peripheral nervous system, providing a supportive growth environment following nerve injury (1). Here we show that rat SCs express the protease-activated receptor-1 (PAR1) both in vivo and in vitro. PAR1 is a G-protein coupled receptor eliciting cellular responses to thrombin and other proteases (2). To investigate if PAR1 activation affects the neurotrophic properties of SCs, this receptor was activated by a specific agonist peptide (TFLLR) and the conditioned medium was transferred to PC12 pheocromocytoma cells for assessing cell survival and neurite outgrowth. Culture medium from SCs treated with 10 µM TFLLR reduced significantly the release of LDH and increased the viability of PC12 cells with respect to the medium of the untreated SCs. Furthermore, conditioned medium from TFLLR-treated SCs increased neurite outgrowth on PC12 cells respect to control medium from untreated cells. To identify putative neurotrophic candidates we performed proteomic analysis on SC secretoma and real time PCR experiments after PAR1 activation. Stimulation of SCs with TFLLR increased specifically the release of a subset of five proteins: Macrophage migration inhibitory factor (Mif), Aldose reductase (Akr1b1), Matrix metalloproteinase-2 (Mmp2), Syndecan-4 (Sdc) and Decorin (Dcn). At the same time there was a significant decrease in the level of three proteins: Complement C1r subcomponent (C1r), Complement component 1 Q subcomponent-binding protein (C1qbp) and Angiogenic factor with G patch and FHA domains 1 (Aggf1). These data indicate that PAR1 stimulation does induce the release by SCs of factors promoting cell survival and neuritogenesis. Among these proteins, Mif, Sdc, Dcn and Mmp2 are of particular interest

Comparing alternative distributional assumptions in mixed models used for small area estimation of income parameter

Linear Mixed Models used in small area estimation usually rely on normality for the estimation of the variance components and the Mean Square Error of predictions. Nevertheless, normality is often inadequate when the target variable is income. For this reason, in this paper we consider Linear Mixed Models for the log-transformed income (which require back-transformation for prediction of means and totals on the variable’s original scale) and a Generalized Linear Mixed Model based on the Gamma distribution. Various prediction methods are compared by means of a simulation study based on the ECHP data. Standard predictors obtained from Linear Mixed Model for the untrasformed income are shown to be preferable to the considered alternatives, confirming their robustness with respect to the failure of the normality assumption

Microstructural, texture, plastic anisotropy and superplasticity development of ZK60 alloy during equal channel angular extrusion processing

In this study, equal channel angular pressing (ECAP) was exploited to refine the grain size of a ZK60 magnesium alloy in multi-processing steps, namely at temperatures of 250˚C, 200˚C and 150˚C, producing an ultrafine-grained (UFG) structure. The microstructural development and texture evolution during ECAP were systemically investigated by electron backscattered diffraction (EBSD) analysis. The microstructure of the ECAP processed alloy was remarkably refined to an average grain size of 600 nm. During ECAP process the original fiber texture of the as-extruded alloy was gradually weakened and eventually replaced by a stronger texture component coinciding with ECAP shear plane. The ECAP processed material showed a proper balance of tensile as well as compression strength and tensile ductility at room temperature. Yield strength of 273 and 253 MPa in tension and compression, respectively, ultimate tensile strength of 298 MPa and fracture elongation of about 30% were obtained in the UFG alloy. A transition from ductile–brittle to ductile fracture consisting of very fine and equiaxed dimples was also found in the ECAP processed material. Compared to the as-received alloy, a combination of grain refinement and texture development in the UFG alloy gave rise to a notable reduction in mechanical asymmetric behavior at room temperature. The superplastic behavior of the as-extruded and ECAP processed alloy was also investigated at 200˚C with strain rate of 1.0×10-3 s-1. The concurrent effect of grain boundary sliding and favorable basal texture in the UFG alloy led to an achievement of elongation value of about 300% while, under similar testing conditions, the elongation of about 140% was obtained in the as-extruded alloy

Autophagy in trimethyltin-induced neurodegeneration

Autophagy is a degradative process playing an important role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria and endoplasmic reticulum, as well as eliminating intracellular pathogens. The autophagic process is important for balancing sources of energy at critical developmental stages and in response to nutrient stress. Recently, autophagy has been involved in the pathophysiology of neurodegenerative diseases although its beneficial (pro-survival) or detrimental (pro-death) role remains controversial. In the present review, we discuss the role of autophagy following intoxication with trimethyltin (TMT), an organotin compound that induces severe hippocampal neurodegeneration associated with astrocyte and microglia activation. TMT is considered a useful tool to study the molecular mechanisms occurring in human neurodegenerative diseases such as Alzheimer’s disease and temporal lobe epilepsy. This is also relevant in the field of environmental safety, since organotin compounds are used as heat stabilizers in polyvinyl chloride polymers, industrial and agricultural biocides, and as industrial chemical catalysts

CFD Model of a Molten Salt Tank with Integrated Steam Generator

Abstract For each solar technology the dispatchable CSP plant scheme that maximizes the solar to electrical energy conversion and minimizes the costs associated to such transformation is searched. In recent years double tank TES systems are evolving towards more simple configurations of a single tank [1] , [2] , [3] , also known as thermocline tank TES systems and, even going beyond, there are already thermocline tanks in process of development where the steam generator (SG) is integrated into the storage tank (European project OPTS). A prototype with integrated SG has been erected for testing purpose in the Casaccia Research Centre of ENEA (Italy) [4] . The model presented in this paper reproduces the experimental data of such prototype using the CFD commercial code STAR-CCM + [5] . Unlike very few published until now [6] . The simulated system account for molten salts behavior, not only for the bulk molten salts, but also for the circulation of the molten salts inside the SG (with three steam coils). The molten salts move by induced natural convection and the steam temperatures and pressures are up to ∼500° C/40 bar. Temperature gauges situated in the bulk and the molten salts mass flow inside the SG are the main variables considered for validating the model. From the numerical point of view is a transient simulation and the model is 2D-axisymmetric. The required features of the system mesh and the physical models used are presented in this work

Thrombin in the peripheral nervous system as regulator of Schwann cell neurotrophic potentials

Coagulation and inflammation are tightly and reciprocally regulated. Inflammation initiates clotting, decreases the activity of natural anticoagulant mechanisms and impairs the fibrinolytic system. Thrombin is the main effector protease in hemostasis and it also plays a role in various non-hemostatic biological and pathophysiologic processes, predominantly mediated through activation of protease-activated receptors (PARs)

PAR1 activation induces the release by Schwann cells of factors promoting cell survival and neuritogenesis

Protease-activated receptor 1 (PAR1) is a member of a family of four G-protein-coupled receptors which are activated by proteolytic cleavage of their N-terminal extracellular domain. The expression and the role of PAR1 in peripheral nervous system (PNS) is still poorly investigated, although high PAR1 mRNA expression was found in the dorsal root ganglia and in the non-compacted Schwann cell myelin microvilli at the nodes of Ranvier. Schwann cells (SCs) are the principal population of glial cells of the PNS which myelinate axons and play a key role in axonal regeneration and remyelination. Aim of the present study was to determine if the activation of PAR1 affects the neurotrophic properties of SCs. By double immunofluorescence we observed a specific staining for PAR1 in S100ȕ-positive cells of rat sciatic nerve and sciatic teased fibers. Moreover, PAR1 was highly expressed in SC cultures obtained from both neonatal and adult rat sciatic nerves. When PAR1 specific agonists were added to these cultures an increased proliferation rate was observed. Moreover, the conditioned medium obtained from primary SCs treated with PAR1 agonists increased cell survival and neurite outgrowth on PC12 cells respect to controls. By proteomics, western blot and RT-PCR analyses we identified five proteins which are released by SCs following PAR1 stimulation: Macrophage migration inhibitory factor (Mif), Aldose reductase (Akr1b1), Matrix metalloproteinase-2 (Mmp2), Syndecan-4 (Sdc) and Decorin (Dcn). Conversely, a significant decrease in the level of three proteins was observed: Complement C1r subcomponent (C1r) and Complement component 1 Q subcomponent-bindingprotein (C1qbp). When PAR1 expression was silenced by siRNA the observed pro-survival and neurotrophic properties of SCs appear to be reduced respect to controls. References PAR1 activation affects the neurotrophic properties of Schwann cells. Pompili E1, Fabrizi C2, Somma F2, Correani V3, Maras B3, Schininà ME3, Ciraci V2, Artico M4, Fornai F5, Fumagalli L2. 2017 Jan 4;79:23-33. doi: 10.1016/j.mcn.2017.01.001.Schwann cells (SCs) regulate a wide variety of axonal functions in the peripheral nervous system, providing a supportive growth environment following nerve injury (1). Here we show that rat SCs express the protease-activated receptor-1 (PAR1) both in vivo and in vitro. PAR1 is a G-protein coupled receptor eliciting cellular responses to thrombin and other proteases (2). To investigate if PAR1 activation affects the neurotrophic properties of SCs, this receptor was activated by a specific agonist peptide (TFLLR) and the conditioned medium was transferred to PC12 pheocromocytoma cells for assessing cell survival and neurite outgrowth. Culture medium from SCs treated with 10 µM TFLLR reduced significantly the release of LDH and increased the viability of PC12 cells with respect to the medium of the untreated SCs. Furthermore, conditioned medium from TFLLR-treated SCs increased neurite outgrowth on PC12 cells respect to control medium from untreated cells. To identify putative neurotrophic candidates we performed proteomic analysis on SC secretoma and real time PCR experiments after PAR1 activation. Stimulation of SCs with TFLLR increased specifically the release of a subset of five proteins: Macrophage migration inhibitory factor (Mif), Aldose reductase (Akr1b1), Matrix metalloproteinase-2 (Mmp2), Syndecan-4 (Sdc) and Decorin (Dcn). At the same time there was a significant decrease in the level of three proteins: Complement C1r subcomponent (C1r), Complement component 1 Q subcomponent-binding protein (C1qbp) and Angiogenic factor with G patch and FHA domains 1 (Aggf1). These data indicate that PAR1 stimulation does induce the release by SCs of factors promoting cell survival and neuritogenesis. Among these proteins, Mif, Sdc, Dcn and Mmp2 are of particular interest