Facilitating Sustainable Career Development in Fragility: A Psycho-Linguistic Intervention for Employability of Individuals with Fragile Literacy Skills

The brief report examines the burgeoning interest in sustainable career development by discussing the role of employability of individuals with fragile literacy skills, i.e., second-language learners (L2), and individuals with developmental dyslexia (DD). Considering sustainable career development as the umbrella of practices facilitating individuals flourishing, we aim to present an integrated flexible intervention to promote the employability of individuals with fragile literacy skills (DD and L2) that combines both the promotion of linguistic skills and psychological resources. Using an experimental research design, we tested our training intervention on language skills (reading and writing) coupled with psychological training intended to enhance psychological resources and psychological capital. A total of 38 individuals with DD took part in our examination (n = 22 in the experimental group) and n = 26 L2 (n = 11 in the experimental group). We measured employability skills and psychological capital pre and post our interventions both in the control and in the experimental groups. Our result show that the intervention led to a significant improvement in L2 and DD. We discuss our results and implications for research and practice

Assessing the long-term effectiveness of channel control works and supporting watershed management through sediment dynamics studies

In risk management of mountain basins, quite often, there is a lack of information on the efficiency of existing structures, the evolution of the ongoing process, and a priori in-depth study to analyse the sediment morphology dynamics and the interaction with existing channel control works. The growing capability of producing High-Resolution Topography data (HRT) greatly simplifies the analysis of geomorphological changes at multiple spatial and temporal scales and enables the development of innovative approaches to monitor sediment morphology dynamics and understand the interaction with channel control works. Indeed, thanks to multi-temporal HRT surveys (e.g., Airborne Laser Scanning - ALS), it is possible to derive accurate multi-temporal Digital Terrain Models (DTMs), and reliable DTMs of Difference (DoDs) useful to quantify the morphological changes also in catchment areas covered by vegetation. However, without a methodological and detailed workflow that considers the differences in terms of accuracy between old “legacy” data sets and recent surveys and the errors associated with the processes of co-registration, it would not have been possible to obtain accurate and valid multi-temporal DoD. The information provided by sediment morphology dynamics (i.e., exploiting multi-temporal DoDs at catchment and reach scale) coupled with a very simple, quick, and user-friendly efficiency index of channel control works, could help to support the development of watershed management strategies, assess afterward the effectiveness of existing structures, and foster a more complete decision-making chain. Therefore, this research aims to introduce a methodological approach based on integrating the sediment morphology dynamics data over large time spans in some mountain catchments with an updated state of efficiency of existing interventions. Various examples of the proposed methodology emphasized the usefulness of providing more complete information, than in the past, by exploiting field surveys and remote sensing data, in a context such as the risk management process where uncertainty and incomplete information on the ongoing phenomena prevails. The realized database could be a starting point for further analysis or provide numerical data for prediction models of the life-cycle of channel control works in risk management processes. Finally, the methodological workflow proposed could provide increasingly up-to-date information to constantly identify the areas most prone to hazards, support effective risk management decisions, improve intervention planning, find more appropriate solutions, or direct the maintenance works

Intervenire nella fragilità: la promozione dell’occupabilità in apprendenti italiano L2 e soggetti con DSA

Max 300 words Introduzione. Nell’intervento per la promozione dell’occupabilità non sempre si incontrano processi naturali e spontanei. Ciò è evidente laddove, alla base del destinatario dell’intervento, si innestano difficoltà nei processi comunicativi e di acquisizione della lingua come nel caso di soggetti con diagnosi di Disturbi dello Sviluppo e dell’Apprendimento (DSA) o di soggetti apprendenti L2. Intervenire in questo contesto, richiede a ricercatori e pratici di proporre piani di lavoro sinergici che intreccino aspetti linguistici e psicologici per la promozione dell’occupabilità. Obiettivi. Posizionato in questo contesto di ricerca, il progetto di cui la comunicazione dà conto, propone un modello psicologico-linguistico per approcciare lo studio e la promozione dell’occupabilità in soggetti apprendenti L2 e soggetti con diagnosi DSA. Metodo. Il progetto di durata triennale, si è articolato secondo classiche metodologie di lavoro (p.e., rassegna della letteratura) per culminare nella proposta finale di interventi per la fragilità. Nello specifico, questo si struttura seconda un preliminare lavoro per la promozione di aspetti linguistici interessati dalle casistiche specifiche (p.e. capacità di lettura, capacità comunicative), seguito poi dal lavoro sul bilancio di competenze, promozione del capitale psicologico e servizio di orientamento. L’intervento è stato testato con disegno sperimentale confrontando le misure pre-post di gruppi sperimentali e gruppi di controllo. Risultati. L’analisi di N=40 soggetti DSA (n=20 gruppo sperimentale) e N=25 (n=9 gruppo sperimentale) mostrano come l’intervento abbia portato ad un miglioramento significativo per le dimensioni del capitale psicologico e dell’occupabilità dei soggetti coinvolti. Tuttavia, non si registra una tendenza particolarmente significativa nel confronto con i gruppi di controllo. Limiti. Data la scarsa partecipazione dovuta a molteplici fattori relativi al reclutamento, il contributo avanza un modello di intervento che necessita ulteriori approfondimenti empirici. Aspetti innovativi. Il lavoro estende lo studio dell’occupabilità approcciando i fattori di linguistici e avanzando un modello di intervento sinergico

Inflammation subverts hippocampal synaptic plasticity in experimental multiple sclerosis.

Abnormal use-dependent synaptic plasticity is universally accepted as the main physiological correlate of memory deficits in neurodegenerative disorders. It is unclear whether synaptic plasticity deficits take place during neuroinflammatory diseases, such as multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). In EAE mice, we found significant alterations of synaptic plasticity rules in the hippocampus. When compared to control mice, in fact, hippocampal long-term potentiation (LTP) induction was favored over long-term depression (LTD) in EAE, as shown by a significant rightward shift in the frequency-synaptic response function. Notably, LTP induction was also enhanced in hippocampal slices from control mice following interleukin-1β (IL-1β) perfusion, and both EAE and IL-1β inhibited GABAergic spontaneous inhibitory postsynaptic currents (sIPSC) without affecting glutamatergic transmission and AMPA/NMDA ratio. EAE was also associated with selective loss of GABAergic interneurons and with reduced gamma-frequency oscillations in the CA1 region of the hippocampus. Finally, we provided evidence that microglial activation in the EAE hippocampus was associated with IL-1β expression, and hippocampal slices from control mice incubated with activated microglia displayed alterations of GABAergic transmission similar to those seen in EAE brains, through a mechanism dependent on enhanced IL-1β signaling. These data may yield novel insights into the basis of cognitive deficits in EAE and possibly of MS

Feedback inhibition of cAMP effector signaling by a chaperone-assisted ubiquitin system

Activation of G-protein coupled receptors elevates cAMP levels promoting dissociation of protein kinase A (PKA) holoenzymes and release of catalytic subunits (PKAc). This results in PKAc-mediated phosphorylation of compartmentalized substrates that control central aspects of cell physiology. The mechanism of PKAc activation and signaling have been largely characterized. However, the modes of PKAc inactivation by regulated proteolysis were unknown. Here, we identify a regulatory mechanism that precisely tunes PKAc stability and downstream signaling. Following agonist stimulation, the recruitment of the chaperonebound E3 ligase CHIP promotes ubiquitylation and proteolysis of PKAc, thus attenuating cAMP signaling. Genetic inactivation of CHIP or pharmacological inhibition of HSP70 enhances PKAc signaling and sustains hippocampal long-term potentiation. Interestingly, primary fibroblasts from autosomal recessive spinocerebellar ataxia 16 (SCAR16) patients carrying germline inactivating mutations of CHIP show a dramatic dysregulation of PKA signaling. This suggests the existence of a negative feedback mechanism for restricting hormonally controlled PKA activities

GABAergic transmission is lower in EAE mice in the presence of forskolin.

<p>A) Pooled (mean ± S.E.M) cumulative distributions of sIPSCs amplitude (left; bin size 10 pA) and inter-event interval (right; bin size 50 ms) recorded from neurons of CFA in the absence and presence of forskolin (30 µM). Histograms in the insets are averages (mean ± S.E.M) of the corresponding median values for neurons of CFA, in control conditions and following forskolin perfusion. On top are representative trace records from CFA (left) or CFA in the presence of forskolin (right). B) Cumulative distributions of sIPSCs amplitude (left) and inter-event interval (right) recorded from EAE slices in control conditions and in response to forskolin. The traces on top are obtained from same neuron, in control conditions and during forskolin application. Histograms in the insets are averages (mean ± S.E.M) of the corresponding median values. C) Histograms (mean ± S.E.M) of the maximal effect on sIPSC amplitude (left) and inter-event interval (right) reached in the presence of forskolin both in CFA (n = 10) and EAE (n = 14) mice.</p

Inhibition of the GABAergic transmission in EAE mice.

<p>A) Pooled (mean ± S.E.M) cumulative distributions of sIPSCs amplitude (left; bin size 10 pA) and inter-event interval (right; bin size 50 ms) recorded from neurons of CFA (n = 11) and EAE (n = 9) mice. Histograms in the insets are averages (mean ± S.E.M) of the corresponding median values for neurons of CFA and EAE mice. On top are representative trace records from CFA (left) or EAE (right) mouse. B) Cumulative distributions of sIPSCs amplitude (left) and inter-event interval (right) recorded from a single CFA neuron in response to IL-1β (30 ng/ml). The traces on top are obtained from same neuron, in control conditions, during IL-1β application and at IL-1β washout. Histograms in the insets are averages (mean ± S.E.M; n = 11) of the corresponding median values. C) Input/Output curves (mean ± S.E.M) of fiber volley amplitude vs. fEPSP slope, from extracellular recordings in the CA1 area of 9 slices of CFA and 12 slices of EAE mice. D) Histograms (mean ± S.E.M) of the AMPA/NMDA ratio of evoked EPSCs recorded in whole-cell from 9 neurons of CFA and 13 neurons of EAE mice. On top are representative traces of EPSCs recorded al −80 mV and +40 mV holding potential from CFA (left) and EAE (right) mouse. E) Pooled (mean ± S.E.M) cumulative distributions of sEPSCs amplitude (left; bin size 10 pA) and inter-event interval (right; bin size 50 ms) recorded from neurons of CFA (n = 9) and EAE (n = 13) mice. Histograms in the insets are averages (mean ± S.E.M) of the corresponding median values for neurons of CFA and EAE mice. * and ** indicate <i>p<</i>0.05 and 0.01 t-test, respectively.</p

Loss of PV⁺ interneurons in the EAE hippocampus.

<p>(A–C) Immunostaining of PV⁺ neurons (green) in hippocampal coronal sections derived from CFA (A) and EAE mice at 20 dpi (B), respectively. The hippocampal structure is defined by fluorescent signal derived from DAPI positive cell nuclei (gray). A loss of PV⁺ neurons characterizes EAE mice. A’ and B’ are high magnifications of the white boxes in A and B panels, respectively. The number of PV⁺ interneurons (lower panels) in the CA1 layer and <i>stratum oriens</i> was reduced in EAE mice relative CFA mice. C) Histogram shows the mean percentage of the PV⁺ density interneurons (1/mm²) which was significantly reduced in EAE mice by about 27% relative to CFA in the acute phase of the disease. ** indicates <i>p<</i>0.01, t- test. Scale bar 200 µm in A and B; 100 µm in A’ and B’.</p

Reduced gamma oscillations in hippocampal slices of EAE mice.

<p>A) Spectrogram against time, showing the increase of PSD in the frequency range of 30 to 50 Hz, induced by Cch (20 µM) in the CA1 area of a CFC mouse hippocampal slice. PSD is expressed with a colorimetric scale, measured in successive 1 min epochs. The traces on top are local field potentials recorded in the CA1 pyramidal layer, before (left) and during (right) Cch perfusion. B) Histograms (mean ± S.E.M) of the change in PSD area in Cch (20 µM), for the range of frequencies indicated on top, relative to corresponding measurements obtained before Cch perfusion, in slices from CFC (n = 9) and EAE (n = 9) mice. The scattered dots on each column are single experimental data. * indicates <i>p<</i>0.05, t-test.</p