Il progetto PNRR presso l’Ufficio GIP-GUP del Tribunale di Milano: primi risultati e capacità di conseguire gli obiettivi 2026

Gli uffici giudiziari hanno stabilito specifici target da raggiungere grazie all’apporto degli addetti all’ufficio per il processo (AUPP) acquisiti grazie ai fondi PNRR. Questo articolo si concentra sulla sezione GIP del Tribunale di Milano, che per le particolari condizioni di criticità vissute nel 2020, ha visto una massiccia iniezione di personale aggiuntivo e un conseguente riassetto organizzativo. L’analisi mostra che tutti gli indicatori di performance appaiono nel 2022 in deciso miglioramento e che gli AUPP contribuiscono alla più rapida gestione delle fasi a cui sono assegnati. Nonostante questi buoni risultati, i target 2026 non saranno raggiunti: l’apporto degli AUPP non è infatti sufficiente a compensare le scoperture di organico e le carenze strutturali e tecnologiche dell’ufficio. Per conseguire l’impatto atteso dal PNRR – riduzione dei tempi di giustizia e eliminazione dell’arretrato – appare cruciale pianificare in modo integrato gli strumenti di policy e monitorarne l’implementazione, ponendo attenzione alla qualità dei dati a supporto della strategia organizzativa

Low loss, high contrast optical waveguides based on CMOS compatible LPCVD processing

A new class of integrated optical waveguide structures is presented, based on low cost CMOS compatible LPCVD processing. This technology allows for medium and high index contrast waveguides with very low channel attenuation. The geometry is basically formed by a rectangular cross-section silicon nitride $(Si_{3}N_{4})$ filled with and encapsulated by silicon dioxide $(SiO_{2})$. The birefringence and minimal bend radius of the waveguide is completely controlled by the geometry of the waveguide layer structures. Experiments on typical geometries will be presented, showing excellent characteristics (channel attenuation ≤0.06 dB/cm, IL ≤0.6 dB, PDL ≤0.2 dB, Bg «1 x $10^{-3}$, bend radius ≤500 μm)

Extracellular release of the ‘differentiation enhancing factor’, a HMG1 protein type, is an early step in murine erythroleukemia cell differentiation

AbstractDifferentiation enhancing factor (DEF) is a 29 kDa protein expressed in murine erythroleukemia (MEL) cells and active in promoting a significant increase in the rate of hexamethylenebisacetamide induced differentiation of these cells. The factor was recently shown to possess an amino acid sequence identical to that reported for one of the HMG1 proteins, designated as ‘amphoterin’ on the basis of its highly dipolar sequence. In the present study, we have expressed DEF cDNA in an E. coli strain and found that the recombinant protein has functional properties identical to those observed with native DEF. Furthermore, we demonstrate that, following MEL cell stimulation with the chemical inducer, DEF is secreted in large amounts in the extracellular medium. In fact, the N-terminal sequence and the partial amino acid sequence of tryptic peptides from the secreted protein correspond to those of DEF isolated from the soluble fraction of resting MEL cells. These results are indicative for an extracellular localization as the site of action of DEF and suggest a novel function for proteins belonging to the HMG1 family. Finally, the early decay of DEF mRNA, in chemical induced MEL cells, support the hypothesis that the involvement of the enhancing factor occurs and is completed in the early phases of cell differentiation

Phosphorylation of rat brain calpastatins by protein kinase C

AbstractCalpastatin, the natural inhibitor of calpain, is present in rat brain in multiple forms, having different molecular masses, due to the presence of one (low Mr form) or four (high Mr form) repetitive inhibitory domains. Recombinant and native calpastatin forms are substrates of protein kinase C, which phosphorylates a single serine residue at their N-terminus. Furthermore, both low and high Mr calpastatins are phosphorylated by protein kinase C at the same site. These calpastatin forms are phosphorylated also by protein kinase A, although with a lower efficiency. The incorporation of a phosphate group determines an increase in the concentration of Ca2+ required to induce the formation of the calpain-calpastatin complex. This effect results in a large decrease of the inhibitory efficiency of calpastatins. We suggest that phosphorylation of calpastatin represents a mechanism capable to balance the actual amount of active calpastatin to the level of calpain to be activated

Surface nanoscale axial photonics: Robust fabrication of high quality factor microresonators

Recently introduced Surface Nanoscale Axial Photonics (SNAP) makes it possible to fabricate high Q-factor microresonators and other photonic microdevices by dramatically small deformation of the optical fiber surface. To become a practical and robust technology, the SNAP platform requires methods enabling reproducible modification of the optical fiber radius at nanoscale. In this Letter, we demonstrate super-accurate fabrication of high Q-factor microresonators by nanoscale modification of the optical fiber radius and refractive index using the CO2 laser and the UV excimer laser beam exposures. The achieved fabrication accuracy is better than 2 angstroms in variation of the effective fiber radius

Cutting edge: extracellular high mobility group box-1 protein is a proangiogenic cytokine.

The chromosomal high mobility group box-1 (HMGB1) protein acts as a proinflammatory cytokine when released in the extracellular environment by necrotic and inflammatory cells. In the present study, we show that HMGB1 exerts proangiogenic effects by inducing MAPK ERK1/2 activation, cell proliferation, and chemotaxis in endothelial cells of different origin. Accordingly, HMGB1 stimulates membrane ruffling and repair of a mechanically wounded endothelial cell monolayer and causes endothelial cell sprouting in a three-dimensional fibrin gel. In keeping with its in vitro properties, HMGB1 stimulates neovascularization when applied in vivo on the top of the chicken embryo chorioallantoic membrane whose blood vessels express the HMGB1 receptor for advanced glycation end products (RAGE). Accordingly, RAGE blockade by neutralizing Abs inhibits HMGB1-induced neovascularization in vivo and endothelial cell proliferation and membrane ruffling in vitro. Taken together, the data identify HMGB1/RAGE interaction as a potent proangiogenic stimulus

EEG correlates of social interaction at distance

This study investigated EEG correlates of social interaction at distance between twenty-five pairs of participants who were not connected by any traditional channels of communication. Each session involved the application of 128 stimulations separated by intervals of random duration ranging from 4 to 6 seconds. One of the pair received a one-second stimulation from a light signal produced by an arrangement of red LEDs, and a simultaneous 500 Hz sinusoidal audio signal of the same length. The other member of the pair sat in an isolated sound-proof room, such that any sensory interaction between the pair was impossible. An analysis of the Event-Related Potentials associated with sensory stimulation using traditional averaging methods showed a distinct peak at approximately 300 ms, but only in the EEG activity of subjects who were directly stimulated. However, when a new algorithm was applied to the EEG activity based on the correlation between signals from all active electrodes, a weak but robust response was also detected in the EEG activity of the passive member of the pair, particularly within 9 – 10 Hz in the Alpha range. Using the Bootstrap method and the Monte Carlo emulation, this signal was found to be statistically significant

TRAIL, OPG, and TWEAK in kidney disease: biomarkers or therapeutic targets?

Ligands and receptors of the tumor necrosis factor (TNF) superfamily regulate immune responses and homeostatic functions with potential diagnostic and therapeutic implications. Kidney disease represents a global public health problem, whose prevalence is rising worldwide, due to the aging of the population and the increasing prevalence of diabetes, hypertension, obesity, and immune disorders. In addition, chronic kidney disease is an independent risk factor for the development of cardiovascular disease, which further increases kidney-related morbidity and mortality. Recently, it has been shown that some TNF superfamily members are actively implicated in renal pathophysiology. These members include TNF-related apoptosis-inducing ligand (TRAIL), its decoy receptor osteoprotegerin (OPG), and TNF-like weaker inducer of apoptosis (TWEAK). All of them have shown the ability to activate crucial pathways involved in kidney disease development and progression (e.g. canonical and non-canonical pathways of the transcription factor nuclear factor-kappa B), as well as the ability to regulate cell proliferation, differentiation, apoptosis, necrosis, inflammation, angiogenesis, and fibrosis with double-edged effects depending on the type and stage of kidney injury. Here we will review the actions of TRAIL, OPG, and TWEAK on diabetic and non-diabetic kidney disease, in order to provide insights into their full clinical potential as biomarkers and/or therapeutic options against kidney disease