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This paper presents a comprehensive methodology to forecast the daily energy demand associated with recharging private electric vehicles in urban areas. The approach is based on plausible scenarios regarding the penetration of battery-powered vehicles and the availability of charging infrastructure. Accurate space and time forecasting of charging activities and power requirements is a critical issue in supporting the transition from conventional to battery-powered vehicles for urban mobility. This technological shift represents a key milestone toward achieving the zero-emissions target set by the European Green Deal for 2050. The methodology leverages Floating Car Data (FCD) samples. The widespread use of On-Board Units (OBUs) in private vehicles for insurance purposes ensures the methodology’s applicability across diverse geographical contexts. In addition to FCD samples, the estimation of charging demand for private electric vehicles is informed by a large-scale, detailed survey conducted by ENEA in Italy in 2023. Funded by the Ministry of Environment and Energy Security as part of the National Research on the Electric System, the survey explored individual charging behaviors during daily urban trips and was designed to calibrate a discrete choice model. To date, the methodology has been applied to the Metropolitan Area of Rome, demonstrating robustness and reliability in its results on two different scenarios of analysis. Each demand/supply scenario has been evaluated in terms of the hourly distribution of peak charging power demand, at the level of individual urban zones or across broader areas. Results highlight the role of the different components of power demand (at home or at other destinations) in both scenarios. Charging at intermediate destinations exhibits a dual peak pattern—one in the early morning hours and another in the afternoon—whereas home-based charging shows a pronounced peak during evening return hours and a secondary peak in the early afternoon, corresponding to a decline in charging activity at other destinations. Power distributions, as expected, sensibly differ from one scenario to the other, conditional to different assumptions of private and public recharge availability and characteristics.

Background Atrial fibrillation (AF) after thoracic surgery is a continuing source of morbidity and mortality. The effect of postoperative AF on long-term survival however has not been studied. Our aim was to evaluate the impact of AF on early outcome and on survival > 5 years after pulmonary lobectomy for lung cancer. Methods From 1996 to June 2009, 454 consecutive patients undergoing lobectomy for lung cancer were enrolled and followed-up until death or study end (October 2010). Patients with postoperative AF were identified; AF was investigated with reference to its predictors and to short- and long-term survival (> 5 years). Results Hospital mortality accounted for 7 patients (1.5%), while postoperative AF occurred in 45 (9.9%). Independent AF predictors were: preoperative paroxysmal AF (odds ratio [OR] 5.91; 95%CI 2.07 to 16.88), postoperative blood transfusion (OR 3.61; 95%CI 1.67 to 7.82) and postoperative fibro-bronchoscopy (OR 3.39; 95%CI 1.48 to 7.79). Patients with AF experienced higher hospital mortality (6.7% vs. 1.0%, p = 0.024), longer hospitalization (15.3 ± 10.1 vs. 12.2 ± 5.2 days, p = 0.001) and higher intensive care unit admission rate (13.3% vs. 3.9%, p = 0.015). The median follow-up was 36 months (maximum: 179 months). Among the 445 discharged subjects with complete follow-up, postoperative AF was not an independent predictor of mortality; however, among the 151 5-year survivors, postoperative AF independently predicted poorer long-term survival (HR 3.75; 95%CI 1.44 to 9.08). Conclusion AF after pulmonary lobectomy for lung cancer, in addition to causing higher hospital morbidity and mortality, predicts poorer long-term outcome in 5-year survivors.

Mobility management is a regulatory framework designed to streamline systematic mobility and mitigate energy, environmental and economic impacts. In this work, we propose a flexible methodology for evaluating the sustainability of home-to-work travel, providing a comprehensive and detailed ex post cost–benefit assessment. Specifically, we analyzed the effectiveness of the shuttle service operating in the ENEA “Casaccia” Research Centre in pre-pandemic times. Initially, we conducted an online survey to collect data with the aim of characterizing the travel behavior of the staff and reconstructing the multi-modal individual mobility patterns. Over 70% of the recipients, which amounted to about 950 individuals, completed the survey. Subsequently, we studied two alternative scenarios—with and without the shuttle service—comparing their total mileage, energy consumption, and pollutant emissions and performing an economic analysis. Our findings suggest that operating the service has a significant impact on air pollutants and greenhouse gas emissions, with reductions of 97% for volatile organic compounds, 72% for particulate matter, and 60% for carbon dioxide. Moreover, the cost–benefit analysis reveals that both users and the community reaped benefits from the provision of the collective service. These benefits are estimated to be almost EUR 1.35 M per year.

Cytopathological analyses of bronchial washings (BWs) collected during fibre‐optic bronchoscopy are often inconclusive for lung cancer diagnosis. To address this issue, we assessed the suitability of conducting molecular analyses on BWs, with the aim to improve the diagnosis and outcome prediction of lung cancer. The methylation status of RASSF1A, CDH1, DLC1 and PRPH was analysed in BW samples from 91 lung cancer patients and 31 controls, using a novel two‐colour droplet digital methylation‐specific PCR (ddMSP) technique. Mutations in ALK, BRAF, EGFR, ERBB2, KRAS, MAP2K1, MET, NRAS, PIK3CA, ROS1 and TP53 and gene fusions of ALK, RET and ROS1 were also investigated, using next‐generation sequencing on 73 lung cancer patients and 14 tumour‐free individuals. Our four‐gene methylation panel had significant diagnostic power, with 97% sensitivity and 74% specificity (relative risk, 7.3; odds ratio, 6.1; 95% confidence interval, 12.7–127). In contrast, gene mutation analysis had a remarkable value for predictive, but not for diagnostic, purposes. Actionable mutations in EGFR, HER2 and ROS1 as well as in other cancer genes (KRAS, PIK3CA and TP53) were detected. Concordance with gene mutations uncovered in tumour biopsies was higher than 90%. In addition, bronchial‐washing analyses permitted complete patient coverage and the detection of additional actionable mutations. In conclusion, BWs are a useful material on which to perform molecular tests based on gene panels: aberrant gene methylation and mutation analyses could be performed as approaches accompanying current diagnostic and predictive assays during the initial workup phase. This study establishes the grounds for further prospective investigation. Diagnostic and predictive assessment remains major challenges in lung cancer management. In this work, we investigate the importance of molecular investigations applied to bronchial washings collected during fibre‐optic bronchoscopy for lung lesions. Using a cancer‐specific DNA methylation panel and gene mutations analyses, we demonstrated that bronchial washing represents a useful material for performing molecular tests in lung cancer patients.

Public Transport (PT) planning requires a detailed evaluation of the fleet energy consumption, usually depending on the specific characteristics of the bus service network. These include topography, climate and operational features. In this work, we focus on the additional air conditioning (AC) energy consumption, proposing a method to evaluate the extra energy consumption based not only on climate variables, but also on the PT planned service. Results are presented for a large part of the provincial capitals and regions of Italy, and clearly show that overconsumption for air conditioning are significantly affected by the daily mileage distribution, with large variance even when climatic conditions are similar. The mileage data are extracted from GTFS databases, widely available for PT applications. The developed tool allows us to apply this methodology to any urban and extra-urban area. Reference AC consumption related to climate conditions are derived from a measurement campaign hold in Cagliari (Sardinia, Italy) during September 2018, within the National Research Program on the Electric System. A discussion on how to optimize the use of climatic data is also presented, resulting in the choice to use Heat Index as unique independent variable for air conditioning energy consumption calculation. A methodology to compute the Heat Index from climatic variables for large domains as, for instance, the Italian regions, was also developed.

– Dall’invenzione del Web, sempre più studiosi si chiedono in quale misura le nuove modalità di scrittura e fruizione delle storie stiano modificando il modo in cui comunichiamo, ci relazioniamo, raccontiamo, e come influiscano sul nostro cervello. Questo contributo mette in luce come le modalità di produzione e pubblicazione dei racconti autobiografici e delle fanfiction all’interno del cyberspazio e la natura ‘convergente’ delle comunità online entro cui vengono creati renderebbero questo fenomeno culturale l’ambiente ideale per la costituzione di una identità ibrida, che contribuisce alla creazione di nuove modalità di formattazione del racconto. Dall’analisi a campione di blog, microblog e fanfiction emerge un nuovo format digitale, che si allontana sempre più dal tradizionale impianto narrativo occidentale.

Rett syndrome (RTT) is an autism spectrum disorder mainly caused by mutations in the X-linked MECP2 gene and affecting roughly 1 out of 10.000 born girls. Symptoms range in severity and include stereotypical movement, lack of spoken language, seizures, ataxia and severe intellectual disability. Notably, muscle tone is generally abnormal in RTT girls and women and the Mecp2-null mouse model constitutively reflects this disease feature. We hypothesized that MeCP2 in muscle might physiologically contribute to its development and/or homeostasis, and conversely its defects in RTT might alter the tissue integrity or function. We show here that a disorganized architecture, with hypotrophic fibres and tissue fibrosis, characterizes skeletal muscles retrieved from Mecp2-null mice. Alterations of the IGF-1/Akt/mTOR pathway accompany the muscle phenotype. A conditional mouse model selectively depleted of Mecp2 in skeletal muscles is characterized by healthy muscles that are morphologically and molecularly indistinguishable from those of wild-type mice raising the possibility that hypotonia in RTT is mainly, if not exclusively, mediated by non-cell autonomous effects. Our results suggest that defects in paracrine/endocrine signaling and, in particular, in the GH/IGF axis appear as the major cause of the observed muscular defects. Remarkably, this is the first study describing the selective deletion of Mecp2 outside the brain. Similar future studies will permit to unambiguously define the direct impact of MeCP2 on tissue dysfunctions.

Embryonic VE-Cadherin-expressing progenitors (eVE-Cad+), including hemogenic endothelium, have been shown to generate hematopoietic stem cells and a variety of other progenitors, including mesoangioblasts, or MABs. MABs are vessel-associated progenitors with multilineage mesodermal differentiation potential that can physiologically contribute to skeletal muscle development and regeneration, and have been used in an ex vivo cell therapy setting for the treatment of muscular dystrophy. There is currently a therapeutic need for molecules that could improve the efficacy of cell therapy protocols; one such good candidate is nitric oxide. Several studies in animal models of muscle dystrophy have demonstrated that nitric oxide donors provide several beneficial effects, including modulation of the activity of endogenous cell populations involved in muscle repair and the delay of muscle degeneration. Here we used a genetic lineage tracing approach to investigate whether the therapeutic effect of nitric oxide in muscle repair could derive from an improvement in the myogenic differentiation of eVE-Cad+ progenitors during embryogenesis. We show that early in vivo treatment with the nitric oxide donor molsidomine enhances eVE-Cad+ contribution to embryonic and fetal myogenesis, and that this effect could originate from a modulation of the properties of yolk sac hemogenic endothelium.

Background and Aim. Portal hypertension has been reported in association with acquired and primary immune deficiencies without a comprehensive description of associated spleno-portal axis abnormalities. Pathological mechanisms are poorly defined. Methods. Observational, single centre study with the aim of assessing the prevalence of spleno-portal axis abnormalities in an unselected cohort of 123 patients with primary antibody deficiencies and without known causes of liver diseases regularly followed up for a mean time of 18 ± 14 years. A cumulative period of 1867 patients-year was analysed. Clinical and immunological data, abdominal ultrasounds, CT scans, and endoscopy features were included in the analysis. Results. Twenty-five percent of patients with primary antibody deficiencies had signs of portal vein enlargement but only 4% of them had portal hypertension, with portal systemic collaterals. Liver biopsies showed liver sinusoids congestive dilatation, endothelization, and micronodularity fulfilling the criteria for noncirrhotic portal hypertension. Patients with portal vein enlargement had severe clinical and immunological phenotypes. Conclusions. In primary antibody deficient patients, infections, inflammations, splenomegaly, increased blood venous flow, and lymphocyte abnormalities contribute to establishment of liver damage possibly leading to noncirrhotic portal hypertension. Patients with primary antibody deficiency should be considered a good model to give insight into the pathological mechanisms underlying noncirrhotic portal hypertension.

Medulloblastoma (MB), one of the most malignant brain tumors of childhood, comprises distinct molecular subgroups, with p53 mutant sonic hedgehog-activated (SHH-activated) MB patients having a very severe outcome that is associated with unfavorable histological large cell/anaplastic (LC/A) features. To identify the molecular underpinnings of this phenotype, we analyzed a large cohort of MB developing in p53-deficient Ptch+/- SHH mice that, unexpectedly, showed LC/A traits that correlated with mTORC1 hyperactivation. Mechanistically, mTORC1 hyperactivation was mediated by a decrease in the p53-dependent expression of mTORC1 negative regulator Tsc2. Ectopic mTORC1 activation in mouse MB cancer stem cells (CSCs) promoted the in vivo acquisition of LC/A features and increased malignancy; accordingly, mTORC1 inhibition in p53-mutant Ptch+/- SHH MB and CSC-derived MB resulted in reduced tumor burden and aggressiveness. Most remarkably, mTORC1 hyperactivation was detected only in p53-mutant SHH MB patient samples, and treatment with rapamycin of a human preclinical model phenocopying this subgroup decreased tumor growth and malignancy. Thus, mTORC1 may act as a specific druggable target for this subset of SHH MB, resulting in the implementation of a stringent risk stratification and in the potentially rapid translation of this precision medicine approach into the clinical setting.