University of Cagliari

The concept of sustainability, as outlined by the United Nations’ Sustainable Development Goals (SDGs), refers to the ability to meet the needs of the present without compromising the ability of future generations to meet their own needs. This vision is addressed by combining goals concerning the environmental , social , and economic spheres. In this context, Recommender Systems (RS) have emerged as tools that can foster these principles by nudging responsible user behavior and promoting sustainable decision-making. However, the interplay between RS and sustainability is inherently complex since it can be analyzed from two different perspectives: (i) RS for Sustainability , which focuses on how recommendation algorithms can support the achievement of SDGs, and (ii) Sustainability of RS , which focuses on developing recommendation models that inherently adhere to sustainability principles. While the integration of both these perspectives is beneficial and crucial, unfortunately, the current literature has addressed these aspects independently. Accordingly, in this survey, we first provide a comprehensive review of the existing literature on RS that either promotes sustainable behaviors aligned with the SDGs or embeds sustainability principles into their algorithmic design. Next, we identify current gaps and propose key research directions toward an integrated, holistic approach that concurrently addresses both aspects to advance the development of sustainable RS. • This survey distinguishes two key dimensions: Recommender Systems (RS) for Sustainability and Sustainability of RS. • The work reviews existing studies that promote sustainable behaviors or embed sustainability principles in their design. • The work identifies critical gaps in current research and outlines a roadmap for developing sustainable recommender systems.

Valorization or recycling of the hydrothermal liquefaction aqueous phase (HTL-AP) pose a substantial obstacle to the commercial use of the HTL process for biomass (especially algal). This is due to its high concentration of organic constituents and nutrients. This article focus on nanofiltration (NF) of acidic and basic synthetic HTL-AP using a DuPont FilmTec™ NF90 membrane in a batch crossflow module. The emphasis is on rejection performance and fouling behavior, supported by membrane autopsy. Overall, almost 90% rejection of COD, NH 4 + , and PO 4 3- , and TDS/conductivity was achieved. HTL-AP(pH=4) led to higher NH 4 + rejection (94±1%) compared with pH=8.5 (83±3%). This can be attributed to the formation of a gel layer and the equilibrium between NH 4 + and NH 3, favoring the more permeable NH 3 at higher pH. Flux monitoring revealed that NF90 performs better (J 30 wt% recovery /J 0 ca. 0.77±0.02) with HTL-AP(pH=8.5) than at pH=4 (0.56±0.06) since at pH=8.5 most of the small organic compounds are deprotonated and therefore exhibit weaker interactions with the negatively charged NF90 surface. At both HTL-AP pH levels irreversible fouling is negligible while gel layer and concentration polarization are major contributors which are reversible through water flushing. Resistance due to the gel layer formation was more prominent for HTL-AP(pH=4). The presence of a thin gel layer was confirmed through attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR), scanning electron microscopy (SEM), water contact angle measurements, and thermal gravimetric analysis (TGA). In addition, fouling resistance due to pore blockage and persistent adsorbed foulants inside the membrane matrix is also a significant contributor. This was removed successfully by basic cleaning (NaOH). • Treatment of complex synthetic HTL-AP using NF90 nanofiltration membrane. • NF90 rejection compared for acidic/basic HTL-AP with up to 30 wt% permeate recovery. • High pollutant rejection; permeate quality similar to untreated urban wastewater. • High flux recovery after NaOH flushing with only slight irreversible fouling. • Membrane autopsy results provided key support for the fouling analysis

Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction and bronchial hyperresponsiveness, affecting millions worldwide and showing heterogeneity in its endotype, clinical presentation, and severity. Following the principles of modern precision medicine, studying an asthmatic patient involves collecting various biomarkers that may assist in diagnosis, management, and characterization of the disease to predict clinical outcomes and treatment responses. Although systemic corticosteroid use should be limited to specific situations, this therapy still plays a crucial role in managing an asthmatic patient, especially during exacerbations. While it is known that steroids can affect biomarkers, the extent of this impact is often unclear. This remains an open issue, particularly in patients with severe asthma, where systemic steroids are more frequently used and biomarker measurement can deeply influence management and even access to therapy. Misinterpreting biomarkers can lead to over- or underestimating asthma severity, potentially resulting in serious consequences. In this comprehensive analysis, we have collected the available literature data on how systemic corticosteroids can affect different biomarkers used in clinical practice and research setting, categorizing them into humoral (eg, blood eosinophil count, total and specific IgE, alfa-1 antitrypsin, interleukins, eosinophil cationic protein, and thymic stromal lymphopoietin), instrumental (eg, spirometry, impulse oscillometry, fractional and multiple flow exhaled nitric oxide, and nasal nitric oxide), and clinical (ear-nose-throat and gastroenterological evaluation). The goal is to provide a practical and concise overview of this impact to assist clinicians in interpreting biomarkers independently of steroid therapy. Research should focus on developing predictive models that adjust individual biomarker readings for steroid dosage and duration, as well as markers less affected by corticosteroid interference. A detailed understanding of steroid-induced biomarker modulation is crucial for accurate asthma phenotyping, personalized treatment choices, and avoiding adverse outcomes caused by both under- and overtreatment. Going forward, integrating improved biomarker correction methods, enhancing patient education on steroid use, and continuing research into new inflammatory markers will be crucial for improving the accuracy and effectiveness of asthma management.

To compare in vitro performance of phacoemulsification platforms during critical surgical phases including aspiration, occlusion and occlusion break. Five phacoemulsification platforms (Alcon Centurion, Bausch & Lomb PC Stellaris, BVI Virtuoso, DORC Eva Nexus and Zeiss Quatera) underwent standardized testing including controlled occlusion within a collapsible test chamber. Tests were conducted with 21G tips, infusion pressure presets 30 and 55 mmHg, flow-rate 30 ml/min and vacuum range 200–600 mmHg. Outcome measures included Intraocular Pressure (IOP) at rest, during aspiration, occlusion and standardized occlusion break as well as chamber volume loss and time to regain 90% of IOP after/during occlusion break. All devices kept target IOP at rest. During aspiration, IOP changed significantly (p < 0.01): Stellaris showed the greatest IOP reduction, Quatera had small decrease, Virtuoso maintained preset, Centurion and Eva Nexus slightly overcompensated. During occlusion, Eva Nexus and Stellaris PC exceeded the preset 55 mmHg (p < 0.05) whereas other machines remained on target. Upon occlusion break, volume loss ranged 35-200μL (p < 0.001) and recovery time to 90% of preset IOP varied between 0.30–2 s (p < 0.001) with Centurion and Virtuoso outperforming others at 30 mmHg IOP and Centurion, Quatera and Virtuoso at 55 mmHg IOP. Phacoemulsifiers exhibited distinct behaviour under standardized conditions and fluidic settings significantly influenced performance. Surgeon must understand machines’ fluidic to master different platforms. What is known What is new

Mentalising skills may be conceptualised as composed by both personal and interpersonal competencies, in turn shaped by early adverse experiences and coping strategies. Although cross-sectional observations described a role for mentalising skills in burnout development, large-scale longitudinal studies on the topic remain limited, especially in relation to psychiatry training. The primary aim was to investigate protective and risk factors for higher burnout scores across time. Secondary aims included testing whether psychiatry exhibited different burnout scores across time in comparison to other medical residents. A cohort of 1803 medical residents (1131 psychiatry residents) was assessed for mentalising skills, conceptualised as composed of emotional regulation (Difficulties in Emotion Regulation Scale), interpersonal competencies (Interpersonal Competence Questionnaire), coping strategies (Coping Orientation to Problems Experienced) and burnout dimensions (Maslach Burnout Inventory). One-year follow-up was available for 520 psychiatry residents (73.03% response rate) and 234 other medical residents (35.94% response rate). Longitudinal mixed models and bivariate latent change models were employed. Across all residents, greater levels of burnout were associated with higher scores in insecure attachment, emotional dysregulation and maladaptive coping, as well as lower scores in interpersonal skills. Attending at least one supervision per month was associated with lower burnout scores across time. According to a bivariate latent change model, emotional regulation improvements through years were associated with lower burnout scores across time. In psychiatry residents, lower burnout scores across time were observed as compared to other medical residents. Psychiatry residents benefited from a higher protective effect of interpersonal competencies (group by moderator by time interaction) and coping strategies against burnout. Mentalising skills may mitigate burnout development. Training in psychiatry emerged as a potential mitigating factor against burnout increases. Structured supervisions may foster professional development and emotional resilience.

Abstract Alzheimer’s disease (AD) is characterized by a prolonged asymptomatic phase before cognitive decline emerges, yet the mechanisms driving symptom onset remain unclear. Here, we hypothesized that the transition from asymptomatic to symptomatic disease is linked to dysfunction of brain–immune communication. Retrograde neuronal tracing in the 5xFAD mouse model of amyloidosis revealed reduced brain–spleen connectivity at advanced disease stages. To probe the functional role of the brain–spleen axis in coping with disease, we denervated the splenic nerve at an early presymptomatic stage. This intervention accelerated cognitive decline, impaired splenic hematopoiesis, diminished monocyte recruitment to the brain, disrupted monocyte–microglia signaling networks, and reduced the transition of microglia from a homeostatic to the disease-associated (DAM) state. Conversely, enhancing splenic noradrenergic input increased hematopoiesis, restored monocyte homing to the brain, and delayed cognitive impairment. The protective role of splenic monocytes was independently validated in a retinal cytotoxic injury model, in which splenic denervation impaired post-insult retinal ganglion cell survival. Together, these findings identify an active brain–spleen circuit in regulating monocyte recruitment and establish peripheral monocytes as key drivers of microglial state transitions and disease progression.

Wilson's disease (WD) is a rare genetic disorder of copper transport due to mutations in the ATP7B gene. This results in copper overload and tissue damage that is most evident in the liver and brain. Over 1000 pathogenic mutations have been found in WD patients, and of these, mutations within the ATP7B coding region predominate. In this study, we perform functional analyses of 7 rare sequence variations in the promoter region of the ATP7B gene. We performed dual luciferase reporter assays in HepG2 and SH-SY5Y cell lines under basal conditions and after the addition of 10 μM or 40 μM concentrations of CuSO4. The results showed that promoter activity varied both according to the haplotype and the cell line used. Our results suggest a potential role of promoter polymorphisms in the variation of ATP7B gene expression with probable implications in copper accumulation in the organism and consequent phenotype variation in WD. In addition, given the association of copper concentration and ATP7B expression in the brain, promoter polymorphisms could act as susceptibility determinants of neurodegeneration in the most common late-onset nervous system diseases. Finally, promoter involvement in ATP7B overexpression and platinum resistance presents new mechanisms of great importance that need to be better understood. Further experimental and clinical studies are necessary to further explore the role of the ATP7B promoter in copper and platinum management. These studies will offer new insights for the development of molecular therapies for brain degenerative and tumor diseases.