The existing literature highlights the importance of psychosexual education for adolescents with autism spectrum disorder (ASD). We developed a group training program on sexuality and affectivity, specifically designed for adolescents with ASD, with the aim of investigating changes in psychosexual functioning after the intervention and evaluating its clinical utility. The program, consisting of 10 sessions and conducted by two expert clinicians, was administered to three small groups (maximum six participants per group), for a total of 17 adolescents (aged 12-18) diagnosed with ASD without intellectual disability or language impairment. Parent-report measures of sociosexual behaviors were collected at baseline (T0), after the intervention (T1), and at a three-month follow-up (T2). Cognitive abilities and ASD symptom severity were also assessed at baseline for each participant. No significant differences emerged among the three groups in terms of cognitive functioning or ASD symptom severity. Analysis of the entire sample revealed a significant improvement in sex education knowledge and a reduction in dysfunctional sexual behaviors following participation in the program, regardless of cognitive level or symptom severity. Conversely, no significant changes were found in social behaviors related to sexuality, privacy awareness, or parental concerns. These findings suggest that participation in a psychosexual group training program tailored for adolescents with ASD may enhance knowledge and reduce problematic behaviors in the sociosexual domain. Future implementations may benefit from increasing the number of sessions, employing both self- and parent-report measures, including satisfaction and fidelity assessments, and involving caregivers in parallel sessions to maximize clinical impact.
Antimicrobial resistance (AMR) is a paramount global health threat. While antibiotic misuse is a recognized driver, other environmental pollutants, particularly non-biodegradable heavy metals, are increasingly implicated in the selection and dissemination of resistance through co-selection mechanisms. This systematic review synthesizes evidence on the role of environmental heavy metal contamination as a driver of AMR evolution and spread. A systematic search was conducted across seven databases (PubMed, Web of Science, Scopus, Cochrane, Biomed Central, Google Scholar, and Embase) between November 2023 and January 2024, following PRISMA guidelines. Studies investigating the impact of heavy metals on AMR in environmental matrices were included. Study quality was assessed using the CASP checklist, and data were synthesized thematically. From 9513 records, 22 studies published between 2018 and 2024 were included. Evidence frequently reported strong associations between heavy metal pollution (e.g., Pb, Cd, Hg) and increased abundance and diversity of antibiotic resistance genes (ARGs) in wastewater, riverine, and soil ecosystems. The dominant mechanism identified in the reviewed studies was co-resistance, with metal resistance genes and ARGs co-located on mobile genetic elements, facilitating horizontal transfer. Cross-resistance and co-regulation were also reported. Importantly, metal pollution was linked to the environmental presence of high-risk multidrug-resistant pathogens. Methodological appraisal revealed a predominance of cross-sectional studies and limited data on metal speciation, constraining causal inference. The reviewed evidence suggests that environmental heavy metal pollution may be an important but underappreciated driver of AMR, potentially acting through co-selection. Effective AMR control requires integrated strategies combining antimicrobial stewardship with environmental governance. Future studies should adopt longitudinal designs and advanced molecular tools to establish causation and quantify risks. Environmental heavy metal pollution from industry and agriculture releases persistent toxins like lead and mercury into ecosystems. This pressure selects for bacteria carrying metal and antibiotic resistance traits that may be linked through multiple mechanisms including co-resistance (genes on shared mobile elements). These resistant traits can spread between microbes via horizontal gene transfer in contaminated water and soil. Ultimately, this process may contribute to the emergence of multidrug-resistant pathogens, threatening to compromise antibiotic efficacy and human health on a global scale
DNA single-strand breaks (SSB) formation coordinates the myogenic program, and defects in SSB repair in post-mitotic cells have been associated with human diseases. However, the DNA damage response by SSB in terminally differentiated cells has not been explored yet. Here we show that mouse post-mitotic muscle cells accumulate SSB after alkylation damage, but they are extraordinarily resistant to the killing effects of a variety of SSB-inducers. We demonstrate that, upon SSB induction, phosphorylation of H2AX occurs in myotubes and is largely ataxia telangiectasia mutated (ATM)-dependent. However, the DNA damage signaling cascade downstream of ATM is defective as shown by lack of p53 increase and phosphorylation at serine 18 (human serine 15). The stabilization of p53 by nutlin-3 was ineffective in activating the cell death pathway, indicating that the resistance to SSB inducers is due to defective p53 downstream signaling. The induction of specific types of damage is required to activate the cell death program in myotubes. Besides the topoisomerase inhibitor doxorubicin known for its cardiotoxicity, we show that the mitochondria-specific inhibitor menadione is able to activate p53 and to kill effectively myotubes. Cell killing is p53-dependent as demonstrated by full protection of myotubes lacking p53, but there is a restriction of p53-activated genes. This new information may have important therapeutic implications in the prevention of muscle cell toxicity.
Numerous research works have tried to evaluate the correlation between inflammation and the onset of prostate cancer. Given the in vitro antioxidant power and the anti-proliferative effects on human prostate cancer cells shown by a Juglans regia L. fresh fruit extract, the aim of this work was the evaluation of its potential in the acute and chronic inflammatory states in vivo, revealing a strong anti-inflammatory activity. In the zymosan-induced edema formation assay, a light and non-significant edema reduction was shown. On the contrary, in the zymosan-induced thermal hyperalgesia assay, the reversion of hyperalgesia after the extract administration was determined. Moreover, in the formalin test, the extract caused a significant decrease in the licking time caused by the aldehyde, especially in the late phase. In silico, quercetin showed the best fit into the enzymatic pocket of AChE (docking score: −11.306 Kcal/mol). Neochlorogenic acid and ellagic acid gave the best docking scores on BChE (−10.292 Kcal/mol and −10.054 Kcal/mol, respectively). Abscisic acid showed a high binding affinity for the glucocorticoid receptor. Finally, quercetin and abscisic acid were quantified to complete the data by HPLC-DAD, giving 0.246 ± 0.003 mg/g of dried extract and 0.036 ± 0.004 mg/g of dried extract, respectively.
Cutaneous melanoma is a highly aggressive type of cancer with a poor prognosis at advanced stages. Accumulating evidence demonstrates that metabolic reprogramming is essential for melanoma, allowing it to adapt to both cellular changes, due to its genetic instability, and to micro-environmental stimuli. This review provides an overview of how melanoma cells remodel membrane lipids during melanoma progression with a focus on how environmental stresses (e.g., UV radiation) affect tumor aggressiveness and therapy resistance by reshaping membrane structure, fluidity, and composition. Dietary lipids, especially omega-3 polyunsaturated fatty acids (PUFAs), further modulate membrane properties and can sensitize melanoma cells to oxidative stress and ferroptosis, revealing potential therapeutic vulnerabilities. Finally, we discuss emerging evidence that lipid signatures, including circulating lipid profiles and melanoma-derived exosomes, have prognostic and predictive value. Together, these insights emphasize the importance of lipid metabolism and membrane architecture as key factors in melanoma biology and as promising targets for personalized interventions.
