Archivio Istituzionale della Ricerca- Università del Piemonte Orientale
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Correction: Serum levels of per- and polyfluoroalkylated substances and methylation of DNA from peripheral blood (Frontiers in Public Health, (2025), 13, (1621495), 10.3389/fpubh.2025.1621495)
No full textIn the published article, there was an error in [Figure 3] as published. [Only the two panels corresponding to PFOS (3B) were displayed, while those related to Figure PFOA (3A) were missing]. The corrected [Figure 3] and its caption [ORIGINAL Caption] appear below. Bar charts for KEGG enrichment analysis of differentially methylated CpG sites associated with (A) PFOA and (B) PFOS at threshold unadjusted p-value < 0.01 in the epigenome-wide association analyses. Pathways were considered significant when the FDR < 0.05. The terms of the KEGG pathways are depicted on the y-axis. On the top figure, the x-axis is the –log10 FDR of the tests of the gene set enrichment in each pathway. On the bottom figure, the x-axis is the ratio between the number of differentially methylated genes and the number of genes in the KEGG term. The different colors represent the –log10 FDR. The original article has been updated
Measurement of the inclusive WZ production cross section in pp collisions at s = 13.6 TeV
No full textThe inclusive WZ production cross section is measured in proton-proton collisions at a centre-of-mass energy of 13.6 TeV, using data collected during 2022 with the CMS detector, corresponding to an integrated luminosity of 34.7 fb−1. The measurement uses multileptonic final states and a simultaneous likelihood fit to the number of events in four different lepton flavour categories: eee, eeμ, μμe, and μμμ. The selection is optimized to minimize the number of background events, and relies on an efficient prompt lepton discrimination strategy. The WZ production cross section is measured in a phase space defined within a 30 GeV window around the Z boson mass, as σtotal (pp → WZ) = 55.2 ± 1.2 (stat) ± 1.2 (syst) ± 0.8 (lumi) ± 0.3 (theo) pb. In addition, the cross section is measured in a fiducial phase space closer to the detector-level requirements. All the measurements presented in this paper are in agreement with standard model predictions
Sex differences in the weight response to GLP-1RA in people with type 2 diabetes. A long-term longitudinal real-world study
No full textSex differences may influence pathophysiology, treatment response, and outcomes of type 2 diabetes (T2D). We assessed whether sex affected clinical response to GLP-1 receptor agonists (GLP-1RA) in a large real-world cohort. Thus, we conducted a multicentre, retrospective, longitudinal study of 7847 individuals with T2D initiating GLP-1RA therapy across 18 Italian diabetes centres. Participants were stratified by self-reported sex. The primary outcome was change in body weight over time; secondary outcomes included changes in HbA1c, renal function, and lipid profile. Analyses were performed using a mixed model for repeated measures, adjusting for baseline imbalances. Participants were 60 % male, with similar age, diabetes duration, and HbA1c (mean 8.0 %). Females had higher BMI but fewer micro- and macrovascular complications. Over a median 4-year follow-up, females experienced significantly greater weight reduction than males (adjusted mean difference: −1.1 kg; p < 0.001), with more females achieving a weight loss of ≥ 5 % (66.5 % vs. 58.0 %, p < 0.001) or ≥ 10 % (40.0 % vs 30.7 %, p < 0.001). This sex difference in weight loss remained unchanged after progressive adjustment for variables that differed between males and females, across GLP-1RA molecules, and after accounting for weight-adjusted drug doses. Instead, HbA1c reductions were comparable between men and women (mean difference 0.4 mmol/mol; p = 0.21). In conclusion, in this real-world cohort, women achieved greater weight loss than men after GLP-1RA initiation, independently of dosing. These findings highlight sex as a potential predictor of GLP-1RA response and support individualized T2D management. Further investigation is needed to clarify the biological mechanisms underlying this sex-specific response
The global, regional, and national burden of cancer, 1990–2023, with forecasts to 2050: a systematic analysis for the Global Burden of Disease Study 2023
No full textBackground: Cancer is a leading cause of death globally. Accurate cancer burden information is crucial for policy planning, but many countries do not have up-to-date cancer surveillance data. To inform global cancer-control efforts, we used the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023 framework to generate and analyse estimates of cancer burden for 47 cancer types or groupings by age, sex, and 204 countries and territories from 1990 to 2023, cancer burden attributable to selected risk factors from 1990 to 2023, and forecasted cancer burden up to 2050. Methods: Cancer estimation in GBD 2023 used data from population-based cancer registration systems, vital registration systems, and verbal autopsies. Cancer mortality was estimated using ensemble models, with incidence informed by mortality estimates and mortality-to-incidence ratios (MIRs). Prevalence estimates were generated from modelled survival estimates, then multiplied by disability weights to estimate years lived with disability (YLDs). Years of life lost (YLLs) were estimated by multiplying age-specific cancer deaths by the GBD standard life expectancy at the age of death. Disability-adjusted life-years (DALYs) were calculated as the sum of YLLs and YLDs. We used the GBD 2023 comparative risk assessment framework to estimate cancer burden attributable to 44 behavioural, environmental and occupational, and metabolic risk factors. To forecast cancer burden from 2024 to 2050, we used the GBD 2023 forecasting framework, which included forecasts of relevant risk factor exposures and used Socio-demographic Index as a covariate for forecasting the proportion of each cancer not affected by these risk factors. Progress towards the UN Sustainable Development Goal (SDG) target 3.4 aim to reduce non-communicable disease mortality by a third between 2015 and 2030 was estimated for cancer. Findings: In 2023, excluding non-melanoma skin cancers, there were 18·5 million (95% uncertainty interval 16·4 to 20·7) incident cases of cancer and 10·4 million (9·65 to 10·9) deaths, contributing to 271 million (255 to 285) DALYs globally. Of these, 57·9% (56·1 to 59·8) of incident cases and 65·8% (64·3 to 67·6) of cancer deaths occurred in low-income to upper-middle-income countries based on World Bank income group classifications. Cancer was the second leading cause of deaths globally in 2023 after cardiovascular diseases. There were 4·33 million (3·85 to 4·78) risk-attributable cancer deaths globally in 2023, comprising 41·7% (37·8 to 45·4) of all cancer deaths. Risk-attributable cancer deaths increased by 72·3% (57·1 to 86·8) from 1990 to 2023, whereas overall global cancer deaths increased by 74·3% (62·2 to 86·2) over the same period. The reference forecasts (the most likely future) estimate that in 2050 there will be 30·5 million (22·9 to 38·9) cases and 18·6 million (15·6 to 21·5) deaths from cancer globally, 60·7% (41·9 to 80·6) and 74·5% (50·1 to 104·2) increases from 2024, respectively. These forecasted increases in deaths are greater in low-income and middle-income countries (90·6% [61·0 to 127·0]) compared with high-income countries (42·8% [28·3 to 58·6]). Most of these increases are likely due to demographic changes, as age-standardised death rates are forecast to change by –5·6% (–12·8 to 4·6) between 2024 and 2050 globally. Between 2015 and 2030, the probability of dying due to cancer between the ages of 30 years and 70 years was forecasted to have a relative decrease of 6·5% (3·2 to 10·3). Interpretation: Cancer is a major contributor to global disease burden, with increasing numbers of cases and deaths forecasted up to 2050 and a disproportionate growth in burden in countries with scarce resources. The decline in age-standardised mortality rates from cancer is encouraging but insufficient to meet the SDG target set for 2030. Effectively and sustainably addressing cancer burden globally will require comprehensive national and international efforts that consider health systems and context in the development and implementation of cancer-control strategies across the continuum of prevention, diagnosis, and treatment. Funding: Gates Foundation, St Jude Children's Research Hospital, and St Baldrick's Foundation
The Chronotope of the Encounter of Nizāmī’s and Dante’s Walking Heroes: The Strength of Human Reality in the Divine Order
No full textThis article intends to examine and compare some examples of representation of the ‘chronotope of the encounter’ (Mikhail Bakhtin) in Nizāmī’s Iskandar Nāma and Dante’s Divina Commedia. In both works, the protagonist is a hero on a journey, a hero who walks and meets many people, whose stories he listens to, and with whom he
enters into dialogical relations that vary according to the situation. We will try to see how the realistic description of these encounters relates to the presence of supernatural elements within the narrated story and to the divine and universal perspective on which the design of the two works is based. In both poets, the force of human reality embodied in the depicted settings, events, and characters tends to press against the didactic, allegorical, and theological framework. On the one hand, as Erich Auerbach writes, ‘Dante’s work made man’s Christian-figural being a reality, and destroyed it in the very process of realizing it. The tremendous pattern was broken by the overwhelming power of the imagery it had to contain.’ On the other hand, Nizāmī offers us a perspective delimiting ‘a sphere and an autonomy for human knowledge’, recognizing its ‘intrinsic value’, and affirming a ‘positive humanity rooted in the experience of the world ..., tending towards the analysis of the concreteness and the active intervention’
(Carlo Saccone
Expanding the Scope of PROTACs: Opportunities and Challenges in Topical Delivery
No full textProteolysis-targeting chimeras (PROTACs) have emerged as a novel therapeutic modality primarily through systemic administration. Recently, their topical use has drawn increasing attention, offering a promising strategy to achieve localized protein degradation while minimizing systemic toxicity. This miniperspective highlights key advances in the development of topical PROTACs, exemplified by AH-001 and GT20029, androgen receptor degraders, both in clinical trials for androgenetic alopecia, with GT20029 also evaluated for acne. We discuss emerging degraders that target clinically relevant proteins, including JAK kinases and BET family members, with applications extending beyond dermatology to pulmonary and ocular diseases and even cosmetic use. Innovative strategies, such as liposomes and microneedle systems, are also enabling effective local delivery. Despite this progress, topical PROTACs face some challenges, such as optimizing the stability, tissue penetration, and selective target engagement under physiological conditions. We conclude by outlining strategic directions that could accelerate the clinical translation of this emerging therapeutic modality
New TNM Staging System Predicts Progression of Small Renal Masses Under Active Surveillance: A Retrospective Analysis of a Single-center Prospective Series
No full text: We validated the newly proposed cT1 classification (new cT1a -tumor size ≤3 cm - vs new cT1b -tumor size >3 cm) for renal masses treated with active surveillance (AS). A prospective AS cohort was retrospectively assessed for growth rate and progression (defined as cTNM upstage, volume doubling time [VDT] 12 mo occurred in 27 patients (11 new cT1b vs 16 new cT1a tumors). Progression-free survival rates at 24, 36, and 60 mo was 73%, 60%, and 40% for new cT1b versus 95%, 88%, and 79% for new cT1a masses, respectively (p < 0.001). In multivariable Cox regression models at a landmark of 12 mo, after adjusting for growth rate, the new TNM classification independently predicted progression (hazard ratio = 4.63, 95% confidence interval: 1.91, 11.2, p < 0.001). The major limitations are the retrospective nature and the lack of renal mass biopsies in a proportion of cases. Our results validated the new cT1a classification system, which may better select patients eligible for AS
Occupational exposure to formaldehyde and risk of lymphoma subtypes: results of a multicentre Italian case-control study
No full textBackground: The International Agency for Research on Cancer classifies formaldehyde as a human carcinogen, with sufficient evidence for nasopharyngeal cancer and leukaemia. However, the association with lymphoma subtypes has been less thoroughly investigated. We explored this link in an Italian multicentre case-control study. Methods: A total of 867 incident lymphoma cases, histologically confirmed using the WHO classification, and 774 controls participated in the study. Occupational experts classified the probability, frequency, and intensity of exposure to formaldehyde for each study subject based on detailed questionnaire data and literature information. We used unconditional regression analysis to model the risk of lymphoma and its main subgroups and subtypes associated with different formaldehyde exposure metrics, adjusting for age, gender, education, and study centre. Results: Ever exposure to formaldehyde was not associated with risk of all lymphomas combined, the non-Hodgkin lymphoma (NHL) and B-cell lymphoma (BCL) subgroups, or the most prevalent BCL subtypes, but multiple myeloma (MM) (OR = 2.0, 95% CI 1.19–3.31). MM risk also showed consistent upward trends with all the exposure metrics (p for trend ranging 0.005–0.034). Hodgkin’s lymphoma risk was also elevated in the top categories of intensity, duration, and cumulative exposure, but no significant increasing trends were observed. Conclusions: Our findings suggest an increased risk of multiple myeloma associated with occupational exposure to formaldehyde. A stronger link was observed for daily exposure lasting 20 years or more. The risk of Hodgkin’s lymphoma was also elevated at high exposure intensities
The interplay between thyrotropic axis, neurological complications, and rehabilitation outcomes in patients with traumatic brain injury
No full textTraumatic brain injury (TBI) is a leading cause of mortality and long-term disability, with its pathophysiology encompassing both primary mechanical damage and secondary neuroinflammatory, metabolic, and biochemical alterations. These complex mechanisms contribute to the observed heterogeneous clinical outcomes, including neuroendocrine dysfunctions, post-traumatic seizures, and disorders of consciousness (DoC). Thyroid hormones (THs) play essential roles in synaptic plasticity, neurogenesis and neuronal homeostasis, and the hypothalamic-pituitary-thyroid (HPT) axis has recently emerged as a potential acute and chronic modulator of neurological and functional recovery following TBI, thereby hinting at the potential involvement of THs in post-TBI outcomes. While evidence suggests that alterations in the HPT axis may influence susceptibility to seizures, progression of DoC, and rehabilitation outcomes, an increased blood-brain barrier permeability in concert with dysregulated deiodinase activity and expanding oxidative stress have all been proposed as mechanisms linking THs to post-TBI neurological complications. This review aims to summarize current evidence on the potential role of the thyrotropic axis in neurological and rehabilitation outcomes following TBI