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Background: Western dietary patterns, characterized by high intake of ultra-processed foods (UPFs), added sugars, and saturated fats, have been increasingly implicated in promoting systemic inflammation and disrupting gut microbiota composition. These mechanisms may influence the onset, progression, and comorbidities of chronic inflammatory arthritides. This systematic scoping review aimed to summarize current evidence on the association between Western diet (WD) or UPF consumption and the risk, activity, and related outcomes in rheumatoid arthritis (RA), axial spondyloarthritis (axSpA), and psoriatic arthritis (PsA). Methods: We conducted a systematic review including randomized controlled trials, observational studies (cohort, case-control, cross-sectional), and preclinical models assessing the relationship between WD or UPF intake and disease-related outcomes in RA, axSpA, or PsA. Exclusion criteria comprised narrative reviews, editorials, case reports, and studies not specifically addressing both the dietary exposure and relevant disease outcomes. A comprehensive literature search was conducted in PubMed, Embase, Scopus, Web of Science, and the Cochrane Library, with the final search on May 18, 2025 and no time limit applied. Reference lists were manually screened, and forward citation tracking was performed using Google Scholar. Risk of bias was not formally assessed, consistent with the exploratory nature of this scoping review. Data were synthesized narratively and tabulated by dietary exposure, outcomes, and key findings. Results: During screening, we assessed 165 papers. Only 10 studies involving over 244,000 individuals were included. Eight studies addressed RA, comprising 7 clinical and 1 preclinical investigation. Across these, greater UPF consumption or adherence to WD was consistently associated with adverse outcomes. Cohort studies reported an increased RA incidence with adjusted hazard ratios between 1.04 and 1.17; case-control analyses found odds ratios up to 1.84. Inflammatory markers were elevated, including CRP (+0.01 to +0.097 mg/L), ESR (+2 to +3.985 mm/h), and HbA1c (+0.02% to +0.04%). Effects on disease activity were variable (DAS28: +0.01 to +0.49; SJC: up to +0.6 joints). Cardiometabolic risk indicators, such as Framingham score, glucose, insulin, and visceral fat, also worsened with higher UPF intake. Alterations in gut microbiota were documented in both clinical and murine RA models. For axSpA, 1 prospective study (n=140) found no significant association between UPF intake and disease activity. No eligible clinical studies were found for PsA, though one preclinical model demonstrated that WD exposure exacerbated joint and skin inflammation and induced dysbiosis. Discussion: Current evidence supports a detrimental association between WD or UPF intake and inflammatory and metabolic outcomes in RA. Data on axSpA are scarce and inconclusive, and clinical evidence in PsA is lacking. These findings underscore the need for targeted dietary research in spondyloarthritis and support the incorporation of nutritional assessment into comprehensive rheumatologic care.

In the Article titled "Robotic resection of mediastinal left vagus neurofibroma" published on June 12, 2022, in the Early Access issue of Monaldi Archives for Chest Disease, an author name was misspelled. In the byline, the fifth author, "Sergio Nicola Fortiparri" should have been "Sergio Nicola Forti Parri." This article was corrected online. Reference Brandolini J, Ambrosi F, Bertoglio P, et al. Robotic resection of mediastinal left vagus neurofibroma. Monaldi Arch Chest Dis 2023;93:2248. https://doi.org/10.4081/monaldi.2022.2248.

The kinetics of the uptake of the fluid phase marker Lucifer Yellow (LY), and its alteration by wortmannin, an inhibitor of phosphatidylinositol-3 kinase (PI-3K), and the PKC modulators: GF 109203 X, an inhibitor, and phorbol ester, an activator was studied in eukaryotic model Paramecium aurelia. Spectrophotometric quantification of LY accumulation was performed in the presence or absence of transferrin, a marker of receptor-mediated endocytosis. Internalization of LY showed a curvilinear kinetics: the high initial rate of LY uptake (575 ng LY/mg protein/hr) decreased almost 5-fold within 15 min, reaching plateau at 126 ng/mg protein/hr. Transferrin induced a small increase (7.5%) in the fluid phase uptake rate (after 5 min) followed by a small decrease at longer incubation times. Lucifer Yellow and transferrin (visualized by streptavidin-FITC) were localized in Paramecium by 3-D reconstruction by confocal microscopy. LY showed a scattered, diffuse fluorescence typical of fluid phase uptake whereas transferrin accumulated in membrane-surrounded endosomes. Wortmannin did not affect LY accumulation but decreased it when transferrin was present in the incubation medium. This suggests an effect on the transferrin uptake pathway, presumably on the stage of internalization in "mixing" endosomes to which transferrin and LY were targeted. Phorbol ester diminished LY accumulation by 22% and this effect persisted up to 25 min of incubation. PKC inhibitor did not affect LY uptake. However, in the presence of transferrin, the LY uptake increased within the first 15 minutes followed by a rapid 20% decrease in comparison to the control. Such an effect of PKC modulators suggests that PMA action on fluid phase uptake is not directly mediated by PKC.

At present, it seems clear that the nucleolus is multifunctional and represents one of the key cell organelles that participate directly or indirectly in cell resting, proliferation, differentiation and maturation states, and possibly also in programmed cell death. Thus, the morphology and cytochemistry of nucleoli may represent a very useful tool not only for the evaluation of nucleolar biosynthetic activities but also for the evaluation of various cell states under physiological, experimental and pathological conditions.