This study investigated the effects of an 8-week daily 2000 IU vitamin D₃ supplementation, administered via orodispersible films, on serum vitamin D, leukocyte count, and performance parameters in healthy recreational runners and non-runners, followed by a 12-week post-supplementation follow-up. Forty-five participants were randomized into four groups: supplemented runners (RUN-SUPPL, n = 13, age 33.4 ± 7.5 y), non-supplemented runners (RUN-CON, n = 10, age 34.8 ± 8.6 y), supplemented non-runners (NON-RUN-SUPPL, n = 11, age 29.3 ± 7.5 y), and non-supplemented non-runners (NON-RUN-CON, n = 11, age 28.3 ± 6.0 y). Assessments were conducted at baseline (T0, October, pre-supplementation), post-intervention (T1, December, after 8 weeks), and follow-up (T2, March, 12-weeks post-supplementation). Supplementation significantly increased serum 25(OH)D₃ in runners (30.45 ± 7.0 to 35.35 ± 8.9 ng/mL, p < 0.001) and non-runners (25.0 ± 8.7 to 30.2 ± 9.7 ng/mL, p < 0.001), while non-supplemented non-runners showed a marked decline (25.93 ± 6.6 to 17.8 ± 7.3 ng/mL, p < 0.001). After follow-up, serum vitamin D decreased significantly in all groups (e.g., RUN-SUPPL 23.52 ± 5.6 ng/mL, p < 0.001). A significant time-by-supplementation interaction was observed for total leukocytes (p = 0.001) and neutrophils (p = 0.03), indicating more stable immune profiles in supplemented participants. No significant changes were found in VO₂max or countermovement jump (p > 0.05), while maximal isometric force showed a trend toward improvement in supplemented subjects (p = 0.056). Despite these physiological benefits, no ergogenic effects on aerobic or explosive performance were observed.

Head and neck cancers (HNCs) represent a major global health burden and remain associated with substantial morbidity and limited therapeutic options, particularly in advanced or recurrent disease. Increasing interest has focused on naturally derived bioactive compounds with potential chemopreventive and therapeutic properties. Sulforaphane, a dietary xenobiotic isothiocyanate derived from glucoraphanin in cruciferous vegetables, has attracted attention due to its ability to modulate redox balance, epigenetic regulation, and multiple oncogenic signaling pathways. This manuscript reviews current evidence regarding the biological effects of sulforaphane in HNCs. Particular attention is given to the molecular mechanisms underlying its modulation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a key regulator of cellular antioxidant and detoxification responses that can be activated by sulforaphane. Several studies indicate that sulforaphane can inhibit tumor growth through several mechanisms beyond Nrf2 activation, including induction of apoptosis, cell cycle arrest, epigenetic modulation, and suppression of oncogenic signaling pathways. In addition, sulforaphane has been shown to enhance the efficacy of conventional treatments, including chemotherapy, radiotherapy, and photodynamic therapy. Overall, the literature suggests that sulforaphane may represent a promising chemopreventive or therapeutic adjunct in HNC, although further clinical investigation is required to clarify its translational potential.

Background: Methyltransferase-like 26 (METTL26) is a poorly characterized member of the METTL family that has been included in previous pan-cancer analyses, but its disease-specific clinical and molecular relevance in head and neck squamous cell carcinoma (HNSCC) and oral squamous cell carcinoma (OSCC) remains poorly defined. The aim of this study was to investigate METTL26 expression and its potential clinical and biological relevance in HNSCC, with particular attention to OSCC. Methods: The TCGA-HNSC dataset was used as a discovery dataset. METTL26 expression and pathological stage were evaluated using GEPIA3, whereas survival associations were analyzed in R. Tumor microenvironment associations were investigated using TIMER3. Genes co-expressed with METTL26 were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, while protein interaction networks were explored using STRING. These discovery analyses were performed using the heterogeneous TCGA-HNSC cohort, whereas two independent OSCC cohorts (GSE37991 and GSE30784) were primarily used to validate differential expression. Results: METTL26 expression was significantly increased in TCGA-HNSC compared to normal tissues and was associated with pathological stage. High METTL26 expression showed a non-significant trend toward poorer OS and PFI and was not independently associated with either outcome after multivariable adjustment. A positive association with cancer-associated fibroblast (CAF) abundance was detected using TIDE, whereas an inverse association with endothelial cell abundance was observed across multiple algorithms. Functional analysis showed enrichment of mitochondrial gene expression, mitochondrial translation, ribosomal functions, oxidative phosphorylation, and reactive oxygen species-related pathways. METTL26 was also positively correlated with several genes involved in therapy response such as PTOV1, MIF, BAD, and EIF3C. Importantly, METTL26 upregulation was independently confirmed in both OSCC cohorts, GSE37991 and GSE30784. Conclusions: METTL26 upregulation was independently confirmed in two OSCC cohorts, supporting its potential relevance as an expression biomarker. In contrast, the observed associations with pathological stage, mitochondrial and redox-related programs, stromal composition, and therapy-response-related genes should be considered exploratory and hypothesis-generating and require independent and functional validation.

Background: Home Enteral Nutrition (HEN) patients, often older adults, are susceptible to gut microbiota dysbiosis and low-grade chronic inflammation (inflammaging), which negatively impacts overall health and intestinal integrity. However, evidence on microbiota-targeted interventions in this population remains limited. The development of targeted nutritional strategies, such as probiotic supplementation, has been proposed to address these age-related changes. Methods: This exploratory randomized, open-label study explored changes in gut microbiota composition following a 30-day probiotic intervention in a cohort of sixteen older HEN patients. Gut microbiota profiles were analyzed at baseline and post-intervention using 16S rRNA gene amplicon sequencing. Results: Significant shifts in the gut microbiota were observed, including a statistically significant increase in alpha diversity after 30 days. At the taxonomic level, the treated group showed an increased relative abundance of Lachnospiraceae and Erysipelotrichaceae, suggesting a modulation of gut microbiota structure following probiotic supplementation. Conclusions: These findings provide preliminary insights into microbiota dynamics in this population and may inform the design of future studies integrating functional and clinical outcomes.