Peripheral neuropathy (PN) is a prevalent condition characterized by damage to peripheral nerves, often linked to risk factors such as diabetes. This condition results from various forms of neural damage, including injury to the cell body, axons, or demyelination, frequently beginning with small and thinly or unmyelinated fibers. Such nerve damage disrupts normal signaling, leading to symptoms like numbness, tingling, and pain. Effective nerve repair and regeneration, particularly through remyelination, are essential therapeutic objectives. While vitamin B12’s role in repair processes has been well established, emerging evidence suggests that other neurotropic vitamins, specifically B1 and B6, also contribute significantly to nerve health and symptom relief in PN. In this study, we demonstrate that a combination treatment of vitamins B1, B6, and B12 enhances repair and oxidative stress responses in co-cultures of neural and Schwann cells, leading to improved cell maturation and connectivity compared to vitamin B12 alone. Furthermore, proteomic analysis supports these observations at the molecular level, with enhanced cellular recycling processes like proteasome enhancement, as well as protein synthesis upregulation, needed to rebuild nerve connections and combatting oxidative stress. Our combined morphological and molecular results highlight the potential therapeutic advantage of the B1, B6, and B12 combination over vitamin B12 alone.

Dullness or lack of radiance in facial appearance is a common concern among females. Previous studies have linked skin dullness to aging and revealed alterations in skin pigments. However, younger individuals (ages ≤ 35) also report concerns about dull skin in their hectic daily lives, which may not involve pigmentation changes. We hypothesized that the mechanisms underlying dullness in youth differ from those associated with aging. To investigate this, we measured cellular and molecular changes in 132 healthy Japanese and Chinese females aged 18 to 35 using biophotonic multiphoton tomography and biochemical tape-strip analysis. Our findings revealed that dull skin exhibited a thicker stratum granulosum and less densely packed keratinocytes in deeper layers. Biochemical analysis showed upregulation of interleukin-36γ and downregulation of E-cadherin in dull skin, with interleukin-36γ levels negatively correlating (p = 0.023) with metabolites of filaggrin. These alterations resemble those observed in inflammatory skin conditions, suggesting an additional mechanism of skin dullness beyond pigmentation. In vitro cultured cell models evaluated the efficacy of three skincare ingredients: galactomyces fermentation filtrate, bisabolol, and batyl alcohol. Galactomyces suppressed interleukin-36γ (p = 0.037), while both batyl alcohol (p = 0.006) and bisabolol (p = 0.049) showed beneficial effects on filaggrin. Targeting these biomarkers may improve the appearance of dull skin.

Aim: Small extracellular vesicles from bovine milk (BEVs) have garnered attention as vehicles for delivering therapeutics to pathological tissues. Theoretically, mRNAs in BEVs might be translated into...

Poor oral health is a neglected epidemic, potentially contributing to systemic health issues. We employed a multi-omics approach to investigate the biological changes associated with gingivitis and the effects of stannous fluoride (SnF₂) dentifrice on microbial composition and salivary proteomics in an eight-week clinical trial involving 39 participants categorized as high (n = 20) and low bleeders (n = 19). Baseline assessments revealed significant microbial dysbiosis in high bleeders, characterized by a higher abundance of Porphyromonas and Fusobacterium, alongside compromised epithelial barriers and increased inflammation. Following SnF₂ treatment, a substantial reduction in these bacteria, and an increase in Rothia and Haemophulis, were observed, correlating with improved clinical measures, including reduced bleeding and inflammation indices. In total, 80 proteins (including pro-inflammatory cytokines, alarmin keratins, and matrix metalloproteinases) showed a significant reduction in high bleeders after treatment, with 29 overlapping the disease biomarkers in the plasma atlas, supporting the role of SnF₂ in mitigating oxidative stress and enhancing epithelial integrity. Furthermore, SnF₂ treatment significantly reduced collagen degradation, suggesting the preservation of tissue integrity. These findings highlight that SnF₂ not only improves local oral health but may also benefit systemic health, showcasing the value of a multi-omics approach in understanding the interconnections among oral microbiota, inflammatory responses, and systemic health outcomes.