Sleep shortage is a major concern in modern life and induces various psycho-physical disorders, including skin problems. In cosmeceutics, females are aware that sleep deprivation worsens their facial skin tone. Here, we measured the effects of sleep deprivation on facial skin yellowness and examined yellow chromophores, such as bilirubin and carotenoids, in blood serum as potential causes of yellowness. Total sleep deprivation (0 h sleep overnight, N = 28) and repeated partial sleep deprivation (4 h sleep for 5 consecutive days, N = 10) induced significant increases in facial skin yellowness. The higher yellowness was sustained even after both sleep deprivation types stopped. However, circulating levels of yellow chromophores were unchanged in the total sleep deprivation study. Neither circulating interleukin-6 nor urinary biopyrrin levels were affected by total sleep deprivation, suggesting that apparent oxidative stress in the body was not detected in the present total deprivation protocol. Facial redness was affected by neither total nor repeated partial sleep deprivation. Therefore, blood circulation may play a limited role in elevated yellowness. In conclusion, facial skin yellowness was indeed increased by sleep deprivation in our clinical studies. Local in situ skin-derived factors, rather than systemic chromophore change, may contribute to the sleep deprivation-induced elevation of facial skin yellowness.

Objective: Previous studies have reported the existence of various topographic structures on the skin surface at different scales: visible and subvisible structures. Surface topography regulates the light reflection profile, and the relationship between light diffusion and human perception, such as soft appearance, has been well studied in the manufacturing industry. However, our understanding of how skin surface topography controls the optical properties of the skin surface and the appearance remains limited.Methods: Two human studies were conducted involving healthy East Asian females. The topography of their skin was evaluated by measuring roughness parameters on skin replicas and roughness attributes on stripped corneocyte samples. These topographical attributes at different scales were compared with their perceived skin appearance, characterized by softness and radiance. Additionally, a novel image analysis algorithm to measure Crista cutis surface reflection (CSR) was developed to assess light reflection on their skin surface. The correlations of light reflection on the skin surface with these skin topographic parameters were also analysed.Results: Through skin replica observations, attributes of subvisible microscale texture on the surface of the crista cutis were defined. This texture showed significant correlations with light diffusion on the skin surface measured as CSR, and this CSR strongly correlated with soft skin appearance and radiant skin appearance. However, neither macro‐topography nor surface roughness on corneocytes showed a clear correlation with these skin attributes.Conclusion: Subvisible microscale texture on the skin's surface is not visible to the naked eye. However, this structure plays a crucial role in regulating the optical properties of the skin's surface, which in turn leads to tangible differences in skin appearance.

Objective: Skin is exposed to multiple external factors such as solar radiation and environmental oxidative stressors. Ageing and the accumulation of stress damage lead to reduced skin health and loss of skin firmness, which contribute to wrinkling and sagging. We investigated if Galactomyces ferment filtrate (GFF) could modulate skin cell mechanical properties through changes to the actin cytoskeleton and anchoring junctions. Methods: Proteomic analysis was performed to identify age‐associated changes in cellular components in skin biopsies and GFF‐mediated changes in full thickness 3D skin equivalent models. Nanoindentation was used to measure the Young's modulus (resistance to elastic deformation) of keratinocyte cells under Latrunculin B (LatB)‐induced destabilization of the actin cytoskeleton. Immunofluorescence and confocal microscopy were performed on skin equivalents to validate the GFF‐induced changes observed in proteomic analysis and identify expression profiles of key structural proteins within the skin. Results: Aged skin had decreased expression of internal cellular components ‘actin cytoskeleton’ and ‘focal adhesion’. Destabilization of actin cytoskeleton by LatB significantly reduced the Young's modulus of keratinocyte cells. Pre‐treatment of keratinocytes with GFF was able to prevent LatB‐induced decline of skin cell mechanical properties. Proteomic analysis of full thickness 3D skin equivalent models revealed that GFF increased the expression of ‘actin cytoskeleton’ and ‘anchoring junctions’, especially the actin‐binding focal adhesion proteins. Immunofluorescence staining confirmed that GFF upregulated expression of the actin stabilizer, calponin 2 and integrin α2 in basal keratinocytes. GFF increased integrin localisation to the dermal‐epidermal junction (DEJ) and colocalised with collagen IV in vitro, suggesting increased linkage between the epidermis and dermis. Conclusion: Our data establish the actin cytoskeleton and anchoring junctions which bind it as important cellular structures which decline with age. We also identified that the cellular structures are required for the maintenance of keratinocyte Young's modulus, which could be an important property impacting skin firmness. Furthermore, we have identified that GFF promotes actin stability and builds a rigid holding structure of the anchoring junctions to increase cell–cell and epidermis–dermis anchoring in skin equivalent models. Therefore, GFF has the potential to help maintain and restore skin firmness in young and old skin, respectively.

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.