Livin is protective in UVB-induced skin photodamage by regulating keratinocyte activation and inflammatory responses.

UVB radiation can lead to skin photodamage, which might arise from keratinocyte (KC) activation. Nuclear factor kappa B (NF-κB) assumes an essential function in the context of UVB-triggered skin photodamage. Initiating the NF-κB cascade leads to the release of inflammatory factors from KCs. Livin can modulate both KC activation and function, yet it remains uncertain whether and how Livin regulates KC activation induced by UVB. To explore the involvement of Livin in UVB-triggered skin photodamage and its impact on skin damage through NF-κB activation. Immunofluorescence staining was used to analyse the expression of Livin in individuals with skin photodamage and in mice treated with UVB radiation. KC-specific Livin knockout (LivinΔKC ) mice and HaCaT cells with Livin knockdown were employed to examine the function of Livin in regulating KC activation induced by UVB radiation. Additionally, the impact of Livin on the NF-κB cascade during KC activation was confirmed via western blot analysis. In patients with skin photodamage, UVB-treated mice and HaCaT cells, Livin expression was reduced in KCs. LivinΔKC mice displayed heightened sensitivity to UVB radiation, resulting in more pronounced skin damage and inflammatory responses compared to the control Livinfl/fl mice. Following UVB exposure, both LivinΔKC mice and Livin-knockdown HaCaT cells released elevated levels of cytokines compared to their respective controls. Moreover, the UVB-induced activation of NF-κB in HaCaT cells was significantly enhanced following Livin knockdown. Our findings propose that Livin within KCs could contribute to reducing UVB-induced skin photodamage by regulating the NF-κB pathway.

Near-Barrierless CO Oxidation Using Phosphotungstic Acid-Supported Single-Atom Catalysts.

Efficient CO oxidation at ambient or low temperatures is essential for environmental purification and selective CO oxidation in H2, yet achieving this remains a challenge with current methodologies. In this research, we extensively evaluated the catalytic performance of phosphotungstic acid (PTA)-supported 11 M1/PTA single-atom catalysts (SACs) using density functional theory calculations across both gas phase and 12 common solvents. The Rh1/PTA, Pd1/PTA, and Pt1/PTA systems exhibit moderate CO adsorption energies, facilitating the feasibility of oxygen vacancy formation. Remarkably, the Pd1/PTA and Pt1/PTA catalysts exhibited negligible energy barriers and demonstrated exceptionally high catalytic rates, with values reaching up to (1 × 1010)11, markedly exceeding the threshold for room temperature reactions, set at 6.55 × 108. This phenomenon is attributed to a transition from the high-energy barrier processes of oxygen dissociation in O2 and N-O bond dissociation in N2O to the more efficient dissociation of H2O2. Orbital analysis and charge variations at metal sites throughout the reaction process provide deeper insights into the role of the three metal catalytic sites in CO activation. Our findings not only reveal key aspects of SACs in facilitating CO oxidation at low temperatures but also provide valuable insights for future catalytic reaction mechanism studies and environmental applications.

Livin expression promotes keratinocyte release of inflammatory mediators in psoriasis.

BACKGROUND: Psoriasis is a prevalent, long-term skin condition characterized by inflammation. Keratinocytes (KCs) are important effector cells that release inflammatory factors and chemokines to promote the inflammatory cascade in psoriasis. However, the mechanisms underlying the activation of KCs in psoriasis remain unclear. Livin suppresses apoptotic proteins and directly affects the growth and spread of cancer cells. Livin expression reportedly increases significantly in lesions of patients with psoriasis; however, its specific role in KC activation remains unknown. This study aimed to examine the impact of Livin on KC activation and the subsequent release of inflammatory mediators. METHODS: Immunofluorescence staining, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting were used to assess Livin expression in patients with psoriasis, an imiquimod (IMQ)-induced psoriasis-like mouse model, and M5-treated HaCaT cells. To investigate the role of Livin in KCs, we performed RNA sequencing and proteomic analysis of Livin-knockdown (knockdown-HaCaT) and negative control (NC-HaCaT) cells. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were used for enrichment analyses. Moreover, the effect of Livin expression on the release of inflammatory mediators in KCs was verified using ELISA. RESULTS: Livin expression was higher in KCs of patients with psoriasis than in those healthy controls. Livin expression in HaCaT cells treated with M5 increased significantly over time. Livin expression was higher in the skin lesions of the IMQ mouse model than in the control group. Proteomic analysis and RNA sequencing used to investigate the function of Livin in HaCaT cells revealed its potential role in mediating KC activation and inflammatory mediator release, which affected the pathology of psoriasis. CONCLUSIONS: Livin expression played an effect on KCs activation, which induced release of inflammatory mediators and up-regulation of keratin. This study provides a new effector molecule for the mechanism of inflammatory response in psoriasis.

Global burden and future trends in psoriasis epidemiology: insights from the global burden of disease study 2019 and predictions to 2030.

BACKGROUND: Millions of people worldwide are affected by psoriasis, one of the most prevalent skin conditions. Currently, there is a lack of high-quality epidemiological reports on psoriasis. OBJECTIVE: This study aimed to reveal trends in psoriasis epidemiology in 1990-2019. METHODS: Using data from the GBD study 2019, we examined psoriasis epidemiology globally and across regions defined by the social-demographic index (SDI). Trends in incidence, prevalence, and disability-adjusted life year (DALY) rates were assessed using estimated annual percentage changes (EAPC)s. Age-period-cohort analysis examined risk variations, and decomposition analysis identified factors impacting the psoriasis burden. A Bayesian Age-Period-Cohort model predicted future incidence. Frontier analysis associated psoriasis outcomes with socio-demographic development. RESULTS: In 2019, the global psoriasis burden included 4,622,594 incidence, 40,805,386 prevalence, and 3,505,736 DALY cases. Despite variations in SDI regions, the overall trend showed a decline in psoriasis rates from 1990 to 2019 (EAPC = - 0.76). The age-specific analysis indicated that the highest incidence of psoriasis was observed among individuals aged 40-64 years (global, 1,606,429). Epidemiological shifts contributed negatively to global incidence and DALYs by - 80.52% and - 103.06%, respectively. Countries like San Marino and Spain displayed the highest effective differences in the decomposition analysis. By 2030, while incidence cases per 10,000 might rise (487.36, 423.62 to 551.10), age-standardized incidence rates per 100,000 were predicted to decline (53.67, 0.00 to 259.99). CONCLUSION: This research revealed a global decline in psoriasis incidence rate from 1990 to 2019, with predictions suggesting this trend continues through 2030. Geographic disparities underscore the importance of tailored healthcare policies.