BackgroundThis phase 3 trial is the first to evaluate the efficacy and safety of treatment with the systemic TNF‐α inhibitor, adalimumab, for Chinese patients with moderate‐to‐severe plaque psoriasis.MethodsIn the 12‐week, double‐blind, placebo‐controlled Period A, patients were randomized 4 : 1 to receive adalimumab 40 mg every‐other‐week (following a single 80 mg dose), or placebo every‐other‐week. In the subsequent 12‐week, open‐label, Period B, all patients received adalimumab 40 mg every‐other‐week starting at week 13, following a single, blinded dose at week 12 of adalimumab 80 mg or matching placebo (for patients receiving placebo or adalimumab in Period A respectively). In Period A, efficacy was analysed for all randomized patients and safety for all patients receiving ≥1 dose of the study drug.ResultsFor the 425 patients in this study (87 placebo; 338 adalimumab), a higher percentage randomized to adalimumab achieved the primary endpoint of ≥75% improvement from baseline in PASI score (PASI 75) at week 12: placebo 11.5% (10/87); adalimumab 77.8% (263/338; P < 0.001). Physician's Global Assessment of clear to minimal was achieved at week 12 by 14.9% placebo (13/87) and 80.5% adalimumab (272/338; P < 0.001). For patients who received adalimumab at any time during the study (All‐adalimumab Population), treatment‐emergent adverse events (AEs) were reported by 63.4%; the most common was upper respiratory infection (16.1%). Serious AEs were reported by 3.5% of the All‐adalimumab Population, and serious infectious AEs by 1.2%, which include lung infection, pneumonia and tuberculosis [2 (0.5%) patients each]. There was one death (chronic heart failure).ConclusionIn these Chinese patients with moderate‐to‐severe psoriasis, a significantly greater percentage treated with adalimumab compared with placebo achieved efficacy endpoints at week 12 and efficacy was sustained to week 24. Safety results were consistent with the known adalimumab safety profile; no new safety signals were identified in the 24 weeks of treatment.

The present study demonstrated that hair follicle stem cells (HFSc) have multidirectional differentiation potential and participate in skin wound healing processes. Long non‑coding RNAs (lncRNAs) are defined as non‑protein coding transcripts longer than 200 nucleotides, which are important in the proliferation and differentiation of cells. The purpose of the present study was to investigate the role of PlncRNA‑1 in the proliferation and differentiation of HFSc. Results revealed that PlncRNA‑1, transforming growth factor (TGF)‑β1, Wnt and β‑catenin expression levels were significantly downregulated in HFSc. PlncRNA‑1 transfection promoted proliferation and differentiation of HFSc. TGF‑β1, Wnt and β‑catenin expression levels were upregulated in HFSc following transfection of PlncRNA‑1. Results demonstrated that TGF‑β1 inhibitor LY2109761 blocked proliferation and differentiation of HFSc promoted by PlncRNA‑1 transfection. In addition, TGF‑β1 inhibitor LY2109761 led to decreased Wnt and β‑catenin expression levels in HFSc. Furthermore, PlncRNA‑1 transfection stimulated the cell cycle of HFSc, whereas TGF‑β1 inhibitor LY2109761 inhibited the cell cycle of HFSc and decreased the acceleration of the cell cycle induced by PlncRNA‑1 transfection. In conclusion, these findings suggest that PlncRNA‑1 may promote proliferation and differentiation of HFSc through upregulation of TGF‑β1‑mediated Wnt/β‑catenin signaling pathway.

Sunscreen protection is not related in one uniform way to the amount of product applied to human skin. Consumers may achieve an even lower than expected sunburn protection from high SPF products than from low SPF sunscreens.

Background:PM2.5 (aerodynamic diameter ≤ 2.5 μm) is a dominant and ubiquitous air pollutant that has become a global concern as PM2.5 exposure has been linked to many adverse health effects including cardiovascular and pulmonary diseases. Emerging evidence supports a correlation between increased air PM2.5 levels and skin disorders although reports on the underlying pathophysiological mechanisms are limited. Oxidative stress is the most common mechanism of PM2.5-induced adverse health effects. This study aimed to investigate PM2.5-induced oxidative damage and apoptosis in immortalized human keratinocyte (HaCaT) cells.Methods:HaCaT cells were exposed to 0, 25, 50, 100, or 200 μg/ml PM2.5 for 24 h. Reactive oxygen species (ROS) generation, lipid peroxidation products, antioxidant activity, DNA damage, apoptotic protein expression, and cell apoptosis were measured.Results:PM2.5 exposure (0–200 μg/ml) for 24 h resulted in increased ROS levels (arbitrary unit: 201.00 ± 19.28, 264.50 ± 17.91, 305.05 ± 19.57, 427.95 ± 18.32, and 436.70 ± 17.77) and malondialdehyde production (0.54 ± 0.05 nmol/mg prot, 0.61 ± 0.06 nmol/mg prot, 0.68 ± 0.05 nmol/mg prot, 0.70 ± 0.05 nmol/mg prot, and 0.76 ± 0.05 nmol/mg prot), diminished superoxide dismutase activity (6.47 ± 0.28 NU/mg prot, 5.97 ± 0.30 NU/mg prot, 5.15 ± 0.42 NU/mg prot, 4.08 ± 0.20 NU/mg prot, and 3.76 ± 0.37 NU/mg prot), and increased DNA damage and apoptosis in a dose-dependent manner in HaCaT cells. Moreover, cytochrome-c, caspase-3, and caspase-9 expression also increased proportionately with PM2.5 dosing.Conclusion:PM2.5 might elicit oxidative stress and mitochondria-dependent apoptosis that likely manifests as skin irritation and damage.

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