Objective To develope a method for determination of hydroxide in depilatory cosmetics and to provide the basis for the establishment of national standard method for determination of hydroxide in depilatory cosmetics. Methods Potentiometric titration method was used in this assay. Results This method revealed good precision(RSD

Objetive To explore the method for determination of titanium dioxide in sunscreen cosmetics by spectrophotometry.Methods The cosmetic sample was undergone ashing treatment at 500 ℃ for dry 4 h,then was added with 2 g ammonium sulfate and 8ml concentrated sulfuric acid,for complete digestion.Titanium dioxide was determined by spectrophotometry with diantipyryl-methane as the chromogenic agent.Results The linear range of the standard curve was 0.1-6.0 ?g/ml.The detectable minimum concentration was 0.1%.Linear correlation coefficient was 0.999 8.The average recovery rates were 97.2%-98.5%.RSDs were 0.62%-1.85%(n=6).Conclusion This method is simple,rapid,accurate and suitable for the determination of titanium dioxide in sunscreen cosmetics.

BACKGROUND:A series of inflammatory signal pathways are activated accompanied by increasing expressions of inflammatory factors after periodontal tissues being stimulated by exogenous substances like bacterium. Inflammation is closely related to periodontal tissue repair and regeneration.
OBJECTIVE:To il ustrate the correlation of immune response of periodontitis and periodontitis-related inflammatory cytokines to p38 mitogen activated protein kinase (p38MAPK) pathway, and to provide a new idea and method for the treatment of periodontitis in the future.
METHODS:The related literatures of periodontitis and p38MAPK pathway published from January 1990 to January 2016 were retrieved from the databases of CBM, CNKI, SWIC and PubMed. The research and progress of periodontal tissue repair and regeneration after periodontitis were analyzed.
RESULTS AND CONCLUSION:Total y 36 literatures were enrol ed final y. Inflammation-regulated and inflammation-associated signaling pathways as wel as subsequent expression of inflammatory mediators can partly control the excessive disease-induced inflammation and immune responses of the host, among which p38MAPK signaling pathway may be involved in the occurrence and development of periodontitis. More studies, however, are needed to validate these findings. The regulation of p38MAPK signaling pathway is stil of great significance in the treatment of periodontal disease, and we hope to provide a new insight and basis for clinical diagnosis and treatment of periodontitis.