OBJECTIVE To provide evidence to establish properly protocol for medical cosmetic institutions.METHODS Through investigation to analyze the current situation and problems of disinfection and isolation in the medical cosmetic institutions.RESULTS There were 86.7% medical cosmetic institutions located in commercial buildings.And there were 33.3% institutions with improper layout of therapeutic room,sterilizing room and dressing room resulting from insufficient space or less rooms.The illumination intensity of the ultraviolet lamp and the disinfection effect of air were not coincident with standards.CONCLUSIONS There are many problems of disinfection and isolation in the medical cosmetic institutions,the disinfection is insufficient,the ultraviolet light is in wild-using,people only focus on using,but ignore irradiation dose and distance.It is very important for strictly observing Hospital Infection Management Methods,Disinfection Technology Standards and Disinfection Management Methods,and strengthening the management of disinfection and isolation in the medical cosmetic institutions.

Both cholinergic dysfunction and protein citrullination are the hallmarks of rheumatoid arthritis (RA), but the relationship between the two phenomena remains unclear. We explored whether and how cholinergic dysfunction accelerates protein citrullination and consequently drives the development of RA. Cholinergic function and protein citrullination levels in patients with RA and collagen-induced arthritis (CIA) mice were collected. In both neuron-macrophage coculture system and CIA mice, the effect of cholinergic dysfunction on protein citrullination and expression of peptidylarginine deiminases (PADs) was assessed by immunofluorescence. The key transcription factors for PAD4 expression were predicted and validated. Cholinergic dysfunction in the patients with RA and CIA mice negatively correlated with the degree of protein citrullination in synovial tissues. The cholinergic or alpha7 nicotinic acetylcholine receptor (α7nAChR) deactivation and activation resulted in the promotion and reduction of protein citrullination in vitro and in vivo, respectively. Especially, the activation deficiency of α7nAChR induced the earlier onset and aggravation of CIA. Furthermore, deactivation of α7nAChR increased the expression of PAD4 and specificity protein-3 (SP3) in vitro and in vivo. Our results suggest that cholinergic dysfunction-induced deficient α7nAChR activation, which induces the expression of SP3 and its downstream molecule PAD4, accelerating protein citrullination and the development of RA.