Objective To evaluate the consistency of global acne grading system (GAGS) and acne lesion counting. Methods After training 3 dermatologists evaluated 60 acne patients by GAGS and skin lesion counting respectively in randomized order sequentially, and evaluated again 5 days later. Results The kappa-value of GAGS (consistency) was 0.675 among 3 different dermatologists, and 0.847 for the same desmatologist. The kappa-value among the 3 different dermatologists and the same dermatologist for the total lesion count was 0.426 and 0.413 respectively; for pustule count was 0.446 and 0.407 respectively. The kappa-value of total number of the inflammatory lesion counting was 0.429 for the 3 different dermatologists and the kappa-value was

A molecularly imprinted two-dimensional photonic crystal hydrogel sensor was developed with erythromycin as imprinted molecule, polystyrene two-dimensional photonic crystal as templates, methanol as solvent, methacrylic acid as monomers and ethylene glycol dimethylacrylate as cross-linkers.The imprinted molecule was removed by methanol/acetic acid (9∶1, V/V).The results showed that the diameter of Debye ring increased 6 mm when the concentration of EM changed from 0 to 1×10-6 mol/L.Namely the lattice spacing decreased 30 nm.In addition, the diameter of Debye ring only increased 1.5 and 2.0 mm when the hydrogel immersed in 1×10-6 mol/L roxithromycin (RM) or erythromycin ethylsuccinate (EEs) solution.The result indicated that the sensor had high selectivity and could be used in determination of erythromycin with low cost and easy operation.

Objective:To investigate the effects of ectodysplasin-A1 (EDA1) on the proliferation and cell cycle of ameloblast-like epithelial cells (LS8 cells).Methods:Wild EDA1 plasmid pCR3-Flag-EDA1-W (wild group), syndrome mutant EDA1 plasmid pCR3-Flag-EDA1-H252L (mutant group) and empty vector plasmid pCR3-Flag (control group) were transfected into LS8 cells. Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay and cell cycle was detected by flow cytometry. All tests were repeated three times.Results:Compared with the control group (0.105±0.032), the proliferation activity of the wild group (0.201±0.009) was significantly higher after 72 h ( P<0.05). Compared with the control group (0.168±0.054) and the mutant group (0.194±0.059), the proliferation activity of the wild group (0.386±0.066) was significantly higher after 96 h ( P<0.05). There was no significant difference between the mutant group and the control group at all time points ( P>0.05). In the G 0/G 1 phase, compared with the control group (65.4%±2.1%) and the mutant group (66.6%±3.1%), the cell distribution ratio of the wild group (51.2%±1.1%) was significantly lower ( P<0.01). In the S phase, compared with the control group (23.1%±2.0%) and the mutant group (21.9%±1.8%), the cell distribution ratio of the wild type group (37.3%±2.4%) was significantly higher ( P<0.01). There was no significant difference in cell cycle distribution between the mutant group and the control group ( P<0.05). Conclusions:Wild EDA1 promotes the proliferation of LS8 cells and the transformation from G 0/G 1 to S phase. The syndrome mutant EDA1 (EDA1-H252L) loses its function of regulating the cell proliferation and cell cycle of LS8 cells.