Objective To investigate the clinical efficacy of topical corticosteroids combined with fusidic acid cream in treating infantile eczema.Methods Four hundreds cases of infantile eczema in the outpatient department of our hospital from March 2012 to January 2015 were collected and divided into observation group (220 cases) and control group (180 cases).The observation group received topical corticosteroids combined with fusidic acid cream,while the control group was treated only by topical corticosteroid.The medication time reaching to clinical cure,effect maintenance time during 30 d observation period and recurrence rate were recorded in the two groups.Results During the 30 days of observation, 50 cases of infantile eczema withdrew from the study,17 cases in the observation group and 33 cases in the control group.The average medication time in the observation group was (2.2±0.9)d,which was shorter than (3.2±1.1)d in the control group.The effect maintenance time during observation period in the observation group was (11.7±5.4) d,which was longer than (7.2±4.0)d in the control group,the difference was statistically significant(P<0.05);74.0% of recurrent cases during the observation period in the observation group manifested by mild eczema,while 57.8% in the control group manifested by mild eczema and had no need to use corticosteroid,the improvement of symptoms during recurrent period for the patients in the observation group was better than that for the patients in the control group,the difference was statistically significant (P<0.05).Conclusion Topical corticosteroids combined with fusidic acid cream for treating infantile eczema can reduce the medication time,prolong the effect maintenance time,and alleviate the recurrent symptoms.

Objective To study the effects of Lentinan on bleomycin A5’s inhibition effects in hemangioma-derived endothelial cell. Methods Hemangioma-derived endothelial cell line EOMA were divided into LTN group (only lentinan treatment), BLE group (only bleomycin A 5 treatment), L+B group (Lentinan and bleomycin A5 treatment) and CON group (no lentinan and bleomycin A5 treatment). Cell proliferation, cell cycle, PI and apoptosis were detected and compared among four groups. Results The differences of absorbance in LBE group was significantly higher than that in L+B group after treatment for d 1-d 7 (P<0.05), but both of them were significantly lower than in CON group and LTN group (P<0.05). The G 0/G 1 stage and apoptosis rate in L+B group was significantly higher than in BLE group(P<0.05), while it was significantly lower in S stage, G 2/M stage and PI(P<0.05). Conclusion Lentinan could significantly promote bleomycin A5’s inhibition effects on hemangioma-derived endothelial cell.

Objective To study the effects of 5-azacytidine’s demethylation for P16 gene on hemangioma cell’s proliferation and apoptosis.Methods Bisulfite sequencing PCR was applied to detect P16 gene′s promoter methylation status in 5-azacytidine treated and untreated EOMA cell line.RT-PCR and western blot were used to detect the P16 gene mRNA and protein expressions.Flow cytometry was used to detect cell proliferation, cell cycle and cell apoptosis.The differences of P16 gene′s promoter methylation status,mRNA and protein expressions,cell proliferation,cell cycle and apoptosis in two groups were compared. Results The methylation rates in 1st and 13th CGs were 0%after 5-azacytidine treatment in EOMA hemangioma cell line,which were lower than in untreated cells.The mRNA and protein expressions increased after 5-azacytidine treatment,which were significantly higher than in untreated cells.The absorbance,S phase and G2/M phase and PI after 5-azacytidine treatment were lower than untreated cells,while the G0/G1 phase and apoptosis rates were higher.Conclusion The P16 gene promoter is hypermethylated in hemangioma cells with silent gene expressions.5-azacytidine could reverse P16 gene′s promoter methylation and silent gene expressions,which inhibit hemangioma cell’s proliferation and promote apoptosis.

The dorsal lingual epithelium, which is composed of taste buds and keratinocytes differentiated from K14⁺ basal cells, discriminates taste compounds and maintains the epithelial barrier. N6-methyladenosine (m⁶A) is the most abundant mRNA modification in eukaryotic cells. How METTL3-mediated m⁶A modification regulates K14⁺ basal cell fate during dorsal lingual epithelium formation and regeneration remains unclear. Here we show knockout of Mettl3 in K14⁺ cells reduced the taste buds and enhanced keratinocytes. Deletion of Mettl3 led to increased basal cell proliferation and decreased cell division in taste buds. Conditional Mettl3 knock-in mice showed little impact on taste buds or keratinization, but displayed increased proliferation of cells around taste buds in a protective manner during post-irradiation recovery. Mechanically, we revealed that the most frequent m⁶A modifications were enriched in Hippo and Wnt signaling, and specific peaks were observed near the stop codons of Lats1 and FZD7. Our study elucidates that METTL3 is essential for taste bud formation and could promote the quantity recovery of taste bud after radiation.
Animals ; Epithelium/metabolism* ; Homeostasis ; Methylation ; Methyltransferases/metabolism* ; Mice ; RNA ; Taste Buds/metabolism*