Objective To study the expression of nicotinamide phosphoribosyl transferase (Nampt) in breast cancer and to investigate the effects of Nampt inhibitor on the growth and chemotherapy sensitivity of breast cancer cells.Methods Nampt mRNA expression in breast cancer tissues and adjacent normal tissues was detected by qRT-PCR method.The effect of Nampt inhibitor on the growth of breast cancer cells and chemotherapy sensitization was detected by MTT and soft agar clonogenic assays.Results Nampt in breast cancer was significantly higher than that in normal breast tissue (P=0.000).Nampt inhibitor FK866 repressed breast cancer cell proliferation (24 h,P=0.003;48 h,P=0.001) and suppressed cell anchorage-independent growth (0.3 nM vs 0 nM,P=0.02;3 nM vs 0.3 nM,P=0.0143;0 nM vs 3 nM,P=0.02).FK866 also increased the chemo-sensitivity of breast cancer cells to fluorouracil by greater inhibition of cell proliferation.Conclusion Our findings indicate that Nampt may be a new therapeutic target for breast cancer.

Objective To investigate the serum C-type lectin domain family 4 member G(CLEC4G)level and its clinical value in patients with Atopic Dermatitis(AD).Methods The blood samples of 60 AD patients and 29 control patients were collected,and CLEC4G,Interleukin-33(IL-33),total immunoglobulin E(tIgE),specific IgE(specific IgE),and eosinophil levels were detected.The correlation between CLEC4G level and clinical data of AD patients and IL-33 was analyzed.The risk of AD was evaluated by Logistic regression analysis of CLEC4G,IL-33 and other indicators.Results Compared with the control group,the serum CLEC4G level in AD patients was significantly decreased(359.4±57.3 vs.521.8±48.1)pg/mL.There was no significant difference in CLEC4G level between child-hood,adolescent and adult,male and female AD patients.Compared with tIgE≤100 kU/L group,CLEC4G level was significantly decreased in 100～200 kU/L group and tIgE≥200 kU/L group,but there was no significant difference between 100～200 kU/L group and tIgE≥200 kU/L group.Serum CLEC4G level decreased significantly only in the moderate AD group,but had no significant difference among the other groups.The serum level of IL-33 was increased in AD patients,but there was no significant correlation between CLEC4G and IL-33(r = 0.090,P = 0.495).Age less than 14 years old and IL-33 were risk factors for the incidence of AD,with OR values of 2.756 and 1.241,95%CI of 1.076～7.060 and 1.030～1.495,respectively.CLEC4G was a protective factor for AD(OR = 0.890,95%CI:0.809～0.979).Conclusion CLEC4G may be a protective factor independent of IL-33 mediated AD pathogenesis.

Objective To investigate the effect of ERH gene knockdown on the proliferation and apoptosis of human bladder cancer T24 cells. Methods T24 cells infected by lentivirus with interference on ERH gene sequence were cloned to establish stable T24 cells clone in ERH gene suppression. The expression of ERH mRNA gene in bladder cancer was detected by using quantitative real time polymerase chain reaction (qPCR). The effects of ERH knockout on the cell proliferation and apoptosis were examined by using methylthiazolyl tetrazolium (MTT) assay, colony formation assay and flow cytometry. The effect of ERH knockout on the tumorigenic effect of T24 cells in vivo was verified by subcutaneous tumor formation in nude mice. Results After lentiviral transfection, qPCR results showed that the knockdown effect of ERH mRNA in ERH normal group (untreated T24 cells) was better than that in ERH gene knockdown group, and the difference was statistically significant [(1.006±0.126) vs. (0.079±0.007); t=12.72, P=0.0002]. After knocking out ERH gene, MTT assay showed that the proliferation ability of T24 cells in ERH gene knockdown group was weakened compared with ERH normal group, and the difference was statistically significant [A490 value: (0.13±0.00) vs. (0.66±0.01);t=104.61, P<0.0001]. Colony formation assay indicated that the ability of clone in ERH normal group was weakened compared with ERH gene knockdown group [(10.5 ±1.2) vs. (196.4 ±4.0); t= 73.63, P< 0.0001]. Flow cytometry showed that the cell apoptosis rate in ERH gene knockdown group was higher than that in ERH normal group [(11.0 ±0.5) ％ vs. (4.2 ±0.5) ％; t= 16.06, P<0.0001]. Imaging results of subcutaneous tumor formation in nude mice showed that the total fluorescence intensity of the tumor area in ERH gene knockdown group was (4.67 ±0.59) × 1010 μW/cm2, and the corresponding part in ERH normal group was (9.54±4.20) × 1010μW/cm2 (t=3.64, P=0.0051);tumor weight in ERH gene knockdown group was (0.80±0.62) g, and in ERH normal group was (1.79±0.71) g (t=3.33, P=0.0037). Conclusion ERH gene knockout can inhibit the proliferation of human bladder cancer T24 cells, and promote the cell apoptosis.