Objective To investigate the effect and mechanism of melatonin on the anoikis of melanoma cells.Methods The drug concentration of melatonin inhibiting melanoma cell line B16-F10 was optimized based on the effect on CCK-8 assay.An anti-anoikis of melanoma cell model was developed and divided it into four groups:The blank control group,the TrkB activator group,the melatonin group and the melatonin+TrkB activator group.Calce-in AM/EthD-1 fluorescence double staining was used to detect the anoikis of melanoma cells.Reactive oxygen spe-cies were detected using the fluorescent probe DCFH-DA.Western blot was used to detect the expression of Nrf2 protein and TrkB protein in each group.Results Melatonin significantly inhibited the proliferation of melanoma cells in a time-and dose-dependent manner with IC50 of 1×10-7 μmol/L.Its inhibitory effect was found to be related to in-duction of anoikis of melanoma cells.Melatonin could upregulate the generation of cellular reactive oxygen species(P<0.05),while addition of TrkB activator antagonized this effect.Melatonin could reduce the expression of Nrf2 protein and TrkB protein in melanoma cells(P<0.05),and the addition of TrkB activator could inhibite the effect of melatonin on the expression of Nrf2 protein and TrkB protein(P<0.05).Conclusions Melatonin can inhibit the pro-liferation of melanoma cell line B16-F10 through the mechanism of inducing anoikis.

Objective: To explore the regulation of interleukin 8(IL-8) secretion by peptidylarginine deiminase 4(PADI4) and its effect on the pathogenesis of systemic lupus erythematosus(SLE). Methods: qRT-PCR was used to compare the expression levels of IL-8 in neutrophils between healthy controls(HC) and SLE patients. ELISA was used to detect IL-8 secretion levels in the serum of HC and SLE patients, the correlation between serum IL-8 and SLE related serological indicators in lupus patients was analyzed. ELISA was used to detect the effect of HC orSLE serum on IL-8 secretion by neutrophils. Using PADI4-specific inhibitor GSK484 in primary neutrophils, or in PADI4-knockdown neutrophil-like HL-60 cells(dHL-60), IL-8 stimulated by N-formyl-met-leu-phe(fMLP) or immune complexes(ICs) was detected. Results: Compared with HC, IL-8 was significantly higher expressed in neutrophils of SLE patients. Serum IL-8 levels significantly increased in lupus patients and were positively correlated with serum IgM levels. Serum from SLE patients induced neutrophils to secrete more IL-8. PADI4 inhibitor could upregulate the production of IL-8 in neutrophils. In dHL-60 cells, knockdown of PADI4 led to a significant increase in IL-8 secretion. Conclusion The proinflammatory cytokine IL-8 is highly expressed in neutrophils and serum of SLE patients, regulated by PADI4 and correlated with lupus serological indicators. IL-8 plays a role in the development of SLE through inflammatory responses, and PADI4/IL-8 provides new thinking for SLE monitoring and therapy.

Objective : To investigate the expression and clinical significance of classic vascular endothelial growth factor A (VEGFA) and vasotropic mimicry factor matrix metalloproteinase 14 (MMP⁃14) in lung adenocarcinoma(LUAD) . Methods : The expression levels of MMP⁃14 and VEGFA genes and proteins in LUAD and their correlation with survival and prognosis were analyzed using TCGA and UALCAN databases . Serum of 69 patients with LUAD and 20 healthy subjects (control group) was collected , and the contents of MMP⁃14 and VEGFA were detected by ELISA and chemiluminescence , respectively , to analyze the correlation between the two and the clinicopathological features of tumors and their value in prediction and diagnosis of LUAD . Results: The levels of MMP⁃14 and VEGFA in LUAD tissues and serum were higher than those in control group . There were significant differences in serum VEGFA and MMP⁃14 expression levels among early stage group , advanced stage group and control group (P< 0. 001) . MMP⁃14 was higher in T3 /T4 stage than that in T1 /T2 stage (P = 0. 045) , higher in N2 /N3 stage than that in N0 /N1 stage (P = 0. 035) , and higher in the pleural metastasis group than that in the non⁃pleural metastasis group (P = 0. 034) . VEGFA level was higher in M 1 than M0 (P = 0. 025) . Elevated VEGFA level was a risk factor for LUAD (P = 0. 002) . The area under the curve (AUC) of MMP⁃14 , VEGFA and CEA alone was 0. 793 , 0. 849 and 0. 851 , respectively , and the AUC of the combined test was 0. 952 . The overall survival ( OS) and disease specific survival (DSS) of MMP⁃14 and VEGFA low expression group were longer than those of MMP⁃14 and VEGFA high expression group (P < 0. 05) . Conclusion High expression of MMP⁃14 and VEGFA in LUAD is associated with the growth , invasion and metastasis of LUAD , respectively , and has implications for survival prognosis determination .

Objective To analyze the clinical characteristics of acinetobacter baumannii infection and drug resistance tendency of our hospital in 2014 ,so as to promote the clinical rational use of antibiotics .Methods The study was a retrospective review ,the re‐sults of clinical distribution and drug resistance of acinetobacter baumannii isolated from our hospital in 2014 were analyzed .The an‐timicrobial susceptibility testing(AST) of acinetobacter baumannii was determined by K‐B disk diffusion method and minimal inhib‐itory concentration(MIC) test ,respectively .The AST was performed as recommended by CLSI 2010 .Results A total of 299 strains of acinetobacter baumannii were isolated from clinical specimens throughout the year .Of the 299 Acinetobacter baumannii isolates , 268 strains(89 .63% ) were isolated from sputum ,165 strains(55 .18% ) of Acinetobacter baumannii were from intensive care unit (ICU) and 52 strains(17 .39% ) were from neurosurgery .The resistance rate of Acinetobacter baumannii to cefoperazone/sulbactam was 5 .02% while its resistance to Imipenem and Meropenem significantly increased to 52 .17% and 56 .86% ,respectively .And the resistance rates ofβ‐lactams ,fluoroquinolones and aminoglycosides were higher than 60% .Conclusion The isolation rate of Acine‐tobacter baumannii is increasing in recent year in our hospital ,as well the resistance rate to the common Antibiotics .Monitoring the resistance of Acinetobacter baumannii should be strengthened for preventing resistant bacteria from spreading .