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Objective@#To evaluate the effect of water-soluble components of atmospheric fine particulate matter PM2.5 on proliferation, migration, tyrosinase activity and melanin content of a human melanocyte line PIG1.@*Methods@#PM2.5 was collected during haze weather in heating seasons, and processed into suspensions. PIG1 melanocytes were cultured and divided into 5 experimental groups and 1 control group. PIG1 melanocytes in the 5 experimental groups were treated with 10, 20, 50, 100 and 200 mg/L PM2.5 suspensions respectively for 48 hours, while cells in the control group were not treated with PM2.5 suspensions. In cell migration assay, there was only 1 experimental group treated with 10 mg/L PM2.5 suspensions. After treatment, methyl thiazol tetrazolium (MTT) assay, micropore filtration assay, DOPA oxidase assay and NaOH lysis method were performed to determine the cell proliferation rate, migration rate, tyrosinase activity and melanin content respectively. Statistical analysis was carried out by using t test for comparison of means of two samples, one-way analysis of variance for means of multiple samples, Student-Newman-Keuls (SNK) -q test for multiple comparisons, and linear correlation analysis for analysis of correlations.@*Results@#Compared with the control group ([100 ± 1.41]%) , the proliferation rate of PIG1 cells significantly decreased in the 20-, 50-, 100- and 200-mg/L PM2.5 groups ([93.41 ± 2.13]%, [88.31 ± 1.3557]%, [79.75 ± 1.89]%, [69.83 ± 2.50]% respectively, all P < 0.05) . Linear correlation analysis showed that the proliferation rate and tyrosinase activity of PIG1 cells decreased with the increase in PM2.5 concentrations (r = -0.98, -0.93, respectively, both P < 0.01) . After the treatment with 10 mg/L PM2.5, the migration rate of PIG1 cells significantly decreased (66.23% ± 1.11%) compared with the control group ([76.86 ± 1.81]%, t = 7.55, P < 0.01) . With the increase in PM2.5 concentrations (50-200 mg/L) , the melanin content of PIG1 cells gradually decreased (r = -0.97, P < 0.01) .@*Conclusion@#Atmospheric fine particulate matter PM2.5 can affect the normal functions of melanocytes by inhibiting their proliferation and migration, and reducing their tyrosinase activity and melanin content.
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Objective To evaluate the effect of water-soluble components of atmospheric fine particulate matter PM2.5 on proliferation,migration,tyrosinase activity and melanin content of a human melanocyte line PIG1.Methods PM2.5 was collected during haze weather in heating seasons,and processed into suspensions.PIG1 melanocytes were cultured and divided into 5 experimental groups and 1 control group.PIG1 melanocytes in the 5 experimental groups were treated with 10,20,50,100 and 200 mg/L PM2.5 suspensions respectively for 48 hours,while cells in the control group were not treated with PM2.5 suspensions.In cell migration assay,there was only 1 experimental group treated with 10 mg/L PM2.5 suspensions.After treatment,methyl thiazol tetrazolium (MTT) assay,micropore filtration assay,DOPA oxidase assay and NaOH lysis method were performed to determine the cell proliferation rate,migration rate,tyrosinase activity and melanin content respectively.Statistical analysis was carried out by using t test for comparison of means of two samples,one-way analysis of variance for means of multiple samples,Student-Newman-Keuls (SNK)-q test for multiple comparisons,and linear correlation analysis for analysis of correlations.Results Compared with the control group ([100 ± 1.41] ％),the proliferation rate of PIG1 cells significantly decreased in the 20-,50-,100-and 200-mg/L PM2.5 groups ([93.41 ± 2.13]％,[88.31 ± 1.3557]％,[79.75 ± 1.89]％,[69.83 ± 2.50]％ respectively,all P ＜ 0.05).Linear correlation analysis showed that the proliferation rate and tyrosinase activity of PIG 1 cells decreased with the increase in PM2.5 concentrations (r =-0.98,-0.93,respectively,both P ＜ 0.01).After the treatment with 10 mg/L PM2.5,the migration rate of PIG1 cells significantly decreased (66.23％ ± 1.11％) compared with the control group ([76.86 ± 1.81]％,t =7.55,P ＜ 0.01).With the increase in PM2.5 concentrations (50-200 mg/L),the melanin content of PIG1 cells gradually decreased (r =-0.97,P ＜ 0.01).Conclusion Atmospheric fine particulate matter PM2.5 can affect the normal functions of melanocytes by inhibiting their proliferation and migration,and reducing their tyrosinase activity and melanin content.
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Objective To explore the correlation of total IgE and childhood atopic dermatitis (AD) in maternal serum and newborn cord blood, as well as its clinical significance of allergen testing. Methods Thirty-five cases diagnosed as AD (AD group) were selected, and other 35 children who were not diagnosed as AD (control group) were randomly selected from a birth cohort established in 2009—2011. The total IgE levels were detected by ELISA in maternal serum and newborn cord blood. The serum specific IgE antibody level was detected by quantitative immunoblotting method. Results The serum total IgE level was significantly higher in mother and newborn cord blood in AD group than that in control group (χ2=16.568 and 14.933, P<0.01). Compared to control group, there was a significantly higher positive rate of mother serum allergen includ?ing dust mites, house dust, ragweed pollen, song kind of pollen, poplar, surname and elm pollen, mould, shrimp, marine fish, in AD group (P<0.05). There was a significantly higher positive rate of artemisia pollen and fungi IgE in newborn cord blood in AD group (P<0.05). Conclusion The increased total IgE in maternal serum may play a predictive effect on infants suf?fering from AD. There is no obvious consistency in allergic state between mothers and infants.
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Objective To compare the efficacy and side effects of S-1 combined with oxaliplatin and capecitabine combined with oxaliplatin in treatment of advanced gastric cancer. Methods From Mar 2011 to Dec 2014, the data of 93 cases with gastric cancer in Zhengzhou Peopleˊs Hospital were studied retrospectively. 48 cases treated by S-1 combined with oxaliplatin (SL group) and 45 cases treated by capecitabine combined with oxaliplatin (XL group). The patients of SL group received S-1 80 mg·m-2·d-1, bid, po, d1-14, L-OHP 130 mg/m2, ivgtt, 2 hours, d1. The patients of XL group received capecitabine 2 000 mg·m-2·d-1, bid, po, d1-14, L-OHP 130 mg/m2, ivgtt, 2 hours, d1. The course was 21 days in two groups. The efficacy and side effects were evaluated after two courses. Results The efficacy rates of SL and XL group were 52.08 % (25/48) and 53.33 % (24/45), respectively there was no significant difference (P > 0.05). The incidence rate of gastrointestinal reaction in SL group was obviously higher than that in XL group [52.08%(25/48) vs 24.44%(11/45), P<0.05]. The incidence rate of oral mucositis in SL group was significantly lower than that in XL group [25.00 % (12/48) vs 51.11 % (23/45), P< 0.05]. Conclusion Both S-1 combined with L-OHP and capecitabine combined with L-OHP for gastric cancer treatment are safe and effective.
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Objective To evaluate the role of C-type lectin domain family 2,member B (CLEC2B) gene in the pathogenesis of vitiligo.Methods Real time fluorescence-based PCR was performed to detect the expression of CLEC2B mRNA in the peripheral blood and lesional skin of 37 patients with vitiligo as well as in the peripheral blood and normal skin of 40 healthy controls.Data were statistically analyzed by t test and chisquare test.Results Among the 37 patients,23 had progressive vitiligo,14 stable vitiligo,31 vitiligo vulgaris,6 segmental vitiligo.The expression level of CLEC2B mRNA was significantly higher in vitiligo lesions than in the control skin (1.21 ± 0.03 vs.1.00,t =4.432,P ＜ 0.05),but was of no significant difference in peripheral blood between the patients and healthy controls (1.02 ± 0.05 vs.1.00,t =1.435,P ＞ 0.05).Increased expression of CLEC2B mRNA was noted in lesions of vulgaris vitiligo compared with those of segmental vitiligo (1.21 ± 0.03 vs.1.02 ± 0.01,t =5.330,P ＜ 0.05),as well as in lesions of progressive vitiligo compared with those of stable vitiligo (1.25 ± 0.05 vs.1.08 ± 0.03,t =3.046,P ＜ 0.05).No significant difference was observed in the expression of CLEC2B mRNA among lesions of vitiligo with different courses (P ＞ 0.05).Conclusion The differential expression of CLEC2B mRNA may take part in the pathogenesis of vitiligo.
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Objective To evaluate the effects of tacrolimus on the secretion of IL-6 and sIL-2R as well as the expression of IL-6 and sIL-2R mRNA by lymphocytes.Methods Jurkat human lymphoma cells were cultured and treated with tacrolimus of different concentrations.Enzyme linked immunosorbent assay was performed to determine the levels of IL-6 and sIL-2R in the supernatant of Jurkat cells at 48 hours after treatment with tacrolimus of 0,10,102,103 and 104 nmol/L,and real time reverse transcription PCR to measure the expression of IL-6 mRNA and sIL-2R mRNA of Jurkat cells at 48 hours after treatment with tacrolimus of 102 nmol/L.Results Tacrolimus of 102 - 104 nmol/L could suppress the secretion of IL-6 and sIL-2R from Jurkat cells (all P＜ 0.05),with a more marked suppressing effect achieved by the use of tacrolimus at 103 - 104 nmol/L.The expressions of IL-6 and sIL-2R mRNA from Jurkat cells were downregulated by tacrolimus of 102 nmol/L (both P ＜ 0.05).Conclusion Tacrolimus at certain concentrations could downregulate the secretion of IL-6 and sIL-2R as well as the expression of IL-6 and sIL-2R mRNA by lymphocytes.
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Objective To investigate the effects of tacrolimus on the expression of SCF mRNA in keratinocytes and c-kit mRNA in melanoma cells.Methods Tacrolimus was used to treat cultured HaCaT keratinocytes and B16 melanoma cells for 48 hours.Subsequently,real-time fluorescence quantitative PCR was performed to determine the mRNA expression of SCF in HaCaT cells and of c-kit in B16 cells.Results A significant change was observed in the expression of SCF mRNA in HaCaT cells and c-kit mRNA in B16 cells treated with tacrolimus compared with untreated HaCaT cells and B16 cells,respectively (both P<0.05).Conclusion Tacrolimus can upregulate SCF mRNA expression in HaCaT cells and c-kit mRNA expression in R16 cells.