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Objective To investigate the relationship of Vaneomycin serum concentration and drug adverse reactions (ADRs) in neonates.Methods Two hundred and thirteen neonates who were treated by Vancomycin and had their serum concentration monitored were recruited.The number of cases which had liver,kidney and hearing damage after treatment was calculated.The correlation between 3 different serum concentrations (＜5 mg/L,5-10 mg/L,＞ 10 mg/L) and ADRs were analyzed.Results The mean level of Vancomycin in serum was (4.36 ± 4.99) mg/L The total incidence of ADRs was 17.8％ (38/213 cases).The main ADRs were liver damage and hearing impairment,whose incidences were 9.9％ (21/213 cases) and 7.5％ (16/213 cases),respectively,and they were were significantly higher than kidney danage (0.5％,1/213 cases) (x2 =19.172,P =0.000;x2 =13.785,P =0.000).There was no significant difference be-tween the inidence ratio of liver damage and that of the hearing impairment (x2 =0.330,P =0.566).The ADRs ratio among 3 different serum concentrations was 17.0％ (24/141 cases),17.6％ (9/51 cases) and 23.8％ (5/21 cases).There was no significant difference between the ADRs ratios and distribution of different serum concentrations (x2 =0.576,P =0.750).Moreover,the ADRs rates didn't increase along with the serum concentrations (Z =0.648,P =0.517).Except for aspartate transaminase,the indicators of liver and kidney function varied significantly after vancomycin treatment (P ＜0.05).But there was no clinical significance because the mean value was in normal range.By Bivariate Correlation analysis,Vancomyein serum concentration had no significant influence on liver and kidney function (P ＞ 0.05).Conclusions Neonates treated by Vancomycin had reatively high ratio of the liver damage and the hearing impairment.There is no significant correlation between Vancomyein serum concentration and ADRs in neonates.
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Objective To explore the association between rs3179060C/A polymorphism in the ex-on 1 of TNF-a gene and hyperandrogenism and polycystic ovary syndrome (PCOS). Methods One hundred thirty PCOS women and one hundred seventy five normal women as controls were enrolled in this study. The genotypes were screened by polymerase chain reaction-On/off switch and the product was isolated by e-lectrophoresis on a 2. 5% agarose gel containing ethidium bromide and visualized using an ultraviolet transil-luminator. The relationship of TNF-a alleles to serum testosterone level was analyzed in PCOS patients. Results Three genotypes were identified, corresponding to CC, CA, AA, and two alleles were screened, corresponding to C and A. The frequencies of the CC, CA, AA genotypes were 58. 4% ,23.1% ,18.5% vs. 72. 0% , 17.7% , 10. 3% in PCOS group and control group, showing statistically significant difference between two groups( P < 0.05 ). The allelic frequency was 70.0% for the C allele and 30.0% for the A in P-COS group, and 80. 9% for the C allele and 19. 1% for the A in control group, respectively, showing statistically significant between two groups ( P <0.05). The relationship was not observed between rs3179060C/ A polymorphism and serum testosterone level in PCOS patients in Han Chinese racial origin ( P >0.05). Conclusions The TNF-a gene rs3179060C/A polymorphism may be a risk factor for the pathogenesis of P-COS in Chinese women, but it was not effect on hyperandrogenism in PCOS women.
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Aim To study the effect of Macrophage colony-stimulating factor(M-CSF) on MMP-9 in RAW 264.7 cell and explore the relationship between atherosclerosis caused by M-CSF and the activity of MMP-9. Methods Gelatin zymography analysis was used to investigate the effect of M-CSF and PD98059 on the activity of MMP-9 in cultured RAW 264.7 cell.Western blot was used to study the effect of M-CSF and PD98059 on the express of p-ERK1/2 in cultured RAW 264.7 cell. Results The enzyme activity of MMP-9 was significantly increased after 24-hour M-CSF treatment.Meanwhile, M-CSF upregulated the expression of p-ERK1/2. Pre-treatment with PD98059 blocked partly the increased expression of p-ERK1/2 and the activity of MMP-9 induced by M-CSF. Conclusion M-CSF can induce the secretion of MMP9 in RAW 264.7 cell, which may be mediated by the phosphorylation of ERK1/2.