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Objective To observe and investigate the efficacy and safety of combining with intrathecal injection of vancomycin and dexamethasone based on intravenous meropenem for treating refractory purulent meningitis in children.Methods Ninety children cases of refractory purulent meningitis from June 2014 to March 2015 were randomized into the observation group (45 cases) and control group (45 cases) according to the random number table method.The control group was given intravenous meropenem therapy,on this basis the observation group was added with intrathecal injection of vancomycin and dexamethasone.The changes of serum inflammatory markers and clinical efficacies after 7 d treatment were compared between the two groups,and the incidence rate of sequelae in the two groups were recorded after 3-months follow up.Results The descend ranges of TNF-a,CRP and PCT after 7 d treatment in the observation group were (87.3±21.8)pg/mL,(47.9±10.7)mg/L and (348.9J67.3)pg/mL,which were significantly higher than (61.5±18.5)pg/mL,(33.0± 7.9)mg/L,(263.7 ± 61.5)pg/mL in the control group(P＜0.05).There was statistically significant difference in clinical efficacy between the two groups (Z=2.086,P=0.037),the total effective rate in the observation group was 93.3 ％,which was higher than 82.2 ％ in the control group (x2 =2.589,P =0.108);the average treatment duration in the observation group was(12.8 ± 3.9)d,which was significantly less than (16.7 ± 4.7)d in the control group,the difference was statistically significant(t=4.216,P＜0.01).There were no statistically significant differences in the incidence rate of adverse drug reactions and sequelae between the two groups (P＞0.05).Conclusion With intrathecal injection of vancomycin and dexamethasone based on intravenous meropenem therapy for treating purulent meningitis,can further inhibit the inflammatory reaction,and increases clinical efficacy without significantly increasing adverse drug reactions.
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Aim To explore the mechanism of E.coli heat-labile enterotoxin B subunit(LTB)as adjuvant by analysis of cellular proteins interacting with LTB. Methods Whole cell proteins were purified from RAW 264.7 cell after treated with LTB or NaCl 12 h, respectively.The cellular proteins were interacted with LTB and the interacting proteins were purified by pull-down assay and identified by mass spectrography.The LTB interaction proteins were conformed with Western blot and immunofluorescence assay.Results 25 LTB interaction proteins were found,and their interaction network was mapped;four proteins (Jup,Dsp,Ddx5 and Vimentin)were indicated to be related with LTB adjuvant activity;immunofluorescence assay indicated that GM130 interacted with LTB,however,Vimentin had no interaction with LTB in vivo.After treated by LTB,the expression of β-actin was upregulated obvi-ously in RAW 264.7 cell,whereras,Hspd1 did not show any change.Conclusions LTB exerts adjuvant activity through binding to GM1 of immune cells,cau-sing endocytosis and transporting to the Golgi apparatus by vesicles.Then LTB might bind to Jup and affect TCF/LEF activity,regulating the expression of Bcl 2, IL-6,and Runx3.The result is promoted T cell and B cell proliferation,differentiation and activation by se-cretion of cytokines and immunoglobulins.
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OBJECTIVE:To study the effects of mifepristone on the expression of inflammatory factors in endometriosis (Ems)model rats. METHODS:SD rats were randomly divided into normal group(normal saline),model group(normal saline), mifepristone low-dose,medium-dose and high-dose groups [0.65,1.30,2.60 mg/(kg·d)],with 10 rats in each group. Except for normal group,Ems model was induced in other groups,and they were given relevant medicine intragastrically for consecutive 4 weeks. The volume of the ectopic focus was compared before and after treatment. The serum contents of TNF-α,IL-6 and IL-8 were detected by ELISA method. The phosphorylation of NF-κB p65 and the expression of COX-2 and PGE2 were detected by West-ern blot. The expression of NF-κB p65 mRNA in ectopic focus was detected by RT-PCR. RESULTS:Compared with normal group,the volume of the ectopic focus,the serum contents of TNF-α,IL-6 and IL-8,the expression of COX-2 and PGE2 protein, the phosphorylation of NF-κB p65 and the expression of NF-κB p65 mRNA in ectopic focus were increased in model group(P<0.01). Compared with model group,the volume of the ectopic focus,the serum contents of TNF-α,IL-6 and IL-8,the expression of COX-2 and PGE2 protein,the phosphorylation of NF-κB p65 and the expression of NF-κB p65 mRNA in ectopic focus were de-creased in mifepristone groups(P<0.01),in dose-dependent manner. CONCLUSIONS:Mifepristone can reduce the volume of the Ems ectopic focus,via blocking NF-κB signaling pathway and reducing the expression of inflammatory factors.
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Proteomic technology has been widely used in the research of differently-expressed proteins under different physiology and pathologic conditions.In the aspect of the human spermatozoa proteomics,many reports have demonstrated the differently expressed proteins and the roles of sperm under different physiology and pathologic state from proteome level,and these results provided reliable theoretic base for well understanding of sperm molecule mechanism in physiology and pathologic conditions.
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Aim To construct a eukaryotic expression vector of human MCHR2 and to analyze the stable expression and signal transduction pathways of MCHR2 in CHO cells. Methods The full-length MCHR2 cDNA fragment was amplified by PCR from the human fetal brain cDNA library and inserted into eukaryotic expres-sion vector pcDNA3.1(+), resulted in the recombinant expression vector pcDNA3.1-MCHR2. The recombinant plasmid was confirmed by the restriction enzymatic digestion and DNA sequencing analysis, and then transfected into CHO cells by lipofectamine. A stably-transfected cell line was obtained by the dominant G418 selection, and the expression of the MCHR2 gene on transcription and translation levels were identified by RT-PCR and Western blot. Signal transduction pathways mediated by MCHR2 were analyzed by measurement of intracellular cAMP and calcium. Results The eukaryotic expression vector pcDNA3.1-MCHR2 was successfully constructed and the MCHR2 gene was stably transfected into CHO cells. A stably-transfected cell line was established and the MCHR2 gene was efficiently transcribed and translated. MCH stimulation had no effect on the production of cAMP, however, it could induce a clear and transient increase of intracellular calcium, suggesting that MCHR2 was only coupled to Gq protein. Conclusion The stable expression of MCHR2 and analysis of its signal transduction pathways in CHO cell line provided a solid experimental foundation for further studies on the function of the MCHR2 gene in vitro.