Objective: To study the corrosion resistance of orthodontic magnet with titanium nitride coating in artificial saliva. Methods: 6 samples of magnet in the size 3 mm?5 mm?7 mm were prepared.3 of them were coated with titanium nitride by plasma enhanced chemical vapor deposition,another 3 without coating were used as controls.The samples were immersed into artificial saliva at 37 ℃ for one month. Then the surface characters of two kinds of magnets were observed with the naked eye and by electron-probe microanalysis (EPMA). Results: The surface of the magnets with titanium nitride coating was fine and close in texture and there were no cleft and disintegrated area. However, that of the magnets without titanium nitride coating was uneven and coarse in texture,and there were evident clefts and disintegrated areas. Conclusion: The corrosion resistance of orthodontic magnets with titanium nitride coating is stronger than that without coating.

Objective: To study the corrosion resistance of the ortho do ntic magnets with titanium nitride (TiN) coating. Methods: The m agnets coated TiN film were immersed into artificial saliva at 37 ℃ for two mon ths. During the immersion, the concentration of iron ion in the artificial saliv a was analyzed with atomic absorption spectrophotometry(AAS). After immersion, t he weight change of the magnets was measured.The magnets coated with nickel film and without coating were used as the controls.Results: In all t he groups, iron ion concentration in the artificial saliva increased with the in crease of immersion time(P

OBJECTIVE:To provide theoretical analysis reference for the entry of Chinese antimalaria artemisia annua compound preparation into Vietnam market.METHODS:By literature review,data summary and comprehensive analysis,we introduced the general situation of Vietnam artemisia annua market and analyzed the necessity,the problems and restriction factors encountered for the entry of Chinese antimalaria artemisia annua compound preparation into Vietnam market.RESUL-TS & CONCLUSIONS:To successfully enter the Vietnam market,Chinese manufactures of antimalaria artemisia annua compound preparation should select proper management model,establish good drug brand,guide marketing,strengthen communication with doctors and patients and develop international cooperation etc.

Objective To investigate the prevalence of primary HIV-1 genotype drug-resistance and viral subtype from 237 treatment-naive patients in China.nethods CD4+ T cell counts,plasma HIV-1 viral load and HIV-1 gene sequencing in total 237 treatment-naive patients enrolled from 20 provinces/regions were detected for the evaluation of primary HIV genotypic drug-resistance.Results The survey of 237 treatment-naive patients from muhicenter areas including Henan Province,Yunan Province,and Shanghai showed that 9 subtypes of HIV-1 strains were finally identified.Most of patients were infected before 2003.Only 3 cases had genotypic mutations associated resistance to antiretroviral drugs,with high resistance to nucleoside reverse transcriptase inhibitors(NRTIs),moderate resistance to protease inhibitors(PIs)and high resistance to non-nucleoside reverse transcriptase inhibitors(NNRTIs).respectively.The prevalence of primary genotypic drug resistance was 1.3%(3/237)in this study.Conclusions The rate of HIV-1 primary genotypic drug-resistance is still relatively low in treatment-naive HIV/AIDS patients while 9 subtypes of HIV-1 strain was diseovered.

Staphylococcus aureus (S. aureus) is an important human pathogen which can cause a chronic condition with a high relapse rate despite the aggressive antimicrobial treatment. Recent studies showed that intracellular pattern recognition receptors (including NOD) in response to bacteria or bacterial products play a proinflammatory role by activating nuclear transcription factor-κB (NF-κB). But how NOD2 mediates the proinflammatory response to S. aureus in mast cells (MCs) is unclear. So, in this study, we attempted to examine the role of NOD2 in inflammatory responses of MCs to S. aureus. P815 cells (a mouse mast cell line) were cultured. Real-time PCR was used to detect the NOD2 mRNA expression in P815 cells during S. aureus infection. The siRNA against NOD2 gene was synthesized and transfected into S. aureus-infected P815 cells. By using the methods of ELISA and flow cytometry, the effects of NOD2 gene silencing on cell phagocytosis, cytokine secretion, NF-κB activation and cell apoptosis of the S. aureus-infected P815 cells were examined. It was found that S. aureus infection could increase the expression of NOD2 mRNA in P815 cells. NOD2 gene interference in P815 cells reduced the number of S. aureus engulfed by P815 cells, the level of cytokines and the activation of NF-κB. In addition, S. aureus could induce the apoptosis of P815 cells, but NOD2 gene silencing did not affect the cell apoptosis rate. Our data suggested that NOD2 plays a key role in pathogen recognition, signal transduction, and NF-κB activation in the inflammatory responses of MCs infected by S. aureus.

Objective To investigate the effect and mechanism of siHybrids technique on inhibiring the efflux pump gene mexB of Pseudomonas aeruginosa PAO1 in vitro. MethodsTargeting the efflux pump gene mexB of Pseudomonas aeruginosa PAO1 ,we designed and synthesized three siHybrids molecule and one negative scamble siHybrids molecule. Pseudomonas aeruginosa PAO1 were intervened by the siHybrids molecules in 50 nmol/L, respectively. And the experiments were made of control groups[blank and scamble (sc) -001]and intervened groups[siHybrids( si ) -001, siHybrids( si ) -002 and siHybrids(si) -003]of Pseudomonas aeruginosa PAO1. The targeting efflux pump gene mexB mRNA expressions of Pseudomonas aeruginosa PAO1, including all groups, were measured by real-time PCR in 12 h and 24 h after interference in vitro. Further, the minimal inhibitory concentration (MIC) of chlormycetinCP, erythrocin( EM ), levofloxacin ( L-OFLX), ceftazidime ( CAZ), meropenem (MER) to those groups were detected by using Mueller-Hinton broth dilution before and after interference. ResultsThe relative mexB mRNA amounts of Pseudomonas aeruginosa PAO1 intervened by different siHybrids were not much more different from each other after 12 h,but the expression of mexB mRNA of the intervened group ( si-001 ,si-002 ,si-003 ) was much lower than control groups after interference for 24 h. The relative mexB mRNA amounts, comparing 12 h with 24 h, we would find the blank control and negative control submit escalating trend. And the intervened control ,three different siHybrids were all with a downward tendency. However, in presence of 50 nmol/L siHybrids, the minimal inhibitory concentration(MIC) of CP, EM, L-OFLX, CAZ, MER to those controls were not much more different before and after interference. Conclusion On level of the mRNA expressions, siHybrids could inhibit the efflux pump gene mexB of Pseudomonas aeruginosa PAO1 in vitro, and within 24 h would be able to function effectively. Further, the effect was time-dependent.

Objective To investigate whether Pseudomonas aeruginosa pvdQ( PA2385 ) gene reveals altered antibiotic susceptibility under swarming conditions. Methods The plasmid pME6032 with pvdQ gene was constructed and identified, then transformed into Pseudomonas aeruginosa PAO1 by the electroporation, building pvdQ overexpression strain. Using the same method building pME6032-PAO1 strain.Bacteria were inoculated in LB overnight , measuring the colony diameter of the swarming zone . Results Strains of pvdQ overexpression was successfully constructed by real-time PCR. Comparison of two strains of the swarming motility of change in diameter: The result showed that PAO1 and pvdQ overexpression strains can both improve the antibiotics resistance. Swarmer cells of pvdQ overexpression strain exhibited a 2- to 4-fold increase in antibiotic resistance toward ceftazidime,ciprofloxacin, meropenem and polymyxin B compared to PAO1 on BM2-swarming agar plates. Conclusion pvdQ gene played an important role in elevating the antibiotics resistance, which through prarticipated in the swarmer cell differentiation.

ObjectiveTo investigate the alteration of MexB protein expression by plasmid containing siRNA template strand was transformed into Pseudomonas aeruginosa.Methods siRNA molecules specifically against mexB were designed and ligated into pGPU6/GFP/Neo vector to construct the recombinant plasmid pGPU6/GFP/Neo-siRNA.MexB gene was cloned into expression vector pET22b+ to construct plasmid pET22b+/mexB,the recombinant expression plasmid was transformed into E.coli BL21 (DE3)plysS and protein MexB was induced to express,then purified protein MexB was used to prepare specific antibodies in rabbits.The plasmids with siRNA molecules specifically against mexB were transformed into wild type strain,clinical multiresistant strain and mexB overexpression strain of Pseudomonas aeruginosa by electroporation respectively,and the changes of the expression of MexB were detected in 8,12,24 h respectively by Western blot.ResultspGPU6/GFP/Neo-siRNA was constructed successfully.Protein MexB was expressed successfully and the rabbit polyclonal antibodies against MexB was prepared well.The gene silence of mexB by siRNA molecules was effective in the three strains of Pseudomonas aeruginosa,but it depended on the silencing time.ConclusionThe expression of MexB was reduced in 8 h and 12 h,but in 24 h,the expression was unchanged.

Staphylococcus aureus (S. aureus) is an important human pathogen which can cause a chronic condition with a high relapse rate despite the aggressive antimicrobial treatment. Recent studies showed that intracellular pattern recognition receptors (including NOD) in response to bacteria or bacterial products play a proinflammatory role by activating nuclear transcription factor-κB (NF-κB). But how NOD2 mediates the proinflammatory response to S. aureus in mast cells (MCs) is unclear. So, in this study, we attempted to examine the role of NOD2 in inflammatory responses of MCs to S. aureus. P815 cells (a mouse mast cell line) were cultured. Real-time PCR was used to detect the NOD2 mRNA expression in P815 cells during S. aureus infection. The siRNA against NOD2 gene was synthesized and transfected into S. aureus-infected P815 cells. By using the methods of ELISA and flow cytometry, the effects of NOD2 gene silencing on cell phagocytosis, cytokine secretion, NF-κB activation and cell apoptosis of the S. aureus-infected P815 cells were examined. It was found that S. aureus infection could increase the expression of NOD2 mRNA in P815 cells. NOD2 gene interference in P815 cells reduced the number of S. aureus engulfed by P815 cells, the level of cytokines and the activation of NF-κB. In addition, S. aureus could induce the apoptosis of P815 cells, but NOD2 gene silencing did not affect the cell apoptosis rate. Our data suggested that NOD2 plays a key role in pathogen recognition, signal transduction, and NF-κB activation in the inflammatory responses of MCs infected by S. aureus.
Animals ; Cell Line ; Cytokines ; immunology ; Inflammation Mediators ; immunology ; Mast Cells ; immunology ; microbiology ; Mice ; NF-kappa B ; immunology ; Nod2 Signaling Adaptor Protein ; immunology ; Staphylococcus aureus ; physiology

Objective:To investigate the effect of metformin on the microRNA (miRNA) expression and screen potential target with network pharmacology analysis in patients with type 2 diabetes.Methods:Fifteen patients with new diagnosed type 2 diabetes admitted to our hospital were selected, who received metformin during hospitalization and after discharge. The expression of serum matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)-β1, and myocardial fibrosis related miRNAs were compared before and 6 month after metformin treatment. In addition, gene ontology (GO) and KEGG pathway enrichment analysis were applied to analyze differential expression miRNAs showing statistical significance. Meanwhile, the network figure was established to reflect the target gene messenger RNA (mRNA) corresponding to differentially expressed miRNA.Results:Compared with pre-medication, the serum level of MMP-9 was significantly decreased after treatment ( P<0.05). Besides, the expression of homo sapiens microRNA (hsa-miR)29a-3p, hsa-miR133a-5p, hsa-miR21-5p, hsa-miR30c-5p, and hsa-miR1-3p in patients with type 2 diabetes were dramatically down-regulated by metformin ( P<0.05 or P<0.01). Results of GO analysis and KEGG pathway enrichment analysis showed that differentially expressed miRNAs were mainly concentrated in endoplasmic reticulum lumen, synapse, basement membrane and other cell components. The molecular functions such as Rho GTPase binding and participation in extracellular matrix structural constituent were exerted through biological processes such as collagen catabolic process, regulation of short-term neuronal synaptic plasticity, and axon extension, which were mainly enriched in advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) signaling pathway in diabetic complications, tumor necrosis factor (TNF) signaling pathway, and Wnt signaling pathway, etc. The outcome of miRNA-mRNA network analysis demonstrated that there were 230 target genes mRNAs corresponding to differentially expressed miRNA. Conclusion:Metformin could play its role in the treatment of type 2 diabetes by down regulating the expression of miRNA, participating in the transduction of related cellular signaling pathways, regulating chromatin, nucleic acid binding, and enzyme activities.