ABSTRACT
A method to generate stable single longitudinal mode (SLM) radiation from a multi-interferometric cavity configuration that can be considered as the combination of one Michelson cavity and two Fox-Smith cavities is presented. A numerical model of the interferometric cavity is investigated to optimize the laser for mode selection, and experimental verification has been carried out in a tunable TEA CO(2) laser. Pulse output energy of 300 mJ at 10.6 mum has been obtained at repetition rate of 20 Hz, corresponding to a repetition of SLM operation of 100%. This result shows that this interferometric cavity gives better performance in mode selection than other cavities based on multibeam interference.
ABSTRACT
Silencing of protein-coding tumor suppressor genes (TSGs) by CpG island hypermethylation is a common occurrence in gastric cancer (GC). Here, we examine if tumor suppressor microRNAs (miRNAs) are silenced in a similar manner. Real-time quantitative PCR (RTQ-PCR) was employed to investigate the expression level of four candidate miRNAs in GC tissues (n=30) and cell lines. Basing on RTQ-PCR results and bioinformatics approach, miR-9 was chosen for further study on epigenetic regulation. Bisulfite genomic sequencing PCR (BSP) was performed to assess the methylation status of miR-9 in GC tissues. In both GC cell lines and animal models, demethylation was performed either by treatment with 5-aza-2'-deoxycytidine (5-AZA-CdR) or by siRNA targeting DNMT1. We also analyzed the relationship between miRNAs and several clinicopathological features. Candidate miRNAs (miR-9, miR-433, miR-19b, and miR-370) were found strongly downregulated in GC tissues and cell lines. Their expression was increased following 5-AZA-CdR treatment. CpG island methylation of miR-9 was significantly higher in GC tissues compared to normal controls. After two demethylation treatments, miR-9 methylation degree was significantly decreased and miR-9 expression was ob-viously restored in GC cells and animal models. Deregulation of miR-9 was positively correlated with tumor lesion size. Three other miRNAs, miR-19b, miR-433, and miR-370 were assοciated with lymph node metastasis, decreased curvature, and poorly differentiated carcinoma. miR-19b and miR-433 were positively correlated with male gender. Of four candidate miRNAs downregulated in GC, miR-9 is epigenetically regulated by DNA methylation both in vitro and in vivo.
Subject(s)
DNA Methylation/genetics , Epigenesis, Genetic , MicroRNAs/genetics , Stomach Neoplasms/genetics , Adult , Aged , Animals , Azacitidine/administration & dosage , Azacitidine/analogs & derivatives , Cell Line, Tumor , CpG Islands/genetics , Decitabine , Female , Gene Expression Regulation, Neoplastic/drug effects , Humans , Male , Mice , MicroRNAs/antagonists & inhibitors , Middle Aged , Promoter Regions, Genetic , Stomach Neoplasms/pathology , Xenograft Model Antitumor AssaysABSTRACT
OBJECTIVE: To compare the efficiency of pamidronate (PAM) and isopentenyl pyrophosphate (IPP) to stimulate γδ T cell expansion from human peripheral blood and explore the optimized expansion conditions. METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll-Paque gradient centrifugation, and then cultured in RPMI1640 medium supplemented with 10% fetal bovine serum, IPP (1.0, 5.0, 10.0, 15.0 µg/mL) or PAM (2.0, 5.0, 8.0, 12.0 µg/mL), and IL-2 (100.0, 200.0, 500.0 IU/mL). The cells were observed and collected. The number and proportion of CD3âºTCRδ2⺠γδ T cells stimulated by PAM or IPP in total lymphocytes were evaluated by flow cytometry and the expansion efficiency was calculated. RESULTS: After 14 days, the ratios of γδ T cells in total lymphocytes in IPP group and PAM group increased to 81.3% and 78.5%, respectively. This indicated that both IPP and PAM could effectively stimulate γδ T cell expansion and there was no significant difference in the efficiency of expansion between the two groups (P>0.05). CONCLUSION: PAM has the similar ability with IPP to stimulate γδ T cell expansion in vitro. PAM could become more economical and practical choice for stimulating γδ T cell expansion.