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@#BACKGROUND: Exosomes and exosomal microRNAs have been implicated in tumor occurrence and metastasis. Our previous study showed that microRNA-761 (miR-761) is overexpressed in hepatocellular carcinoma (HCC) tissues and that its inhibition affects mitochondrial function and inhibits HCC metastasis. The mechanism by which exosomal miR-761 modulates the tumor microenvironment has not been elucidated. METHODS: Exosomal miR-761 was detected in six cell lines. Cell counting kit-8 (CCK-8) and transwell migration assays were performed to determine the function of exosomal miR-761 in HCC cells. The luciferase reporter assay was used to analyze miR-761 target genes in normal fibroblasts (NFs). The inhibitors AZD1480 and C188-9 were employed to determine the role of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the transformation of cancer-associated fibroblasts (CAFs). RESULTS: In this study, we characterized the mechanism by which miR-761 reprogrammed the tumor microenvironment. We found that HCC-derived exosomal miR-761 was taken up by NFs. Moreover, HCC exosomes affected the tumor microenvironment by activating NFs via suppressor of cytokine signaling 2 (SOCS2) and the JAK2/STAT3 signaling pathway. CONCLUSIONS: These results demonstrated that exosomal miR-761 modulated the tumor microenvironment via SOCS2/JAK2/STAT3 pathway-dependent activation of CAFs. Our findings may inspire new strategies for HCC prevention and therapy.
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Robotic surgical systems are becoming increasingly popular for the treatment of cardiovascular diseases. However, most of them have been designed without considering techniques and skills of natural surgical manipulations, which are key factors to clinical success of percutaneous coronary intervention. This paper proposes an HMM-based framework to recognize six typical endovascular manipulations for surgical skill analysis. A simulative surgical platform is built for endovascular manipulations assessed by five subjects (1 expert and 4 novices). The performances of the proposed framework are evaluated by three experimental schemes with the optimal model parameters. The results show that endovascular manipulations are recognized with high accuracy and reliable performance. Furthermore, the acceptable results can also be applied to the design of next generation vascular interventional robots.
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Procedimentos EndovascularesRESUMO
<p><b>OBJECTIVE</b>To study the transfection of pancreatic cancer cells BxPC-3 with recombinant plasmid pSilencer4.1-CMV neo-hTERT-siRNA and its silencing effects.</p><p><b>METHODS</b>Pancreatic cancer cells BxPC-3 transfected with recombinant plasmid pSilencer4.1-CMV neo-hTERT-siRNA were selected as target and divided into five groups: (1) T1 group (pSilencer4.1CMV neo-hTERT1-siRNA), (2) T2 group (pSilencer4.1CMV neo-hTERT2-siRNA), (3) Lipofectamine (Lipofectamine), (4) mismatch group(pSilence4.1CMV, as negative control), (5) cell control group(without transfection). The expression of hTERT mRNA was detected by RT-PCR. The viability of cells was measured by MTT method. The cell cycle and cell apoptosis was measured by flow cytometry. The expression of telomerase protein was measured by Western blot.</p><p><b>RESULTS</b>Compared with Lipofectamine group, negative control group and cell control group, the expression of hTERT-mRNA and telomerase protein in cells was downregulated significantly(P<0.05), the viability of BxPC-3 cells was decreased significantly (P<0.05), the ratio of cells in G0/G1 stage was increased, the ratio of cells in S stage and G2/M stage was decreased, and the ratio of apoptotic cells was increased significantly in T1 group and T2 group.</p><p><b>CONCLUSION</b>Recombinant plasmid T1 and T2 can downregulate the expression of hTERT mRNA and telomerase protein in BxPC-3 cells , and has good RNAi silencing effects. T1 and T2 can also inhibit the growth of BxPC-3 cells, block the cell cycle, promote the apoptosis of cells, and has anti-pancreatic cancer effects in vitro.</p>
