[Efficacy of drug coated balloon versus conventional balloon in the treatment of coronary de novo bifurcation lesions: a meta-analysis].

Objective: To systematically evaluate the efficacy of drug coated balloon (DCB) versus conventional balloon in the treatment of coronary de novo bifurcation lesions. Methods: The databases of PubMed, Embase, Cochrane Library, Web of science, CNKI (China National Knowledge Infrastructure), Wanfang database, VIP, China Biology Medicine disc, Chinese clinical trial registry, American clinical trial registry and cardiovascular related websites until September 2020 were retrieved for collecting the randomized controlled trials (RCT) comparing DCB versus conventional balloon in the treatment of coronary de novo bifurcation lesions. The risk of bias of included studies was assessed using the Cochrane risk assessment tool. The meta-analysis was performed by using Revman 5.3 and Stata 14.0 software. Results: Seven RCTs with a total of 613 patients were included in this meta-analysis. Among the included studies, 4 articles reached the low risk of bias, and the other 3 articles reached the medium risk of bias. The results of meta-analysis showed that there was no significant difference in the major adverse cardiac events (RR=0.65, 95%CI 0.39-1.08, P=0.10), myocardial infarction (RR=0.68, 95%CI 0.25-1.80, P=0.43), target lesion revascularization (RR=0.94, 95%CI 0.53-1.67, P=0.83) between DCB group and conventional balloon group. Late lumen loss of side branch was less in the DCB group than that in the conventional balloon group (WMD=-0.25, 95%CI -0.41--0.09, P<0.01) and the risk of side branch restenosis was also lower in the DCB group than that in the conventional balloon group (RR=0.47, 95%CI 0.22-0.98, P<0.05). However, subgroup analysis showed that the conclusions of domestic studies and foreign studies on late lumen loss and side branch restenosis were inconsistent. The meta-analysis based on domestic literature showed that the risk of side branch restenosis after DCB treatment was lower compared with conventional balloon group (RR=0.29, 95%CI 0.15-0.57, P<0.05), while this parameter derived from foreign literatures remained unchanged between two groups (P=0.53). The meta-analysis results of domestic literature showed that late lumen loss in DCB group was less than that in conventional balloon group (WMD=-0.32, 95%CI -0.51--0.13, P<0.05), but this phenomenon was not observed in foreign literatures (P=0.30). Conclusions: The use of DCB in the treatment of coronary de novo bifurcation lesions has the potential to reduce the rate of restenosis and late lumen loss of side branch compared with conventional balloon group. However, due to the limitation on quantity, quality and results of published studies, more high-quality and large scale RCTs are still needed to confirm these findings.

Propofol suppresses proliferation, migration and invasion of gastric cancer cells via regulating miR-29/MMP-2 axis.

The article "Propofol suppresses proliferation, migration and invasion of gastric cancer cells via regulating miR-29/MMP-2 axis" by Y.-J. Ni, J. Lu, H.-M. Zhou, published in Eur Rev Med Pharmacol Sci 2019; 23(19): 8606-8615 has been withdrawn.

Propofol suppresses proliferation, migration and invasion of gastric cancer cells via regulating miR-29/MMP-2 axis.

OBJECTIVE: Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent. Previous studies suggested that propofol might act as anti-tumor drug in various cancers, including gastric cancer. However, the underlying mechanism is still largely unknown. MATERIALS AND METHODS: 1, 5, 10 and 20 µg/ml of propofol were used to treat gastric cancer cell MKN45 for 24, 48 or 72 hours. MTT assay was used to detect the proliferation. Transwell assay was employed to measure the invasion and migration with or without matrigel. The expression of miR-29a, 29b and 29c was assessed by quantitative real time polymerase chain reaction (qRT-PCR). Luciferase assay was introduced to confirm the relationship between miR-29 family member and MMP-2. Western blot was adopted to measure the expression of MMP-2 protein. RESULTS: The proliferation, migration and invasion of gastric cancer cell MKN45 were gradually decreased after propofol treatment in time- and dose- dependent manners. MiR-29a, b and c were downregulated in MKN45 cells compared with normal gastric mucosa epithelial cell GES-1 and upregulated by propofol. Inhibition of miR-29a, b or c promoted cell proliferation, migration and invasion of MKN45 cells under propofol treatment. MMP-2 was a target and regulated by miR-29 family and propofol. MMP-2 silencing reversed the stimulative effects of miR-29 inhibitor. CONCLUSIONS: Propofol inhibited cell proliferation, migration and invasion by upregulating miR-29a, miR-29b and miR-29c and downregulating MMP-2.

Syncytium formation is induced in the murine neuroblastoma cell cultures which produce pathogenic type G proteins of the rabies virus.

We investigated comparatively the interactions of host cells with two types of rabies virus G protein, an avirulent type G (Gln) and a virulent type G (Arg) protein, having glutamine and arginine at position 333, respectively. For this purpose, we established four types of cell lines (referred to as G(Gln)-NA, G(Arg)-NA, G(Gln)-BHK, and G(Arg)-BHK cells, respectively) by transfecting either the G(Gln)-cDNA or G(Arg)-cDNA into two kinds of cells, murine neuroblastoma C1300 (clone NA) and nonneuronal BHK-21. Both G(Gln)-NA and G(Arg)-NA cells produced G proteins when they were treated with 5 mM sodium butyrate, but only G(Arg)-NA cells formed syncytia at the neutral pH, which was suppressed by anti-G antiserum. The sodium butyrate-treated G(Arg)-NA cells fused also with sodium butyrate-treated NA cells under coculture conditions, but neither with untreated NA cells nor with BHK-21 cells. On the other hand, both G(Gln)-BHK and G(Arg)-BHK cells constitutively produced G proteins, but no syncytium was produced at the neutral pH. G(Arg)-BHK cells, however, formed syncytia with the sodium butyrate-treated NA cells when they were cocultured. These results suggest that only G(Arg) has a potential ability to produce syncytia of NA cells regardless of cell types by which G(Arg) protein was produced and also suggest that a certain cellular factor(s) is required for the syncytium formation, the factor(s) which is lacking in BHK-21 and untreated NA cells but is produced by the sodium butyrate-treated NA cells.