Background Coronary artery disease (CAD) is associated with gut microbiota alterations in different populations. Gut microbe-derived metabolites have been proposed as markers of major adverse cardiac events. However, the relationship between the gut microbiome and the different stages of CAD pathophysiology remains to be established by a systematic study. Results Based on multi-omic analyses (sequencing of the V3-V4 regions of the 16S rRNA gene and metabolomics) of 161 CAD patients and 40 healthy controls, we found that the composition of both the gut microbiota and metabolites changed significantly with CAD severity. We identified 29 metabolite modules that were separately classified as being positively or negatively correlated with CAD phenotypes, and the bacterial co-abundance group (CAG) with characteristic changes at different stages of CAD was represented by Roseburia , Klebsiella , Clostridium IV and Ruminococcaceae . The result revealed that certain bacteria might affect atherosclerosis by modulating the metabolic pathways of the host, such as taurine, sphingolipid and ceramide, and benzene metabolism. Moreover, a disease classifier based on differential levels of microbes and metabolites was constructed to discriminate cases from controls and was even able to distinguish stable coronary artery disease from acute coronary syndrome accurately. Conclusion Overall, the composition and functions of the gut microbial community differed from healthy controls to diverse coronary artery disease subtypes. Our study identified the relationships between the features of the gut microbiota and circulating metabolites, providing a new direction for future studies aiming to understand the host–gut microbiota interplay in atherosclerotic pathogenesis. Electronic supplementary material The online version of this article (10.1186/s40168-019-0683-9) contains supplementary material, which is available to authorized users.

BackgroundRobotic-assisted total hip arthroplasty (THA) allows for accurate preoperative planning and component positioning, potentially enhancing implant survival and long-term outcomes. The relative efficacy and safety of robotic-assisted and conventional THA, however, are unclear. This systematic review and meta-analysis compared the safety and efficacy of robotic-assisted and conventional THA.MethodsMedline, Embase and the Cochrane Library were comprehensively searched in September 2017 to identify studies comparing the safety and efficacy of robotic-assisted and conventional THA. Seven studies were included. Data of interest were extracted and analysed using Review Manager 5.3.ResultsThe seven included studies involved 1516 patients, with 522 undergoing robotic-assisted and 994 undergoing conventional THA. Compared with conventional THA, robotic-assisted THA was associated with longer surgical time (not significant); lower intraoperative complication rates (OR: 0.12, 95% CI: 0.05 to 0.34, p<0.0001 I2); better cup placement, stem placement and global offset and a higher rate of heterotopic ossifications. Functional scores, limb length discrepancy and rates of revision and stress shielding were similar in the two groups. The relative amount of blood loss was unclear.ConclusionThe results of this meta-analysis suggest that robotic-assisted THA has certain advantages over conventional THA, including the results of component positioning and rates of intraoperative complications. Additional comparative studies are required to determine the long-term clinical outcomes of robotic-assisted THA.

Anti-dsDNA Ab is reported to be the central pathogenic autoantibody involved in systemic lupus erythematosus (SLE) pathogenesis. However, the mechanisms involved in anti-dsDNA Ab production remain unclear. Recent evidence indicated that DNA-containing immune complexes (ICs) in circulation (termed “circulating DNA-containing ICs”), which are one of the hallmarks of SLE, might be involved in autoantibody production. In this study, we explored their potential role in anti-dsDNA Ab production and the underlying mechanisms in patients with SLE. We demonstrated that circulating DNA-containing ICs were able to induce anti-dsDNA Ab. Of note, HMGB1 in circulating DNA-containing ICs was crucial for anti-dsDNA Ab induction. The HMGB1 content of circulating DNA-containing ICs also correlated positively with anti-dsDNA Ab production in patients with SLE. Further, we revealed that the TLR2/MyD88/microRNA-155 (miR-155) pathway was pivotal for HMGB1 to confer anti-dsDNA Ab induction, and Ets-1 was a functional target of miR-155 in the induction of anti-dsDNA Ab by circulating DNA-containing ICs. Finally, we validated the expression of miR-155 and Ets-1 and their correlation with anti-dsDNA Ab production in patients with SLE. To our knowledge, this is the first report of the crucial role of HMGB1 in autoantibody production mediated by the TLR2/MyD88/miR-155/Ets-1 pathway. These findings identify a novel mechanism to account for the persistent production of anti-dsDNA Ab in SLE and a clue for developing a novel therapeutic strategy against SLE.