Performance evaluation with the leave-one-out cross-validation (LOOCV) procedure showed that the RF-25lncRNA achieved a good performance in distinguishing high- and low-bone mineral density (BMD) subjects in different osteoporosis datasets. Our study for the first time revealed a global view of lncRNA-associated ceRNA regulation in osteoporosis and provided novel lncRNAs with ceRNA activity as candidate epigenetic diagnostic biomarkers for early detection of osteoporosis risk. Copyright © 2020 Zhang, Cheng and Zhang.Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) is an evolutionally conserved and unique enzyme that specifically catalyzes the cis-trans isomerization of phosphorylated serine/threonine-proline (pSer/Thr-Pro) motif and, subsequently, induces the conformational change of its substrates. Mounting evidence has demonstrated that Pin1 is widely overexpressed and/or overactivated in cancer, exerting a critical influence on tumor initiation and progression via regulation of the biological activity, protein degradation, or nucleus-cytoplasmic distribution of its substrates. Moreover, Pin1 participates in the cancer hallmarks through activating some oncogenes and growth enhancers, or inactivating some tumor suppressors and growth inhibitors, suggesting that Pin1 could be an attractive target for cancer therapy. In this review, we summarize the findings on the dysregulation, mechanisms, and biological functions of Pin1 in cancer cells, and also discuss the significance and potential applications of Pin1 dysregulation in human cancer. Copyright © 2020 Pu, Zheng and Peng.Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Most lncRNAs have been proven to have biological and clinical significance in acute myeloid leukemia (AML), but further investigation remains necessary. In this study, we investigated lncRNA NR-104098 in AML and its specific mechanism. The microarray analysis was performed on NB4 cells. Based on the related analysis results, we identified that lncRNA NR-104098 is a suppressor gene that is significantly upregulated in AML cells. LncRNA NR-104098 could inhibit proliferation and induce differentiation in AML cells in vitro and also play main role in the mouse xenografts. Mechanically, it was confirmed that lncRNA NR-104098 may effectively inhibit EZH2 transcription by directly binding to E2F1 and recruiting E2F1 to the EZH2 promoter. In addition, ATPR can significantly increase the expression of lncRNA NR-104098, whereas knocking down NR104098 can inhibit the inhibitory effect of ATPR on the proliferation and induction differentiation of AML cells. Taken together, these results lead to deeper insight into the mechanism of ATPR-induced AML differentiation and prevent proliferation by inhibiting EZH2 on the transcriptional level. Copyright © 2020 Feng, Hu, Li, Zhang, Liu, Xu, Zhang, Du, Du, Peng and Chen.Intestinal floras influence a lot of biological functions of the organism. Although animal model are strong tools for researches on the relationship between host and microbe, a physiologically relevant in vitro human gut model was still required. Here, a novel human gut-vessel microfluidic system was established to study the host-microbial interaction. Peristaltic motion of the cells on the chip was driven by a pneumatic pump. When intestinal epithelial cells (Caco2) were co-cultured with vascular endothelial cells (HUVECs) on the peristaltic microfluidic chip, Caco2 showed normal barrier and absorption functions after 5 days cultivation, which generally took 21 days in static Transwell models. Intestinal microvilli and glycocalyx layer were seen after 4 days cultivation, and Lactobacillus casei was successfully co-cultured for a week in the intestinal cavity. https://www.selleckchem.com/products/glutathione.html A model for intestinal damage and inflammatory responses caused by E. coli was set up on this chip, which were successfully suppressed by Lactobacillus casei or antibiotic. In summary, this human gut-vessel microfluidic system showed a good potential for investigating the host-microbial interaction and the effect and mechanism of microbiome on intestinal diseases in vitro. Copyright © 2020 Jing, Wang, Zhang, Deng, Wei, Luo, Zhang, Li and Du.Inflammatory intestinal diseases such as Crohn's disease and ulcerative colitis have seen an increase in their prevalence in developing countries throughout the current decade. These are caused by a combination of genetic and environmental factors, altered immune response, intestinal epithelium disruption and dysbiosis in the gut microbiome. Current therapies are mainly focused on treating symptoms and are often expensive and ineffective in the long term. Recently, there has been an increase in our understanding of the relevance of the gut microbiome and its impact on human health. Advances in the use of probiotics and synthetic biology have led to the development of intestinal biosensors, bacteria engineered to detect inflammation biomarkers, that work as diagnostic tools. Additionally, live biotherapeutics have been engineered as delivery vehicles to produce treatment in situ avoiding common complications and side effects of current therapies. These genetic constructs often express a therapeutic substance constitutively, but others could be regulated externally by specific substrates, making the production of their treatment more efficient. Additionally, certain probiotics detecting specific biomarkers in situ and responding by generating a therapeutic substance are beginning to be developed. While most studies are still in the laboratory stage, a few modified probiotics have been tested in humans. These advances indicate that live biotherapeutics could have great potential as new treatments for inflammatory intestinal diseases. Copyright © 2020 Barra, Danino and Garrido.Saccharomyces cerevisiae is a common platform for production of therapeutic proteins, but it is not intrinsically suited for the manufacturing of antibodies. Antibodies are naturally produced by plasma cells (PCs) and studies conducted on PC differentiation provide a comprehensive blueprint for the cellular transformations needed to create an antibody factory. In this study we mined transcriptomics data from PC differentiation to improve antibody secretion by S. cerevisiae. Through data exploration, we identified several new target genes. We tested the effects of 14 genetic modifications belonging to different cellular processes on protein production. Four of the tested genes resulted in improved antibody expression. The ER stress sensor IRE1 increased the final titer by 1.8-fold and smaller effects were observed with PSA1, GOT1, and HUT1 increasing antibody titers by 1. 6-, 1. 4-, and 1.4-fold. When testing combinations of these genes, the highest increases were observed when co-expressing IRE1 with PSA1, or IRE1 with PSA1 and HUT1, resulting in 3.