Together, these results suggest that lncRNA SNHG5 may predict ccRCC patient clinical outcome and serve as a novel anti-ccRCC therapeutic target. AJTR Copyright © 2020.Head and neck squamous cell carcinoma (HNSCC) is an aggressive epithelial malignancy characterized by frequent mutations and metastasis. Long noncoding RNAs (lncRNAs) have been implicated in tumorigenesis and serve as novel prognostic biomarkers in different cancers. To enhance our understanding of lncRNAs that may have biological significance in HNSCC and may serve as prognostic biomarkers, we globally profiled lncRNAs in HNSCC by analyzing the RNA-seq data from The Atlas of Noncoding RNAs in Cancer (TANRIC) database. Of 3576 lncRNAs, we identified 926 (higher-688, lower-238) lncRNAs with a 2-fold abundance difference among the forty HNSCC and paired adjacent normal tissue. We investigated differential abundance of lncRNAs based on TP53 mutation and p16 status. https://www.selleckchem.com/products/corticosterone.html We found 133 lncRNAs to have differential abundance by 2-fold among the mutant vs wild-type TP53 samples, whereas among p16-negative vs positive samples, we identified 710 lncRNAs with the same criteria. Meanwhile, analysis of the 15 most abundant lncRNAs in the tumor samples identified five lncRNAs whose higher abundance was associated with poor overall patient survival. Among these five, higher abundance of LINC00460 associated with poor patient survival in an independent cohort of 82 HNSCC patients. To further evaluate the potential function of LINC00460, we performed lncRNA-mRNAs co-expression analysis and found that higher abundance of LINC00460 associated with cancer-related biological pathways including EMT and other inflammatory response pathways. In summary, we report LINC00460 is more abundant in tumors compared to adjacent normal tissue and that it may serve as a potential prognostic biomarker in HNSCC. AJTR Copyright © 2020.To investigate whether p16 deletion can prevent osteoporosis caused by estrogen deficiency, we first confirmed that p16 protein expression levels were significantly up-regulated in bony tissue of ovariectomized (OVX) wild-type mice. Eight-week-old wild-type and p16-/- mice were then sham-operated or bilateral OVX. After 12 weeks, the bone phenotypes of all models were analyzed by radiography, micro-computed tomography, histology, immunohistochemistry, and molecular biology. The results showed that p16 deficiency could rescue OVX-induced osteoporosis by significantly increased bone mineral density, trabecular bone volume, total collagen positive area, osteoblast number, type I collagen positive area, fibroblast colony-forming unit (CFU-f) and alkaline phosphatase-positive CFU-f with up-regulation of the mRNA expression levels of Alp, Runx2, type I collagen and osteocalcin, and significantly reduced osteoclast surface and the ratio of RANKL/OPG mRNA expression level. Furthermore, we also demonstrated that p16 deletion inhibited OVX-induced oxidative stress and bone cell senescence, such as a significant decrease in reactive oxygen species levels, up-regulation of superoxide dismutase 1 and 2 protein expression levels, and reduction of the percentage of β-galactosidase-positive osteocytes and p21 protein expression levels in bony tissue. Our results indicate that p16 deletion can prevent estrogen deficiency-induced osteoporosis by inhibiting oxidative stress, osteocyte senescence and osteoclastic bone resorption, stimulating osteogenesis and osteoblastic bone formation. Therefore, this study provides new insights into the potential of p16 as a novel therapeutic target for estrogen deficiency-induced osteoporosis. AJTR Copyright © 2020.Estrogen plays critical roles in apical periodontitis and subsequent bone loss, however the mechanism is not clear yet. In this study, we aimed to study the underlying mechanism of estrogen in apical periodontitis using both clinic samples and animal model. Clinically, as estrogen physiologically declines in elder female patients (premenopausal verses postmenopausal patients), we found that the expression level of NLRP3/Caspase-1/IL-1β signaling pathway was elevated in the infected apical tissues of postmenopausal patients as compared to the premenopausal patients, suggesting that this pathway is involved in the estrogen-mediated apical periodontitis. Furthermore, by analyzing the well-established OVX (estrogen deficiency model) animal model, we confirmed that the expression level of NLRP3/Caspase-1/IL-1β signaling pathway was also elevated in the infection areas of apical periodontitis in OVX animals. Importantly, as the periodontitis progressed, the subsequent bone loss was aggravated significantly. Thus, taken all these data together, our results demonstrated that the NLRP3/Caspase-1/IL-1β signaling pathway is involved in the estrogen-mediated apical periodontitis and the consequent bone loss in both human being and animal model. This study may provide a potential target for female apical periodontitis therapy. AJTR Copyright © 2020.For the development of Lupus nephritis, environmental factors are reasoned to be one of the risk factors. In recent years, the role of bisphenol A (BPA) in kidney injury has attracted wide attention. In this study, we explored the nephrotoxicity and its possible mechanism of BPA exposure to lupus-prone MRL/lpr mice. Orally exposure of BPA increased serum anti-dsDNA level and urinary protein, and aggravated renal pathological injury in MRL/lpr mice. BPA increased the expression of NF-κB protein and activated the inflammatory response in both MRL/lpr and C57 mice. Unlike C57 mice, BPA exposure partially activated autophagy associated proteins, but the autophagy signaling pathway lacked the regulation of Becline1 and LC3-associated phagocytosis deficiency, and decreased Nrf2 protein expression in renal tissue of MRL/lpr mice. Therefore, exacerbating lupus nephritis induced by BPA exposure was associated with the activation of inflammation, abnormal autophagy and decreased antioxidant ability. AJTR Copyright © 2020.INTRODUCTION Coronary artery disease (CAD) is a major global health problem with high incidence and mortality. Despite many advances in treatment, the prognosis of patients with CAD still remains poor. Therefore, this study aimed to identify potential biomarkers and targets associated with the progression of CAD. METHODS Two gene expression profile datasets (GSE20681 and GSE12288), and two microRNA (miRNA) expression profile datasets (GSE59421 and GSE105449) were downloaded from the Gene Expression Omnibus (GEO) database; R language was used to screen out the differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs), respectively. In addition, five online bioinformatics tools (miRWalk et al.) were used to identify the target genes of DEMs, and miRNA-gene network was constructed using Cytoscape software. Moreover, CCK-8, flow cytometry assays were used to detect the cell proliferation and apoptosis in human umbilical vein endothelial cells (HUVECs). Meanwhile, the dual luciferase reporter system assay was used to explore the interaction of miR-376a-3p and NRIP1 in HUVECs.