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All four species were present from the Southeast United States to Greenland; humpback whales were also present in the Caribbean. All species occurred throughout all regions in the winter, suggesting that baleen whales are widely distributed during these months. Each of the species showed significant changes in acoustic occurrence after 2010. Similar to NARWs, sei whales had higher acoustic occurrence in mid-Atlantic regions after 2010. Fin, blue, and sei whales were more frequently detected in the northern latitudes of the study area after 2010. Despite this general northward shift, all four species were detected less on the Scotian Shelf area after 2010, matching documented shifts in prey availability in this region. A decade of acoustic observations have shown important distributional changes over the range of baleen whales, mirroring known climatic shifts and identifying new habitats that will require further protection from anthropogenic threats like fixed fishing gear, shipping, and noise pollution.Background Nasopharyngeal carcinoma (NPC), a subclass of neck and head cancers, is the predominant cause of cancer-associated death globally. LncRNA MAGI2-AS3 has been previously reported to be associated with multiple cancers, but its molecular mechanism in NPC has not been fully explained. Hence, the purpose of this study is to identify the role and regulatory mechanism of MAGI2-AS3 in NPC. Methods Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB) were employed to examine gene levels. The biologic function of MAGI2-AS3 in NPC was estimated by cell counting, EdU, Transwell, and WB assays. Luciferase reporter and radioimmunoprecipitation (RIP) assays were carried out to determine the combination between miR-218-5p and MAGI2-AS3, GDPD5, and SEC61A1. Results MAGI2-AS3 is expressed at a high level in NPC cell lines. Moreover, MAGI2-AS3 knockdown-suppressed NPC progression in vitro and in vivo. Furthermore, MAGI2-AS3 functioned as a competing endogenous RNA (ceRNA) by sponging miR-218-5p to increase the expression of GDPD5 in NPC. Importantly, it was found that MAGI2-AS3 regulated NPC progression and cisplatin resistance via modulating GDPD5. In addition, MAGI2-AS3 could also promote the proliferation and migration in NPC cells by regulating SEC61A1. Conclusion MAGI2-AS3/miR-218-5p/GDPD5/SEC61A1 axis drove cell proliferation, migration, and epithelial-mesenchymal transition, and conferred cisplatin resistance in NPC, which may provide a novel insight into the development of NPC.Hydrometeorological phenomena have increased in intensity and frequency in last decades, with Europe as one of the most affected areas. This accounts for considerable economic losses in the region. Regional adaptation strategies for costs minimization require a comprehensive assessment of the disasters' economic impacts at a multiple-region scale. This article adapts the flood footprint method for multiple-region assessment of total economic impact and applies it to the 2009 Central European Floods event. The flood footprint is an impact accounting framework based on the input-output methodology to economically assess the physical damage (direct) and production shortfalls (indirect) within a region and wider economic networks, caused by a climate disaster. Here, the model is extended through the capital matrix, to enable diverse recovery strategies. According to the results, indirect losses represent a considerable proportion of the total costs of a natural disaster, and most of them occur in nonhighly directly impacted industries. learn more For the 2009 Central European Floods, the indirect losses represent 65% out of total, and 70% of it comes from four industries business services, manufacture general, construction, and commerce. Additionally, results show that more industrialized economies would suffer more indirect losses than less-industrialized ones, in spite of being less vulnerable to direct shocks. This may link to their specific economic structures of high capital-intensity and strong interindustrial linkages.Introduction Alterations of the epigenome may influence cancer initiation and progression. At the cellular level, histones are key regulators of chromatin accessibility and gene transcription; thus, the inhibition of histone deacetylase enzymes (HDACs) constitutes an attractive target for therapy. In this study, we investigated the effects of the HDAC inhibitor entinostat on oral squamous cell carcinoma (OSCC). Materials and methods We tested the effects of entinostat on OSCC cell lines. Cell viability and growth were analyzed using MTT assay. Cell cycle analysis, cell apoptosis, cancer stem cell (CSC) content, and the concentration of reactive oxygen species (ROS) in OSCC tumor cells were assessed using flow cytometry. The expression of histones and cell cycle regulatory proteins was examined by Western blot. Results The administration of entinostat resulted in reduced proliferation of OSCC cells, followed by cell cycle arrest at the G0/G1 phase, as well as substantial tumor apoptosis. We found an increase in ROS production and significant reductions in CSCs. We also found that entinostat caused increased acetylation histone H3 and histone H4, and changes in the expression of cell cycle-associated proteins such as p21. Conclusion This study indicates that entinostat is a potential novel therapeutic agent for OSCC by halting tumor proliferation, inducing cytotoxicity and intracellular ROS, and attacking the CSCs.Background Glutathione peroxidase 3 (Gpx3) protects cells from oxidative stress and its reduced expression in human prostate cancer has been reported. Objectives We hypothesized that Gpx3 might play an important role in the development of prostatic intraepithelial neoplasia (PIN), a pre-cancerous state of the prostate, and aimed to highlight the underlying molecular mechanism. Materials and methods The following double-knockout mice Nkx3.1-/-; Gpx3+/+, Nkx3.1-/-; Gpx3+/-, Nkx3.1-/-; Gpx3-/- were produced. Randomly divided animals were weighed, and their genitourinary tract (GUT) weights were determined after euthanasia at 4, 8, and 12 months. The mRNA expression of the genes involved in oxidative stress and Wnt signaling were analyzed in the prostate. Histopathology, ROS, and superoxide dismutase (SOD) activities were also measured. Results Loss of Gpx3 did not affect body weight and GUT weight in Nkx3.1 knockout mice. The mRNA expression of SOD3, iNOS, Hmox, and CISD2, which are associated with oxidative stress, were increased in Nkx3.