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Ocean currents exert notable influences on surface wave height through wave-current coupling. In this paper, we provide solid evidences that ocean currents can regulate the significant wave height (SWH) by comparing measurements of a fleet of surface drifting wave buoys (DrWBs) with GFS-WW3 model product. In the Kuroshio Extension (KE) of Northwestern Pacific, the SWH observed by DrWBs are shown to be generally lower (higher) than that simulated by GFS-WW3 when waves propagate towards (against) the direction of surface currents. It is indicated that the GFS-WW3 product could be underestimated/overestimated by up to 5% compared with observed SWH if the forcing from current field is not involved. Adopting altimeter derived data, further analysis shows consistent relationship between observed and modelled SWH in the global ocean, except for regions where ocean swells dominate. The findings may help improve wave model simulations without increasing computational burdens if this relationship is considered. • Wave buoy observations show SWH is lower (higher) than GFS-WW3 product as waves propagate towards (against) surface currents. • SWH is underestimated/overestimated by up to 5% if current effect is absent in GFS-WW3 product. • Surface currents effect on waves is universal, but different mechanisms dominate in the wind-wave and swell regions. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) regulate gene expression to participate in carcinogenesis and tumor progression. Therefore, identification of a malignant phenotype associated with miRNAs and therapeutic targets will contribute substantially in improving nasopharyngeal carcinoma (NPC) treatment. In this study, we demonstrated that overexpression of let-7i-5p promotes the malignant phenotype by acting as an autophagy suppressor by targeting ATG10 and ATG16L1 in NPC. Expression levels of let-7i-5p were markedly increased in NPC and head and neck cancers based on an analysis of the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Using a cohort comprising 150 NPC tissues, we found that let-7i-5p was correlated with advanced stage, recurrence, metastasis, lymph node metastasis, and poor clinical outcomes. In addition to a series of in vitro cellular analyses, in vivo mouse tumor models revealed that let-7i-5p inhibits autophagy and promotes the malignant phenotype of NPC by targeting ATG10 and ATG16L1. Our findings demonstrate that let-7i-5p may represent a promising therapeutic target for NPC treatment. [ABSTRACT FROM AUTHOR]