Description: Current climate models systematically underestimate the strength of oceanic fronts associated with strong western boundary currents, such as the Kuroshio and Gulf Stream Extensions, and have difficulty simulating their positions at the mid-latitude ocean’s western boundaries1. Even with an enhanced grid resolution to resolve ocean mesoscale eddies—energetic circulations with horizontal scales of about a hundred kilometres that strongly interact with the fronts and currents—the bias problem can still persist2; to improve climate models we need a better understanding of the dynamics governing these oceanic frontal regimes. Yet prevailing theories about the western boundary fronts are based on ocean internal dynamics without taking into consideration the intense air–sea feedbacks in these oceanic frontal regions. Here, by focusing on the Kuroshio Extension Jet east of Japan as the direct continuation of the Kuroshio, we show that feedback between ocean mesoscale eddies and the atmosphere (OME-A) is fundamental to the dynamics and control of these energetic currents. Suppressing OME-A feedback in eddy-resolving coupled climate model simulations results in a 20–40 per cent weakening in the Kuroshio Extension Jet. This is because OME-A feedback dominates eddy potential energy destruction, which dissipates more than 70 per cent of the eddy potential energy extracted from the Kuroshio Extension Jet. The absence of OME-A feedback inevitably leads to a reduction in eddy potential energy production in order to balance the energy budget, which results in a weakened mean current. The finding has important implications for improving climate models’ representation of major oceanic fronts, which are essential components in the simulation and prediction of extratropical storms and other extreme events3, 4, 5, 6, as well as in the projection of the effect on these events of climate change.

Description: Well-known problems trouble coupled general circulation models of the eastern Atlantic and Pacific Ocean basins. Model climates are significantly more symmetric about the equator than is observed. Model sea surface temperatures are biased warm south and southeast of the equator, and the atmosphere is too rainy within a band south of the equator. Near-coastal eastern equatorial SSTs are too warm, producing a zonal SST gradient in the Atlantic opposite in sign to that observed. The U.S. Climate Variability and Predictability Program (CLIVAR) Eastern Tropical Ocean Synthesis Working Group (WG) has pursued an updated assessment of coupled model SST biases, focusing on the surface energy balance components, on regional error sources from clouds, deep convection, winds, and ocean eddies; on the sensitivity to model resolution; and on remote impacts. Motivated by the assessment, the WG makes the following recommendations: 1) encourage identification of the specific parameterizations contributing to the biases in individual models, as these can be model dependent; 2) restrict multimodel intercomparisons to specific processes; 3) encourage development of high-resolution coupled models with a concurrent emphasis on parameterization development of finer-scale ocean and atmosphere features, including low clouds; 4) encourage further availability of all surface flux components from buoys, for longer continuous time periods, in persistently cloudy regions; and 5) focus on the eastern basin coastal oceanic upwelling regions, where further opportunities for observational–modeling synergism exist.

Description: BACKGROUND Prostate cancer is one of the most prevalent cancers in men worldwide. Aberrant activation of c-Met/signal transducer and activator of transcription-3 (STAT3) signaling is involved in prostate carcinogenesis, underscoring the demand for developing c-Met/STAT3-targeting drugs. Thus, we first utilized virtual screening strategy to identify STAT3-inhibiting marine compound, heteronemin, and then validated the STAT3-inhibiting function of heteronemin in prostate cancer cells. METHODS Human prostate cancer LNCaP, DU145, and PC-3 cell lines were treated with heteronemin for 24 hr, then the cell viability was evaluated by MTT assay. Flow cytometry was performed to analyze the apoptosis in heteronemin-treated cells. Western blot and quantitative real-time PCR were executed to further confirm the c-Met/STAT3 signaling inhibition by heteronemin in DU145 and PC-3 cells. RESULTS In this study, we employed the virtual screening strategy to identify heteronemin, a spongean sesterterpene, as a potential STAT3 inhibitor from Taiwan marine drugs library. Application of heteronemin potently suppressed the viability and anchorage-independent growth of human prostate cancer cells. Besides, heteronemin induced apoptosis in prostate cancer cells by activation of both intrinsic (caspase-9) and extrinsic (caspase-8) apoptotic pathways. By luciferase assay and expression analysis, it was confirmed that heteronemin inhibited the phosphorylation of c-Met/src/STAT3 signaling axis, STAT3-driven luciferase activities and expression of STAT3-regulated genes including Bcl-xL, Bcl-2, and Cyclin D1. Finally, heteronemin effectively antagonized the hepatocyte growth factor (HGF)-stimulated c-Met/STAT3 activation as well as the proliferation and colonies formation in refractory prostate cancer cells. CONCLUSIONS These findings suggest that heteronemin may constitute a novel c-Met/STAT3-targeting agent for prostate cancer. Prostate © 2016 Wiley Periodicals, Inc.

Description: Integrated multi-omics analyses reveal the biochemical mechanisms and phylogenetic relevance of anaerobic androgen biodegradation in the environment The ISME Journal 10, 1967 (August 2016). doi:10.1038/ismej.2015.255 Authors: Fu-Chun Yang, Yi-Lung Chen, Sen-Lin Tang, Chang-Ping Yu, Po-Hsiang Wang, Wael Ismail, Chia-Hsiang Wang, Jiun-Yan Ding, Cheng-Yu Yang, Chia-Ying Yang & Yin-Ru Chiang