We compared the temporal variability of the heat content of the world ocean, of the global atmosphere, and of components of Earth's cryosphere during the latter half of the 20th century. Each component has increased its heat content (the atmosphere and the ocean) or exhibited melting (the cryosphere). The estimated increase of observed global ocean heat content (over the depth range from 0 to 3000 meters) between the 1950s and 1990s is at least one order of magnitude larger than the increase in heat content of any other component. Simulation results using an atmosphere-ocean general circulation model that includes estimates of the radiative effects of observed temporal variations in greenhouse gases, sulfate aerosols, solar irradiance, and volcanic aerosols over the past century agree with our observation-based estimate of the increase in ocean heat content. The results we present suggest that the observed increase in ocean heat content may largely be due to the increase of anthropogenic gases in Earth's atmosphere.

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Anillin (ANLN) is an actin-binding protein essential for assembly of cleavage furrow during cytokinesis. Although reportedly overexpressed in various human cancers, its role in hepatocellular carcinoma (HCC) is unclear. To address this issue, we confirmed that in 436 liver samples obtained from surgically removed HCC tissues, higher ANLN expression was detected in tumor tissues than in adjacent non-tumor tissues of HCC as measured by immunohistochemistry, quantitative real-time PCR and western blotting. Correlation and Kaplan-Meier analysis revealed that patients with higher ANLN expression were associated with worse clinical outcomes and a shorter survival time, respectively. Moreover, ANLN inhibition resulted in growth restraint, reduced colony formation, and a lower sphere number in suspension culture. Mechanistically, ANLN deficiency induced an increasing number of multinucleated cells along with the activation of apoptosis signaling and DNA damage checkpoints. Furthermore, HBV infection increased ANLN expression by inhibiting the expression of microRNA (miR)-15a and miR-16-1, both of which were identified as ANLN upstream repressors by targeting its 3’ untranslated region. Thus, we conclude that ANLN promotes tumor growth by ways of decreased apoptosis and DNA damage. Expression level of ANLN significantly influences the survival probability of HCC patients and may represent a promising prognostic biomarker.