Heat-duty reduction is the major challenge in CO 2 desorption and amine regeneration. The use of a combination of heterogeneous catalytic desorption with improved amine solvents is a novel approach to address this issue. We studied CO 2 -desorption tests of noncatalytic diethylamine (DEA) solvents as a benchmark and focused on five blended amines (DEA−monoethanolamine, MEA; 4.5:0.5 to 2.5:2.5 M) with three types of catalysts (γ-Al 2 O 3 , H-ZSM-5, and 2:1 blended γ-Al 2 O 3 −H-ZSM-5) to explore the synergy effects of DEA-based amine blends with solid catalysts. The heat duty and CO 2 production of each case scenario were tested for six sets of solutions with initial loading of 0.5 mol of CO 2 per mole of amine at 363−378 K and were compared with those of 5 M DEA solvents. The results showed that the three catalyst conditions (blended catalyst, H-ZSM-5, and γ-Al 2 O 3 ) followed different trends at rich and lean loadings. Finally, both 5 M DEA and 4.5:0.5 M DEA−MEA with blended catalysts exhibited very low heat duties of 151.2 and 168.0 kJ per mole of CO 2 at loadings of 0.50− 0.20 mol per mole of amine at 378 K among the six solutions. Both approaches proved to be the most-energy-efficient amine solutions whereas the blended amine with blended catalysts was the best strategy that was applicable in the CO 2 desorber.

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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.

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