CO2 Capture Test for A Moving-bed System Utilizi g Low-temperature Steam

AbstractIn the process of capturing CO2 from flue gas (combustion exhaust gas), the lowering of CO2 capture energy is considered a significant issue. If some or all of the CO2 capture energy can be compensated with the waste heat, a significant energy saving is possible. In our proposed CO2 adsorption process, because the CO2 is captured using low-temperature steam, an energy-s ving process that makes it is easy to utilize the waste heat can be created. In this paper, we conduct bench tests aimed at developing a mo ing-bed system suitable for large-scale plants in order to verify the performance of the adsorbent. The results demonstrated that an moving-bed system could be established to capture 1.6t/day of CO2 from coal combustion exhaust gas

Diverse Basis of β-Catenin Activation in Human Hepatocellular Carcinoma: Implications in Biology and Prognosis

<div><p>Aim</p><p>β-catenin signaling is a major oncogenic pathway in hepatocellular carcinoma (HCC). Since β-catenin phosphorylation by glycogen synthase kinase 3β (GSK3β) and casein kinase 1ε (CK1ε) results in its degradation, mutations affecting these phosphorylation sites cause β-catenin stabilization. However, the relevance of missense mutations in non-phosphorylation sites in exon 3 remains unclear. The current study explores significance of such mutations in addition to addressing the clinical and biological implications of β-catenin activation in human HCC.</p><p>Methods</p><p>Gene alteration in exon3 of <i>CTNNB1</i>, gene expression of β-catenin targets such as <i>glutamate synthetase (GS)</i>, <i>axin2</i>, <i>lect2</i> and <i>regucalcin (RGN)</i>, and protein expression of β-catenin were examined in 125 human HCC tissues.</p><p>Results</p><p>Sixteen patients (12.8%) showed conventional missense mutations affecting codons 33, 37, 41, and 45. Fifteen additional patients (12.0%) had other missense mutations in codon 32, 34, and 35. Induction of exon3 mutation caused described β-catenin target gene upregulation in HCC cell line. Interestingly, conventional and non-phosphorylation site mutations were equally associated with upregulation of β-catenin target genes. Nuclear localization of β-catenin was associated with poor overall survival (<i>p</i> = 0.0461). Of these patients with nuclear β-catenin localization, loss of described β-catenin target gene upregulation showed significant poorer overall survival than others (<i>p</i> = 0.0001).</p><p>Conclusion</p><p>This study suggests that both conventional and other missense mutations in exon 3 of <i>CTNNB1</i> lead to β-catenin activation in human HCC. Additionally, the mechanism of nuclear β-catenin localization without upregulation of described β-catenin target genes might be of clinical importance depending on distinct mechanism.</p></div

β-catenin signaling assessed by protein expression in human HCC.

<p>A. Representative pictures for β-catenin expression in human. B. Occurrence of β-catenin nuclear translocation in each group is shown. C. In patients with β-catenin nuclear translocation (n = 28), occurrence of β-catenin target gene upregulation in each group is shown. D. Patients with β-catenin nuclear translocation in tumor could be divided into two groups; patients with <i>CTNNB1</i> mutation and without it. Furthermore, patients without <i>CTNNB1</i> mutation were classified into two subgroups; patients with determined β-catenin target gene upregulation and patients without it.</p

Regulation of β-catenin target genes by <i>CTNNB1</i> exon3 mutation in human HCC cell line.

<p>A. Stable cell line expressing <i>CTNNB1</i> exon3 mutation (Hep3B-S33Y) is established. Control cell line is shown as Hep3B-pCI. Immunofluorescent staining is performed with β-catenin antibody. Nuclear staining is performed with Hoechst33342. Arrow heads show nuclear translocation of β-Catenin. B. TOP-Flash activity is compared between Hep3B-S33Y and Hep3B-pCI. C. β-catenin target protein expressions (GS, Regucalcin and Lect2) of Hep3B-S33Y and Hep3B-pCI are shown by Western blot.</p

Prognostic impact of β-catenin signaling in human HCC.

<p>A. Overall survival is compared between patients with β-catenin nuclear translocation in tumor (n = 28) and patients without it (n = 78). B. Overall survival was compared between patients with described target gene upregulation (n = 22) and others without it (n = 6) in patients with β-catenin nuclear translocation.</p

β-catenin signaling based on target gene expressions in human HCC.

<p>A. Correlations of β-catenin target gene expressions. B. Heat map is shown based on β-catenin target gene expressions. Patients were classified into 4 groups; patients with conventional mutations (C); patients with other site mutations (O); patients with β-catenin target gene upregulation but no-mutation (NA); patients without mutation or signal activation (N). C. Percentage of β-catenin signal activation is compared among three groups, HCC patients with conventional mutation, patients with other site mutation, and patients without mutations. *<i>p</i> < 0.05. D. quantitative expressions of β-catenin targets, <i>GS</i>, <i>Axin2</i>, <i>Lect2</i>, and <i>Regucalcin</i>, are shown. *, <i>p</i> < 0.05. **, <i>p</i> < 0.01.</p