Stakeholder Views on Financing Carbon Capture and Storage Demonstration Projects in China

Chinese stakeholders (131) from 68 key institutions in 27 provinces were consulted in spring 2009 in an online survey of their perceptions of the barriers and opportunities in financing large-scale carbon dioxide capture and storage (CCS) demonstration projects in China. The online survey was supplemented by 31 follow-up face-to-face interviews. The National Development and Reform Commission (NDRC) was widely perceived as the most important institution in authorizing the first commercial-scale CCS demonstration project and authorization was viewed as more similar to that for a power project than a chemicals project. There were disagreements, however, on the appropriate size for a demonstration plant, the type of capture, and the type of storage. Most stakeholders believed that the international image of the Chinese Government could benefit from demonstrating commercial CCS and that such a project could also create advantages for Chinese companies investing in CCS technologies. In more detailed interviews with 16 financial officials, we found striking disagreements over the perceived risks of demonstrating CCS. The rate of return seen as appropriate for financing demonstration projects was split between stakeholders from development banks (who supported a rate of 5–8%) and those from commercial banks (12–20%). The divergence on rate alone could result in as much as a 40% difference in the cost of CO₂ abatement and 56% higher levelized cost of electricity based on a hypothetical case study of a typical 600-MW new build ultrasupercritical pulverized coal-fired (USCPC) power plant. To finance the extra operational costs, there were sharp divisions over which institutions should bear the brunt of financing although, overall, more than half of the support was expected to come from foreign and Chinese governments

Correlations between Galectin-3 expression and chemotherapeutic resistance in breast cancers (n = 135).

<p>CR: complete response; PR: partial response; SD: stable disease; PD: progressive disease.</p><p>Correlations between Galectin-3 expression and chemotherapeutic resistance in breast cancers (n = 135).</p

Cell viability was reduced by combined galectin-3 knockdown and ATO treatment.

<p>Cell viability was reduced by combined galectin-3 knockdown and ATO treatment.</p

ATO treatment (2.5 µM) significantly increased endogenous galectin-3 expression in MDA-MB-231 cells.

<p>Cells were treated with ATO and anti-galectin-3 antibody (1∶1000) was used to detect endogenous galectin-3 proteins. GAPDH was used as loading control. The results shown are the mean of at least 3 independent experiments. *P<0.01.</p

Galectin-3 knockdown sensitized MDA-MB-231 cells to ATO-induced apoptosis.

<p>Cells were labeled with annexin V (x-axis) and PI (y-axis), and apoptosis was analyzed using a flow cytometer.</p

Immunohistochemical analysis revealed that galectin-3 was located in the cytoplasm and membrane of breast cancer cells (A). Galectin-3 protein is expressed at a significantly higher level in breast cancer tissues compared to paracancerous tissue (B).

<p>Immunohistochemical analysis revealed that galectin-3 was located in the cytoplasm and membrane of breast cancer cells (A). Galectin-3 protein is expressed at a significantly higher level in breast cancer tissues compared to paracancerous tissue (B).</p

The protein level of galectin-3 was reduced after shRNA treatment.

<p>Three independent shRNAs against galectin-3 were used to construct stable cell lines.</p

UMI-77 Modulates the Complement Cascade Pathway and Inhibits Inflammatory Factor Storm in Sepsis Based on TMT Proteomics and Inflammation Array Glass Chip

Sepsis is a systemic inflammatory response syndrome caused by infection, which has no specific drug at present. UMI-77 can significantly improve the survival rate of septic mice; the detailed role of UMI-77 and its underlying mechanisms in sepsis are not clear. Inflammation array glass chip and proteomic analyses were performed to elucidate the latent mechanism of UMI-77 in the treatment of sepsis. The results showed that 7.0 mg/kg UMI-77 improved the 5 day survival rate in septic mice compared to the LPS group (60.964 vs 9.779%) and ameliorated the pathological conditions. Inflammation array glass chip analysis showed that sepsis treatment with UMI-77 may eventually through the suppression of the characteristic inflammatory storm-related cytokines such as KC, RANTES, LIX, IL-6, eotaxin, TARC, IL-1β, and so on. Proteomics analysis showed that 213 differential expression proteins and complement and coagulation cascades were significantly associated with the process for the UMI-77 treatment of sepsis. The top 10 proteins including Apoa2, Tgfb1, Serpinc1, Vtn, Apoa4, Cat, Hp, Serpinf2, Fgb, and Serpine1 were identified and verified, which play important roles in the mechanism of UMI-77 in the treatment of sepsis. Our findings indicate that UMI-77 exerts an antisepsis effect by modulating the complement cascade pathway and inhibiting inflammatory storm factors

Multivariate analysis of the factors related to post-operative distant metastasis.

<p>CI = confidence interval.</p><p>Multivariate analysis of the factors related to post-operative distant metastasis.</p

UMI-77 Modulates the Complement Cascade Pathway and Inhibits Inflammatory Factor Storm in Sepsis Based on TMT Proteomics and Inflammation Array Glass Chip

Sepsis is a systemic inflammatory response syndrome caused by infection, which has no specific drug at present. UMI-77 can significantly improve the survival rate of septic mice; the detailed role of UMI-77 and its underlying mechanisms in sepsis are not clear. Inflammation array glass chip and proteomic analyses were performed to elucidate the latent mechanism of UMI-77 in the treatment of sepsis. The results showed that 7.0 mg/kg UMI-77 improved the 5 day survival rate in septic mice compared to the LPS group (60.964 vs 9.779%) and ameliorated the pathological conditions. Inflammation array glass chip analysis showed that sepsis treatment with UMI-77 may eventually through the suppression of the characteristic inflammatory storm-related cytokines such as KC, RANTES, LIX, IL-6, eotaxin, TARC, IL-1β, and so on. Proteomics analysis showed that 213 differential expression proteins and complement and coagulation cascades were significantly associated with the process for the UMI-77 treatment of sepsis. The top 10 proteins including Apoa2, Tgfb1, Serpinc1, Vtn, Apoa4, Cat, Hp, Serpinf2, Fgb, and Serpine1 were identified and verified, which play important roles in the mechanism of UMI-77 in the treatment of sepsis. Our findings indicate that UMI-77 exerts an antisepsis effect by modulating the complement cascade pathway and inhibiting inflammatory storm factors