Simulation and Economic Analysis of Indirect Coal-to-Liquid Technology Coupling Carbon Capture and Storage

Because the liquid fuel market in China is growing rapidly compared to the capacity for liquid fuel production, interest of coal-to-liquid technology is growing for producing liquid fuel. Several processes have not yet been industrialized. Among these, the Fischer–Tropsch (FT) process for fuel production from coal was chosen for simulation and analysis. We consider carbon capture and storage (CCS) technology because of the importance of CO₂ emissions in climate change. Systems with and without CCS coupling were simulated using Aspen Plus software. We used the simulation results to estimate costs, investment per unit of product, net present value, internal rate of return, and the static investment recovery period as economic indicators. The economic benefits of CCS technology were estimated in terms of CO₂ emission reductions cost and the cost for CO₂ capture. We also performed a price sensitivity analysis. The results reveal that CCS coupling to indirect coal liquefaction is economically feasible. With the pressure to limit CO₂ emissions, CCS coupling systems for FT fuel production are expected to be competitive

Withanolides cause thiol oxidation and aggregation of Hsp90 in MDA-MB-231 cells.

<p>(A) Cells were treated with WA (5 µM), TA (5 µM), HW (20 µM), AA (20 µM) or PH (20 µM) for 12 h. The Triton-insoluble fractions of cell lysates were prepared as described under “Experimental Procedures.” The protein levels of the disulfide-linked-Hsp 90 were analyzed by nonreducing SDS-PAGE. (B, C) The thiol-reducing agent NAC prevents the degradation of Hsp90 client proteins and cell death caused by withanolides. MDA-MB-231 cells were pretreated with or without NAC (2.5 mM) for 1 h before challenged with withanolides for 12 h (B) or 48 h (C). The protein levels of heat shock proteins and client proteins were analyzed by western blot (B). The viability of MDA-MB-231 cells was determined by the MTT assay (C). Results are presented as means ± S.E.M. (n = 3). **<i>P</i><0.01, ***<i>P</i><0.001 as compared with each group without NAC pretreated.</p

Effect of the withanolides on ER-positive human breast cancer cells.

<p>(A) Withanolides reduce the viability of MCF-7 cells. MCF-7 cells were treated with the indicated concentrations of WA, HW, AA, or PH for 48 h, and cell viability was determined by the MTT assay. (B) Withanolides induce caspase-7 activation and PARP cleavage. MCF-7 cells were treated with the withanolides for 48 h. After treatment, cells were harvested and analyzed for caspase-7 and PARP by Western blot. (C) Withanolides induce degradation of Hsp90 client proteins and induction of Hsp70. MCF-7 cells were treated with the withanolides or GM for 12 h. Levels of Hsp90 client proteins and Hsp70 were determined by Western blot. (D) Withanolides induce IKK degradation and inhibit NF-κB activation. MCF-7 cells were treated with the withanolides or GM for 12 h. After treatment, cells were harvested and analyzed for the proteins involved in the NF-κB pathway by Western blot.</p

Withanolides induce apoptosis in MDA-MB-231 cells.

<p>(A) Cells were treated with the indicated concentrations of WA, HW, AA, and geldanamycin (GM) for 48 h. After treatment, cells were harvested and analyzed for PARP and caspase-3 by Western blot. (B) Cells were treated with WA (5 µM), HW (20 µM), AA (20 µM), or GM (10 µM) for 48 h. Harvested cells were then stained with annexin V-FITC and PI and analyzed by flow cytometry. Percentages of annexin V-positive cells were calculated by combining annexin V⁺/PI⁻ (lower right quadrants) and annexin V⁺/PI⁺ (upper right quadrants) cells. Results are presented as means ± S.E.M. (n = 3).</p

Effect of the withanolides on the viability of MDA-MB-231 cells.

<p>(A) MDA-MB-231 cells were treated with the indicated concentrations of various withanolide compounds for 48 h, and cell viability was determined by the MTT assay. (B) The IC₅₀ values of the withanolides on the viability of MDA-MB-231 cells. Results are presented as means ± S.E.M. (n = 3).</p

Effect of heat shock on luciferase expressed in vivo in the presence of withanolides.

<p>MDA-MB-231 cells expressed luciferase were pretreated DMSO or withanolides in 96-well plates for 30 min before incubation at 42°C for 15 min. After heat shock treatment, cells were left to recover at 37°C for 10 or 60 min. Luciferase activity was assayed on whole-cell lysates. Results are presented as means ± S.E.M. (n = 3). *<i>P</i><0.05, **<i>P</i><0.01, **<i>P</i><0.001 as compared with the no heat shock group. ^#<i>P</i><0.05, ^##<i>P</i><0.01, ^###<i>P</i><0.001 as compared with the DMSO group which was recovered for 60 min after heat shock.</p

Effect of withanolide on the IKK/NF-κB pathway.

<p>(A) Withanolides induce IKK degradation and inhibit NF-κB activation. MDA-MB-231 cells were treated with WA (5 µM), HW (20 µM), AA (20 µM), PH (20 µM) or GM (10 µM) for 12 h. After treatment, cells were harvested and analyzed for the proteins involved in the NF-κB pathway by Western blotting. (B) Withanolides decrease anti-apoptotic proteins that are regulated by NF-κB. Cells were treated with withanolides for 48 h. After treatment, cells were harvested and analyzed for Bcl-2, Bcl-xL, and c-FLIP by Western blotting. (C) NAC prevents IKK degradation and NF-κB inhibition by WA. Cells were treated with WA (5 µM) or GM (10 µM) in the absence or presence of NAC (2.5 mM) for 12 h. After treatment, cells were harvested and subjected to Western blotting.</p

Withanolides induce degradation of Hsp90 client proteins and induction of Hsp70 in MDA-MB-231 cells.

<p>(A) Cells were treated with the indicated concentrations of various withanolide compounds for 12 h. After treatment, cells were harvested and analyzed for the Hsp90 client proteins (Raf-1, CDK4, and Akt), a non-Hsp90 client protein p85, and Hsp70 by Western blot. (B) Concentration-dependent effect of WA, HW, and AA on the Hsp90 client proteins and Hsp70. GM (10 µM) was used as a positive control. (C, D) Knockdown of Hsp70 enhances the pro-apoptotic effect of the withanolides. MDA-MB-231 cells were transfected with shRNA plasmid against Hsp70 or control plasmid for 48 h. The knockdown efficiency of shRNA for Hsp70 was confirmed by Western blot (C). The transfected cells were treated with WA (2 µM), HW (5 µM), or AA (20 µM) for another 48 h for determining apoptosis (D).</p

Buprenorphine had negligible effects on learning/memory and locomotor activity in pups.

<p>Prenatal buprenorphine (0, 0.3, and 1 mg/kg/day) exposure was started from gestation day 7 and lasted for 14 days. After birth, the male and female pups were collected at postnatal day 21 and subjected to neurobehavioral test. The time required to reach the hidden platform (latency) was recorded in Morris water maze task (n = 6 per group). Each animal underwent three sessions (test 1–3) per day for three consecutive days (A). The spontaneous locomotion (n = 6 per group), including travel distance and moving time, was measured for a period of 20 min using open field test (B).</p

Imipramine attenuated buprenorphine-induced depression-like neurobehaviors in pups.

<p>Prenatal buprenorphine (0 and 1 mg/kg/day) exposure was started from gestation day 7 and lasted for 14 days. After birth, the male and female pups were collected at postnatal day 21 and subjected to neurobehavioral test. Male and female pups (n = 6 per group) were subjected to intraperitoneal imipramine (0 and 20 mg/kg) administration 1 h before forced swimming test (A) and tail suspension test (B). **p<0.01 vs. each vehicle group and ##p<0.01 vs. each buprenorphine group.</p