The purification of bioethanol fuel involves an energy-intensive separation process to concentrate the diluted streams obtained in the fermentation stage and to overcome the azeotropic behavior of the ethanol–water mixture. The conventional separation sequence employs three distillation columns that carry out several tasks, penalized by high-energy requirements: preconcentration of ethanol, extractive distillation, and solvent recovery. To solve this problem, we propose here a novel heat-pump-assisted extractive distillation process taking place in a dividing-wall column (DWC). In this configuration, the ethanol top vapor stream of the extractive DWC is recompressed from atmospheric pressure to over 3.1 bar (thus to a higher temperature) and used to drive the side reboiler of the DWC, which is responsible for the water vaporization. For a fair comparison with the previously reported studies, we consider here a mixture of 10 wt % ethanol (100 ktpy plant capacity) that is concentrated and dehydrated using ethylene glycol as mass-separating agent. Rigorous process simulations of the proposed vapor recompression (VRC) heat-pump-assisted extractive DWC were carried out in AspenTech Aspen Plus. The results show that the specific energy requirements drop from 2.07 kWh/kg (classic sequence) to only 1.24 kWh/kg ethanol (VRC-assisted extractive DWC); thus, energy savings of over 40% are possible. Considering the requirements for a compressor and use of electricity in the case of the heat-pump-assisted alternative, it is possible to reduce the total annual cost by approximately 24%, despite the 29% increase of the capital expenditures, for the novel process as compared to the optimized conventional separation process.

The ring finger protein 8 (RNF8), a key component of protein complex crucial for DNA-damage response, consists of a forkhead-associated (FHA) domain and a really interesting new gene (RING) domain that enables it to function as an E3 ubiquitin ligase. However, the biological functions of RNF8 in estrogen receptor α (ERα)-positive breast cancer and underlying mechanisms have not been fully defined. Here, we have explored RNF8 as an associated partner of ERα in breast cancer cells, and co-activates ERα-mediated transactivation. Accordingly, RNF8 depletion inhibits the expression of endogenous ERα target genes. Interestingly, our results have demonstrated that RNF8 increases ERα stability at least partially if not all via triggering ERα monoubiquitination. RNF8 functionally promotes breast cancer cell proliferation. RNF8 is highly expressed in clinical breast cancer samples and the expression of RNF8 positively correlates with that of ERα. Up-regulation of ERα-induced transactivation by RNF8 might contribute to the promotion of breast cancer progression by allowing enhancement of ERα target gene expression. Our study describes RNF8 as a co-activator of ERα increases ERα stability via post-transcriptional pathway, and provides a new insight into mechanisms for RNF8 to promote cell growth of ERα-positive breast cancer.

Mediator of DNA damage checkpoint protein 1 (MDC1) is essential for DNA damage response. However, the role of MDC1 in modulating gene transcription independently of DNA damage and the underlying mechanisms have not been fully defined. Androgen receptor (AR) is the central signaling pathway in prostate cancer (PCa) and its target genes are involved in both promotion and suppression of PCa. Here, we functionally identified MDC1 as a co-activator of AR. We demonstrate that MDC1 facilitates the association between AR and histone acetyltransferase GCN5, thereby increasing histone H3 acetylation level on cis-regulatory elements of AR target genes. MDC1 knockdown promotes PCa cells growth and migration. Moreover, depletion of MDC1 results in decreased expression of a subset of the endogenous androgen-induced target genes, including cell cycle negative regulator p21 and PCa metastasis inhibitor Vinculin, in AR positive PCa cell lines. Finally, the expression of MDC1 and p21 correlates negatively with aggressive phenotype of clinical PCa. These studies suggest that MDC1 as an epigenetic modifier regulates AR transcriptional activity and MDC1 may function as a tumor suppressor of PCa, and provide new insight into co-factor-AR-signaling pathway mechanism and a better understanding of the function of MDC1 on PCa.