Ionic liquids (ILs) have been proposed to simultaneously capture a variety of condensable gases for the first time. The hydrophobic IL [EMIM][Tf 2 N] was selected as a suitable absorbent screened by the COSMO-RS (conductor-like screening model for real solvents) model, which in combination with the quantum chemistry calculation provided some theoretical insight into mechanisms with respect to condensable gas capture. Considering the simultaneous capture of volatile organic compounds (VOCs) and water, we selected benzene, toluene, and pxylene (BTX) as three kinds of VOC representatives, measured the vapor− liquid equilibrium (VLE) of BTX + [EMIM][Tf 2 N] mixture systems, and compared them with the predicted results by the UNIFAC−Lei model. The experiment of capturing condensable gases with [EMIM][Tf 2 N] as the absorbent was conducted. Furthermore, the conceptual design of continuous processes with [EMIM][Tf 2 N] and the conventional benchmark solvent triethylene glycol as absorbents at the industrial scale was performed using a rigorous equilibrium stage model with the UNIFAC− Lei model parameter input. It reveals that condensable gas capture with an IL belongs to a typical process intensification technology in chemical engineering.
Liver transplantation is currently the most effective method for treating end-stage liver disease. However, recipients still need long-term immunosuppressive drug treatment to control allogeneic immune rejection, which may cause various complications and affect the long-term survival of the recipient. Many liver transplant researchers constantly pursue the induction of immune tolerance in liver transplant recipients, immunosuppression withdrawal, and the maintenance of good and stable graft function. Although allogeneic liver transplantation is more tolerated than transplantation of other solid organs, and it shows a certain incidence of spontaneous tolerance, there is still great risk for general recipients. With the gradual progress in our understanding of immune regulatory mechanisms, a variety of immune regulatory cells have been discovered, and good results have been obtained in rodent and non-human primate transplant models. As immune cell therapies can induce long-term stable tolerance, they provide a good prospect for the induction of tolerance in clinical liver transplantation. At present, many transplant centers have carried out tolerance-inducing clinical trials in liver transplant recipients, and some have achieved gratifying results. This article will review the current status of liver transplant tolerance and the research progress of different cellular immunotherapies to induce this tolerance, which can provide more support for future clinical applications.
The excessive accumulation of extracellular matrix (ECM) is a key feature of liver fibrosis and the activated hepatic stellate cells (HSCs) are the major producer of ECM proteins. However, the precise mechanisms and target molecules that are involved in liver fibrosis remain unclear. In this study, we reported that activating transcription factor 3 (ATF3) was over-expressed in mice and human fibrotic livers, in activated HSCs and injured hepatocytes (HCs). Both in vivo and in vitro study have revealed that silencing ATF3 reduced the expression of pro-fibrotic genes and inhibited the activation of HSCs, thus alleviating the extent of liver fibrosis, indicating a potential protective role of ATF3 knockdown. However, ATF3 was not involved in either the apoptosis or proliferation of HCs. In addition, our data illustrated that increased nuclear localization of ATF3 promoted the transcription of fibrogenic genes and lnc-SCARNA10, which functioned as a novel positive regulator of TGF-β signaling in liver fibrogenesis by recruiting SMAD3 to the promoter of these genes. Interestingly, further study also demonstrated that lnc-SCARNA10 promoted the expression of ATF3 in a TGF-β/SMAD3-dependent manner, revealing a TGF-β/ATF3/lnc-SCARNA10 axis that contributed to liver fibrosis by activating HSCs. Taken together, our data provide a molecular mechanism implicating induced ATF3 in liver fibrosis, suggesting that ATF3 may represent a useful target in the development of therapeutic strategies for liver fibrosis.
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