A variety of natural mineral sorbents were synthesized and tested on a lab-scale fixed-bed system to evaluate mercury removal efficiencies under a simulated flue gas condition that contains 84% N 2 , 4% O 2 , and 12% CO 2 in volume fraction. Three types of natural minerals, bentonite (Ben), mordenite (Mor), and attapulgite (Atp), were selected as raw sorbents, and several chemical promoters, such as CuCl 2 , NaClO 3 , KBr, and KI, were employed to enhance mercury removal abilities of the raw sorbents. The physical-chemical characteristics of these minerals were analyzed by an X-ray diffractometer (XRD), an accelerated surface area and porosimeter (ASAP) using the N 2 isotherm adsorption/desorption method, and X-ray fluorescence (XRF) spectrometry. The mercury concentration was detected continuously using a VM3000 online mercury analyzer. The results showed that CuCl 2 -impregnated Atp (Cu-Atp) and CuCl 2 -impregnated Ben (Cu-Ben) presented about 90% average Hg 0 removal efficiencies at 120 °C, respectively. In addition, as the temperature increased, the removal efficiencies decreased. Although NaClO 3 -impregnated Atp showed an average Hg 0 removal efficiency more than 90% at 120 °C, its performance was limited by the testing temperature, and that was probably due to the high iron oxide content in Atp. For the KI-impregnated sorbents, high mercury removal efficiencies could be observed, and the efficiencies increased steadily with the temperature increased from 70 to 150 °C. The three natural minerals presented poor adsorption abilities for bromine, which resulted in the disappointing mercury removal efficiencies. Generally, Cu-Atp, Cu-Ben, and KI-impregnated sorbents were promising costeffective mercury sorbents.

Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extra-pancreatic organ dysfunction; however, the underlying mechanisms remain unclear. The present study was designed to evaluate the effect of dexamethasone (DXM) on pancreatic damage and to investigate the role of high-mobility group box-1 (HMGB1) and nuclear factor-κB (NF-κBp65) in the development of SAP in animal and cell models. For the in vivo experiment, 35 Sprague-Dawley rats were randomly assigned to three groups: The sham-operation control group, the SAP group and the DXM treatment group. Histological analysis revealed that, when DXM was infused into SAP rats, edema formation and structural alterations with necrosis were reduced, and the number of apoptotic cells was markedly reduced. In addition, compared with the SAP group, the expression level of HMGB1 was significantly decreased in the nucleus and the expression level of NF-κBp65 was significantly decreased in the cytoplasm from rats treated with DXM. In vitro, DXM was able to suppress the apoptosis and cell death induced by caerulein (CAE), and DXM could suppress the expression of NF-κBp65 and HMGB1 induced by CAE, as demonstrated by western blotting and immunofluorescence analysis. Therefore, these results provide an experimental basis for investigating the underlying therapeutic mechanisms of DXM treatment for SAP.

Cholangiocarcinoma (CCA) is the second most common type of hepatocellular carcinoma characterized by high aggressiveness and extremely poor patient prognosis. The germ cell-specific gene 2 protein (GSG2) is a histone H3 threonine-3 kinase required for normal mitosis. Nevertheless, the role and mechanism of GSG2 in the progression and development of CCA remain elusive. In the present study, the association between GSG2 and CCA was elucidated. Firstly, we demonstrated that GSG2 was overexpressed in CCA specimens and HCCC-9810 and QBC939 cells by immunohistochemical (IHC) staining. It was further revealed that high expression of GSG2 in CCA had significant clinical significance in predicting disease deterioration. Subsequently, cell proliferation, apoptosis, cell cycle distribution and migration were measured by MTT, flow cytometry, and wound healing assays, respectively in vitro . The results demonstrated that downregulation of GSG2 decreased proliferation, promoted apoptosis, arrested the cell cycle and weakened migration in the G2 phase of CCA cells. Additionally, GSG2 knockdown inhibited CCA cell migration by suppressing epithelial-mesenchymal transition (EMT)-related proteins, such as N-cadherin and vimentin. Mechanistically, GSG2 exerted effects on CCA cells by modulating the PI3K/Akt, CCND1/CDK6 and MAPK9 signaling pathways. In vivo experiments further demonstrated that GSG2 knockdown suppressed tumor growth. In summary, GSG2 was involved in the progression of CCA, suggesting that GSG2 may be a potential therapeutic target for CCA patients.