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The injection of carbon dioxide (CO2) into gob contributes to the geological sequestration of CO2. The chemical inhibitors, which are used for fire protection, can promote the sequestration of CO2. High pressure adsorption tests, swelling experiments and scanning electron microscopy were used to analyze the effects of several chemical inhibitors on the CO2 adsorption and on the coal pore structure. The adsorption capacity of CO2 and its pore volume increase after spaying an inhibitor solution. The treatment of coal in an inhibitor solution increases its pore size distribution from 0.4 nm to 0.6 nm in coal. Moreover, pore sizes lower than 0.419 nm increase together with the adsorption capacity of CO2. Based on the swelling experiments, soaking coal in an inhibitor solution induces a swelling effect on the compound, which leads to an increase in the size of its pores and cracks. This increasing trend of the pores and cracks has been verified by a series of adsorption experiments. The results obtained in this paper provide a basis for the development of further applications based on the CO2 storage technology. [ABSTRACT FROM AUTHOR]

The construction of electrode materials for lithium-ion batteries (LIBs) and sodium-ion batteries (SIBs) has gradually been an appealing and attractive technology in energy storage research field. In the present work, a facile strategy of synthesizing ultrathin amorphous/nanocrystal dual-phase P-doped Bi2MoO6 (denoted as P-BiMO) nanosheets via a one-step wet-chemical synthesis approach is explored. Quite distinct from conventional two-dimensional (2D) nanosheets, our newly developed ultrathin P-BiMO nanosheets exhibit a unique tunable amorphous/nanocrystalline dual-phase structure with several compelling advantages including fast ion exchange ability and superb volume change buffer capability. The experimental results reveal that our prepared P-BiMO-6 electrode delivers an excellent reversible capacity of 509.6 mA·g−1 after continuous 1,500 cycles at the current densities of 1,500 mA·g−1 and improved rate performance for LIBs. In the meanwhile, the P-BiMO-6 electrode also shows a reversible capacity of 300.6 mA·g−1 after 100 cycles at 50 mA·g−1 when being used as the SIBs electrodes. This present work uncovers an effective dual-phase nanosheet structure to improve the performance of batteries, providing an attractive paradigm to develop superior electrode materials. [ABSTRACT FROM AUTHOR]

Moment tensors are key to seismic discrimination but often require accurate Green's functions for estimation. This limits the regions, frequency bands and wave types in moment tensor inversions. In this study, we propose a differential moment tensor inversion (diffMT) method that uses relative measurements to remove the path effects shared by clustered events, thereby improving the accuracy of source parameters. Using results from regular inversions as a priori distribution, we apply Bayesian Markov Chain Monte Carlo to invert the body- and surface wave amplitude ratios of an event pair for refined moment tensors of both events. Applications to three North Korea nuclear tests from 2013 to 2016 demonstrate that diffMT reduces the uncertainties substantially compared with the traditional waveform-based moment tensor inversion. Our results suggest high percentages of explosive components with similar double-couple components for the North Korea nuclear tests. [ABSTRACT FROM AUTHOR]

11-Deoxy-16,16-dimethyl PGE2 (DDM-PG[E.sub.2]) protects renal proximal tubule epithelial cells (LLC-P[K.sub.1) against the toxicity induced by 2,3,5-tris(glutathion-S-yl)hydroquinone (TGHQ), a potent nephrotoxic and nephrocarcinogenic metabolite of hydroquinone. We have now determined the ability of DDM-PGE2 to protect against other renal toxicants and report that DDM-PG[E.sub.2] only protects against oncotic cell death, induced by [H.sub.2][O.sub.2], iodoacetamide, and TGHQ, but not against apoptotic cell death induced by cisplatin, mercuric chloride, or tumor necrosis factor-[alpha]. DDM-PG[E.sub.2]-mediated cytoprotection is associated with the upregulation of at least five proteins, including the major endoplasmic reticulum (ER) chaperone glucose-regulated protein 78 (Grp78). To elucidate the role of Grp78 in oncotic cell death, we used LLC-P[K.sub.1] cells in which induction of grp78 expression was disrupted by stable expression of an antisense grp78 RNA (pkASgrp78). As anticipated, DDM-PG[E.sub.2] failed to induce Grp78 in pkASgrp78 cells, with a concomitant inability to provide cytoprotection. In contrast, DDM-PG[E.sub.2] induced Grp78 and afforded cytoprotection against [H.sub.2][O.sub.2], iodoacetamide, and TGHQ in empty vector transfected cells (pkNEO). These data suggest that Grp78 plays an essential role in DDM-PG[E.sub.2]-mediated cytoprotection. Moreover, TGHQ-induced p38 MAPK activation is disrupted under conditions of a compromised ER stress response in pkASgrp78 cells, which likely contributes to the loss of cytoprotection. Finally, using two-dimensional gel electrophoresis coupled to matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy, we found that DDM-PG[E.sub.2] induced several proteins in pkNEO cells, but not in pkASgrp78 ceils, including retinol-binding protein, myosin light chain, and heat shock protein 27. The findings suggest that additional proteins may act in concert with Grp78 during DDM-PG[E.sub.2]-mediated cytoprotection against oncotic cell death. quinone-thioether; endoplasmic reticulum stress; heat shock protein 27; thromboxane receptor; proteomics

EGFR-independent activation of p38 MAPK and EGFR-dependent activation of ERK1/2 are required for ROS-induced renal cell death. Am J Physiol Renal Physiol 287:F1049-Fl058, 2004. First published June 29, 2004; doi:10.1152/ajprenal.00132.2004.--2,3,5-Tris-(glutathion-S-yl)hydroquinone (TGHQ), a reactive metabolite of the nephrotoxicant hydroquinone, induces the ROS-dependent activation of MAPKs, followed by histone H3 phosphorylation and oncotic cell death in renal proximal tubule epithelial cells (LLC-P[K.sub.1]). Cell death and histone H3 phosphorylation are attenuated by pharmacological inhibition of p38 MAPK or ERK1/2 pathways. Because TGHQ, but not epidermal growth factor (EGF), induces histone H3 phosphorylation and cell death in LLC-P[K.sub.1] cells, we hypothesized that there are differences in the mechanisms by which TGHQ and EGF induce activation of the EGF receptor (EGFR). We therefore compared the relative ability of TGHQ, [H.sub.2][O.sub.2], and EGF to activate EGFR and MAPKs and found that p38 MAPK activation is EGFR independent, whereas ERK1/2 activation occurs mainly through EGFR activation. TGHQ, [H.sub.2][O.sub.2], and EGF induce different EGFR tyrosine phosphorylation profiles that likely influence the subsequent differential kinetics of MAPK activation. We next transfected LLC-P[K.sub.1] cells with a dominant negative p38 MAPK-expressing plasmid (pcDNA3-DNp38). TGHQ failed to induce phosphorylation of p38 MAPK and its substrate, MK-2, in pcDNA3-DNp38-transfected cells, indicating loss of function of p38 MAPK. In untransfected, pcDNA3 or pcDNA3-p38 (native)-transfected LLC-P[K.sub.1] cells, Hsp27 was intensively phosphorylated after TGHQ treatment, whereas in pcDNA3-DNp38-transfected cells, TGHQ failed to induce Hsp27 phosphorylation. Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin. reactive oxygen species; epidermal growth factor receptor; mitogen-activated protein kinase; histone H3; heat shock protein 27

Background: With the global pandemic of obesity and nonalcoholic fatty liver disease (NAFLD), the incidence of cirrhosis associated with nonalcoholic steatohepatitis (NASH) has greatly increased. This study aimed to evaluate the efficacy and safety of bariatric surgery in obese cirrhotic patients. Methods: PubMed, EMBASE, and the Cochrane Library were searched for relevant studies. Effectiveness outcomes were weight loss, remission of comorbidities, and improvement in liver function. Safety outcomes were procedural complications and mortality. Results: A total of 15 studies were included in this meta-analysis. Patients with compensated cirrhosis lost weight significantly after surgery, and the percentage of excess weight loss was 60.44 (95% CI, 44.34 to 76.55). Bariatric surgery resulted in remission of NAFLD in 57.9% (95% CI, 27.5% to 88.3%), T2DM in 58.4% (95% CI, 48.4% to 68.4%), hypertension in 53.1% (95% CI, 43% to 63.3%), dyslipidemia in 59.8% (95% CI, 41.1% to 78.5%) of patients with cirrhosis. Bariatric surgery reduced the levels of alanine aminotransferase and aspartate aminotransferase. The incidence of surgical complications in patients with cirrhosis was about 19.2% (95% CI, 11.7% to 26.6%), which was higher than that in patients without cirrhosis (OR 2.67 [95% CI, 1.26 to 5.67]). Patients with cirrhosis had an overall mortality rate of 1.3%, and the mortality rates for compensated cirrhosis and decompensated cirrhosis were 0.9% and 18.2%, respectively. Conclusions: Bariatric surgery is effective for weight loss, remission of comorbidities, and reversal of liver damage. Although cirrhotic patients have a higher risk of complications and death, bariatric surgery is relatively safe for well-compensated cirrhosis. [ABSTRACT FROM AUTHOR]