Peat is one of the most challenging and problematic soils in the fields of geotechnical and environmental engineering. The most critical problems related to peat soils are extremely low strength and high compressibility, resulting in poor inhabitancy and infrastructural developments in their vicinity. Thus far, peat soils were stabilized using Portland cement; however, the production of Portland cement causes significant emission of greenhouse gases, which is not environmentally desirable. Microbial-induced carbonate precipitation (MICP) is an innovative technique for improving the mechanical properties of soil through potentially environmentally friendly processes. This article presents a laboratory study carried out with the aim of investigating the viability and effect of scallop shell powder (SSP) on enhancing the mechanical properties of the MICP-treated amorphous peat. The hypothesis was that the distribution of SSP (as-derived calcite particles) would (i) provide more nucleation sites to precipitates and (ii) increase the connectivity of MICP bridges to facilitate mineral skeleton to amorphous peat, accompanied by an increase in its compressive strength. Specimens were treated at varying combinations of SSP and MICP reagents, and the improvement was comprehensively assessed through a series of unconfined compression tests and supported by microscale and chemical analyses such as scanning electron microscopy, energy-dispersive X-ray analysis, and X-ray diffraction analysis. The outcomes showed that incorporating SSP in MICP treatment would be a promising approach to treat amorphous peat soils. The proposed approach could improve the unconfined compressive strength by over 200% after a 7-day curing period, while the conventional MICP could not exhibit any significant improvements.
The endothelin-A receptor antagonist BQ123 is an effective treatment agent for hypertension and obese cardiomyopathy. However, the role of BQ123 in controlling acute inflammatory diseases and its underlying mechanisms are not well understood. Here, we showed that BQ123 activated polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) in mice and that the IL13/STAT6/Arg1 signaling pathway is involved in this process. Importantly, both treatment with BQ123 and the transfer of BQ123-induced PMN-MDSCs (BQ123-MDSCs) were effective in relieving inflammation, including dextran sulfate sodium (DSS)-induced colitis, papain-induced pneumonia, and concanavalin A (ConA)-induced hepatitis, in mice. The treatment effects were mediated by the attenuation of the inflammation associated with the accumulation of PMN-MDSCs in the colon, lung, and liver. However, concurrent injection of Gr1 agonistic antibody with BQ123 induced PMN-MDSC aggravated the observed acute inflammation. Interestingly, no remission of inflammation was observed in Rag2 knockout mice administered BQ123-MDSCs, but co-injection with CD3+ T cells significantly relieved acute inflammation. In summary, BQ123-induced PMN-MDSCs attenuated acute inflammation in a T cell-dependent manner, providing a novel potential strategy to prevent the occurrence of acute inflammation.
Background
Hepatocellular carcinoma (HCC) is a common malignant tumor with characteristics of poor prognosis, high morbidity and mortality worldwide. In particular, only a few systemic treatment options are available for advanced HCC patients, and include sorafenib and the recently described atezolizumab plus bevacizumab regimen as possible first-line treatments. We here propose acteoside, a phenylethanoid glycoside widely distributed in many medicinal plants as a potential candidate against advanced HCC.
Methods
Cell proliferation, colony formation and migration were analyzed in the three human HCC cell lines BEL7404, HLF and JHH-7. Angiogenesis assay was performed using HUVESs. The BEL7404 or JHH-7 xenograft nude mice model was established to analyze the possible antitumor effects of acteoside. qRT-PCR and western blotting were used to reveal the potential antitumor mechanisms of acteoside.
Results
Acteoside inhibited cell proliferation, colony formation and migration in all the three human HCC cell lines BEL7404, HLF and JHH-7. The prohibition of angiogenesis by acteoside was revealed by the inhibition of tube formation and cell migration of HUVECs. The combination of acteoside and sorafenib produced stronger inhibition of cell colony formation and migration of the HCC cells as well as of angiogenesis of HUVECs. The in vivo antitumor efficacy of acteoside was further demonstrated in BEL7404 or JHH-7 xenograft nude mice model, with an enhancement when combined with sorafenib in inhibiting the growth of JHH-7 xenograft. Further treatment of JHH-7 cells with acteoside revealed an increase in the level of tumor suppressor protein p53 as well as a decrease of kallikrein-related peptidase (KLK1, 2, 4, 9 and 10) gene level with no significant changes of the rest of KLK1–15 genes.
Conclusions
Acteoside exerts an antitumor effect possibly through its up-regulation of p53 levels as well as inhibition of KLK expression and angiogenesis. Acteoside could be useful as an adjunct in the treatment of advanced HCC in the clinic.
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