Performance of C\u3csub\u3e2\u3c/sub\u3eH\u3csub\u3e4\u3c/sub\u3e Reductant in Activated-Carbon-Supported MnOx-Based SCR Catalyst at Low Temperatures

Hydrocarbons as reductants show promising results for replacing NH3 in SCR technology. Therefore, considerable interest exists for developing low-temperature (\u3c 200 °C) and environmentally friendly HC-SCR catalysts. Hence, C2H4 was examined as a reductant using activated-carbon-supported MnOx-based catalyst in low-temperature SCR operation. Its sensitivity to Mn concentration and operating temperature was parametrically studied, the results of which showed that the catalyst activity followed the order of 130 °C \u3e 150 °C \u3e 180 °C with an optimized Mn concentration near 3.0 wt.%. However, rapid deactivation of catalytic activity also occurred when using C2H4 as the reductant. The mechanism of deactivation was explored and is discussed herein in which deactivation is attributed to two factors. The manganese oxide was reduced to Mn3O4 during reaction testing, which contained relatively low activity compared to Mn2O3. Also, increased crystallinity of the reduced manganese and the formation of carbon black occurred during SCR reaction testing, and these constituents on the catalyst’s surface blocked pores and active sites from participating in catalytic activity

Extracellular depolymerisation triggers fermentation of tamarind xyloglucan and wheat arabinoxylan by a porcine faecal inoculum

Arabinoxylan (AX) and xyloglucan (XG) are important components of primary cell walls of cereal grains and vegetables/fruits, respectively. Despite the established health benefits of these non-starch polysaccharides, the mechanisms of their utilisation by the gut microbiota are poorly understood. In this study, the mechanisms of solubilised wheat AX and tamarind XG degradation were investigated under in vitro fermentation conditions using a porcine faecal inoculum. Through structural analysis of the polymers, we demonstrate that depolymerisation by microbial surface accessible endo-degrading enzymes occurs prior to active fermentation of AX or XG. Breakdown products are released into the medium and potentially utilised cooperatively by other microbes. Acetate and propionate are the main fermentation products and are produced concurrently with polysaccharide depletion. Butyrate, however, is produced more slowly consistent with it being a secondary metabolite

Growth behaviour of Ge nano-islands on the nanosized Si{111} facets bordering on two {100} planes

Abstract Si(100) substrates were used to fabricate various nanosized {111} facets between the (100) planes using photolithography and anisotropic wet chemical etching. Following simultaneous Ge chemical vapour deposition on the neighbouring (100) and {111} facets, the Ge nano-island formation and distribution was observed on both the (100) terraces and the {111} side walls using a dynamical atomic force microscope. The nano-island formation on the nanosized {111} strip facets was found to be strongly suppressed upon reducing the strip width due primarily to the interaction of adatoms on the neighbouring facets. Specifically, the difference in the effective chemical potential of Ge adatoms on the two neighbouring facets leads to the depletion of nano-islands on the {111} strip with width <500 nm under the growth condition used in this study

Benefits of Huang Lian mediated by gut microbiota on HFD/STZ-induced type 2 diabetes mellitus in mice

BackgroundHuang Lian (HL), one of the traditional Chinese medicines (TCMs) that contains multiple active components including berberine (BBR), has been used to treat symptoms associated with diabetes for thousands of years. Compared to the monomer of BBR, HL exerts a better glucose-lowering activity and plays different roles in regulating gut microbiota. However, it remains unclear what role the gut microbiota plays in the anti-diabetic activity of HL.MethodsIn this study, a type 2 diabetes mellitus (T2DM) mouse model was induced with a six-week high-fat diet (HFD) and a one-time injection of streptozotocin (STZ, 75 mg/kg). One group of these mice was administrated HL (50 mg/kg) through oral gavage two weeks after HFD feeding commenced and continued for four weeks; the other mice were given distilled water as disease control. Comprehensive analyses of physiological indices related to glycolipid metabolism, gut microbiota, untargeted metabolome, and hepatic genes expression, function prediction by PICRUSt2 were performed to identify potential mechanism.ResultsWe found that HL, in addition to decreasing body fat accumulation, effectively improved insulin resistance by stimulating the hepatic insulin-mediated signaling pathway. In comparison with the control group, HL treatment constructed a distinct gut microbiota and bile acid (BA) profile. The HL-treated microbiota was dominated by bacteria belonging to Bacteroides and the Clostridium innocuum group, which were associated with BA metabolism. Based on the correlation analysis, the altered BAs were closely correlated with the improvement of T2DM-related markers.ConclusionThese results indicated that the anti-diabetic activity of HL was achieved, at least partly, by regulating the structure of the gut microbiota and the composition of BAs

Honokiol Crosses BBB and BCSFB, and Inhibits Brain Tumor Growth in Rat 9L Intracerebral Gliosarcoma Model and Human U251 Xenograft Glioma Model

BACKGROUND: Gliosarcoma is one of the most common malignant brain tumors, and anti-angiogenesis is a promising approach for the treatment of gliosarcoma. However, chemotherapy is obstructed by the physical obstacle formed by the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB). Honokiol has been known to possess potent activities in the central nervous system diseases, and anti-angiogenic and anti-tumor properties. Here, we hypothesized that honokiol could cross the BBB and BCSFB for the treatment of gliosarcoma. METHODOLOGIES: We first evaluated the abilities of honokiol to cross the BBB and BCSFB by measuring the penetration of honokiol into brain and blood-cerebrospinal fluid, and compared the honokiol amount taken up by brain with that by other tissues. Then we investigated the effect of honokiol on the growth inhibition of rat 9L gliosarcoma cells and human U251 glioma cells in vitro. Finally we established rat 9L intracerebral gliosarcoma model in Fisher 344 rats and human U251 xenograft glioma model in nude mice to investigate the anti-tumor activity. PRINCIPAL FINDINGS: We showed for the first time that honokiol could effectively cross BBB and BCSFB. The ratios of brain/plasma concentration were respectively 1.29, 2.54, 2.56 and 2.72 at 5, 30, 60 and 120 min. And about 10% of honokiol in plasma crossed BCSFB into cerebrospinal fluid (CSF). In vitro, honokiol produced dose-dependent inhibition of the growth of rat 9L gliosarcoma cells and human U251 glioma cells with IC(50) of 15.61 µg/mL and 16.38 µg/mL, respectively. In vivo, treatment with 20 mg/kg body weight of honokiol (honokiol was given twice per week for 3 weeks by intravenous injection) resulted in significant reduction of tumor volume (112.70±10.16 mm(3)) compared with vehicle group (238.63±19.69 mm(3), P = 0.000), with 52.77% inhibiting rate in rat 9L intracerebral gliosarcoma model, and (1450.83±348.36 mm(3)) compared with vehicle group (2914.17±780.52 mm(3), P = 0.002), with 50.21% inhibiting rate in human U251 xenograft glioma model. Honokiol also significantly improved the survival over vehicle group in the two models (P<0.05). CONCLUSIONS/SIGNIFICANCE: This study provided the first evidence that honokiol could effectively cross BBB and BCSFB and inhibit brain tumor growth in rat 9L intracerebral gliosarcoma model and human U251 xenograft glioma model. It suggested a significant strategy for offering a potential new therapy for the treatment of gliosarcoma