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Three types of biochar (BC) (mulberry biochar (MB), wheat straw biochar, and pine tree sawdust biochar) were prepared and used to stabilize hydrophobic organic compounds (HOCs) in contaminated sediment. The kinetics of HOC adsorption to the BCs had two distinct stages. The second stage adsorption process was longer for MB than the other BCs, presumably because MB contained large pores, mesopores, and micropores. The adsorption isotherms for the three BCs were described well by the Freundlich model. The adsorption capacities of MB, WS and PT for HOCs ranged between 106.7 and 1202 μg/g, 135.1 and 1002 μg/g, and 255.6 and 909 μg/g, respectively. The apparent HOC adsorption coefficients (KBC-w) for the three BCs were determined from the isotherm data and were similar. The HOC logKOW values correlated well with the logKBC-w values. In sediment slurry experiments, HOCs were much more effectively stabilized by MB than wheat straw and pine tree sawdust biochar. This was probably because of the MB pore characteristics that favored adsorption of HOCs of various molecular sizes. The Fourier-transform infrared and Raman spectra indicated that the main binding mechanisms were hydrogen boding, hydrophobic interactions, and π-π interactions. MB was found to be a possible agent for stabilizing HOCs in contaminated sediment. HOCs in sediment slurry continued to become adsorbed to MB for a long time, indicating that relatively long reaction times should be allowed for in situ remediation using MB.To understand isotope distributions of PM2.5 in residential buildings and apply them for source identification, carbon (δ13C) and lead (Pb) isotope ratios in indoor and outdoor air of residential buildings were analyzed. Moreover, factor analysis (FA) was employed to investigate sources, which were compared through isotopic analyses. The average δ13C values of indoor air are -26.94 ± 1.22‰ and -27.04 ± 0.44‰ in warm (August to October) and cold (February to March) seasons, respectively, and the corresponding values for outdoor air are -26.77 ± 0.54‰ and -26.57 ± 0.39‰. The average 206Pb/207Pb (208Pb/207Pb) ratios of indoor air are 1.1584 ± 0.0091 (2.4309 ± 0.0125) and 1.1529 ± 0.0032 (2.4227 ± 0.0081) in warm and cold seasons, respectively, and the corresponding values for outdoor air are 1.1594 ± 0.0069 (2.4374 ± 0.0103) and 1.1538 ± 0.0077 (2.4222 ± 0.0085). Seasonal variation in δ13C values or Pb isotope ratios of indoor air was not significant, and similar results were obtained for outdoor air. Significant differences were not observed between δ13C values or Pb isotope ratios of indoor and outdoor air. Traffic emission is the major contributor to indoor and outdoor PM2.5 based on isotopic analyses; this result was consistent with the results of FA. The δ13C values of indoor air in buildings with poor ventilation conditions were significantly lighter than those of outdoor air. In summary, the spatial and seasonal variations of isotopes were similar in residential buildings, which can be used to identify sources of indoor PM2.5, and ventilation condition is an influencing factor.Natural organic matters (NOMs), omnipresent in natural water, challenge the toxicity assessment of pollutants to aquatic organisms due to their complex interactions with chemicals and organisms. Here, we investigated the combined toxicity of one solid NOM (black carbon, BC) or one soluble NOM (humic acid, HA) with antibiotics, roxithromycin (RTM) or gatifloxacin (GAT), to the cyanobacterium Synechocystis sp.. The NOMs alleviated the toxicity of RTM and GAT to Synechocystis sp., and BC had greater alleviation effects than HA due to its stronger adsorption to antibiotics. Antibiotics disturbed the photosynthesis of Synechocystis sp. significantly, which were also mitigated by BC and HA. Proteomic analysis showed that BC up-regulated the pathway of ribosome and photosynthetic antenna protein. GAT down-regulated the pathways of ABC transporter and oxidative phosphorylation. RTM interfered the pathway of porphyrin and chlorophyll metabolism. Furthermore, the addition of BC reduced the number of differentially expressed proteins caused by antibiotics, corroborating its mitigation effects on the toxicity of antibiotics. The disturbance of HA on the pathway of ABC transporters inhibited the internalization of RTM, thus decreasing its toxicity. This study underscores the significance of NOMs in mediating the toxicity of organic pollutants to aquatic organisms in natural waters.Black carbon (BC) is released into the atmosphere in large quantities from different emission sources each year and poses a serious threat to human health. These BC possessed a variety of characteristics and different mediation abilities for the reactive oxygen species (ROS) generation. In this study, we collected BC (i.e., diesel BC, coal BC and wood BC) from three typica emission sources, and examined their mediation abilities to the oxidation of glutathione (GSH). Results showed that all three BC significantly promoted the GSH oxidation, and the mediation efficiencies were as follows diesel BC > coal BC > wood BC. In comparison with the water-soluble fraction, the mediation abilities of three BC mainly came from their solid phase fractions. In the coal BC and wood BC systems, the oxidation of GSH was attributed to the catalysis of transition metals in BC. By contrast, the transition metals, phenolic -OH and persistent free radicals in diesel BC were identified as the active sites responsible for the GSH oxidation. In addition, the graphitic surface of diesel BC could synergize with these active sites to accelerate the oxidation of GSH. Under the catalysis of BC, dissolved oxygen was first reduced to ROS (O2•- and H2O2) and then caused the GSH oxidation. These findings not only help to better assess the adverse health effects of different BC, but also deepen the understanding of the reaction mechanisms.Microplastics (MPs) are emerging as a class of pollutants that are a potential threat to biological and human health. Aggregation and settling are crucial to controlling MPs transport and environmental fate. However, the influence of clay minerals in the aqueous environment on the aggregation-settling processes of larger size MPs and its mechanisms remain unclear. In this study, homoaggregation of pristine and aged polyethylene microplastics (PEs) and heteroaggregation-settling of PEs with typical clay minerals (chlorite, illite, kaolinite, montmorillonite) under different hydrochemical conditions (NaCl, CaCl2, MgCl2) were systematically investigated. The results showed that the cation type has a greater influence on the homoaggregation system. In detail, the aged PEs is more stable than pristine PEs in monovalent electrolyte solutions, but not in divalent electrolytes. In heteroaggregation systems, electrostatic repulsion dominates the interaction of PEs (pristine, aged) with clay minerals. However, the settling ratio of PEs (pristine, aged) contributed by clay minerals is not very dependent on the clay mineral type. Conversely, high NaCl concentrations are more conducive to the heteroaggregation-settling of PEs, which can be explained by the DLVO theory. The findings of this study provide new insights into the environmental fate and distribution of MPs in natural waters.

The dedifferentiation of tubular epithelial cells has been identified as an important trigger of renal fibrosis. The Hippo pathway is a crucial regulator of cell proliferation and differentiation. In this study, we determined the role of Hippo proteins in tubular dedifferentiation in diabetic nephropathy (DN).

In this study, we measured dedifferentiation markers and Hippo proteins in db/db mice and high glucose treated tubular epithelial cells. Then, verteporfin and knockdown of large tumor suppressor kinase (LATS) 1 and 2 were performed to uncover therapeutic targets for DN.

Here, we found dedifferentiation and upregulated Hippo proteins in tubular epithelial cells in DN model both in vivo and in vitro. Both verteporfin and LATS knockdown could inhibit the tubular mesenchymal transition, but verteporfin showed broad inhibitory effect on Hippo proteins, especially nuclear YAP, and exacerbated podocyte loss of DN. LATS2 knockdown did not reverse the tubular E-Cadherin loss while it also induced podocyte apoptosis. Overall, intervention of LATS1 inhibited tubular dedifferentiation efficiently without affecting YAP and bringing podocyte apoptosis. Further mechanistic investigations revealed that the TGF-β1/Smad, instead of the YAP-TEAD-CTGF signaling, might be the underlying pathway through which verteporfin and LATS1 engaged in the tubular dedifferentiation.

In conclusion, verteporfin is not a suitable treatment for DN owing to evitable podocyte loss and apoptosis. Bucladesine order Targeting LATS1 is a better choice worthy of further investigation for DN therapy.

In conclusion, verteporfin is not a suitable treatment for DN owing to evitable podocyte loss and apoptosis. Targeting LATS1 is a better choice worthy of further investigation for DN therapy.

Nephrotoxicity is one of the most serious health consequences of cadmium (Cd) toxic exposure. Cd was associated with nephrotoxicity through different mechanisms including apoptosis, inflammation, and oxidative stress. This study investigated the effects of glimepiride on renal inflammatory reactions and oxidative stress in response to Cd in mice animal model, pointing to the possible role of JNK/NF-кB and PI3K/AKT signaling.

Four groups of animals were created; the control group, the glimepiride group (4mg/kg; i.p.), CdCl

nephrotoxic group (6.5mg/kg; i.p.), and the CdCl

/glimepiride group. On the other hand, molecular docking studies were used to investigate the affinity of glimepiride towards JNK, AKT, and PI3K targets.

The CdCl

group's serum creatinine and urea levels were found to have a significant increase when compared to the normal group. High expression of 8-OHDG, JNK, AKT, and NGAL was also detected in the CdCl

group. In addition, coagulative necrosis of the renal tubules and increased iuced by the toxic effects of CdCl2.We have previously reported the inhibition of thioredoxin reductase (TrxR) and invasion by tricyclohexylphosphine gold (I) n-mercaptobenzoate (n = 2, 3, 4) labeled as 1-3 towards MCF-7 cells, in vitro. Nevertheless, the mode of death and its apoptotic pathway has yet to be revealed. The main aim of this study is to investigate the anti-neoplastic activity of this phosphanegold (I) thiolates against breast adenocarcinoma cells, MCF-7. Herein, we explored the role of gold(I) series, 1-3 for their apoptosis-inducing ability against MCF-7 cells. They were scrutinized for their antiproliferative activities which exhibited their IC50 values of 8.14 μM ± 0.10, 7.26 μM ± 0.33, and 9.03 μM ± 0.69, respectively, and indicated better cytotoxicities than that of cisplatin (positive control). Further, the mechanisms of their actions were studied by analyzing the status of ROS generation (by DCFH-DA), cytochrome c release (by ELISA), and activation of caspases 3/7, 8, 9, and 10, annexin V staining and cell cycle analysis by flow cytometry, respectively. It was observed that the compounds, 1-3 can promote ROS generation, cytochrome c release, and activation of caspases 3/7, caspase 8, caspase 9, and caspase 10 on MCF-7 cells. In addition, the compounds are shown to induce MCF-7 cell arrest at S-phase. Gene analysis via PCR array further clarified their effects by modulating the related genes upon the compounds' treatment. Further investigation on other breast cancer cells as well as in vivo studies on these compounds will further increase their potential as anti-breast cancer agents.

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