Search

Aims: Left ventricular remodelling subsequent to myocardial infarction (MI) constitutes a pivotal underlying cause of heart failure. Intervention with the nontoxic endogenous aryl hydrocarbon receptor (AHR) agonist 2‐(1′H‐indole‐3′‐carbonyl)‐thiazole‐4‐carboxylic acid methyl ester (ITE) in the acute phase of MI has been shown to ameliorate cardiac function, but its role in the chronic phase remains obscured. This study explores the beneficial role of ITE in delaying the progression of heart failure in the chronic phase of MI. Methods and results: MI rats established by ligating the left anterior descending coronary artery were treated with the indicated concentration of the AHR agonist ITE or vehicle alone. Echocardiography was performed to determine cardiac structure and function; myocardial morphology and fibrosis were observed by haematoxylin and eosin and Masson's trichrome staining; serum biochemical indices, BNP, and inflammatory cytokine levels were detected by enzyme‐linked immunosorbent assay; F4/80+iNOS+M1 macrophages and F4/80+CD206+M2 macrophages were detected by immunofluorescence; the terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling assay was used to detect the apoptosis of cardiomyocytes; ultrastructural changes in myocardial tissue were observed by transmission electron microscopy; and Cyp1a1, Akt, P‐Akt, p70S6K, P‐p70S6K, Bcl‐2, Bax, caspase‐3, and cleaved caspase‐3 protein levels were determined via Western blotting. We found that therapy with the AHR agonist ITE rescued cardiac remodelling and dysfunction in rats with MI and attenuated myocardial fibrosis, inflammation, and mitochondrial damage. Further studies confirmed that ITE dose‐dependently improved myocardial cell apoptosis after MI, as demonstrated by reduced levels of the apoptosis‐related proteins cleaved caspase‐3 and Bax but increased expression levels of Bcl‐2. These effects were attributed to ITE‐induced activation of AHR receptors, leading to the down‐regulation of Akt and p70S6K phosphorylation. Conclusions: The AHR agonist ITE alleviates cardiomyocyte apoptosis through the Akt/p70S6K signalling pathway, thereby rescuing left ventricular adverse remodelling and cardiac dysfunction after MI. [ABSTRACT FROM AUTHOR]

Herein, two CeO2 samples dominantly decorated with surface and bulk sulfates were constructed and their distinct effects on high-temperature NH3-SCR were investigated by strictly controlling the sulfate content at a comparable level. The obtainment of surface and bulk sulfates was revealed using a designed leaching experiment, and further evidenced by the characterization results from XPS and H2-TPR. In comparison with CeO2 modified with bulk sulfates (B-CeS), sufficient acid sites with strong intensity were generated on CeO2 modified with surface sulfates (S-CeS). In addition, due to electron-withdrawing effect from S=O in sulfate species, NH3 oxidation over S-CeS was greatly suppressed, providing an additional contribution to enhanced performance in high-temperature NH3-SCR. [ABSTRACT FROM AUTHOR]

The application of iron oxide to NH3-SCR is attractive but largely hindered by its poor acid properties, and surface sulfation is proven to be a prominent way of enhancing the acidity. As such, the method of enriching the sulfate species on iron oxide is crucial for improving the NH3-SCR performance. In the present study, by employing ammonium bisulfate (ABS) as the source of gaseous SO2 for the purpose of trapping, we reported an effective strategy for enhancing the SO42− immobilization on α-Fe2O3 catalyst via spatial confinement in a mesoporous SBA-15 framework. Interestingly, although the presence of the mesopore channel had an adverse effect on the ABS decomposition, which was expected to produce less available SO2, the measured SO42− immobilized on α-Fe2O3 in the mesoporous SBA-15 system was significantly greater than that of the regular SiO2, demonstrating the promoting effect of the spatial confinement on the SO42− enrichment. Further characterizations of the NH3-TPD, NO oxidation, and NH3-SCR performance tests proved that, as a result of the enhanced acidity, the enrichment of SO42− on α-Fe2O3 displayed a clear correlation with the SCR activity. The results of the present study provide an effective strategy for boosting the catalytic performance of iron oxide in NH3-SCR via SO42− enrichment. [ABSTRACT FROM AUTHOR]

To meet the growing demand for potable water, desalinated water is becoming a significant component of the overall water supply. As a result, there is an increased need to understand how the addition of desalinated water within aging water distribution systems impacts water quality and the ability to deliver safe drinking water when unlined cast iron pipes and cement mortar-lined cast iron pipes are both present in the distribution systems. In this paper, we studied the relationship of turbidity, total iron content, and the effects of pH, alkalinity, and hardness on the dissolved silica. Then, we presented the mathematical and pilot-scale empirical development and quantification of three nonlinear regression models and used pH, alkalinity, total hardness, temperature, and hydraulic retention time as water quality variables. The dependent variables were the total iron concentration, the increase in turbidity, and the concentration of dissolved silica. Based on the three models, which use a genetic algorithm, an integrated solution for simultaneously minimizing the release of iron, the increase of turbidity, and the dissolved silica content was presented. This solution provides an economical and efficient method for water plants to identify specific water quality parameters that require adjustment to maintain an acceptable water quality. [ABSTRACT FROM PUBLISHER]

The therapeutic effects and mechanism of umbilical cord mesenchymal stem cells (UC-MSC) on kidney injury in MRL/Ipr mice were studied. UC-MSC, methylprednisolone (MP), and their combination were used to treat MRL/Ipr mice. The therapeutic effects were evaluated by renal function assessment, and HE, PAS, and Masson staining were carried out on renal tissues and visualized by electron microscopy. Subsequently, podocyte injury was detected by the presence of podocin in renal tissues by immunofluorescence. To further explore the mechanism, serum TGF-β1 was measured, and TGF-β1, p-Smad3, and TRAF6 in the renal tissue were detected by Western blotting. In vitro , TGF-β1 was used to stimulate podocytes, and the podocyte activity and changes in synaptopodin were observed after UC-MSC treatment. Significant improvements in renal function and pathological injury were observed in the UC-MSC group compared to the lupus nephritis (LN) model group. UC-MSC and MP treatment improved podocyte injury in MRL/Ipr mice. Western blot examination showed a significant increase in TGF-β1, p-Smad3, and TRAF6 expression in renal tissues of the LN model group, while significant downregulation of those proteins was observed in the UC-MSC group. After TGF-β1 stimulation in vitro , podocyte activity decreased, and UC-MSC treatment improved podocyte activity and restored synaptopodin expression. UC-MSC therapy could improve the deterioration of renal function and the pathological changes of the renal tissues in MRL/Ipr mice. Our study suggested that UC-MSC may improve kidney injury and podocyte injury in LN mice by inhibiting the TGF-β1 pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Huang, Meng, Li, Liu, Li, Su, Gao, He, Zhao, Zhang, Hou, Wang and Wang.)