Research on the Prediction Model of Blasting Vibration Velocity in the Dahuangshan Mine

In order to improve the prediction accuracy of blast vibration velocity, the model for predicting the peak particle velocity of blast vibration using the XGBoost (Extreme Gradient Boosting) method is improved, and the EWT–XGBoost model is established to predict the peak particle velocity of blast vibration by combining it with the EWT (Empirical Wavelet Transform) method. Calculate the relative error and root mean square error between the predicted value and measured value of each test sample, and compare the prediction performance of the EWT–XGBoost model with the original model. There is a large elevation difference between each vibration measurement location of high and steep slopes, but high and steep slopes are extremely dangerous, which is not conducive to the layout of blasting vibration monitoring equipment. The vibration velocity prediction model adopts the numerical simulation method, selects the center position of the small platform as the measurement point of the peak particle velocity, and studies the variation law of the blasting vibration velocity of the high and steep slopes under the action of top blasting. The research results show that the EWT–XGBoost model has a higher accuracy than the original model in the prediction of blasting vibration velocity; the simultaneous detonation method on adjacent high and steep slopes cannot meet the relevant requirements of safety regulations, and the delayed detonation method can effectively reduce the blasting vibration of high and steep slopes. The shock absorption effect of the elevation difference within 45 m is obvious

Macrophage origin, phenotypic diversity, and modulatory signaling pathways in the atherosclerotic plaque microenvironment

Atherosclerosis is the main pathological basis of most cardiovascular diseases and the leading health threat in the world. Of note, lipid-lowering therapy cannot completely retard atherosclerosis progression, even in patients treated with combined statins and PCSK9 inhibitors. This failure further impels researchers to explore other underlying therapeutic strategies except for lipid-lowering. Monocytes and macrophages are the major immune cell groups in atherosclerotic plaques. They play important roles in all stages of atherosclerosis, including the occurrence, advance, and regression. It is interesting that macrophages are demonstrated to have plastic and heterogenous characteristics within the dynamic atherosclerotic plaque microenvironment. Furthermore, the phenotype of macrophages can switch upon different microenvironmental stimulus. Therefore, macrophages have become a potential therapeutic target for anti-atherosclerosis treatment. This article reviews the phenotypic diversity of macrophages and their roles in dynamic atherosclerotic plaque microenvironment, especially the related signaling pathways involved in macrophage polarization and compounds exhibiting therapeutic effects

Exogenous supplement of N-acetylneuraminic acid improves macrophage reverse cholesterol transport in apolipoprotein E-deficient mice

Abstract Background N-acetylneuraminic acid (NANA) is the major form of sialic acid in mammals, and the plasma NANA level is increased in patients with cardiovascular diseases. Exogenous supplement of NANA has been demonstrated to reduce hyperlipidaemia and the formation of atherosclerotic lesions; however, the underlying mechanisms have not yet been clarified. The aim of this study is to investigate whether exogenous supplement of NANA improves reverse cholesterol transprot (RCT) in vivo. Methods Apolipoprotein E-deficient mice fed a high-fat diet were used to investigate the effect of NANA on RCT by [3H]-cholesterol-loaded macrophages, and the underlying mechanism was further investigated by various molecular techniques using fenofibrate as a positive control. Results Our novel results demonstrated that exogenous supplement of NANA significantly improved [3H]-cholesterol transfer from [3H]-cholesterol-loaded macrophages to the plasma (an increase of > 42.9%), liver (an increase of 35.8%), and finally to the feces (an increase of 50.4% from 0 to 24 h) for excretion in apolipoprotein E-deficient mice fed a high-fat diet. In addition, NANA up regulated the protein expression of ATP-binding cassette (ABC) G1 and peroxisome proliferator-activated receptor α (PPARα), but not the protein expression of ABCA1and scavenger receptor B type 1 in the liver. Therefore, the underlying mechanism of NANA in improving RCT may be partially due to the elevated protein levels of PPARα and ABCG1. Conclusion Exogenous supplement of NANA improves RCT in apolipoprotein E-deficient mice fed a high-fat diet mainly by improving the protein expression of PPARα and ABCG1. These results are helpful in explaining the lipid-lowering effect of NANA

Niacin Inhibits Vascular Inflammation via Downregulating Nuclear Transcription Factor-κB Signaling Pathway

The study aimed to investigate the effect of niacin on vascular inflammatory lesions in vivo and in vitro as well as its lipid-regulating mechanism. In vivo study revealed that niacin downregulated the levels of inflammatory factors (IL-6 and TNF-α) in plasma, suppressed protein expression of CD68 and NF-κB p65 in arterial wall, and attenuated oxidative stress in guinea pigs that have been fed high fat diet. In vitro study further confirmed that niacin decreased the secretion of IL-6 and TNF-α and inhibited NF-κB p65 and notch1 protein expression in oxLDL-stimulated HUVECs and THP-1 macrophages. Moreover, niacin attenuated oxLDL-induced apoptosis of HUVECs as well. In addition, niacin significantly lessened lipid deposition in arterial wall, increased HDL-C and apoA levels and decreased TG and non-HDL-C levels in plasma, and upregulated the mRNA amount of cholesterol 7α-hydroxylase A1 in liver of guinea pigs. These data suggest for the first time that niacin inhibits vascular inflammation in vivo and in vitro via downregulating NF-κB signaling pathway. Furthermore, niacin also modulates plasma lipid by upregulating the expression of factors involved in the process of reverse cholesterol transport

Retraction of “Fucosylated Chondroitin Sulfate from Sea Cucumber Apostichopus japonicus Retards Atherosclerosis in Apolipoprotein-E-Deficient Mice”

Retraction of “Fucosylated Chondroitin Sulfate from Sea Cucumber Apostichopus japonicus Retards Atherosclerosis in Apolipoprotein-E-Deficient Mice