Gas-Solid Flow Characteristics of Airflow and Dust Particles in Blasting Excavation of Underground Metal Mine Tunnels.

Effective dust removal has long been a challenge in the blasting mining of underground metal mine tunnels, and uncontrolled dust diffusion seriously endangers workers' respiratory systems and the underground space safety environment. However, the vast majority of existing numerical studies on dust diffusion are focused on coal mine fully mechanized mining, which is different from metal mine blasting excavation in terms of stope structure and dust properties. Furthermore, the mechanism by which the forced and exhaust ventilation modes affect the diffusion characteristics of inhalable particles is unclear. In this work, gas-solid flow characteristics for dust diffusion in a typical metal mine blasting tunnel were numerically investigated based on the Euler-Lagrange method, where the blasting face instantly released 6.37 × 107 particles with 100 different sizes, ranging from 0.8 to 200 µm. The interphase forces between airflow and dust particles are comprehensively modeled, and the particle diffusion effect caused by fluid turbulence is described by a discrete random walk model. Detailed information for airflow turbulence and particle migration was revealed, and dust removal efficiencies for inhalable particulate matter (PM10) by forced, exhaust, and hybrid ventilation were analyzed. Numerical results predict a complex airflow pattern in the working roadway, including the jet-flow region, return airflow core region, airflow disorder region, and secondary flow region. Dust diffusion temporal characteristics can be divided into three stages, namely, the initial stage of dust generation, the efficient ventilation and dust removal stage, and the later stage of dust diffusion. Dust diffusion spatial characteristics indicate that under the Coanda wall attachment effect, the dust concentration exhibits nonuniform distribution in both vertical and horizontal directions of the return air roadway. The dust removal efficiency of hybrid ventilation on inhalable particles above respiratory height is better than that of forced ventilation, especially in the return air roadway. The additional exhaust air duct based on forced ventilation can discharge more inhalable particles from the tunnel.

Long-term stability and immunogenicity of lipid nanoparticle COVID-19 mRNA vaccine is affected by particle size.

Messenger ribonucleic acid (mRNA) technology has been rapidly applied for the development of the COVID-19 vaccine. However, naked mRNA itself is inherently unstable. Lipid nanoparticles (LNPs) protect mRNAs from extracellular ribonucleases and facilitate mRNA trafficking. For mRNA vaccines, antigen-presenting cells utilize LNPs through uptake to elicit antigen-specific immunity. There are reports on the impact of various physical characteristics of LNPs, particularly those with sizes less than 200 nm, especially 50 to 150 nm, on the overall stability and protective efficacy of mRNA vaccines. To address this, a single change in the size of LNPs using the same mRNA stock solution was assessed for the physicochemical characterization of the resulting mRNA-LNPs vaccine, along with the evaluation of their protective efficacy. Particles of smaller sizes generally disperse more effectively in solutions, with minimized occurrence of particle precipitation and aggregation. Here, we demonstrate that the vaccine containing 80-100 nm mRNA-LNPs showed the best stability and protection at 4°C and -20°C. Furthermore, we can conclude that freezing the vaccine at -20°C is more appropriate for maintaining stability over the long term. This effort is poised to provide a scientific basis for improving the quality of ongoing mRNA vaccine endeavors and providing information on the development of novel products.

Rap1GAP exacerbates myocardial infarction by regulating the AMPK/SIRT1/NF-κB signaling pathway.

Rap1 GTPase-activating protein (Rap1GAP) is an important tumor suppressor. The purpose of this study was to investigate the role of Rap1GAP in myocardial infarction (MI) and its potential mechanism. Left anterior descending coronary artery ligation was performed on cardiac-specific Rap1GAP conditional knockout (Rap1GAP-CKO) mice and control mice with MI. Seven days after MI, Rap1GAP expression in the hearts of control mice peaked, the expression of proapoptotic markers (Bax and cleaved caspase-3) increased, the expression of antiapoptotic factors (Bcl-2) decreased, and the expression of the inflammatory factors IL-6 and TNF-α increased; thus, apoptosis occurred, inflammation, infarct size, and left ventricular dysfunction increased, while the heart changes caused by MI were alleviated in Rap1GAP-CKO mice. Mouse heart tissue was obtained for transcriptome sequencing, and gene set enrichment analysis (GSEA) was used to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. We found that Rap1GAP was associated with the AMPK and NF-κB signaling pathways and that Rap1GAP inhibited AMPK/SIRT1 and activated the NF-κB signaling pathway in model animals. Similar results were observed in primary rat myocardial cells subjected to oxygen-glucose deprivation (OGD) to induce ischemia and hypoxia. Activating AMPK with the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) reversed the damage caused by Rap1GAP overexpression in cardiomyocytes. In addition, the coimmunoprecipitation results showed that exogenous Rap1GAP interacted with AMPK. Rap1GAP was verified to regulate the AMPK SIRT1/NF-κB signaling pathway and exacerbate the damage to myocardial cells caused by ischemia and hypoxia. In conclusion, our results suggest that Rap1GAP promotes MI by modulating the AMPK/SIRT1/NF-κB signaling pathway and that Rap1GAP may be a therapeutic target for MI treatment in the future.

Phosphoglycerate mutase 2 is elevated in serum of patients with heart failure and correlates with the disease severity and patient's prognosis.

BACKGROUND: Heart failure (HF) is a serious and advanced stage of various cardiac diseases with high mortality and rehospitalization rates. Phosphoglycerate mutase 2 (PGAM2) overexpression was identified in the serum of patients with HF. MATERIAL/METHODS: One hundred and fifty-three cases of HF were included in the present work. According to New York Heart Association (NYHA) classification, 22 were grade II, 84 were grade III, and 47 were grade IV. Serum PGAM2, NT-proBNP, B-type natriuretic peptide (BNP), troponin T (TNT), and Cys-C of HF patients were detected using ELISA assay. Left ventricular ejection fraction, left ventricular end-diastolic inner diameter, and left atrium (LA) inner diameter of the included cases were also detected by the cardiac color Doppler. RESULTS: The number of patients with atrial fibrillation was significantly higher in NYHA IV group than in groups II and III with statistical difference (p < 0.05). The serum PGAM2, NT-proBNP, and Cys-C were significantly higher in NYHA IV group than in NYHA II and NYHA III groups (p all < 0.05). NT-proBNP had the highest prediction efficacy of HF severity and PGAM2 was also a potential biomarker for HF severity evaluation with relatively high sensitivity, specificity, and area under the ROC. The overall survival among NYHA II, III, and IV groups were statistically different (p = 0.04) with the median survival time of 25 months for NYHA III and IV groups. CONCLUSION: PGAM2 is a new promising biomarker for evaluation of the severity of HF. Combination detection using multiple serum factors such as PGAM2, NT-proBNP, BNP, TNT, and Cys-C can improve the HF severity differential diagnosis performance.

IL-18 and IL-35 in the serum of patients with sepsis thrombocytopenia and the clinical significance.

Expression levels of interleukin-18 (IL-18) and IL-35 in the serum of patients with sepsis and without thrombocytopenia and patients with sepsis thrombocytopenia (TCP) were detected to preliminarily investigate their clinical significance. One hundred and sixty-six patients admitted to Jinan Central Hospital Affiliated to Shandong University from July 2013 to September 2015 were retrospectively analysed. There were 96 patients with sepsis without thrombocytopenia in the sepsis group, and 70 patients with sepsis TCP in the sepsis TCP group. In the same period, 80 healthy subjects were selected as the control group. Fluorescent quantitative PCR was used for the detection the expression of mRNA levels of IL-18 and IL-35, and Enzyme-linked immunosorbent assay for the detection of the protein concentrations of IL-18 and IL-35 in the serum of peripheral blood. The correlation between IL-18, IL-35 and platelets was analyzed. There were significant differences in albumin, creatinine, total bilirubin and platelet count between the sepsis group and the sepsis TCP group (P<0.05); the expression levels of mRNA of IL-18 and IL-35 in a karyocyte in peripheral blood in the sepsis group and the sepsis TCP group were higher than those in the control group (P<0.05); the expression of mRNA of IL-18 and IL-35 in the sepsis TCP group was higher than those in the sepsis group (P<0.05). The concentration of IL-18 and IL-35 in the sepsis TCP group was higher than in the sepsis group (P<0.05); IL-18 and IL-35 were negatively correlated with platelets (r=-0.8749, -0.6228, P<0.001). There was a significant positive correlation between serum IL-18 and IL-35 in the control group, sepsis group, and sepsis TCP group (r=0.5124, 0.5718, 0.5511, P<0.001). IL-18 and IL-35 were negatively correlated with the reduced degree of platelets in patients with sepsis and are likely to play an important role in the pathogenetic process of sepsis TCP.

[Effects of population density and culture volume on the growth and reproduction of Moina irrasa].

A laboratory experiment was conducted to study the effects of different population density (D1 : 100 ind x L(-1), D2 : 150 ind x L(-1), D3 : 300 ind x L(-1)) and culture volume (V1: 50 mL, V2 : 100 mL, V3 : 400 mL) on the growth and reproduction of Moina irrasa at 25 degrees C. At the same culture density, the body length of the M. irrasa females at their first pregnancy, the first brood, and the total offsprings per female decreased with the increase of culture volumes, while the sex ratio (male/female) of the offsprings was in adverse. At the same culture volumes, the total offsprings per female decreased with the increase of culture density. At D1 V1, the body length of the females at their first pregnancy (0.95 +/- 0.10 mm) and the total offsprings (171.3 +/- 19.8 ind) per female were the maximum. At D3V2, the sex ratio was the maximum (0.54 +/- 0.05). Culture density, culture volume, and their interactions significantly affected the total offsprings per female and the sex ratio (P < 0.001).

Effect of oral atorvastatin on CD4+CD25+ regulatory T cells, FoxP3 expression, and prognosis in patients with ST-segment elevated myocardial infarction before primary percutaneous coronary intervention.

OBJECTIVE: Our objective was to explore the effects of atorvastatin on changes of CD4+CD25+ regulatory T cells (Tregs), FoxP3 expression in the infarct-related coronary artery, and peripheral venous blood of patients with ST-segment elevation myocardial infarction. METHODS: We recorded 112 cases of patients with ST-segment elevation myocardial infarction who were randomly assigned to receive either atorvastatin 80 mg (n = 52) or placebo (n = 60) before primary percutaneous coronary intervention. Blood samples were obtained from the infarct-related coronary artery and peripheral vein during percutaneous coronary intervention. The proportion of CD4+CD25+ Tregs, FoxP3 mRNA expression in blood and concentrations of transforming growth factor-ß and interferon-γ in plasma of the samples were measured or detected by flow cytometry, real-time polymerase chain reaction, or enzyme-linked immunosorbent assay, respectively. RESULTS: In comparison with the control group, the proportions of CD4+CD25+ Tregs and the mRNA level of FoxP3 and transforming growth factor-ß significantly increased; however, interferon-γ decreased with atorvastatin therapy. In the controls, the proportions of CD4+CD25+ Tregs and the mRNA level of FoxP3 and transforming growth factor-ß were significantly decreased, but the level of interferon-γ increased more in the infarct-related coronary artery than in the peripheral vein. CONCLUSION: : The inhibition of CD4+CD25+ Tregs in patients with ST-segment elevation myocardial infarction could be regulated with atorvastatin given before percutaneous coronary intervention.