N2O emission factors in bubbling fluidized bed incineration of municipal sewage sludge: The China case.

The N2O emissions resulting from sludge incineration are estimated using the default values published by the Intergovernmental Panel on Climate Change (IPCC), which may differ significantly from the actual emissions. In this investigation, N2O emissions from four sludge incineration lines in two plants were monitored for varying durations. The variation in N2O emission factors (EFs) between incineration lines of the same plant was much smaller than the difference between different plants. Data on N2O EFs obtained from brief monitoring may contain variabilities of up to 30%. N2O EFs were more sensitive to temperature changes at low temperatures, necessitating extended monitoring periods to improve the reliability of N2O monitoring outcomes in cases of low furnace temperatures. Excessive use of the SNCR system to reduce NOx emissions resulted in concentrations of N2O and NH3 in the exhaust gases exceeding NOx levels. In the case of furnace temperature control and advanced reburning technology, it is advisable to utilize actual monitoring data or the smaller default values provided by the IPCC in China. Otherwise, the estimated N2O emissions may exceed the actual emissions.

Role of MEG3 in Cellular Physiology of Atherosclerosis.

OBJECTIVE: To investigate the role of the lncRNA MEG3 (MEG3) in opposing the biochemical processes thought to be involved in the development of atherosclerosis (AS). METHODS: Thirty patients with AS and thirty healthy control subjects were enrolled in this study. The expression of MEG3, miR-200b-3p and ABCA1 was analyzed by RT-qPCR in the individuals and the macrophages-derived foam cells. Lipid accumulation was detected by oil red O staining. Cholesterol efflux was measured by ELISA assay in the foam cells. Expression of miR-200b-3p was identified by sequencing. Targeting relationships were determined by dual luciferase assay between MEG3 and miR-200b-3p, miR-200b-3p and ABCA1. RESULTS: In the patients with AS, MEG3 and ABCA1 expression were decreased and miR-200b-3p expression was upregulated. Foam cells transfected with an expression vector (pcDNA3.1) containing MEG3 (pcDNA3.1-MEG3) induced decrease of lipid accumulation and increase of cholesterol efflux compared to cells transfected with control plasmid alone. Foam cells transfected by pcDNA3.1-MEG3 also showed decreased miR-200b-3p and increased ABCA1 expression. Interestingly, co-expression of miR-200b-3p partially prevented these effects of MEG3 expression. CONCLUSION: Expression of MEG3 is downregulated in the patients with AS and foam cells. Overexpressed MEG3 may act as an anti-atherosclerotic factor by reducing lipid accumulation and accelerating cholesterol efflux through the miR-200b-3p/ABCA1 axis.

Acid gas emission and ash fusion characteristics of multi-component leather solid waste incineration in bubbling fluidized bed.

The tanning sludge (TS) and other tanning solid wastes are produced in significant quantities by the leather industry. To evaluate the combustion properties, acid gaseous pollutant conversion, and ash management, co-firing of TS with various wastes was investigated in a bubbling fluidized bed. TG-FTIR test indicated that tanning solid wastes had superior combustion properties and include more gaseous pollutants than TS. The leather mixed solid waste (LMSW) formed by mixing had better fuel characteristics than TS. The conversion rates of SO2 and HCl of LMSW incineration were 67% and 40%, respectively. The co-combustion of TS and solid wastes reduces the conversion rate of acid gas. Increasing the proportion of high-inorganic chlorine raw material could further reduce the conversion rate and increase the ash fusion temperature appropriately. Because ash and slag were primarily composed of Ca and Fe elements, the addition of calcium carbonate (CaCO3) can increase ash melting point while reducing acid gas emissions. When CaCO3 was added at a calcium to sulfur (Ca/S) ratio of 2, the acid gas emission was reduced by more than 80% and the softening temperature was raised by 90 °C. When Ca/S is greater than 2, the economics of adding CaCO3 decreased.

The relationship between dyslipidemia and inflammation among adults in east coast China: A cross-sectional study.

Objective: Dyslipidemia is one of the major public health problems in China. It is characterized by multisystem dysregulation and inflammation, and oxidant/antioxidant balance has been suggested as an important factor for its initiation and progression. The objective of this study was to determine the relationship between prevalence of dyslipidemia and measured changes in the levels of proinflammatory cytokines (IL-6, TNF-a, and MCP-1), thiobarbituric acid-reactant substances (TBARS), and serum total antioxidant capacity (TAC) in serum samples. Study design: A cross-sectional survey with a purposive sampling of 2,631 enrolled participants (age 18-85 years) was performed using the adult population of long-term residents of the municipality of east coast China in Fujian province between the years 2017 and 2019. Information on general health status, dyslipidemia prevalence, and selected mediators of inflammation was collected through a two-stage probability sampling design according to socioeconomic level, sex, and age. Methods: The lipid profile was conducted by measuring the levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) with an autoanalyzer. Dyslipidemia was defined according to National Cholesterol Education Program Adult Treatment Panel III diagnostic criteria, and patients with it were identified by means of a computerized database. Serum parameters including IL-6/TNF-a/MCP-1, TBARS, and TAC were measured in three consecutive years. Familial history, education level, risk factors, etc. were determined. The association between dyslipidemia and serum parameters was explored using multivariable logistic regression models. Sociodemographic, age, and risk factors were also investigated among all participants. Results: The mean prevalence of various dyslipidemia in the population at baseline (2017) was as follows: dyslipidemias, 28.50%; hypercholesterolemia, 26.33%; high LDL-C, 26.10%; low HDL-C, 24.44%; and hypertriglyceridemia, 27.77%. A significant effect of aging was found among all male and female participants. The mean levels of serum Il-6/TNF-a/MCP-1 were significantly higher in all the types of dyslipidemia among male participants. Female participants with all types of dyslipidemia but low HDL-C showed an elevation of IL-6 and MCP-1 levels, and those with dyslipidemias and hypercholesterolemia presented higher levels of TNF-a compared to the normal participants. The oxidative stress marker TBARS increased among all types of dyslipidemia except hypertriglyceridemia. All participants with different types of dyslipidemia had a lower total antioxidant capacity. Correlation analysis showed that cytokines and TBARS were positively associated with age, obesity, and diabetes mellitus, but not sex, sedentary leisure lifestyle, hypertension, and CVD/CHD history. The activity of TAC was negatively associated with the above parameters. Conclusions: The correlation between the prevalence of dyslipidemia and the modification of inflammation status was statistically significant. The levels of proinflammatory cytokines, oxidative stress, and antioxidant capacity in serum may reflect the severity of the lipid abnormalities. These promising results further warrant a thorough medical screening in enhanced anti-inflammatory and reduced oxidative stress to better diagnose and comprehensively treat dyslipidemia at an early stage.

Agomelatine prevents angiotensin II-induced endothelial and mononuclear cell adhesion.

Agomelatine is a non-selective melatonin receptor agonist and an atypical antidepressant with anti-inflammatory, neuroprotective, and cardioprotective effects. The renin-angiotensin system modulates blood pressure and vascular homeostasis. Angiotensin II (Ang II) and its receptor Ang II type I receptor (AT1R) are recognized as contributors to the pathogenesis of cardiovascular and cardiometabolic diseases, including diabetes, obesity, and atherosclerosis. The recruitment and attachment of monocytes to the vascular endothelium is a major event in the early stages of atherosclerosis and other cardiovascular diseases. In the present study, we demonstrate that agomelatine reduced Ang II-induced expression of AT1R while significantly inhibiting the attachment of monocytes to endothelial cells induced by Ang II and mediated by ICAM-1 and VCAM-1. Additionally, Ang II inhibited the expression of the chemokines CXCL1, MCP-1, and CCL5, which are critical in the process of immune cell recruitment and invasion. Agomelatine also suppressed the expression of TNF-α, IL-8, and IL-12, which are proinflammatory cytokines that promote endothelial dysfunction and atherogenesis. Importantly, we demonstrate that the inhibitory effect of agomelatine against the expression of adhesion molecules is mediated through the downregulation of Egr-1 signaling. Together, our findings provide evidence of a novel mechanism of agomelatine that may be practicable in the treatment and prevention of cardiovascular diseases.

Microvesicles Derived from TGF-ß1 Stimulated Hepatic Stellate Cells Aggravate Hepatocellular Injury.

Hepatic stellate cells (HSCs) are liver-specific cells playing critical roles in liver physiological and pathophysiological processes. Transforming growth factor-ß1 (TGF-ß1) is an inflammatory cytokine secreted by both hepatocytes and HSCs. We have previously shown that microvesicles (MVs) derived from quiescent HSCs protect hepatocyte functions. In this study, we investigated the effects of MVs released from TGF-ß1-stimulated HSCs (HSC-MVs) on xenobiotic-injured hepatocytes. Two hepatocyte cell lines (BRL-3A and HL-7702) were treated with N-acetyl-p-aminophenol or H2O2 to build the injury models. Different concentrations of HSC-MVs were used to coculture with injured hepatocytes. MTT, Hochest33258 staining, and flow cytometry were used to determine their effects on the viability and apoptosis of hepatocytes. Liver injury indicators, alanine aminotransferase (ALT) and aspartate amino transferase (AST), were assessed by enzyme-linked immune sorbent assay kits. The phosphoinositide 3-kinase (PI3K) activator (740Y-P) and extracelluar signal regulated kinase (Erk)1/2 activator (platelet-derived growth factor-BB) were used for pathway analysis. The expression levels of p-PI3K/PI3K, p-Akt/Akt, and activated caspase-3 were measured by western blot. Results showed that (i) HSC-MVs dose dependently impaired the viability of hepatocytes in both injury models, (ii) moreover, HSC-MVs dose dependently increased the apoptosis in those cell models, (iii) HSC-MVs also elevated the levels of ALT and AST in the coculture media, and (iv) these effects were accompanied by a decrease in p-PI3K/PI3K and p-Akt/Akt, which could be partially abolished by 740Y-P. Meanwhile, the proapoptotic effect of HSC-MVs was associated with p-Erk1/2/Erk1/2 downregulation and activated caspase-3 upregulation, and could be inhibited by Erk1/2 activation. Our findings demonstrate that HSC-MVs are involved in inflammatory hepatocytes injury probably through the PI3K/Akt, Erk1/2, and caspase-3 pathways.