Using sodium alginate aided bio-treatment for improving the uniformity of precipitates on recycled aggregates.

The recycled concrete aggregates have high porosity and water absorption, which hinders their utilization in concrete production. Microbial-induced calcium carbonate precipitation was regarded as a very promising method for strengthening recycled aggregates. However, the uneven distribution of CaCO3 on surface of aggregates encountered in the current bio-deposition treatment weakened the efficiency, especially in the aspect of the decrease of water absorption. Therefore, this study innovatively applied a sodium alginate aided bio-deposition treatment to improve the uniform distribution of biogenic CaCO3. The principle was that sodium alginate was used to uniformly "fix" the bio-agents (urea or bacterial cells) on the surface of recycled aggregates, which was supposed to promote the uniform in-situ precipitation of CaCO3 on the surface of aggregates, and hence effectively blocking surface pores, and reducing the water absorption of the aggregates. Two concentrations of sodium alginate (0.2w% and 0.5w%) and four sodium alginate aided bio-deposition treatments were studied. It was found that CaCO3 (a mass increase of 4.05%) was formed on the aggregates after the suitable sodium alginate aided bio-deposition treatment. The participation of sodium alginate made CaCO3 uniformly deposited on full surface of the aggregates, resulting in a significant decrease (42.10%) of water absorption. The biogenic CaCO3 showed limited mass loss under ultrasonic attack, indicated a strong cohesion and bonding strength with aggregates. The results demonstrated that sodium alginate-aided bio-deposition treatment can enhance the efficiency, which was beneficial to improve the quality of recycled aggregates and their utilization of recycled aggregates in concrete production. KEY POINTS: • The SA-aided bio-treatment promoted the distribution uniformity of CaCO3 on aggregates. • The water absorption of aggregates decreased by 42.10%. • The formed CaCO3 showed excellent cohesion and adhesion.

Integrating proteomic, lipidomic and metabolomic data to construct a global metabolic network of lethal ventricular tachyarrhythmias (LVTA) induced by aconitine.

Lethal ventricular tachyarrhythmias (LVTA)-related sudden cardiac death (SCD) is one of the major causes of death worldwide. However, the mechanisms underlying LVTA induced by myocardial ion channel diseases (MICDs) are not yet fully understood. Here, we produced an LVTA rat model induced by aconitine, to mimic MICDs-elicited LVTA, and constructed a global pathway network via integrating proteomic and lipidomic data, and our previously published metabolomic data. Results showed that both proteome and lipidome were disturbed during the LVTA process. Most of the differentially expressed proteins and lipid species were correlated. Proteomic data indicated disturbance of energy metabolism (e.g. fatty acid ß-oxidation and the tricarboxylic acid cycle) and activation of the protein kinase C and nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase pathway; these alterations led to lowered ATP and elevated ROS, respectively. Altered levels of the Ca2+ handling proteins suggested aberrant intracellular Ca2+ homeostasis, which might also be secondary to the shortage of ATP and oxidative stress. Significantly, the disrupted pathways implied by proteomic data were largely confirmed by lipidomic and metabolomic data. Collectively, we have constructed a metabolic pathway network of aconitine-induced LVTA using a multi-omics strategy, which confers great promise for the deeper interpretation of the mechanisms underlying LVTA. SIGNIFICANCE: In this study, we integrated proteomics, lipidomics and metabolomics to explore the pathophysiological processes of LVTA induced by aconitine. It is innovative to try to integrate these three omics in a study exploring the relative mechanisms. Here, based on the DEPs and differentially abundant lipid species (DALPs) between the LVTA groups and the controls, and the different metabolites discovered previously from the same model, we have successfully constructed a global metabolic network. Taken together, the multi-omics integration strategies used in this study show the potential for a new interpretation of the pathophysiological processes of LVTA induced by different conditions and open the possibility to explore deeper and broader mechanisms of other diseases.

Serum metabolic characteristics and biomarkers of early-stage heart failure.

Aim: We aimed to identify metabolic characteristics of early-stage heart failure (HF) and related biomarkers. Patients & methods: One hundred and forty-three patients with New York Heart Association class I-IV HF and 34 healthy controls were recruited. Serum metabolic characteristics of class I HF were analyzed and compared with those of class II-IV HF. Potential biomarkers of class I HF with normal N-terminal-pro-B-type natriuretic peptide (NT-proBNP) level were screened and validated in additional 72 subjects (46 class I patients and 26 controls). Results & conclusion: Eleven metabolites were found disturbed in class I HF, and five of which were also disturbed in class II-IV HF. Glutamine and tyrosine showed high value to identify class I HF with normal NT-proBNP level. The diagnostic potential of glutamine was partially confirmed in the validate set, holding a promise to detect early HF with normal NT-proBNP level.

Integrative analyses of myocardial lipidome and proteome implicate mitochondrial dysfunction in lethal ventricular tachyarrhythmia (LVTA) induced by acute myocardial ischemia (AMI).

Lethal ventricular tachyarrhythmia (LVTA) is the most prevalent electrophysiological event leading to sudden cardiac death (SCD). In this study, the myocardial lipidome and proteome were analysed in rats experiencing LVTA as a consequence of acute myocardial ischemia (AMI). Results showed that 257 lipid species and 814 myocardial proteins were disrupted during LVTA. Cardiolipin (CL), phosphatidylcholine (PC), phosphatidylethanolamine (PE), ceramide (Cer), lysophosphatidylethanolamine (LPE), lysophosphatidylcholine (LPC), phosphatidylglycerol (PG), and lysophosphatidylserine (LPS) were down-regulated; whereas sphingosine (SO) and diacylglycerol (DG) were up-regulated. Enrichment analysis of these proteins suggested mitochondrial dysfunction. Most of the differential lipids showed a high degree of interaction with the core differentially expressed proteins. Seven lipid pathways, including DG → PE, PE → LPE, PA → DG, PC → DG, PE → PA, Cer → SM, and LPE → LPC, were active during the process. Activation of LPE → PE could be partially confirmed by proteomic results. CL (72:7), PE (42:4), and LPE (P-18:0) jointly represent a promising diagnostic markers for LVTA. Collectively, we discovered marked disturbances of the lipidome and proteome in the myocardia of LVTA rats, mainly involving dysfunction of the mitochondrial respiratory chain.