Co-accumulation characteristics and interaction mechanism of microplastics and PFASs in a large shallow lake.

Microplastics (MPs) and per- and polyfluoroalkyl substances (PFASs) coexist widely in lakes and affect ecological security. The coexistence characteristics and adsorption-desorption mechanisms between MPs and typical PFASs were explored in a typical eutrophic shallow lake (Taihu Lake). Polyvinyl chloride (PVC) and polyethylene (PE) are the primary types of MPs in Taihu Lake, with average abundances in water and sediment of 18630 n/m3 and 584 n/kg, respectively. The average concentrations of PFASs in water and sediment are 288.93 ng/L and 4.33 ng/g, with short-chain PFASs (C4-C7) being the main pollutants. Perfluorobutanoic acid (PFBA) in both water and sediment contributed 38.48 % and 44.53 %, respectively, followed by hexafluoropropylene oxide dimer acid (HFPO-DA). The morphological characteristics of MPs influence the distribution of long-chain PFAS in lake water, while the presence of HFPO-DA and perfluorohexanoic acid (PFHxA) in sediment is directly linked to the concentration and size of MPs. A combination of field investigations and indoor experiments revealed that the irreversible adsorption characteristics between MPs and HFPO-DA may promote the high cumulative flux of HFPO-DA in sediment, and the biofilm on the surface of MPs significantly accelerates this accumulation process. The results provide a new perspective on the co-transport behavior of emerging pollutants in aquatic environments.

Identification of miR-1 and miR-499 in chronic atrial fibrillation by bioinformatics analysis and experimental validation.

Background: Atrial fibrillation (AF) is one of the most prevalent arrhythmias and is characterized by a high risk of heart failure and embolic stroke, yet its underlying mechanism is unclear. The primary goal of this study was to establish a miRNA-mRNA network and identify the miRNAs associated with chronic AF by bioinformatics and experimental validation. Methods: The GSE79768 dataset was collected from the Gene Expression Omnibus(GEO) database to extract data from patients with or without persistent AF. Differentially expressed genes (DEGs) were identified in left atrial appendages (LAAs). The STRING platform was utilized for protein-protein interaction (PPI) network analysis. The target miRNAs for the top 20 hub genes were predicted by using the miRTarBase Web tool. The miRNA-mRNA network was established and visualized using Cytoscape software. The key miRNAs selected for verification in the animal experiment were confirmed by miRwalk Web tool. We used a classic animal model of rapid ventricular pacing for chronic AF. Two groups of animals were included in the experiment, namely, the ventricular pacing group (VP group), where ventricular pacing was maintained at 240-280 bpm for 2 weeks, and the control group was the sham-operated group (SO group). Finally, we performed reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to validate the expression of miR-1 and miR-499 in LAA tissues of the VP group and the SO group. Left atrial fibrosis and apoptosis were evaluated by Masson staining and caspase-3 activity assays, respectively. Results: The networks showed 48 miRNAs in LAA tissues. MiR-1 and miR-499 were validated using an animal model of chronic AF. The expression level of miR-1 was increased, and miR-499 was decreased in VP group tissues compared to SO group tissues in LAAs (P < 0.05), which were correlated with left atrial fibrosis and apoptosis in AF. Conclusion: This study provides a better understanding of the alterations in miRNA-1 and miR-499 in chronic AF from the perspective of the miRNA-mRNA network and corroborates findings through experimental validation. These findings may offer novel potential therapeutic targets for AF in the future.

Induction of cardiomyocyte proliferation and angiogenesis protects neonatal mice from pressure overload-associated maladaptation.

Cardiac pressure overload (for example due to aortic stenosis) induces irreversible myocardial dysfunction, cardiomyocyte hypertrophy and interstitial fibrosis in patients. In contrast to adult, neonatal mice can efficiently regenerate the heart after injury in the first week after birth. To decipher whether insufficient cardiac regeneration contributes to the progression of pressure overload dependent disease, we established a transverse aortic constriction protocol in neonatal mice (nTAC). nTAC in the non-regenerative stage (at postnatal day P7) induced cardiac dysfunction, myocardial fibrosis and cardiomyocyte hypertrophy. In contrast, nTAC in the regenerative stage (at P1) largely prevented these maladaptive responses and was in particular associated with enhanced myocardial angiogenesis and increased cardiomyocyte proliferation, which both supported adaptation during nTAC. A comparative transcriptomic analysis between hearts after regenerative versus non-regenerative nTAC suggested the transcription factor GATA4 as master regulator of the regenerative gene-program. Indeed, cardiomyocyte specific deletion of GATA4 converted the regenerative nTAC into a non-regenerative, maladaptive response. Our new nTAC model can be used to identify mediators of adaptation during pressure overload and to discover novel potential therapeutic strategies.