[Operation Performance of a Bioaugmented Membrane-aerated Biofilm Reactor Treating Atrazine Wastewater].

A hydrophobic SPG (shirasu porous glass) membrane-aerated biofilm reactor (MABR) with genetically engineered microorganism (GEM) biofilm formed on the SPG membrane surface was applied to treat atrazine wastewater. The contaminant removal performance and its influencing factors were investigated during the stable operation of this MABR. The results indicated that the oxygen supply capacity could be increased in the SPG membrane aeration when the membrane pore size and the aeration pressure increased, which could improve the performance of COD and atrazine removals.

Foam cells in atherosclerosis.

Atherosclerosis is a chronic disease characterized by the deposition of excessive cholesterol in the arterial intima. Macrophage foam cells play a critical role in the occurrence and development of atherosclerosis. The generation of these cells is associated with imbalance of cholesterol influx, esterification and efflux.

Posttranscriptional regulation of ATP-binding cassette transporter A1 in lipid metabolism.

Aim: Several lines of evidence have shown that posttranscriptional regulations play an important role in the modulation of ATP-binding cassette transporter A1 (ABCA1) expression and function.

Results: The clearance of ABCA1 mRNA as well as the trafficking, stability, degradation, and activity of the ABCA1 protein are regulated by diverse posttranscriptional mechanisms. ABCA1 mRNA clearance is induced by several microRNAs that result in translational repression and reduction of ABCA1 protein expression.

Apolipoprotein A-I inhibits LPS-induced atherosclerosis in ApoE(-/-) mice possibly via activated STAT3-mediated upregulation of tristetraprolin.

Aim: To investigate the effects of the major component of high-density lipoprotein apolipoprotein A-I (apoA-I) on the development of atherosclerosis in LPS-challenged ApoE(-/-) mice and the underlying mechanisms.

Methods: Male ApoE-KO mice were daily injected with LPS (25 μg, sc) or PBS for 4 weeks. The LPS-challenged mice were intravenously injected with rAAV-apoA-I-GFP or rAAV-GFP.

PAPP-A negatively regulates ABCA1, ABCG1 and SR-B1 expression by inhibiting LXRα through the IGF-I-mediated signaling pathway.

Pregnancy-associated plasma protein-A (PAPP-A) has been involved in the atherosclerotic process through regulation of local expression of IGF-1 that mediates the activation of the phosphatidylinositol-3 (PI3-K) and Akt kinase (Akt) signaling cascades which lead to constitutive nitric oxide formation, with its attending vasodilator, antiplatelet and insulin-sensitizing actions. In addition, IGF-1 may decreased cholesterol efflux through reductions of expression in ABCA1 and SR-B1 by the PI3-K/Akt signaling pathway. In the current study, we examined whether PAPP-A was involved in LXRα regulation and in expression of ABCA1, ABCG1 or SR-B1 through the IGF-I-mediated signaling pathway (IGF/PI3-K/Akt).

The magic and mystery of microRNA-27 in atherosclerosis.

Atherosclerosis (As) is now widely appreciated to represent a chronic inflammatory reaction of the vascular wall in response to dyslipidemia and endothelial distress involving the inflammatory recruitment of leukocytes and the activation of resident vascular cells. MicroRNAs (miRNAs) are a group of endogenous, small (~22 nucleotides in length) non-coding RNA molecules, which function specifically by base pairing with mRNA of genes, thereby induce translation repressions of the genes within metazoan cells. Recently, the function of miR-27, one of the miRNAs, in the initiation and progression of atherosclerosis has been identified.

The interaction of ApoA-I and ABCA1 triggers signal transduction pathways to mediate efflux of cellular lipids.

Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATP-binding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1.