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Addition of conductive materials to anaerobic sludge systems is an attractive strategy to enhance anaerobic metabolism and methane production. The presence of direct interspecies electron transfer (DIET) in microbial communities is commonly used to improve methane production, while the underlying mechanisms remain under debate. Though DIET has distinct advantages, the interspecies H2/formate transfer in syntrophic metabolism is believed to be the main electron transfer pathway. This chapter presents an overview on fundamental mechanisms on interspecies electron transfer and the boosting effect of some conductive materials in bioengineered system with a particular focus on the improvement in methane production.

Herein, an expanded granular sludge bed (EGSB) reactor with activated carbon (AC)-nano manganese dioxide (MnO2) added was employed for azo dye wastewater treatment to investigate its effectiveness at decolorizing of azo dyes and removing COD. The results showed that the treatment of azo dye wastewater with the AC-MnO2 modified EGSB reactor gave an 83% average decolorization efficiency, which was more efficient than the pure AC modified EGSB reactor. Moreover, the COD removal and changes in the intermediate products were controlled by AC-MnO2. Additionally, there was a sharp increase in the sludge conductivity, while there was a significant decrease in the coenzyme F420 concentration with long-term operation. Moreover, electrochemical analysis showed that the addition of AC-MnO2 can enhance electron transfer in anaerobic system. The AC-MnO2 can act as redox mediator; in the presence of the Mn4+/Mn2+ cycle, accelerating the electron transfer between the microbial cells and dyes, thereby promoting the decolorization of azo dyes. This caused a decrease in the methanogenic activity. Furthermore, high-throughput sequencing showed that the relative abundances of Pseudomonas and Desulfovibrio were significantly high among the acidogenic bacteria community, while Methanobacterium and Methanosaeta had very low abundances from among the methanogenic archaea community.

Inhibitory effects of phosphate on zero-valent iron (ZVI) dissolution have been studied mainly focusing on a single chemical system. Little is known about inhibitory effects and the mechanism of phosphate on ZVI dissolution within a bioreactor during long-term operation. This study demonstrates the feasibility of achieving energy recovery from phosphate-containing domestic sewage using an efficient anaerobic reactor with micro-sized or nano-sized ZVI addition. The results indicate that the chemical oxygen demand (COD) removal and methane production are enhanced by ZVI addition. A maximum COD removal efficiency of 89% and methane content of 60% was achieved. However, the strengthening effect of ZVI on methane production is weakened by the presence of phosphate in domestic sewage. Analyzing the variations of Fe2+ ions and phosphate concentrations and characterizing the micro-morphology of corroded ZVI proved that the generated Fe2+ ions reacts with phosphate and forms a passivation layer on the ZVI surface, inhibiting further dissolution of ZVI. As an improved alternative, we chose the double layered core-shell structured ZVI@carbon composite as an excellent candidate to reduce the inhibitory effects of phosphate on ZVI dissolution. In this way, the direct formation of precipitates on the ZVI surface can be avoided due to the protective carbon layer which adjusts the ion transfer. Adding ZVI@carbon composites accelerate the methane content by 16%. To our knowledge, this is the first report on adding ZVI@carbon composites to promote the anaerobic metabolism in studies, which are focusing on reducing the inhibition of ZVI by phosphate.

Background Urotensin II (UII) is a potent vasoconstrictive peptide. Our previous study found that UII could stimulate adventitial fibroblasts phenotypic conversion and collagen synthesis, suggesting that UII plays an important role in vascular fibrosis. The aim of this study was to test the hypothesis that smad 2/3 is involved in UII-induced adventitial fibroblasts phenotypic conversion. Design Growth-arrested adventitial fibroblasts from rat aorta were incubated in serum-free medium with UII, and SB710411, the antagonist of UII receptor. The Smad2/3 phosphorylation was evaluated by western blot. In another experiment, the adventitial fibroblasts were transfected with Smad2 and smad3-specific siRNA, and the α-smooth muscle-actin (α-SM-actin) expression was also evaluated by western blot. Results UII stimulated smad2/3 phosphorylation in cultured adventitial fibroblasts in a time-dependent manner. After 3, 6, 12 or 24 h incubation with UII (10 −8 mol/l), the Smad 2/3 phosphorylation were increased by 21.6%, 68.1%, 117.8%, and 147.2% (p −10 ∼10 −8 mol/l) also stimulated Smad 2/3 phosphorylation in a concentration dependent manner (p Conclusion These data show that UII activates the Smad2/3 phosphorylation via its receptor, and the Smad2/3 pathways are involved in UII-induced a-SM-Actin expression in adventitial fibroblasts. The novel finding suggests that Smad2/3 activation could be involved in the profibrogenic effects of UII in vascular diseases.

Background Recent studies reported that vascular adventitial fibroblasts (AFs) are involved in the development of vascular inflammatory diseases, such as atherosclerosis. Urotensin II (UII), a potent vasoconstrictive peptide, could stimulate phenotype differentiation and proliferation of the AFs. The goal of this study was to investigate the effect of UII on the expression of monocyte chemoattractant protein-1 (MCP-1) in rat aortic AFs, and to study the signal transduction pathways of it. Methods Growth-arrested AFs were incubated in serum-free medium with UII (10 −10 –10 −7 mol/l). In order to explore the mechanism of UII effect, the cells were pretreated with some inhibitors of signal transduction pathways for 30 m, and then incubated with UII (10 −8 mol/l) for 3 h to 24 h. The MCP-1 mRNA and protein expression induced by UII were evaluated by the reverse transcriptase PCR and Western Blotting, respectively. The MCP-1 secretion from the cells was determined by ELISA. Results UII could upregulate MCP-1 expression significantly. The MCP-1 mRNA expression increased after 1 h (p −8 mol/l) treatment and reached a peak at 3 h (p −8 mol/l at 3 h (p −10 mol/l, 10 −9 mol/l, 10 −8 mol/l and 10 −7 mol/l group, respectively, as compared with the control group (without UII stimulation), and the upregulation was significant (p −6 mol/l), Rho protein kinase inhibitor Y27632 (10 −5 mol/l), protein kinase C inhibitor H7 (10 −5 mol/l), mitogen-activated protein kinase inhibitor PD98059 (10 −5 mol/l), calcineurin inhibitor Cyclosporine A (10 −5 mol/l) and Ca 2+ channel blocker nicardipine (10 −5 mol/l), (p −8 mol/l at 12 h (in the level of protein secretion from the cells, p Conclusion Urotensin II may stimulate the expression of monocyte chemoattractant protein-1 in rat aortic adventitial fibroblasts, through its receptor and the Ca 2+ channel, protein kinase C, mitogen-activated protein kinase, calcineurin and Rho kinase signal transduction pathways, contributing to the vascular inflammation.

Background Recent studies suggest osteopontin (OPN) plays a critical role in the progression of vascular remodelling, and that Urotensin II (UII) is a potent vasoconstrictor and stimulator of cellular migration. The goal of this study was to test the hypothesis that OPN is involved in UII-induced migration of rat aortic adventitial fibroblasts (AFs), and examine the effect and mechanisms of UII on OPN expression. Design Growth-arrested AFs were incubated in serum-free medium with UII and some inhibitors of signal transduction pathways. Cell migration was determined by a transwell technique. The OPN mRNA expression and protein secretion induced by UII were evaluated by the reverse transcriptase PCR and ELISA method, respectively. Results OPN antisense oligonucleotides inhibited UII-induced AFs migration significantly compared with UII (10 −8 mol/l) group (p −8 mol/l at 3 h for mRNA expression, or at 24 h for protein secretion, respectively (p −6 mol/l), Ca 2+ channel blocker nicardipine (10 −5 mol/l), protein kinase C inhibitor H7 (10 −5 mol/l), calcineurin inhibitor cyclosporine A (10 −5 mol/l), Rho kinase inhibitor Y-27632 (10 −5 mol/l) and mitogen activated protein kinase (MAPK) inhibitor PD98059 (10 −5 mol/l) inhibited the UII effects significantly. Conclusion This study indicated that UII may up-regulate OPN expression in AFs through the UII receptor, protein kinase C, MAPK, calcineurin, Rho kinase and Ca2+ signal transduction pathways, and OPN is involved in UII-induced AFs migration.