Role of Microorganisms in Microbial Fuel Cells for Bioelectricity Production

The catalytic microorganisms oxidise the organic matter to produce electrical energy in microbial fuel cells (MFCs). The microorganisms that can shuttle the electrons exogenously to the electrode surface without utilising artificial mediators are referred as exoelectrogens. The microorganisms produce specific proteins or genes for their inevitable performance towards electricity generation in MFCs. Multiple studies have confirmed the expression of certain genes for outer membrane multiheme cytochromes (e.g. OmcZ), redox-active compounds (e.g. pyocyanin), conductive pili, and their potential roles in the exoelectrogenic activity of various microorganisms, particularly in the members of Geobacteraceae and Shewanellaceae family. This chapter explores the various mechanisms of microorganisms that are advantageous for the technology: biofilm formation, metabolism, electron transfer mechanisms from inside the microorganisms to the electrodes and vice versa

Ephrin-B2 reverse signaling regulates progression and lymph node metastasis of oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC) is a common malignant tumor of the head and neck and frequently metastasizes to cervical lymph nodes. Aggressive local invasion and metastasis of OSCC are significant factors for poor prognosis. In this study, we investigated whether ephrin-B2 expressed in OSCC contributed to tumor progression and lymph node metastasis. Clinical specimens from patients with OSCC had robust ephrin-B2-positive tumor cells and ephrin-B2 protein level was associated with clinical stage, lymph node metastasis, and poor survival outcomes. We also determined that ephrin-B2 protein level was increased in OSCC cell lines compared to normal human oral keratinocytes and that its levels were associated with the migratory and invasive potential of OSCC cell lines. Transfection of an EFNB2-specific small interfering RNA (siRNA) into SAS-L1 cells significantly reduced proliferation, attachment, migration, and invasion through phosphorylation of the epidermal growth factor receptor, FAK, ERK1/2, p38, AKT, and JNK1/2 pathways. Furthermore, knockdown of EFNB2 significantly suppressed adhesion and transmigration of SAS-L1 cells toward human lymphatic endothelial cells. In addition, the growth rate of tumor xenografts and cervical lymph node metastases of OSCC were suppressed by local injection of EFNB2 siRNA. These results suggest that ephrin-B2 overexpression and activation of the ephrin-B2 reverse signaling pathway in tumor microenvironment in OSCC facilitates progression and lymph node metastasis via enhancement of malignant potential and interaction with surrounding cells