Use of biochar-based cathodes and increase in the electron flow by pseudomonas aeruginosa to improve waste treatment in microbial fuel cells

In this paper, we tested the combined use of a biochar-based material at the cathode and of Pseudomonas aeruginosa strain in a single chamber, air cathode microbial fuel cells (MFCs) fed with a mix of shredded vegetable and phosphate buffer solution (PBS) in a 30% solid/liquid ratio. As a control system, we set up and tested MFCs provided with a composite cathode made up of a nickel mesh current collector, activated carbon and a single porous poly tetra fluoro ethylene (PTFE) diffusion layer. At the end of the experiments, we compared the performance of the two systems, in the presence and absence of P. aeruginosa, in terms of electric outputs. We also explored the potential reutilization of cathodes. Unlike composite material, biochar showed a life span of up to 3 cycles of 15 days each, with a pH of the feedstock kept in a range of neutrality. In order to relate the electric performance to the amount of solid substrates used as source of carbon and energy, besides of cathode surface, we referred power density (PD) and current density (CD) to kg of biomass used. The maximum outputs obtained when using the sole microflora were, on average, respectively 0.19 Wm(-2)kg(-1) and 2.67 Wm(-2)kg(-1), with peaks of 0.32 Wm(-2)kg(-1) and 4.87 Wm(-2)kg(-1) of cathode surface and mass of treated biomass in MFCs with biochar and PTFE cathodes respectively. As to current outputs, the maximum values were 7.5 Am-2 kg(-1) and 35.6 Am(-2)kg(-1) in MFCs with biochar-based material and a composite cathode. If compared to the utilization of the sole acidogenic/acetogenic microflora in vegetable residues, we observed an increment of the power outputs of about 16.5 folds in both systems when we added P. aeruginosa to the shredded vegetables. Even though the MFCs with PTFE-cathode achieved the highest performance in terms of PD and CD, they underwent a fouling episode after about 10 days of operation, with a dramatic decrease in pH and both PD and CD. Our results confirm the potentialities of the utilization of biochar-based materials in waste treatment and bioenergy production

Pancreatic cancer-associated diabetes mellitus: an open field for proteomic applications.

Background: Diabetes mellitus is associated with pancreatic cancer in more than 80% of the cases. Clinical, epidemiological, and experimental data indicate that pancreatic cancer causes diabetes mellitus by releasing soluble mediators which interfere with both beta-cell function and liver and muscle glucose metabolism. Methods: We analysed, by matrix-assisted laser desorption ionization time of flight (MALDI-TOF), a series of pancreatic cancer cell lines conditioned media, pancreatic cancer patients' peripheral and portal sera, comparing them with controls and chronic pancreatitis patients' sera. Results: MALDI-TOF analysis of pancreatic cancer cells conditioned media and patients' sera indicated a low molecular weight peptide to be the putative pancreatic cancer-associated diabetogenic factor. The sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of tumor samples from diabetic and non-diabetic patients revealed the presence of a 1500 Da peptide only in diabetic patients. The amino acid sequence of this peptide corresponded to the N-terminal of an S-100 calcium binding protein, which was therefore suggested to be the pancreatic cancer-associated diabetogenic factor. Conclusions: We identified a tumor-derived peptide of 14 amino acids sharing a 100% homology with an S-100 calcium binding protein, which is probably the pancreatic cancer-associated diabetogenic facto

Pancreatic cancer-derived S-100A8 N-terminal peptide: a diabetes cause?

BACKGROUND: Our aim was to identify the pancreatic cancer diabetogenic peptide. METHODS: Pancreatic tumor samples from patients with (n=15) or without (n=7) diabetes were compared with 6 non-neoplastic pancreas samples using SDS-PAGE. RESULTS: A band measuring approximately 1500 Da was detected in tumors from diabetics, but not in neoplastic samples from non-diabetics or samples from non-neoplastic subjects. Sequence analysis revealed a 14 amino acid peptide (1589.88 Da), corresponding to the N-terminal of the S100A8. At 50 nmol/L and 2 mmol/L, this peptide significantly reduced glucose consumption and lactate production by cultured C(2)C(12) myoblasts. The 14 amino acid peptide caused a lack of myotubular differentiation, the presence of polynucleated cells and caspase-3 activation. CONCLUSIONS: The 14 amino acid peptide from S100A8 impairs the catabolism of glucose by myoblasts in vitro and may cause hyperglycemia in vivo. Its identification in biological fluids might be helpful in diagnosing pancreatic cancer in patients with recent onset diabetes mellitus

After a perfect myectomy for obstructive hypertrophic cardiomyopathy, which patients should need more? That is the question

International audienceNo abstract availabl