The flat-plate plant-microbial fuel cell: the effect of a new design on internal resistances

Due to a growing world population and increasing welfare, energy demand worldwide is increasing. To meet the increasing energy demand in a sustainable way, new technologies are needed. The Plant-Microbial Fuel Cell (P-MFC) is a technology that could produce sustainable bio-electricity and help meeting the increasing energy demand. Power output of the P-MFC, however, needs to be increased to make it attractive as a renewable and sustainable energy source. To increase power output of the P-MFC internal resistances need to be reduced. With a flat-plate P-MFC design we tried to minimize internal resistances compared to the previously used tubular P-MFC design. With the flat-plate design current and power density per geometric planting area were increased (from 0.15 A/m² to 1.6 A/m² and from 0.22 W/m² to and 0.44 W/m²)as were current and power output per volume (from 7.5 A/m³ to 122 A/m³ and from 1.3 W/m³ to 5.8 W/m³). Internal resistances times volume were decreased, even though internal resistances times membrane surface area were not. Since the membrane in the flat-plate design is placed vertically, membrane surface area per geometric planting area is increased, which allows for lower internal resistances times volume while not decreasing internal resistances times membrane surface area. Anode was split into three different sections on different depths of the system, allowing to calculate internal resistances on different depths. Most electricity was produced where internal resistances were lowest and where most roots were present; in the top section of the system. By measuring electricity production on different depths in the system, electricity production could be linked to root growth. This link offers opportunities for material-reduction in new designs. Concurrent reduction in material use and increase in power output brings the P-MFC a step closer to usable energy density and economic feasibility.     

Inhibition of trypsin by the beta-amyloid protein precursor. A comparative study between transfected cells, human brain and cerebrospinal fluid.

Soluble beta-amyloid protein precursors (beta-APPs) were studied in human brain and cerebrospinal fluid (CSF) after partial purification by ion exchange chromatography. Proteins were analysed in immunoblotting experiments using a monoclonal antibody directed against the N-terminal segment of the beta-APP 770, and by reverse enzymography. In the human brain and CSF, a protein which comigrates with the beta-APP 770 expressed by transfected CHO cells was able to inhibit trypsin.     

The monod equation: A revisit and a generalization to product inhibition situations

This paper shows how to treat the substrate-limiting Monod equation in a straight forward manner for different types of fermentors (plug-flow, batch, and mixed-flow) using the general language of chemical reaction engineering. Straight-line plots are developed for directly finding the kinetic constants of the equation, and an example using Monod's original data illustrates the procedure. The Monod equation is then generalized to account for the effects of both substrate and inhibitory toxic wastes. Finally, for pure product inhibition performance, expressions are derived for various reactor types, and correlation graphs are developed for finding the kinetic constants of the reaction. An example from the recent literature shows that this equation form fits the data extremely well.     

Transferrin protein and iron uptake by cultured hepatocytes

The binding and uptake of ⁵⁹Fe-loaded ³H-labelled rat transferrin by cultured rat hepatocytes was investigated. At 4°C, there is no evidence for a specific binding of transferrin which could be related to the association of neo-synthesized transferrin with plasma membrane receptors. At 37°C, iron uptake is much more important than transferrin uptake; it proceeds linearly over the time of incubation, is largely proportional to the extracellular transferrin concentration, and is compatible with uptake by fluid phase endocytosis. The difference observed between iron and transferrin uptake implies the existence of a mechanism allowing the reutilization of transferrin after iron delivery.     

Lack of Rapid Desensitization of Ca2+ Responses in Transfected CHO Cells Expressing the Rat Neurotensin Receptor Despite Agonist-Induced Internalization

Abstract: Transfected Chinese hamster ovary cells were used as a model for the study of the desensitization of the neurotensin receptor at the second messenger level. Stimulation with nanomolar concentrations of neurotensin elicited rapid rises in the cytosolic calcium concentration ([Ca²⁺]_i), which remained elevated throughout the peptide application. A significant response was already detected with neurotensin concentrations as low as 0.01 nM. This high efficiency of neurotensin in mediating this calcium response contrasts with the nanomolar affinity of the peptide for its receptor measured in binding experiments. Evidence indicated that the initial elevation of the [Ca²⁺]_i resulted from release of Ca²⁺ from intracellular stores, whereas the sustained response involved an influx of extracellular origin. Return to the basal level was only reached after extensive washing of the peptide or its displacement with the neurotensin receptor antagonist SR48692. After washing, further stimulations were still able to mediate an increase in the [Ca²⁺]_i, indicating an apparent absence of rapid desensitization of the intracellular signaling pathway that mediates calcium mobilization. In contrast with this absence of response desensitization, the neurotensin receptors were found to internalize after stimulation with the peptide. This internalization was maximal after 30 min and accounted for ～70% of the number of neurotensin binding sites located at the cell surface. These results indicate that despite the functional properties of the rat neurotensin receptor present in Chinese hamster ovary cells after transfection, the intracellular signaling pathway triggered by stimulation with neurotensin seems to be resistant to desensitization. This might be related to the high efficiency of the intracellular signaling pathway coupled to the neurotensin receptor observed in these cells. A possible absence of desensitization of the neurotensin receptor itself is also discussed.