Hydration properties and rate determining steps of the oxygen reduction reaction of perovskite-related oxides as H+-SOFC cathodes

Four mixed ionic-electronic conducting (MIEC) perovskite-related oxides were studied as potential H+-SOFC cathode materials: La0.6Sr0.4Fe0.8Co0.2O3−, Ba0.5Sr0.5Co0.8Fe0.2O3−, PrBaCo2O5+ and Pr2NiO4+. Their hydration properties were measured by TGA: Ba0.5Sr0.5Co0.8Fe0.2O3− shows the largest water uptake. Their electrochemical performances were characterized using BaCe0.9Y0.1O3− as electrolyte; polarization resistances as low as 0.5 cm2 were found at 600°C, for PrBaCo2O5+ and Pr2NiO4+. The rate determining steps of the oxygen reduction reaction were determined on the basis of electrochemical studies performed as a function of pH2O, in air. Proton transfer and water release appear to be the rate determining steps for Ba0.5Sr0.5Co0.8Fe0.2O3−, PrBaCo2O5+ and Pr2NiO4+. No rate determining step involving proton was found for La0.6Sr0.4Fe0.8Co0.2O3−. On the basis of this study, one can suggest that Ba0.5Sr0.5Co0.8Fe0.2O3−, PrBaCo2O5+ and Pr2NiO4+ show some protonic conduction as well as oxide diffusivity and can be labeled Triple Conducting (e-/O2−/H+) Oxides, so-called TCO

The riddle of the dual expression of IgM and IgD

Signalling through the B cell antigen receptor (BCR) is required for peripheral B lymphocyte maturation, maintenance, activation and silencing. In mature B cells, the antigen receptor normally consists of two isotypes, membrane IgM and IgD (mIgM, mIgD). Although the signals initiated from both isotypes differ in kinetics and intensity, in vivo, the BCR of either isotype seems to be able to compensate for the loss of the other, reflected by the mild phenotypes of mice deficient for mIgM or mIgD. Thus, it is still unclear why mature B cells need expression of mIgD in addition to mIgM. In the current review we suggest that the view that IgD has a simpIy definable function centred around the basic signalling function should be replaced by the assumption that IgD fine tunes humoral responses, modulates B cell selection and homeostasis and thus shapes the B cell repertoire, defining IgD to be a key modulator of the humoral immune response

IgD attenuates the IgM-induced anergy response in transitional and mature B cells

Self-tolerance by clonal anergy of B cells is marked by an increase in IgD and decrease in IgM antigen receptor surface expression, yet the function of IgD on anergic cells is obscure. Here we define the RNA landscape of the in vivo anergy response, comprising 220 induced sequences including a core set of 97. Failure to co-express IgD with IgM decreases overall expression of receptors for self-antigen, but paradoxically increases the core anergy response, exemplified by increased Sdc1 encoding the cell surface marker syndecan-1. IgD expressed on its own is nevertheless competent to induce calcium signalling and the core anergy mRNA response. Syndecan-1 induction correlates with reduction of surface IgM and is exaggerated without surface IgD in many transitional and mature B cells. These results show that IgD attenuates the response to self-antigen in anergic cells and promotes their accumulation. In this way, IgD minimizes tolerance-induced holes in the pre-immune antibody repertoire