11 research outputs found
Physics in Riemann's mathematical papers
Riemann's mathematical papers contain many ideas that arise from physics, and
some of them are motivated by problems from physics. In fact, it is not easy to
separate Riemann's ideas in mathematics from those in physics. Furthermore,
Riemann's philosophical ideas are often in the background of his work on
science. The aim of this chapter is to give an overview of Riemann's
mathematical results based on physical reasoning or motivated by physics. We
also elaborate on the relation with philosophy. While we discuss some of
Riemann's philosophical points of view, we review some ideas on the same
subjects emitted by Riemann's predecessors, and in particular Greek
philosophers, mainly the pre-socratics and Aristotle. The final version of this
paper will appear in the book: From Riemann to differential geometry and
relativity (L. Ji, A. Papadopoulos and S. Yamada, ed.) Berlin: Springer, 2017
Prolonged Swimming Exercise Training Induce Hypophosphatemic Osteopenia in Stroke-Prone Spontaneously Hypertensive Rats (SHRSP).
Inflammatory processes have differential effects on claudins 2, 3 and 4 in colonic epithelial cells
Claudin proteins comprise a recently described family of tight junction proteins that differentially regulate paracellular permeability. Since other tight junction proteins show alterations in distribution or expression in inflammatory bowel disease (IBD) we assessed expression of claudins (CL) 2, 3 and 4 in IBD. CL 2 was strongly expressed along the inflamed crypt epithelium, whilst absent or barely detectable in normal colon. In contrast, CL 3 and 4 were present throughout normal colonic epithelium and were reduced or redistributed in the diseased surface epithelium. In a T84-cell culture model of the gut barrier, paracellular permeability decreased with time after plating and correlated with a marked decrease in the expression of CL 2. Addition of IFN/TNF led to further decreases in CL 2 and 3, the redistribution of CL 4 and a marked increase in paracellular permeability. Conversely, IL-13 dramatically increased CL 2, with little effect on CL 3 or 4, but also resulted in increased paracellular permeability. Expression of CL 2 did not correlate with proliferation or junctional reorganisation after calcium ion depletion. Re-expression of CL 2 in response to IL-13 was inhibited by phophatidylinositol 3 kinase inhibitor, LY294002, which also restored the ion permeability to previous levels. CL 2 expression could be stimulated in the absence of IL-13 by activation of phospho-Akt in the phophatidylinositol 3 kinase pathway. These results suggest that INF/TNF and IL-13 have differential effects on CL 2, 3 and 4 in tight junctions, which may lead to increased permeability via different mechanisms