UV and IR behaviour in QFT and LCQFT with fields as Operator Valued Distributions:Epstein and Glaser revisited

Following Epstein-Glaser's work we show how a QFT formulation based on operator valued distributions (OPVD) with adequate test functions treats original singularities of propagators on the diagonal in a mathematically rigourous way.Thereby UV and/or IR divergences are avoided at any stage, only a finite renormalization finally occurs at a point related to the arbitrary scale present in the test functions.Some well known UV cases are examplified.The power of the IR treatment is shown for the free massive scalar field theory developed in the (conventionally hopeless) mass perturbation expansion.It is argued that the approach should prove most useful for non pertubative methods where the usual determination of counterterms is elusiveComment: 6 pages 2 columns per pag

Sub-lethal concentrations of CdCl2 disrupt cell migration and cytoskeletal proteins in cultured mouse TM4 Sertoli cells

The aims of this study were to examine the effects of CdCl2 on the viability, migration and cytoskeleton of cultured mouse TM4 Sertoli cells. Time- and concentration-dependent changes were exhibited by the cells but 1 µM CdCl2 was sub-cytotoxic at all time-points. Exposure to 1 and 12 µM CdCl2 for 4 h resulted in disruption of the leading edge, as determined by chemical staining. Cell migration was inhibited by both 1 and 12 µM CdCl2 in a scratch assay monitored by live cell imaging, although exposure to the higher concentration was associated with cell death. Western blotting and immunofluorescence staining indicated that CdCl2 caused a concentration dependent reduction in actin and tubulin levels. Exposure to Cd2+ also resulted in significant changes in the levels and/or phosphorylation status of the microtubule and microfilament destabilising proteins cofilin and stathmin, suggesting disruption of cytoskeletal dynamics. Given that 1-12 µM Cd2+ is attainable in vivo, our findings are consistent with the possibility that Cd2+ induced impairment of testicular development and reproductive health may involve a combination of reduced Sertoli cell migration and impaired Sertoli cell viability depending on the timing, level and duration of exposure