d-wave superconductivity near charge instabilities

We investigate the symmetry of the superconducting order parameter in the proximity of a phase-separation or of an incommensurate charge-density-wave instability. The attractive effective interaction at small or intermediate transferred momenta is singular near the instability. This strongly $q$-dependent interaction, together with a residual local repulsion between the quasiparticles and an enhanced density of states for band structures appropriate for the high temperature superconducting oxides, strongly favors the formation of $d$-wave superconductivity. The relative stability with respect to superconductivity in the $s$-wave channel is discussed in detail, finding this latter hardly realized in the above conditions. The superconducting temperature is mostly determined by the closeness to the quantum critical point associated to the charge instability and displays a stronger dependence on doping with respect to the simple proximity to a Van Hove singularity. The relevance of this scenario and the generic agreement of the resulting phase diagram with the properties displayed by high temperature superconducting oxides is discussed.Comment: 1 revtex file and 12 postscript figure

Association of Insulin Receptor Substrate 1 (IRS-1) Y895 with Grb-2 Mediates the Insulin Signaling Involved in IRS-1-Deficient Brown Adipocyte Mitogenesis

We have recently generated immortalized fetal brown adipocyte cell lines from insulin receptor substrate 1 (IRS-1) knockout mice and demonstrated an impairment in insulin-induced lipid synthesis as compared to wild-type cell lines. In this study, we investigated the consequences of IRS-1 deficiency on mitogenesis in response to insulin. The lack of IRS-1 resulted in the inability of insulin-stimulated IRS-1-deficient brown adipocytes to increase DNA synthesis and enter into S/G(2)/M phases of the cell cycle. These cells showed a severe impairment in activating mitogen-activated protein kinase kinase (MEK1/2) and p42-p44 mitogen-activated protein kinase (MAPK) upon insulin stimulation. IRS-1-deficient cells also lacked tyrosine phosphorylation of SHC and showed no SHC–Grb-2 association in response to insulin. The mitogenic response to insulin could be partially restored by enhancing IRS-2 tyrosine phosphorylation and its association with Grb-2 by inhibition of phosphatidylinositol 3-kinase activity through a feedback mechanism. Reconstitution of IRS-1-deficient brown adipocytes with wild-type IRS-1 restored insulin-induced IRS-1 and SHC tyrosine phosphorylation and IRS-1–Grb-2, IRS-1–SHC, and SHC–Grb-2 associations, leading to the activation of MAPK and enhancement of DNA synthesis. Reconstitution of IRS-1-deficient brown adipocytes with the IRS-1 mutant Tyr895Phe, which lacks IRS-1–Grb-2 binding, restored SHC–IRS-1 association and SHC–Grb-2 association. However, the lack of IRS-1–Grb-2 association impaired MAPK activation and DNA synthesis in insulin-stimulated mutant cells. These data provide strong evidence for an essential role of IRS-1 and its direct association with Grb-2 in the insulin signaling pathway leading to MAPK activation and mitogenesis in brown adipocytes

Von mises approximation of the critical value of a test

Robustness in hypotheses testing, von Mises expansion, influence function, tail area influence function, saddlepoint approximation, Primary 62F35, secondary 62E17, 62F03,