Higher-order supersymmetric contributions to electroweak precision observables

The dominant electroweak two-loop corrections to the precision observables M(_w) and sin(^2) θ off are calculated in the MSSM. They are obtained by evaluating the two loop Yukawa contributions of ϭ (aas) and ϭ (at2), ϭ (a2ab), ϭ (a2b), to the quantity Ap. A review of the one-loop Standard Model calculation is given in the large Top-Yukawa coupling limit. The 0{aļ), 0{atab), 0{al) result, involving the contributions from Standard Model fermions, sfermions, Higgs bosons and higgsinos, is derived in the gauge- less limit for arbitrary values of the lightest CP-even Higgs boson mass. A thorough discussion of the parameter relations enforced by super symmetry is given. Two different renormalisation schemes are applied. Compared to the previously known result for the quark-loop contribution we find a shift of up to +8 MeV in Mw and —4 X 10—5 in sin2 ^eff- Detailed numerical estimates of the remaining uncertainties of Mw and sin2 もff from unknown higher-order contributions are obtained for different values of the supersymmetric mass scale. The calculations are preceded by a review of EWPO and super symmetry. The electroweak precision variable Ap is defined. We renormalise using both dimensional regularisation and dimensional reduction

ROS-mediated PI3K activation drives mitochondrial transfer from stromal cells to hematopoietic stem cells in response to infection

Hematopoietic stem cells (HSCs) undergo rapid expansion in response to stress stimuli. Here we investigate the bioenergetic processes which facilitate the HSC expansion in response to infection. We find that infection by Gram-negative bacteria drives an increase in mitochondrial mass in mammalian HSCs, which results in a metabolic transition from glycolysis toward oxidative phosphorylation. The initial increase in mitochondrial mass occurs as a result of mitochondrial transfer from the bone marrow stromal cells (BMSCs) to HSCs through a reactive oxygen species (ROS)-dependent mechanism. Mechanistically, ROS-induced oxidative stress regulates the opening of connexin channels in a system mediated by phosphoinositide 3-kinase (PI3K) activation, which allows the mitochondria to transfer from BMSCs into HSCs. Moreover, mitochondria transfer from BMSCs into HSCs, in the response to bacterial infection, occurs before the HSCs activate their own transcriptional program for mitochondrial biogenesis. Our discovery demonstrates that mitochondrial transfer from the bone marrow microenvironment to HSCs is an early physiologic event in the mammalian response to acute bacterial infection and results in bioenergetic changes which underpin emergency granulopoiesis