Nucleon resonances in the fourth resonance region

Nucleon and $\Delta$ resonances in the fourth resonance region are studied in a multichannel partial-wave analysis which includes nearly all available data on pion- and photo-induced reactions off protons. In the high-mass range, above 1850\,MeV, several alternative solutions yield a good description of the data. For these solutions, masses, widths, pole residues and photo-couplings are given. In particular, we find evidence for nucleon resonances with spin-parities $J^P=1/2^+...7/2^+$. For one set of solutions, there are four resonances forming naturally a spin-quartet of resonances with orbital angular momentum L=2 and spin S=3/2 coupling to $J=1/2,...,7/2$. Just below 1.9\,GeV we find a spin doublet of resonances with $J^P=1/2^-$ and $3/2^-$. Since a spin partner with $J^P=5/2^-$ is missing at this mass, the two resonances form a spin doublet which must have a symmetric orbital-angular-momentum wave function with L=1. For another set of solutions, the four positive-parity resonances are accompanied by mass-degenerate negative-parity partners -- as suggested by the conjecture of chiral symmetry restoration. The possibility of a $J^P=1/2^+, 3/2^+$ spin doublet at 1900\,MeV belonging to a 20-plet is discussed.Comment: 16 page

Regulation of immune cell function and differentiation by the NKG2D receptor

NKG2D is one of the most intensively studied immune receptors of the past decade. Its unique binding and signaling properties, expression pattern, and functions have been attracting much interest within the field due to its potent antiviral and anti-tumor properties. As an activating receptor, NKG2D is expressed on cells of the innate and adaptive immune system. It recognizes stress-induced MHC class I-like ligands and acts as a molecular sensor for cells jeopardized by viral infections or DNA damage. Although the activating functions of NKG2D have been well documented, recent analysis of NKG2D-deficient mice suggests that this receptor may have a regulatory role during NK cell development. In this review, we will revisit known aspects of NKG2D functions and present new insights in the proposed influence of this molecule on hematopoietic differentiation

Properties of baryon resonances from a multichannel partial wave analysis

Properties of nucleon and $\Delta$ resonances are derived from a multichannel partial wave analysis. The statistical significance of pion and photo-induced inelastic reactions off protons are studied in a multichannel partial-wave analysis.Comment: 12 pages, 8 Table

Diabetes Alters the Expression and Translocation of the Insulin-Sensitive Glucose Transporters 4 and 8 in the Atria

We would like to thank Dr. Emilie Martinez and Jill Murray for their excellent technical assistance and animal care.Although diabetes has been identified as a major risk factor for atrial fibrillation, little is known about glucose metabolism in the healthy and diabetic atria. Glucose transport into the cell, the rate-limiting step of glucose utilization, is regulated by the Glucose Transporters (GLUTs). Although GLUT4 is the major isoform in the heart, GLUT8 has recently emerged as a novel cardiac isoform. We hypothesized that GLUT-4 and -8 translocation to the atrial cell surface will be regulated by insulin and impaired during insulin-dependent diabetes. GLUT protein content was measured by Western blotting in healthy cardiac myocytes and type 1 (streptozotocin-induced, T1Dx) diabetic rodents. Active cell surface GLUT content was measured using a biotinylated photolabeled assay in the perfused heart. In the healthy atria, insulin stimulation increased both GLUT-4 and -8 translocation to the cell surface (by 100% and 240%, respectively, P<0.05). Upon insulin stimulation, we reported an increase in Akt (Th308 and s473 sites) and AS160 phosphorylation, which was positively (P<0.05) correlated with GLUT4 protein content in the healthy atria. During diabetes, active cell surface GLUT-4 and -8 content was downregulated in the atria (by 70% and 90%, respectively, P<0.05). Akt and AS160 phosphorylation was not impaired in the diabetic atria, suggesting the presence of an intact insulin signaling pathway. This was confirmed by the rescued translocation of GLUT-4 and -8 to the atrial cell surface upon insulin stimulation in the atria of type 1 diabetic subjects. In conclusion, our data suggest that: 1) both GLUT-4 and -8 are insulin-sensitive in the healthy atria through an Akt/AS160 dependent pathway; 2) GLUT-4 and -8 trafficking is impaired in the diabetic atria and rescued by insulin treatment. Alterations in atrial glucose transport may induce perturbations in energy production, which may provide a metabolic substrate for atrial fibrillation during diabetes.Yeshttp://www.plosone.org/static/editorial#pee