Measurement of the p-pbar -> Wgamma + X cross section at sqrt(s) = 1.96 TeV and WWgamma anomalous coupling limits

The WWgamma triple gauge boson coupling parameters are studied using p-pbar -> l nu gamma + X (l = e,mu) events at sqrt(s) = 1.96 TeV. The data were collected with the DO detector from an integrated luminosity of 162 pb^{-1} delivered by the Fermilab Tevatron Collider. The cross section times branching fraction for p-pbar -> W(gamma) + X -> l nu gamma + X with E_T^{gamma} > 8 GeV and Delta R_{l gamma} > 0.7 is 14.8 +/- 1.6 (stat) +/- 1.0 (syst) +/- 1.0 (lum) pb. The one-dimensional 95% confidence level limits on anomalous couplings are -0.88 < Delta kappa_{gamma} < 0.96 and -0.20 < lambda_{gamma} < 0.20.Comment: Submitted to Phys. Rev. D Rapid Communication

Measurement of the Lambda^0_b lifetime in the decay Lambda^0_b -> J/psi Lambda^0 with the D0 Detector

We present measurements of the Lambda^0_b lifetime in the exclusive decay channel Lambda^0_{b}->J/psi Lambda^0, with J/psi to mu+ mu- and Lambda^0 to p pi-, the B^0 lifetime in the decay B^0 -> J/psi K^0_S with J/psi to mu+ mu- and K^0_S to pi+ pi-, and the ratio of these lifetimes. The analysis is based on approximately 250 pb^{-1} of data recorded with the D0 detector in pp(bar) collisions at sqrt{s}=1.96 TeV. The Lambda^0_b lifetime is determined to be tau(Lambda^0_b) = 1.22 +0.22/-0.18 (stat) +/- 0.04 (syst) ps, the B^0 lifetime tau(B^0) = 1.40 +0.11/-0.10 (stat) +/- 0.03 (syst) ps, and the ratio tau(Lambda^0_b)/tau(B^0) = 0.87 +0.17/-0.14 (stat) +/- 0.03 (syst). In contrast with previous measurements using semileptonic decays, this is the first determination of the Lambda^0_b lifetime based on a fully reconstructed decay channel.Comment: 7 pages, 4 figures, Submitted to Physical Review Letters, v2: Added FNAL Pub-numbe

Measurement of the WW production cross section in p anti-p collisions at s**(1/2) = 1.96 TeV

We present a measurement of the W boson pair-production cross section in p anti-p collisions at a center-of-mass energy of sqrt{s}=1.96 TeV. The data, collected with the Run II DO detector, correspond to an integrated luminosity of 224-252 pb^-1 depending on the final state (ee, emu or mumu). We observe 25 candidates with a background expectation of 8.1+/-0.6(stat)+/-0.6(syst)+/-0.5(lum) events. The probability for an upward fluctuation of the background to produce the observed signal is 2.3x10^-7, equivalent to 5.2 standard deviations.The measurement yields a cross section of 13.8+4.3/-3.8(stat)+1.2/-0.9(syst)+/-0.9(lum) pb, in agreement with predictions from the standard model.Comment: submitted to PR

Expression and induction of anaphylatoxin C5a receptors in the rat liver

The C5a-anaphylatoxin which is generated by limited proteolysis upon activation of the fifth component of complement may be induced by the classical, the alternative or the lectin pathway. C5a has been shown, under normal conditions, to induce the release of prostanoids from Kupffer cells (KC) and hepatic stellate cells (HSC) and thereby indirectly to increase glucose output from hepatocytes (HC). A direct action of C5a on HC would require the expression of the specific C5a receptor (C5aR). In studies using quantitative RT-PCR it was shown that non-stimulated HC lack C5aR, in contrast to KC, HSC and sinusoidal endothelial cells (SEC) all of which contained mRNA for the C5aR in decreasing amounts. FACS analyses, immunohisto- and immunocytochemistry as well as functional analyses confirmed the results of the RT-PCR assays. Under inflammatory situations the C5aR was found to be upregulated in various organs and tissues which included the liver. Interleukin-6 (IL-6) as a main inflammatory mediator in the liver induced a de novo expression of functional C5aR in HC in-vitro and invivo. In contrast, LPS failed to induce C5aR directly in cultured HC in-vitro but induced C5aR in HC in vivo and in co-cultures of HC and KC which release IL-6 upon stimulation with LPS. So far, the only known effector function of C5a on HSC was the induction of prostanoid release. In an approach to reveal new functions of C5aR in HSC, the cells responsible for liver fibrosis, it could be shown that C5a upregulated fibronectin-specific mRNA five-fold whereas entactin, collagen IV and the structure protein smooth muscle actin were not affected. In addition, C5a did not upregulate specific mRNA for the profibrotic cytokine TGF-ß1 in either isolated KC or HSC. Thus, C5a alone appears to have only a limited role in the induction of liver fibrosis

Integrin α1β1 (VLA-1) mediates adhesion of activated intraepithelial lymphocytes to collagen

Intraepithelial lymphocytes (IELs) from human intestinal epithelium are memory CD8+ T cells that bind to epithelial cells through human mycosal lymphocyte (HML)-1 and to mesenchymal cells through very late activation antigen-4 (VLA-4). Their binding of extracellular matrix proteins and the mechanism involved were tested. Activated 51Cr-labelled lymphocytes were incubated in protein-coated microwells with various additives. After washing, the adherent cells were detected by radioactivity. The percentages of activated IELs that bound to collagen types I and IV were 20 and 31%, respectively; fewer bound to fibronectin or laminin. Compared to interleukin-2-activated peripheral blood CD8+ T lymphocytes, more IELs bound collagen IV and fewer bound fibronectin. IEL adhesion to collagen (but not fibronectin or laminin) was up-regulated by antibody ligation of CD2 or by protein kinase C stimulation by phorbol ester; staurosporine reduced binding, while herbimycin, phytohaemagglutinin and CD3 ligation had no effect. Antibody-blocking of integrin VLA-1 subunits α1 (CD49a) and β1 (CD18) inhibited adhesion to collagen type I by 82±6% and to type IV by 94±1% (P < 0·001), implicating VLA-1 as the main collagen receptor for IELs. Cell adhesion was dependent on extracellular divalent cations, a characteristic event of VLA-1 never before shown for IELs: manganese and magnesium ions supported binding in a dose-dependent manner; calcium ions inhibited their effectiveness. Therefore, IELs bind collagen through integrin α1β1 after protein kinase C activation. Adhesion is modulated by divalent cations

T-cell populations in the pig intestinal lamina propria: memory cells with unusual phenotypic characteristics

We have previously presented evidence of a highly organized and compartmentalized structure of the small intestinal lamina propria of the pig. In this study, we conducted a detailed analysis of the T-cell populations found at this site, and compared these T cells with cell populations found in other tissue sites and the periphery. We showed that the CD4+ and CD8+ T-cell populations found in the pig gut are of memory phenotype, defined by CD45 isoform expression, but show few signs of recent activation. They show a high degree of phenotypic and therefore presumably functional homogeneity. Both CD4- and CD8-positive cells show strong parallels in the patterns of surface molecule expression, suggesting similar pressures on differentiation. The unique combination of surface molecules found on lamina propria T cells is found only infrequently on cells in other lymphoid sites