Coherent states for compact Lie groups and their large-N limits

The first two parts of this article surveys results related to the heat-kernel coherent states for a compact Lie group K. I begin by reviewing the definition of the coherent states, their resolution of the identity, and the associated Segal-Bargmann transform. I then describe related results including connections to geometric quantization and (1+1)-dimensional Yang--Mills theory, the associated coherent states on spheres, and applications to quantum gravity. The third part of this article summarizes recent work of mine with Driver and Kemp on the large-N limit of the Segal--Bargmann transform for the unitary group U(N). A key result is the identification of the leading-order large-N behavior of the Laplacian on "trace polynomials."Comment: Submitted to the proceeding of the CIRM conference, "Coherent states and their applications: A contemporary panorama.

Evidence for the h_b(1P) meson in the decay Upsilon(3S) --> pi0 h_b(1P)

Using a sample of 122 million Upsilon(3S) events recorded with the BaBar detector at the PEP-II asymmetric-energy e+e- collider at SLAC, we search for the $h_b(1P)$ spin-singlet partner of the P-wave chi_{bJ}(1P) states in the sequential decay Upsilon(3S) --> pi0 h_b(1P), h_b(1P) --> gamma eta_b(1S). We observe an excess of events above background in the distribution of the recoil mass against the pi0 at mass 9902 +/- 4(stat.) +/- 2(syst.) MeV/c^2. The width of the observed signal is consistent with experimental resolution, and its significance is 3.1sigma, including systematic uncertainties. We obtain the value (4.3 +/- 1.1(stat.) +/- 0.9(syst.)) x 10^{-4} for the product branching fraction BF(Upsilon(3S)-->pi0 h_b) x BF(h_b-->gamma eta_b).Comment: 8 pages, 4 postscript figures, submitted to Phys. Rev. D (Rapid Communications

Delineation of the Innate and Adaptive T-Cell Immune Outcome in the Human Host in Response to Campylobacter jejuni Infection

BACKGROUND: Campylobacter jejuni is the most prevalent cause of bacterial gastroenteritis worldwide. Despite the significant health burden this infection presents, molecular understanding of C. jejuni-mediated disease pathogenesis remains poorly defined. Here, we report the characterisation of the early, innate immune response to C. jejuni using an ex-vivo human gut model of infection. Secondly, impact of bacterial-driven dendritic cell activation on T-cell mediated immunity was also sought. METHODOLOGY: Healthy, control paediatric terminal ileum or colonic biopsy tissue was infected with C. jejuni for 8-12 hours. Bacterial colonisation was followed by confocal microscopy and mucosal innate immune responses measured by ELISA. Marked induction of IFNγ with modest increase in IL-22 and IL-17A was noted. Increased mucosal IL-12, IL-23, IL-1β and IL-6 were indicative of a cytokine milieu that may modulate subsequent T-cell mediated immunity. C. jejuni-driven human monocyte-derived dendritic cell activation was followed by analyses of T cell immune responses utilising flow cytometry and ELISA. Significant increase in Th-17, Th-1 and Th-17/Th-1 double-positive cells and corresponding cytokines was observed. The ability of IFNγ, IL-22 and IL-17 cytokines to exert host defence via modulation of C. jejuni adhesion and invasion to intestinal epithelia was measured by standard gentamicin protection assay. CONCLUSIONS: Both innate and adaptive T cell-immunity to C. jejuni infection led to the release of IFNγ, IL-22 and IL-17A; suggesting a critical role for this cytokine triad in establishing host anti-microbial immunity during the acute and effectors phase of infection. In addition, to their known anti-microbial functions; IL-17A and IL-17F reduced the number of intracellular C. jejuni in intestinal epithelia, highlighting a novel aspect of how IL-17 family members may contribute to protective immunity against C. jejuni

The effect of enteral and parenteral feeding on secretion of orexigenic peptides in infants

<p>Abstract</p> <p>Background</p> <p>The feeding in the first months of the life seems to influence the risks of obesity and affinity to some diseases including atherosclerosis. The mechanisms of these relations are unknown, however, the modification of hormonal action can likely be taken into account. Therefore, in this study the levels of ghrelin and orexin A - peripheral and central peptide from the orexigenic gut-brain axis were determined.</p> <p>Methods</p> <p>Fasting and one hour after the meal plasma concentrations of ghrelin and orexin were measured in breast-fed (group I; n = 17), milk formula-fed (group II; n = 16) and highly hydrolyzed, hypoallergic formula-fed (group III; n = 14) groups, age matched infants (mean 4 months) as well as in children with iv provision of nutrients (glucose - group IV; n = 15; total parenteral nutrition - group V; n = 14). Peptides were determined using EIA commercial kits.</p> <p>Results</p> <p>Despite the similar caloric intake in orally fed children the fasting ghrelin and orexin levels were significantly lower in the breast-fed children (0.37 ± 0.17 and 1.24 ± 0.29 ng/ml, respectively) than in the remaining groups (0.5 ± 0.27 and 1.64 ± 0.52 ng/ml, respectively in group II and 0.77 ± 0.27 and 2.04 ± 1.1 ng/ml, respectively, in group III). The postprandial concentrations of ghrelin increased to 0.87 ± 0.29 ng/ml, p < 0.002 and 0.76 ± 0.26 ng/ml, p < 0.01 in groups I and II, respectively as compared to fasting values. The decrease in concentration of ghrelin after the meal was observed only in group III (0.47 ± 0.24 ng/ml). The feeding did not influence the orexin concentration. In groups IV and V the ghrelin and orexin levels resembled those in milk formula-fed children.</p> <p>Conclusion</p> <p>The highly hydrolyzed diet strongly affects fasting and postprandial ghrelin and orexin plasma concentrations with possible negative effect on short- and long-time effects on development. Also total parenteral nutrition with the continuous stimulation and lack of fasting/postprandial modulation might be responsible for disturbed development in children fed this way.</p

Observation of CP violation in B ->eta/K-0 decays

We present measurements of the time-dependent CP-violation parameters S and C in B-0 -> eta K-'(0) decays. The data sample corresponds to 384 x 10(6) B (B) over bar pairs produced by e(+)e(-) annihilation at the Upsilon(4S). The results are S = 0.58 +/- 0.10 +/- 0.03 and C = -0.16 +/- 0.07 +/- 0.03. We observe mixing-induced CP violation with a significance of 5.5 standard deviations in this b -> s penguin dominated mode

Measurement of the CP asymmetry and branching fraction of B-0 ->rho K-0(0)

We present a measurement of the branching fraction and time-dependent CP asymmetry of B-0 -> POKO. The results are obtained from a data sample of 227 x 10(6) Y(4S) -> BB decays collected with the BABAR detector at the PEP-II asymmetric-energy B factory at Stanford Linear Accelerator Center. From a time-dependent maximum likelihood fit yielding 111 +/- 19 signal events, we find B(B-0 -> rho K-0(0)) = (4.9 +/- 0.8 +/- 0.9) x 10(-6), where the first error is statistical and the second systematic. We report the measurement of the CP parameters S-rho 0KS0 = 0.20 +/- 0.52 +/- 0.24 and C-rho 0KS0 = 0.64 +/- 0.41 +/- 0.20

Measurements of CP-violating asymmetries in B-0 -> a(1)(+/-)(1260)pi(-/+) decays

We present measurements of CP-violating asymmetries in the decay B-0 -> a(1)(+/-)(1260)pi(-/+) with a(1)(+/-)(1260)->pi(-/+)pi(+/-)pi(+/-). The data sample corresponds to 384x10(6) B(b) over bar pairs collected with the BABAR detector at the PEP-II asymmetric B factory at SLAC. We measure the CP-violating asymmetry A(CP)(a1 pi)=-0.07 +/- 0.07 +/- 0.02, the mixing-induced CP violation parameter S-a1 pi=0.37 +/- 0.21 +/- 0.07, the direct CP violation parameter C-a1 pi=-0.10 +/- 0.15 +/- 0.09, and the parameters Delta C-a1 pi=0.26 +/- 0.15 +/- 0.07 and Delta S-a1 pi=-0.14 +/- 0.21 +/- 0.06. From these measured quantities we determine the angle alpha(eff)=78.6 degrees +/- 7.3 degrees

Measurement of branching fractions and charge asymmetries in B decays to an eta meson and a K-* meson

We present measurements of branching fractions and charge asymmetries for the decays B ->eta K-*, where K-* indicates a spin 0, 1, or 2 K pi system. The data sample corresponds to 344x10(6) B (B) over bar pairs collected with the BABAR detector at the PEP-II asymmetric-energy e(+)e(-) collider at SLAC. We measure the branching fractions (in units of 10(-6)): B(B-0 ->eta K-*0(892))=16.5 +/- 1.1 +/- 0.8, B(B+->eta K*+(892))=18.9 +/- 1.8 +/- 1.3, B(B-0 ->eta(K pi)(0)(*0))=11.0 +/- 1.6 +/- 1.5, B(B+->eta(K pi)(0)(*+))=18.2 +/- 2.6 +/- 2.6, B(B-0 ->eta K-2(*0)(1430))=9.6 +/- 1.8 +/- 1.1, and B(B+->eta K-2(*+)(1430))=9.1 +/- 2.7 +/- 1.4. We also determine the charge asymmetries for all decay modes

Branching fraction measurements of B+->rho(+)gamma, B-0 ->rho(0)gamma, and B-0 ->omega gamma

We present a study of the decays B+->rho(+)gamma, B-0 ->rho(0)gamma, and B-0 ->omega gamma. The analysis is based on data containing 347x10(6) B (B) over bar events recorded with the BABAR detector at the PEP-II asymmetric B factory. We measure the branching fractions B(B+->rho(+)gamma)=(1.10(-0.33)(+0.37)+/- 0.09)x10(-6) and B(B-0 ->rho(0)gamma)=(0.79(-0.20)(+0.22)+/- 0.06)x10(-6), and set a 90% C.L. upper limit B(B-0 ->omega gamma)(rho/omega)gamma)=(1.25(-0.24)(+0.25)+/- 0.09)x10(-6), from which we determine vertical bar V-td/V-ts vertical bar=0.200(-0.020)(+0.021)+/- 0.015, where the first uncertainty is experimental and the second is theoretical