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Results of the search for the rare decay $B_s^0 \to \mu^+ \mu^-$ using data collected by the D0 detector at the Fermilab Tevatron collider are presented. This analysis covers the full Run II data set, corresponding to approximately 10.4~fb$^{-1}$ of integrated luminosity in $p\bar{p}$ collisions at a center of mass energy of 1.96 TeV. The analysis used new variables and a multivariate technique to improve the background reduction. After seeing fewer events than expected from background, a new Tevatron best observed limit was set on the branching fraction of the decay at $\cal{B}$($B_s^0 \to \mu^+ \mu^-$) $< 15 \times 10^{-9}$ ($12 \times 10^{-9}$) at the 95\% (90\%) C.L.

<p>Several HIV-1 neutralizing antibodies (e.g. 2F5, 4E10) have been shown to react with self-antigens, suggesting that effective humoral responses to HIV-1 may be constrained by the tolerization of HIV-reactive B cells that also recognize self-antigens. I have tracked the development of 2F5-like HIV-1 gp41 membrane proximal external region (MPER)-reactive B cells throughout ontogeny using B-cell tetramer reagents. In BL/6 mice, MPER-binding populations are lost during normal B-cell development and immunization with HIV-1 MPER antigen does not elicit robust humoral responses. I have identified Kynureninase as a self-antigen that is recognized by 2F5 antibody and, therefore, is a molecule that could mediate the developmental loss of B cells reactive to an epitope shared by HIV gp41 and Kynureninase. To recover these MPER-reactive cells, I describe and characterize a stromal-cell independent culture system that efficiently supports pro-B cell to IgM+ B-cell development with near normal levels of IgH and Igkappa diversity. B-cell development in vitro closely follows the patterns of development in vivo with culture derived (CD) B cells demonstrating characteristic patterns of surface antigen expression and gene activation. Immature and transitional B-cell compartments are reduced, due to the induction of tolerance, in the bone marrow of 3H9 IgH knockin mice ; however, cultures of 3H9 IgH knockin pro-B cells yields high frequencies of "forbidden", autoreactive IgM+ B cells. Furthermore, serum IgG autoantibody exceeded that present in autoimmune, C4-/- animals following the reconstitution of RAG-1-/- mice with IgM+ CD cells derived from BL/6 mice. I show that HIV-1 MPER-reactive B cells are recovered from both BL/6 and 2F5 IgH knockin bone marrow using this in vitro culture system. RAG-1-/- mice reconstituted with these culture-derived B and T cells generate strong germinal center and antibody responses to HIV-1 MPER antigens. These data demonstrate that the humoral immune response to this HIV-1 gp41 MPER antigen can be restored in mice when the constraints of B-cell tolerance have been relaxed.</p> / Dissertation

This work presents a precision determination of the mass difference of neutral and charged B mesons, m(B0) - m(B+). The measurement is based on a data sample of about 232 million B-meson pairs recorded with the BABAR detector at the e+e- storage-ring system PEP-II. In events of e+e- --&amp;gt; Upsilon(4S) --&amp;gt; B Bbar, B0 and B+ mesons are fully reconstructed in decays B+ --&amp;gt; J/psi K+ and B0 --&amp;gt; J/psi K*0 using the subsequent decays J/psi --&amp;gt; l+ l- and K*0 --&amp;gt; K+ pi- for the reconstruction of J/psi mesons and K*0 resonances, respectively. The determination of the mass difference from the measurement of the invariant B-meson masses suffers from detector-resolution effects. To reach the desired sensitivity, the B-meson momenta are measured in the center-of-mass system, the Upsilon(4S) rest frame. Since their energy is also known in the center-of-mass system, this method leads to the mass difference using the relativistic energy-momentum relation. For this purpose, three different fit methods are performed to the spectra of the B momenta. The obtained result is m(B0) - m(B+) = (+0.33 +- 0.05 +- 0.03) MeV/c^2, where the first error is statistical and the second estimates the systematic uncertainty of this measurement, which agrees well with the current world average. However, the combined error of this measurement is substantially smaller than that in the current world average, and the significance of m(B0) - m(B+) being non-zero has exceeded the 5 sigma level.

Despite evidence that viral hepatitis poses a significant risk to public health, universal vaccination has not yet been implemented. The risk for viral hepatitis infection is particularly high among injection drug users and other individuals who do not attend regular health care visits. Jails provide a structural opportunity to vaccinate these high risk individuals. HAV and HBV vaccines administered on an accelerated three week schedule could dramatically decrease the lifetime risk for contracting viral hepatitis among jail detainees. Assuming that 75% of detainees would accept vaccination, 33% have previous exposure to HAV, 25% have previous exposure to HBV, and independent future healthcare costs were US $317,000, the US health care system would save $12 per individual with a vaccinate upon entry program in comparison to no intervention. This savings translates into an economic benefit amounting to about US$ 5,000,000 saved if all new jail inmates in a given year were immunized. A vaccination upon entry program for HAV/HBV in jails should be widely implemented with coordination between the corrections system and public health agencies to reduce the growing cost of viral hepatitis infection.

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / "December 2000." Typescript. Vita. Includes bibliographical references (leaves 177-206). Also available on the Internet.

Thesis (Ph. D.)--University of Washington, 2000. / Vita. Includes bibliographical references (leaves 89-105).

B virus (Cercopithecine herpesvirus 1) is an alphaherpesvirus indigenous to macaque monkeys and is closely related to herpes simplex virus type 1 (HSV-1). Disease caused by B virus, which is often mild or asymptomatic in its natural host, the macaque monkey, is similar in infected macaques to HSV-1 infection in humans. When B virus zoonotically infects foreign hosts, e.g., humans, high morbidity and mortality are evidenced in > 80% of untreated cases. To explore the underlying reasons for differences in pathogenesis between B virus and HSV-1 infection in humans, human microarrays were used to comparatively examine global cellular gene expression patterns engaged as a result of infection of human foreskin fibroblasts (HFFs). Our results demonstrate that these closely related simplexvirus family members have divergent strategies to thwart host cell pathways related to innate defenses. In these studies, B virus did not induce detectable interferon, cytokine or chemokine genes, in sharp contrast to HSV-1, which induced innate immune responsive genes in infected cells. Although no innate immune response genes were found to be up-regulated by B virus infection, B virus induced I£eB£a, which was the only gene found to be involved in the NF-£eB signaling pathway within the innate immunity biological network. Quantification of NF-£eB p50 DNA binding activity in virus-infected nuclear extracts demonstrated that NF-£eB p50 DNA binding activity was lower in B virus-infected cells. Suppression of I£eB£a in B virus infected cells by siRNA restored NF-£eB-induced cytokine and chemokine expressions. Data presented here support the model that I£eB£a inhibits NF-£eB regulated immune responsive genes in B virus-infected HFF cells, and this response differs from that observed in HFF cells infected with HSV-1. The result is that B virus alters the NF-£eB regulated expression of cytokine and chemokine genes of HFF cells differently from HSV-1 early after infection. These differences in cytokine and chemokine expression may be associated with the delayed or reduced host responses observed in B virus infected humans and underlie the failure of adaptive responses in zoonotically infected humans.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 4 uppsatser.

Title: Measurement of the B0 d meson lifetime at ATLAS detector Author: Pavel Řezníček Department: Institute of Particle and Nuclear Physics Supervisor of the doctoral thesis: Dr. Zdeněk Doležal Supervisor's e-mail address: Zdenek.Dolezal@mff.cuni.cz Abstract: The lifetime of B0 d mesons is determined from their decays B0 d → J/ψK∗0 reconstructed in ATLAS experiment at the LHC using pp collision data at a center-of-mass energy of 7 TeV and corresponding to integrated luminosity of 40 pb−1 . The lifetime, extracted from the simultaneous unbinned maximum likelihood mass-lifetime fit, is 1.51±0.04 (stat.)±0.04 (syst.) ps. A total number of 2750±90 (stat.) signal B0 d decays are observed in the measurement, with a fit- ted B0 d mass of 5363.7 ± 1.2 (stat.) MeV. Both the extracted B0 d meson mass and lifetime are within the determined errors consistent with the world average values. Although the achieved precision is still significantly lower than the one of the world average value, the measurement successfully tested the feasibility of the fit-method and allowed to cross-check ATLAS detector performance. Keywords: CERN, LHC, ATLAS, B-physics, B-hadron, Lifetime