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R Winston

Publications and source records attributed to R Winston.

At least 19 recordsLinked to original sources

Measurement of the K0 charge radius and a CP-violating asymmetry and a search for CP-violating E1 direct photon emission in the rare decay KL--> pi+ pi- e+ e-.

Using the complete KTeV data set of 5,241 candidate K(L)--> pi(+) pi(-) e(+) e(-) decays (including an estimated background of 204 +/- 14 events), we have measured the coupling g(CR)= 0.163 +/- 0.0149(stat) +/- 0.023(syst) of the CP conserving charge radius process and from it determined a K(0) charge radius of = [-0.077 +/- 0.007(stat) +/- 0.011(syst)]fm(2). We have determined a first experimental upper limit of 0.04 (90% C.L.) /g(e1)/ / /g(M1)/ of the couplings for the E1 and M1 direct photon emission processes. We also report the measurement of /g(M1)/ including a vector form factor /g(M1)/(1 + (a(1)/a(2))/((M(2)(p)-(M(2)(k))= 2M(K)E(gamma*)), where vector /g(M1)/= 1.11+/- 0.12(stat) +/- 0.08(syst) and a(1)/a(2) = [-0.744 +/- 0.027(stat) +/- 0.032(syst)] GeV(2)/c(2). Finally, a CP-violating asymmetry of [13.6 +/- 1.4(stat) +/- 1.5(syst)]% in the CP and T odd angle phi between the decay planes of the e(+) e(-) and pi(+) pi(-) pairs in the K(L) center of mass is reported.

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Observation of the decay xi0 --> sigma+ mu- nu(mu).

The xi0 muon semileptonic decay has been observed for the first time with nine identified events using the KTeV beam line and detector at Fermilab. The decay is normalized to the xi0 beta decay mode and yields a value for the ratio of decay rates gamma(xi0 --> sigma+ mu- nu(mu))/gamma(xi0 --> sigma+ e- nu(e)) of [1.8(-0.5)(+0.7)(stat) +/- 0.2(syst)] x 10(-2). This is in agreement with the SU(3) flavor symmetric quark model.

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A determination of the Cabibbo-Kobayashi-Maskawa parameter |V us| using KL decays.

We present a determination of the Cabibbo-Kobayashi-Maskawa parameter |V(us)| based on new measurements of the six largest K(L) branching fractions and semileptonic form factors by the KTeV (E832) experiment at Fermilab. We find |V(us)|=0.2252+/-0.0008(KTeV)+/-0.0021(ext), where the errors are from KTeV measurements and from external sources. We also use the measured branching fractions to determine the CP violation parameter |eta(+-)|=(2.228+/-0.005(KTeV)+/-0.009(ext))x10(-3).

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Search for the rare decay K(L)-->pi(0)e(+)e(-).

The KTeV/E799 experiment at Fermilab has searched for the rare kaon decay K(L)-->pi(0)e(+)e(-). This mode is expected to have a significant CP violating component. The measurement of its branching ratio could support the standard model or could indicate the existence of new physics. This Letter reports new results from the 1999-2000 data set. One event is observed with an expected background at 0.99+/-0.35 events. We set a limit on the branching ratio of 3.5x10(-10) at the 90% confidence level. Combining with the previous result based on the data set taken in 1997 yields the final KTeV result: BR(K(L)-->pi(0)e(+)e(-))<2.8x10(-10) at 90% C.L.

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Multiple sclerosis: etiological mechanisms and future directions.

Multiple sclerosis (MS) is a complex human autoimmune-type disease with a predominantly unknown etiology. Immunologic destruction of myelin basic protein (MBP) throughout the nervous system is the major pathology of multiple sclerosis. This review will attempt to update new information about basic mechanisms and therapeutic management of the disease. The significance of the structure of MBP is discussed with respect to the contribution of such structures to the disease process. A number of MBP peptides that serve as the immunodominant antigens in MS patients have been identified. These peptides have been studied in animal models for their antigenic characteristics and ability to induce disease. Evidence for genetic contributions is reviewed with multigenerational twin studies providing the best evidence for susceptible haplotypes. The role of microorganisms/viruses and environmental agents are discussed as potential etiological factors but are now thought to be of minor importance to the primary causal development of the disease. Of major consideration are immunological mechanisms that contribute to the development of autoimmunity. In particular, antigen expression, cytokine and leukocyte interactions, and regulatory T-cells are discussed. Particular attention is given to regulatory T-cells (Treg), which help balance/modulate other T-cells such as Th1 and Th2 cells, and how such Treg regulate autoimmunity is addressed. The importance of the role of Tregs is exemplified by the demonstration that administration of oral antigens can induce specific Tregs that counteract experimental autoimmune encephalomyelitis in animal models. The significance of animal studies to human multiple sclerosis is discussed. A potential role for natural antibodies and innate immune mechanisms to help provide resistance to disease development is also reviewed. Finally, a variety of therapeutic agents that have been and continue to be utilized for multiple sclerosis is reviewed. Trials with oral antigens, such as glatirmer acetate (copolymer 1) especially in combination with interferon-beta, have shown promise. Antibody therapy and bone marrow transplantation are also briefly discussed.

Animals↗

Measurements of the Decay KL-->e+ e- mu+ mu-.

The KTeV experiment at Fermilab has isolated a total of 132 events from the rare decay K(L)-->e+ e- mu+ mu-, with an estimated background of 0.8 events. The branching ratio of this mode is determined to be [2.69+/-0.24(stat)+/-0.12(syst)]x10(-9), with a radiative cutoff of M(2)(ee mu mu)/M(2)(K)>0.95. The first measurement using this mode of the parameter alpha from the D'Ambrosio-Isidori-Portolès (DIP) model of the K(L)gamma*gamma* vertex yields a result of -1.59+/-0.37, consistent with values obtained from other decay modes. Because of the limited statistics, no sensitivity is found to the DIP parameter beta. We use this decay mode to set limits on CP and lepton violation.

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Search for the KL-->pi 0 pi 0 e+e- decay in the KTeV experiment.

The recent discovery of a large CP violating asymmetry in KL-->pi+pi-e+e- mode has prompted us to seach for the associated KL-->pi 0 pi 0 e+e- decay mode in the KTeV-E799 experiment at Fermilab. In 2.7 x 10(11) K(L) decays, one candidate event has been observed with an expected background of 0.3 event, resulting in an upper limit for the KL-->pi 0 pi 0 e+e- branching ratio of 6.6 x 10(-9) at the 90% C.L.

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Radiative decay width measurements of neutral kaon excitations using the primakoff effect.

We use K(L)'s in the 100-200 GeV energy range to produce 147 candidate events of the axial vector pair K1(1270)-K1(1400) in the nuclear Coulomb field of a Pb target and determine the radiative widths Gamma(K1(1400)-->K0+gamma)=280.8+/-23.2(stat)+/-40.4(syst) keV and Gamma(K1(1270)-->K0+gamma)=73.2+/-6.1(stat)+/-28.3(syst) keV. These first measurements appear to be lower than the quark-model predictions. We also place upper limits on the radiative widths for K(*)(1410) and K(*)(2)(1430) and find that the latter is vanishingly small in accord with SU(3) invariance in the naive quark model.

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Measurement of the K(L) charge asymmetry.

We present a measurement of the charge asymmetry delta(L) in the mode K(L)-->pi(+/-)e(-/+)nu based on 298 x 10(6) analyzed decays. We measure a value of delta(L) = [3322+/-58(stat)+/-47(syst)]x10(-6), in good agreement with previous measurements and 2.4 times more precise than the current best published result. The result is used to place more stringent limits on CPT and DeltaS = DeltaQ violation in the neutral kaon system.

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First measurement of form factors of the decay Xi(0) --> Sigma(+)e(-)nu macro(e).

We present the first measurement of the form factor ratios g(1)/f(1) (direct axial vector to vector), g(2)/f(1) (second class current), and f(2)/f(1) (weak magnetism) for the decay Xi(0)-->Sigma(+)e(-)nu macro(e) using the KTeV (E799) beam line and detector at Fermilab. From the Sigma(+) polarization measured with the decay Sigma(+)-->p pi(0) and the e(-)-nu; correlation, we measure g(1)/f(1) to be 1.32+/-(0.21)(0.17)(stat)+/-0.05(syst), assuming the SU(3)(f) (flavor) values for g(2)/f(1) and f(2)/f(1). Our results are all consistent with exact SU(3)(f) symmetry.

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Branching ratio measurement of the decay K(L) --> e(+)e(-)mu(+)mu(-).

We have collected a 43 event sample of the decay K(L)-->e(+)e(-)mu(+)mu(-) with negligible backgrounds and measured its branching ratio to be (2.62+/-0.40+/-0.17)x10(-9). We see no evidence for CP violation in this decay. In addition, we set the 90% confidence upper limit on the combined branching ratios for the lepton flavor violating decays K(L)-->e(+/-)e(+/-)mu(-/+)mu(-/+) at B(K(L)-->e(+/-)e(+/-)mu(-/+)mu(-/+))< or =1.23x10(-10), assuming a uniform phase space distribution.

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Measurement of the branching ratio and form factor of K(L)-->mu(+)mu(-)gamma.

We report on the analysis of the rare decay K(L)-->mu(+)mu(-)gamma the 1997 data from the KTeV experiment at Fermilab. A total of 9327 candidate events are observed with 2.4% background, representing a factor of 40 increase in statistics over the current world sample. We find that B(K(L)-->mu(+)mu(-)gamma) = (3.62 +/- 0.04(stat) +/- 0.08(syst)) x 10(-7). The form factor parameter alpha(K*) is measured to be alpha(K*) = -0.160(+0.026)(-0.028). In addition, we make the first measurement of the parameter alpha from the D'Ambrosio-Isidori-Portolés form factor, finding alpha = -1.54 +/- 0.10. In that model, this alpha measurement limits the Cabibbo-Kobayashi-Maskawa parameter rho>-0.2.

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Measurements of the rare decay K(L) --> e(+)e(-)e(+)e(-).

We observe 441 K(L)-->e(+)e(-)e(+)e(-) candidate events with a background of 4.2 events and measure B(K(L)-->e(+)e(-)e(+)e(-)) = [3.72+/-0.18(stat)+/-0.23(syst)]x10(-8) in the KTeV/E799II experiment at Fermilab. Using the distribution of the angle between the planes of the e(+)e(-) pairs, we measure the CP parameters beta(CP) = -0.23+/-0.09(stat)+/-0.02(syst) and gamma(CP) = -0.09+/-0.09(stat)+/-0.02(syst). We also present the first detailed study of the e(+)e(-) invariant mass spectrum in this decay mode.

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Measurement of the branching ratio and asymmetry of the decay Xi degrees -->Sigma degrees gamma.

We have studied the rare weak radiative hyperon decay Xi degrees -->Sigma degrees gamma in the KTeV experiment at Fermilab. We have identified 4045 signal events over a background of 804 events. The dominant Xi degrees -->Lambdapi degrees decay, which was used for normalization, is the only important background source. An analysis of the acceptance of both modes yields a branching ratio of B(Xi degrees -->Sigma degrees gamma)/B(Xi degrees -->Lambdapi degrees ) = (3.34+/-0.05+/-0.09)x10(-3). By analyzing the final state decay distributions, we have also determined that the Sigma degrees emission asymmetry parameter for this decay is alpha(XiSigma) = -0.63+/-0.09.

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Study of the K(0)(L) --> pi(+)pi(-)gamma Direct Emission Vertex.

We have performed studies of the K(0)(L)-->pi(+)pi(-)gamma direct emission ( DE) and inner Bremsstrahlung ( IB) vertices, based on data collected by KTeV during the 1996 Fermilab fixed target run. We find a(1)/a(2) = -0.737+/-0.034 GeV2 for the DE form-factor parameter in the rho-propagator parametrization, and report on fits of the form factor to linear and quadratic functions as well. We concurrently measure gamma(K(0)(L)-->pi(+)pi(-)gamma,E(*)(gamma)>20 MeV)/gamma(K(0)(L)-->pi(+)pi(-)) = (20.8+/-0.3)x10(-3), and a K(0)(L)-->pi(+)pi(-)gamma DE/(DE+IB) branching ratio of 0.683+/-0.011.

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Search for the decay KL --> pi(0)e+e-.

We report on a search for the decay KL-->pi(0)e+e- carried out by the KTeV/E799 experiment at Fermilab. This decay is expected to have a significant CP violating contribution and the measurement of its branching ratio could support the Cabibbo-Kobayashi-Maskawa mechanism for CP violation or could point to new physics. Two events were observed in the 1997 data with an expected background of 1.06+/-0.41 events, and we set an upper limit B(KL-->pi(0)e+e-)<5.1 x 10(-10) at the 90% confidence level.

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Clinical experience with recombinant follicle-stimulating hormone (FSH) and urinary FSH: a retrospective case- controlled analysis.

OBJECTIVE: To compare the efficacy and efficiency of recombinant FSH (rFSH) and urinary FSH (uFSH). DESIGN: Retrospective case controlled analysis. SETTING: An assisted reproduction unit at a university center. PATIENT(S): 1388 patients undergoing long protocol in vitro fertilization/embryo transfer (IVF-ET) using buserelin acetate from day 2 of the cycle and either rFSH (follitropin beta) (n = 694) or uFSH (n = 694) with equal number of ampules started (rFSH: 50 IU, uFSH: 75 IU). INTERVENTION(S): Patients were included in the two groups of treatment after matching for similarity in age and type of treatment (IVF or intracytoplasmic sperm injection). MAIN OUTCOME MEASURE(S): Total dose of FSH, ovarian response, and IVF outcome. RESULT(S): Patients who received uFSH experienced a shorter period of stimulation, and a higher number of oocytes were collected. The total FSH used was lower in the rFSH group, and they required a lower FSH dose per oocyte retrieved. The implantation and pregnancy rates were similar between the uFSH and rFSH groups. In both groups implantation and pregnancy rates were higher when intracytoplasmic sperm injection was performed as compared with IVF. CONCLUSION(S): The implantation and pregnancy rates are similar when either rFSH or uFSH is used (when compared on an ampule-to-ampule basis, rFSH: 50 IU, and uFSH: 75 IU). However, a significantly lower total FSH dose was used in the rFSH group with a lower FSH dose per oocyte collected.

Adult↗

Circulating natural IgM antibodies and their corresponding human cord blood cell-derived Mabs specifically combat the Tat protein of HIV.

OBJECTIVE: IgM antibodies reactive with each of two specifically defined sequences of HIV Tat protein have been identified in sera from both HIV(+) and normal (HIV(-)) humans. This study was designed to confirm that those antibodies are innate immune factors capable of restriction of specific mechanisms of HIV pathogenicity attributed to the Tat protein. MATERIALS AND METHODS: Antibody-secreting hybridomas were generated from human cord blood cells and processed for monoclonality. Those Mabs reactive with each of the sequences of Tat with which the circulating antibodies are reactive were isolated and their heavy and light chains identified and DNA sequenced. Pools of IgM isolated from blood of normal humans, chimpanzees, rhesus macaques, and mice and the isolated Tat reactive Mabs were tested for capacity to inhibit Tat-induced human T-cell apoptosis. RESULTS: Human and chimpanzee IgM pools, as well as the human cord blood cell-derived Mabs, showed a definite capacity to inhibit the Tat-induced apoptosis, while the IgM pools of rhesus macaques or of mice did not. CONCLUSIONS: These studies establish that the circulating IgM of normal humans include innate antibodies capable of restriction of HIV Tat-induced pathogenesis. That capacity is shared by chimpanzee IgM but not by IgM of other primates or of mice. The identification of those human circulating antibodies as innate is confirmed by the display of similar epitopic identity and apoptosis inhibition capacity by Mabs from human cord blood cell hybridomas. Thus, the arsenal of human cord blood cell hybridomas provides a resource by which, specifically, the potential therapeutic role of the identified HIV Tat-reactive Mabs and, broadly, the fundamental role of innate antibodies in infection control may be explored.

Adult↗