372 research outputs found

    A search for the decay modes B+/- to h+/- tau l

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    We present a search for the lepton flavor violating decay modes B+/- to h+/- tau l (h= K,pi; l= e,mu) using the BaBar data sample, which corresponds to 472 million BBbar pairs. The search uses events where one B meson is fully reconstructed in one of several hadronic final states. Using the momenta of the reconstructed B, h, and l candidates, we are able to fully determine the tau four-momentum. The resulting tau candidate mass is our main discriminant against combinatorial background. We see no evidence for B+/- to h+/- tau l decays and set a 90% confidence level upper limit on each branching fraction at the level of a few times 10^-5.Comment: 15 pages, 7 figures, submitted to Phys. Rev.

    Evidence for an excess of B -> D(*) Tau Nu decays

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    Based on the full BaBar data sample, we report improved measurements of the ratios R(D(*)) = B(B -> D(*) Tau Nu)/B(B -> D(*) l Nu), where l is either e or mu. These ratios are sensitive to new physics contributions in the form of a charged Higgs boson. We measure R(D) = 0.440 +- 0.058 +- 0.042 and R(D*) = 0.332 +- 0.024 +- 0.018, which exceed the Standard Model expectations by 2.0 sigma and 2.7 sigma, respectively. Taken together, our results disagree with these expectations at the 3.4 sigma level. This excess cannot be explained by a charged Higgs boson in the type II two-Higgs-doublet model. We also report the observation of the decay B -> D Tau Nu, with a significance of 6.8 sigma.Comment: Expanded section on systematics, text corrections, improved the format of Figure 2 and included the effect of the change of the Tau polarization due to the charged Higg

    Search for the decay modes D^0 → e^+e^-, D^0 → μ^+μ^-, and D^0 → e^±μ∓

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    We present searches for the rare decay modes D^0→e^+e^-, D^0→μ^+μ^-, and D^0→e^±μ^∓ in continuum e^+e^-→cc events recorded by the BABAR detector in a data sample that corresponds to an integrated luminosity of 468  fb^(-1). These decays are highly Glashow–Iliopoulos–Maiani suppressed but may be enhanced in several extensions of the standard model. Our observed event yields are consistent with the expected backgrounds. An excess is seen in the D^0→μ^+μ^- channel, although the observed yield is consistent with an upward background fluctuation at the 5% level. Using the Feldman–Cousins method, we set the following 90% confidence level intervals on the branching fractions: B(D^0→e^+e^-)<1.7×10^(-7), B(D^0→μ^+μ^-) within [0.6,8.1]×10^(-7), and B(D^0→e^±μ^∓)<3.3×10^(-7)

    Study of the reaction e^{+}e^{-} -->J/psi\pi^{+}\pi^{-} via initial-state radiation at BaBar

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    We study the process e+eJ/ψπ+πe^+e^-\to J/\psi\pi^{+}\pi^{-} with initial-state-radiation events produced at the PEP-II asymmetric-energy collider. The data were recorded with the BaBar detector at center-of-mass energies 10.58 and 10.54 GeV, and correspond to an integrated luminosity of 454 fb1\mathrm{fb^{-1}}. We investigate the J/ψπ+πJ/\psi \pi^{+}\pi^{-} mass distribution in the region from 3.5 to 5.5 GeV/c2\mathrm{GeV/c^{2}}. Below 3.7 GeV/c2\mathrm{GeV/c^{2}} the ψ(2S)\psi(2S) signal dominates, and above 4 GeV/c2\mathrm{GeV/c^{2}} there is a significant peak due to the Y(4260). A fit to the data in the range 3.74 -- 5.50 GeV/c2\mathrm{GeV/c^{2}} yields a mass value 4244±54244 \pm 5 (stat) ±4 \pm 4 (syst)MeV/c2\mathrm{MeV/c^{2}} and a width value 11415+16114 ^{+16}_{-15} (stat)±7 \pm 7(syst)MeV\mathrm{MeV} for this state. We do not confirm the report from the Belle collaboration of a broad structure at 4.01 GeV/c2\mathrm{GeV/c^{2}}. In addition, we investigate the π+π\pi^{+}\pi^{-} system which results from Y(4260) decay

    Experimental Mycobacterium bovis infection in three white rhinoceroses (Ceratotherium simum):Susceptibility, clinical and anatomical pathology

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    Tuberculosis caused by Mycobacterium bovis is endemic in the African buffalo (Syncerus caffer) population in the Kruger National Park and other conservation areas in South Africa. The disease has been diagnosed in a total of 21 free ranging or semi-free ranging wildlife species in the country with highly variable presentations in terms of clinical signs as well as severity and distribution of tuberculous lesions. Most species are spillover or dead-end hosts without significant role in the epidemiology of the disease. White rhinoceroses (Ceratotherium simum) are translocated from the Kruger National Park in substantial numbers every year and a clear understanding of their risk to manifest overt tuberculosis disease and to serve as source of infection to other species is required. We report the findings of experimental infection of three white rhinoceroses with a moderately low dose of a virulent field isolate of Mycobacterium bovis. None of the animals developed clinical signs or disseminated disease. The susceptibility of the white rhinoceros to bovine tuberculosis was confirmed by successful experimental infection based on the ante mortem isolation of M. bovis from the respiratory tract of one rhinoceros, the presence of acid-fast organisms and necrotizing granulomatous lesions in the tracheobronchial lymph nodes and the detection of M. bovis genetic material by PCR in the lungs of two animals

    The genesis of cerebellar interneurons and the prevention of neural DNA damage require XRCC1

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    Defective responses to DNA single strand breaks underlie various neurodegenerative diseases. However, the exact role of this repair pathway during the development and maintenance of the nervous system is unclear. Using murine neural-specific inactivation of Xrcc1, a factor that is critical for the repair of DNA single strand breaks, we found a profound neuropathology that is characterized by the loss of cerebellar interneurons. This cell loss was linked to p53-dependent cell cycle arrest and occurred as interneuron progenitors commenced differentiation. Loss of Xrcc1 also led to the persistence of DNA strand breaks throughout the nervous system and abnormal hippocampal function. Collectively, these data detail the in vivo link between DNA single strand break repair and neurogenesis and highlight the diverse consequences of specific types of genotoxic stress in the nervous system

    A Single-Step Sequencing Method for the Identification of Mycobacterium tuberculosis Complex Species

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    The Mycobacterium tuberculosis complex (MTC) comprises several closely related species responsible for strictly human and zoonotic tuberculosis. Some of the species are restricted to Africa and were responsible for the high prevalence of tuberculosis. However, their identification at species level is difficult and expansive. Accurate species identification of all members is warranted in order to distinguish between strict human and zoonotic tuberculosis, to trace source exposure during epidemiological studies, and for the appropriate treatment of patients. In this paper, the Exact Tandem Repeat D (ETR-D) intergenic region was investigated in order to distinguish MTC species. The ETR-D sequencing unambiguously identified MTC species type strain except M. pinnipedii and M. microti, and the results agreed with phenotypic and molecular identification. This finding offers a new tool for the rapid and accurate identification of MTC species in a single sequencing reaction, replacing the current time-consuming polyphasic approach. Its use could assist public health interventions and aid in the control of zoonotic transmission in African countries, and could be of particular interest with the current emergence of multidrug-resistant and extended-resistance isolates

    Wnt signaling in triple-negative breast cancer

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    Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC. We review the complex molecular nature of TNBC and the emerging therapies that are currently under investigation for the treatment of this disease
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