200 research outputs found
Observation of and Evidence for
We report the first observation of and first
evidence for , which are CP eigenstate decay modes.
These results are obtained from of data collected at
the resonance with the Belle detector at the KEKB
collider. We measure the branching fractions with a significance of , and
with a significance of . The last error
listed is due to uncertainty in the number of produced pairs.Comment: 5 pages, 2 figures, 2 tables, published in PR
Belle II Technical Design Report
The Belle detector at the KEKB electron-positron collider has collected
almost 1 billion Y(4S) events in its decade of operation. Super-KEKB, an
upgrade of KEKB is under construction, to increase the luminosity by two orders
of magnitude during a three-year shutdown, with an ultimate goal of 8E35 /cm^2
/s luminosity. To exploit the increased luminosity, an upgrade of the Belle
detector has been proposed. A new international collaboration Belle-II, is
being formed. The Technical Design Report presents physics motivation, basic
methods of the accelerator upgrade, as well as key improvements of the
detector.Comment: Edited by: Z. Dole\v{z}al and S. Un
Total disc replacement for chronic back pain in the presence of disc degeneration
Scientific Assessment and Innovation in Neurosurgical Treatment Strategie
Evidence for the Suppressed Decay B- -> DK-, D -> K+pi-
The suppressed decay chain B- -> DK-, D -> K+pi-, where D indicates a anti-D0
or D0 state, provides important information on the CP-violating angle phi_3. We
measure the ratio R_{DK} of the decay rates to the favored mode B- -> DK-, D ->
K-pi+ to be R_{DK} = [1.63^{+0.44}_{-0.41}(stat)^{+0.07}_{-0.13}(syst)] x
10^{-2}, which indicates the first evidence of the signal with a significance
of 4.1sigma. We also measure the asymmetry A_{DK} between the charge-conjugate
decays to be A_{DK} = -0.39^{+0.26}_{-0.28}(stat)^{+0.04}_{-0.03}(syst). The
results are based on the full 772 x 10^6 B anti-B pair data sample collected at
the Upsilon(4S) resonance with the Belle detector.Comment: 6 pages, 2 figures, 2 tables, accepted by Physical Review Letter
O movimento ortodôntico não induz reabsorção cervical externa ou O movimento ortodôntico não altera cor, volume e nem induz inflamação gengival
Nesse trabalho, procurou-se explicar - anatômica e funcionalmente - como se estrutura e se organiza a região cervical dos dentes, para fundamentar os seguintes questionamentos: 1) Por que ocorre Reabsorção Cervical Externa na dentição humana?; 2) Por que na gengivite e na periodontite não se tem Reabsorção Cervical Externa?; 3) Por que depois do traumatismo dentário e da clareação interna pode ocorrer a Reabsorção Cervical Externa?; 4) Por que o movimento ortodôntico não altera a cor e o volume gengival durante o tratamento?; 5) Por que o movimento ortodôntico não induz Reabsorção Cervical Externa, mesmo sabendo-se que a região cervical pode ser muito exigida? A existência de antígenos sequestrados na dentina, a presença de janelas de dentina na região cervical de todos os dentes, a reação do epitélio juncional e a distribuição dos vasos sanguíneos gengivais podem justificar por que a Reabsorção Cervical Externa não ocorre e nem a cor e o volume gengival são alterados no movimento ortodôntico.This study sought to explain, both anatomically and functionally, how the cervical region of human teeth is structured and organized in order to address the following questions: 1) Why does External Cervical Resorption (ECR) occur in human dentition? 2) Why is there no ECR in gingivitis and periodontitis? 3) Why ECR can occur after dental trauma and internal bleaching? 4) Why does orthodontic movement not change the gingival color and volume during treatment? 5) Why does orthodontic movement not induce ECR although it is common knowledge that the cervical region can undergo much stress? The existence of sequestered antigens in the dentin, the presence of dentin gaps in the cervical region of all teeth, the reaction of the junctional epithelium and the gingival distribution of blood vessels may explain why ECR does not occur, nor do gingival color and volume change when teeth are orthodontically moved
The Physics of the B Factories
This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C
Proteomic Profile of Reversible Protein Oxidation Using PROP, Purification of Reversibly Oxidized Proteins
Signal transduction pathways that are modulated by thiol oxidation events are beginning to be uncovered, but these discoveries are limited by the availability of relatively few analytical methods to examine protein oxidation compared to other signaling events such as protein phosphorylation. We report here the coupling of PROP, a method to purify reversibly oxidized proteins, with the proteomic identification of the purified mixture using mass spectrometry. A gene ontology (GO), KEGG enrichment and Wikipathways analysis of the identified proteins indicated a significant enrichment in proteins associated with both translation and mRNA splicing. This methodology also enabled the identification of some of the specific cysteine residue targets within identified proteins that are reversibly oxidized by hydrogen peroxide treatment of intact cells. From these identifications, we determined a potential consensus sequence motif associated with oxidized cysteine residues. Furthermore, because we identified proteins and specific sites of oxidation from both abundant proteins and from far less abundant signaling proteins (e.g. hepatoma derived growth factor, prostaglandin E synthase 3), the results suggest that the PROP procedure was efficient. Thus, this PROP-proteomics methodology offers a sensitive means to identify biologically relevant redox signaling events that occur within intact cells
Antipsychotic-Induced Metabolic and Cardiovascular Side Effects in Schizophrenia: A Novel Mechanistic Hypothesis
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