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

Observation of Bs0→J/ψf0(980)B_s^0\to J/\psi f_0(980) and Evidence for Bs0→J/ψf0(1370)B_s^0\to J/\psi f_0(1370)

We report the first observation of $B_s^0\to J/\psi f_0(980)$ and first evidence for $B_s^0\to J/\psi f_0(1370)$, which are CP eigenstate decay modes. These results are obtained from $121.4\;\mathrm{fb}^{-1}$ of data collected at the $\Upsilon(5S)$ resonance with the Belle detector at the KEKB $e^+e^-$ collider. We measure the branching fractions $\mathcal{B}(B_s^0\to J/\psi f_0(980);f_0(980)\to\pi^+\pi^-)=(1.16^{+0.31}_{-0.19}(\mathrm{stat.})^{+0.15}_{-0.17}(\mathrm{syst.})^{+0.26}_{-0.18}(N_{B_s^{(*)}\bar B_s^{(*)}})) \times 10^{-4}$ with a significance of $8.4\sigma$, and $\mathcal{B}(B_s^0\to J/\psi f_0(1370);f_0(1370)\to\pi^+\pi^-)=(0.34^{+0.11}_{-0.14}(\mathrm{stat.})^{+0.03}_{-0.02}(\mathrm{syst.})^{+0.08}_{-0.05}(N_{B_s^{(*)}\bar B_s^{(*)}})) \times 10^{-4}$ with a significance of $4.2\sigma$. The last error listed is due to uncertainty in the number of produced $B_s^{(*)}\bar B_s^{(*)}$ pairs.Comment: 5 pages, 2 figures, 2 tables, published in PR

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

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

Functional characterization of a multi-cancer risk locus on chr5p15.33 reveals regulation of TERT by ZNF148

Genome wide association studies (GWAS) have mapped multiple independent cancer susceptibility loci to chr5p15.33. Here, we show that fine-mapping of pancreatic and testicular cancer GWAS within one of these loci (Region 2 in CLPTM1L) focuses the signal to nine highly correlated SNPs. Of these, rs36115365-C associated with increased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity. Transcriptional gene silencing of this regulatory element repressed TERT expression in an allele-specific manner. Proteomic analysis identifies allele-preferred binding of Zinc finger protein 148 (ZNF148) to rs36115365-C, further supported by binding of purified recombinant ZNF148. Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length. Our results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele

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