Experimental Signature of Medium Modifications for rho and omega Mesons in the 12 GeV p + A Reactions

The invariant mass spectra of e+e- pairs produced in 12-GeV proton-induced nuclear reactions are measured at the KEK Proton-Synchrotron. On the low-mass side of the omega meson peak, a significant enhancement over the known hadronic sources has been observed. The mass spectra, including the excess, are well reproduced by a model that takes into account the density dependence of the vector meson mass modification, as theoretically predicted.Comment: 4 pages, 3 figures, Version accepted for Physical Review Lette

Nuclear mass number dependence of inclusive production of omega and phi mesons in 12 GeV p + A collisions

The inclusive production of omega and phi mesons is studied in the backward region of the interaction of 12 GeV protons with polyethylene, carbon, and copper targets. The mesons are measured in e^+ e^- decay channels. The production cross sections of the mesons are presented as functions of rapidity y and transverse momentum p_T. The nuclear mass number dependences (A dependences) are found to be A^{0.710 +/- 0.021(stat) +/- 0.037(syst)} for omega mesons and A^{0.937 +/- 0.049(stat) +/- 0.018(syst)} for phi mesons in the region of 0.9 < y < 1.7 and p_T < 0.75 GeV/c.Comment: 12 pages, 8 figures; typos adde

Nuclear-matter modification of decay widths in the ϕ→e+e−\phi \to e^{+}e^{-} and ϕ→K+K−\phi \to K^{+}K^{-} channels

The invariant mass spectra of $\phi \to K^{+}K^{-}$ are measured in 12 GeV $p+A$ reactions in order to search for the in-medium modification of $\phi$ mesons. The observed $K^{+}K^{-}$ spectra are well reproduced by the relativistic Breit-Wigner function with a combinatorial background shape in three $\beta\gamma$ regions between 1.0 and 3.5. The nuclear mass-number dependence of the yields of the $K^{+}K^{-}$ decay channel is compared to the simultaneously measured $e^{+}e^{-}$ decay channel for carbon and copper targets. We parameterize the production yields as $\sigma (A) = \sigma_0 \times A^\alpha$ and obtain $\alpha_{\phi\to K^+K^-} - \alpha_{\phi\to e^+e^-}$ to be 0.14 $\pm$ 0.12. Limits are obtained for the partial decay widths of $\phi$ mesons in nuclear matter.Comment: 5 pages, 4 figure

Cardiac involvement in Beagle-based canine X-linked muscular dystrophy in Japan (CXMD(J)): electrocardiographic, echocardiographic, and morphologic studies

BACKGROUND: Cardiac mortality in Duchenne muscular dystrophy (DMD) has recently become important, because risk of respiratory failure has been reduced due to widespread use of the respirator. The cardiac involvement is characterized by distinctive electrocardiographic abnormalities or dilated cardiomyopathy, but the pathogenesis has remained obscure. In research on DMD, Golden retriever-based muscular dystrophy (GRMD) has attracted much attention as an animal model because it resembles DMD, but GRMD is very difficult to maintain because of their severe phenotypes. We therefore established a line of dogs with Beagle-based canine X-linked muscular dystrophy in Japan (CXMD(J)) and examined the cardiac involvement. METHODS: The cardiac phenotypes of eight CXMD(J )and four normal male dogs 2 to 21 months of age were evaluated using electrocardiography, echocardiography, and histopathological examinations. RESULTS: Increases in the heart rate and decreases in PQ interval compared to a normal littermate were detected in two littermate CXMD(J )dogs at 15 months of age or older. Distinct deep Q-waves and increase in Q/R ratios in leads II, III, and aVF were detected by 6–7 months of age in all CXMD(J )dogs. In the echocardiogram, one of eight of CXMD(J )dogs showed a hyperechoic lesion in the left ventricular posterior wall at 5 months of age, but the rest had not by 6–7 months of age. The left ventricular function in the echocardiogram indicated no abnormality in all CXMD(J )dogs by 6–7 months of age. Histopathology revealed myocardial fibrosis, especially in the left ventricular posterobasal wall, in three of eight CXMD(J )dogs by 21 months of age. CONCLUSION: Cardiac involvement in CXMD(J )dogs is milder and has slower progression than that described in GRMD dogs. The distinct deep Q-waves have been ascribed to myocardial fibrosis in the posterobasal region of the left ventricle, but our data showed that they precede the lesion on echocardiogram and histopathology. These findings imply that studies of CXMD(J )may reveal not only another causative mechanism of the deep Q-waves but also more information on the pathogenesis in the dystrophin-deficient heart

Genome-wide association of multiple complex traits in outbred mice by ultra low-coverage sequencing

The authors wish to acknowledge excellent technical assistance from A. Kurioka, L. Swadling, C. de Lara, J. Ussher, R. Townsend, S. Lionikaite, A.S. Lionikiene, R. Wolswinkel and I. van der Made. We would like to thank T.M. Keane and A.G. Doran for their help in annotating variants and adding the FVB/NJ strain to the MGP. We thank the High-Throughput Genomics Group at the Wellcome Trust Centre for Human Genetics and the Wellcome Trust Sanger Institute for the generation of the sequencing data. This work was funded by Wellcome Trust grant 090532/Z/09/Z (J.F.). Primary phenotyping of the mice was supported by the Mary Lyon Centre and Mammalian Genetics Unit (Medical Research Council, UK Hub grant G0900747 91070 and Medical Research Council, UK grant MC U142684172). D.A.B. acknowledges support from NIH R01AR056280. The sleep work was supported by the state of Vaud (Switzerland) and the Swiss National Science Foundation (SNF 14694 and 136201 to P.F.). The ECG work was supported by the Netherlands CardioVascular Research Initiative (Dutch Heart Foundation, Dutch Federation of University Medical Centres, Netherlands Organization for Health Research and Development and the Royal Netherlands Academy of Sciences) PREDICT project, InterUniversity Cardiology Institute of the Netherlands (ICIN; 061.02; C.A.R. and C.R.B.). N.C. is supported by the Agency of Science, Technology and Research (A*STAR) Graduate Academy. R.W.D. is supported by a grant from the Wellcome Trust (097308/Z/11/Z).Peer reviewedPostprin