J/Psi Suppression in Heavy Ion Collisions at the CERN SPS

We reexamine the production of J/Psi and other charmonium states for a variety of target-projectile choices at the SPS. For this study we use a newly constructed cascade code LUCIFER II, which yields acceptable descriptions of both hard and soft processes, specifically Drell-Yan and hidden charm production, and soft energy loss and meson production, at the SPS. Glauber calculations of other authors are redone, and compared directly to the cascade results. The modeling of the charmonium states differs from that of earlier workers in its unified treatment of the hidden charm meson spectrum, which is introduced from the outset as a set of coupled states. The result is a description of the NA38 and NA50 data in terms of a conventional hadronic picture. The apparently anomalous suppression found in the most massive Pb+Pb system arises from three sources: destruction in the initial nucleon-nucleon cascade, use of coupled channels to exploit the larger breakup in the less bound Chi and Psi' states, and comover interaction in the final low energy phase.Comment: 36 pages (15 figures

Exotic ρ±ρ0\rho^\pm\rho^0 state photoproduction

It is shown that the list of unusual mesons planned for a careful study in photoproduction can be extended by the exotic states $X^\pm(1600)$ with $I^G(J ^{PC})=2^+(2^{++})$ which should be looked for in the $\rho^\pm\rho^0$ decay channels in the reactions $\gamma N\to\rho^\pm\rho^0N$ and $\gamma N\to\rho^\pm \rho^0\Delta$. The full classification of the $\rho^\pm\rho^0$ states by their quantum numbers is presented. A simple model for the spin structure of the $\gamma p\to f_2(1270)p$, $\gamma p\to a^0_2(1320)p$, and $\gamma N\to X^\pm (N, \Delta)$ reaction amplitudes is formulated and the tentative estimates of the corresponding cross sections at the incident photon energy $E_\gamma\approx 6$ GeV are obtained: $\sigma(\gamma p\to f_2(1270)p)\approx0.12$ $\mu$b, $\sigma(\gamma p\to a^0_2(1320)p)\approx0.25$ $\mu$b, $\sigma(\gamma N\to X^\pm N\to\rho^\pm\rho^0N)\approx0.018$ $\mu$b, and $\sigma(\gamma p\to X^-\Delta^{++ }\to\rho^-\rho^0\Delta^{++})\approx0.031$ $\mu$b. The problem of the $X^\pm$ signal extraction from the natural background due to the other $\pi^\pm\pi^0 \pi^+\pi^-$ production channels is discussed. In particular the estimates are presented for the $\gamma p\to h_1(1170)\pi^+n$, $\gamma p\to\rho'^{+}n\to \pi^+\pi^0\pi^+\pi^-n$, and $\gamma p\to\omega\rho^0p$ reaction cross sections. Our main conclusion is that the search for the exotic $X^\pm(2^+(2^{++}))$ states is quite feasible at JEFLAB facility. The expected yield of the $\gamma N\to X^\pm N\to\rho^\pm\rho^0N$ events in a 30-day run at the 100% detection efficiency approximates $2.8\times10^6$ events.Comment: 19 pages, revtex, 1 figure in postscipt, some comments and references added, a few minor typos corrected, to be published in Phys. Rev.

Some psychosocial and cultural factors in the Arab-Israeli conflict: a review of the literature

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66497/2/10.1177_002200277201600210.pd

A de novo paradigm for male infertility

Genetics of Male Infertility Initiative (GEMINI) consortium: Donald F. Conrad, Liina Nagirnaja, Kenneth I. Aston, Douglas T. Carrell, James M. Hotaling, Timothy G. Jenkins, Rob McLachlan, Moira K. O’Bryan, Peter N. Schlegel, Michael L. Eisenberg, Jay I. Sandlow, Emily S. Jungheim, Kenan R. Omurtag, Alexandra M. Lopes, Susana Seixas, Filipa Carvalho, Susana Fernandes, Alberto Barros, João Gonçalves, Iris Caetano, Graça Pinto, Sónia Correia, Maris Laan, Margus Punab, Ewa Rajpert-De Meyts, Niels Jørgensen, Kristian Almstrup, Csilla G. Krausz & Keith A. Jarvi.De novo mutations are known to play a prominent role in sporadic disorders with reduced fitness. We hypothesize that de novo mutations play an important role in severe male infertility and explain a portion of the genetic causes of this understudied disorder. To test this hypothesis, we utilize trio-based exome sequencing in a cohort of 185 infertile males and their unaffected parents. Following a systematic analysis, 29 of 145 rare (MAF < 0.1%) protein-altering de novo mutations are classified as possibly causative of the male infertility phenotype. We observed a significant enrichment of loss-of-function de novo mutations in loss-of-function-intolerant genes (p-value = 1.00 × 10−5) in infertile men compared to controls. Additionally, we detected a significant increase in predicted pathogenic de novo missense mutations affecting missense-intolerant genes (p-value = 5.01 × 10−4) in contrast to predicted benign de novo mutations. One gene we identify, RBM5, is an essential regulator of male germ cell pre-mRNA splicing and has been previously implicated in male infertility in mice. In a follow-up study, 6 rare pathogenic missense mutations affecting this gene are observed in a cohort of 2,506 infertile patients, whilst we find no such mutations in a cohort of 5,784 fertile men (p-value = 0.03). Our results provide evidence for the role of de novo mutations in severe male infertility and point to new candidate genes affecting fertility.This project was funded by The Netherlands Organization for Scientific Research (918-15-667) to J.A.V. as well as an Investigator Award in Science from the Wellcome Trust (209451) to J.A.V. a grant from the Catherine van Tussenbroek Foundation to M.S.O. a grant from MERCK to R.S. a UUKi Rutherford Fund Fellowship awarded to B.J.H. and the German Research Foundation Clinical Research Unit “Male Germ Cells” (DFG, CRU326) to C.F. and F.T. This project was also supported in part by funding from the Australian National Health and Medical Research Council (APP1120356) to M.K.O.B., by grants from the National Institutes of Health of the United States of America (R01HD078641 to D.F.C. and K.I.A., P50HD096723 to D.F.C.) and from the Biotechnology and Biological Sciences Research Council (BB/S008039/1) to D.J.E.info:eu-repo/semantics/publishedVersio