Study of Cronin effect and nuclear modification of strange particles in d-Au and Au-Au collisions at 200 GeV in PHENIX

Effects of strangeness on nuclear modification in d-Au and Au-Au collisions at 200 GeV are studied, in order to quantify the effects of quark content and mass. Measurements of ratios of the yields in central collisions to the yields in peripheral collisions are performed for lambda baryon and phi meson. Found results show little dependence of particle suppression or enhancement on mass and strange content, but rather prominent difference in nuclear modification between mesons and baryons.Comment: 4 pages, 4 figures, proceedings of the Seventeenth International Conference on Ultra-Relativistic Nucleus-Nucleus Collisions (Quark Matter 2004

PHENIX Highlights

Recent highlights of measurements by the PHENIX experiment at RHIC are presented.Comment: 8 pages, 9 figures. Talk at Quark Matter 200

Human neuroblastoma cells with acquired resistance to the p53 activator RITA retain functional p53 and sensitivity to other p53 activating agents

Adaptation of wild-type p53 expressing UKF-NB-3 cancer cells to the murine double minute 2 inhibitor nutlin-3 causes de novo p53 mutations at high frequency (13/20) and multi-drug resistance. Here, we show that the same cells respond very differently when adapted to RITA, a drug that, like nutlin-3, also disrupts the p53/Mdm2 interaction. All of the 11 UKF-NB-3 sub-lines adapted to RITA that we established retained functional wild-type p53 although RITA induced a substantial p53 response. Moreover, all RITA-adapted cell lines remained sensitive to nutlin-3, whereas only five out of 10 nutlin-3-adapted cell lines retained their sensitivity to RITA. In addition, repeated adaptation of the RITA-adapted sub-line UKF-NB-3rRITA10 μM to nutlin-3 resulted in p53 mutations. The RITA-adapted UKF-NB-3 sub-lines displayed no or less pronounced resistance to vincristine, cisplatin, and irradiation than nutlin-3-adapted UKF-NB-3 sub-lines. Furthermore, adaptation to RITA was associated with fewer changes at the expression level of antiapoptotic factors than observed with adaptation to nutlin-3. Transcriptomic analyses indicated the RITA-adapted sub-lines to be more similar at the gene expression level to the parental UKF-NB-3 cells than nutlin-3-adapted UKF-NB-3 sub-lines, which correlates with the observed chemotherapy and irradiation sensitivity phenotypes. In conclusion, RITA-adapted cells retain functional p53, remain sensitive to nutlin-3, and display a less pronounced resistance phenotype than nutlin-3-adapted cells

Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

Drug resistance to chemotherapy is often associated with increased malignancy in neuroblastoma (NB). In pursuit of alternative treatments for chemoresistant tumour cells, we tested the response of multidrug-resistant SKNSH and of vincristine (VCR)-, doxorubicin (DOX)-, or cisplatin (CDDP)-resistant UKF-NB-2, UKF-NB-3 or UKF-NB-6 NB tumour cell lines to valproic acid (VPA), a differentiation inducer currently in clinical trials. Drug resistance caused elevated NB adhesion (UKF-NB-2VCR, UKF-NB-2DOX, UKF-NB-2CDDP, UKF-NB-3VCR, UKF-NB-3CDDP, UKF-NB-6VCR, UKF-NB-6CDDP) to an endothelial cell monolayer, accompanied by downregulation of the adhesion receptor neural cell adhesion molecule (NCAM). Based on the UKF-NB-3 model, N-myc proteins were enhanced in UKF-NB-3VCR and UKF-NB-3CDDP, compared to the drug naïve controls. p73 was diminished, whereas the p73 isoform deltaNp73 was upregulated in UKF-NB-3VCR and UKF-NB-3CDDP. Valproic acid blocked adhesion of UKF-NB-3VCR and UKF-NB-3CDDP, but not of UKF-NB-3DOX, and induced the upregulation of NCAM surface expression, NCAM protein content and NCAM coding mRNA. Valproic acid diminished N-myc and enhanced p73 protein level, coupled with downregulation of deltaNp73 in UKF-NB-3VCR and UKF-NB-3CDDP. Valproic acid also reverted enhanced adhesion properties of drug-resistant UKF-NB-2, UKF-NB-6 and SKNSH cells, and therefore may provide an alternative approach to the treatment of drug-resistant NB by blocking invasive processes

Identified Hadron Spectra From pp, dA and AA collisions

The experimental data for identified hadron spectra from pp,d+A and AA collisions are reviewed. Three regions with different dominant production mechanisms are considered: soft region (pt <2 GeV/c) - with large degree of collectivity and thermalization, hard particle production which exhibits jet-quenching in Au+Au collisions at RHIC and intermediate region (2 < pt <5 GeV/c) with distinct baryon dynamics. Cronin effect, nuclear modification factors and jet-like correlations are studied with the goal of understanding the baryon dynamics at RHIC.Comment: 8 pages, 9 figures, Plenary talk at Quark Matter 2004, Oakland, Jan 11-1

Invariant-mass and fractional-energy dependence of inclusive production of di-hadrons in e+e−e^+e^- annihilation at s=\sqrt{s}= 10.58 GeV

The inclusive cross sections for di-hadrons of charged pions and kaons ($e^+e^- \rightarrow hhX$) in electron-positron annihilation are reported. They are obtained as a function of the total fractional energy and invariant mass for any di-hadron combination in the same hemisphere as defined by the thrust event-shape variable and its axis. Since same-hemisphere di-hadrons can be assumed to originate predominantly from the same initial parton, di-hadron fragmentation functions are probed. These di-hadron fragmentation functions are needed as an unpolarized baseline in order to quantitatively understand related spin-dependent measurements in other processes and to apply them to the extraction of quark transversity distribution functions in the nucleon. The di-hadron cross sections are obtained from a $655\,{\rm fb}^{-1}$ data sample collected at or near the $\Upsilon(4S)$ resonance with the Belle detector at the KEKB asymmetric-energy $e^+ e^-$ collider.Comment: 21 pages, 18 figures plus 25 figures in supplemental material, submitted to PR

The comparison of cytotoxicity of the anticancer drugs doxorubicin and ellipticine to human neuroblastoma cells

Ellipticine is an antineoplastic agent, whose mode of action is based mainly on DNA intercalation, inhibition of topoisomerase II and formation of covalent DNA adducts mediated by cytochromes P450 and peroxidases. Here, the cytotoxicity of ellipticine to human neuroblastoma derived cell lines IMR-32 and UKF-NB-4 was investigated. Treatment of neuroblastoma cells with ellipticine was compared with that of these cancer cells with doxorubicin. The toxicity of ellipticine was essentially the same as that of doxorubicin to UKF-NB-4 cells, but doxorubicin is much more effective to inhibit the growth of the IMR-32 cell line than ellipticine. Hypoxic conditions used for the cell cultivation resulted in a decrease in ellipticine and/or doxorubicin toxicity to IMR-32 and UKF-NB-4 neuroblastoma cells

Studies of charmed strange baryons in the ΛD\Lambda D final state at Belle

We report the discovery of $\Xi_{c}(3055)^{0}$, observed by its decay into the final state $\Lambda D^{0}$, and present the first observation and evidence of the decays of $\Xi_c(3055)^{+}$ and $\Xi_c(3080)^{+}$ into $\Lambda D^{+}$. We also perform a combined analysis of the $\Lambda D^{+}$ with the $\Sigma_{c}^{++}K^{-}$ and $\Sigma_{c}^{\ast ++}K^{-}$ decay modes to measure the ratios of branching fractions, masses and widths with improved accuracy. We measure the ratios of branching fractions ${\cal B}(\Xi_{c}(3055)^{+} \to \Lambda D^{+})/{\cal B}(\Xi_{c}(3055)^{+} \to \Sigma_{c}^{++}K^{-})=5.09\pm1.01\pm0.76$, ${\cal B}(\Xi_{c}(3080)^{+} \to \Lambda D^{+})/{\cal B}(\Xi_{c}(3080)^{+} \to \Sigma_{c}^{++}K^{-})=1.29\pm0.30\pm0.15$, and ${\cal B}(\Xi_{c}(3080)^{+} \to \Sigma_{c}^{\ast ++}K^{-})/{\cal B}(\Xi_{c}(3080)^{+} \to \Sigma_{c}^{++}K^{-})=1.07\pm0.27\pm0.01$, where the uncertainties are statistical and systematic. The analysis is performed using a 980 fb$^{-1}$ data sample collected with the Belle detector at the KEKB asymmetric-energy $e^{+}e^{-}$ collider.Comment: Submitted to PR

Measurement of eta_c(1S), eta_c(2S) and non-resonant eta' pi+ pi- production via two-photon collisions

We report the measurement of gamma gamma to eta_c(1S), eta_c(2S) to eta' pi+ pi- with eta' decays to gamma rho and eta pi+ pi- using 941 fb^{-1} of data collected with the Belle detector at the KEKB asymmetric-energy e+e- collider. The eta_c(1S) mass and width are measured to be M = [2984.6\pm0.7 (stat.)\pm2.2 (syst.)] MeV/c^{2} and \Gamma = [30.8^{+2.3}_{-2.2}~(stat.) \pm 2.5~(syst.)] MeV, respectively. First observation of eta_c(2S) to eta' pi+ pi- with a significance of 5.5sigma including systematic error is obtained, and the eta_c(2S) mass is measured to be M = [3635.1\pm3.7~(stat.)\pm2.9~(syst.)] MeV/c^{2}. The products of the two-photon decay width and branching fraction (B) of decays to eta'pi+ pi- are determined to be \Gamma_{gamma gamma}B = [65.4\pm2.6~(stat.)\pm6.9~(syst.)] eV for eta_c(1S) and [5.6^{+1.2}_{-1.1}~(stat.)\pm1.1~(syst.)] eV for eta_c(2S). A new decay mode for the eta_c(1S) to eta'f_0(2080) with f_0(2080) to pi+ pi- is observed with a statistical significance of 20sigma. The f_0(2080) mass and width are determined to be M = [2083^{+63}_{-66}~(stat.)\pm 32~(syst.)] MeV/c^{2} and \Gamma = [178^{+60}_{-178}~(stat.) \pm 55~(syst.)] MeV. The cross sections for gamma gamma to eta' pi+ pi- and eta'f_{2}(1270) are measured for the first time.Comment: 19 pages, 14 figure

Inclusive study of bottomonium production in association with an η\eta meson in e+e−e^+e^- annihilations near Υ(5S)\Upsilon(5S)

We study bottomonium production in association with an $\eta$ meson in $e^+e^-$ annihilations near the $\Upsilon(5S)$, at a center of mass energy of $\sqrt{s}=10.866\,$GeV. The results are based on the $121.4\,$fb$^{-1}$ data sample collected by the Belle experiment at the asymmetric energy KEKB collider. Only the $\eta$ meson is reconstructed and the missing-mass spectrum of $\eta$ candidates is investigated. We observe the $e^+e^-\to\eta\Upsilon_J(1D)$ process and find evidence for the $e^+e^-\to\eta\Upsilon(2S)$ process, while no significant signals of $\Upsilon(1S)$, $h_b(1P)$, nor $h_b(2P)$ are found. Cross sections for the studied processes are reported.Comment: Submitted to EPJ-