Flow coefficients v_{n} for n=2, 3, 4, characterizing the anisotropic collective flow in Au+Au collisions at sqrt[s_{NN}]=200  GeV, are measured relative to event planes Ψ_{n}, determined at large rapidity. We report v_{n} as a function of transverse momentum and collision centrality, and study the correlations among the event planes of different order n. The v_{n} are well described by hydrodynamic models which employ a Glauber Monte Carlo initial state geometry with fluctuations, providing additional constraining power on the interplay between initial conditions and the effects of viscosity as the system evolves. This new constraint can serve to improve the precision of the extracted shear viscosity to entropy density ratio η/s.

Back-to-back hadron pair yields in d+Au and p+p collisions at √s(NN)=200 GeV were measured with the PHENIX detector at the Relativistic Heavy Ion Collider. Rapidity separated hadron pairs were detected with the trigger hadron at pseudorapidity |η|<0.35 and the associated hadron at forward rapidity (deuteron direction, 3.0<η<3.8). Pairs were also detected with both hadrons measured at forward rapidity; in this case, the yield of back-to-back hadron pairs in d+Au collisions with small impact parameters is observed to be suppressed by a factor of 10 relative to p+p collisions. The kinematics of these pairs is expected to probe partons in the Au nucleus with a low fraction x of the nucleon momenta, where the gluon densities rise sharply. The observed suppression as a function of nuclear thickness, p(T), and η points to cold nuclear matter effects arising at high parton densities.

We present measurements of J/ψ yields in d+Au collisions at sqrt[s(NN)]=200  GeV recorded by the PHENIX experiment and compare them with yields in p+p collisions at the same energy per nucleon-nucleon collision. The measurements cover a large kinematic range in J/ψ rapidity (-2.2<y<2.4) with high statistical precision and are compared with two theoretical models: one with nuclear shadowing combined with final state breakup and one with coherent gluon saturation effects. In order to remove model dependent systematic uncertainties we also compare the data to a simple geometric model. The forward rapidity data are inconsistent with nuclear modifications that are linear or exponential in the density weighted longitudinal thickness, such as those from the final state breakup of the bound state.

Large parity-violating longitudinal single-spin asymmetries A(L)(e+)=-0.86(-0.14)(+0.30) and A(L)(e-)= 0.88(-0.71)(+0.12) are observed for inclusive high transverse momentum electrons and positrons in polarized p+p collisions at a center-of-mass energy of sqrt[s]= 500 GeV with the PHENIX detector at RHIC. These e± come mainly from the decay of W± and Z0 bosons, and their asymmetries directly demonstrate parity violation in the couplings of the W± to the light quarks. The observed electron and positron yields were used to estimate W± boson production cross sections for the e± channels of σ(pp → W+ X) × BR(W+ → e+ ν(e))= 144.1 ± 21.2(stat)(-10.3)(+3.4)(syst) ± 21.6(norm)  pb, and σ(pp → W- X) × BR(W- → e- ν[over ¯](e))= 31.7 ± 12.1(stat)(-8.2)(+10.1)(syst) ± 4.8(norm)  pb.

HASH(0x29a4e8f0)

Glaucoma is a distinct neuropathy characterized by the chronic and progressive death of retinal ganglion cells (RGCs). The etiology of RGC death remains unknown. Risk factors for glaucomatous RGC death are elevated intraocular pressure and glial production of tumor necrosis factor-alpha (TNF-α). Previously, the authors showed that glaucoma causes a rapid upregulation of a neurotrophin receptor truncated isoform lacking the kinase domain, TrkC.T1, in retina. Here they examined the biological role of TrkC.T1 during glaucoma progression. Rat and mouse models of chronic ocular hypertension were used. Immunofluorescence Western blot analysis and in situ mRNA hybridization were used to identify cells upregulating TrkC.T1. A genetic model of engineered mice lacking TrkC.T1 (TrkC.T1(-/-)) was used to validate a role for this receptor in glaucoma. Pharmacologic studies were conducted to evaluate intravitreal delivery of agonists or antagonists of TrkC.T1, compared with controls, during glaucoma. Surviving RGCs were quantified by retrograde-labeling techniques. Production of neurotoxic TNF-α and α2 macroglobulin were quantified. TrkC.T1 was upregulated in retinal glia, with a pattern similar to that of TNF-α. TrkC.T1(-/-) mice had normal retinas. However, during experimental glaucoma, TrkC.T1(-/-) mice had lower rates of RGC death and produced less TNF-α than wild-type littermates. In rats with glaucoma, the pharmacologic use of TrkC antagonists delayed RGC death and reduced the production of retinal TNF-α. TrkC.T1 is implicated in glaucomatous RGC death through the control of glial TNF-α production. Overall, the data point to a paracrine mechanism whereby elevated intraocular pressure upregulated glial TrkC.T1 expression in glia; TrkC.T1 controlled glial TNF-α production, and TNF-α caused RGC death.

The production of e;{+}e;{-} pairs for m_{e;{+}e;{-}}<0.3 GeV/c;{2} and 1<p_{T}<5 GeV/c is measured in p+p and Au+Au collisions at sqrt[s_{NN}]=200 GeV. An enhanced yield above hadronic sources is observed. Treating the excess as photon internal conversions, the invariant yield of direct photons is deduced. In central Au+Au collisions, the excess of the direct photon yield over p+p is exponential in transverse momentum, with an inverse slope T=221+/-19;{stat}+/-19;{syst} MeV. Hydrodynamical models with initial temperatures ranging from T_{init} approximately 300-600 MeV at times of approximately 0.6-0.15 fm/c after the collision are in qualitative agreement with the data. Lattice QCD predicts a phase transition to quark gluon plasma at approximately 170 MeV.

Bose-Einstein correlations of charged kaons are used to probe Au+Au collisions at sqrt[s_{NN}]=200 GeV and are compared to charged pion probes, which have a larger hadronic scattering cross section. Three-dimensional Gaussian source radii are extracted, along with a one-dimensional kaon emission source function. The centrality dependences of the three Gaussian radii are well described by a single linear function of N_{part};{1/3} with a zero intercept. Imaging analysis shows a deviation from a Gaussian tail at r greater, similar10 fm, although the bulk emission at lower radius is well described by a Gaussian. The presence of a non-Gaussian tail in the kaon source reaffirms that the particle emission region in a heavy-ion collision is extended, and that similar measurements with pions are not solely due to the decay of long-lived resonances.

The momentum distribution of electrons from semileptonic decays of charm and bottom quarks for midrapidity |y|<0.35 in p+p collisions at square root of s=200 GeV is measured by the PHENIX experiment at the Relativistic Heavy Ion Collider over the transverse momentum range 2<pT<7 GeV/c. The ratio of the yield of electrons from bottom to that from charm is presented. The ratio is determined using partial D/D-->e(+/-)K(-/+)X (K unidentified) reconstruction. It is found that the yield of electrons from bottom becomes significant above 4 GeV/c in pT. A fixed-order-plus-next-to-leading-log perturbative quantum chromodynamics calculation agrees with the data within the theoretical and experimental uncertainties. The extracted total bottom production cross section at this energy is sigma(bb)=3.2(-1.1)(+1.2)(stat)(-1.3)(+1.4)(syst)mub.

A new method suitable for single nucleotide polymorphism (SNP) detection using differential oligonucleotide probe extension has been developed. Sulfur-linked laser-cleavable trityl labels are implemented in this protocol. The method is based on mass spectrometry and utilizes a single surface for affinity purification of extended probes and matrix-independent desorption-ionization of the cleavable labels. The usefulness of this method for SNP genotyping is demonstrated.