Charged and strange hadron elliptic flow in Cu plus Cu collisions at root s(NN)=62.4 and 200 GeV

We present the results of an elliptic flow, v(2), analysis of Cu + Cu collisions recorded with the solenoidal tracker detector (STAR) at the BNL Relativistic Heavy Ion Collider at root s(NN) = 62.4 and 200 GeV. Elliptic flow as a function of transverse momentum, v(2)(p(T)), is reported for different collision centralities for charged hadrons h(+/-) and strangeness-ontaining hadrons K(S)(0), Lambda, Xi, and phi in the midrapidity region vertical bar eta vertical bar < 1.0. Significant reduction in systematic uncertainty of the measurement due to nonflow effects has been achieved by correlating particles at midrapidity, vertical bar eta vertical bar < 1.0, with those at forward rapidity, 2.5 < vertical bar eta vertical bar < 4.0. We also present azimuthal correlations in p + p collisions at root s = 200 GeV to help in estimating nonflow effects. To study the system-size dependence of elliptic flow, we present a detailed comparison with previously published results from Au + Au collisions at root s(NN) = 200 GeV. We observe that v(2)(p(T)) of strange hadrons has similar scaling properties as were first observed in Au + Au collisions, that is, (i) at low transverse momenta, p(T) < 2 GeV/c, v(2) scales with transverse kinetic energy, m(T) - m, and (ii) at intermediate p(T), 2 < p(T) < 4 GeV/c, it scales with the number of constituent quarks, n(q.) We have found that ideal hydrodynamic calculations fail to reproduce the centrality dependence of v(2)(p(T)) for K(S)(0) and Lambda. Eccentricity scaled v(2) values, v(2)/epsilon, are larger in more central collisions, suggesting stronger collective flow develops in more central collisions. The comparison with Au + Au collisions, which go further in density, shows that v(2)/epsilon depends on the system size, that is, the number of participants N(part). This indicates that the ideal hydrodynamic limit is not reached in Cu + Cu collisions, presumably because the assumption of thermalization is not attained.

Spectrum and Prevalence of FP/TMEM127 Gene Mutations in Pheochromocytomas and Paragangliomas

Context Pheochromocytomas and paragangliomas are genetically heterogeneous neural crest-derived neoplasms. We recently identified germline mutations of the novel transmembrane-encoding gene FP/TMEM127 in familial and sporadic pheochromocytomas consistent with a tumor suppressor effect. Objectives To examine the prevalence and spectrum of FP/TMEM127 mutations in pheochromocytomas and paragangliomas and to test the effect of mutations in vitro. Design, Setting, and Participants We sequenced the FP/TMEM127 gene in 990 individuals with pheochromocytomas and/or paragangliomas, including 898 previously unreported cases without mutations in other susceptibility genes from 8 independent worldwide referral centers between January 2009 and June 2010. A multiplex polymerase chain reaction-based method was developed to screen for large gene deletions in 545 of these samples. Confocal microscopy of 5 transfected mutant proteins was used to determine their subcellular localization. Main Outcome Measures The frequency and type of FP/TMEM127 mutation or deletion was assessed and correlated with clinical variables; the subcellular localization of 5 overexpressed mutants was compared with wild-type FP/TMEM127 protein. Results We identified 19 potentially pathogenic FP/TMEM127 germline mutations in 20 independent families, but no large deletions were detected. All mutation carriers had adrenal tumors, including 7 bilateral (P=2.7 x 10(-4)) and/or with familial disease (5 of 20 samples; P=.005). The median age at disease onset in the FP/TMEM127 mutation group was similar to that of patients without a mutation (41.5 vs 45 years, respectively; P=.54). The most common presentation was that of a single benign adrenal tumor in patients older than 40 years. Malignancy was seen in 1 mutation carrier (5%). Expression of 5 novel FP/TMEM127 mutations in cell lines revealed diffuse localization of the mutant proteins in contrast with the discrete multiorganelle distribution of wild-type TMEM127. Conclusions Germline mutations of FP/TMEM127 were associated with pheochromocytoma but not paraganglioma and occured in an age group frequently excluded from genetic screening algorithms. Disease-associated mutations disrupt intracellular distribution of the FP/TMEM127 protein. JAMA. 2010;304(23):2611-2619 www.jama.com