Longitudinal spin transfer to Lambda and Lambda hyperons in polarized proton-proton collisions at s=200 GeV

The longitudinal spin transfer, D(LL), from high energy polarized protons to Lambda and Lambda hyperons has been measured for the first time in proton-proton collisions at s=200 GeV with the STAR detector at the Relativistic Heavy Ion Collider. The measurements cover pseudorapidity, eta, in the range |eta|< 1.2 and transverse momenta, p(T), up to 4 GeV/c. The longitudinal spin transfer is found to be D(LL)=-0.03 +/- 0.13(stat)+/- 0.04(syst) for inclusive Lambda and D(LL)=-0.12 +/- 0.08(stat)+/- 0.03(syst) for inclusive Lambda hyperons with <>=0.5 and << p(T)>>=3.7 GeV/c. The dependence on eta and p(T) is presented.

Growth of Long Range Forward-Backward Multiplicity Correlations with Centrality in Au plus Au Collisions at root s(NN)=200 GeV

Forward-backward multiplicity correlation strengths have been measured with the STAR detector for Au + Au and p + p collisions at root s(NN) = 200 GeV. Strong short- and long-range correlations (LRC) are seen in central Au + Au collisions. The magnitude of these correlations decrease with decreasing centrality until only short-range correlations are observed in peripheral Au + Au collisions. Both the dual parton model (DPM) and the color glass condensate (CGC) predict the existence of the long-range correlations. In the DPM, the fluctuation in the number of elementary (parton) inelastic collisions produces the LRC. In the CGC, longitudinal color flux tubes generate the LRC. The data are in qualitative agreement with the predictions of the DPM and indicate the presence of multiple parton interactions.

Neutral pion production in Au plus Au collisions at root s(NN)=200 GeV

The results of midrapidity (0 < y < 0.8) neutral pion spectra over an extended transverse momentum range (1 < p(T) < 12 GeV/c) in root s(NN) = 200 GeV Au + Au collisions, measured by the STAR experiment, are presented. The neutral pions are reconstructed from photons measured either by the STAR Barrel Electro-Magnetic Calorimeter or by the Time Projection Chamber via tracking of conversion electron-positron pairs. Our measurements are compared to previously published pi(+/-) and pi(0) results. The nuclear modification factors R(CP) and R(AA) of pi(0) are also presented as a function of p(T). In the most central Au + Au collisions, the binary collision scaled pi(0) yield at high p(T) is suppressed by a factor of about 5 compared to the expectation from the yield of p + p collisions. Such a large suppression is in agreement with previous observations for light quark mesons and is consistent with the scenario that partons suffer considerable energy loss in the dense medium formed in central nucleus-nucleus collisions at the Relativistic Heavy Ion Collider.

J/psi production at high transverse momenta in p plus p and Cu plus Cu collisions at root s(NN)=200 GeV

The STAR Collaboration at the Relativistic Heavy Ion Collider presents measurements of J/psi e(+) e(-) at midrapidity and high transverse momentum (pT > 5 GeV/c) in p + p and central Cu + Cu collisions at root s(NN) = 200 GeV. The inclusive J/psi production cross section for Cu + Cu collisions is found to be consistent at high p(T) with the binary collision-scaled cross section for p + p collisions. At a confidence level of 97%, this is in contrast to a suppression of J/psi production observed at lower p(T). Azimuthal correlations of J/psi with charged hadrons in p + p collisions provide an estimate of the contribution of B-hadron decays to J/psi production of 13% +/- 5%.

K/pi Fluctuations at Relativistic Energies

We report K/pi fluctuations from Au+Au collisions at s(NN)=19.6, 62.4, 130, and 200 GeV using the STAR detector at the Relativistic Heavy Ion Collider. K/pi fluctuations in central collisions show little dependence on incident energy and are on the same order as those from NA49 at the Super Proton Synchrotron in central Pb+Pb collisions at s(NN)=12.3 and 17.3 GeV. We report results for the collision centrality dependence of K/pi fluctuations and results for charge-separated fluctuations. We observe that the K/pi fluctuations scale with the charged particle multiplicity density.

Pion interferometry in Au plus Au and Cu plus Cu collisions at s(NN)=62.4 and 200 GeV

We present a systematic analysis of two-pion interferometry in Au+Au collisions at s(NN)=62.4 GeV and Cu+Cu collisions at s(NN)=62.4 and 200 GeV using the STAR detector at the Relativistic Heavy Ion Collider (RHIC). The multiplicity and transverse momentum dependences of the extracted correlation lengths (radii) are studied. The scaling with charged particle multiplicity of the apparent system volume at final interaction is studied for the RHIC energy domain. The multiplicity scaling of the measured correlation radii is found to be independent of colliding system and collision energy.

Measurement of D* mesons in jets from p plus p collisions at root s=200 GeV

We report the measurement of charged D* mesons in inclusive jets produced in proton-proton collisions at a center-of-mass energy root s = 200 GeV with the STAR experiment at the Relativistic Heavy Ion Collider. For D* mesons with fractional momenta 0.2< z< 0.5 in inclusive jets with 11.5 GeV mean transverse energy, the production rate is found to be N(D*(+) + D*(-))/N(jet) = 0.015 +/- 0.008(stat) +/- 0.007(sys). This rate is consistent with perturbative QCD evaluation of gluon splitting into a pair of charm quarks and subsequent hadronization.

Observation of Two-Source Interference in the Photoproduction Reaction AuAu -> AuAu rho(0)

In ultraperipheral relativistic heavy-ion collisions, a photon from the electromagnetic field of one nucleus can fluctuate to a quark-antiquark pair and scatter from the other nucleus, emerging as a rho(0). The rho(0) production occurs in two well-separated (median impact parameters of 20 and 40 F for the cases considered here) nuclei, so the system forms a two-source interferometer. At low transverse momenta, the two amplitudes interfere destructively, suppressing rho(0) production. Since the rho(0) decays before the production amplitudes from the two sources can overlap, the two-pion system can only be described with an entangled nonlocal wave function, and is thus an example of the Einstein-Podolsky-Rosen paradox. We observe this suppression in 200 GeV per nucleon-pair gold-gold collisions. The interference is 87%+/- 5%(stat.)+/- 8%(syst.) of the expected level. This translates into a limit on decoherence due to wave function collapse or other factors of 23% at the 90% confidence level.

Hadronic resonance production in d+Au collisions at root S(NN) = 200 GeV measured at the BNL Relativistic Heavy Ion Collider

We present the first measurements of the rho(770)(0),K(*)(892),Delta(1232)(++),Sigma(1385), and Lambda(1520) resonances in d+Au collisions at s(NN)=200 GeV, reconstructed via their hadronic decay channels using the STAR detector (the solenoidal tracker at the BNL Relativistic Heavy Ion Collider). The masses and widths of these resonances are studied as a function of transverse momentum p(T). We observe that the resonance spectra follow a generalized scaling law with the transverse mass m(T). The < p(T)> of resonances in minimum bias collisions are compared with the < p(T)> of pi,K, and p. The rho(0)/pi(-),K(*)/K(-),Delta(++)/p,Sigma(1385)/Lambda, and Lambda(1520)/Lambda ratios in d+Au collisions are compared with the measurements in minimum bias p+p interactions, where we observe that both measurements are comparable. The nuclear modification factors (R(dAu)) of the rho(0),K(*), and Sigma(*) scale with the number of binary collisions (N(bin)) for p(T)> 1.2 GeV/c.

Pion femtoscopy in p plus p collisions at root s=200 GeV

The STAR Collaboration at the BNL Relativistic Heavy Ion Collider has measured two-pion correlation functions from p + p collisions at root s = 200 GeV. Spatial scales are extracted via a femtoscopic analysis of the correlations, though this analysis is complicated by the presence of strong nonfemtoscopic effects. Our results are put into the context of the world data set of femtoscopy in hadron-hadron collisions. We present the first direct comparison of femtoscopy in p + p and heavy ion collisions, under identical analysis and detector conditions.

Salicylates dilate blood vessels through inhibiting PYK2-mediated RhoA/Rho-kinase activation

Aims Compared with other non-steroid anti-inflammatory drugs (NSAIDs), aspirin is not correlated to hypertension. It has been shown that aspirin has unique vasodilator action in vivo, offering an explanation for the unique blood pressure effect of aspirin. In the present study, we investigate the mechanism whereby salicylates (aspirin and sodium salicylate) dilate blood vessels. Methods and results Rat aortic or mesenteric arterial rings were used to test the vascular effect of salicylates and other NSAIDs. RhoA translocation and the phosphorylation of MYPT1, the regulatory subunit of myosin light chain phosphatase, were measured by western blot, as evidenced for RhoA/Rho-kinase activation. Salicylates, but not other NSAIDs, relaxed contraction induced by most tested constrictors except for calyculin A, indicating that RhoA/Rho-kinase-mediated calcium sensitization is involved. The involvement of RhoA/Rho kinase in vasodilation by salicylates was confirmed by measurements of RhoA translocation and MYPT1 phosphorylation. The calculated half maximal inhibitory concentration (IC(50)) of vasodilation was apparently higher than that of cyclooxygenase inhibition, but comparable to that of proline-rich tyrosine kinase 2 (PYK2) inhibition. Over-expression of PYK2 induced RhoA translocation and MYPT1 phosphorylation, and these effects were markedly inhibited by sodium salicylate treatment. Consistent with the ex vitro vascular effects, sodium salicylate acutely decreased blood pressure in spontaneous hypertensive rats but not in Wistar Kyoto rats. Conclusion Salicylates dilate blood vessels through inhibiting PYK2-mediated RhoA/Rho-kinase activation and thus lower blood pressure.

TNF-alpha Infusion Impairs Corpora Cavernosa Reactivity

Introduction. Erectile dysfunction (ED), as well as cardiovascular diseases (CVDs), is associated with endothelial dysfunction and increased levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha). Aim. We hypothesized that increased TNF-alpha levels impair cavernosal function. Methods. In vitro organ bath studies were used to measure cavernosal reactivity in mice infused with vehicle or TNF-alpha-(220 ng/kg/min) for 14 days. Gene expression of nitric oxide synthase isoforms was evaluated by real-time polymerase chain reaction. Results. Cavernosal strips from the TNF-alpha-infused mice displayed decreased nonadrenergic-noncholinergic (NANC)-induced relaxation (59.4 +/- 6.2 vs. control: 76.2 +/- 4.7; 16 Hz) compared with the control animals. These responses were associated with decreased gene expression of eNOS and nNOS (P < 0.05). Sympathetic-mediated, as well as phenylephrine (PE)-induced, contractile responses (PE-induced contraction; 1.32 +/- 0.06 vs. control: 0.9 +/- 0.09, mN) were increased in cavernosal strips from TNF-alpha-infused mice. Additionally, infusion of TNF-alpha increased cavernosal responses to endothelin-1 and endothelin receptor A subtype (ET(A)) receptor expression (P < 0.05) and slightly decreased tumor necrosis factor-alpha receptor 1 (TNFRI) expression (P=0.063). Conclusion. Corpora cavernosa from TNF-alpha-infused mice display increased contractile responses and decreased NANC nerve-mediated relaxation associated with decreased eNOS and nNOS gene expression. There changes may trigger ED and indicate that TNF-alpha plays a detrimental role in erectile function. Blockade of TNF-alpha actions may represent an alternative therapeutic approach for ED, especially in pathologic conditions associated with increased levels of this cytokine. Carneiro FS, Zemse S, Giachini FRC, Carneiro ZN, Lima W, Clinton Webb R, and Tostes RC. TNF-alpha infusion impairs corpora cavernosa reactivity. J Sex Med 2009;6(suppl 3):311-319.

TNF-alpha Knockout Mice Have Increased Corpora Cavernosa Relaxation

Erectile dysfunction is considered an early clinical manifestation of vascular disease and an independent risk factor for cardiovascular events associated with endothelial dysfunction and increased levels of pro-inflammatory cytokines. Tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine, suppresses endothelial nitric oxide synthase (eNOS) expression. Considering that nitric oxide (NO) is of critical importance in penile erection, we hypothesized that blockade of TNF-alpha actions would increase cavernosal smooth muscle relaxation. In vitro organ bath studies were used to measure cavernosal reactivity in wild type and TNF-alpha knockout (TNF-alpha KO) mice and NOS expression was evaluated by western blot. In addition, spontaneous erections (in vivo) were evaluated by videomonitoring the animals (30 minutes). Collagen and elastin expression were evaluated by Masson trichrome and Verhoff-van Gieson stain reaction, respectively. Corpora cavernosa from TNF-alpha KO mice exhibited increased NO-dependent relaxation, which was associated with increased eNOS and neuronal NOS (nNOS) cavernosal expression. Cavernosal strips from TNF-alpha KO mice displayed increased endothelium-dependent (97.4 +/- 5.3 vs. Control: 76.3 +/- 6.3, %) and nonadrenergic-noncholinergic (93.3 +/- 3.0 vs. Control: 67.5 +/- 16.0; 16 Hz) relaxation compared to control animals. These responses were associated with increased protein expression of eNOS and nNOS (P < 0.05). Sympathetic-mediated (0.69 +/- 0.16 vs. Control: 1.22 +/- 0.22; 16 Hz) as well as phenylephrine-induced contractile responses (1.6 +/- 0.1 vs. Control: 2.5 +/- 0.1, mN) were attenuated in cavernosal strips from TNF-alpha KO mice. Additionally, corpora cavernosa from TNF-alpha KO mice displayed increased collagen and elastin expression. In vivo experiments demonstrated that TNF-alpha KO mice display increased number of spontaneous erections. Corpora cavernosa from TNF-alpha KO mice display alterations that favor penile tumescence, indicating that TNF-alpha plays a detrimental role in erectile function. A key role for TNF-alpha in mediating endothelial dysfunction in ED is markedly relevant since we now have access to anti-TNF-alpha therapies. Carneiro FS, Sturgis LC, Giachini FRC, Carneiro ZN, Lima VV, Wynne BM, Martin SS, Brands MW, Tostes RC, and Webb RC. TNF-alpha knockout mice have increased corpora cavernosa relaxation. J Sex Med 2009;6:115-125.

Activation of the ET-1/ETA Pathway Contributes to Erectile Dysfunction Associated with Mineralocorticoid Hypertension

The cavernosal tissue is highly responsive to endothelin-1 (ET-1), and penile smooth muscle cells not only respond to but also synthesize ET-1. Considering that ET-1 is directly involved in end-organ damage in salt-sensitive forms of hypertension, we hypothesized that activation of the ET-1/ET(A) receptor pathway contributes to erectile dysfunction (ED) associated with mineralocorticoid hypertension. Wistar rats were uninephrectomized and submitted to deoxycorticosterone acetate (DOCA)-salt treatment for 5 weeks. Control (Uni [uninephrectomized control]) animals were uninephrectomized and given tap water. Uni and DOCA-salt rats were simultaneously treated with vehicle or atrasentan (ET(A) receptor antagonist, 5 mg/Kg/day). Cavernosal reactivity to ET-1, phenylephrine (PE), ET(B) receptor agonist (IRL-1620) and electric field stimulation (EFS) were evaluated in vitro. Expression of ROCK alpha, ROCK beta, myosin phosphatase target subunit 1 (MYPT-1), and extracellular signal-regulated kinase 1/2 (ERK 1/2) were evaluated by western blot analysis. ET-1 and ET(A) receptor mRNA expression was evaluated by real-time reverse-transcriptase polymerase chain reaction. Voltage-dependent increase in intracavernosal pressure/mean arterial pressure (ICP/MAP) was used to evaluate erectile function in vivo. ET(A) receptor blockade prevents DOCA-salt-associated ED. Cavernosal strips from DOCA-salt rats displayed augmented preproET-1 expression, increased contractile responses to ET-1 and decreased relaxation to IRL-1620. Contractile responses induced by EFS and PE were enhanced in cavernosal tissues from DOCA-salt hypertensive rats. These functional changes were associated with increased activation of the RhoA/Rho-kinase and ERK 1/2 pathways. Treatment of rats with atrasentan completely prevented changes in cavernosal reactivity in DOCA-salt rats and restored the decreased ICP/MAP, completely preventing ED in DOCA-salt rats. Activation of the ET-1/ET(A) pathway contributes to mineralocorticoid hypertension-associated ED. ET(A) receptor blockade may represent an alternative therapeutic approach for ED associated with salt-sensitive hypertension and in pathological conditions where increased levels of ET-1 are present. Carneiro FS, Nunes KP, Giachini FRC, Lima VV, Carneiro ZN, Nogueira EF, Leite R, Ergul A, Rainey WE, Webb RC, and Tostes RC. Activation of the ET-1/ETA pathway contributes to erectile dysfunction associated with mineralocorticoid hypertension. J Sex Med **;**:**-**.

Murine and rat cavernosal responses to endothelin-1 and urotensin-II Vasoactive Peptide Symposium

Endothelin-1 (ET-1) and urotensin-II (U-II) are the most potent constrictors of human vessels. Although the cavernosal tissue is highly responsive to ET-1, no information exists on the effects of U-II on cavernosal function. The aim of this study was to characterize ET-1 and U-II responses in corpora cavernosa from rats and mice. Male Wistar rats and C57/BL6 mice were used at 13 weeks. Cumulative concentration-response curves to ET-1, U-II, and IRL-1620, an ET(B) agonist, were performed. ET-1 increased force generation in cavernosal strips from mice and rats, but no response to U-II was observed in the presence or absence of N(omega)-nitro-L-arginine methyl ester (L-NAME), or in strips prestimulated with 20 mM KCI. IRL-1620 did not induce cavernosal contraction even in presence of L-NAME, but induced a cavernosal relaxation that was greater in rats than mice. No relaxation responses to U-II were observed in cavernosal strips precontracted with phenylephrine. mRNA expression of ET-1, ET(A), ET(B), and U-II receptors, but not U-II was observed in cavernosal strips. ET-1, via ET(A) receptors activation, causes contractile responses in cavernosal strips from rats and mice, whereas ET(B) receptor activation produces relaxation. Although the cavernosal tissue expresses U-II receptors, U-II does not induce contractile responses in corpora cavernosa from mice or rats. J Am Soc Hypertens 2008;2(6): 439-447. Published by Elsevier Inc. on behalf of the American Society of Hypertension.