Heavy quarkonium: progress, puzzles, and opportunities

A golden age for heavy quarkonium physics dawned a decade ago, initiated by the confluence of exciting advances in quantum chromodynamics (QCD) and an explosion of related experimental activity. The early years of this period were chronicled in the Quarkonium Working Group (QWG) CERN Yellow Report (YR) in 2004, which presented a comprehensive review of the status of the field at that time and provided specific recommendations for further progress. However, the broad spectrum of subsequent breakthroughs, surprises, and continuing puzzles could only be partially anticipated. Since the release of the YR, the BESII program concluded only to give birth to BESIII; the $B$-factories and CLEO-c flourished; quarkonium production and polarization measurements at HERA and the Tevatron matured; and heavy-ion collisions at RHIC have opened a window on the deconfinement regime. All these experiments leave legacies of quality, precision, and unsolved mysteries for quarkonium physics, and therefore beg for continuing investigations. The plethora of newly-found quarkonium-like states unleashed a flood of theoretical investigations into new forms of matter such as quark-gluon hybrids, mesonic molecules, and tetraquarks. Measurements of the spectroscopy, decays, production, and in-medium behavior of c\bar{c}, b\bar{b}, and b\bar{c} bound states have been shown to validate some theoretical approaches to QCD and highlight lack of quantitative success for others. The intriguing details of quarkonium suppression in heavy-ion collisions that have emerged from RHIC have elevated the importance of separating hot- and cold-nuclear-matter effects in quark-gluon plasma studies. This review systematically addresses all these matters and concludes by prioritizing directions for ongoing and future efforts.Comment: 182 pages, 112 figures. Editors: N. Brambilla, S. Eidelman, B. K. Heltsley, R. Vogt. Section Coordinators: G. T. Bodwin, E. Eichten, A. D. Frawley, A. B. Meyer, R. E. Mitchell, V. Papadimitriou, P. Petreczky, A. A. Petrov, P. Robbe, A. Vair

Improved Measurement of Branching Fractions for pipi Transitions among Upsilon(nS)States

Using samples of (5.93 +/- 0.10) x 10^6 Upsilon(3S) decays and (9.11 +/- 0.14) x 10^6 Upsilon(2S) decays collected with the CLEO detector, we report improved measurements of the branching fractions for the following five transitions: B(Upsilon(3S)-->Upsilon(1S) pi^+ pi^-) = (4.46 +/- 0.01 +/- 0.13)%, B(Upsilon(2S)-->Upsilon(1S) pi^+ pi^-) = (18.02 +/- 0.02 +/- 0.61)%, B(Upsilon(3S)-->Upsilon(1S) pi^0 pi^0) = (2.24 +/- 0.09 +/- 0.11)%, B(Upsilon(2S)-->Upsilon(1S) pi^0 pi^0) = (8.43 +/- 0.16 +/- 0.42)% and B(Upsilon(3S)-->Upsilon(2S) pi^0 pi^0) = (1.82 +/- 0.09 +/- 0.12)%. In each case the first uncertainty reported is statistical, while the second is systematic.Comment: 11 pages, available at http://www.lns.cornell.edu/public/CLNS/, Accepted for Publication in Phys. Rev.

PGC-1α Agonist Rescues Doxorubicin-Induced Cardiomyopathy by Mitigating the Oxidative Stress and Necroptosis

Cardiomyopathy (particularly dilated cardiomyopathy (DCM)) significantly contributes to development and progression of heart failure (HF), and inflammatory factors further deteriorate the symptoms. Morphological and functional defects of the heart in doxorubicin (DOX)-induced cardiomyopathy (cardiotoxicity) are similar to those of DCM. We used anagonist of PGC-1α (PPAR (peroxisome proliferator-activated receptor-gamma)-γ coactivator-1α) that is considered as the ‘master regulator’ of mitochondrial biogenesis with an aim to rescue the DOX-induced deleterious effects on the heart. Forty male C57BL/6J mice (8 weeks old) were divided in four groups, Control, DOX, ZLN005, and ZLN005 + DOX (n = 10 each group). The DOX-induced (10 mg/kg, single dose) cardiomyopathy mimics a DCM-like phenotype with marked morphologic alteration in cardiac tissue and functional derangements. Significant increased staining was observed for Masson Trichrome/Picrosirius red and α-Smooth Muscle Actinin (α-SMA) that indicated enhanced fibrosis in the DOX group compared to the control that was attenuated by (peroxisome proliferator-activated receptor-gamma (PPAR-γ) coactivator) (PGC)-1α (alpha) agonist (four doses of 2.5 mg/kg/dose; cumulative dose = 10 mg/kg). Similarly, elevated expression of necroptosis markers along with enhanced oxidative stress in the DOX group were alleviated by PGC-1α agonist. These data collectively suggested the potent therapeutic efficacy of PGC-1α agonist in mitigating the deleterious effects of DOX-induced cardiomyopathy, and it may be targeted in developing the future therapeutics for the management of DCM/HF

Enzymatic and transport studies in cholesterol-fed Guinea Pigs using Intestinal Brush Border Membrane Vesicles

The intestinal absorptive and digestive functions using the brush border membrane (BBM) vesicles were evaluated in guinea pigs receiving cholesterol-supplemented diet for 12 weeks. The Na+-gradient-dependent transport of D-glucose (p < 0.001), L-alanine and L-phenylalanine (p < 0.01) was decreased significantly the BBM of cholesterol-fed animals. The maximal velocity (Vmax) value of the sucrase and leucine aminopeptidase was decreased without any change in the affinity constant (Km) value, demonstrating that the enzyme contents were reduced in response to cholesterol-rich diet. However, both the Km and Vmax values of the alkaline phosphatase decreased markedly, suggesting that a new enzyme of increased substrate affinity had been formed due to intestinal adaptation of cholesterol load in diet. The present study demonstrated that cholesterol feeding caused a significant alteration in nutrients absorption, membrane enzymes and chemical composition of the small intestine

Differential cross sections for excitation of H2 by low-energy electron impact

Experimental and theoretical differential cross sections (DCS) for the electron-impact excitation of molecular hydrogen to the B S+u 1 sc Pu 3 sa S+g 3 sC Pu 1 sand the E(F) S+g 1 states are presented at incident energies near to threshold. The experimental DCSs were taken at incident energies of 14, 15, 16 and 17.5 eV and for scattering angles from 10° to 130°. The theoretical DCSs are from the convergent close-coupling method which has recently successfully modeled differential electron scattering from H2 when compared with available experiment at energies of 17.5 eV and above

Mapping binding sites for the PDE4D5 cAMP-specific phosphodiesterase to the N- and C-domains of beta-arrestin using spot-immobilized peptide arrays

Beta2-ARs (beta2-adrenoceptors) become desensitized rapidly upon recruitment of cytosolic beta-arrestin. PDE4D5 (family 4 cAMP-specific phosphodiesterase, subfamily D, isoform 5) can be recruited in complex with beta-arrestin, whereupon it regulates PKA (cAMP-dependent protein kinase) phosphorylation of the beta2-AR. In the present study, we have used novel technology, employing a library of overlapping peptides (25-mers) immobilized on cellulose membranes that scan the entire sequence of beta-arrestin 2, to define the interaction sites on beta-arrestin 2 for binding of PDE4D5 and the cognate long isoform, PDE4D3. We have identified a binding site in the beta-arrestin 2 N-domain for the common PDE4D catalytic unit and two regions in the beta-arrestin 2 C-domain that confer specificity for PDE4D5 binding. Alanine-scanning peptide array analysis of the N-domain binding region identified severely reduced interaction with PDE4D5 upon R26A substitution, and reduced interaction upon either K18A or T20A substitution. Similar analysis of the beta-arrestin 2 C-domain identified Arg286 and Asp291, together with the Leu215-His220 region, as being important for binding PDE4D5, but not PDE4D3. Transfection with wild-type beta-arrestin 2 profoundly decreased isoprenaline-stimulated PKA phosphorylation of the beta2-AR in MEFs (mouse embryo fibroblasts) lacking both beta-arrestin 1 and beta-arrestin 2. This effect was negated using either the R26A or the R286A mutant form of beta-arrestin 2 or a mutant with substitution of an alanine cassette for Leu215-His220, which showed little or no PDE4D5 binding, but was still recruited to the beta2-AR upon isoprenaline challenge. These data show that the interaction of PDE4D5 with both the N- and C-domains of beta-arrestin 2 are essential for beta2-AR regulation