Finite Size Scaling, Fisher Zeroes and N=4 Super Yang-Mills

We investigate critical slowing down in the local updating continuous-time Quantum Monte Carlo method by relating the finite size scaling of Fisher Zeroes to the dynamically generated gap, through the scaling of their respective critical exponents. As we comment, the nonlinear sigma model representation derived through the hamiltonian of our lattice spin model can also be used to give a effective treatment of planar anomalous dimensions in N=4 SYM. We present scaling arguments from our FSS analysis to discuss quantum corrections and recent 2-loop results, and further comment on the prospects of extending this approach for calculating higher twist parton distributions.Comment: Lattice 2004(spin), Fermilab, June 21-26, 2004; 3 pages, 4 figure

A simplified procedure to trace triglyceride-rich lipoprotein metabolism in vivo

Glycerol tri[H-3]oleate and [C-14]cholesteryl oleate double-labeled triglyceride-rich lipoprotein (TRL)-like particles are a well-established tool to trace the effect of lipid-modulating interventions on TRL metabolism. The routine generation of these particles involves sonication of a lipid mixture and subsequent fractionation of resulting particles into populations of different average size through density gradient ultracentrifugation. Here, we describe a simplified and more time-efficient procedure for preparing TRL-like particles without the need of fractionation. The simplified procedure shortened the preparation of particles from over 4 h to less than 2 h and generated particles with a higher yield, although with a smaller average size and more heterogeneous size distribution. In C57Bl/6J mice housed at thermoneutrality (30 degrees C), the two preparations showed highly comparable plasma clearance and organ distribution of glycerol tri[H-3]oleate-derived [H-3]oleate and [C-14]cholesteryl oleate, as measures of lipolysis and core remnant uptake, respectively. Upon a cold challenge (14 degrees C), plasma clearance was accelerated due to enhanced uptake of glycerol tri[H-3]oleate-derived [H-3]oleate by brown adipose tissue. The simplified procedure resulted in a modestly increased particle uptake by the spleen, while uptake by other organs was comparable between the two preparations. In conclusion, the simplified procedure accelerates the preparation of TRL-like particles for tracing in vivo TRL metabolism. We anticipate that this time-efficient procedure will be useful for incorporation of PET-traceable lipids to obtain more insight into human lipoprotein metabolism.Diabetes mellitus: pathophysiological changes and therap

Early but not late exercise training in mice exacerbates hepatic inflammation in developing nonalcoholic fatty liver disease

Host-parasite interactio

Hepatic scavenger receptor class B type 1 knockdown reduces atherosclerosis and enhances the antiatherosclerotic effect of brown fat activation in APOE*3-Leiden.CETP mice

Objective:Brown fat activation attenuates atherosclerosis development by accelerating triglyceride-rich lipoprotein turnover and/or stimulation of reverse cholesterol transport via the SRB1 (scavenger receptor class B type 1). The aim of this study was to investigate the specific role of hepatic SRB1 in the atheroprotective properties of brown fat activation.Approach and Results:APOE*3-Leiden.CETP mice, a well-established model of human-like lipoprotein metabolism and atherosclerosis, were treated with vehicle or adenoassociated virus serotype 8-short hairpin RNA, which decreased hepatic SRB1 protein levels by 40% to 55%. After 2 weeks, mice without or with hepatic SRB1 knockdown were treated with vehicle or the beta 3-adrenergic receptor agonist CL316 243 to activate brown fat for 4 weeks to determine HDL (high-density lipoprotein) catabolism and for 9 weeks to evaluate atherosclerosis. Surprisingly, hepatic SRB1 knockdown additively improved the beneficial effects of beta 3-adrenergic receptor agonism on atherosclerosis development. In fact, hepatic SRB1 knockdown per se not only increased HDL-cholesterol levels but also reduced plasma triglyceride and non-HDL-cholesterol levels, thus explaining the reduction in atherosclerosis development. Mechanistic studies indicated that this is due to increased lipolytic processing and hepatic uptake of VLDL (very low density lipoprotein) by facilitating VLDL-surface transfer to HDL.Conclusions:Hepatic SRB1 knockdown in a mouse model with an intact ApoE (apolipoprotein E)-LDLR (low density lipoprotein receptor) clearance pathway, relevant to human lipoprotein metabolism, reduced atherosclerosis and improved the beneficial effect of brown fat activation on atherosclerosis development, explained by pleiotropic effects of hepatic SRB1 knockdown on lipolytic processing and hepatic uptake of VLDL. Brown fat activation could thus be an effective strategy to treat cardiovascular disease also in subjects with impaired SRB1 function.Functional Genomics of Systemic Disorder

Cannabinoid type 1 receptor inverse agonism attenuates dyslipidemia and atherosclerosis in APOE∗3-Leiden.CETP mice

Pharmacological blockade of the cannabinoid type 1 receptor, a G protein-coupled receptor expressed in the central nervous system and various peripheral tissues, reverses diet-induced obesity and dyslipidemia through the reduction of food intake and altered nutrient partitioning. This strategy is being explored for a number of therapeutic applications; however, its potency for the treatment of atherosclerotic cardiovascular disease via improvements in lipid metabolism remains unclear. Therefore, here, we aimed to investigate whether inhibition of the endocannabinoid system can attenuate atherosclerosis development through improvement of dyslipidemia. Lean, dyslipidemic female APOE∗3-Leiden.CETP transgenic mice were fed a Western-type diet supplemented with or without the cannabinoid type 1 receptor inverse agonist rimonabant (20 mg·kg body weight-1 day-1) for up to 20 weeks. Plasma lipids and bile acids were determined, and atherosclerotic lesions were scored in the aortic valve region. Rimonabant lowered plasma levels of triglyceride (TG) (-56%) and non-HDL-C (-19%) and increased HDL-C (+57%). These effects were explained by decreased VLDL-TG production (-52%) and accelerated VLDL-TG turnover accompanied by pronounced browning of white adipose tissue. In addition, rimonabant attenuated reverse cholesterol transport (-30%), increased plasma bile acid levels (+160%), and increased hepatic cholesterol accumulation (+88%). Importantly, rimonabant markedly lowered atherosclerotic lesion size (-64%), which coincided with decreased lesion severity (28% vs. 56% severe lesions) and which strongly correlated with non-HDL-C exposure (R2 = 0.60). Taken together, inhibition of the endocannabinoid system potently reverses dyslipidemia and prevents atherogenesis, even in the absence of obesity.Molecular Physiolog

Measurements of the Mass and Full-Width of the ηc\eta_c Meson

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five different decay channels: $\gamma K^+K^-\pi^+\pi^-$, $\gamma\pi^+\pi^-\pi^+\pi^-$, $\gamma K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\gamma \phi\phi$ (with $\phi\to K^+K^-$) and $\gamma p\bar{p}$. From a combined fit of all five channels, we determine the mass and full-width of $\eta_c$ to be $m_{\eta_c}=2977.5\pm1.0 ({stat.})\pm1.2 ({syst.})$ MeV/$c^2$ and $\Gamma_{\eta_c} = 17.0\pm3.7 ({stat.})\pm7.4 ({syst.})$ MeV/$c^2$.Comment: 9 pages, 2 figures and 4 table. Submitted to Phys. Lett.

A Measurement of Psi(2S) Resonance Parameters

Cross sections for e+e- to hadons, pi+pi- J/Psi, and mu+mu- have been measured in the vicinity of the Psi(2S) resonance using the BESII detector operated at the BEPC. The Psi(2S) total width; partial widths to hadrons, pi+pi- J/Psi, muons; and corresponding branching fractions have been determined to be Gamma(total)= (264+-27) keV; Gamma(hadron)= (258+-26) keV, Gamma(mu)= (2.44+-0.21) keV, and Gamma(pi+pi- J/Psi)= (85+-8.7) keV; and Br(hadron)= (97.79+-0.15)%, Br(pi+pi- J/Psi)= (32+-1.4)%, Br(mu)= (0.93+-0.08)%, respectively.Comment: 8 pages, 6 figure

Holographic \Lambda(t)CDM model in a non-flat universe

The holographic $\Lambda(t)$CDM model in a non-flat universe is studied in this paper. In this model, to keep the form of the stress-energy of the vacuum required by general covariance, the holographic vacuum is enforced to exchange energy with dark matter. It is demonstrated that for the holographic model the best choice for the IR cutoff of the effective quantum field theory is the event horizon size of the universe. We derive the evolution equations of the holographic $\Lambda(t)$CDM model in a non-flat universe. We constrain the model by using the current observational data, including the 557 Union2 type Ia supernovae data, the cosmic microwave background anisotropy data from the 7-yr WMAP, and the baryon acoustic oscillation data from the SDSS. Our fit results show that the holographic $\Lambda(t)$CDM model tends to favor a spatially closed universe (the best-fit value of $\Omega_{k0}$ is -0.042), and the 95% confidence level range for the spatial curvature is $-0.101<\Omega_{k0}<0.040$. We show that the interaction between the holographic vacuum and dark matter induces an energy flow of which the direction is first from vacuum to dark matter and then from dark matter to vacuum. Thus, the holographic $\Lambda(t)$CDM model is just a time-varying vacuum energy scenario in which the interaction between vacuum and dark matter changes sign during the expansion of the universe.Comment: 8 pages, 4 figures. version for publication in EPJC. arXiv admin note: text overlap with arXiv:1112.235

Measurement of Branching Ratios for ηc\eta_c Hadronic Decays

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five decay channels: $\eta_c \to K^+K^-\pi^+\pi^-$, $\pi^+\pi^-\pi^+\pi^-$, $K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\phi\phi$ (with $\phi\to K^+K^-$) and $p\bar{p}$. From these signals, we determine $Br(J/\psi\to\gamma\eta_c)\times Br(\eta_c\to K^+K^-\pi^+\pi^-)$ $=(1.5\pm0.2\pm0.2)\times10^{-4}$, $Br(J/\psi\to\gamma\eta_c)\times Br(\eta_c\to \pi^+\pi^-\pi^+\pi^-)$ $=(1.3\pm0.2\pm0.4)\times10^{-4}$, $Br(J/\psi\to\gamma\eta_c)\times Br(\eta_c\to K^\pm K_{S}^{0}\pi^\mp)$ $=(2.2\pm0.3\pm0.5)\times10^{-4}$, $Br(J/\psi\to\gamma\eta_c)\times Br(\eta_c\to \phi\phi)$ $=(3.3\pm0.6\pm0.6)\times10^{-5}$ and $Br(J/\psi\to\gamma\eta_c)\times Br(\eta_c\to p\bar{p})$ $=(1.9\pm0.3\pm0.3)\times10^{-5}$.Comment: 8 pages, 1 figures and 4 table. Submitted to Phys. Lett.