Hadronic contribution to the muon g-2: a theoretical determination

The leading order hadronic contribution to the muon g-2, $a_{\mu}^{HAD}$, is determined entirely from theory using an approach based on Cauchy's theorem in the complex squared energy s-plane. This is possible after fitting the integration kernel in $a_{\mu}^{HAD}$ with a simpler function of $s$. The integral determining $a_{\mu}^{HAD}$ in the light-quark region is then split into a low energy and a high energy part, the latter given by perturbative QCD (PQCD). The low energy integral involving the fit function to the integration kernel is determined by derivatives of the vector correlator at the origin, plus a contour integral around a circle calculable in PQCD. These derivatives are calculated using hadronic models in the light-quark sector. A similar procedure is used in the heavy-quark sector, except that now everything is calculable in PQCD, thus becoming the first entirely theoretical calculation of this contribution. Using the dual resonance model realization of Large $N_{c}$ QCD to compute the derivatives of the correlator leads to agreement with the experimental value of $a_\mu$. Accuracy, though, is currently limited by the model dependent calculation of derivatives of the vector correlator at the origin. Future improvements should come from more accurate chiral perturbation theory and/or lattice QCD information on these derivatives, allowing for this method to be used to determine $a_{\mu}^{HAD}$ accurately entirely from theory, independently of any hadronic model.Comment: Several additional clarifying paragraphs have been added. 1/N_c corrections have been estimated. No change in result

B meson decay constants f(Bc), f(Bs) and f(B) from QCD sum rules

Finite energy QCD sum rules with Legendre polynomial integration kernels are used to determine the heavy meson decay constant f(Bc), and revisit f(B) and f(Bs). Results exhibit excellent stability in a wide range of values of the integration radius in the complex squared energy plane, and of the order of the Legendre polynomial. Results are f(Bc) = 528 +/- 19 MeV, f(B) = 186 +/- 14 MeV, and f(Bs) = 222 +/- 12 MeV

Precise Charm- and Bottom-Quark Masses: Theoretical and Experimental Uncertainties

Recent theoretical and experimental improvements in the determination of charm and bottom quark masses are discussed. A new and improved evaluation of the contribution from the gluon condensate $$ to the charm mass determination and a detailed study of potential uncertainties in the continuum cross section for $b\bar b$ production is presented, together with a study of the parametric uncertainty from the $\alpha_s$-dependence of our results. The final results, $m_c(3 \text{GeV})=986(13)$MeV and $m_b(m_b)=4163(16)$MeV, represent, together with a closely related lattice determination $m_c(3\;{\rm GeV})=986(6)$MeV, the presently most precise determinations of these two fundamental Standard Model parameters. A critical analysis of the theoretical and experimental uncertainties is presented.Comment: 12 pages, presented at Quarks~2010, 16th International Seminar of High Energy Physics, Kolomna, Russia, June 6-12, 2010; v2: references adde

Higgs and non-universal gaugino masses: no SUSY signal expected yet?

So far, no supersymmetric particles have been detected at the Large Hadron Collider (LHC). However, the recent Higgs results have interesting implications for the SUSY parameter space. In this paper, we study the consequences of an LHC Higgs signal for a model with non-universal gaugino masses in the context of SU(5) unification. The gaugino mass ratios associated with the higher representations produce viable spectra that are largely inaccessible to the current LHC and direct dark matter detection experiments. Thus, in light of the Higgs results, the non-observation of SUSY is no surprise.Comment: supplementary file containing plots with log priors in ancillary files. v2: added some comments on more general settings and references, accepted for publication in JHE

LYL1 Degradation by the Proteasome Is Directed by a N-Terminal PEST Rich Site in a Phosphorylation-Independent Manner

Background: The Lymphoblastic leukemia 1 (LYL1) gene is a proto-oncogenic transcription factor found upregulated in patients with T-cell acute lymphoblastic leukemia (T-cell ALL). Initially, the upregulation was described to be as a result of a translocation. However, further studies revealed that transcriptional upregulation of LYL1could also occur without translocations. In addition, post-translational mechanisms, such as protein degradation could influence LYL1 expression as well. Methodology/Principal Findings: In this study, we considered possible post-translational regulation of Lyl1, and investigated fundamental mechanisms governing LYL1 degradation in cell-based culture assays. We identify a PEST sequence motif located in the N-terminus of LYL1, which determines the efficiency of LYL1 degradation by the proteasome. The absence of the PEST degradation site leads to accumulation or upregulation of LYL1. We also show that LYL1 is phosphorylated by MAPK at S36, and determined that proteasomal degradation of LYL1 occurs in a phosphorylationindependent manner. Conclusions/Significance: Understanding LYL1 degradation is a step forward not only towards deciphering the normal function and regulation of LYL1, but could suggest post-translational mechanisms for upregulation of LYL1 that ma

The Ontogeny and Evolution of Sex-Biased Gene Expression in Drosophila melanogaster

Sexually dimorphic phenotypes are thought to largely result from sex differences in gene expression, and genes with sex-biased expression have been well characterized in adults of many species. Although most sexual dimorphisms manifest in adults, many result from sex-specific developmental trajectories, implying that juveniles may exhibit significant levels of sex-biased expression. However, it is unclear how much sex-biased expression occurs before reproductive maturity and whether preadult sex-biased genes should exhibit the same evolutionary dynamics observed for adult sex-biased genes. In order to understand the continuity, or lack thereof, and evolutionary dynamics of sex-biased expression throughout the life cycle, we examined sex-biased genes in pre-gonad tissue of two preadult stages and compared them with the adult gonad of Drosophila melanogaster. We found that the majority of the genome is sex-biased at some point in the life cycle, with some genes exhibiting conserved sex-biased expression and others displaying stage-specific sex bias. Our results also reveal a far more complex pattern of evolution for sex-biased genes throughout development. The most rapid evolutionary divergence occurred in genes expressed only in larvae within each sex, compared with continuously expressed genes. In females—but not males—this pattern appeared to be due to relaxed purifying selection in larva-limited genes. Furthermore, genes that retained male bias throughout life evolved more rapidly than stage-specific male-biased genes, due to stronger purifying selection in stage-specific genes. However, female-biased genes that were specific to larvae evolved most rapidly, a pattern that could not be definitively attributed to differences in adaptive evolution or purifying selection, suggesting that pleiotropic constraints on protein-coding sequences can arise when genes are broadly expressed across developmental stages. These results indicate that the signature of sex-specific selection can be detected well before reproductive maturity and is strongest during development

MEKK1-MKK4-JNK-AP1 Pathway Negatively Regulates Rgs4 Expression in Colonic Smooth Muscle Cells

Background: Regulator of G-protein Signaling 4 (RGS4) plays an important role in regulating smooth muscle contraction, cardiac development, neural plasticity and psychiatric disorder. However, the underlying regulatory mechanisms remain elusive. Our recent studies have shown that upregulation of Rgs4 by interleukin (IL)-1b is mediated by the activation of NFkB signaling and modulated by extracellular signal-regulated kinases, p38 mitogen-activated protein kinase, and phosphoinositide-3 kinase. Here we investigate the effect of the c-Jun N-terminal kinase (JNK) pathway on Rgs4 expression in rabbit colonic smooth muscle cells. Methodology/Principal Findings: Cultured cells at first passage were treated with or without IL-1b (10 ng/ml) in the presence or absence of the selective JNK inhibitor (SP600125) or JNK small hairpin RNA (shRNA). The expression levels of Rgs4 mRNA and protein were determined by real-time RT-PCR and Western blot respectively. SP600125 or JNK shRNA increased Rgs4 expression in the absence or presence of IL-1b stimulation. Overexpression of MEKK1, the key upstream kinase of JNK, inhibited Rgs4 expression, which was reversed by co-expression of JNK shRNA or dominant-negative mutants for MKK4 or JNK. Both constitutive and inducible upregulation of Rgs4 expression by SP600125 was significantly inhibited by pretreatment with the transcription inhibitor, actinomycin D. Dual reporter assay showed that pretreatment with SP600125 sensitized the promoter activity of Rgs4 in response to IL-1b. Mutation of the AP1-binding site within Rgs