Revisiting B\to\pi K, \pi K^{\ast} and \rho K decays: CP violations and implication for New Physics

Combining the up-to-date experimental information on $B\to\pi K, \pi K^{\ast}$ and $\rho K$ decays, we revisit the decay rates and CP asymmetries of these decays within the framework of QCD factorization. Using an infrared finite gluon propagator of Cornwall prescription, we find that the time-like annihilation amplitude could contribute a large strong phase, while the space-like hard spectator scattering amplitude is real. Numerically, we find that all the branching ratios and most of the direct CP violations, except $A_{CP}(B^{\pm}\to K^{\pm}\pi^{0})$, agree with the current experimental data with an effective gluon mass $m_g\simeq0.5 {\rm GeV}$. Taking the unmatched difference in direct CP violations between $B\to\pi^{0} K^{\pm}$ and $\pi^{\mp}K^{\pm}$ decays as a hint of new physics, we perform a model-independent analysis of new physics contributions with a set of $\bar{s}(1+\gamma_{5})b\otimes\bar{q}(1+\gamma_{5})q$ (q=u,d) operators. Detail analyses of the relative impacts of the operators are presented in five cases. Fitting the twelve decay modes, parameter spaces are found generally with nontrivial weak phases. Our results may indicate that both strong phase from annihilation amplitude and new weak phase from new physics are needed to resolve the $\pi K$ puzzle. To further test the new physics hypothesis, the mixing-induced CP violations in $B\to\pi^{0}K_{S}$ and $\rho^{0}K_{S}$ are discussed and good agreements with the recent experimental data are found.Comment: Version published in JHE

Efficacy and Safety of Emricasan in Liver Cirrhosis and/or Fibrosis

This study aimed to perform a meta-analysis to determine the efficacy and safety of emricasan. Nine databases were searched for clinical trials investigating the efficacy of emricasan treatment in patients with liver cirrhosis or fibrosis. A manual search was conducted to identify the missing trials. The quality of the included studies was assessed using the revised Cochrane risk of bias tool. Efficacy of emricasan treatment was defined as a positive change in apoptosis-related parameters from baseline to the last follow-up visit. Overall, emricasan treatment is more effective in patients with liver cirrhosis or fibrosis than placebo (standardized mean difference [SMD] [95% confidence intervals (CI)]=0.28 [0.14; 0.41]). No significant change in model for end-stage liver disease (MELD) score between the emricasan and placebo groups was noted (SMD [95% CI]=0.18 [-0.01; 0.36]; p=0.058). A 50 mg dose of emricasan had the highest efficacy rate compared to placebo (SMD [95% CI]=0.28 [0.06; 0.50]; p=0.012), followed by the 5 mg dosing regimen (SMD [95% CI]=0.28 [0.06; 0.50]; p=0.012). Treatment with emricasan resulted in significant reductions in ALT (mean difference (MD) [95% CI]=-5.89 [-10.59; -1.20]; p=0.014) and caspase3/7 levels (MD [95%CI]=-1215.93 [-1238.53; -1193.33]; p<0.001), respectively. No significant increase in the rate of overall adverse events was noted (OR [95% CI]=1.52 [0.97; 2.37]; p=0.069). Treatment with emricasan is more effective in improving liver function and apoptosis parameters compared to placebo, with a well-tolerated safety profile. However, due to the poor quality of the analyzed studies, the small number of trials and patients, and the short follow-up periods, more robust trials are still warranted

Family Non-universal Z^\prime effects on \bar{B}_q-B_q$ mixing, B\to X_s \mu^+\mu^- and B_s\to \mu^+\mu^- Decays

Motivated by the large discrepancy of CP-violating phase in $\bar{B}_s-B_s$ mixing between the experimental data and the Standard Model prediction, we pursue possible solutions within a family non-universal $Z^{\prime}$ model. Within such a specific model, we find that both the $\bar{B}_s-B_s$ mixing anomaly and the well-known "$\pi K$ puzzle" could be moderated simultaneously with a nontrivial new weak phase, $\phi^L_s\sim-72^{\circ}$ (S1) or $-82^{\circ}$ (S2). With the stringently constrained $Z^{\prime}$ coupling $B_{sb}^{L}$, we then study the $Z^{\prime}$ effects on the rare $B\to X_s \mu^+\mu^-$ and $B_s\to \mu^+\mu^-$ decays, which are also induced by the same $b\to s$ transition. The observables of $B\to X_s \mu^+\mu^-$, at both high and low $q^2$ regions, are found to be able to put strong constraints on the $\mu-\mu-Z^{\prime}$ coupling, $B_{\mu\mu}^{L,R}\sim10^{-2}$. It is also shown that the combined constraints from $\bar{B}_s-B_s$ mixing, $B\to \pi K$ and $B\to X_s \mu^+\mu^-$ do not allow a large $Z^{\prime}$ contribution to the pure leptonic $B_s\to\mu^+\mu^-$ decay.Comment: 29 pages, 10 figs and 6 tables. References and discussions added. To appear in JHE

B→K∗l+l−B \to K^{\ast} l^+ l^-, Kl+l−K l^+ l^- decays in a family non-universal Z′Z^{\prime} model

Motivated by the observed forward-backward asymmetry in $B\to K^{\ast} l^+ l^-$ decay, we perform a detailed analysis of this decay mode within a family non-universal $Z^{\prime}$ model. With the related coupling $Z^{\prime}-\bar{s}b$ constrained by $\bar{B}_s-B_s$ mixing, $B\to \pi K$, and $B\to X_s \mu^{+}\mu^{-}$ decays, we look for further constraint on the couplings $Z^{\prime}-\mu^{+}\mu^{-}$ from $A_{FB}(B\to K^{\ast} \mu^{+}\mu^{-})_{0 {\rm GeV}^2\leqslant q^2\leqslant 2 {\rm GeV}^2}$ and get numerically $B_{\mu\mu}^{L,R}\sim{\cal O}(10^{-2})$. Moreover, we find that the relations, $B_{\mu\mu}^{L}<B_{\mu\mu}^{R}$ and $B_{\mu\mu}^{L}+B_{\mu\mu}^{R}<0$, with a small negative $\phi_{s}^{L}$, are crucial to moderate the discrepancy for $A_{FB}(B\to K^{\ast} \mu^{+}\mu^{-})$ between the SM prediction and the experimental data. Numerically, comparing with the SM prediction, we find that $A_{FB}(B\to K^{\ast} \mu^{+}\mu^{-})_{0 {\rm GeV}^2\leqslant q^2\leqslant 2 {\rm GeV}^2}$ could be enhanced about 80% and 50% by $Z^{\prime}$ contribution at most in scenarios S1 and S2, corresponding to the two fitted results of $\phi_{s}$ by UTfit collaboration, respectively. However, the results are still about $1.5\sigma$ lower than the experimental measurement.Comment: 20 pages, 3 figures. To appear in JHE

On the measurement of the Hubble constant in a local low-density universe

Astrophysical observations indicate that the ``Local Universe" has a relatively lower matter density ($\Omega_0$) than the predictions of the standard inflation cosmology and the large-scale motions of galaxies which provide a mean mass density to be very close to unity. In such a local underdense region the Hubble expansion may not be representative of the global behaviour. Utilizing an underdense sphere embedded in a flat universe as the model of our ``Local Universe", we show that the local Hubble constant would be 1.2 -- 1.4 times larger than the global value on scale of $\sim80$ Mpc, depending on the variation of $\Omega_0$. This may account for the recent measurements of the unpleasantly large Hubble constant of $\sim$80 km/s/Mpc using the Cepheid variables in the Virgo cluster and the relative distance between Virgo and Coma cluster and removes the resulted apparent paradox of the age of our universe.Comment: 9 pages, Latex file, 3 figures available by reques

catena-Poly[[[aqua­bis­(1H-imidazole-κN 3)copper(II)]-μ-furan-2,5-di­car­boxylato-κ2 O 2:O 5] trihydrate]

In the title cooridnation polymer, {[Cu(C6H2O5)(C3H4N2)2(H2O)]·3H2O}n, an infinite chain is formed along [001] by linking of the Cu(C3N2H4)2(H2O) entities with two bridging monodentate carboxyl­ate groups of two different furan-2,5-dicarboxyl­ate dianions. The geometry of the Cu2+ ion is a square-based pyramid with the water atom in the apical position and the ligand O and N atoms in a trans orientation. The dihedral angle between the imidazole planes is 83.96 (14)°. Ow–H⋯O and Ni–H⋯O (w = water and i = imidazole) hydrogen bonds help to establish the packing

NGX6 gene mediated by promoter methylation as a potential molecular marker in colorectal cancer

<p>Abstract</p> <p>Background</p> <p>Nasopharyngeal carcinoma associated gene 6 (NGX6) is down-regulated in most colon cancer cell lines and tumor tissues when compared with their normal tissue samples. As a novel suppress tumor gene, it could inhibit colon cancer cell growth and cell cycle progression. However, little is known about the transcriptional mechanisms controlling NGX6 gene expression. Recent findings suggest that epigenetic inactivation of multiple tumor suppressor genes plays an important role in the tumorigenesis of colorectal carcinoma (CRC). In this study, we explored the role of DNA methylation in regulation of NGX6 transcription.</p> <p>Methods</p> <p>In the present study, we cloned the NGX6 promoter with characteristics of a CpG island by luciferase reporter assay. Then, the CpG methylation status around the NGX6 promoter region in colon cancer cell lines and colorectal tumor tissues was examined by methylation-specific PCR and bisulfite DNA sequencing. Finally, 5-Aza-2'-deoxycytidine (5-Aza-dC) treatment was used to confirm the correlation between NGX6 promoter methylation and its gene inactivation.</p> <p>Results</p> <p>The sequence spanning positions -157 to +276 was identified as the NGX6 promoter, in which no canonical TATA boxes were found, while two CAAT boxes and GC boxes were discovered. Methylation status was observed more frequently in 40 colorectal cancer samples than in 40 adjacent normal mucosa samples (18/40 versus 7/40; P < 0.05). An analysis correlating gene methylation status with clinicopathological cancer features revealed that dense methylation of the NGX6 promoter was associated with colorectal cancer patients age (P < 0.05). Moreover, a trend was shown toward metastasis status and primary site in colorectal carcinomas with NGX6 promoter methylation (p = 0.056 and P = 0.067, respectively). In addition, 5-Aza-dC could induce NGX6 mRNA expression and NGX6 promoter demethylation in HT-29 cells.</p> <p>Conclusions</p> <p>Down-regulation of NGX6 gene is related to the promoter methylation. DNA methylation of NGX6 promoter might be a potential molecular marker for diagnosis or prognosis, or serve as a therapeutic target.</p

(E)-1-(4-Bromo­phen­yl)-3-(2-fur­yl)prop-2-en-1-one

In the title compound, C13H9BrO2, the benzene and furan rings form a dihedral angle of 44.35 (14)°. The crystal packing exhibits no significantly short inter­molecular contacts