3,500 research outputs found
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 and 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
, agree with the current experimental data
with an effective gluon mass . Taking the unmatched
difference in direct CP violations between and
decays as a hint of new physics, we perform a
model-independent analysis of new physics contributions with a set of
(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 puzzle. To further test the new physics hypothesis, the
mixing-induced CP violations in and 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
mixing between the experimental data and the Standard Model prediction, we
pursue possible solutions within a family non-universal model.
Within such a specific model, we find that both the mixing
anomaly and the well-known " puzzle" could be moderated simultaneously
with a nontrivial new weak phase, (S1) or
(S2). With the stringently constrained coupling
, we then study the effects on the rare and decays, which are also induced by the same
transition. The observables of , at both high and
low regions, are found to be able to put strong constraints on the
coupling, . It is also shown
that the combined constraints from mixing, and
do not allow a large contribution to the
pure leptonic decay.Comment: 29 pages, 10 figs and 6 tables. References and discussions added. To
appear in JHE
, decays in a family non-universal model
Motivated by the observed forward-backward asymmetry in decay, we perform a detailed analysis of this decay mode within a family
non-universal model. With the related coupling
constrained by mixing, , and
decays, we look for further constraint on the
couplings from and get
numerically . Moreover, we find that the
relations, and
, with a small negative , are
crucial to moderate the discrepancy for
between the SM prediction and the experimental data. Numerically, comparing
with the SM prediction, we find that could be enhanced about 80%
and 50% by contribution at most in scenarios S1 and S2,
corresponding to the two fitted results of by UTfit collaboration,
respectively. However, the results are still about 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 () 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 Mpc,
depending on the variation of . This may account for the recent
measurements of the unpleasantly large Hubble constant of 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
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