Comment on "Chiral Suppression of Scalar Glueball Decay"

Comment on ``Chiral Suppression of Scalar Glueball Decay''Comment: Comment published in Phys. Rev. Lett. 98, 149103(2007

Superposition coded modulation with peak-power limitation

We apply clipping to superposition coded modulation (SCM) systems to reduce the peak-to-average power ratio (PAPR) of the transmitted signal. The impact on performance is investigated by evaluating the mutual information driven by the induced peak-power-limited input signals. It is shown that the rate loss is marginal for moderate clipping thresholds if optimal encoding/decoding is used. This fact is confirmed in examples where capacityapproaching component codes are used together with the maximum a posteriori probability (MAP) detection. In order to reduce the detection complexity of SCM with a large number of layers, we develop a suboptimal soft compensation (SC) method that is combined with soft-input soft-output (SISO) decoding algorithms in an iterative manner. A variety of simulation results for additive white Gaussian noise (AWGN) and fading channels are presented. It is shown that with the proposed method, the effect of clipping can be efficiently compensated and a good tradeoff between PAPR and bit-error rate (BER) can be achieved. Comparisons with other coded modulation schemes demonstrate that SCM offers significant advantages for high-rate transmissions over fading channels

Fragmentation function of g→QQˉ(3S1[8])g\to Q\bar{Q}(^3S_1^{[8]}) in soft gluon factorization and threshold resummation

We study the fragmentation function of the gluon to color-octet $^3S_1$ heavy quark-antiquark pair using the soft gluon factorization (SGF) approach, which expresses the fragmentation function in a form of perturbative short-distance hard part convoluted with one-dimensional color-octet $^3S_1$ soft gluon distribution (SGD). The short distance hard part is calculated to next-to-leading order in $\alpha_s$ and a renormalization group equation for the SGD is derived. By solving the renormalization group equation, threshold logarithms are resummed to all orders in perturbation theory. The comparison with gluon fragmentation function calculated in NRQCD factorization approach indicates that the SGF formula resums a series of velocity corrections in NRQCD which are important for phenomenological study.Comment: 38 pages, 8 figure

The role and possible molecular mechanism of valproic acid in the growth of MCF-7 breast cancer cells

Aim To investigate the role of valproic acid (VPA), a class I selective histone deacetylase inhibitor, on Michigan Cancer Foundation (MCF)-7 breast cancer cells, named and explore its possible molecular mechanism. Methods MCF-7 cells were cultured with sodium valproate (0. 5-4.0 mmol/L) for 24 h, 48 h, and 72 h in vitro, respectively. The cell viability, apoptosis, and cell cycle were examined. The activities and protein expressions of caspase-3, caspase-8, and caspase-9 were subsequently assayed. Finally, mRNA and protein expressions of cyclin A, cyclin D1, cyclin E, and p21 were analyzed. Results Sodium valproate suppressed MCF-7 cell growth, induced cell apoptosis, and arrested G1 phase in a timeand concentration- dependent manner, with the relative cell viabilities decreased, cell apoptosis ratios increased, and percentage of G1 phase enhanced (P < 0.05). Increased activity of caspase-3 and caspase-9, but not caspase-8, and increased protein levels were found under sodium valproate (2.0 mmol/L, 48h). P21 was up-regulated and cyclin D1 was down-regulated at both mRNA and protein levels under sodium valproate (2.0 mmol/L, 48h)(P < 0.05), although cyclin E and cyclin A remained changed. Conclusion These results indicate that VPA can suppress the growth of breast cancer MCF-7 cells by inducing apoptosis and arresting G1 phase. Intrinsic apoptotic pathway is dominant for VPA-induced apoptosis. For G1 phase arrest, p21 up-regulation and down-regulation of cyclin D1 may be the main molecular mechanism