QCD Factorization Based on Six-Quark Operator Effective Hamiltonian from Perturbative QCD and Charmless Bottom Meson Decays B(s)→ππ,πK,KKB_{(s)}\to \pi\pi,\pi K, KK

The charmless bottom meson decays are systematically investigated based on an approximate six quark operator effective Hamiltonian from perturbative QCD. It is shown that within this framework the naive QCD factorization method provides a simple way to evaluate the hadronic matrix elements of two body mesonic decays. The singularities caused by on mass-shell quark propagator and gluon exchanging interaction are appropriately treated. Such a simple framework allows us to make theoretical predictions for the decay amplitudes with reasonable input parameters. The resulting theoretical predictions for all the branching ratios and CP asymmetries in the charmless $B^0, B^+, B_s\to \pi\pi, \pi K, KK$ decays are found to be consistent with the current experimental data except for a few decay modes. The observed large branching ratio in $B\to \pi^0\pi^0$ decay remains a puzzle though the predicted branching ratio may be significantly improved by considering the large vertex corrections in the effective Wilson coefficients. More precise measurements of charmless bottom meson decays, especially on CP-violations in $B\to K K$ and $B_s\to \pi\pi, \pi K, KK$ decay modes, will provide a useful test and guide us to a better understanding on perturbative and nonperturbative QCD.Comment: 36 pages, 5 figures, typos correcte

Life fingerprints of nuclear reactions in the body of animals

Nuclear reactions are a very important natural phenomenon in the universe. On the earth, cosmic rays constantly cause nuclear reactions. High energy beams created by medical devices also induce nuclear reactions in the human body. The biological role of these nuclear reactions is unknown. Here we show that the in vivo biological systems are exquisite and sophisticated by nature in influence on nuclear reactions and in resistance to radical damage in the body of live animals. In this study, photonuclear reactions in the body of live or dead animals were induced with 50-MeV irradiation. Tissue nuclear reactions were detected by positron emission tomography (PET) imaging of the induced beta+ activity. We found the unique tissue "fingerprints" of beta+ (the tremendous difference in beta+ activities and tissue distribution patterns among the individuals) are imprinted in all live animals. Within any individual, the tissue "fingerprints" of 15O and 11C are also very different. When the animal dies, the tissue "fingerprints" are lost. The biochemical, rather than physical, mechanisms could play a critical role in the phenomenon of tissue "fingerprints". Radiolytic radical attack caused millions-fold increases in 15O and 11C activities via different biochemical mechanisms, i.e. radical-mediated hydroxylation and peroxidation respectively, and more importantly the bio-molecular functions (such as the chemical reactivity and the solvent accessibility to radicals). In practice biologically for example, radical attack can therefore be imaged in vivo in live animals and humans using PET for life science research, disease prevention, and personalized radiation therapy based on an individual's bio-molecular response to ionizing radiation

QCD Approach to B->D \pi Decays and CP Violation

The branching ratios and CP violations of the $B\to D\pi$ decays, including both the color-allowed and the color-suppressed modes, are investigated in detail within QCD framework by considering all diagrams which lead to three effective currents of two quarks. An intrinsic mass scale as a dynamical gluon mass is introduced to treat the infrared divergence caused by the soft collinear approximation in the endpoint regions, and the Cutkosky rule is adopted to deal with a physical-region singularity of the on mass-shell quark propagators. When the dynamical gluon mass $\mu_g$ is regarded as a universal scale, it is extracted to be around $\mu_g = 440$ MeV from one of the well-measured $B\to D\pi$ decay modes. The resulting predictions for all branching ratios are in agreement with the current experimental measurements. As these decays have no penguin contributions, there are no direct $CP$ asymmetries. Due to interference between the Cabibbo-suppressed and the Cabibbo-favored amplitudes, mixing-induced CP violations are predicted in the $B\to D^{\pm}\pi^{\mp}$ decays to be consistent with the experimental data at 1-$\sigma$ level. More precise measurements will be helpful to extract weak angle $2\beta+\gamma$.Comment: 21pages,5 figures,3 tables, typos corrected and numerical result for one of decay channels is improve

Exclusive B→VVB \to VV Decays and CP Violation in the General two-Higgs-doublet Model

Using the general factorization approach, we present a detailed investigation for the branching ratios, CP asymmetries and longitudinal polarization fractions in all charmless hadronic $B \to VV$ decays (except for the pure annihilation processes) within the most general two-Higgs-doublet model with spontaneous CP violation. It is seen that such a new physics model only has very small contributions to the branching ratios and longitudinal polarization fractions. However, as the model has rich CP-violating sources, it can lead to significant effects on the CP asymmetries, especially on those of penguin-dominated decay modes, which provides good signals for probing new physics beyond the SM in the future B-physics experiments.Comment: 17 pages, no figure

Charmless Bs→PP,PV,VVB_s\to PP, PV, VV Decays Based on the six-quark Effective Hamiltonian with Strong Phase Effects II

We provide a systematic study of charmless $B_s \to PP, PV, VV$ decays ($P$ and $V$ denote pseudoscalar and vector mesons, respectively) based on an approximate six-quark operator effective Hamiltonian from QCD. The calculation of the relevant hard-scattering kernels is carried out, the resulting transition form factors are consistent with the results of QCD sum rule calculations. By taking into account important classes of power corrections involving "chirally-enhanced" terms and the vertex corrections as well as weak annihilation contributions with non-trivial strong phase, we present predictions for the branching ratios and CP asymmetries of $B_s$ decays into PP, PV and VV final states, and also for the corresponding polarization observables in VV final states. It is found that the weak annihilation contributions with non-trivial strong phase have remarkable effects on the observables in the color-suppressed and penguin-dominated decay modes. In addition, we discuss the SU(3) flavor symmetry and show that the symmetry relations are generally respected

Synthesis of Large-Area MoS2 Atomic Layers with Chemical Vapor Deposition

Large-area MoS2 atomic layers are synthesized on SiO2 substrates by chemical vapor deposition using MoO3 and S powders as the reactants. Optical, microscopic and electrical measurements suggest that the synthetic process leads to the growth of MoS2 monolayer. The TEM images verify that the synthesized MoS2 sheets are highly crystalline.Comment: First submitted on 12-Dec-2011. Accepted in Adv. Mate

Low oxygen tension primes aortic endothelial cells to the reparative effect of tissue-protective cytokines

Erythropoietin (EPO) has both erythropoietic and tissue-protective properties. The EPO analogues carbamylated EPO (CEPO) and pyroglutamate helix B surface peptide (pHBSP) lack the erythropoietic activity of EPO but retain the tissue-protective properties that are mediated by a heterocomplex of EPO receptor (EPOR) and the β common receptor (βCR). We studied the action of EPO and its analogues in a model of wound healing where a bovine aortic endothelial cells (BAECs) monolayer was scratched and the scratch closure was assessed over 24 h under different oxygen concentrations. We related the effects of EPO and its analogues on repair to their effect on BAECs proliferation and migration (evaluated using a micro-Boyden chamber). EPO, CEPO and pHBSP enhanced scratch closure only at lower oxygen (5%), while their effect at atmospheric oxygen (21%) was not significant. The mRNA expression of EPOR was doubled in 5% compared to 21% oxygen, and this was associated with increased EPOR assessed by immunofluorescence and Western blot. By contrast βCR mRNA levels were similar in 5% and 21% oxygen. EPO and its analogues increased both BAECs proliferation and migration, suggesting that both may be involved in the reparative process. The priming effect of low oxygen tension on the action of tissue-protective cytokines may be of relevance to vascular disease, including atherogenesis and restenosis

Design principles for riboswitch function

Scientific and technological advances that enable the tuning of integrated regulatory components to match network and system requirements are critical to reliably control the function of biological systems. RNA provides a promising building block for the construction of tunable regulatory components based on its rich regulatory capacity and our current understanding of the sequence–function relationship. One prominent example of RNA-based regulatory components is riboswitches, genetic elements that mediate ligand control of gene expression through diverse regulatory mechanisms. While characterization of natural and synthetic riboswitches has revealed that riboswitch function can be modulated through sequence alteration, no quantitative frameworks exist to investigate or guide riboswitch tuning. Here, we combined mathematical modeling and experimental approaches to investigate the relationship between riboswitch function and performance. Model results demonstrated that the competition between reversible and irreversible rate constants dictates performance for different regulatory mechanisms. We also found that practical system restrictions, such as an upper limit on ligand concentration, can significantly alter the requirements for riboswitch performance, necessitating alternative tuning strategies. Previous experimental data for natural and synthetic riboswitches as well as experiments conducted in this work support model predictions. From our results, we developed a set of general design principles for synthetic riboswitches. Our results also provide a foundation from which to investigate how natural riboswitches are tuned to meet systems-level regulatory demands

The regulatory subunit of PKA-I remains partially structured and undergoes β-aggregation upon thermal denaturation

Background: The regulatory subunit (R) of cAMP-dependent protein kinase (PKA) is a modular flexible protein that responds with large conformational changes to the binding of the effector cAMP. Considering its highly dynamic nature, the protein is rather stable. We studied the thermal denaturation of full-length RIα and a truncated RIα(92-381) that contains the tandem cyclic nucleotide binding (CNB) domains A and B. Methodology/Principal Findings: As revealed by circular dichroism (CD) and differential scanning calorimetry, both RIα proteins contain significant residual structure in the heat-denatured state. As evidenced by CD, the predominantly α-helical spectrum at 25°C with double negative peaks at 209 and 222 nm changes to a spectrum with a single negative peak at 212-216 nm, characteristic of β-structure. A similar α→β transition occurs at higher temperature in the presence of cAMP. Thioflavin T fluorescence and atomic force microscopy studies support the notion that the structural transition is associated with cross-β-intermolecular aggregation and formation of non-fibrillar oligomers. Conclusions/Significance: Thermal denaturation of RIα leads to partial loss of native packing with exposure of aggregation-prone motifs, such as the B' helices in the phosphate-binding cassettes of both CNB domains. The topology of the β-sandwiches in these domains favors inter-molecular β-aggregation, which is suppressed in the ligand-bound states of RIα under physiological conditions. Moreover, our results reveal that the CNB domains persist as structural cores through heat-denaturation. © 2011 Dao et al

Transforming growth factor beta signaling: The master sculptor of fingers

Transforming growth factor beta (TGF?) constitutes a large and evolutionarily conserved superfamily of secreted factors that play essential roles in embryonic development, cancer, tissue regeneration, and human degenerative pathology. Studies of this signaling cascade in the regulation of cellular and tissue changes in the three-dimensional context of a developing embryo have notably advanced in the understanding of the action mechanism of these growth factors. In this review, we address the role of TGF? signaling in the developing limb, focusing on its essential function in the morphogenesis of the autopod. As we discuss in this work, modern mouse genetic experiments together with more classical embryological approaches in chick embryos, provided very valuable information concerning the role of TGF? and Activin family members in the morphogenesis of the digits of tetrapods, including the formation of phalanxes, digital tendons, and interphalangeal joints. We emphasize the importance of the Activin and TGF? proteins as digit inducing factors and their critical interaction with the BMP signaling to sculpt the hand and foot morphology