Agricultural policies exacerbate honeybee pollination service supply-demand mismatches across Europe

Declines in insect pollinators across Europe have raised concerns about the supply of pollination services to agriculture. Simultaneously, EU agricultural and biofuel policies have encouraged substantial growth in the cultivated area of insect pollinated crops across the continent. Using data from 41 European countries, this study demonstrates that the recommended number of honeybees required to provide crop pollination across Europe has risen 4.9 times as fast as honeybee stocks between 2005 and 2010. Consequently, honeybee stocks were insufficient to supply >90% of demands in 22 countries studied. These findings raise concerns about the capacity of many countries to cope with major losses of wild pollinators and highlight numerous critical gaps in current understanding of pollination service supplies and demands, pointing to a pressing need for further research into this issue

Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes. Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid. Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers. A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals. Future research, including appropriate clinical investigation, should clarify these emerging concepts in the context of both genetic and epigenetic mechanisms dysregulated in cancer, and the pros and cons of specific dietary intervention strategies

Search for the decay B0→a1±ρ

DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF and DFG (Germany), INFN (Italy), FOM (The Netherlands), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from CONACyT (Mexico), Marie Curie EIF (European Union), the A. P. Sloan Foundation, the Research Corporation, and the Alexander von Humboldt Foundation

Measurement of branching fractions and charge asymmetries in B decays to an eta meson and a K-* meson

We present measurements of branching fractions and charge asymmetries for the decays B ->eta K-*, where K-* indicates a spin 0, 1, or 2 K pi system. The data sample corresponds to 344x10(6) B (B) over bar pairs collected with the BABAR detector at the PEP-II asymmetric-energy e(+)e(-) collider at SLAC. We measure the branching fractions (in units of 10(-6)): B(B-0 ->eta K-*0(892))=16.5 +/- 1.1 +/- 0.8, B(B+->eta K*+(892))=18.9 +/- 1.8 +/- 1.3, B(B-0 ->eta(K pi)(0)(*0))=11.0 +/- 1.6 +/- 1.5, B(B+->eta(K pi)(0)(*+))=18.2 +/- 2.6 +/- 2.6, B(B-0 ->eta K-2(*0)(1430))=9.6 +/- 1.8 +/- 1.1, and B(B+->eta K-2(*+)(1430))=9.1 +/- 2.7 +/- 1.4. We also determine the charge asymmetries for all decay modes

Measurement of the branching fraction ratios and CP asymmetries in B-→ D0 CP K-decays

We present a preliminary study of $B^- \to D^0_{CP} \pi^-$ and $B^- \to D^0_{CP} K^-$ decays, with the $D^0_{CP}$ reconstructed in the CP-odd eigenstates $K_s \pi^0$, $K_s \omega$, in the CP-even eigenstates $K^+ K^-$, $\pi^+ \pi^-$, and in the (non-CP) flavor eigenstate $K^\mp \pi^\pm$. Using a sample of about 382 million Y(4S) decays into BBbar pairs, collected with the BABAR detector operating at the PEP-II asymmetric-energy B Factory at SLAC, we measure the ratios of the branching fractions R_CP+- and the direct CP asymmetries A_CP+-. The results are: R_CP- = 0.81 \pm 0.10 (stat) \pm 0.05 (syst) R_CP+ = 1.07 \pm 0.10 (stat) \pm 0.04 (syst) A_CP- = -0.19 \pm 0.12 (stat) \pm 0.02 (syst) A_CP+ = 0.35 \pm 0.09 (stat) \pm 0.05 (syst