Radiative Leptonic BcB_c Decays

We analyze the radiative leptonic $B_c$ decay mode: $B_c \to \ell \nu \gamma$ ($\ell=e, \mu$) using a QCD-inspired constituent quark model. The prediction: ${\cal B}(B_c \to \ell \nu \gamma)\simeq 3 \times 10^{-5}$ makes this channel experimentally promising in view of the large number of $B_c$ mesons which are expected to be produced at the future hadron facilities.Comment: LaTex, 12 pages, 2 figures. A discussion on gauge invariance added. Numerical results update

Observation of the rare eta->e+e-e+e- decay with the KLOE experiment

We report the first observation of the rare eta->e+e-e+e- decay based on 1.7 fb^{-1} collected by the KLOE experiment at the DAFNE phi-factory. The selection of the e+e-e+e- final state is fully inclusive of radiation. We have identified 362 +- 29 events resulting in a branching ratio of (2.4 +- 0.2_stat+bckg +- 0.1_syst) x 10^{-5}.Comment: 12 pages, 3 figures, to be published on PL

A Novel Role of RASSF9 in Maintaining Epidermal Homeostasis

The physiological role of RASSF9, a member of the Ras-association domain family (RASSF), is currently unclear. Here, we report a mouse line in which an Epstein-Barr virus Latent Membrane Protein 1 (LMP1) transgene insertion has created a 7.2-kb chromosomal deletion, which abolished RASSF9 gene expression. The RASSF9-null mice exhibited interesting phenotypes that resembled human ageing, including growth retardation, short lifespan, less subcutaneous adipose layer and alopecia. In the wild-type mice, RASSF9 is predominantly expressed in the epidermal keratinocytes of skin, as determined by quantitative reverse-transcription PCR, immunofluorescence and in situ hybridization. In contrast, RASSF9−/− mice presented a dramatic change in epithelial organization of skin with increased proliferation and aberrant differentiation as detected by bromodeoxyuridine incorporation assays and immunofluorescence analyses. Furthermore, characteristic functions of RASSF9−/− versus wild type (WT) mouse primary keratinocytes showed significant proliferation linked to a reduction of p21Cip1 expression under growth or early differentiation conditions. Additionally, in RASSF9−/− keratinocytes there was a drastic down-modulation of terminal differentiation markers, which could be rescued by infection with a recombinant adenovirus, Adv/HA-RASSF9. Our results indicate a novel and significant role of RASSF9 in epidermal homeostasis

A Unified Approach to Distance-Two Colouring of Graphs on Surfaces

In this paper we introduce the notion of $\Sigma$-colouring of a graph $G$: For given subsets $\Sigma(v)$ of neighbours of $v$, for every $v\in V(G)$, this is a proper colouring of the vertices of $G$ such that, in addition, vertices that appear together in some $\Sigma(v)$ receive different colours. This concept generalises the notion of colouring the square of graphs and of cyclic colouring of graphs embedded in a surface. We prove a general result for graphs embeddable in a fixed surface, which implies asymptotic versions of Wegner's and Borodin's Conjecture on the planar version of these two colourings. Using a recent approach of Havet et al., we reduce the problem to edge-colouring of multigraphs, and then use Kahn's result that the list chromatic index is close to the fractional chromatic index. Our results are based on a strong structural lemma for graphs embeddable in a fixed surface, which also implies that the size of a clique in the square of a graph of maximum degree $\Delta$ embeddable in some fixed surface is at most $\frac32\,\Delta$ plus a constant.Comment: 36 page

NIBBS-Search for Fast and Accurate Prediction of Phenotype-Biased Metabolic Systems

Understanding of genotype-phenotype associations is important not only for furthering our knowledge on internal cellular processes, but also essential for providing the foundation necessary for genetic engineering of microorganisms for industrial use (e.g., production of bioenergy or biofuels). However, genotype-phenotype associations alone do not provide enough information to alter an organism's genome to either suppress or exhibit a phenotype. It is important to look at the phenotype-related genes in the context of the genome-scale network to understand how the genes interact with other genes in the organism. Identification of metabolic subsystems involved in the expression of the phenotype is one way of placing the phenotype-related genes in the context of the entire network. A metabolic system refers to a metabolic network subgraph; nodes are compounds and edges labels are the enzymes that catalyze the reaction. The metabolic subsystem could be part of a single metabolic pathway or span parts of multiple pathways. Arguably, comparative genome-scale metabolic network analysis is a promising strategy to identify these phenotype-related metabolic subsystems. Network Instance-Based Biased Subgraph Search (NIBBS) is a graph-theoretic method for genome-scale metabolic network comparative analysis that can identify metabolic systems that are statistically biased toward phenotype-expressing organismal networks. We set up experiments with target phenotypes like hydrogen production, TCA expression, and acid-tolerance. We show via extensive literature search that some of the resulting metabolic subsystems are indeed phenotype-related and formulate hypotheses for other systems in terms of their role in phenotype expression. NIBBS is also orders of magnitude faster than MULE, one of the most efficient maximal frequent subgraph mining algorithms that could be adjusted for this problem. Also, the set of phenotype-biased metabolic systems output by NIBBS comes very close to the set of phenotype-biased subgraphs output by an exact maximally-biased subgraph enumeration algorithm ( MBS-Enum ). The code (NIBBS and the module to visualize the identified subsystems) is available at http://freescience.org/cs/NIBBS

Cell Death or Survival Promoted by Alternative Isoforms of ErbB4

The report demonstrates that two distinct isoforms of the ErbB4 receptor tyrosine kinase stimulate either proliferation or apoptosis by mechanisms involving differential transcriptional regulation of the PDGFRA gene. These data have implications for developing approaches to target ErbB4 signaling in cancer

Epoxyeicosanoids promote organ and tissue regeneration

Epoxyeicosatrienoic acids (EETs), lipid mediators produced by cytochrome P450 epoxygenases, regulate inflammation, angiogenesis, and vascular tone. Despite pleiotropic effects on cells, the role of these epoxyeicosanoids in normal organ and tissue regeneration remains unknown. EETs are produced predominantly in the endothelium. Normal organ and tissue regeneration require an active paracrine role of the microvascular endothelium, which in turn depends on angiogenic growth factors. Thus, we hypothesize that endothelial cells stimulate organ and tissue regeneration via production of bioactive EETs. To determine whether endothelial-derived EETs affect physiologic tissue growth in vivo, we used genetic and pharmacological tools to manipulate endogenous EET levels. We show that endothelial-derived EETs play a critical role in accelerating tissue growth in vivo, including liver regeneration, kidney compensatory growth, lung compensatory growth, wound healing, corneal neovascularization, and retinal vascularization. Administration of synthetic EETs recapitulated these results, whereas lowering EET levels, either genetically or pharmacologically, delayed tissue regeneration, demonstrating that pharmacological modulation of EETs can affect normal organ and tissue growth. We also show that soluble epoxide hydrolase inhibitors, which elevate endogenous EET levels, promote liver and lung regeneration. Thus, our observations indicate a central role for EETs in organ and tissue regeneration and their contribution to tissue homeostasis