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12 páginas, 4 tablas, 11 figuras, 1 apéndice., Tandem runs are a form of recruitment in ants. During a tandem run, a single leader teaches one follower the route to important resources such as sources of food or better nest sites. In the present study, we investigate what tandem leaders and followers do, in the context of nest emigration, if their partner goes missing. Our experiments involved removing either leaders or followers at set points during tandem runs. Former leaders first stand still and wait for their missing follower but then most often proceed alone to the new nest site. By contrast, former followers often first engage in a Brownian search, for almost exactly the time that their former leader should have waited for them, and then former followers switch to a superdiffusive search. In this way, former followers first search their immediate neighbourhood for their lost leader before becoming ever more wide ranging so that in the absence of their former leader they can often find the new nest, re-encounter the old one or meet a new leader. We also show that followers gain useful information even from incomplete tandem runs. These observations point to the important principle that sophisticated communication behaviours may have evolved as anytime algorithms, i.e. procedures that are beneficial even if they do not run to completion., T.O.R. and A.B.S.-F. gratefully acknowledge EPSRC grant EP/E061796/1. F.B. acknowledges a Ramon y Cajal contract from the Spanish Ministry of Science and Innovation. N.R.F. wishes to thank both the EPSRC (grant no EP/D076226/1) and the BBSRC (grant no. BB/G02166X/1) for their support.

1. Protease activated receptor-2 (PAR2) is a seven transmembrane domain G protein coupled receptor proteolytically activated. PAR2, together with other PARs, can be also activated by peptides mimicking the sequence of the receptor tethered ligand. We have evaluated the effect of systemic administration of a peptide activating PAR2 (PAR2-AP, SLIGRL) on histamine-induced increase in lung resistances in the guinea-pig. 2. Intravenous administration of PAR2-AP (1 mg kg(-1)) significantly inhibited histamine-induced increase in lung resistance in a time-dependent fashion that was not abolished by indomethacin or vagotomy. 3. Bronchoprotective effect of PAR2-AP was not reversed by the cyclo-oxygenase inhibitor, indomethacin, the nitric oxide synthetase inhibitor, L-NAME, nor by the non-selective beta-antagonist, propranolol. 4. Indomethacin augmented the bronchoconstriction to histamine which was inhibited by PAR2-AP. Furthermore, in vagotomized animals, the bronchial hyper-responsiveness to histamine was significantly reduced, and in these circumstances, PAR2-AP still retained the capacity to provide bronchoprotection against histamine. 5. PAR2-AP also produced a modest reduction in histamine-induced protein leakage in trachea and upper bronchi. 6. Our results indicated that PAR2 might have a bronchoprotective role in the guinea-pig in vivo independent of prostaglandin or nitric oxide release.

Glioblastoma is one of the most challenging forms of cancer to treat. Here we describe a computational platform that integrates the analysis of copy number variations and somatic mutations and unravels the landscape of in-frame gene fusions in glioblastoma. We found mutations with loss of heterozygosity in LZTR1, encoding an adaptor of CUL3-containing E3 ligase complexes. Mutations and deletions disrupt LZTR1 function, which restrains the self renewal and growth of glioma spheres that retain stem cell features. Loss-of-function mutations in CTNND2 target a neural-specific gene and are associated with the transformation of glioma cells along the very aggressive mesenchymal phenotype. We also report recurrent translocations that fuse the coding sequence of EGFR to several partners, with EGFR-SEPT14 being the most frequent functional gene fusion in human glioblastoma. EGFR-SEPT14 fusions activate STAT3 signaling and confer mitogen independence and sensitivity to EGFR inhibition. These results provide insights into the pathogenesis of glioblastoma and highlight new targets for therapeutic intervention. © 2013 Nature America, Inc. All rights reserved.