The Ecology of fear: host foraging behavior varies with the spatio-temporal abundance of a dominant ectoparasite.

Prey engage in myriad behaviors to avoid predation, and these indirect effects of predators on their prey are often measured by the amount of food abandoned by a forager (the "giving-up density", or GUD) in a given habitat. Recent evidence suggests that hosts may engage in comparable behaviors to avoid exposure to parasites. We investigated changes in local foraging and regional space use by mammal hosts for the lone star tick (Amblyomma americanum), using GUDs as an indicator of the perceived risk of parasitism. At eight study sites at the Tyson Research Center (Eureka, MO), we placed two feeding trays, one on the ground and one at 1.5 m height in a tree, in order to assess how the emergence of ground-dwelling ticks affected foraging by several mammal species both locally (between the two GUD stations) and regionally (among the eight sites, mean distance 1064 m apart). Though GUDs did not differ between the ground and tree GUD stations, we did find that greater amounts of food were "given-up" at sites with higher abundances of ticks. This increase in food abandonment suggests that hosts respond to the risk of parasitism and alter their space use accordingly, potentially affecting a cascade of other ecological interactions across large spatial scales.

Fibroblast growth factor (FGF) and FGF receptor-mediated autocrine signaling in non-small-cell lung cancer cells.

Despite widespread expression of epidermal growth factor (EGF) receptors (EGFRs) and EGF family ligands in non-small-cell lung cancer (NSCLC), EGFR-specific tyrosine kinase inhibitors (TKIs) such as gefitinib exhibit limited activity in this cancer. We propose that autocrine growth signaling pathways distinct from EGFR are active in NSCLC cells. To this end, gene expression profiling revealed frequent coexpression of specific fibroblast growth factors (FGFs) and FGF receptors (FGFRs) in NSCLC cell lines. It is noteworthy that FGF2 and FGF9 as well as FGFR1 IIIc and/or FGFR2 IIIc mRNA and protein are frequently coexpressed in NSCLC cell lines, especially those that are insensitive to gefitinib. Specific silencing of FGF2 reduced anchorage-independent growth of two independent NSCLC cell lines that secrete FGF2 and coexpress FGFR1 IIIc and/or FGFR2 IIIc. Moreover, a TKI [(+/-)-1-(anti-3-hydroxy-cyclopentyl)-3-(4-methoxy-phenyl)-7-phenylamino-3,4-dihydro-1H-pyrimido-[4,5-d]pyrimidin-2-one (RO4383596)] that targets FGFRs inhibited basal FRS2 and extracellular signal-regulated kinase phosphorylation, two measures of FGFR activity, as well as proliferation and anchorage-independent growth of NSCLC cell lines that coexpress FGF2 or FGF9 and FGFRs. By contrast, RO4383596 influenced neither signal transduction nor growth of NSCLC cell lines lacking FGF2, FGF9, FGFR1, or FGFR2 expression. Thus, FGF2, FGF9 and their respective high-affinity FGFRs comprise a growth factor autocrine loop that is active in a subset of gefitinib-insensitive NSCLC cell lines.