70 research outputs found
Spatial Guilds in the Serengeti Food Web Revealed by a Bayesian Group Model
Food webs, networks of feeding relationships among organisms, provide
fundamental insights into mechanisms that determine ecosystem stability and
persistence. Despite long-standing interest in the compartmental structure of
food webs, past network analyses of food webs have been constrained by a
standard definition of compartments, or modules, that requires many links
within compartments and few links between them. Empirical analyses have been
further limited by low-resolution data for primary producers. In this paper, we
present a Bayesian computational method for identifying group structure in food
webs using a flexible definition of a group that can describe both functional
roles and standard compartments. The Serengeti ecosystem provides an
opportunity to examine structure in a newly compiled food web that includes
species-level resolution among plants, allowing us to address whether groups in
the food web correspond to tightly-connected compartments or functional groups,
and whether network structure reflects spatial or trophic organization, or a
combination of the two. We have compiled the major mammalian and plant
components of the Serengeti food web from published literature, and we infer
its group structure using our method. We find that network structure
corresponds to spatially distinct plant groups coupled at higher trophic levels
by groups of herbivores, which are in turn coupled by carnivore groups. Thus
the group structure of the Serengeti web represents a mixture of trophic guild
structure and spatial patterns, in contrast to the standard compartments
typically identified in ecological networks. From data consisting only of nodes
and links, the group structure that emerges supports recent ideas on spatial
coupling and energy channels in ecosystems that have been proposed as important
for persistence.Comment: 28 pages, 6 figures (+ 3 supporting), 2 tables (+ 4 supporting
Combination of temozolomide with immunocytokine F16βIL2 for the treatment of glioblastoma
Glioblastoma patients are still not cured by the treatments available at the moment. We investigated the therapeutic properties of temozolomide in combination with F16-IL2, a clinical-stage immunocytokine consisting of human interleukin (IL)-2 fused to the human antibody F16, specific to the A1 domain of tenascin-C
Resveratrol Induces Growth Arrest and Apoptosis through Activation of FOXO Transcription Factors in Prostate Cancer Cells
Resveratrol, a naturally occurring phytopolyphenol compound, has attracted extensive interest in recent years because of its diverse pharmacological characteristics. Although resveratrol possesses chemopreventive properties against several cancers, the molecular mechanisms by which it inhibits cell growth and induces apoptosis have not been clearly understood. The present study was carried out to examine whether PI3K/AKT/FOXO pathway mediates the biological effects of resveratrol.Resveratrol inhibited the phosphorylation of PI3K, AKT and mTOR. Resveratrol, PI3K inhibitors (LY294002 and Wortmannin) and AKT inhibitor alone slightly induced apoptosis in LNCaP cells. These inhibitors further enhanced the apoptosis-inducing potential of resveratrol. Overexpression of wild-type PTEN slightly induced apoptosis. Wild type PTEN and PTEN-G129E enhanced resveratrol-induced apoptosis, whereas PTEN-G129R had no effect on proapoptotic effects of resveratrol. Furthermore, apoptosis-inducing potential of resveratrol was enhanced by dominant negative AKT, and inhibited by wild-type AKT and constitutively active AKT. Resveratrol has no effect on the expression of FKHR, FKHRL1 and AFX genes. The inhibition of FOXO phosphorylation by resveratrol resulted in its nuclear translocation, DNA binding and transcriptional activity. The inhibition of PI3K/AKT pathway induced FOXO transcriptional activity resulting in induction of Bim, TRAIL, p27/KIP1, DR4 and DR5, and inhibition of cyclin D1. Similarly, resveratrol-induced FOXO transcriptional activity was further enhanced when activation of PI3K/AKT pathway was blocked. Over-expression of phosphorylation deficient mutants of FOXO proteins (FOXO1-TM, FOXO3A-TM and FOXO4-TM) induced FOXO transcriptional activity, which was further enhanced by resveratrol. Inhibition of FOXO transcription factors by shRNA blocked resveratrol-induced upregulation of Bim, TRAIL, DR4, DR5, p27/KIP1 and apoptosis, and inhibition of cyclin D1 by resveratrol.These data suggest that FOXO transcription factors mediate anti-proliferative and pro-apoptotic effects of resveratrol, in part due to activation of extrinsic apoptosis pathway
History matters: childhood weight trajectories as a basis for planning community-based obesity prevention to adolescents
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