Avifauna discard packages and bone damage resulting from human consumption processes

Few actualistic studies of the patterns resulting from human preparation and consumption of birds inform interpretations of archeological avifauna assemblages. This study focuses on developing new and adding to existing interpretive models. We examine differences in bone modifications produced by a culturally homogeneous group of eaters consuming medium-sized birds cooked using three cross-culturally common methods. We use the analytical concept of discard packages to capture variability in how groups of skeletal elements might be deposited into the archeological record. We also examine chop/cut marks, burn marks, and chew marks as these are variables that archeologists frequently use to identify and interpret anthropogenic avifaunal assemblages. We find that the creation of discard packages appears to be culturally motivated and varies little within our group of eaters, but the degree to which the associated elements are disaggregated during consumption is highly variable and depends on individual preference. Additionally, we find that while the presence and locations of chop marks are consistent across cooking methods and individual consumption preferences, the presence and locations of cut marks, burn marks, and chew marks are affected by cooking methods, individual preferences, or both

Interview with Dr. James Osborne, 2011-2012 IEMA Postdoctoral Fellow

Dr. James F. Osborne is currently the Postdoctoral Fellow at the Institute for European and Mediterranean Archaeology at the University of Buffalo, SUNY. He received a Bachelor’s of Arts with honors in Ancient Near Eastern Studies from the University of Toronto. James attended Harvard University for his graduate work, earning a Master’s of Arts and Doctor of Philosophy in Archaeology of the Levant, with the latter being awarded with distinction. He has recently been awarded the Andrew W. Mellon Postdoctoral Fellowship in the Humanities at Johns Hopkins University. Drawing from multiple disciplines, such as Geographical Information System and built environment studies, Dr. Osborne explores issues of territoriality and politics in Iron Age Turkey

TLR4/MyD88/PI3K interactions regulate TLR4 signaling

TLRs activate immune responses by sensing microbial structures such as bacterial LPS, viral RNA, and endogenous “danger” molecules released by damaged host cells. MyD88 is an adapter protein that mediates signal transduction for most TLRs and leads to activation of NF-κB and MAPKs and production of proinflammatory cytokines. TLR4-mediated signaling also leads to rapid activation of PI3K, one of a family of kinases involved in regulation of cell growth, apoptosis, and motility. LPS stimulates phosphorylation of Akt, a downstream target of PI3K, in wild-type (WT) mouse macrophages. LPS-induced phosphorylation of Akt serine 473 was blunted in MyD88−/− macrophages and was completely TLR4-dependent. MyD88 and p85 were shown previously to co-immunoprecipitate, and a YXXM motif within the Toll-IL-1 resistance (TIR) domain of MyD88 was suggested to be important for this interaction. To test this hypothesis, we compared expressed MyD88 variants with mutations within the YXXM motif or lacking the TIR domain or death domain and measured their capacities to bind PI3K p85, MyD88, and TLR4 by co-immunoprecipitation analyses. The YXXM → YXXA mutant MyD88 bound more strongly to p85, TLR4, and WT MyD88 than the other variants, yet was significantly less active than WT MyD88, suggesting that sustained interaction of MyD88/PI3K with the TLR4 intracellular “signaling platform” negatively regulates signaling. We propose a hypothetical model in which sustained PI3K activity at the membrane limits the availability of the PI3K substrate, thereby negatively regulating signaling