Dangerous Speech: A Cross-Cultural Study of Dehumanization and Revenge

Dehumanization is routinely invoked in social science and law as the primary factor in explaining how propaganda encourages support for, or participation in, violence against targeted outgroups. Yet the primacy of dehumanization is increasingly challenged by the apparent influence of revenge on collective violence. This study examines critically how various propaganda influence audiences. Although previous research stresses the dangers of dehumanizing propaganda, a recently published study found that only revenge propaganda significantly lowered outgroup empathy. Given the importance of these findings for law and the behavioral sciences, this research augments that recent study with two additional samples that were culturally distinct from the prior findings, showing again that only revenge propaganda was significant. To explore this effect further, we also conducted a facial electromyography (fEMG) among a small set of participants, finding that revenge triggered significantly stronger negative emotions against outgroups than dehumanization

Suppressor of sable [Su(s)] and Wdr82 down-regulate RNA from heat-shock-inducible repetitive elements by a mechanism that involves transcription termination

Although RNA polymerase II (Pol II) productively transcribes very long genes in vivo, transcription through extragenic sequences often terminates in the promoter-proximal region and the nascent RNA is degraded. Mechanisms that induce early termination and RNA degradation are not well understood in multicellular organisms. Here, we present evidence that the suppressor of sable [su(s)] regulatory pathway of Drosophila melanogaster plays a role in this process. We previously showed that Su(s) promotes exosome-mediated degradation of transcripts from endogenous repeated elements at an Hsp70 locus (Hsp70-αβ elements). In this report, we identify Wdr82 as a component of this process and show that it works with Su(s) to inhibit Pol II elongation through Hsp70-αβ elements. Furthermore, we show that the unstable transcripts produced during this process are polyadenylated at heterogeneous sites that lack canonical polyadenylation signals. We define two distinct regions that mediate this regulation. These results indicate that the Su(s) pathway promotes RNA degradation and transcription termination through a novel mechanism

Contributions on the development of the reproductive system in Sternotherus odoratus (latreille)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47667/1/441_2004_Article_BF00572100.pd

Glycogen metabolic genes are involved in trehalose-6-phosphate synthase-mediated regulation of pathogenicity by the rice blast fungus Magnaporthe oryzae.

© 2013 Badaruddin et al.Editor - Peter N. Dodds, Commonwealth Scientific and Industrial Research Organisation (CSIRO), AustraliaThis work was funded by the Biotechnology and Biological Sciences Research Council and a European Research Council Advanced Investigator Award to NJT. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.The filamentous fungus Magnaporthe oryzae is the causal agent of rice blast disease. Here we show that glycogen metabolic genes play an important role in plant infection by M. oryzae. Targeted deletion of AGL1 and GPH1, which encode amyloglucosidase and glycogen phosphorylase, respectively, prevented mobilisation of glycogen stores during appressorium development and caused a significant reduction in the ability of M. oryzae to cause rice blast disease. By contrast, targeted mutation of GSN1, which encodes glycogen synthase, significantly reduced the synthesis of intracellular glycogen, but had no effect on fungal pathogenicity. We found that loss of AGL1 and GPH1 led to a reduction in expression of TPS1 and TPS3, which encode components of the trehalose-6-phosphate synthase complex, that acts as a genetic switch in M. oryzae. Tps1 responds to glucose-6-phosphate levels and the balance of NADP/NADPH to regulate virulence-associated gene expression, in association with Nmr transcriptional inhibitors. We show that deletion of the NMR3 transcriptional inhibitor gene partially restores virulence to a Δagl1Δgph1 mutant, suggesting that glycogen metabolic genes are necessary for operation of the NADPH-dependent genetic switch in M. oryzae.Biotechnology and Biological Sciences Research Council (BBSRC)European Research Council (ERC

Studies on germ cells. I. The history of the germ cells in insects with special reference to the Keimbahn-determinants. II. The origin and significance of the Keimbahn-determinants in animals

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50235/1/1050250302_ftp.pd

Racial and Spatial Relations as Fundamental Determinants of Health in Detroit

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71561/1/1468-0009.00028.pd

SCD1 Inhibition Causes Cancer Cell Death by Depleting Mono-Unsaturated Fatty Acids

Increased metabolism is a requirement for tumor cell proliferation. To understand the dependence of tumor cells on fatty acid metabolism, we evaluated various nodes of the fatty acid synthesis pathway. Using RNAi we have demonstrated that depletion of fatty-acid synthesis pathway enzymes SCD1, FASN, or ACC1 in HCT116 colon cancer cells results in cytotoxicity that is reversible by addition of exogenous fatty acids. This conditional phenotype is most pronounced when SCD1 is depleted. We used this fatty-acid rescue strategy to characterize several small-molecule inhibitors of fatty acid synthesis, including identification of TOFA as a potent SCD1 inhibitor, representing a previously undescribed activity for this compound. Reference FASN and ACC inhibitors show cytotoxicity that is less pronounced than that of TOFA, and fatty-acid rescue profiles consistent with their proposed enzyme targets. Two reference SCD1 inhibitors show low-nanomolar cytotoxicity that is offset by at least two orders of magnitude by exogenous oleate. One of these inhibitors slows growth of HCT116 xenograft tumors. Our data outline an effective strategy for interrogation of on-mechanism potency and pathway-node-specificity of fatty acid synthesis inhibitors, establish an unambiguous link between fatty acid synthesis and cancer cell survival, and point toward SCD1 as a key target in this pathway

Reactivation of tectonics, crustal underplating, and uplift after 60 Myr of passive subsidence, Raukumara Basin, Hikurangi-Kermadec fore arc, New Zealand: implications for global growth and recycling of continents

We use seismic reflection and refraction data to determine crustal structure, to map a fore-arc basin containing 12 km of sediment, and to image the subduction thrust at 35 km depth. Seismic reflection megasequences within the basin are correlated with onshore geology: megasequence X, Late Cretaceous and Paleogene marine passive margin sediments; megasequence Y, a similar to 10,000 km(3) submarine landslide emplaced during subduction initiation at 22 Ma; and megasequence Z, a Neogene subduction margin megasequence. The Moho lies at 17 km beneath the basin center and at 35 km at the southern margin. Beneath the western basin margin, we interpret reflective units as deformed Gondwana fore-arc sediment that was thrust in Cretaceous time over oceanic crust 7 km thick. Raukumara Basin has normal faults at its western margin and is uplifted along its eastern and southern margins. Raukumara Basin represents a rigid fore-arc block > 150 km long, which contrasts with widespread faulting and large Neogene vertical axis rotations farther south. Taper of the western edge of allochthonous unit Y and westward thickening and downlap of immediately overlying strata suggest westward or northwestward paleoslope and emplacement direction rather than southwestward, as proposed for the correlative onshore allochthon. Spatial correlation between rock uplift of the eastern and southern basin margins with the intersection between Moho and subduction thrust leads us to suggest that crustal underplating is modulated by fore-arc crustal thickness. The trench slope has many small extensional faults and lacks coherent internal reflections, suggesting collapse of indurated rock, rather than accretion of > 1 km of sediment from the downgoing plate. The lack of volcanic intrusion east of the active arc, and stratigraphic evidence for the broadening of East Cape Ridge with time, suggests net fore-arc accretion since 22 Ma. We propose a cyclical fore-arc kinematic: rock moves down a subduction channel to near the base of the crust, where underplating drives rock uplift, oversteepens the trench slope, and causes collapse toward the trench and subduction channel. Cyclical rock particle paths led to persistent trench slope subsidence during net accretion. Existing global estimates of fore-arc loss are systematically too high because they assume vertical particle paths. Citation: Sutherland, R., et al. (2009), Reactivation of tectonics, crustal underplating, and uplift after 60 Myr of passive subsidence, Raukumara Basin, Hikurangi-Kermadec fore arc, New Zealand: Implications for global growth and recycling of continents, Tectonics, 28, TC5017, doi: 10.1029/2008TC002356