Who do I say I am? Evangelical identity and academic writing

This dissertation explores how evangelical Christian students negotiate their identities in their academic writing. Specifically, this study addresses two overarching questions: 1. What happens to evangelical students when they write academically? 2. How are evangelical students\u27 identities integrated into and implicated by their academic writing? In answering these questions, this project seeks to bridge two key scholarly discussions in rhetoric and composition, namely the discussions about writing and identity and about evangelical discourse. This project also seeks to challenge reductive stereotypes about evangelicals perpetuated in rhetoric and composition and in the academy at large. The research for this project comes from case studies conducted with four evangelical students---two undergraduates and two graduates. The case studies involved a series of interviews and focused on the academic writing participants completed for their first-year writing courses or their graduate programs in rhetoric and composition. The results of this study suggest that faith shapes academic writing in highly idiosyncratic ways. Even pieces of writing that don\u27t appear to have anything to do with faith are often shaped by the motives and beliefs supplied by these students\u27 evangelical identities. Equally important, this study shows that the act of participating in academic discourse---of writing academically---shapes these students\u27 identities. Each participant acknowledged that they had to accommodate the conventions of academic discourse that led them to construct their identities in ways that don\u27t align with their evangelical senses of self. These students\u27 experiences speak to the truth behind Donna LeCourt\u27s conclusion in Identity Matters: academic discourse does influence the construction of self (143). How it does so is the focus of this dissertation

VMY-1-103 is a novel CDK inhibitor that disrupts chromosome organization and delays metaphase progression in medulloblastoma cells

Medulloblastoma is the most prevalent of childhood brain malignancies, constituting 25% of childhood brain tumors. Craniospinal radiotherapy is a standard of care, followed by a 12 mo regimen of multi-agent chemotherapy. For children less than 3 y of age, irradiation is avoided due to its destructive effects on the developing nervous system. Long-term prognosis is worst for these youngest children and more effective treatment strategies with a better therapeutic index are needed. VMY-1-103, a novel dansylated analog of purvalanol B, was previously shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. In the current study, we have identified new mechanisms of action by which VMY-1-103 affected cellular proliferation in medulloblastoma cells. VMY-1-103, but not purvalanol B, significantly decreased the proportion of cells in s phase and increased the proportion of cells in G2/M. VMY-1-103 increased the sub G1 fraction of apoptotic cells, induced paRp and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. p21CIp1/WaF1 levels were greatly suppressed. Importantly, we found that while both VMY and flavopiridol inhibited intracellular CDK1 catalytic activity, VMY-1-103 was unique in its ability to severely disrupt the mitotic spindle apparatus, significantly delaying metaphase and disrupting mitosis. Our data suggest that VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma

Arsenic trioxide inhibits human cancer cell growth and tumor development in mice by blocking Hedgehog/GLI pathway

The Hedgehog (Hh) pathway is activated in some human cancers, including medulloblastoma. The glioma-associated oncogene homolog (GLI) transcription factors are critical mediators of the activated Hh pathway, and their expression may be elevated in some tumors independent of upstream Hh signaling. Thus, therapies targeting GLI transcription factors may benefit a wide spectrum of patients with mutations at different nodal points of the Hh pathway. In this study, we present evidence that arsenic trioxide (ATO) suppresses human cancer cell growth and tumor development in mice by inhibiting GLI1. Mechanistically, ATO directly bound to GLI1 protein, inhibited its transcriptional activity, and decreased expression of endogenous GLI target genes. Consistent with this, ATO inhibited the growth of human cancer cell lines that depended on upregulated GLI expression in vitro and in vivo in a xenograft model of Ewing sarcoma. Furthermore, ATO improved survival of a clinically relevant spontaneous mouse model of medulloblastoma with activated Hh pathway signaling. Our results establish ATO as a Hh pathway inhibitor acting at the level of GLI1 both in vitro and in vivo. These results warrant the clinical investigation of ATO for tumors with activated Hh/GLI signaling, in particular patients who develop resistance to current therapies targeting the Hh pathway upstream of GLI

Evaluation of cloud and water vapor simulations in CMIP5 climate models Using NASA "A-Train" satellite observations

International audience[1] Using NASA's A-Train satellite measurements, we evaluate the accuracy of cloud water content (CWC) and water vapor mixing ratio (H2O) outputs from 19 climate models submitted to the Phase 5 of Coupled Model Intercomparison Project (CMIP5), and assess improvements relative to their counterparts for the earlier CMIP3. We find more than half of the models show improvements from CMIP3 to CMIP5 in simulating column-integrated cloud amount, while changes in water vapor simulation are insignificant. For the 19 CMIP5 models, the model spreads and their differences from the observations are larger in the upper troposphere (UT) than in the lower or middle troposphere (L/MT). The modeled mean CWCs over tropical oceans range from ~3% to ~15× of the observations in the UT and 40% to 2× of the observations in the L/MT. For modeled H2Os, the mean values over tropical oceans range from ~1% to 2× of the observations in the UT and within 10% of the observations in the L/MT. The spatial distributions of clouds at 215 hPa are relatively well-correlated with observations, noticeably better than those for the L/MT clouds. Although both water vapor and clouds are better simulated in the L/MT than in the UT, there is no apparent correlation between the model biases in clouds and water vapor. Numerical scores are used to compare different model performances in regards to spatial mean, variance and distribution of CWC and H2O over tropical oceans. Model performances at each pressure level are ranked according to the average of all the relevant scores for that level. © 2012. American Geophysical Union