Aerodynamic roughness measured in the field and simulated in a wind tunnel

This study evaluates how well values of aerodynamic surface roughness, z sub 0, measured over scale models in wind tunnels correlate with values of z sub 0 measured at full scale in the field. A field experiment was conducted in which values of z sub 0 and u* (wind friction speed) were measured over three arrays of non-erodible roughness elements on a dry lake bed. Wind profiles were measured by ten anemometers on a 15 m mast under thermally neutral atmospheric conditions. Values of z sub 0 increased from .00014 m (dry lake bed only) to .026 m with increasing roughness element density. The three roughness element arrays were simulated at 1/10 and 1/20 scale in an open-circuit atmospheric boundary-layer wind tunnel. Velocities were measured with a boundary-layer pitot-tube rake from the same relative position within the scale model arrays as the anemometers were relative to the field arrays. Each array at each scale was sampled three times at five freestream velocities. Average values of z sub 0 for each model array at each scale were compared with full-scale values of z sub 0 obtained in the field. The field vs. wind tunnel correspondence of z sub 0 is found to be z sub 0 field = 0.2661 x (z sub(0 model) x scale(exp -1))exp .8159

Development of wind tunnel techniques for the solution of problems in planetary Aeolian processes

Kutzbach reports wind profiles over a series of roughness elements on a frozen lake and how the wind profile changed as the surface roughness was varied. The approach of the current study was to duplicate Kutzbach's roughness arrays in the wind tunnel at 1/20 and 1/40 scales, and to compare the wind profiles over these scale models to those derived by Kutzbach at full scale in the field. The effects of scale differences and data reduction techniques are discussed. Although the study suggests that wind tunnel scale models can predict parameters measured in the field, the development of more definitive guidelines requires a field experiment designed specifically for comparison with wind tunnel results

Regulation of arginine transport by GCN2 eIF2 kinase is important for replication of the intracellular parasite Toxoplasma gondii

Toxoplasma gondii is a prevalent protozoan parasite that can infect any nucleated cell but cannot replicate outside of its host cell. Toxoplasma is auxotrophic for several nutrients including arginine, tryptophan, and purines, which it must acquire from its host cell. The demands of parasite replication rapidly deplete the host cell of these essential nutrients, yet Toxoplasma successfully manages to proliferate until it lyses the host cell. In eukaryotic cells, nutrient starvation can induce the integrated stress response (ISR) through phosphorylation of an essential translation factor eIF2. Phosphorylation of eIF2 lowers global protein synthesis coincident with preferential translation of gene transcripts involved in stress adaptation, such as that encoding the transcription factor ATF4 (CREB2), which activates genes that modulate amino acid metabolism and uptake. Here, we discovered that the ISR is induced in host cells infected with Toxoplasma. Our results show that as Toxoplasma depletes host cell arginine, the host cell phosphorylates eIF2 via protein kinase GCN2 (EIF2AK4), leading to induced ATF4. Increased ATF4 then enhances expression of the cationic amino acid transporter CAT1 (SLC7A1), resulting in increased uptake of arginine in Toxoplasma-infected cells. Deletion of host GCN2, or its downstream effectors ATF4 and CAT1, lowers arginine levels in the host, impairing proliferation of the parasite. Our findings establish that Toxoplasma usurps the host cell ISR to help secure nutrients that it needs for parasite replication

GCN2-like eIF2α kinase manages the amino acid starvation response in Toxoplasma gondii

The apicomplexan protozoan Toxoplasma gondii is a significant human and veterinary pathogen. As an obligate intracellular parasite, Toxoplasma depends on nutrients provided by the host cell and needs to adapt to limitations in available resources. In mammalian cells, translational regulation via GCN2 phosphorylation of the alpha subunit of eukaryotic translation initiation factor 2 (eIF2α) is a key mechanism for adapting to nutrient stress. Toxoplasma encodes two GCN2-like protein kinases, TgIF2K-C and TgIF2K-D. We previously showed that TgIF2K-D phosphorylates T. gondii eIF2α (TgIF2α) upon egress from the host cell, which enables the parasite to overcome exposure to the extracellular environment. However, the function of TgIF2K-C remained unresolved. To determine the functions of TgIF2K-C in the parasite, we cloned the cDNA encoding TgIF2K-C and generated knockout parasites of this TgIF2α kinase to study its function during the lytic cycle. The TgIF2K-C knockout did not exhibit a fitness defect compared with parental parasites. However, upon infection of human fibroblasts that were subsequently cultured in glutamine-free medium, the intracellular TgIF2K-C knockout parasites were impeded for induced phosphorylation of TgIF2α and showed a 50% reduction in the number of plaques formed compared with parental parasites. Furthermore, we found that this growth defect in glutamine-free media was phenocopied in parasites expressing only a non-phosphorylatable TgIF2α (TgIF2α-S71A), but not in a TgIF2K-D knockout. These studies suggest that Toxoplasma GCN2-like kinases TgIF2K-C and TgIF2K-D evolved to have distinct roles in adapting to changes in the parasite’s environment

OCC Letter from Michael Sullivan and Ron Frake to John Lyons Re Subprime CDO Valuation and Oversight Review Conculsion Memorandum

This letter is addressed to John Lyon

Thoughts on Commercial Speech: A Roundtable Discussion

Adam Liptak, the legal affairs writer for The New York Times, moderates a lively discussion about commercial speech between three esteemed constitutional scholars: Professor Erwin Chemerinsky of Duke University School of Law; Professor Kathleen Sullivan of Stanford Law School; and Professor Steve Shiffrin of Cornell Law School. These scholars debate the proper definition of defining commercial speech, how the corporate identity of a speaker and the content of the speech determines the level of First Amendment protection, whether it is possible to demarcate commercial speech from political speech, and the problems of paternalism and viewpoint discrimination in this complex and conflicted area

Thoughts on Commercial Speech: A Roundtable Discussion

Adam Liptak, the legal affairs writer for The New York Times, moderates a lively discussion about commercial speech between three esteemed constitutional scholars: Professor Erwin Chemerinsky of Duke University School of Law; Professor Kathleen Sullivan of Stanford Law School; and Professor Steve Shiffrin of Cornell Law School. These scholars debate the proper definition of defining commercial speech, how the corporate identity of a speaker and the content of the speech determines the level of First Amendment protection, whether it is possible to demarcate commercial speech from political speech, and the problems of paternalism and viewpoint discrimination in this complex and conflicted area