POTENTIAL BENEFITS OF RICE VARIETY AND WATER MANAGEMENT IMPROVEMENTS IN THE TEXAS GULF COAST

The welfare benefits from potential rice yield-enhancing and water-saving research programs and their distributional implications under alternative farm program provisions are compared. This is done in an ex ante surplus maximization framework by using a multiregional, price endogenous mathematical programming model of U.S. agriculture. The simulation results indicate that government price support policies have profound impacts on the distribution of research benefits and distort interest group incentives and rankings for allocation of resources to research.Agricultural and Food Policy, Research and Development/Tech Change/Emerging Technologies,

A First Person Shooter/Real Time Strategy Hybrid: Lessons Learned

Today's military training bears little resemblance to the methods of previous generations. The Cold War is over and the enemy has changed. Doctrine that was once useful is now woefully out of date. No longer are we confronting a predictable nation but instead a diverse collection of independent fighters spread out over several countries. The enemy has changed, his tactics have changed amI cin.:urnsLance dictates that we must change as well. The wars in Iraq and Afghanistan have tested virtually all aspects of the military's support infrastructure. After fighting continuously for over a decade, many weaknesses have been revealed by the steady grind of war. Chief among them is the inability of the military to rapidly and adequately train its soldiers in the latest doctrines. In response to the enemy developing new strategies on a near monthly basis, the Joint Training Counter-IED Operations Integration Center (JTCOIC) was first created. Designed to supplement the current training system, it would attempt to address the current training shortfalls. As a result, new methods were devised to streamline training

Cytochrome P4501A is Induced in Endothelial Cell Lines From the Kidney and Lung of the Bottlenose Dolphin, \u3ci\u3eTursiops truncatus\u3c/i\u3e

Marine mammals respond to the presence of polycyclic and planar halogenated aromatic hydrocarbons (PAH or PHAH) with the induced expression in endothelium of cytochrome P4501A1, regulated through the aryl hydrocarbon receptor (AHR) transcription factor. Physiological responses in other animals, such as edema and inflammation indicate that the endothelium may be compromised by exposure to AHR agonists, which are ubiquitous in the marine environment. In other mammals and fish the cellular and molecular consequences of exposure to AHR agonists have been elucidated in cultured endothelial cells. We have cultured and characterized cetacean endothelial cells (EC) and used them in induction studies. Endothelial cells were cultured from the lung and kidney of the bottlenose dolphin, Tursiops truncates, and exposed to the AHR agonists β-naphthoflavone (βNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). βNF (1–3 μM) induced significant increases in CYP1A1 (O-deethylation of 7-ethoxyresorufin to resorufin; EROD) activity to 3.6 and 0.92 pmol/mg/min in lung and kidney EC, respectively. TCDD was more potent than βNF, and more efficacious, with maximum induction of CYP1A1 activity of 10.1 and 15.2 pmol/mg/min in lung and kidney EC at 3–10 nM TCDD. The differential response indicates that the lung and kidney endothelial cells in culture retain the ability to respond in a selective manner to specific stimuli. Both the molecular mechanisms of induction and the physiological consequences, especially in the vasculature, of toxicant exposure can be studied in this system

Cytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin, Tursiops truncatus

Author Posting. © The Authors, 2005. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Aquatic Toxicology 76 (2006): 295-305, doi:10.1016/j.aquatox.2005.10.005.Marine mammals respond to the presence of polycyclic and planar halogenated aromatic hydrocarbons (PAH or PHAH) with the induced expression in endothelium of cytochrome P4501A1, regulated through the aryl hydrocarbon receptor (AHR) transcription factor. Physiological responses in other animals, such as edema and inflammation indicate that the endothelium may be compromised by exposure to AHR agonists, which are ubiquitous in the marine environment. In other mammals and fish the cellular and molecular consequences of exposure to AHR agonists have been elucidated in cultured endothelial cells. We have cultured and characterized cetacean endothelial cells (EC) and used them in induction studies. Endothelial cells were cultured from the lung and kidney of the bottlenose dolphin Tursiops truncatus and exposed to the AHR agonists β-naphthoflavone (βNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). βNF (1-3 μM) induced significant increases in CYP1A1(O-deethylation of 7-ethoxyresorufin to resorufin;EROD) activity to 3.6 and 0.92 pmol/mg/min in lung and kidney EC, respectively. TCDD was more potent than βNF, and more efficacious, with maximum induction of CYP1A1activity of 10.1 and 15.2 pmol/mg/min in lung and kidney EC at 3-10 nM TCDD. The differential response indicates that the lung and kidney endothelial cells in culture retain the ability to respond in a selective manner to specific stimuli. Both the molecular mechanisms of induction and the physiological consequences, especially in the vasculature, of toxicant exposure can be studied in this system.Part of this work was completed during a faculty fellowship from Fordham University for RAG. The Faculty Research Council of Fordham University provided partial support for RAG. This research was supported by NIH grant 5- P42-ES07381 and by U.S.EPA grant R827102-01-0. This research is an outgrowth and continuing impact of Sea Grant Number Grant No. NA90- AA-D-SG480, project NA86RG0075-R/P61

LOW-DOSE GAMMA-RADIATION INHIBITS BENZO[A]PYRENE-INDUCED LUNG ADENOMA DEVELOPMENT IN A/J MICE

Low-dose ionizing radiation (LDR) may lead to suppression of smoking-related lung cancer. We examined the effects of a known cigarette smoke carcinogen Benzo[a]pyrene (B[a]P) alone or in combination with fractionated low-dose gamma radiation (60 – 600 mGy total dose) on the induction of lung neoplasms in the A/J mouse. Our results show that 600 mGy of gamma radiation delivered in six biweekly fractions of 100 mGy starting 1 month after B[a]P injection significantly inhibits the development of lung adenomas per animal induced by B[a]P. Our data also indicated that the six biweekly doses suppressed the occurrence of spontaneous hyperplastic foci in the lung, although this suppression failed to reach statistical significance when analyzed as average foci per lung possibly related to the small sample sizes used for the control and test groups

Genetic Improvement @ ICSE 2020

Following Prof. Mark Harman of Facebook's keynote and formal presentations (which are recorded in the proceedings) there was a wide ranging discussion at the eighth international Genetic Improvement workshop, GI-2020 @ ICSE (held as part of the International Conference on Software En- gineering on Friday 3rd July 2020). Topics included industry take up, human factors, explainabiloity (explainability, jus- tifyability, exploitability) and GI benchmarks. We also con- trast various recent online approaches (e.g. SBST 2020) to holding virtual computer science conferences and workshops via the WWW on the Internet without face to face interac- tion. Finally we speculate on how the Coronavirus Covid-19 Pandemic will a ect research next year and into the future

Genetic variation in CFH predicts phenytoin-induced maculopapular exanthema in European-descent patients

Objective To characterize, among European and Han Chinese populations, the genetic predictors of maculopapular exanthema (MPE), a cutaneous adverse drug reaction common to antiepileptic drugs. Methods We conducted a case-control genome-wide association study of autosomal genotypes, including Class I and II human leukocyte antigen (HLA) alleles, in 323 cases and 1,321 drug-tolerant controls from epilepsy cohorts of northern European and Han Chinese descent. Results from each cohort were meta-analyzed. Results We report an association between a rare variant in the complement factor H–related 4 (CFHR4) gene and phenytoin-induced MPE in Europeans (p = 4.5 × 10–11; odds ratio [95% confidence interval] 7 [3.2–16]). This variant is in complete linkage disequilibrium with a missense variant (N1050Y) in the complement factor H (CFH) gene. In addition, our results reinforce the association between HLA-A*31:01 and carbamazepine hypersensitivity. We did not identify significant genetic associations with MPE among Han Chinese patients. Conclusions The identification of genetic predictors of MPE in CFHR4 and CFH, members of the complement factor H–related protein family, suggest a new link between regulation of the complement system alternative pathway and phenytoin-induced hypersensitivity in European-ancestral patients