Executive Order Number Fifteen, March 2000

Executive order signed by Governor Thomas Vilsck

Executive Order Number Sixteen, March 2000

Executive order signed by Governor Thomas Vilsck

Executive Order Number Seventeen, February 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Eighteen, March 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Nineteen, May 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty, May 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-One, July 2001

Executive order signed by Governor Thomas Vilsck

Dose optimization approach to fast X-ray microtomography of the lung alveoli.

A basic prerequisite for in vivo X-ray imaging of the lung is the exact determination of radiation dose. Achieving resolutions of the order of micrometres may become particularly challenging owing to increased dose, which in the worst case can be lethal for the imaged animal model. A framework for linking image quality to radiation dose in order to optimize experimental parameters with respect to dose reduction is presented. The approach may find application for current and future in vivo studies to facilitate proper experiment planning and radiation risk assessment on the one hand and exploit imaging capabilities on the other.

Executive Order Number Twenty-Two, October 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Three, October 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Four, November 2001

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Five, June 2002

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Six, June 2002

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Seven, February 2003

Executive order signed by Governor Thomas Vilsck

Genome-wide screen of genes required for caffeine tolerance in fission yeast

Background: An excess of caffeine is cytotoxic to all eukaryotic cell types. We aim to study how cells become tolerant to atoxic dose of this drug, and the relationship between caffeine and oxidative stress pathways.Methodology/Principal Findings: We searched for Schizosaccharomyces pombe mutants with inhibited growth on caffeinecontainingplates. We screened a collection of 2,700 haploid mutant cells, of which 98 were sensitive to caffeine. The genes mutated in these sensitive clones were involved in a number of cellular roles including the H2O2-induced Pap1 and Sty1 stress pathways, the integrity and calcineurin pathways, cell morphology and chromatin remodeling. We have investigated the role of the oxidative stress pathways in sensing and promoting survival to caffeine. The Pap1 and the Sty1 pathways are both required for normal tolerance to caffeine, but only the Sty1 pathway is activated by the drug. Cells lacking Pap1 aresensitive to caffeine due to the decreased expression of the efflux pump Hba2. Indeed, ?hba2 cells are sensitive to caffeine, and constitutive activation of the Pap1 pathway enhances resistance to caffeine in an Hba2-dependent manner. Conclusions/Significance: With our caffeine-sensitive, genome-wide screen of an S. pombe deletion collection, we havedemonstrated the importance of some oxidative stress pathway components on wild-type tolerance to the drug.