Selection by herbicides has resulted in widespread evolution of herbicide resistance in agricultural weeds. In California, resistance to glyphosate was first confirmed in rigid ryegrass in 1998. Objectives of this study were to determine the current distribution and level of glyphosate resistance in Italian ryegrass, and to assess whether resistance could be due to an altered target site. Seeds were sampled from 118 populations and seedlings were treated with glyphosate at 866 g ae ha−1. Percentage of survivors ranged from 5 to 95% in 54 populations. All plants from 64 populations died. One susceptible (S) population, four putatively resistant (R) populations, and one S accession from Oregon were used for pot dose–response experiments, shikimic acid analyses, and DNA sequencing. Seedlings were treated with glyphosate at eight rates, ranging from 108 to 13,856 g ae ha−1. Shoot biomass was evaluated 3 wk after treatment and fit to a log-logistic regression equation. On the basis of GR50(herbicide rate required to reduce growth by 50%) values, seedlings from putatively R populations were roughly two to 15 times more resistant to glyphosate than S plants. Shikimic acid accumulation was similar in all plants before glyphosate treatment, but at 4 and 7 DAT, S plants from California and Oregon accumulated approximately two and three times more shikimic acid, respectively, than R plants. Sequencing of a cDNA fragment of the EPSPS coding region revealed two different codons, both of which encode proline at amino acid position 106 in S individuals. In contrast, all R plants sequenced exhibited missense mutations at site 106. Plants from one population revealed a mutation resulting in a proline to serine substitution. Plants from three R populations exhibited a mutation corresponding to replacement of proline with alanine. Our results indicate that glyphosate resistance is widespread in Italian ryegrass populations of California, and that resistance is likely due to an altered target enzyme.

Progression from URI to LRD occurred in up to 60% of HCT recipients with risk factors such as systemic corticosteroid use or low lymphocyte counts. Further studies are needed to define the role of viral load in the pathogenesis of progressive disease.

Objectives: To explore the sources of variability in evaluator ratings among third year medical students in the Internal Medicine clinical rotation. Also, to examine systematic effects and variability introduced by differences in the various student, evaluator, and evaluation settings. Methods: A multilevel model was used to estimate the amount of between-student, between-rater and raterstudent interaction variability present in the students' clinical evaluations in a third year internal medicine clinical rotation. Within this model, linear regression analysis was used to estimate the effect of variables on the students' numerical evaluation scores and the reliability of those scores. Results: A total of 2,747 evaluation surveys were collected from 389 evaluators on 373 students over 4.5 years. All surveys used a nine-point grading scale, and therefore all results are reported on this scale. The calculated betweenrater, between-student and rater-student interaction variance components were 0.50, 0.27 and 0.62, respectively. African American/Black students had lower scores than Caucasian students by 0.58 points (t=-3.28; P=0.001). No gender effects were noted. Conclusions: These between-rater and between-student variance components imply that the evaluator plays a larger role in the students' scores than the students themselves. The residual rater-student interaction variance was larger and did not change by accounting for the measured demographic variables. This implies there is significant variability in each rater-student interaction that remains unexplained. This could contribute to unreliability in the system, requiring that students receive between 8 and 17 clinical evaluations to achieve 80% reliability.

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