The Relationship Between Resistance to the Fungal Toxin Cercosporin and Grey Leaf Spot Disease Resistance in Corn (ZEA MAYS L.)

65 leaves. Advisor: Michael E. MyszewskiThe problem. Corn is infected by the fungus "Cerospora zeae-maydis" which causes the disease Grey Leaf Spot. The fungus produces a toxin, cercosporin, whose role in the pathogenicity of the disease is not known. The first step in determining the importance of the toxin to the fungus is to screen corn inbreds to see if any disease resistant inbreds are also resistant to the toxin. Procedure. Thirteen corn inbreds were tested for their degree of resistance to the fungal toxin cercosporin. The level of tolerance to cercosporin for each inbred was then compared to the inbred's level of resistance to Grey Leaf Spot. Resistance to cercosporin was determined by measuring the increases in the conductivity of water containing leaf tissue slices following exposure to cercosporin. Ion leakage is an indicator of cellular damage, so resistant tissue would be expected ro have a lower level of conductivity increase than susceptible tissue. Resistance to Grey Leaf Spot disease had been previously determined by field test conducted by Pioneer Hi-Bred International, Inc. Findings. The ion leakage assay showed that the inbreds which were more disease resistant tended to have a lower tolerance for cercosporin than did the less disease resistant inbreds (correlation coefficient = 0.5524). Conclusion. Based on the lack of a positivc relationship between disease susceptibility and cercosporin susceptibility it was concluded that cercosporin resistance does not have a significant role in the prevention of Grey Leaf Spot infections among the tested inbreds

Results of a planned interim toxicity analysis with trimodality therapy, including carboplatin AUC = 4, paclitaxel, 5-fluorouracil, amifostine, and radiation for locally advanced esophageal cancer: preliminary analyses and treatment recommendations from the North Central Cancer Treatment Group

PURPOSE: An aggressive trimodality approach from the Minnie Pearl Cancer Research Network [carboplatin AUC = 6, days 1 and 22; 5-fluorouracil 225 mg/m2 continuous infusion, days 1–42, paclitaxel 200 mg/m2, days 1 and 22; 45 Gy] has resulted in remarkable pathologic response rates but notable toxicity. This trial was designed to mitigate this toxicity by starting with a lower carboplatin dose, AUC = 4, and by adding subcutaneous amifostine. METHODS: This phase II trial included patients with locally advanced, potentially resectable esophageal cancer. All were to receive the above regimen with modifications of carboplatin AUC = 4 and amifostine 500 mg subcutaneously before radiation. All were then to undergo an esophagectomy. A planned interim toxicity analysis after the first 10 patients was to determine whether the carboplatin dose should escalate to AUC = 6. RESULTS: Ten patients were enrolled, and all required dose reductions/omissions during neoadjuvant therapy. One patient died from paclitaxel anaphylaxis. Six patients manifested a complete pathologic response. CONCLUSION: With this regimen, carboplatin AUC = 4 for patients with locally advanced esophageal cancer is appropriate