Dusky Sap Beetle Mediated Dispersal of Bacillus subtilis to Inhibit Aspergillus flavus and Aflatoxin Production in Maize Zea mays L.

Laboratory assays were performed with detached milk stage maize ( Zea mays L.) ears and dusky sap beetles ( Carpophilus lugubris Murray) carrying the Kodiak Concentrate formulation of the bacterium, Bacillus subtilis (Ehrenberg) Cohn. After 1 day of exposure to the B. subtilis- contaminated C. lugubris , the colonization of mechanically damaged kernels by Aspergillus flavus Link ex. Fries was reduced from 82% (if the A. flavus was inoculated first) to 41% (if B. subtilis was added by C. lugubris before the A. flavus ). Field cage studies were performed with an autoinoculative device containing B. subtilis into which C. lugubris beetles were introduced. C. lugubris -dispersed B. subtilis reduced visible A. flavus colonization by 97% when the A. flavus was added to purposely damaged maize ears 4 days after C. lugubris were released from the autoinoculator. In 1993 field studies, none of the purposely damaged ears that allowed access to C. lugubris beetles emerging from autoinoculators containing B. subtilis had visible sporulating A. flavus compared with 92% of ears that did not allow access of C. lugubris but that subsequently had the A. flavus inoculum added. In 1994 field studies, 70% of the ears that excluded C. lugubris had aflatoxin levels greater than 200 ppb in purposely damaged kernels, as opposed to less than 10% of kernels that permitted access by natural populations of C. lugubris that probably acquired B. subtilis from a single autoinoculator. Aflatoxin levels in these ears were negatively correlated with the presence of both B. subtilis and C. lugubris . The B. subtilis was widely dispersed over a 16-ha area as indicated by maize ear and C. lugubris trap sampling. These studies indicate that autoinoculative dispersal of B. subtilis by natural populations of C. lugubris is a potentially useful means for reducing A. flavus and aflatoxin in maize.     

Hepatic vascular lesions associated with dacarbazine treatment.

Dacarbazine is widely used in the treatment of melanoma. Transient abnormalities of liver function tests are well-recognised side effects of the drug, but acute liver failure due to vascular occlusion in patients receiving single-agent chemotherapy with dacarbazine has been noted only rarely. Two cases are reported in which hepatic vascular lesions developed during treatment with dacarbazine and were confirmed at necropsy. Hepatic vascular occlusion due to treatment with dacarbazine may be less rare than was previously thought. Greater caution may be needed when dacarbazine is prescribed, particularly as an adjuvant agent in stage I and II disease.