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Unacceptable levels of contamination by aflatoxin, a carcinogenic toxin, produced by Aspergillus flavus Link:Fr can halt the sale and shipment of maize (Zea mays L.) grain. Our objectives were to: (i) determine the relative resistance to A. flavus and aflatoxin accumulation in [F.sub.1] hybrids produced by crossing promising resistant maize inbreds, regardless of heterotic pattern; (ii) investigate the genetic basis of resistance for this subset of inbreds through diallel analysis; and (iii) determine which inbreds are the most promising sources of resistance for molecular marker mapping and breeding programs. Two historically important inbreds and six inbreds tentatively associated with reduced ear rot and inhibition of aflatoxin production were crossed in all combinations. The resulting [F.sub.1] hybrids were evaluated for two years. Ears were inoculated 20 to 24 d after midsilk by a pinboard method and a mixture of conidia of Aspergillus flavus Link:Fr. isolates. Individual ears from each plot were rated by scoring the percent visible rot in the inoculated area. Aflatoxin [B.sub.1] levels in harvested ears were determined by an indirect competitive ELISA. The highest level of resistance for ear rot and aflatoxin accumulation was detected for resistant inbred x resistant inbred [F.sub.1] hybrids, but they were not significantly different from many resistant inbred x historically important inbred [F.sub.1] hybrids. Diallel analysis indicated general combining ability (GCA) effects for ear rot and aflatoxin levels were highly significant among hybrids overall, and for the inbreds Tex6 and Oh516. The results indicate that Tex6 and Oh516 are promising resistance sources for molecular marker mapping and breeding programs in diverse genetic backgrounds., THE ACCUMULATION OF aflatoxin, a secondary metabolite produced by the fungus Aspergillus flavus Link:Fr., in maize grain in the U.S. midwest and elsewhere continues to be a problem, especially during [...]

Critically ill patients exhibit a range of organ dysfunctions and often require treatment with a variety of drugs including sedatives, analgesics, neuromuscular blockers, antimicrobials, inotropes and gastric acid suppressants. Understanding how organ dysfunction can alter the pharmacokinetics of drugs is a vital aspect of therapy in this patient group. Many drugs will need to be given intravenously because of gastrointestinal failure. For those occasions on which the oral route is possible, bioavailability may be altered by hypomotility, changes in gastrointestinal pH and enteral feeding. Hepatic and renal dysfunction are the primary determinants of drug clearance, and hence of steady-state drug concentrations, and of efficacy and toxicity in the individual patient. Oxidative metabolism is the main clearance mechanism for many drugs and there is increasing recognition of the importance of decreased activity of the hepatic cytochrome P450 system in critically ill patients. Renal failure is equally important with both filtration and secretion clearance mechanisms being required for the removal of parent drugs and their active metabolites. Changes in the steady-state volume of distribution are often secondary to renal failure and may lower the effective drug concentrations in the body. Failure of the central nervous system, muscle, the endothelial system and endocrine system may also affect the pharmacokinetics of specific drugs. Time-dependency of alterations in pharmacokinetic parameters is well documented for some drugs. Understanding the underlying pathophysiology in the critically ill and applying pharmacokinetic principles in selection of drug and dose regimen is, therefore, crucial to optimising the pharmacodynamic response and outcome. [ABSTRACT FROM AUTHOR]