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Notes: Although kernel infection by Aspergillus flavus Link ex Fries and subsequent pre-harvest aflatoxin contamination of maize (Zea mays L.) grain are major production problems in the south-eastern United States and elsewhere in the world, limited progress has been made in developing and identifying sources for resistance. Genetics of kernel infection by A. flavus remains poorly understood. A 10-parent diallel experiment was conducted in 1992 and 1994 to study the genetic nature of percentage kernel infection (PKI) by A. flavus. General combining ability (GCA), specific combining ability (SCA), and reciprocal mean squares for PKI were significant. The GCA and SCA sums of squares were about equal. The GCA, SCA, and reciprocal effects varied across years, which implied that percentage kernel infection was greatly influenced by environments. The percentage kernel infection was always greater when Mo 17 was the male parent in a cross than when it was the female parent. The percentage kernel infection mean for female Mo 17 was 38.5% lower than that for male Mol7. Similarly, percentage kernel infection mean for female L668 was 23.7% lower than that for male L668. The use of inbred lines L729 and B73 as female parents should be avoided, as they showed significant, positive maternal reciprocal effects.

Notes: Previous genetic studies on resistance to aflatoxin production in maize (Zea mays L.) only used a limited amount of germplasm. The objective of this study was to determine general (GCA) and specific combining abilities (SCA) for resistance to prehar-vest aflatoxin accumulation in grain, utilizing A619 Lfy syn, A632 Lfy syn, B73 Lfy syn, Hy Lfy syn, Mol7 Lfy syn, Wf9 Lfy syn, and 914 Lfy syn. We evaluated 21 F1 crosses (diallel) for aflatoxin accumulation in grain in three environments. Twenty-one days after mid-silk, ears were slash-inoculated with Aspergillus parasiticus (Speare). Samples were analyzed for aflatoxins Bl B2, G1 and G2. Significant differences for aflatoxin accumulation were detected among environments, with the environment that experienced drought stress showing the highest concentration for all four aflatoxins. The GCA and crosses mean squares were not significant for any aflatoxin and the SCA mean square was significant (P = 0.1) only for aflatoxin G2. Relatively small quantities of aflatoxin accumulation on, and nonsignificant differences among the 21 F1 crosses might be indicative of their inherently high resistance levels. The SCA sums of squares constituted two thirds or more of crosses sums of squares, which indicated a preponderance of dominance and/or epistatic effects for aflatoxin accumulation. The Hy Lfy syn GCA effect tended to increase aflatoxin Bl and Wf9 Lfy syn tended to reduce aflatoxin accumulation as it showed a significant (P = 0.1), negative GCA effect for aflatoxin G1. The F1 cross Wf9 Lfy syn × 914 Lfysyn showed significant, negative SCA effect for af-latoxins B1 and G1, whereas A619 Lfy syn × 914 Lfy syn and Mo17 Lfy syn × Wf9 Lfy syn tended to increase one or more aflatoxins. For aflatoxin Br, a significant environments (E) × crosses (C) interaction was largely due to E × GCA interaction, which, in turn, was due to an interaction of the B73 Lfy syn GCA effect with E. This interaction effect tended to reduce aflatoxin BS. The E × C interaction for aflatoxin G2 was due to both E × GCA and E × SCA interactions. B73 Lfy syn GCA × E tended to reduce aflatoxin G, and Mo17 Lfy syn GCA × E tended to increase aflatoxin G. Additive genetic correlations based on GCA effects among the four aflatoxins were significant (0.76 to 0.96), except the correlation between aflatoxins B, and G2 (0.43), suggesting that, in general, increasing resistance to one toxin may lead to resistance to the other three toxins.

Notes: Background Histone deacetylase (HDAC) inhibition has been demonstrated to change the expression of a restricted set of cellular genes. T cells are essential in the pathogenesis of allergen-induced airway inflammation. It was recently reported that treatment with HDAC inhibitors induces a T cell-suppressive effect.Objective The purpose of this study was to determine whether treatment with trichostatin A (TSA), a representative HDAC inhibitor, would reduce allergen-induced airway inflammation in a mouse asthma model.Methods BALB/c mice were intraperitoneally sensitized to ovalbumin (OVA) and challenged with an aerosol of OVA. TSA (1 mg/kg body weight) was injected intraperitoneally every 2 days beginning on day 1. Mouse lungs were assayed immunohistochemically for HDAC1, a major HDAC subtype, and for infiltration of CD4+ cells. The effect of TSA on airway hyper-responsiveness (AHR) was determined, and the bronchoalveolar lavage fluid (BALF) of these mice was assayed for the number and types of inflammatory cells, and for the concentrations of IL-4, IL-5, and IgE.Results HDAC1 was localized within most airway cells and infiltrating inflammatory cells of asthmatic lungs. Treatment with TSA significantly attenuated AHR, as well as the numbers of eosinophils and lymphocytes in BALF. TSA also reduced infiltration of CD4+ and inflammatory cells and mucus occlusions in lung tissue, and decreased the concentrations of IL-4, IL-5, and IgE in BALF.Conclusion TSA attenuated the development of allergic airway inflammation by decreasing expression of the Th2 cytokines, IL-4 and IL-5, and IgE, which resulted from reduced T cell infiltration. Our results suggest that HDAC inhibition may attenuate the development of asthma by a T cell suppressive effect.

Notes: Genotype × environment (GE) interactions are a major problem in plant breeding programs that involve testing in diverse environments. These interactions can reduce progress from selection. Few studies have characterized the effects of weather variables on GE interactions in sorghum (Sorghum bicolor [L.] Moench). The present investigation estimated the contribution of environmental index, (Ȳ, or mean yield of all cultivars in jth environment minus Ȳ. xor overall mean yield for all cultivars and all environments), rainfall, minimum and maximum temperature, and relative humidity, to GE interaction. Yield means of 5 full-season and 10 medium-season grain sorghum hybrids grown during 1986—1988 at four locations were used in the study. The GE interaction was significant and partitioned into σ2i, components assignable to each genotype. Weather variables (covariates) were used to remove heterogeneity from the GE interaction. The remainder of the GE interaction variance was partitioned into variance components (s2i) assignable to each genotype. In both maturity groups, the environmental index removed most, although non-significant, heterogeneity from the GE interaction sums of squares. Of all weather variables, preseason and seasonal rainfall contributed most to the GE interaction sums of squares.

Notes: Preharvest aflatoxin contamination of maize (Lea mays L.) gram by Aspergillns spp. is a concern to both producers and consumers of maize. Aflatoxms are carcinogenic to animals and have been linked to liver cancer in humans. The most desirable solution for eliminating or reducing aflatoxin contamination is to identify and/or develop sources of resistance. However, only a few genetic studies, which utilized a limited amount of genetic material, have been conducted. A thorough review and consolidation of information from these studies was deemed necessary. The purpose of this paper is to present a current, critical review on aspects of infection by Aspergillus, role of insects, inoculation techniques, and sources and genetics of resistance as they relate to aflatoxin production in maize. Damage to maize kernels by insects, especially the European corn borer (Ostrinia nubilalis Hübner), fall armyworm (Spodoptera frugiperda J. E. Smith), and corn ear-worm (Helicoverpa zea Boddie), has been associated with high aflatoxin levels. Artificial inoculation techniques that damage maize kernels generally result in the highest and most consistent aflatoxin levels. Although, a relatively large amount of maize germplasm has been screened for resistance and varying levels of resistance have been identified, additional germplasm needs to be systematically evaluated. To date, there are no known genotypes with complete resistance. Results from the few genetic studies indicated that additive genetic effects controlled resist-Preharvest aflatoxin contamination of maize (Zea mays L.) gram by Aspergillns spp. is a concern to both producers and consumers of maize. Aflatoxms are carcinogenic to animals and have been linked to liver cancer in humans. The most desirable solution for eliminating or reducing aflatoxin contamination is to identify and/or develop sources of resistance. However, only a few genetic studies, which utilized a limited amount of genetic material, have been conducted. A thorough review and consolidation of information from these studies was deemed necessary. The purpose of this paper is to present a current, critical review on aspects of infection by Aspergillus, role of insects, inoculation techniques, and sources and genetics of resistance as they relate to aflatoxin production in maize. Damage to maize kernels by insects, especially the European corn borer (Ostrinia nubilalis Hübner), fall armyworm (Spodoptera frugiperda J. E. Smith), and corn ear-worm (Helicoverpa Zea Boddie), has been associated with high aflatoxin levels. Artificial inoculation techniques that damage maize kernels generally result in the highest and most consistent aflatoxin levels. Although, a relatively large amount of maize germ-plasm has been screened for resistance and varying levels of resistance have been identified, additional germplasm needs to be systematically evaluated. To date, there are no known genotypes with complete resistance. Results from the few genetic studies indicated that additive genetic effects controlled resistance to aflatoxin contamination in maize. Aflatoxin production on maize grain appeared to be greatly influence by the environment. Further genetic studies, utilizing additional germplasm, are warranted for a better understanding of the nature of resistance to asflatoxin contamination in maize. Future research needs and plans relative to resistance to aflatoxin contaminaton in maize are presented.

Notes: Two new cell cultures from flounder, Paralichthys olivaceus (Temminck & Schlegel), flounder fin (FFN) cells from fin tissue and flounder spleen (FSP) cells from spleen tissue, were established and characterized. The cells multiplied well in Eagle's minimum essential medium, supplemented with 10% foetal bovine serum, and have been subcultured more than 100 times, becoming continuous cell lines. Modal diploid chromosome number of FFN and FSP cells was 64 and 62, respectively. Polymerase chain reaction products were obtained from FFN and FSP cells with primer sets of microsatellite markers of flounder. Optimal growth temperature was 20 °C and consisted of epithelioid cells. FFN and FSP cells showed cytopathic effects after inoculation of infectious pancreatic necrosis virus, marine birnavirus, chum salmon virus, infectious haematopoietic necrosis virus, spring viraemia of carp virus and hirame rhabdovirus. Thus these new cell lines may be useful for studying a wide range of fish viruses.