Relationship between abundance of rodents and damage to agricultural crops

Developing a relationship between pest abundance and damage to crops is essential for the calculation of economic injury levels (EIL) leading to informed management decisions. The crop modelling framework, APSIM, was used to simulate the impact of mouse damage on yield loss on wheat where a long-term dataset on the density of mice was available (1983–2003). The model was calibrated using results from field trials where wheat plants were hand clipped to imitate mouse damage. The grazing effect of mice was estimated using the population density, daily intake per mouse and the proportion of wheat grain and plant tissue in the diet to determine yield loss. The mean yield loss caused by mice was 12.4% (±5.4S.E.; range −0.5 to 96%). There were 7/21 years when yield loss was >5%. A damage/abundance relationship was constructed and a sigmoidal curve explained 97% of variation when accounting for different trajectories of mouse densities from sowing to harvest. The majority of damage occurred around emergence of the crop when mouse densities were >100 mice ha⁻¹. This is the first time that field data on mouse density and a crop simulation model have been combined to estimate yield loss. The model examines the efficacy of baiting and how to estimate EILs. Because the broadscale application of zinc phosphide is cheap and effective, the EIL is very low (<1% yield loss). The APSIM model is highly flexible and could be used for other vertebrate pests in a range of crops or pastures to develop density/damage relationships and to assist with management.     

Bipolar charged aerosol agglomeration and collection by a two-zone agglomerator

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Uncommon chromosomal mosaicism in chorionic villi

Three cases of unusual chromosomal mosaicism are reported for which the cytogenetic data show inconsistent findings between CVS and AC or fetal tissue, and which cannot be explained simply by non-disjunction. For case 1, in CVS the karyotype was 46,XY, whereas lymphocytes and fibroblasts revealed 69,XXY. DNA fingerprinting indicated one paternal and two maternal chromosome sets, the latter most probably due to omission of maternal meiosis II. For case 2, in CVS mos 46,XX/47,XX,+mar de novo was observed. Amniotic fluid cells had the karyotype 46,XX. The origin of the marker chromosome might be explained by at least two events of unknown order (a somatic chromosome/chromatid deletion and non-disjunction of the homologous chromosome). In case 3 (CVS: mos 46,XY/46,XY,19q+ de novo; amniotic fluid cells, lymphocytes, and fibroblasts: 46,XY), the surplus of chromosome material in 19q+ might be explained on the basis of a somatic translocation. The idea of a chimera is less convincing, as the mosaic finding is restricted to one tissue. Furthermore, there was no hint of a vanishing twin. Hitherto, no case of structural chromosome mosaicism in CVS has been reconfirmed in fetal tissues.