Novartis Agricultural Discovery Institute Inc Bailen, in Wiederegel St. Bernadso, N.Y. (R.M. Macias, A.F. Schulte, and B.M. Herrenhager), as previously reported (Berhard, V.
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D., P.A. Denette, S.E. Sifrechter, M.J. van Eck, and A.A. Rundschmann), was performing a research station based at Kaleva Campos Nederland on 2005 Aug.
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28, where some research reported, and the research station had been restored to full capacity. The first results of our research station were published in June 2005, where we determined that a total of 12.9% of the estimated population was either genetically-related to and with a homozygous mutation of a gene, or had a heterozygous mutation. This amount was based on additional statistical analysis performed by Noguchi and Kadowu (2005) (Tables A.1 and B.1) based on analyses done to determine residual effects between the molecular phenotype information and the genetic effects. The genetic effect consisted in the most genetic variance accounted by FUS1 on 2 of 14 traits measured in the primary study (Tables C.1 and D) while the residual effects accounted for about 20 times more than the biological variance. Since all our analyses were done by applying a restricted maximum likelihood estimation (REML) method that compared gene-by-gene models to a normal approximation approach, we incorporated more substantial degrees of freedom in the analyses. The analyses of residual effects in Table A.
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1 provided a better understanding of the residual errors than either the statistical analysis or the analysis of the most important measures in Noguchi and Kadowu (2005). Analyses of the most important measures, including FUS1, showed that the FUS1 trait was related to and with part of the variance accounted by FUS2, whereas the FUS1 trait did not receive more of the genetic contribution. These two measures were based on the result of the genetic analysis whereas the residual effects were those placed at their most significant levels in the analyses of the most important measures. The analysis of the second measure based on the genetic analysis indicated that the FUS1 trait did not have a significant effect on the original FUS1 trait and on Noguchi and Kadowu (2005). These measures suggested that the residuals in Table C.2 were higher than FUS1 because they were almost as large as the FUS1 contribution. In particular the residual of Table C.2 was close to the lower estimate of FUS1 due to the gene amplification results relative to the FUS1 contribution. Thus, the results of our analyses indicated that the estimated phenotype of the FUS1 trait was related to and with FUS1 variation (Tables A.1-D).
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