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A field experiment was set up in an old field in Michigan in spring and summer 1964, to test whether or not litter determines the abundance of soil microarthropods. Treatments were established to distinguished the importance of litter as a nutritional substance from its importance as a moderator of the microclimate or as a refuge for prey organisms. Treatments were: 1) no litter; 2) high litter; and 3) natural litter replaced with dacron polyester fiberfill, a nondecomposing insulative substance. The first fall the abundance and distribution of microarthropods in the dacron treatment were most similar to that in the high—litter treatment, whereas with respect to the amount of decomposable litter present, the dacron treatment was identical to that in the no—litter treatment. At this time the physical factors in the environment were more favorable in the high—litter and dacron treatments than in the no—litter treatment. The following spring, differences in physical factors among treatments were minimal, and there were no detectable effects of treatment on abundance of microarthropods. The following summer there were significant effects of treatment on physical factors, and the dacron treatment was again most similar to the high—litter treatment with respect to the abundance and distribution of microarthropods. The results demonstrated that physical factors in the environment were of major importance in determining the vertical distribution and abundance of soil microarthropods. Evidently, these organisms were not limited by the nutritional properties of the litter, at least over the 14—month period of the study.

Previous studies have shown that approximately 30% of adult acute myeloid leukaemias and 20% of adult acute lymphoid leukaemias contain point mutated ras oncogenes. In order to assess whether ras oncogenes are also involved in childhood leukaemias, we have used polymerase chain reaction (PCR) amplification and synthetic oligonucleotide probes to study the nature and frequency of ras gene mutations in childhood leukaemias, concentrating largely on the acute myeloid leukaemias (AML). Thirty-four childhood presentation AML DNAs were screened for mutations in and around codons 12, 61 and 117 of N-, K- and H-ras. Eight of these samples (24%) contained ras mutations. As in the adult disease, the gene predominantly involved was N-ras (6/8), with occasional activation of K-ras (2/6). The most common base change was a G----A transition at codon 12 or 13 (4/8). Of the patients with mutant ras, 4/8 were diagnosed as AML FAB subtype M5. Five of the 34 childhood AMLs analysed displayed abnormalities of chromosome 7. However, none of these cases contained a mutant ras gene. One AML patient was studied at relapse, 14 months after initial presentation. The presentation mutation (N61p3) was not detectable, although a new mutation (N13Cys) was readily identified. This observation extends our original finding with presentation and relapse samples of adult AML, in which it was uncommon for the relapse sample to contain the same ras mutation as the presentation DNA. In addition, two out of five patients diagnosed as juvenile CML, were found to harbour mutant ras.

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