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The transposable genetic element Tn9 consists of two direct repeats of the insertion sequence IS1 flanking a region of 1,102 base pairs which determines chloramphenicol resistance. Transposition of Tn9 leads to the duplication of a 9-base pair sequence which preexists at the site of insertion. One copy of this sequence is found at each end of the inserted element. The chloramphenicol resistance determined by Tn9, and by various other R plasmids, is due to the synthesis of the enzyme chloramphenicol acetyl transferase (CAT). This enzyme catalyses the formation of acetylated derivatives of chloramphenicol which are inactive as inhibitors of protein synthesis. By using the chain termination technique of DNA sequencing, we have now determined the nucleotide sequence of the 1,102 base pair region between the directly repeated IS1 sequence in the bacterial transposon Tn9 (encoding chloramphenicol resistance). The amino acid sequence of CAT predicted from the nucleotide sequence is identical to that determined by Shaw and coworkers. An analysis of the sequence suggests that the internal 1,102 base pair region is not directly involved in transposition.

Summary Twelve patients with small cell lung cancer were treated with recombinant human granulocyte colony-stimulating factor, rhG-CSF, given by continuous infusion at doses ranging from 1 to 40 ig kg-'day-'. Patients received the rhG-CSF before the start of intensive chemotherapy and after alternate cycles of chemotherapy. Several in vitro assays were performed using peripheral blood neutrophils and marrow progenitor cells collected from patients prior to and after infusion of the growth factor. Peripheral blood neutrophils were tested for mobility and phagocytic activity. In addition, in vitro clonogenic assays of marrow haemopoietic progenitor cells and analysis of bone marrow trephines and aspirates were carried out. We found that rhG-CSF in vivo has at least two main effects: (a) an early fall in peripheral neutrophils, within the first hour, followed by a rapid influx of mature neutrophils into the circulatory pool; (b) stimulation of proliferation and differentiation of neutrophil precursors in the bone marrow. Neutrophils released into the circulation were normal in tests of their mobility and phagocytic activity.

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