The distribution of P-glycoprotein in human placenta has been examined by immunohistochemistry using a battery of monoclonal antibodies (MRK-16, C219 and JSB-1). P-glycoprotein was located on the syncytiotrophoblast microvillus border in first-trimester placentas and some of the placental macrophages (Hofbauer cells) showed weak cytoplasmic staining. In term placentas, however, staining was not observed in the trophoblast but most of the Hofbauer cells displayed strong cytoplasmic staining. In situ hybridization with specific gene probes suggested that both human multidrug resistance genes were expressed in the placenta, although only the multidrug resistance-1 gene product would have been detected by the MRK and JSB-1 antibodies. These results point to distinct functions for P-glycoprotein during the different stages of placental development and indicate that its expression may be under developmental control.

Defining the variation of tissue properties across the bovine carpometacarpal joint and the lack of variation in biosynthetic activity will enable proper matching of experimental and control groups of biopsies in studies of the effects of mechanical stimuli on the composition and mechanical properties of articular cartilage. In addition, the lack of correlation between stiffness, water and glycosaminoglycan contents is further evidence that the mechanical properties of the tissue depend significantly on factors other than these broad measures of composition.

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White blood cells from a total of 19 patients diagnosed as having acute lymphoblastic (ALL) or acute myeloid (AML) leukaemia were analysed (36 samples) for amplification and expression of the mdr1 and mdr3 genes. Nine of the patients had samples analysed at presentation and at subsequent stages of the disease (24 samples, including 4 at second relapse). Patients received standard MRC UK Trial remission-induction treatment protocols appropriate to disease and age. No amplification of either the mdr1 or mdr3 gene was found in any of the samples, and neither were mdr3 transcripts detected by dot-blot analysis using gene-specific probes. Transcripts of the mdr1 gene were found in only 2 ALL samples (of 10). However, mdr1 transcripts were detected in all AML patients and there was a significant increase in the transcript levels in these patients who went on to first and second relapse, compared with levels measured at presentation (P < 0.001). The results support the hypothesis that P-glycoprotein-mediated drug resistance may be a significant factor in tumour cell resistance to chemotherapy at relapse following initial induction-remission therapy for acute myeloid leukemia.