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The irradiation of human lymphocytes with five doses of 250 kV X-rays and five doses of d(42MeV)-Be neutrons was performed in order to obtain dose-response curves for both radiation qualities. By using the FPC technique, aberration scoring was confined to first division cells only and dose-response curves were obtained at three sampling times. Sampling time independence was observed for chromosome-type aberrations and common curves could be fitted, confirming homogeneity of the initial lymphocyte population. R.b.e. values between 1x1 and 8x8 were obtained for dicentric yields between 0x01 and 2x0 per cell. Some variabilities were encountered for other aberration types. Mitotic delay showed an r.b.e. of 1x75. There was no evidence for any induction of SCE by either X-rays or neutrons, up to the highest doses used.

Cytogenetic analyses were performed on dividing cells from the peritoneal effluent of 26 patients undergoing chronic peritoneal dialysis (CPD). Numerical and structural abnormalities of karyotype served as the diagnostic criteria for “atypical cells.” The following cytogenetic abnormalities were observed in 7 patients: hyperdiploidy (in 6 patients), hypodiploidy (in 2 patients), and marker chromosomes (in 2 patients). In 3 patients more than one chromosome abnormality was present. Dividing cells with normal mitoses were observed in 11 patients, while in the remaining 8 patients no dividing cells could be found. There were no differences in age, sex, duration of dialysis, and peritonitis incidence between patients with pathological mitoses and those without it. The question whether this unexpected finding is a consequence of immunosuppressed uremic status, dialysis procedure, or some other factor remains to be elucidated.

Pathogenesis of diabetes is still a mystery for medicine, the real challenge currently being the identification of genetic factors and specific mutations that cause the disease. Heterogeneity of diabetes hampers research, only a few loci inside the human genome being correlated with predisposition for disease till now. Insulin-dependent diabetes - IDDM (T1DM) develops through autoimmune destruction of pancreatic beta cells. HLA complex on the short arm of chromosome 6 (6p21), where very important genes responsible for immunological condition of the person are located, plays a very important role in genetic predisposition for T1DM. Beside this region, there are also other loci in the human genome (on chromosomes 1, 2 and 11) where a correlation with T1DM has been shown. Correlation between HLA systems and T1DM was first described for class I alleles, but recently attention has been drawn to class II loci which seem to be the cause of primary predisposition for T1DM. In the case of non-insulin-dependent diabetes - NIDDM (T2DM), the situation proved to be even more complex. Only a few genetic loci on chromosomes 11, 13 and 20 and MODY variant on chromosomes 7 and 12 have been identified by now. There are two theories about genetic basis of T2DM: the first stipulates that the genetic predisposition is determined through numerous loci, each individually responsible for a small part of predisposition; the second claims that there are a limited number of "major" genes probably functioning on a polygenic basis. Further research in this area is definitely needed to enable an accurate calculation of the risks of the disease and possible consequences during a lifetime of a person