A 21-year-old mentally retarded female with 10p12 trisomy is reported. She presented a slight craniofacial dysmorphism very similar to that found in the full 10p-trisomy syndrome. Other features usually found in full 10p trisomy, however, such as failure to thrive and internal malformations, were absent.

The somatic chromosome numbers of 67 hybrid tuberous begonia cultivars (Begonia x tuberhybrida Voss) have been determined. The material concerned was collected in Belgium and England and represents several distinct groups, comprising both cultivars originated at the turn of this century and those introduced recently.The old 'Pendula' group is characterized by the diploid chromosome number 28. Among the 'Multiflora' group diploid, triploid and tetraploid cultivars are represented almost equally, while the investigated 'Multiflora maxima' and large-flowered begonias proved to be tetraploid except for one triploid.Mitotic instability, to the extent reported by some authors, was not observed. The variation of the diploid number between 27 and 28, the triploid number between 41 and 42 and of the tetraploid number between 52 and 56 can be explained as a consequence of the fact that in the original hybridization wild tuberous species with 2n = 26 and 2n = 28 were involved.

A 10-year-old girl with partial deletion of the short arm of chromosome 9 is reported; karyotype: 46,XX,del(9)(p22). This syndrome results in a distinctive craniofacial dysmorphism with trigonocephaly and contrasting midfacial hypoplasia. Partial monosomy 9p was the result of a paternal de novo germinal deletion in this case.

In this report we summarize the results of a genetic‐diagnostic survey of an institutionalized population of 158 severely mentally retarded patients. The etiological study was based on a clinical genetic approach with special attention to dysmorphology and neurological findings. In 72 patients a constitutional cause of their mental impairment was found: a chromosomal abnormality in 21, a Mendelian disorder in 36 (autosomal recessive disorder: 23; autosomal dominant: 12; and X‐linked recessive: 1), a MCA/MR syndrome in 9, and a CNS malformation in 6 patients. In 33 patients, a pre‐ or perinatal cause was found, and 20 patients presented a pre‐ or perinatal infection of the CNS. Finally, no etiological diagnosis was detected in 28 patients; 6 of them presented a hitherto unclassifiable type of familial mental retardation.