Congenital diaphragmatic hernia: Bochdalek type

Congenital Bochdalek hernias result in significant mortality in the newborn period. Forty-four cases over a nineteen year period are presented. The overall mortality is 34 per cent; however, it has decreased from 41 to 25 per cent in the last five years. The mortality of those patients less than 24 hours old remains high (33 per cent) but improved. We prefer the abdominal approach and believe that prolonged respiratory support will salvage a significant number of these critically ill infants.     

Retroperitoneal germinoma marked by elevated serum lactic dehydrogenase

A case of primary retroperitoneal germinoma is presented in which markedly elevated serum lactic dehydrogenase levels were present before diagnosis, but declined to normal with abdominal irradiation. It is the first report of lactic dehydrogenase serving as a tumor marker in germinoma.     

Weekly doxorubicin in the treatment of patients with AIDS-related Kaposi''s sarcoma. AIDS Clinical Trials Group

It has been shown that the X-ray-sensitive Chinese hamster V79 mutants (V-E5, V-C4 and V-G8) are similar to ataxia-telangiectasia (A-T) cells. To determine whether the AT-like rodent cell mutants are defective in the gene homologous to A-T (group A, C or D), human chromosome 11 was introduced to the V-E5 and V-G8 mutant cells by microcell-mediated chromosome transfer. Forty independent hybrid clones were obtained in which the presence of chromosome 11 was determined by in situ hybridization. The presence of the region of chromosome 11q22-23 was shown by molecular analysis using polymorphic DNA markers specific for the ATA, ATC and ATD loci. Seventeen of the obtained monochromosomal Chinese hamster hybrids contained a cytogenetically normal human chromosome 11, but only twelve hybrid cell lines were shown to contain an intact 11q22-23 region. Despite the complementation of the X-ray sensitivity by a normal chromosome 11 introduced to A-T cells (complementation group D), these twelve Chinese hamster hybrid clones showed lack of complementation of X-ray and streptonigrin hypersensitivity. The observed lack of complementation does not seem to be attributable to hypermethylation of the human chromosome 11 in the rodent cell background, since 5-azacytidine treatment had no effect on the streptonigrin hypersensitivity of the hybrid cell lines. These results indicate that the gene defective in the AT-like rodent cell mutants is not homologous to the ATA, ATC or ATD genes and that the human gene complementing the defect in the AT-like mutants seems not to be located on human chromosome 11.