Peripheral primitive neuroectodermal tumour in a dog.

A 1-year-old German shepherd dog was presented with paraparesis quickly progressing to paraplegia. Magnetic resonance imaging revealed a large mass beneath the thoracolumbar vertebral column infiltrating the spinal canal and resulting in severe extradural compression of the spinal cord. Microscopically, this comprised a cell-rich unencapsulated tumour supported by fine bands of a fibrovascular stroma and occasionally forming primitive rosettes. Immunohistochemistry showed the tumour cells to express synaptophysin and neuron-specific enolase. Ultrastructurally, the neoplastic cells had low to moderate numbers of intracytoplasmic neurosecretory granules. A peripheral primitive neuroectodermal tumour was diagnosed. This is a rare embryonal tumour of neural origin that may have arisen from adrenal medulla, autonomic ganglia or peripheral nerves.

Influence of thiols and oxygen on the survival of gamma-irradiated plasmid DNA and cells.

Some of the recent progress made in the understanding of the quantitative aspects of the oxygen effect in radiation biology by several groups is summarized. Examples are: the importance of unrepairable damage for the quantitative description of the oxygen effect; proof that protein thiols hardly contribute to protection in cells in the absence of oxygen; the proposal that protection by thiols in concentration ranges where all DNA radicals react with oxygen is due to the formation of hydroperoxides which can be repaired enzymatically by glutathione peroxydase; the finding that unscavengeable damage in plasmid DNA is mainly due to spur-induced clustered damages, but that the precursors of the scavengeable and the unscavengeable damage are comparably well repaired by thiols; the result that E. coli repair wild type strains are better protected by addition of thiols than strains with deficiencies in enzymatic repair capacities.

Irradiation of plasmid and phage DNA in water-alcohol mixtures: strand breaks and lethal damage as a function of scavenger concentration.

We have measured the yields of strand break formation and biological inactivation as a function of OH scavenger concentration for 60Co gamma-irradiated pBR322 plasmid and M13mp9 RF phage DNA. The yields of single-strand breaks (ssbs), double-strand breaks formed proportionally to dose (alpha dsbs), and lethal damage (LD) decrease with increasing scavenging capacity sigma, their ratios remaining approximately constant up to sigma approximately 10(8) s-1. On a double-logarithmic plot the yields decrease linearly with sigma in parallel lines. At higher scavenging capacities, the yields, while still decreasing, level off to a different extent. Our results for the yields of ssbs and alpha dsbs confirm those of Krisch et al. (1991) using SV40 DNA. The data were analysed assuming that DNA damage is brought about by OH radicals, and a non-scavengeable portion arising from the direct radiation effect. Using a model based on non-homogeneous scavenging kinetics, the dependence on scavenging capacity of the ssb yield could be quantitatively accounted for. From the scavenging dependence of the yield of dsbs which are formed quadratically with dose (beta dsbs) and which are the result of two independent ssbs within a critical distance h, a value of about 13 basepairs was obtained for h. The parallel decrease in the yield of ssbs and alpha dsbs with scavenging capacity was rationalized in terms of the Siddiqi-Bothe mechanism (Siddiqi and Bothe 1987). The efficiency of this mechanism was found to be approximately 0.01. From the analysis of the LD yields it was shown that up to sigma approximately 10(8) s-1, inactivation is predominantly due to single OH radicals which lead to LD with an efficiency of 0.12 per OH-induced ssb. At higher scavenging capacities, a non-scavengeable spur effect similar to the locally multiply damaged sites mechanism of Ward (1988) mainly contributes to LD.