We conducted a large record-based case-control study testing associations between childhood cancer and natural background radiation. Cases (27 447) born and diagnosed in Great Britain during 1980–2006 and matched cancer-free controls (36 793) were from the National Registry of Childhood Tumours. Radiation exposures were estimated for mother’s residence at the child’s birth from national databases, using the County District mean for gamma-rays, and a predictive map based on domestic measurements grouped by geological boundaries for radon. There was 12% excess relative risk (95% CI 3, 22; 2-sided p=0.01) of childhood leukaemia per millisievert of cumulative red-bone-marrow dose from gamma-radiation; the analogous association for radon was not significant, excess relative risk 3% (95% CI −4, 11; p=0.35). Associations for other childhood cancers were not significant for either exposure. Excess risk was insensitive to adjustment for measures of socio-economic status. The statistically significant leukaemia risk reported in this reasonably-powered study (power ~50%) is consistent with high dose-rate predictions. Substantial bias is unlikely, and we cannot identify mechanisms by which confounding might plausibly account for the association, which we regard as likely to be causal. The study supports the extrapolation of high dose-rate risk models to protracted exposures at natural background exposure levels.

This paper discusses the doses from radon and from its short-lived decay products to a number of organs and tissues and to the foetus. The aim is to put all these doses into context rather than concentrating only on the largest contributions. There is also a brief discussion of the evidence from epidemiology on the risks of exposure to radon and its decay products. As is well known, under normal circumstances the greatest hazard is to the respiratory tract from inhalation of radon decay products. Radon decay products may also give substantial doses to skin. Under some circumstances it seems likely that ingested radon could give significant doses to the stomach. Other risks appear to be smaller; the results given here allow them to be compared.

No abstract

A Trypanosoma cruzi expression vector has been constructed using sequences derived from the flanking regions of the glyceraldehyde 3-phosphate dehydrogenase (gGAPDH) genes. The neomycin phosphotransferase (neor) gene was incorporated as a selectable marker. Using electroporation we have introduced this vector into both T. cruzi and Leishmania cells and conferred G418 resistance. Transformation is mediated by large extrachromosomal circular elements composed of head-to-tail tandem repeats of the vector. The transformed phenotype is stable for at least 6 months in the absence of G418 and can be maintained during passage through the T. cruzi life-cycle. Foreign genes inserted into an expression site within the vector (pTEX) can be expressed at high levels in transformed cells. To our knowledge this paper describes the first trypanosome shuttle vector and the first vector which functions in both trypanosomes and Leishmania.

The heat shock protein (HSP) 27 is constitutively expressed at low levels in medium-sized lumbar dorsal root ganglion (DRG) cells in adult rats. Transection of the sciatic nerve results in a ninefold upregulation of HSP27 mRNA and protein in axotomized neurons in the ipsilateral DRG at 48 hr, without equivalent changes in the mRNAs encoding HSP56, HSP60, HSP70, and HSP90. Dorsal rhizotomy, injuring the central axon of the DRG neuron, does not upregulate HSP27 mRNA levels. After peripheral axotomy, HSP27 mRNA and protein are present in small, medium, and large DRG neurons, and HSP27 protein is transported anterogradely, accumulating in the dorsal horn and dorsal columns of the spinal cord, where it persists for several months. Axotomized motor neurons also upregulate HSP27. Only a minority of cultured adult DRG neurons are HSP27-immunoreactive soon after dissociation, but all express HSP27 after 24 hr in culture with prominent label throughout the neuron, including the growth cone. HSP27 differs from most axonal injury-regulated and growth-associated genes, which are typically present at high levels in early development and downregulated on innervation of their targets, in that its mRNA is first detectable in the DRG late in development and only approaches adult levels by postnatal day 21. In non-neuronal cells, HSP27 has been shown to be involved both in actin filament dynamics and in protection against necrotic and apoptotic cell death. Therefore, its upregulation after adult peripheral nerve injury may both promote survival of the injured neurons and contribute to alterations in the cytoskeleton associated with axonal growth.