The effects of low doses of ionising radiation on the viability of mammalian cells

The clonogenic response of V79-379A cells to single doses of X-rays (0.01-10 Gy) and neutrons (0.02-3 Gy) was determined using a computerised microscope (DMIPS) for locating and identifying cells. Survival estimates over the X-ray dose range 1 Gy to 10 Gy showed a good fit to a Linear-Quadratic (LQ) model. For X-ray doses below 0.6 Gy, an increased X-ray sensitivity was observed, with survival below the LX prediction. This phenomenon was not seen withneutrons, and cell survival decreased exponentially with dose. The increased X-ray effectiveness was reflected by a decrease in the RBE from -4.1 to 1.7 as the X-ray dose decreased from 1 Gy to below 0.05 Gy. Comparing the survival measurements from a DMIPS recognition assay with those obtained from a conventional assay suggest that this phenomenon cannot be attributed to the use of the recognition assay for measuring cell survival. Experiments performed on synchronised populations of cells indicate that the low-dose X-ray hypersensitivity is unlikely to be due to either cell cycle effects or a static subpopulation of X-ray sensitive cells. The X-ray dose response over the range 0.04-1 Gy was altered by repair modifiers in three ways. 3-aminobenzamide reduced the increase in radioresistance that occurred in non drug-treated cells as the X-ray dose was increased over the range 0.2-0.6 Gy, but did not affect the response below 0.2 Gy. Exposure to P-ara-A sensitised the cells to X-rays over the whole dose range (0.04-1 Gy) but did not prevent an increase in radioresistance with increasing X-ray dose. Hydrogen peroxide increased the radioresistance of cells to subsequent doses of X-rays below 0.6 Gy. The dose response was also modified by X-rays; a 0.05 Gy, 0.2 Gy or 1 Gy X-ray 'priming' treatment, given 4-6 hours before the 'test' doses of X-rays, eliminated the low-dose X-ray hypersensitivity that was seen in cells not given the priming treatment. This was not seen when the priming dose was administered 24 hours before the subsequent 'test' X-ray doses. These data are consistent with a hypothesis that the increase in radioresistance as the X-ray dose increases from 0.2-0.6 Gy is due to the manifestation of "induced repair" or a stress response: low doses (0.2 Gy) is there sufficient damage to trigger the protective mechanism. An induced-repair model fitted to the X-ray data predicts that repair is activated in the dose range 0.2-0.6 Gy with a 2 fold decrease in the sensitivity between the very low-dose response (0.6 Gy). Treatment with the protein synthesis inhibitor, cycloheximide, following a single dose of radiation reduced the increase in radioresistance that is seen normally over the X-ray dose range 0.2-0.6 Gy. Similarly, cycloheximide present during the interval between a priming dose and a subsequent X-ray dose eliminated the effect of the priming treatment. These data suggest that de novo protein synthesis is required to express the protective mechanism, possibly for the production of repair enzymes. A novel protein was detected in an irradiated sample of cells (1 Gy of X-rays) using 2D gel electrophoresis that was not present in unirradiated cells. These data appear to indicate that an inducible radioprotective mechanism exists in V79-379A cells that is triggered by H2O2 or small radiation doses and requires the synthesis of new proteins to induce radioresistance, possibly through a biochemical pathway affected by 3AB. The mechanism is induced within 4 hours of being triggered but is absent after 24 hours

AVONET: morphological, ecological and geographical data for all birds

Functional traits offer a rich quantitative framework for developing and testing theories in evolutionary biology, ecology and ecosystem science. However, the potential of functional traits to drive theoretical advances and refine models of global change can only be fully realised when species‐level information is complete. Here we present the AVONET dataset containing comprehensive functional trait data for all birds, including six ecological variables, 11 continuous morphological traits, and information on range size and location. Raw morphological measurements are presented from 90,020 individuals of 11,009 extant bird species sampled from 181 countries. These data are also summarised as species averages in three taxonomic formats, allowing integration with a global phylogeny, geographical range maps, IUCN Red List data and the eBird citizen science database. The AVONET dataset provides the most detailed picture of continuous trait variation for any major radiation of organisms, offering a global template for testing hypotheses and exploring the evolutionary origins, structure and functioning of biodiversity

Low-Dose Hyper-Radiosensitivity: Past, Present, and Future

This review article discusses the biology of low-dose hyper-radiosensitivity (HRS) with reference to the molecular regulation of DNA repair and cell cycle control processes. Particular attention is paid to the significance of G2-phase cell cycle checkpoints in overcoming low-dose hyper-radiosensitivity and the impact of HRS on low-dose rate radiobiology. The history of HRS from the original in vivo discovery to the most recent in vitro and clinical data are examined to present a unifying hypothesis concerning the molecular control and regulation of this important low dose radiation response. Finally, preclinical and clinical data are discussed, from a molecular viewpoint, to provide theoretical approaches to exploit HRS biology for clinical gain