ObjectivesThe objective of this study was to examine the associations of brain tumours with radio frequency (RF) fields from mobile phones.MethodsPatients with brain tumour from the Australian, ...Canadian, French, Israeli and New Zealand components of the Interphone Study, whose tumours were localised by neuroradiologists, were analysed. Controls were matched on age, sex and region and allocated the ‘tumour location’ of their matched case. Analyses included 553 glioma and 676 meningioma cases and 1762 and 1911 controls, respectively. RF dose was estimated as total cumulative specific energy (TCSE; J/kg) absorbed at the tumour's estimated centre taking into account multiple RF exposure determinants.ResultsORs with ever having been a regular mobile phone user were 0.93 (95% CI 0.73 to 1.18) for glioma and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for glioma were below 1 in the first four quintiles of TCSE but above 1 in the highest quintile, 1.35 (95% CI 0.96 to 1.90). The OR increased with increasing TCSE 7+ years before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to 3.47 in the highest quintile). A complementary analysis in which 44 glioma and 135 meningioma cases in the most exposed area of the brain were compared with gliomas and meningiomas located elsewhere in the brain showed increased ORs for tumours in the most exposed part of the brain in those with 10+ years of mobile phone use (OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for meningioma were similar, but ORs were lower, many below 1.0.ConclusionsThere were suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk. The uncertainty of these results requires that they be replicated before a causal interpretation can be made.
Ionizing radiation (IR) is regarded as an abiotic stressor for plants because it causes oxidative stress and changes the expression of genes. We investigated RNA sequencing-based global transcriptome ...changes induced by three different types of IR (gamma rays (GR), ion beams (IB), and proton beams (PB)) at different doses in rice. On average, 489 upregulated and 234 downregulated differentially expressed genes (DEGs) were found per sample. The union of the DEGs for each IR type was collected to simplify the comparison of effects among the different IR treatments. This resulted to a total of 1,558 DEGs after GR irradiation, 1,865 DEGs after IB irradiation, and 1,347 DEGs after PB irradiation. The gene ontology (GO) enrichment analysis of the union DEG sets revealed 69 and 12 commonly enriched GO terms for up- and downregulated DEGs, respectively, many of which were closely related to oxidative stress responses. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapping and enrichment analysis of the union DEG sets also showed that most of the DEGs fell into common pathways related to oxidative stress, stress signaling, and redox reactions. A total of 137 transcription factor (TF) genes were differentially expressed, and many belong to families associated with stress responses. Our results suggest that different types and doses of IR can induce universal gene expression changes in response to oxidative stress. This study contributes to our understanding of the molecular response mechanisms to IR in plants.
In mammalian cells, the mediator protein, 53BP1, exerts distinct impacts on the repair of DNA double strand breaks (DSBs) depending on the setting, for example whether the DSBs arise at telomeres or ...during replication or class switch recombination. Here, we focus on two roles of 53BP1 in response to ionising radiation (IR)-induced DSBs (IR-DSBs). Canonical DNA non-homologous end-joining (c-NHEJ) is the major DSB repair pathway with homologous recombination (HR) contributing to DSB repair in S/G2 phase. ATM signalling promotes histone modifications and protein assembly in the DSB vicinity, which can be visualised as irradiation induced foci (IRIF). 53BP1 assembles at DSBs in a complex manner involving the formation of nano-domains. In G1 and G2 phase, X- or gamma-ray induced DSBs are repaired with biphasic kinetics. 70–80 % of DSBs are repaired with fast kinetics in both cell cycle phases by c-NHEJ; the remaining DSBs are repaired with slower kinetics in G2 phase via HR and in G1 by a specialised form of c-NHEJ termed Artemis and resection-dependent c-NHEJ, due to a specific requirement for the nuclease, Artemis and resection factors. 53BP1 is essential for the repair of DSBs rejoined with slow kinetics in G1 and G2 phase. This 53BP1 function requires its tandem BRCT domain and interaction with NBS1. As a distinct function, 53BP1 suppresses resection during both HR and Artemis and resection-dependent c-NHEJ. This latter role requires RIF1 and is counteracted by BRCA1. 53BP1 appears to be dispensable for the rejoining of the fast c-NHEJ repair process.
Indoor radon exposure increases the risk of lung cancer. Radon concentration in workplaces is regulated in EU countries, including Spain, based on a reference level of 300 Bq/m3. The objective of ...this study is to describe workplace radon exposure in Spain and its influencing factors. To do this, we collected long-term radon measurements with alpha track detectors in 3140 workplaces mainly located in radon prone areas. Radon concentration exceeded 300 Bq/m3 in 1 out of 5 workplaces. Median radon concentration was 107 Bq/m3 in radon prone areas, 28 Bq/m3 off radon prone areas, and 101 Bq/m3 globally for the complete sample. Our results indicate that excessive radon concentrations can be expected in radon prone areas at all floor levels, especially below ground. Floor level, working sector, and location significantly influence radon concentration. The highest radon concentrations were found in the Education & Culture sector, comprising schools, universities, libraries, or cultural centers. These results indicate that radon should no longer be considered a risk for marginal occupations, but a risk everyone has if located in a radon prone area. Immediate action, including radon testing and mitigation, is needed to protect workers in Spain against radon exposure. This is already mandatory since EU regulation for radon has been recently transposed in Spain. Competent authorities should enforce this regulation without further delay, and employers must address their responsibility and communicate with workers about this risk.
We have analysed the role of homologous recombination (HR) genes on the repair of double‐strand breaks induced by γ‐ionising radiation in Candida albicans. Depletion of either CaRad51 or CaRad52 ...caused a dramatic drop in the number of survivors compared with wild type, whereas depletion of CaRad59 caused a moderate decrease. Besides, compared with Saccharomyces cerevisiae, C. albicans relies more on HR proteins for repair of ionising radiation lesions. Pulse‐field electrokaryotypes of survivors identified genetic alterations mainly in the form of aneuploidy in HR mutants and chromosome length polymorphism and ectopic translocation in wild type. Increasing irradiation (4 to 80 krad) of both cycling and nocodazole‐treated (G2/M‐arrested) cells revealed a gradual loss of chromosomes, larger chromosomes being more affected than smaller ones. For cycling wild‐type cells, shattered chromosomes were progressively restored following incubation in yeast extract, peptone, dextrose medium, but not in phosphate‐buffered saline, and this accompanied by a moderate increase in colony‐forming units, suggesting that repair was followed by replication of survivors. Irradiated G2/M arrested cells from wild type but not from HR mutants partially restored the chromosome ladder following incubation (4–8 hr) in yeast peptone dextrose–nocodazole. However, HR mutants showed a chromosome shattering pattern similar to wild type, an indication that lesions other than double‐strand breaks, likely single‐strand break, are responsible for their drastically reduced survivability.
Polymer used in satellite manufacturing are exposed to surface charging phenomenon due to electronic irradiations. This phenomenon can induce electrostatic discharges (ESD) which can lead to ...failures. In order to limit this phenomenon, we propose to develop PEEK composite reinforced with Short Carbon Fibres (SCF). We studied the behaviour of these composites in pristine state and after electronic irradiations compared to PEEK. In pristine state, fibres induce a faster surface electron relaxation. This behaviour shows that SCF can reduce ESD risks in space which is a first validation of the concept. After irradiations, PEEK ageing mechanisms are not modified by the presence of fibres. However, SCF stabilise both the evolution of mechanical behaviour and surface potential relaxation compared to irradiated PEEK. This stabilisation comes from two contributions: fibres stabilise the ageing of the matrix and hides the influence of this ageing on composite mechanical and electrical behaviours.
Humans can be exposed to non-ionizing and ionizing radiation for diagnostic, therapeutic, accidental, and occupational reasons. Consequently, the effect of radiation on biological systems has ...attracted the attention of researchers for a rather long time. This review is about the mid-infrared Fourier Transform Infrared (FTIR) spectroscopic characterization of non-ionizing and ionizing radiation-induced changes in DNA, lipids, and proteins, as isolated or synthetic macromolecules, and in biological membranes, cells, and tissues. Here, the context of radiation was limited with electromagnetic radiation including gamma rays. The review first outlines introductory information about non-ionizing and ionizing radiation and their interaction with biological systems. Afterwards, FTIR spectroscopy and spectroscopic analysis are briefly discussed. Finally, FTIR spectroscopic analysis of DNA, lipids, proteins, membranes, cells, and tissues that were exposed to radiation are presented. The findings show that FTIR spectroscopy can be successfully used as a novel method to monitor radiation-induced alteratios in biological systems.
Previous studies have found indications that exposure to ionising radiation (IR) results in DNA methylation changes in plants. However, this phenomenon is yet to be studied across multiple ...generations. Furthermore, the exact role of these changes in the IR-induced plant response is still far from understood. Here, we study the effect of gamma radiation on DNA methylation and its effect across generations in young
plants. A multigenerational set-up was used in which three generations (Parent, generation 1, and generation 2) of 7-day old
plants were exposed to either of the different radiation treatments (30, 60, 110, or 430 mGy/h) or to natural background radiation (control condition) for 14 days. The parental generation consisted of previously non-exposed plants, whereas generation 1 and generation 2 plants had already received a similar irradiation in the previous one or two generations, respectively. Directly after exposure the entire methylomes were analysed with UPLC-MS/MS to measure whole genome methylation levels. Whole genome bisulfite sequencing was used to identify differentially methylated regions (DMRs), including their methylation context in the three generations and this for three different radiation conditions (control, 30 mGy/h, and 110 mGy/h). Both intra- and intergenerational comparisons of the genes and transposable elements associated with the DMRs were made. Taking the methylation context into account, the highest number of changes were found for cytosines followed directly by guanine (CG methylation), whereas only limited changes in CHG methylation occurred and no changes in CHH methylation were observed. A clear increase in IR-induced DMRs was seen over the three generations that were exposed to the lowest dose rate, where generation 2 had a markedly higher number of DMRs than the previous two generations (Parent and generation 1). Counterintuitively, we did not see significant differences in the plants exposed to the highest dose rate. A large number of DMRs associated with transposable elements were found, the majority of them being hypermethylated, likely leading to more genetic stability. Next to that, a significant number of DMRs were associated with genes (either in their promoter-associated region or gene body). A functional analysis of these genes showed an enrichment for genes related to development as well as various stress responses, including DNA repair, RNA splicing, and (a)biotic stress responses. These observations indicate a role of DNA methylation in the regulation of these genes in response to IR exposure and shows a possible role for epigenetics in plant adaptation to IR over multiple generations.
The targeting of DNA methylation in cancer using DNA hypomethylating drugs has been well known to sensitize cancer cells to chemotherapy and immunotherapy by affecting multiple pathways. Herein, we ...investigated the combinational effects of DNA hypomethylating drugs and ionizing radiation (IR) in human sarcoma cell lines both in vitro and in vivo. Clonogenic assays were performed to determine the radiosensitizing properties of two DNA hypomethylating drugs on sarcoma cell lines we tested in this study with multiple doses of IR. We analyzed the effects of 5-aza-dC or SGI-110, as DNA hypomethylating drugs, in combination with IR in vitro on the proliferation, apoptosis, caspase-3/7 activity, migration/invasion, and Western blotting using apoptosis- or autophagy-related factors. To confirm the combined effect of DNA hypomethylating drugs and IR in our in vitro experiment, we generated the sarcoma cells in nude mouse xenograft models. Here, we found that the combination of DNA hypomethylating drugs and IR improved anticancer effects by inhibiting cell proliferation and by promoting synergistic cell death that is associated with both apoptosis and autophagy in vitro and in vivo. Our data demonstrated that the combination effects of DNA hypomethylating drugs with radiation exhibited greater cellular effects than the use of a single agent treatment, thus suggesting that the combination of DNA hypomethylating drugs and radiation may become a new radiotherapy to improve therapeutic efficacy for cancer treatment.