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Clustered DNA damage is considered a signature of ionizing radiation: “clustered DNA damage sites, which may be considered as a signature of ionising radiation, underlie the deleterious biological consequences of ionising radiation…ionising radiation creates significant levels of clustered DNA damage, including complex double-strand breaks (DSB)” See: “Biological Consequences of Radiation-induced DNA Damage: Relevance to Radiotherapy“, by M.E. Lomax et. al. Clinical Oncology 25 (2013) 578-585

The formation of clustered damage distinguishes ionising radiation-induced damage from normal endogenous damage“. https://cordis.europa.eu/pub/fp5-euratom/docs/non_dsb_lesions_projrep_en.pdf (See more details further below, after political commentary.)

When watching US Congressman from Illinois, Hultgren: http://youtu.be/UkN4Ss5LcrI witchhunting renewable energy researcher Dr. Sharlene Weatherwax over removal of Noelle Metting and closure of the US DOE’s so-called low dose program, which at 100 mSv (10,000 mrem) isn’t even low dose, one needs to bear in mind facts. With the information found further below, we will leave it to the reader to conclude if Hulgren is being misled or doing the bidding of his (nuclear utility) Exelon donors (workers and PAC) to the tune of $19,000: https://www.opensecrets.org/politicians/contrib.php?cid=N00031104 Some of the others involved have funding from Honeywell and Lockheed Martin, which benefit from perpetuating nuclear energy, nuclear research, and/or weapons. It is apparently Noelle Metting who was attempting to mislead Congress about the benefits of her research program on “low dose”, rather than the contrary as alleged. Need for any additional research is strictly academic or for the purposes of pharmaceutical research and has no place in a Department of Energy.

As explained to US Congress in September by Dr. Weatherwax, Ph.D. in biochemistry: “To date, there are no studies that have been able to establish with sufficient certainty a threshold level of radiation below which a risk of cancer is zero, despite decades of research in this area. In the absence of sufficient data to the contrary, the LNT [Linear No-Threshold] model continues to be the accepted, albeit conservative, standard on which current radiation worker protection standards are based. Current National and International bodies (National Council on Radiation Protection and. Measurements, NCRP; International Commission on Radiological Protection, (ICRP)) continue to recommend the use of the LNT.http://docs.house.gov/meetings/SY/SY21/20160921/105345/HHRG-114-SY21-Wstate-WeatherwaxS-20160921.pdf

It is almost comic that the Republicans present themselves as railing against Obama’s plan, whereas Obama’s Exelon funding and entourage show him up to be a high priced prostitute, whereas these Congressmen are simply cheap ones. In fact, Exelon has been called “The President’s Utility” for that reason. And, it may be why the US NRC has put Exelon’s competitor, Entergy, under more scrutiny. “Nuclear Energy Company Backs Obama’s Bid“: https://www.opensecrets.org/news/2008/02/nuclear-energy-company-backs-o/ Thus, the following is a pure, unadulterated, lie: “The Committee concludes that the DOE placed its own priorities to further the President’s Climate Action Plan before its Constitutional obligations to be candid with Congress.“, in “U.S. Department of Energy Misconduct Related to the Low Dose Radiation Research Program “, December 20, 2016, Staff Report, Committee on Science, Space, and Technology, Chairman Lamar Smith. When looking at funding of politicians, it is worth noting that the petroleum industry has an interest in increased radiation exposure, because of their usage of x-ray equipment and because of concentration of naturally occurring radionuclides (TeNORM) by them.

The US DOE’s own Los Alamos National [Nuclear] Lab (LANL) wrote the following in 1995, several years before the Dept. of Energy’s “Low Dose” program begin. It clearly shows that nuclear discharges are lethal and hence criminal. Thus, the almost 20 year long “low dose” program never should have been funded by the Dept. of Energy in the first place. Any funding should have been NIH or CDC. From LANL, 1995: “Although single-strand breaks, abasic sites, and base alterations are induced by both ionizing radiation and normal metabolic processes, one particularly dangerous type of DNA lesion, the double-strand break, is induced preferentially by ionizing radiation. This is due to the manner in which radiation creates radical species within the cell, versus that of metabolic processes. Normal metabolism generates radicals one at a time and at essentially random locations throughout the cell volume. DNA lesions resulting from metabolically derived radicals, therefore, tend to occur at relatively isolated positions along the DNA molecule. Ionizing radiation, in contrast, deposits energy unevenly along the narrow track that is traversed by the ionizing photon or particle. As a result, many radical species are formed in a relatively limited area and tend to form clusters of radicals. If a radical cluster of this type envelops a DNA molecule, then multiple independent lesions might be induced within a localized region of the DNA and both DNA strands might become damaged, broken, or both. Not surprisingly, ionizing radiation can induce very complex lesions comprised of abasic sites and base alterations in addition to strand breaks, as illustrated in Figure 13…
Figure 13. DNA Damage II:  Double-Strand Breaks Double-strand breaks result from two single-strand breaks that are induced at closely opposed positions in the com-plementary strands.  Simple double-strand breaks (upper red box) can often be repaired by a simple end-joining procedure.  Ionizing radiation often in-duces a complex lesion (lower red box) with base alterations and base dele-tions accompanying the breaks.
Figure 13. DNA Damage II: Double-Strand Breaks: Double-strand breaks result from two single-strand breaks that are induced at closely opposed positions in the complementary strands. Simple double-strand breaks (upper red box) can often be repaired by a simple end-joining procedure. Ionizing radiation often induces a complex lesion (lower red box) with base alterations and base dele-tions accompanying the breaks.

It has been estimated from cell-culture studies that approximately twenty to forty double-strand breaks occur per genome at 100 rad of exposure. At that rate, exposures equivalent to ordinary background radiation (typically about 0.3 rad per year) should produce only one double-strand break per ten cells per year… A double-strand break is usually a mess, and repairing it can be problematic. Even a fairly clean double-strand break, wherein the two backbones are broken directly opposite from each other, results in at least a one-base-pair deletion and a disruption of the linkage between the two DNA segments. The passage of densely ionizing particles, such as alpha particles or neutrons, may break several proximal DNA molecules and cause base damage within each strand that can span several nanometers, or fifteen to twenty base pairs. Not surprisingly, the damaged bases are often excised as the free DNA ends are made ready for repair. The excision permanently removes bases. Simple rejoining of the exposed DNA ends is probably the major mechanism for the repair of double-strand breaks, but this mecha-nism would result in a loss of genetic informationDouble-strand breaks are often rapidly repaired by the simple mechanism of joining free ends, and this is likely to be a significant source of DNA mutations. In nonhomologous recombination, the free ends of broken DNA molecules are brought together and joined without reference to an intact partner. There are several mechanisms by which this can occur, the simplest employing a DNA ligase that ligates the two ends together… Although these mechanisms serve to rescue parts of a broken chromosome, they do so at the risk of introducing mutational changes and random genetic rearrangements“,(pp. 77, 79 Number 23 1995 Los Alamos Science)

The “current estimation of human total cell number calculated for a variety of organs and cell types is presented. These partial data correspond to a total number of 3.72 × 10(13).“, i.e. 37,200,000,000,000 or 37.2 trillion cells. “An estimation of the number of cells in the human body“, Bianconi E et. al., Ann Hum Biol. 2013 Nov-Dec;40(6):463-71. doi: 10.3109/03014460.2013.807878. Thus, the number of double strand breaks for 3 mSv alone is estimated to be 3.7 TRILLION BREAKS. Not surprisingly, Swiss researchers, Spycher et.al., published research in a US government publication, in 2015, showing that there is an increase in childhood cancers even from background radiation (which now includes nuclear discharges): http://dx.doi.org/10.1289/ehp.1510111R Refers to http://dx.doi.org/10.1289/ehp.1408548

Cancer is a gross distortion of cell behavior caused by numerous gene mutations and numerous abnormalities in the production and functioning of proteins…

A substantial body of evidence now suggests that cancer initiates from a single cell that has been transformed due to a particular change in its DNA. Some event, such as exposure to radiationcreates a change in the genome. This may be a DNA mutation, or an epigenetic modification. Then, either through direct action or indirectly through a complex web of interacting proteins, the mutation changes the overall expression of some of the cell’s genes. The cell continues to function, albeit slightly differently. Typically, the initial behavioral modification may be difficult to detect, but the functional change is passed on to future cell generations…” (p. 74)
Los Alamos Science Number 23 1995, “Radiation, Cell Cycle, and Cancer

Click to access getfile

Dicentric chromosomes US health and human services gov

The European Commission has funded multiple rounds of research, which provide even more evidence that nuclear discharges into the environment are a heinous crime. The dangers have been known for around 100 years, and suspected for much longer. Nonetheless, additional research has continued. The EU research from 1994 to 2002 dealt with double-stranded DNA breaks. Recall that the US DOE “low dose” program was started in 1998, although similar research was underway since before the nuclear age.

From the European Commission, about research projects from 1994 to 2002:
2. Research within the 4th and 5th Framework Programmes (FP4: 1994-1998; FP5: 1998-2002)

Cellular studies on DNA damage-response

The foundations for research on DNA damage response and repair were established in previous FPs and the new work sought to build upon the critical mass of EU expertise and knowledge that had been developed. At the level of initial radiation damage to DNA, the FP4 programme greatly strengthened the view that the appearance of excess gene/chromosomal mutations in cells was principally driven by the induction of double strand breaks in the helical DNA molecules that make up the chromosomes. Work was undertaken on the dependence of DNA double strand breaks induction by radiations of different qualities (different linear energy transfer LET).

An important finding was that the complexity of this initial damage appeared to strongly influence the quality of DNA repair that was possible. During this period of research the biologically important DNA double strand breaks were suggested to be associated with multiply damaged sites which also contained local damage to other constituents of the molecule, i.e. clustered damage (see note 5 ). This feature seemed likely to be related to the types of gene and chromosomal mutations that arose after radiation.
In this general area of biophysics, technical developments allowed for the irradiation of single cells by single ionising particles of high LET radiation. This technique allowed study of the induction of cellular effects by the lowest possible dose of radiation and also revealed evidence of the potential for transfer of damage signals between cells the bystander effect.

A number of projects addressed the specific mechanisms whereby radiation tracks caused initial DNA damage which was then misrepaired to form chromosomal exchanges (translocations). These studies benefited greatly from a new technique, termed FISH, that allowed differential molecular staining of different chromosomes using this technique and another that prematurely condenses chromosomes (PCC) it became possible to approach mechanistic problems of chromosome damage that had previously been inaccessible, for example the rate of repair of initial DNA double strand breaks in relation to chromosome damage. FISH techniques coupled with cellular/molecular analyses were also used to explore relationships between cellular radiation response, chromosomal instability and the specialised DNA sequences termed telomeres that cap the ends of chromosomes and occupy certain internal chromosomal sites. This and other work highlighted the potential importance of higher order DNA structure as a factor in chromosome stability and radiation response.

The response of cells to radiation include the imposition of checkpoints in the reproductive cycle in order to promote DNA repair also as part of the mechanism of programmed cell death (apoptosis) that serves to eliminate heavily damaged cells. A number of projects succeeded in clarifying the above relationships and some of the genes/enzymes involved in the responses.

The potential role of telomeric sequences in radiation response, highlighted in studies on chromosomal instability in tumorigenesis, was investigated in mouse germ cells. These studies revealed up-regulation of the telomere elongating enzyme telomerase in response to radiation and evidence that some DNA double strand breaks can be healed by addition of telomeric sequences.

The study of mutant cells with altered radiation response had become a most important component of radiation biology and was used widely in many fundamental studies in FP4. Such mutants were selected from cell cultures or derived from carriers of radiosensitive human genetic disorders e.g. ataxia-telangiectasia. A major contribution was made to the characterisation of these mutants including the isolation of the responsible genes and others of related structure/function. Other advances included the elucidation of the relevant biochemical pathways and, latterly, the genetic manipulation of mice to carry the mutant genes. Progress in this whole area was most notable and the EU-supported work on DNA repair is acknowledged world-wide. The characterisation of the repair pathways for DNA double strand breaks repair and associated radiation responses has made a significant contribution to our understanding of the degree of error-prone DNA repair expected after radiation. In turn, this provides important input to the low dose cancer risk debate stated simply, the error-prone repair of sometimes complex DNA double strand breaks may be used as one element in a scientific argument against the presence of a low dose threshold for cancer risk

The characterisation of DNA damage response genes in FP4 has also provided information on candidate genes determining heritable sensitivity to radiation tumorigenesis. This theme appears in a number of cellular projects including studies on the potential association between heritable cellular radiosensitivity and breast cancer risk.

FP5 research in this area represents a more focused approach to key issues associated with initial DNA damage and the nature, control and consequences of the relevant DNA damage response pathways. The ongoing studies underway include detailed consideration of complex DNA lesions; post-irradiation protein-protein and protein-DNA interactions; DNA repair fidelity; and studies with recombinant (gene knock-out) mice to explore the consequences of DNA repair deficiency in whole animals. The induction of persistent genomic instability in cells and the transfer of damage signals from irradiated to unirradiated cells (bystander effects) are also being investigated.”
© European Union, 1995-2016: https://cordis.europa.eu/fp5-euratom/src/effects-health/part1-2-2.htm

From a 2008 summary of research. Note that as with LANL they tend to have pro-nuclear affiliations, whether nuclear medicine or nuclear power or both.
EUROPEAN COMMISSION: nuclear science and technology
Radiation-specific DNA non-double strand break lesions: repair mechanisms and biological effects (Non-DSB Lesions) Contract No FIGH-CT2002-00207
Final report (summary) Work performed as part of the European Atomic Energy Community’s research and training programme in the field of nuclear energy 1998-2002 (Fifth Framework Programme) Generic research in radiological sciencesDirectorate-General for Research 2008 Euratom
Project coordinator L. H. F. Mullenders, Leiden University Medical Centre (LUMC), Department of Toxicogenetics, NL
Project partners P Jeggo, A.Carr, and A. lehman, Genome Damage and Stability Centre, University of Sussex, UK ; J. Hoeijmakers, R. Kanaar, and D. van Gent, Department of Cell Biology and Genetics, Erasmus University, NL ; G. Almouzni and D. Papadopoulo, Institut Curie, FR ; J. Thacker and P. O’Neill, MRC, Radiation and Genome Stability Unit, UK; F. Eckardt-Schupp, GSF, DE ; S. Boiteux, CEA, FR
To make rational judgements in radiation protection, it is necessary to extrapolate from the biological effects of radiation at low doses and low dose rates, and to have an appreciation of variation in response to ionising radiation (IR) among the human population. Therefore, a detailed knowledge of the basic mechanisms by which radiation induces cancer and genetic disorders is essential. DNA damage induced by ionising radiations is formed by direct energy deposition in DNA and by water radicals generated in the vicinity of DNA. The nature of ionising radiation-induced DNA lesions (such as 8-oxo-guanine, thymine glycols and single strand DNA breaks (SSBs)) overlaps substantially with lesions produced by endogenous oxidative metabolism in unirradiated cells. These endogenous damages are effectively repaired by the base excision repair (BER) pathway and this has led to suggest a threshold effect for radiation risk at low dose exposure. However, there is now clear evidence that the random energy deposition by IR not only induces isolated single DNA lesions but in addition a unique form of DNA lesions termed clustered DNA damage. This type of damage consists of two or more closely spaced lesions formed within about one helical turn in the DNA backbone and may include different combinations of base lesions and single strand breaks. The existence of clustered DNA damage caused by ionising radiation was first predicted from theoretical studies of radiation track structures and later demonstrated experimentally. The formation of clustered damage distinguishes ionising radiation-induced damage from normal endogenous damage. If processing of clustered DNA base damage differs from endogenous damage, then the linear-no threshold model might be the most appropriate model for the risk assessment of adverse effects of ionising radiation. Hence it is important to unravel the mechanisms underlying the biological effects of clustered DNA base damage-induced radiation exposures and allow better quantification of the risks of radiation.

Strategic aspects and research performed

In order to achieve the goals of the current project, we utilised the following general approach:

(1) different treatments to induced non-DSB damage (IR, UVA, hydrogen peroxide)
(2) different organisms/cell lines (human, mouse, chicken, yeast) with defined mutations in relevant repair pathways and cell-cycle checkpoints to dissect the mechanistic pathways
(3) genetics and biochemistry to investigate the precise functions of the proteins involved in the various repair pathways and their response to DNA damage using novel techniques (fluorescent redistribution after photo-bleaching, chromatin assemblage at individual DNA molecules, local damage induction)
(4) measurement of the fidelity of repair and the role of translesion synthesis employing cells and transgenic mice with defined mutations in repair genes and substrates with defined lesions
(5) high-density microarrays to obtain a catalogue of genes that respond to non-DSB damage
(6) ultimately, our goal was to understand the consequences of deficiencies in radiation damage responses in man. To this end, we aimed to use our knowledge to screen for polymorphisms in damage response genes within the human population and expression/mutagenesis in human tumour material.

The research carried out in this project was organised in the following five work packages:
• Work package 1: Nature and repair of radiation-induced DNA non-double strand break lesions;
• Work package 2: Interactions of radiation-induced DNA non-double strand break lesions with replication and transcription;
• Work package 3: Role of chromatin structure in repair of radiation-induced DNA non-double strand break lesions;
• Work package 4: Biological effects of radiation-induced DNA non-double strand break lesions;
• Work package 5: Stress responses dependent on DNA non-double strand break lesions.

Main achievements

IR-induced DNA damage constitutes a broad spectrum of purine and pyrimidine modifications, sites of base loss, single strand DNA breaks (SSB) of different kinds (see figure below). We have studied the repair mechanism and biological consequences of these modifications either as single entities or as clusters of DNA damage.

IMAGE EC Contract No FIGH-CT2002-00207         From single lesions to clustered damage

Defect in SSB repair may lead to a neurodegenerative disease. This project has contributed with much new information concerning how one type of lesions, i.e. chromosomal SSBs, is repaired in mammalian cells. We have expressed and purified two new human repair proteins (TDP1 and aprataxin). In addition, this project has contributed to the identification of a defect in SSB repair in a neurodegenerative disease, raising the possibility that SSBs are a significant factor in the etiology of neurological disease, possibly including non-pathological conditions such as ageing.

Frequency of IR-induced DNA base damage in human cells is relatively low. We have demonstrated by different approaches that the frequency of IR-induced DNA base damage in human cells is relatively low and certainly not high enough to explain some of the hazardous effects of IR by known mechanisms. Although low in number, the clustering of IR-induced (p 3) DNA base damage might lead to serious problems to cells and organisms as we have shown that clustered DNA lesions pose a significant challenge to repair systems and replication.

Clustered damage sites might pose problems to repair.
We studied the reparability of clustered lesions by different BER pathways and showed that the damaging effect of such lesions depends on the sequence in which they occur as well as on the relative positioning of primary lesions within a cluster. The processing of clustered DNA damage (using cell extracts) is significantly retarded when compared with the rate of processing of the individual lesions. Some lesions such as 8-oxoguanine within a repair gap do not inhibit short-patch BER, however they block long-patch repair. In contrast, thymine glycol is a much more harmful lesion: when located within a cluster, thymine glycol causes a substantial delay in short-patch BER of the opposing lesion. We also find that repair of tandem lesions (2 or more DNA lesions at short distance on the same DNA strand) could lead to accumulation of strand breaks during repair. Generally the processing of the DNA lesions occurs sequentially thereby minimising the formation of potentially lethal DNA double strand breaks (DSB). This was confirmed in mammalian cells where it was estimated that approximately 15 % of the clustered damage sites are converted into DSB. We also found that DSBs can arise after treatment with agents that generate ROS. Such DSBs can have “dirty” ends that require additional processing prior to rejoining and specific genetic factors for repair.

Clustered damage sites might be highly mutagenic and thereby contribute to the health consequences of low-dose radiation. The type of clusters which are converted into DSB, contains 2 or more DNA lesions on opposite strands of the DNA double helix (bistranded clusters) and may cause infidelity of repair, resulting in mutations, as well as deletions and chromosome rearrangements. These genetic changes are known to play key roles in the multiple steps of the process leading to cancer. That delays in processing of repair intermediates can cause a significant increase in genomic instability and can affect cellular resistance to IR was evident from the observation that clustered damage sites are highly mutagenic relative to the individual lesions and that 2 AP-containing bistranded clusters are precursors to formation of DSB. These mutation studies confirmed that clustered damage sites might be highly mutagenic and thereby contribute to the health consequences of low-dose radiation. These findings are relevant to developing mechanistic models of low dose effects. At low doses of radiation (due to the higher yields of radiation-induced clustered damage to that of DSB) the probability that only a non-DSB clustered site or a single DSB is induced in any one cell is high relative to higher doses when a mixture of both types of damage are formed in any given cell. Overall, our data suggest that clustered lesions are repaired slower than single lesions of the same type and are likely to be responsible for the deleterious effect of IR. During the course of the project, it became clear from studies with mammalian cells lacking certain BER proteins, that non-repaired DNA base damage i.e. IR-induced oxidised pyrimidines, confers severe radiosensitivity to cells (An et al., 2005).

Radiosensitivity is most likely not related to transcription blocks. Impaired transcription of genes, of which expression is essential for viability, by IR-induced base damage has been suggested to be a serious threat to the cell leading to radiosensitivity and aging. Cells have developed a specialised repair pathway that preferentially removes transcription-blocking lesions called transcription-coupled repair (TCR). Although TCR deficiency might leads to radiosensitivity, both experiments with TCR deficient cells and the known IR-induced lesion frequency make it unlikely that interference of IR induced base damage with transcription plays a major role in the toxic effects of IR. The transcription response to base damage appears to act mainly through the stress-activated MAP kinase pathways and be caused by (p. 4) oxidative damage. The characterisation of genes induced in this way was initiated. Surprisingly, the most dramatically induced gene did not lead to a sensitivity phenotype, whereas the less induced gene did. Ultimately we anticipate that new players in the response to IR-induced oxidative stress will be identified and used to characterise the non-DSB response to IR.

Transcription response: indications that oxidative damage plays a role. The transcription response to base damage appears to act mainly through the stress activated MAP kinase pathways and be caused by oxidative damage. The characterisation of genes induced in this way was initiated. Surprisingly, the most dramatically induced gene did not lead to a sensitivity phenotype, whereas the less induced gene did. Ultimately we anticipate that new players in the response to ionising radiation-induced oxidative stress will be identified and used to characterise the non-DSB response to ionising radiation.

We assessed the gene expression profiling of IR exposed human lymphocytes from 39 individuals to investigate the radiation response (2 Gy X-rays, 0.5 Gy/min). Overall fold changes were not dramatic. Only few genes (4.2 % or 940 genes per individual) had changed more than twofold after irradiation. The mean of the magnitude of changes is approximately 1.2-fold. It has been shown before that genotoxic stress induces substantial alterations at transcription level. The 200 most significantly changed genes had an average fold-change of 1.3. There is much variation in the radiation response of the individuals but the overall radiation response turned out to be largely comparable to other studies. All patients had a p53 dependent response and the apoptotic pathway seemed to be turned on, judging by the up- and down-regulated genes.

Polymorphisms in damage response genes within the human population and expression/mutagenesis in human tumour material. At the beginning of the project we intended to focus on cancer analysis for the BER gene Ogg1, since somatic mutations including several polymorphisms in hOgg1 have been identified in a fraction (< 5 %) of human lung and kidney tumour. The involvement of these alterations of hOgg1 in the cancer process is not yet clear. We suggested that inactivation of hOgg1 may be involved in late stages of carcinogenesis. Unfortunately, inactivation of Ogg1 in mice leads to the accumulation of 8-OxoG in the liver, but not to increased tumorigenesis. This disappointing finding has set the priority on other more promising mechanistic issues in the project.

Implications and future perspectives

The picture that emerges is that the ionising radiation induces clustered DNA damage that poses special problems to the cell both with respect to repair by BER and perhaps (during replication) by other repair systems such as recombination repair. Both the impaired repair and replication errors lead to mutagenic events and hence there is a requirement for further investigation into frequencies of clustered lesions by various radiation qualities and DNA repair mechanisms. To understand more precisely the hazardous impact of clustered DNA base damage for cellular function warrants model DNA templates harbouring defined clustered DNA base damage and various in vivo radiation protocols that enriched for clustered DNA base damage. This strategy will allow assessment of the biological consequences of limited (or even a single cluster, equivalent to the lowest dose possible) numbers of DNA base damage for the cell in terms of reparability, toxicity and mutagenesis. In addition, cell lines with knockdown of BER genes will provide the tools to study the role of these genes in (p. 5) counteracting hazardous effects of IR exposure. Further development of mouse models with defects in these genes provide further the way to understand the role played by these genes in mitigating the development of cancer. Indeed, novel findings point to an important role of BER genes in radiosensitivity. In addition, screens for polymorphisms in these and other genes involved in radiation responses might reveal enhanced risk for cancer and ultimately identify individual susceptibility to IR.

Exploitation and dissemination

The results obtained in this period of the contract have been reported in 49 publications in peer-reviewed journals and presented at numerous national and international scientific meetings.(p. 5). © European Union, 1995-2016: https://cordis.europa.eu/pub/fp5-euratom/docs/non_dsb_lesions_projrep_en.pdf

The above, from 8 plus years ago, makes clear that there is ample research to show that nuclear discharges into the environment are lethal. While it lists further research which may be done, and probably has already been done by now, this is also what people are taught to write from Graduate School: How research fits into pre-existing literature; what's important about the research in the context of the literature; and what future research is needed-shortcomings of the research. Any further research funding should be related to public health issues, and by pharmaceutical companies or for purely academic purposes. It has no relationship to energy. That radioactive materials are unacceptably dangerous has been known for around 100 years and suspected for hundreds of years, in relation to mining. The more recent research only confirms additional details.

EMPHASIS ADDED TO TEXT THROUGHOUT THIS BLOG POST. NB: In the last document original a couple of sentences appear twice, whether intentionally or unintentionally and it was left this way.