Environmental assessment for the satellite power system-concept development and evaluation program-microwave health and ecological effects

Potential health and ecological effects of the microwave beam from the microwave power transmission system (MPTS) of the satellite power system (SPS) are discussed. A detailed critical review of selected scientific articles from the published literature on the biological effects of nonionizing electromagnetic radiation is provided followed by an assessment of the possible effects of the SPS, based on exposure values for the reference system

The Largest Unethical Medical Experiment in Human History

This monograph describes the largest unethical medical experiment in human history: the implementation and operation of non-ionizing non-visible EMF radiation (hereafter called wireless radiation) infrastructure for communications, surveillance, weaponry, and other applications. It is unethical because it violates the key ethical medical experiment requirement for “informed consent” by the overwhelming majority of the participants. The monograph provides background on unethical medical research/experimentation, and frames the implementation of wireless radiation within that context. The monograph then identifies a wide spectrum of adverse effects of wireless radiation as reported in the premier biomedical literature for over seven decades. Even though many of these reported adverse effects are extremely severe, the true extent of their severity has been grossly underestimated. Most of the reported laboratory experiments that produced these effects are not reflective of the real-life environment in which wireless radiation operates. Many experiments do not include pulsing and modulation of the carrier signal, and most do not account for synergistic effects of other toxic stimuli acting in concert with the wireless radiation. These two additions greatly exacerbate the severity of the adverse effects from wireless radiation, and their neglect in current (and past) experimentation results in substantial under-estimation of the breadth and severity of adverse effects to be expected in a real-life situation. This lack of credible safety testing, combined with depriving the public of the opportunity to provide informed consent, contextualizes the wireless radiation infrastructure operation as an unethical medical experiment

A review of the ecological effects of radiofrequency electromagnetic fields (RF-EMF)

Industrial EcologyEnvironmental Biolog

DTYMK is essential for genome integrity and neuronal survival

Nucleotide metabolism is a complex pathway regulating crucial cellular processes such as nucleic acid synthesis, DNA repair and proliferation. This study shows that impairment of the biosynthesis of one of the building blocks of DNA, dTTP, causes a severe, early-onset neurodegenerative disease. Here, we describe two unrelated children with bi-allelic variants in DTYMK, encoding dTMPK, which catalyzes the penultimate step in dTTP biosynthesis. The affected children show severe microcephaly and growth retardation with minimal neurodevelopment. Brain imaging revealed severe cerebral atrophy and disappearance of the basal ganglia. In cells of affected individuals, dTMPK enzyme activity was minimal, along with impaired DNA replication. In addition, we generated dtymk mutant zebrafish that replicate this phenotype of microcephaly, neuronal cell death and early lethality. An increase of ribonucleotide incorporation in the genome as well as impaired responses to DNA damage were observed in dtymk mutant zebrafish, providing novel pathophysiological insights. It is highly remarkable that this deficiency is viable as an essential component for DNA cannot be generated, since the metabolic pathway for dTTP synthesis is completely blocked. In summary, by combining genetic and biochemical approaches in multiple models we identified loss-of-function of DTYMK as the cause of a severe postnatal neurodegenerative disease and highlight the essential nature of dTTP synthesis in the maintenance of genome stability and neuronal survival

The comet assay in animal models: From bugs to whales : (Part 2 Vertebrates)

The comet assay has become one of the methods of choice for the evaluation and measurement of DNA damage. It is sensitive, quick to perform and relatively affordable for the evaluation of DNA damage and repair at the level of individual cells. The comet assay can be applied to virtually any cell type derived from different organs and tissues. Even though the comet assay is predominantly used on human cells, the application of the assay for the evaluation of DNA damage in yeast, plant and animal cells is also quite high, especially in terms of biomonitoring. The present extensive overview on the usage of the comet assay in animal models will cover both terrestrial and water environments. The first part of the review was focused on studies describing the comet assay applied in invertebrates. The second part of the review, (Part 2) will discuss the application of the comet assay in vertebrates covering cyclostomata, fishes, amphibians, reptiles, birds and mammals, in addition to chordates that are regarded as a transitional form towards vertebrates. Besides numerous vertebrate species, the assay is also performed on a range of cells, which includes blood, liver, kidney, brain, gill, bone marrow and sperm cells. These cells are readily used for the evaluation of a wide spectrum of genotoxic agents both in vitro and in vivo. Moreover, the use of vertebrate models and their role in environmental biomonitoring will also be discussed as well as the comparison of the use of the comet assay in vertebrate and human models in line with ethical principles. Although the comet assay in vertebrates is most commonly used in laboratory animals such as mice, rats and lately zebrafish, this paper will only briefly review its use regarding laboratory animal models and rather give special emphasis to the increasing usage of the assay in domestic and wildlife animals as well as in various ecotoxicological studies

The role of the folate and methylation cycles in neural tube closure.

Neural tube defects (NTD) are congenital malformations caused by abnormalities in the developmental process of neurulation. Folate metabolism appears to be a determinant of risk of NTD since periconceptional supplementation with folic acid has been shown to reduce the frequency of NTD in humans while sub-optimal folate levels are a risk factor. The mechanisms underlying prevention of NTD by folic acid or susceptibility owing to reduced levels are not known. The aims of this thesis were to understand the role of the folate and, the closely linked, methylation cycle in the cause and prevention of NTD. The effect of methylation cycle intermediates, homocysteine and methionine, on cranial neural tube closure were investigated in cultured mouse embryos. Homocysteine exposure was embryotoxic but did not increase the incidence of NTD, which suggests that increased levels of homocysteine are not a direct cause of cranial NTD. Embryos cultured with high levels of methionine or methylation cycle inhibitors specifically developed cranial NTD in the absence of other developmental defects. These results suggest that the integrity of the methylation cycle is essential for cranial neural tube closure to occur. Mouse embryos that are homozygous for the Splotch211 mutation exhibit NTD that are preventable by folic acid. In Splotch mice, increased apoptosis has been suggested to be responsible for the production of NTD in homozygous embryos. However, in this study immunohistochemical measurement of apoptosis and proliferation in the neuroepithelium in the cranial region of neurulation-stage embryos suggest that the Splotch mutation does not result in increased apoptosis. Finally, in order to test whether there is an underlying defect in folate metabolism in human NTD fetuses, a series of human embryonic cell lines were analysed. The deoxyuridine monophosphate (dUMP) suppression test was modified for use with mammalian fibroblast cell lines and the efficiency and sensitivity of the modified test were analysed by the use of inhibitors of one-carbon metabolism. The test was then applied to human NTD and control cell lines and the results indicate that a subset of the NTD cases have a diminished response, suggestive of an abnormality of folate metabolism