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Koyama, S., Narita, E., Shinohara, N., & Miyakoshi, J. (2014). Effect of an intermediate-frequency magnetic field of 23 kHz at 2 mT on chemotaxis and phagocytosis in neutrophil-like differentiated human HL-60 cells. International journal of environmental research and public health, 11, 9649–9659.
Abstract: Public concerns about potential health risks of intermediate-frequency (IF) electromagnetic fields are increasing, especially as the use of induction-heating cooktops has spread extensively in Japan and Europe. In order to investigate the properties of IF electromagnetic fields, we examined the effect of exposure to a 23-kHz IF magnetic field of 2 mT for 2, 3, or 4 h on neutrophil chemotaxis and phagocytosis using differentiated human HL-60 cells. Compared with sham exposure, exposure to the IF magnetic field had no effect on neutrophil chemotaxis or phagocytosis. Previous studies demonstrated that exposure to a 23-kHz IF magnetic field of 2 mT (about 74-times the maximum value recommended by the International Commission for Nonionizing Radiation Protection guidelines) may affect the first-line immune responses in humans. To our knowledge, this is the first study to evaluate the effects of IF magnetic fields on cellular immune responses. We found that exposure to an IF magnetic field of 2 mT has minimal if any effect on either the chemotaxis or phagocytic activity of neutrophil-like human HL-60 cells.
Keywords: chemotaxis; cooktop; if; ih; induction-heating; induction-heating (IH) cooktop; intermediate-frequency; intermediate-frequency (IF) magnetic field; magnetic field; neutrophil; phagocytosis
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Kulkarni GA, G. W. Z. (2014). Numerical calculation of internal induced fields in humans due to high voltage trasmission lines. Acta Electrotechnica et Informatica, 14(3), 22–27.
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López-DÃaz, B., Mercado-Sáenz, S., MartÃnez-Morillo, M., Sendra-Portero, F., & Ruiz-Gómez, M. J. (2014). Long-term exposure to a pulsed magnetic field (1.5 mT, 25 Hz) increases genomic DNA spontaneous degradation. Electromagnetic biology and medicine, 33(3), 228–235.
Abstract: The aim of this work is to investigate whether long-term pulsed magnetic field (MF) has genotoxic activity by induction of DNA damage on DNA molecules in vitro, in the absence of repair mechanisms. Yeast genomic DNA prepared by phenol extraction from S. cerevisiae cultures and the commercial DNA molecular weight marker Hyperladder I (HL-I) were exposed to 1.5 mT peak, pulsed 25 Hz MF, 8 h/day, 16 days. The total content of DNA (undamaged and damaged DNA) decreased during the exposure of genomic DNA to MF. On day 16 of exposure the DNA content was 41 ± 8.1%. In addition, the undamaged DNA decreases until 6.2 ± 3.1% for unexposed control samples and until 0.3 ± 0.1% for pulsed MF-treated samples at day 16 of exposure. Therefore, the pulsed MF induced at day 16 an increase of 20.7-fold more degradation of DNA molecules >10 000 bp (undamaged DNA) than that observed for unexposed control samples. However, no effect was observed for HL-I DNA marker exposures. We conclude that long-term exposure to a pulsed MF (1.5 mT peak, 25 Hz, 8 h/day, 16 days) induces an increment in the DNA spontaneous degradation of yeast genomic DNA.
Keywords: dna damage; dna strand break; genomic instability; genotoxicity; magnetic field
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Lee, A. A., Lau, J. C. S., Hogben, H. J., Biskup, T., Kattnig, D. R., & Hore, P. J. (2014). Alternative radical pairs for cryptochrome-based magnetoreception. Journal of The Royal Society Interface, 11(95).
Abstract: Alpha A. Lee†, Jason C. S. Lau, Hannah J. Hogben, Till Biskup‡, Daniel R. Kattnig and P. J. Hore⇑Department of Chemistry, Physical and Theoretical Chemistry Laboratory, University of Oxford, Oxford OX1 3QZ, UKe-mail: peter.hore{at}chem.ox.ac.uk↵†Present address: Mathematical Institute, University of Oxford, Oxford OX2 6GG, UK.↵‡ Present address: Institut für Physikalische Chemie, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.Abstract
There is growing evidence that the remarkable ability of animals, in particular birds, to sense the direction of the Earth's magnetic field relies on magnetically sensitive photochemical reactions of the protein cryptochrome. It is generally assumed that the magnetic field acts on the radical pair [FAD•− TrpH•+] formed by the transfer of an electron from a group of three tryptophan residues to the photo-excited flavin adenine dinucleotide cofactor within the protein. Here, we examine the suitability of an [FAD•− Z•] radical pair as a compass magnetoreceptor, where Z• is a radical in which the electron spin has no hyperfine interactions with magnetic nuclei, such as hydrogen and nitrogen. Quantum spin dynamics simulations of the reactivity of [FAD•− Z•] show that it is two orders of magnitude more sensitive to the direction of the geomagnetic field than is [FAD•− TrpH•+] under the same conditions (50 µT magnetic field, 1 µs radical lifetime). The favourable magnetic properties of [FAD•− Z•] arise from the asymmetric distribution of hyperfine interactions among the two radicals and the near-optimal magnetic properties of the flavin radical. We close by discussing the identity of Z• and possible routes for its formation as part of a spin-correlated radical pair with an FAD radical in cryptochrome.
animal navigationflavinmagnetic compassradical pair mechanismspin dynamicsReceived November 15, 2013.Accepted March 3, 2014.© 2014 The Author(s) Published by the Royal Society. All rights reserved.
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Lento, W., Ito, T., Zhao, C., Harris, J. R., Huang, W., Jiang, C., et al. (2014). Loss of beta-catenin triggers oxidative stress and impairs hematopoietic regeneration. Genes Dev, 28(9), 995–1004.
Abstract: Accidental or deliberate ionizing radiation exposure can be fatal due to widespread hematopoietic destruction. However, little is known about either the course of injury or the molecular pathways that regulate the subsequent regenerative response. Here we show that the Wnt signaling pathway is critically important for regeneration after radiation-induced injury. Using Wnt reporter mice, we show that radiation triggers activation of Wnt signaling in hematopoietic stem and progenitor cells. beta-Catenin-deficient mice, which lack the ability to activate canonical Wnt signaling, exhibited impaired hematopoietic stem cell regeneration and bone marrow recovery after radiation. We found that, as part of the mechanism, hematopoietic stem cells lacking beta-catenin fail to suppress the generation of reactive oxygen species and cannot resolve DNA double-strand breaks after radiation. Consistent with the impaired response to radiation, beta-catenin-deficient mice are also unable to recover effectively after chemotherapy. Collectively, these data indicate that regenerative responses to distinct hematopoietic injuries share a genetic dependence on beta-catenin and raise the possibility that modulation of Wnt signaling may be a path to improving bone marrow recovery after damage.
Keywords: Wnt signaling; hematopoietic stem cells; oxidative stress; regeneration; β-catenin
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