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European Health Risk Assessment Network on Electromagnetic Fields Exposure |
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D3 – Report on the analysis of risks associated to exposure to EMF: in vitro and in vivo (animals) studies |
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2010 |
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EFHRAN |
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IT'IS @ kuster @ |
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53 |
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Keshet, Y.; Seger, R. |
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The MAP kinase signaling cascades: a system of hundreds of components regulates a diverse array of physiological functions |
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Journal Article |
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2010 |
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Methods in Molecular Biology (Clifton, N.J.) |
Abbreviated Journal |
Methods Mol Biol |
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661 |
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3-38 |
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Animals; Extracellular Signal-Regulated MAP Kinases/metabolism; Humans; JNK Mitogen-Activated Protein Kinases/metabolism; *MAP Kinase Signaling System; p38 Mitogen-Activated Protein Kinases/metabolism |
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Sequential activation of kinases within the mitogen-activated protein (MAP) kinase (MAPK) cascades is a common, and evolutionary-conserved mechanism of signal transduction. Four MAPK cascades have been identified in the last 20 years and those are usually named according to the MAPK components that are the central building blocks of each of the cascades. These are the extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-Terminal kinase (JNK), p38, and ERK5 cascades. Each of these cascades consists of a core module of three tiers of protein kinases termed MAPK, MAPKK, and MAP3K, and often two additional tiers, the upstream MAP4K and the downstream MAPKAPK, which can complete five tiers of each cascade in certain cell lines or stimulations. The transmission of the signal via each cascade is mediated by sequential phosphorylation and activation of the components in the sequential tiers. These cascades cooperate in transmitting various extracellular signals and thus control a large number of distinct and even opposing cellular processes such as proliferation, differentiation, survival, development, stress response, and apoptosis. One way by which the specificity of each cascade is regulated is through the existence of several distinct components in each tier of the different cascades. About 70 genes, which are each translated to several alternatively spliced isoforms, encode the entire MAPK system, and allow the wide array of cascade's functions. These components, their regulation, as well as their involvement together with other mechanisms in the determination of signaling specificity by the MAPK cascade is described in this review. Mis-regulation of the MAPKs signals usually leads to diseases such as cancer and diabetes; therefore, studying the mechanisms of specificity-determination may lead to better understanding of these signaling-related diseases. |
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Department of Biological Regulation, The Weizmann Institute of Science, Rehovot, Israel |
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1064-3745 |
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WP5 In vitro |
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PMID:20811974 |
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CBM.UAM @ ccobaleda @ |
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66 |
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Maslanyj, M.; Lightfoot, T.; Schuz, J.; Sienkiewicz, Z.; McKinlay, A. |
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A precautionary public health protection strategy for the possible risk of childhood leukaemia from exposure to power frequency magnetic fields |
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Journal Article |
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2010 |
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BMC Public Health |
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BMC Public Health |
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10 |
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673 |
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Adolescent; Child; Dose-Response Relationship, Radiation; Electromagnetic Fields/*adverse effects; Humans; Leukemia, Radiation-Induced/*epidemiology/prevention & control; Odds Ratio; *Public Health; Radio Waves/adverse effects; Risk Assessment/methods; Risk Factors |
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BACKGROUND: Epidemiological evidence showing a consistent association between the risk of childhood leukaemia and exposure to power frequency magnetic fields has been accumulating. This debate considers the additional precautionary intervention needed to manage this risk, when it exceeds the protection afforded by the exposure guidelines as recommended by the International Commission on Non-Ionizing Radiation Protection. METHODS: The Bradford-Hill Criteria are guidelines for evaluating the scientific evidence that low frequency magnetic fields cause childhood leukaemia. The criteria are used for assessing the strength of scientific evidence and here have been applied to considering the strength of evidence that exposures to extremely low frequency magnetic fields may increase the risk of childhood leukaemia. The applicability of precaution is considered using the risk management framework outlined in a European Commission (EC) communication on the Precautionary Principle. That communication advises that measures should be proportionate, non-discriminatory, consistent with similar measures already taken, based on an examination of the benefits and costs of action and inaction, and subject to review in the light of new scientific findings. RESULTS: The main evidence for a risk is an epidemiological association observed in several studies and meta-analyses; however, the number of highly exposed children is small and the association could be due to a combination of selection bias, confounding and chance. Corroborating experimental evidence is limited insofar as there is no clear indication of harm at the field levels implicated; however, the aetiology of childhood leukaemia is poorly understood. Taking a precautionary approach suggests that low-cost intervention to reduce exposure is appropriate. This assumes that if the risk is real, its impact is likely to be small. It also recognises the consequential cost of any major intervention. The recommendation is controversial in that other interpretations of the data are possible, and low-cost intervention may not fully alleviate the risk. CONCLUSIONS: The debate shows how the EC risk management framework can be used to apply the Precautionary Principle to small and uncertain public health risks. However, despite the need for evidence-based policy making, many of the decisions remain value driven and therefore subjective. |
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Health Protection Agency, Chilton, Didcot, Oxfordshire OX110RQ, UK. myron.maslanyj@hpa.org.uk |
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1471-2458 |
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WP9 Epidemiology |
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PMID:21054823 |
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IARC @ ErdmannF @ |
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93 |
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Juutilainen, J. |
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Title |
Developmental effects of electromagnetic fields |
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Journal Article |
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2005 |
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Bioelectromagnetics |
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Bioelectromagnetics |
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Suppl 7 |
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S107-15 |
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Aging/*physiology/*radiation effects; Animals; Behavior, Animal/*physiology/*radiation effects; *Electromagnetic Fields; Female; Growth/*radiation effects; Pregnancy; Prenatal Exposure Delayed Effects/*physiopathology; Radiation Dosage |
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This paper reviews experimental studies on the effects of radiofrequency (RF), extremely low frequency (ELF), and intermediate frequency (IF) electromagnetic fields on animal development. Numerous studies have shown that RF fields are teratogenic at exposure levels sufficiently high to cause significant increase of temperature. There is no consistent evidence of RF field effects at nonthermal exposure levels. Only a few studies have evaluated possible effects on postnatal development using sensitive endpoints, such as behavioral effects. ELF electric fields up to 150 kV/m have been evaluated in several mammalian species. The results are rather consistent and do not suggest adverse developmental effects. The results of studies on ELF magnetic fields suggest effects on bird embryo development, but not consistently in all studies. Results from experiments with other non-mammalian experimental models have also suggested subtle effects on developmental stability. In mammals, most studies have shown no effects of prenatal exposure to ELF or IF magnetic on gross external, visceral, or skeletal malformations. The only finding that shows some consistency is increase of minor skeleton alterations in several experiments. Taken as a whole, the results do not show robust adverse effects of ELF and IF fields on development. However, additional studies on the suggested subtle effects on developmental stability might increase our understanding of the sensitivity of biological organisms to weak low-frequency magnetic fields. |
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Department of Environmental Sciences, University of Kuopio, Kuopio, Finland. jukka.juutilainen@uku.fi |
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0197-8462 |
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WP6 In vivo |
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PMID:16037961 |
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ITEM @ geertje.lewin @ |
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104 |
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Zangrando, A.; Dell'orto, M.C.; Te Kronnie, G.; Basso, G. |
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MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures |
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2009 |
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BMC Medical Genomics |
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BMC Med Genomics |
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2 |
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36 |
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BACKGROUND: The presence of MLL rearrangements in acute leukemia results in a complex number of biological modifications that still remain largely unexplained. Armstrong et al. proposed MLL rearrangement positive ALL as a distinct subgroup, separated from acute lymphoblastic (ALL) and myeloblastic leukemia (AML), with a specific gene expression profile. Here we show that MLL, from both ALL and AML origin, share a signature identified by a small set of genes suggesting a common genetic disregulation that could be at the basis of mixed lineage leukemia in both phenotypes. METHODS: Using Affymetrix(R) HG-U133 Plus 2.0 platform, gene expression data from 140 (training set) + 78 (test set) ALL and AML patients with (24+13) and without (116+65) MLL rearrangements have been investigated performing class comparison (SAM) and class prediction (PAM) analyses. RESULTS: We identified a MLL translocation-specific (379 probes) signature and a phenotype-specific (622 probes) signature which have been tested using unsupervised methods. A final subset of 14 genes grants the characterization of acute leukemia patients with and without MLL rearrangements. CONCLUSION: Our study demonstrated that a small subset of genes identifies MLL-specific rearrangements and clearly separates acute leukemia samples according to lineage origin. The subset included well-known genes and newly discovered markers that identified ALL and AML subgroups, with and without MLL rearrangements. |
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Laboratory of HematoOncology, Department of Pediatrics “Salus Pueri”, University of Padova, Padova, Italy. andrea.zangrando@unipd.it |
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1755-8794 |
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WP6 In vivo |
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PMID:19549311 |
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ITEM @ geertje.lewin @ |
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108 |
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