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Cameron, I.L.; Sun, L.-Z.; Short, N.; Hardman, W.E.; Williams, C.D. |
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Title |
Therapeutic Electromagnetic Field (TEMF) and gamma irradiation on human breast cancer xenograft growth, angiogenesis and metastasis |
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Journal Article |
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Year |
2005 |
Publication |
Cancer Cell International |
Abbreviated Journal |
Cancer Cell Int |
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Volume |
5 |
Issue |
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Pages |
23 |
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Abstract |
BACKGROUND: The effects of a rectified semi-sinewave signal (15 mT amplitude, 120 pulses per second, EMF Therapeutics, Inc.) (TEMF) alone and in combination with gamma irradiation (IR) therapy in nude mice bearing a human MDA MB231 breast cancer xenograft were tested. Green fluorescence protein transfected cancer cells were injected into the mammary fat pad of young female mice. Six weeks later, mice were randomly divided into four treatment groups: untreated controls; 10 minute daily TEMF; 200 cGy of IR every other day (total 800 cGy); IR plus daily TEMF. Some mice in each group were euthanized 24 hours after the end of IR. TEMF treatment continued for 3 additional weeks. Tumor sections were stained for: endothelial cells with CD31 and PAS or hypoxia inducible factor 1alpha (HIF). RESULTS: Most tumors <35 mm3 were white but tumors >35 mm3 were pink and had a vascularized capsule. The cortex within 100 microns of the capsule had little vascularization. Blood vessels, capillaries, and endothelial pseudopods were found at >100 microns from the capsule (subcortex). Tumors >35 mm3 treated with IR 24 hours previously or with TEMF had decreased blood vessels in the subcortex and more endothelial pseudopods projecting into hypoxic, HIF positive areas than tumors from the control group. Mice that received either IR or TEMF had significantly fewer lung metastatic sites and slower tumor growth than did untreated mice. No harmful side effects were attributed to TEMF. CONCLUSION: TEMF therapy provided a safe means for retarding tumor vascularization, growth and metastasis. |
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Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA. cameron@uthscsa.edu |
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ISSN |
1475-2867 |
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PMID:16045802 |
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Call Number |
IT'IS @ evaj @ |
Serial |
289 |
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Author |
Cao, Y.; Xu, Q.; Jin, Z.-D.; Zhou, Z.; Nie, J.-H.; Tong, J. |
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Title |
Induction of adaptive response: pre-exposure of mice to 900 MHz radiofrequency fields reduces hematopoietic damage caused by subsequent exposure to ionising radiation |
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Journal Article |
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Year |
2011 |
Publication |
International Journal of Radiation Biology |
Abbreviated Journal |
Int J Radiat Biol |
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Volume |
87 |
Issue |
7 |
Pages |
720-728 |
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Keywords |
Adaptation, Physiological/*physiology/*radiation effects; Animals; Cell Survival/radiation effects; Cells, Cultured; Dose-Response Relationship, Radiation; Gamma Rays; Hematopoietic Stem Cells/*physiology/*radiation effects; Male; Mice; Radiation Dosage; Radiation Tolerance/*physiology/*radiation effects; Whole-Body Irradiation |
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Abstract |
PURPOSE: To investigate whether an adaptive response can be induced in mice which were pre-exposed to 900 MHz radiofrequency fields. MATERIALS AND METHODS: Adult male Kunming mice were exposed to 900 MHz radiofrequency fields (RF) at power intensities of 12, 120 and 1200 muW/cm(2) for 1 h/day for 14 days and then subjected to whole body gamma-irradiation. The results were compared with those in unexposed control animals and those exposed to gamma-irradiation alone (without pre-exposure to RF). The extent of survival and hematopoietic tissue damage (assessed in the form of nucleated colony forming cells in the bone marrow and colony forming cells in the spleen of lethally irradiated 'recipient' mice) as well as the expression of cell cycle-related genes were investigated. RESULTS: The results indicated a significant increase in survival time, reduction in the hematopoietic tissue damage in RF pre-exposed mice which were gamma-irradiated (as compared with those exposed to gamma-radiation alone). This was accompanied by significantly increased expression of cell cycle-related genes, namely, cyclin-D1, cyclin-E, cyclin-DK4 and cyclin-DK2 in hematopoietic cells. CONCLUSIONS: Pre-exposure of mice to 900 MHz radiofrequency fields has resulted in a significant reduction in hematopoietic damage caused by subsequent exposure to ionising radiation. This phenomenon appears to be similar to that of the 'adaptive response' which is well documented in scientific literature. |
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School of Radiation Medicine and Public Health, Soochow University, Suzhou, China |
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0955-3002 |
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PMID:21294690 |
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CBM.UAM @ ccobaleda @ |
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478 |
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Author |
Capri, M.; Mesirca, P.; Remondini, D.; Carosella, S.; Pasi, S.; Castellani, G.; Franceschi, C.; Bersani, F. |
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Title |
50 Hz sinusoidal magnetic fields do not affect human lymphocyte activation and proliferation in vitro |
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Journal Article |
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Year |
2004 |
Publication |
Physical Biology |
Abbreviated Journal |
Phys Biol |
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1 |
Issue |
3-4 |
Pages |
211-219 |
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Adult; Aged; Cell Cycle; Cell Proliferation/*radiation effects; Flow Cytometry; Humans; Lymphocyte Activation/*radiation effects; *Magnetics; Phenotype |
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In the last 30 years, an increasing public concern about the possible harmful effects of electromagnetic fields generated by power lines and domestic appliances has pushed the scientific community to search for a correct and comprehensive answer to this problem. In this work the effects of exposure to 50 Hz sinusoidal magnetic fields, with a magnetic flux density of 0.05 mT and 2.5 mT (peak values), were studied on human peripheral blood mononuclear cells (PBMCs) collected from healthy young and elderly donors. Cell activation and proliferation were investigated by using flow cytometry techniques and 3H-TdR incorporation assays, respectively. The results obtained indicated that exposure to the fields altered neither DNA synthesis nor the capacity of lymphocytes to enter the activation phase and progress into the cell cycle. Thus, the conclusions are that two important functional phases of human lymphocytes, such as activation and proliferation, are not affected by exposures to 50 Hz magnetic fields similar to those found under power lines. |
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Department of Experimental Pathology, Via S Giacomo 12, University of Bologna, 40126 Bologna, Italy |
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1478-3967 |
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PMID:16204841 |
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Call Number |
IT'IS @ evaj @ |
Serial |
291 |
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Capstick, M.; Schar, P.; Schuermann, D.; Romann, A.; Kuster, N. |
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Title |
ELF exposure system for live cell imaging |
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Journal Article |
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Year |
2012 |
Publication |
Bioelectromagnetics |
Abbreviated Journal |
Bioelectromagnetics |
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A programmable system has been developed for the study of both transient and persistent effects of extremely low frequency (ELF) magnetic field exposure of cell cultures. This high-precision exposure system enables experimental blinding and fully characterized exposure while simultaneously allowing live cell imaging. It is based on a live imaging cell around which two asymmetrical coils are wound in good thermal contact to a temperature-controlled water jacket, and is mounted on a microscope stage insert. The applied B-field uniformity of the active volume is better than 1.2% with an overall exposure uncertainty of less than 4.3% with very low transient field levels. The computer-controlled apparatus allows signal waveforms that are sinusoidal or composed of several harmonics, blind protocols, and monitoring of exposure and environmental conditions. B-fields up to 4 mT root mean square amplitude are possible with minimal temperature variation and no recognizable temperature differences between exposure and sham states. Sources of artifacts have been identified and quantified. There are no visible vibrations observable even at the highest magnifications and exposure levels. Bioelectromagnetics. (c) 2012 Wiley Periodicals, Inc. |
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IT'IS Foundation, Zurich, Switzerland. capstick@itis.ethz.ch |
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0197-8462 |
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PMID:23125057 |
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CBM.UAM @ ccobaleda @ |
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228 |
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Author |
Caraglia, M.; Marra, M.; Mancinelli, F.; D'Ambrosio, G.; Massa, R.; Giordano, A.; Budillon, A.; Abbruzzese, A.; Bismuto, E. |
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Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-chaperone complex in human epidermoid cancer cells |
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Journal Article |
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Year |
2005 |
Publication |
Journal of Cellular Physiology |
Abbreviated Journal |
J Cell Physiol |
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Volume |
204 |
Issue |
2 |
Pages |
539-548 |
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Apoptosis/*radiation effects; Carcinoma, Squamous Cell/metabolism/pathology/*physiopathology; Cell Line, Tumor; Cell Survival; *Cellular Phone; *Electromagnetic Fields; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism; HSP90 Heat-Shock Proteins/antagonists & inhibitors/metabolism; Humans; Molecular Chaperones/*antagonists & inhibitors; Proteasome Endopeptidase Complex/metabolism; Proto-Oncogene Proteins c-raf/metabolism; Signal Transduction/radiation effects; Ubiquitin/metabolism; ras Proteins/metabolism |
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The exposure to non-thermal microwave electromagnetic field (MW-EMF) at 1.95 MHz, a frequency used in mobile communication, affects the refolding kinetics of eukaryotic proteins (Mancinelli et al., 2004). On these basis we have evaluated the in vivo effect of MW-EMF in human epidermoid cancer KB cells. We have found that MW-EMF induces time-dependent apoptosis (45% after 3 h) that is paralleled by an about 2.5-fold decrease of the expression of ras and Raf-1 and of the activity of ras and Erk-1/2. Although also the expression of Akt was reduced its activity was unchanged likely as a consequence of the increased expression of its upstream activator PI3K. In the same experimental conditions an about 2.5-fold increase of the ubiquitination of ras and Raf-1 was also found and the addition for 12 h of proteasome inhibitor lactacystin at 10 microM caused an accumulation of the ubiquitinated isoforms of ras and Raf-1 and counteracted the effects of MW-EMF on ras and Raf-1 expression suggesting an increased proteasome-dependent degradation induced by MW-EMF. The exposure of KB cells to MW-EMF induced a differential activation of stress-dependent pathway with an increase of JNK-1 activity and HSP70 and 27 expression and with a reduction of p38 kinase activity and HSP90 expression. The overexpression of HSP90 induced by transfection of KB cells with a plasmid encoding for the factor completely antagonized the apoptosis and the inactivation of the ras --> Erk-dependent survival signal induced by MW-EMF. Conversely, the inhibition of Erk activity induced by 12 h exposure to 10 mM Mek-1 inhibitor U0126 antagonized the effects induced by HSP90 transfection on apoptosis caused by MW-EMF. In conclusion, these results demonstrate for the first time that MW-EMF induces apoptosis through the inactivation of the ras --> Erk survival signaling due to enhanced degradation of ras and Raf-1 determined by decreased expression of HSP90 and the consequent increase of proteasome dependent degradation. |
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Department of Biochemistry and Biophysics, Second University of Naples, Italy |
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0021-9541 |
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PMID:15754340 |
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Call Number |
IT'IS @ evaj @ |
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292 |
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