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(Database last updated on Mar 27, 2024)
| ID Number | 2006 | |
| Study Type | In Vitro | |
| Model | Effects of pulsed ELF and RF fields (PEMF) on cells exposed in vitro (chondrocytes, cell growth, nitric oxide, dopaminergic MN9D cultures, etc.). | |
| Details | Isolated chondrocytes were exposed to 1-100 Hz pulsed electromagnetic field (PEMF) for 30 minutes. The authors report an increase in DNA content, nitric oxide, and cGMP levels after 72 hrs post-exposure suggesting proliferation. Nitric oxide and cGMP production was enhanced with added calcium, the Ca++ ionophor A23187, or a nitric oxide donor and blocked with the calcium/calmodulin inhibitor W7, the nitric oxide synthase inhibitor L-NAME, and the guanylate cyclase inhibitor LY83583. The authors suggest these findings indicate PEF-stimulated chondrocyte proliferation via nitric oxide as a result of a cascade that involves calcium, calmodulin, and cGMP production. AUTHOR'S ABSTRACT: Pilla 2012 (IEEE #6210): This study shows that a non-thermal pulse-modulated RF signal (PRF), configured to modulate calmodulin (CaM) activation via acceleration of Ca(2+) binding kinetics, produced an immediate nearly 3-fold increase in nitric oxide (NO) from dopaminergic MN9D cultures (P < 0.001). NO was measured electrochemically in real-time using a NO selective membrane electrode, which showed the PRF effect occurred within the first seconds after lipopolysaccharide (LPS) challenge. Further support that the site of action of PRF involves CaM is provided in human fibroblast cultures challenged with low serum and exposed for 15 min to the identical PRF signal. In this case a CaM antagonist W-7 could be added to the culture 3 h prior to PRF exposure. Those results showed the PRF signal produced nearly a two-fold increase in NO, which could be blocked by W-7 (P < 0.001). To the authors' knowledge this is the first report of a real-time effect of non-thermal electromagnetic fields (EMF) on NO release from challenged cells. The results provide mechanistic support for the many reported bioeffects of EMF in which NO plays a role. Thus, in a typical clinical application for acute post operative pain, or chronic pain from, e.g., osteoarthritis, EMF therapy could be employed to modulate the dynamics of NO via Ca/CaM-dependent constitutive nitric oxide synthase (cNOS) in the target tissue. This, in turn, would modulate the dynamics of the signaling pathways the body uses in response to the various phases of healing after physical or chemical insult or injury. AUTHORS' ABSTRACT: Pilla et al. 2011 (IEEE #2011): BACKGROUND: The transduction mechanism for non-thermal electromagnetic field (EMF) bioeffects has not been fully elucidated. This study proposes that an EMF can act as a first messenger in the calmodulin-dependent signaling pathways that orchestrate the release of cytokines and growth factors in normal cellular responses to physical and/or chemical insults. METHODS: Given knowledge of Ca(2+) binding kinetics to calmodulin (CaM), an EMF signal having pulse duration or carrier period shorter than bound Ca(2+) lifetime may be configured to accelerate binding, and be detectable above thermal noise. New EMF signals were configured to modulate calmodulin-dependent signaling and assessed for efficacy in cellular studies. RESULTS: Configured EMF signals modulated CaM-dependent enzyme kinetics, produced several-fold increases in key second messengers to include nitric oxide and cyclic guanosine monophosphate in chondrocyte and endothelial cultures and cyclic adenosine monophosphate in neuronal cultures. Calmodulin antagonists and downstream blockers annihilated these effects, providing strong support for the proposed mechanism. CONCLUSIONS: Knowledge of the kinetics of Ca(2+) binding to CaM, or for any ion binding specific to any signaling cascade, allows the use of an electrochemical model by which the ability of any EMF signal to modulate CaM-dependent signaling can be assessed a priori or a posteriori. Results are consistent with the proposed mechanism, and strongly support the Ca/CaM/NO pathway as a primary EMF transduction pathway. GENERAL SIGNIFICANCE: The predictions of the proposed model open a host of significant possibilities for configuration of non-thermal EMF signals for clinical and wellness applications that can reach far beyond fracture repair and wound healing. AUTHORS' ABSTRACT: Muehsam et al. 2013 (IEEE #6281): The growing body of clinical and experimental data regarding electromagnetic field (EMF) bioeffects and their therapeutic applications has contributed to a better understanding of the underlying mechanisms of action. This study reports that two EMF modalities currently in clinical use, a pulse-modulated radiofrequency (PRF) signal, and a static magnetic field (SMF), applied independently, increased the rate of deoxygenation of human hemoglobin (Hb) in a cell-free assay. Deoxygenation of Hb was initiated using the reducing agent dithiothreitol (DTT) in an assay that allowed the time for deoxygenation to be controlled (from several min to several hours) by adjusting the relative concentrations of DTT and Hb. The time course of Hb deoxygenation was observed using visible light spectroscopy. Exposure for 10-30 min to either PRF or SMF increased the rate of deoxygenation occurring several min to several hours after the end of EMF exposure. The sensitivity and biochemical simplicity of the assay developed here suggest a new research tool that may help to further the understanding of basic biophysical EMF transduction mechanisms. If the results of this study were to be shown to occur at the cellular and tissue level, EMF-enhanced oxygen availability would be one of the mechanisms by which clinically relevant EMF-mediated enhancement of growth and repair processes could occur. |
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| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | The Technical Basis LLC - biocore1@aol.com | |
| Funding Agency | Private/Instit. | |
| Country | UNITED STATES | |
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