ID Number		2567
Study Type		In Vivo
Model		Evaluation of claim that anthropogenic-strength RF EMFs are capable of eliciting post-neurotomy pain by adopting a modification of the tibial neuroma transposition (TNT) model for behavioral assessment of post-neurotomy pain in rats. (RETRACTED by PLOS ONE Editors in 2018, see IEEE #6924)
Details		AUTHORS' ABSTRACT: Black et al. 2016 (IEEE #6319): Anecdotal and clinical reports have suggested that radio-frequency electromagnetic fields (RF EMFs) may serve as a trigger for neuropathic pain. However, these reports have been widely disregarded, as the epidemiological effects of electromagnetic fields have not been systematically proven, and are highly controversial. Here, we demonstrate that anthropogenic RF EMFs elicit post-neurotomy pain in a tibial neuroma transposition model. Behavioral assays indicate a persistent and significant pain response to RF EMFs when compared to SHAM surgery groups. Laser thermometry revealed a transient skin temperature increase during stimulation. Furthermore, immunofluorescence revealed an increased expression of temperature sensitive cation channels (TRPV4) in the neuroma bulb, suggesting that RF EMF-induced pain may be due to cytokine-mediated channel dysregulation and hypersensitization, leading to thermal allodynia. Additional behavioral assays were performed using an infrared heating lamp in place of the RF stimulus. While thermally-induced pain responses were observed, the response frequency and progression did not recapitulate the RF EMF effects. In vitro calcium imaging experiments demonstrated that our RF EMF stimulus is sufficient to directly contribute to the depolarization of dissociated sensory neurons. Furthermore, the perfusion of inflammatory cytokine TNF-± resulted in a significantly higher percentage of active sensory neurons during RF EMF stimulation. These results substantiate patient reports of RF EMF-pain, in the case of peripheral nerve injury, while confirming the public and scientific consensus that anthropogenic RF EMFs engender no adverse sensory effects in the general population. THE PLOS ONE Editors RETRACTION of Black et al. 2016 (IEEE #6319): After the publication of this article, readers raised concerns about several aspects of the methodology for this study and the conclusions drawn. Follow-up discussions with the authors and consultation with editorial board members identified the following concerns: The analysis of skin temperature was found to be incorrect due to interference of the RFID-900-SC antenna with the ThermoWorks TW2 Thermometer, invalidating the measured skin temperatures during the reported experiments. Dosimetry measurements in the paper were not obtained using appropriate equipment at the time the experiments were conducted, and thus the validity of the published data for RF-EMF exposure experiments has been called into question. The authors agree that the temperature data in the published article are not valid, and they conducted additional experiments post-publication in an effort to address the dosimetry concern. However, the PLOS ONE editors determined that in light of the above issues the integrity of the published article is compromised, and the further work needed to address the dosimetry and temperature measurement errors and their impact on the conclusions drawn would necessitate full review as a new submission. For these reasons, we retract this published article. The journal editors notified the articles authors of this retraction. All co-authors BB, RGV, BRJ, EJ, and MRO expressed that they do not agree with the retraction. References 1. Black B, Granja-Vazquez R, Johnston BR, Jones E, Romero-Ortega M (2016). Anthropogenic Radio-Frequency Electromagnetic Fields Elicit Neuropathic Pain in an Amputation Model. PLOS ONE 11(1): e0144268. pmid:26760033
Findings		Effects (only at thermal levels)
Status		Completed With Publication
Principal Investigator		U of Texas at Dallas, Richardson, Texas
Funding Agency		None Noted or Reported None
Country		UNITED STATES
References		Black, B et al. PLoS ONE., (2016) 11:e0144268.-doi:10.1371/journal. The PLOS ONE Editors, PLoS ONE., (2018) 13:1 page- e0191082
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