The day was opened with tutorial on genomic stability and signaling pathways.
The first talk by Robert Kanaar had some interesting statements and suggestions.
The spontaneously occurring DNA damage is very common in cells and it requires efficient repair mechanisms to continuously repair this damage. Some rough numbers were as follows:
- single strand breaks – 50,000/day
- abasic sites – 10,000/day
- deamination – 600/day
- oxidized bases – 2,000/day
- alkalized bases – 5,000/day
- replication errors – several tens/day
Sensitivity of different methods detecting DNA breaks varies dramatically:
- pulsed field electrophoresis – damage to be detected requires energy equal to energy of 10Gy
- comet assay – 1Gy
- focus formation by proteins in sites of damage – 0.4Gy
In the lab of the speaker has been developed more sensitive method relaying on transfection of cells with plasmids.
With none of the above methods was possible to confirm that RF induces DNA damage (breaks) more efficiently as compared with the spontaneous damage.
In case of ELF Primo Schär observed higher level of damaged DNA in exposed cells but it was not due to actual damage but rather due to inhibition of DNA repair processes by the ELF exposure.
In some studies saw suggested that there is higher level of DNA damage in exposed cells. It might be possible that similarly as with ELF exposures; the RF exposures might, in certain cell types affect the DNA repair process?
In the second talk Rony Seger presented effect of RF exposures on ERK kinase pathway and the “antenna” molecule was determined as NADH oxidase. How RF affects function of NADH oxidase remains undetermined (see my comment on classic heating at 43oC on the activity of ERK in earlier blog). These results were already published several years ago.
Interestingly, in pilot experiments with ELF exposure (50Hz, 1mT) there was only very weak effect on ERK pathway. This effect seemed to be cell type-dependent: observed in transformed cells but absent in non-transformed cells. In respect to the ELF exposures (Kuster set up) used in the ERK study, someone from the audience commented that in sham exposures there is low level of ELF = 6 microT what may mean that sham samples are also activated and therefore the difference between sham and exposed might be more difficult to detect.
Following the tutorial plenary session was session on anti-cancer clinical applications of EMF. In this session was presented the in vitro part of the clinical/animal study from Boris Pashe’s group. The presentation suggested that the IP3/DAG signaling pathway is activated what leads to an increase of cytoplasmic calcium. Unfortunately, the evidence concerning calcium level was poor and unconvincing. There was shown only a single sham exposed cell that looked not very healthy, with a couple of large vacuoles that absorbed green stain. In the other part of the cell was seen small diffuse area of green stain indicating area where calcium was located. To me this control cell looked “unhealthy”, in fact having appearance of apoptotic death. In the exposed sample were shown only 2 cells. The smaller one was clearly in advanced stage of apoptosis with extensive surface blebbing. The other cell, much larger in size, was clearly dying by necrosis and swollen by intake of water. There was clearly seen a very large bleb/vacuole. In both cells was seen diffuse green staining indicating location of calcium.
Unfortunately the evidence concerning IP3/DAG and calcium was absolutely unconvincing. Pashe needs a better qualified cell biologist to view the cell cultures and to determine which cells are alive and which are already dead or dying. Also, showing only 1-2 cells, without any numerical analysis is far too little.
BRHP - Between a Rock and a Hard Place 
None of you mentioned the Cam and Seyhan study: Single strand DNA breaks in human hair root cells exposed to mobile phone radiation. I’m wondering what you thought about that. Study found increased DNA breaks in hairs plucked from around the cellphone-used ear after 15 and 30 minutes of exposure as compared with non-exposed controls.
Thank you for your postings, and alos your patience. The field of EMF research must be dreary indeed. In this society people often use the phrase “reinventing the wheel”.
The DNA work as far as I can glean seems to have missed the point and lost its way. As my iterative tweets have stated, the essential DNA mutagenicity work was done 20 years ago. 1993 Lai and Singh did the original COMET assay showing DNA breaks in rat brain tissue after whole animal irradiation to MW. We know the exposure was cosher since the system was designed by Bill Guy. Subsequent work confirmed this, and the mechanism was proposed and tested (Lai and Singh 97). The DNA breakage findings were confirmed by Phillips et al 1998. A very interesting and thought provoking paper, which I suggest shows most of what we want to see.
It would seem this work was unhappened. So subsequently the REFLEX program, funded by the EU, repeats it. Not surprisingly with the same findings.
Is there still doubt about this?
Xu et al 2009 exactly tests the findings of these earlier authors, and completely validate their findings. Note also the de Iluiis et al paper from NSW also does this, here lookng at DNA stability in human sperm.
It is from this published work entirely to be expected that MW will cause DNA breakage at certain levels, they will also supress DNA breakage at other levels. If following levels of DNA breakage you will not expext a clear dose relationship, you will on the other hand expect windowing, the very windowing EMF scientists have been talking about for years.
While the biology must be elucidated here, the fact is that a highly respected oncology investigator, Boris Pasche MD PhD, has reported and published remarkable results with a significant percent patients that live who would normally die, after undergoing a regime using specific frequencies. Thus, we are faced with real human data in need of a theory. As the young presenter acknowledged, the Pasche laboratories are actively seeking explanations for these results and have begun to explore the experimental foundations for these clinical results using the evaluated methods presented this morning.
Traditionally, oncology drug development rested on studies of a single animal responding to an unusual treatment. But modern science requires the use of multiple animals, doses and approaches. This audience may not have been the best suited to reviewing these data as few of those in attendance had experience with oncology, gene-sequencing, etc. It will be fascinating to follow this work as it evolves.
Clearly as the Bioelectromagnetics Society develops with increasing attention to the uses of electricity in medicine it will be important to engage clinical investigators and biostatisticians to review this
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