Carly A. Buckner

Biophoton emissions from cell cultures: biochemical evidence for the plasma membrane as the primary source.

Photon emissions were measured at ambient temperature (21°C) in complete darkness once per min from cultures of 10(6) cells during the 12 h following removal from 37°C. The energy of emission was about 10(-20) J/s/cell. Of 8 different cell lines, B16-BL6 (mouse melanoma cells) demonstrated the most conspicuous emission profile. Acridine orange and ethidium bromide indicated the membranes were intact with no indication of (trypan blue) cell necrosis. Treatments with EGF and ionomycin produced rapid early (first 3 h) increases in energy emission while glutamine-free, sodium azide and wortmanin-treated cells showed a general diminishment 3 to 9 h later. The results suggested the most probable origin of the photon emission was the plasma cell membrane. Measures from cells synchronized at the M- and S-phase supported this inference.

Photon emissions from human brain and cell culture exposed to distally rotating magnetic fields shared by separate light-stimulated brains and cells

Light flashes delivered to one aggregate of cells evoked increased photon emission in another aggregate of cells maintained in the dark in another room if both aggregates shared the same temporospatial configuration of changing rate, circular magnetic fields. During the presentation of the same shared circumcerebral magnetic fields increases in photon emission occurred beside the heads of human volunteers if others in another room saw light flashes. Both cellular and human photon emissions during the light flashes did not occur when the shared magnetic fields were not present. The summed energy emissions from the dark location during light stimulation to others was about 10(-11) W/m(2) and calculated to be in the order of 10(-20) J per cell which is coupled to membrane function. These results support accumulating data that under specific conditions changes in photon emissions may reflect intercellular and interbrain communications with potential quantum-like properties.

Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels

Electromagnetic field (EMF) exposures affect many biological systems. The reproducibility of these effects is related to the intensity, duration, frequency, and pattern of the EMF. We have shown that exposure to a specific time-varying EMF can inhibit the growth of malignant cells. Thomas-EMF is a low-intensity, frequency-modulated (25-6 Hz) EMF pattern. Daily, 1 h, exposures to Thomas-EMF inhibited the growth of malignant cell lines including B16-BL6, MDA-MB-231, MCF-7, and HeLa cells but did not affect the growth of non-malignant cells. Thomas-EMF also inhibited B16-BL6 cell proliferation in vivo. B16-BL6 cells implanted in syngeneic C57b mice and exposed daily to Thomas-EMF produced smaller tumours than in sham-treated controls. In vitro studies showed that exposure of malignant cells to Thomas-EMF for > 15 min promoted Ca2+ influx which could be blocked by inhibitors of voltage-gated T-type Ca2+ channels. Blocking Ca2+ uptake also blocked Thomas-EMF-dependent inhibition of cell proliferation. Exposure to Thomas-EMF delayed cell cycle progression and altered cyclin expression consistent with the decrease in cell proliferation. Non-malignant cells did not show any EMF-dependent changes in Ca2+ influx or cell growth. These data confirm that exposure to a specific EMF pattern can affect cellular processes and that exposure to Thomas-EMF may provide a potential anti-cancer therapy.

Growth of injected melanoma cells is suppressed by whole body exposure to specific spatial-temporal configurations of weak intensity magnetic fields

Purpose: To measure the effect of exposure to a specific spatial-temporal, hysiologically-patterned electromagnetic field presented using different geometric configurations on the growth of experimental tumours in mice. Methods: C57b male mice were inoculated subcutaneously with B16-BL6 melanoma cells in two blocks of experiments separated by six months (to control for the effects of geomagnetic field). The mice were exposed to the same time-varying electromagnetic field nightly for 3 h in one of six spatial configurations or two control conditions and tumour growth assessed. Results: Mice exposed to the field that was rotated through the three spatial dimensions and through all three planes every 2 sec did not grow tumours after 38 days. However, the mice in the sham-field and reference controls showed massive tumours after 38 days. Tumour growth was also affected by the intensity of the field, with mice exposed to a weak intensity field (1–5 nT) forming smaller tumours than mice exposed to sham or stronger, high intensity (2–5 μT) fields. Immunochemistry of tumours from those mice exposed to the different intensity fields suggested that alterations in leukocyte infiltration or vascularisation could contribute to the differences in tumour growth. Conclusions: Exposure to specific spatial-temporal regulated electromagnetic field configurations had potent effects on the growth of experimental tumours in mice.

Digitized quantitative electroencephalographic patterns applied as magnetic fields inhibit melanoma cell proliferation in culture

Weak (1 μT) physiologically patterned magnetic fields produce changes in behavioral, physiological, and cellular activity. In the present experiments 12 temporal samples of the electroencephalographic anomaly and normal activity of a person (SLH) whose proximity reliably affected the brain activity of others were extracted from QEEG data, digitized, and presented as equivalent magnetic field patterns to B16 mouse melanoma cells. Only two of the patterns, both originating from the primary source (right temporal lobe) of the EEG anomaly reduced the cell growth by one-third compared to the other patterns extracted from his QEEG or sham field exposures. In previous experiments these EEG transients were also associated with marked increases in photon emissions from the right side of SLHs head. The results suggest that the intrinsic complexity of electroencephalographic patterns of some people, when amplified appropriately and applied as computer-generated magnetic fields in the three spatial planes, could diminish cancer cell growth.

Cell adhesion and cancer: is there a potential for therapeutic intervention?

Carcinogenesis involves a disruption in adhesion molecule expression and tissue architecture, and tumour invasion requires adhesion-dependent migration into surrounding tissues. Therefore, a variety of peptide and antibody-based reagents that block integrins, cadherins, immunoglobulin superfamily and selectin adhesion molecules have been developed to treat cancers. Therapeutics directed at adhesion molecules can block interactions between tumour cells, endothelial cells and immune cells to prevent tumour cell invasiveness and metastasis. Blocking the adhesion molecules that facilitate the invasion of tumours by endothelial cells and immune cells can prevent tumour-associated angiogenesis and the recruitment of immune-mediated growth factors which are required for tumour growth and spread. In addition, targeted therapies using anticancer agents attached to antibodies or peptides directed as tumour-specific adhesion molecules are being developed.

The effects of electromagnetic fields on B16-BL6 cells are dependent on their spatial and temporal character

Exposure to low intensity, low frequency electromagnetic fields (EMF) has effects on several biological systems. Spatiotemporal characteristics of these EMFs are critical. The effect of several complex EMF patterns on the proliferation of B16-BL6 mouse melanoma cells was tested. Exposure to one of these patterns, the Thomas-EMF, inhibited cell proliferation and promoted calcium uptake. The Thomas-EMF is coded from a digital-to-analog file comprised of 849 points, which provides power to solenoids and can be set to alter timing, intensity, and duration of variable EMF. Setting the point duration to 3 ms generated a time-varying EMF pattern which began at 25 Hz and slowed to 6 Hz over a 2.5 s repeat. Exposing B16-BL6 cells to Thomas-EMF set to 3 ms for 1 h/day inhibited cell proliferation by 40% after 5 days, while setting the point duration to 1, 2, 4, or 5 ms had no effect on cell proliferation. Similarly, exposing cells to Thomas-EMF set to 3 ms promoted a three-fold increase in calcium uptake after 1 h, while the other timings had no effect. Exposure to Thomas-EMF for as short as 15 min/day slowed cell proliferation, but exposure for 1 h/day was optimal. This corresponded to the effect on calcium uptake where uptake was detected after 15 min exposure and was maximal by 1 h of treatment. Studies show that the specific spatiotemporal character of EMF is critical in mediating their biological activities. Bioelectromagnetics. 38:165-174, 2017.

Photon Emissions as Differential Indicators for Different Components of Protein Kinase A (PKA) in Transfected Murine Melanoma Cells

Increased emissions of photons or shifts in spectral power densities of photons have been reliably measured from malignant cells compared to non-malignant cells. Previous experiments have shown that specific wavelengths within the visible spectrum emitted from melanoma cells were associated with the activation or inhibition of specific molecular structures or pathways. To discern if numbers of photons could differentiate the dynamic state of a critical protein (enzyme), Protein Kinase A (PKA), melanoma cells were transfected with either catalytic subunits, regulatory subunits, or a mutant dominant negative PKA. Compared to typical melanoma cells those transfected with the regulatory subunit exhibited a marked (10 to 100) increase in photon emissions for several hours. The small but significant increase in photon emissions from cells transfected with the catalytic subunit was more brief (first 20 min) and less intense. Photon emissions from cells transfected with inhibitory components did not differ from typical melanoma cells. The vectorial characteristics of the photon emissions were sufficient to clearly differentiate activation of various components of PKA domains.