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Effects of Biofield Therapy on Calcium Release in Immortalized Mouse Keratinocyte HaCaT Cells
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Objective: Observe the response on the release of calcium into mouse keratinocyte HaCaT cells subjected to biofield therapy (BT) through a pranic healing technique. Design: This was a pilot experimental study. Settings/location: The study was conducted in a laboratory at Simon Bolivar University. Subjects: Mouse keratinocyte HaCaT cells. Interventions: The intervention consisted of a 15-minute biofield therapy using a pranic healing technique. Outcome measures: Cells were loaded with 5 μM calcium indicator Fura 2-AM to monitor changes in intracellular calcium concentration. Cell population was separated into two groups: a control group where cells received no stimulation and the other experimental group where pranic healing was applied. Results: The cells that were treated with pranic healing showed a significant increase in intracellular calcium concentration as compared with untreated cells. Such increase in calcium concentration is consistent with the depletion of intracellular stores. By the action of Thapsigargin (TG) peak, calcium release is equivalent to cells exposed to pranic healing in comparison to control cells. One possible explanation for this observed result is that store of intracellular calcium had been stimulated by pranic healing and hence the resulting drain is lower. These results allow us to infer that pranic healing has an action on intracellular calcium storage but does not allow us to clarify how calcium has been stimulated.
Keywords:Fura-2 AM; Mouse Keratinocyte HaCaT Cells; [Ca]i; Issuing Biofield Therapy (BT); Pranic Healing Technique; Information Theory; Biofield
Author: Silva Ricardo1, Herrera Alvaro2, Velásquez Hordep2
1.Prometeo Program, Coordinación Zonal 5 y 8, Senescyt, Av. Carlos Luis Plaza Da?ín, Edificio del Sector Público del Sector Social, quinto piso, Guayaquil, Ecuador
2.Laboratorio de Biociencias Integradas, Universidad Simon Bolivar, Sartenejas, Baruta, Edo. Miranda - Apartado 89000 Cable Unibolivar, Caracas, Venezuela
  1. WHO, “General Guidelines for Methodologies on Research and Evaluation of Traditional Medicine,” Geneva, 2000.
  2. NCCAM. National Centre for Complementary and Alternative Medicine. [Online]. Available:
  3. C.K. Sui, Miracles Through Pranic Healing, formely published as “The Ancient Science and Art of Pranic Healing”, 4th ed., Sterling Publishers Pvt. Ltd, 2004.
  4. H.S. Mayberg, T.D. Wager, C.S. Stohler, J.K. Zubieta, and F. Benedetti, “Neurobiological Mechanisms of the Placebo Effect,” The Journal of Neuroscience, vol. 25, no. 45, pp. 10390-10402, November 2005.
  5. N.C. Gordon, H.L. Fields, and J.D. Levine, “The mechanism of placebo analgesia,” Lancet, vol. 8091, no. 2, pp. 654-657, September 1978.
  6. J.M. Jarcho, S. Berman, B.D. Naliboff, B.Y. Suyenobu, M. Mandelkern, E.A. Mayer, and M.D. Lieberman, “The neural correlates of placebo effects: a disruption account,” Neuroimage, vol. 22, no. 1, pp. 447-455, May 2004.
  7. M. Zhuo, “Central inhibition and placebo analgesia,” Molecular Pain, vol. 1, no. 21, 4 pages, 2005, DOI: 10.1186/1744-8069-1-21.
  8. D.A. Seminowicz, E. Jaeger, G.H. Duncan, M.C. Bushnell, and P. Schweinhardt, “The Anatomy of the Mesolimbic Reward System: A Link between Personality and the Placebo Analgesic Response,” The Journal of Neuroscience, vol. 29, no. 15, pp. 4882-4887, April 2009.
  9. G. Rein, “Bioinformation within the biofield: beyond bioelectromagnetics,” The Journal of Alternative & Complementary Medicine, vol. 10, no. 1, pp. 59-68, February 2004.
  10. B. Rubik, “The biofield hypothesis: Its biophysical basis and role in medicine,” The Journal of Alternative & Complementary Medicine, vol. 8, no. 6, pp. 703-717, December 2002.
  11. Ives JA, Jonas WB, and Kiang JG, “External bioenergy-induced increases in intracellular free calcium concentrations are mediated by Na+/Ca2+ exchanger and L-type calcium channel,” Molecular Cellular Biochemistry, vol. 271, no. 1-2, pp. 51-59, March 2005.
  12. D. Marotta, M. Wirkus, M. Wirkus, W.B. Jonas, and J.G. Kiang, “External bioenergy increases intracellular free calcium concentration and reduces cellular response to heat stress,” Journal of investigative medicine, vol. 50, no. 1, pp. 38-45, January 2002.
  13. R.T. Petrussevska, D. Breitkreutz, J. Hornung, A. Markham, N.E. Fusenig, and P. Boukamp, “Normal keratinization in a spontaneously immortalized aneuploid human keratinocyte cell line,” Journal of Cell Biology, vol. 106, no. 3, pp. 761-771, March 1988.
  14. S. Popp, S. Altmeyer, A. Hülsen, C. Fasching, T. Cremer, N.E. Fusenig, and P. Boukamp, “Sustained nontumorigenic phenotype correlates with a largely stable chromosome content during long-term culture of the human keratinocyte line HaCaT,” Genes Chromosomes Cancer, vol. 19, no. 4, pp. 201-214, August 1997.
  15. A.F. Deyrieux and V.G. Wilson, “In vitro culture conditions to study keratinocyte differentiation using the HaCaT cell line,” Cytotechnology, vol. 54, no. 2, pp. 77-83, June 2007.
  16. M. Poenie, R.Y. Tsien, and G. Grynkiewicz, “A new generation of Ca2+ indicators with greatly improved fluorescence properties,” The Journal of Biological Chemistry, vol. 260, no. 6, pp. 3440-3450, March 1985.
  17. V.A. Ziboh and W. Tang, “Agonist/inositol trisphosphate-induced release of calcium from murine keratinocytes: a possible link with keratinocyte differentiation,” The Journal of investigative dermatology, vol. 96, no. 1, pp. 134-138, January 1991.
  18. A. Flores, H. Rojas, A. Acosta, C. Castillo, M.R. Garrido, A. Israel, R. DiPolo, G. Benaim, and C. Colina, “Ceramide increase cytoplasmic Ca2+ concentration in Jurkat T cells by liberation of calcium from intracellular stores and activation of a store-operated calcium channel,” Archives of Biochemistry and Biophysics, vol. 436, no. 2, pp. 333-345, April 2005.