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      Comparative analysis of coherent light action (laser) versus non-coherent light (light-emitting diode) for tissue repair in diabetic rats

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          Abstract

          The already known benefits produced by the interaction of coherent light (laser) with biologic tissues determine its use as an adjuvant in the treatment of several complications associated with diabetes. Non-coherent light, such as that emitted by light emitting diodes (LEDs), becomes a promising alternative, because of its low cost and easy handling in these applications. Thirty-six rats were given surgical dorsum lesions. The lesions for the control group did not receive any supporting therapy. The other groups were irradiated only once, 30 min after the establishment of the lesion, with LED (640 nm with 40 nm full bandwidth at half maximum) or laser (660 nm). The histomorphological and histomorphometrical parameters were quantified. The coherent and non-coherent lights produced similar effects during a period of 168 h after the lesions had been made. For the group composed of diabetic animals, 72 h after creation of the lesion, it was observed that the therapy with LEDs had been more efficient than that with the laser in the reduction of the wounds' diameters.

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          Effect of NASA light-emitting diode irradiation on wound healing.

          The purpose of this study was to assess the effects of hyperbaric oxygen (HBO) and near-infrared light therapy on wound healing. Light-emitting diodes (LED), originally developed for NASA plant growth experiments in space show promise for delivering light deep into tissues of the body to promote wound healing and human tissue growth. In this paper, we review and present our new data of LED treatment on cells grown in culture, on ischemic and diabetic wounds in rat models, and on acute and chronic wounds in humans. In vitro and in vivo (animal and human) studies utilized a variety of LED wavelength, power intensity, and energy density parameters to begin to identify conditions for each biological tissue that are optimal for biostimulation. LED produced in vitro increases of cell growth of 140-200% in mouse-derived fibroblasts, rat-derived osteoblasts, and rat-derived skeletal muscle cells, and increases in growth of 155-171% of normal human epithelial cells. Wound size decreased up to 36% in conjunction with HBO in ischemic rat models. LED produced improvement of greater than 40% in musculoskeletal training injuries in Navy SEAL team members, and decreased wound healing time in crew members aboard a U.S. Naval submarine. LED produced a 47% reduction in pain of children suffering from oral mucositis. We believe that the use of NASA LED for light therapy alone, and in conjunction with hyperbaric oxygen, will greatly enhance the natural wound healing process, and more quickly return the patient to a preinjury/illness level of activity. This work is supported and managed through the NASA Marshall Space Flight Center-SBIR Program.
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            The efficacy of laser therapy in wound repair: a meta-analysis of the literature.

            We determined the overall effects of laser therapy on tissue healing by aggregating the literature and subjecting studies meeting the inclusion and exclusion criteria to statistical meta-analysis. Low-level laser therapy (LLLT) devices have been in use since the mid sixties, but their therapeutic value remains doubtful, as the literature seems replete with conflicting findings. Pertinent original research papers were gathered from library sources, online databases and secondary sources. The papers were screened and coded; those meeting every inclusion and exclusion criterion were subjected to meta-analysis, using Cohen's d. statistic to determine the treatment effect size of each study. Twenty-four studies with 31 effect sizes met the stringent inclusion and exclusion criteria. The overall mean effect of laser therapy on wound healing was highly significant (d = +2.22). Sub-analyses of the data revealed significant positive effects on wound healing in animal experiments (d = +1.97) as well as human clinical studies (d = +0.54). The analysis further revealed significant positive effects on specific indices of healing, for example, acceleration of inflammation (d = +4.45); augmentation of collagen synthesis (d = +1.80); increased tensile strength (d = +2.37), reduced healing time (d = +3.24); and diminution of wound size (d = +0.55). The Fail-Safe number associated with the overall effect of laser therapy was 509; a high number representing the number of additional studies-in which laser therapy has negative or no effect on wound healing-required to negate the overall large effect size of +2.22. The corresponding Fail-Safe number for clinical studies was 22. We conclude that laser therapy is an effective tool for promoting wound repair.
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              Irradiation with He-Ne laser increases ATP level in cells cultivated in vitro.

              A monolayer of HeLa cells was irradiated with an He-Ne laser (632.8 nm, 100 J m-2, 10 s) and the amount of adenosine triphosphate (ATP) was measured by the luceferin-luciferase bioluminescent assay technique at different times (5-45 min) after irradiation. The amount of ATP in the log phase of cultured cells remained at the control level (0.79 +/- 0.09) x 10(-15) mol per cell) during the first 15 min after irradiation; it then increased sharply and, after reaching a maximum (170.8%) 20 min after irradiation, decreased slowly to the control level. The ability of monochromatic red light to induce an increase in the cellular ATP level was found to depend on the growth phase of the culture, being insignificant in the lag phase of cultured cells, increasing in the log phase of cultured cells and reaching a maximum (about 190%) in cells at the late logarithmic and early plateau phase.
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                Author and article information

                Journal
                Lasers in Medical Science
                Lasers Med Sci
                Springer Nature
                0268-8921
                1435-604X
                November 2009
                February 24 2009
                : 24
                : 6
                : 909-916
                Article
                10.1007/s10103-009-0648-5
                19238507
                cdde0153-2afc-455b-b59c-b1bf815d23cb
                © 2009
                History

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