Ellen Buchmann

Medical College of Wisconsin, Milwaukee, WI, United States

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Publications (14)26.48 Total impact

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    ABSTRACT: The purpose of this was to evaluate the neuroprotective effects of near-infrared (NIR) light using an in-vivo rodent model of traumatic brain injury (TBI), controlled cortical impact (CCI), and to characterize changes at the behavioral and biochemical levels. NIR upregulates mitochondrial function, and decreases oxidative stress. Mitochondrial oxidative stress and apoptosis are important in TBI. NIR enhanced cell viability and mitochondrial function in previous in-vitro TBI models, supporting potential NIR in-vivo benefits. Sprague-Dawley rats were divided into three groups: severe TBI, sham surgery, and anesthetization only (behavioral response only). Cohorts in each group were administered either no NIR or NIR. They received two 670 nm LED treatments (5 min, 50 mW/cm(2), 15 J/cm(2)) per day for 72 h (chemical analysis) or 10 days (behavioral). During the recovery period, animals were tested for locomotor and behavioral activities using a TruScan device. Frozen brain tissue was obtained at 72 h and evaluated for apoptotic markers and reduced glutathione (GSH) levels. Significant differences were seen in the TBI plus and minus NIR (TBI+/-) and sham plus and minus NIR (S+/-) comparisons for some of the TruScan nose poke parameters. A statistically significant decrease was found in the Bax pro-apoptotic marker attributable to NIR exposure, along with lesser increases in Bcl-2 anti-apoptotic marker and GSH levels. These results show statistically significant, preclinical outcomes that support the use of NIR treatment after TBI in effecting changes at the behavioral, cellular, and chemical levels.
    Photomedicine and laser surgery 07/2012; 30(9):523-9. · 1.76 Impact Factor
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    ABSTRACT: Parkinson's disease (PD) is a neurodegenerative disorder that affects large numbers of people, particularly those of a more advanced age. Mitochondrial dysfunction plays a central role in PD, especially in the electron transport chain. This mitochondrial role allows the use of inhibitors of complex I and IV in PD models, and enhancers of complex IV activity, such as NIR light, to be used as possible therapy. PD models fall into two main categories; cell cultures and animal models. In cell cultures, primary neurons, mutant neuroblastoma cells, and cell cybrids have been studied in conjunction with NIR light. Primary neurons show protection or recovery of function and morphology by NIR light after toxic insult. Neuroblastoma cells, with a gene for mutant alpha-synuclein, show similar results. Cell cybrids, containing mtDNA from PD patients, show restoration of mitochondrial transport and complex I and IV assembly. Animal models include toxin-insulted mice, and alpha-synuclein transgenic mice. Functional recovery of the animals, chemical and histological evidence, and delayed disease progression show the potential of NIR light in treating Parkinson's disease.
    Frontiers in bioscience (Elite edition) 01/2012; 4:818-23.
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    ABSTRACT: The aim of this study was to investigate the effect of near-infrared (NIR) photobiomodulation on the proliferation and glutathione levels in murine Hertwig's epithelial root sheath (HERS) cells after poisoning with vinblastine. Photobiomodulation has been shown to improve wound healing in a number of animal models. There have been no studies on the effect of photobiomodulation on cancer-related chemotherapy injury to the cells that initiate tooth root growth. Control groups consisted of murine HERS cells without vinblastine (VB-) and cells with vinblastine at 10, 20, and 30 ng/mL (VB10, VB20, and VB30). Experimental groups consisted of these same groups with light therapy (VB-L, VB10L, VB20L, and VB30L). The cells were exposed to vinblastine for 1 h. Photobiomodulation consisted of a 75-cm(2) gallium-aluminum-arsenide light-emitting diode (LED) array at an energy density of 12.8 J/cm(2), delivered with 50 mW/cm(2) power over 256 s. Vinblastine alone significantly decreased HERS cell proliferation and glutathione levels at all concentrations (VB10 [-55%, p < 1.0 × 10(-8)]; VB20 [-72%, p < 1.0 × 10(-9)]; VB30 [-80%, p < 1.0 × 10(-10)]; and VB10 [-36%, p < 0.0001]; VB20 [-49%, p < 1.0 × 10(-6)]; VB30 [-53%, p < 1.0 × 10(-7)] respectively). Photobiomodulation significantly increased cell proliferation at all levels of vinblastine exposure (VB10L [+50%, p < 0.0001]; VB20L [+45%, p < 0.05]; VB30 [+39%, p < 0.05]) but not of the control (+22%, p = 0.063). The photobiomodulation significantly increased glutathione production in all concentrations of vinblastine except 20 ng/mL (VB10L [+39%, p = 0.007]; VB20L [+19%, p = 0.087]; VB30 [+14%, p = 0.025]) and the control (+12%, p = 0.13). Photobiomodulation demonstrated an improvement in proliferation and glutathione levels in vinblastine-poisoned murine HERS cells.
    Photomedicine and laser surgery 12/2010; 29(4):233-7. · 1.76 Impact Factor
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    ABSTRACT: In rat pituitary somatotrophs, cytochrome oxidase is co-packaged with growth hormone (GH) in some storage granules. Because this enzyme is thought to be the molecular photoacceptor of red-near infrared light, and because exposure of diverse tissue systems to 670 nm visible light affects their biological responses (e.g., wound healing), we tested the idea that exposure of rat pituitary cells, rat hemi-pituitary glands and rat pituitary homogenates to 670 nm light in vitro might alter GH storage and/or release. In this report we offer evidence to show that light treatment (670 nm, 80s, intensity 50 mW/cm(2), energy density 4 J/cm(2)) up-regulates GH release, in part by breakdown of intracellular, oligomeric GH as determined by gel filtration chromatography.
    Growth hormone & IGF research: official journal of the Growth Hormone Research Society and the International IGF Research Society 01/2009; 19(3):274-9. · 2.35 Impact Factor
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    ABSTRACT: Studies in our laboratory demonstrate that the action spectrum for stimulation of cytochrome oxidase activity and cellular ATP parallels the near-infrared absorption spectrum of cytochrome oxidase and that 660-680 nm irradiation upregulates cytochrome oxidase activity in cultured neurons. Treatment with nearinfrared light augments cellular energy production and neuronal viability following mitochondrial injury linking the actions of red to near-infrared light on mitochondrial metabolism in vitro and cell injury in vivo. NIR light treatment represents an innovative therapeutic approach for disease processes in which mitochondrial dysfunction is postulated to play a role including Parkinson's disease, laser eye injury and Age-related macular degeneration.
    Proc SPIE 01/2009;
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    ABSTRACT: Near-IR light treatment modifies cellular function, promotes cell survival, and improves outcomes in laboratory and mouse models of Parkinson's disease.
    SPIENewsroom 03/2008; 2008:1-3.
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    ABSTRACT: Near-infrared light via light-emitting diode treatment has documented therapeutic effects on neurons functionally inactivated by tetrodotoxin or methanol intoxication. Light-emitting diode pretreatment also reduced potassium cyanide-induced cell death, but the mode of death via the apoptotic or necrotic pathway was unclear. The current study tested our hypothesis that light-emitting diode rescues neurons from apoptotic cell death. Primary neuronal cultures from postnatal rat visual cortex were pretreated with light-emitting diode for 10 min at a total energy density of 30 J/cm2 before exposing to potassium cyanide for 28 h. With 100 or 300 microM potassium cyanide, neurons died mainly via the apoptotic pathway, as confirmed by electron microscopy, Hoechst 33258, single-stranded DNA, Bax, and active caspase-3. In the presence of caspase inhibitor I, the percentage of apoptotic cells in 300microM potassium cyanide was significantly decreased. Light-emitting diode pretreatment reduced apoptosis from 36% to 17.9% (100 microM potassium cyanide) and from 58.9% to 39.6% (300 microM potassium cyanide), representing a 50.3% and 32.8% reduction, respectively. Light-emitting diode pretreatment significantly decreased the expression of caspase-3 elicited by potassium cyanide. It also reversed the potassium cyanide-induced increased expression of Bax and decreased expression of Bcl-2 to control levels. Moreover, light-emitting diode decreased the intensity of 5-(and -6) chloromethy-2', 7-dichlorodihydrofluorescein diacetate acetyl ester, a marker of reactive oxygen species, in neurons exposed to 300 microM potassium cyanide. These results indicate that light-emitting diode pretreatment partially protects neurons against cyanide-induced caspase-mediated apoptosis, most likely by decreasing reactive oxygen species production, down-regulating pro-apoptotic proteins and activating anti-apoptotic proteins, as well as increasing energy metabolism in neurons as reported previously.
    Neuroscience 06/2006; 139(2):639-49. · 3.12 Impact Factor
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    ABSTRACT: This review presents current research on the use of far-red to near-infrared (NIR) light treatment in various in vitro and in vivo models. Low-intensity light therapy, commonly referred to as "photobiomodulation," uses light in the far-red to near-infrared region of the spectrum (630-1000 nm) and modulates numerous cellular functions. Positive effects of NIR-light-emitting diode (LED) light treatment include acceleration of wound healing, improved recovery from ischemic injury of the heart, and attenuated degeneration of injured optic nerves by improving mitochondrial energy metabolism and production. Various in vitro and in vivo models of mitochondrial dysfunction were treated with a variety of wavelengths of NIR-LED light. These studies were performed to determine the effect of NIR-LED light treatment on physiologic and pathologic processes. NIRLED light treatment stimulates the photoacceptor cytochrome c oxidase, resulting in increased energy metabolism and production. NIR-LED light treatment accelerates wound healing in ischemic rat and murine diabetic wound healing models, attenuates the retinotoxic effects of methanol-derived formic acid in rat models, and attenuates the developmental toxicity of dioxin in chicken embryos. Furthermore, NIR-LED light treatment prevents the development of oral mucositis in pediatric bone marrow transplant patients. The experimental results demonstrate that NIR-LED light treatment stimulates mitochondrial oxidative metabolism in vitro, and accelerates cell and tissue repair in vivo. NIR-LED light represents a novel, noninvasive, therapeutic intervention for the treatment of numerous diseases linked to mitochondrial dysfunction.
    Photomedicine and Laser Surgery 05/2006; 24(2):121-8. · 1.63 Impact Factor
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    ABSTRACT: Far red and near infrared (NIR) light promotes wound healing, but the mechanism is poorly understood. Our previous studies using 670 nm light-emitting diode (LED) arrays suggest that cytochrome c oxidase, a photoacceptor in the NIR range, plays an important role in therapeutic photobiomodulation. If this is true, then an irreversible inhibitor of cytochrome c oxidase, potassium cyanide (KCN), should compete with LED and reduce its beneficial effects. This hypothesis was tested on primary cultured neurons. LED treatment partially restored enzyme activity blocked by 10-100 microm KCN. It significantly reduced neuronal cell death induced by 300 microm KCN from 83.6 to 43.5%. However, at 1-100 mm KCN, the protective effects of LED decreased, and neuronal deaths increased. LED significantly restored neuronal ATP content only at 10 microm KCN but not at higher concentrations of KCN tested. Pretreatment with LED enhanced efficacy of LED during exposure to 10 or 100 microm KCN but did not restore enzyme activity to control levels. In contrast, LED was able to completely reverse the detrimental effect of tetrodotoxin, which only indirectly down-regulated enzyme levels. Among the wavelengths tested (670, 728, 770, 830, and 880 nm), the most effective ones (830 nm, 670 nm) paralleled the NIR absorption spectrum of oxidized cytochrome c oxidase, whereas the least effective wavelength, 728 nm, did not. The results are consistent with our hypothesis that the mechanism of photobiomodulation involves the up-regulation of cytochrome c oxidase, leading to increased energy metabolism in neurons functionally inactivated by toxins.
    Journal of Biological Chemistry 03/2005; 280(6):4761-71. · 4.65 Impact Factor
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    ABSTRACT: The purpose of this study was to assess the changes in gene expression of near-infrared light therapy in a model of impaired wound healing. Background Data: 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 present the effects of LED treatment on wounds in a genetically diabetic mouse model. Polyvinyl acetal (PVA) sponges were subcutaneously implanted in the dorsum of BKS.Cg-m +/+ Lepr(db) mice. LED treatments were given once daily, and at the sacrifice day, the sponges, incision line and skin over the sponges were harvested and used for RNA extraction. The RNA was subsequently analyzed by cDNA array. Our studies have revealed certain tissue regenerating genes that were significantly upregulated upon LED treatment when compared to the untreated sample. Integrins, laminin, gap junction proteins, and kinesin superfamily motor proteins are some of the genes involved during regeneration process. These are some of the genes that were identified upon gene array experiments with RNA isolated from sponges from the wound site in mouse with LED treatment. We believe that the use of NASA light-emitting diodes (LED) for light therapy 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 Defense Advanced Research Projects Agency (DARPA) and NASA Marshall Space Flight Center-SBIR Program.
    Journal of Clinical Laser Medicine & Surgery 05/2003; 21(2):67-74.
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    ABSTRACT: Methanol intoxication produces toxic injury to the retina and optic nerve, resulting in blindness. The toxic metabolite in methanol intoxication is formic acid, a mitochondrial toxin known to inhibit the essential mitochondrial enzyme, cytochrome oxidase. Photobiomodulation by red to near-IR radiation has been demonstrated to enhance mitochondrial activity and promote cell survival in vitro by stimulation of cytochrome oxidase activity. The present studies were undertaken to test the hypothesis that exposure to monochromatic red radiation from light-emitting diode (LED) arrays would protect the retina against the toxic actions of methanol-derived formic acid in a rodent model of methanol toxicity. Using the electroretinogram as a sensitive indicator of retinal function, we demonstrated that three brief (2 min, 24 s) 670-nm LED treatments (4 J/cm(2)), delivered at 5, 25, and 50 h of methanol intoxication, attenuated the retinotoxic effects of methanol-derived formate. Our studies document a significant recovery of rod- and cone-mediated function in LED-treated, methanol-intoxicated rats. We further show that LED treatment protected the retina from the histopathologic changes induced by methanol-derived formate. These findings provide a link between the actions of monochromatic red to near-IR light on mitochondrial oxidative metabolism in vitro and retinoprotection in vivo. They also suggest that photobiomodulation may enhance recovery from retinal injury and other ocular diseases in which mitochondrial dysfunction is postulated to play a role.
    Proceedings of the National Academy of Sciences 04/2003; 100(6):3439-44. · 9.81 Impact Factor
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    ABSTRACT: The purpose of this study was to determine the effects of prophylactic near-infrared light therapy from light-emitting diodes (LEDs) in pediatric bone marrow transplant (BMT) recipients. Oral mucositis (OM) is a frequent side effect of chemotherapy that leads to increased morbidity. Near-infrared light has been shown to produce biostimulatory effects in tissues, and previous results using near-infrared lasers have shown improvement in OM indices. However, LEDs may hold greater potential for clinical applications. We recruited 32 consecutive pediatric patients undergoing myeloablative therapy in preparation for BMT. Patients were examined by two of three pediatric dentists trained in assessing the Schubert oral mucositis index (OMI) for left and right buccal and lateral tongue mucosal surfaces, while the patients were asked to rate their current left and right mouth pain, left and right xerostomia, and throat pain. LED therapy consisted of daily treatment at a fluence of 4 J/cm(2) using a 670-nm LED array held to the left extraoral epithelium starting on the day of transplant, with a concurrent sham treatment on the right. Patients were assessed before BMT and every 2-3 days through posttransplant day 14. Outcomes included the percentage of patients with ulcerative oral mucositis (UOM) compared to historical epidemiological controls, the comparison of left and right buccal pain to throat pain, and the comparison between sides of the buccal and lateral tongue OMI and buccal pain. The incidence of UOM was 53%, compared to an expected rate of 70-90%. There was also a 48% and 39% reduction of treated left and right buccal pain, respectively, compared to untreated throat pain at about posttransplant day 7 (p < 0.05). There were no significant differences between sides in OMI or pain. Although more studies are needed, LED therapy appears useful in the prevention of OM in pediatric BMT patients.
    Journal of Clinical Laser Medicine & Surgery 12/2002; 20(6):319-24.
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    ABSTRACT: Light close to and in the near-infrared range has documented benefits for promoting wound healing in human and animals. However, mechanisms of its action on cells are poorly understood. We hypothesized that light treatment with a light-emitting diode array at 670 nm (LED) is therapeutic in stimulating cellular events involving increases in cytochrome oxidase activity. LED was administered to cultured primary neurons whose voltage-dependent sodium channels were blocked by tetrodotoxin. The down-regulation of cytochrome oxidase activity by TTX was reverted to control levels by LED. LED alone also up-regulated enzyme activity. Thus, the results are consistent with our hypothesis that LED has a stimulating effect on cytochrome oxidase in neurons, even when they have been functionally silenced by TTX.
    Neuroreport 11/2001; 12(14):3033-7. · 1.40 Impact Factor
  • Kristina Desmet, Ellen Buchmann

Publication Stats

626 Citations
26.48 Total Impact Points

Institutions

  • 2001–2012
    • Medical College of Wisconsin
      • • Department of Neurology
      • • Department of Cell Biology, Neurobiology & Anatomy
      Milwaukee, WI, United States
  • 2010
    • Marquette University
      Milwaukee, Wisconsin, United States
  • 2009
    • William Penn University
      University Park, Florida, United States
  • 2006
    • University of Wisconsin - Milwaukee
      • College of Health Sciences
      Milwaukee, Wisconsin, United States