iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavi Asmussen, Erik; Peutzfeldt, Anne (2005): Temperature rise induced by some light emitting diode and quartz-tungsten-halogen curing units. In: European journal of oral sciences, Jg. 113, H. 1, S. 96–98. Online verfügbar unter doi:10.1111/j.1600-0722.2004.00181.x. AbstractBecause of the risk of thermal damage to the pulp, the temperature rise induced bylight-curing units should not be too high. LED (light emitting diode) curing units havethe main part of their irradiation in the blue range and have been reported togenerate less heat than QTH (quartz-tungsten-halogen) curing units. This study hadtwo aims: first, to measure the temperature rise induced by ten LED and three QTHcuring units; and, second, to relate the measured temperature rise to the power density of the curing units. The light-induced temperature rise was measured bymeans of a thermocouple embedded in a small cylinder of resin composite. Thepower density was measured by using a dental radiometer. For LED units, thetemperature rise increased with increasing power density, in a statisticallysignificant manner. Two of the three QTH curing units investigated resulted in ahigher temperature rise than LED curing units of the same power density. Previousfindings, that LED curing units induce less temperature rise than QTH units, doesnot hold true in general.Schlagwörter Composite Resinschemistryradiation effects; Equipment Design; Humans;Lightinginstrumentation; Materials Testing; Temperature; ThermometersBoatright, Jeffrey H.; Moring, Anisha G.; McElroy, Clinton; Phillips, Michael J.; Do, Vi T.; Chang, Bo et al. (2007):Tool from ancient pharmacopoeia prevents vision loss. In: Molecular vision, Jg. 12, S. 1706–1714. AbstractPURPOSE: Bear bile has been used in Asia for over 3,000 years to treat visualdisorders, yet its therapeutic potential remains unexplored in Western visionresearch. The purpose of this study was to test whether treatment of miceundergoing retinal degeneration with tauroursodeoxycholic acid (TUDCA), a primaryconstituent of bear bile, alters the course of degeneration. METHODS: Two retinaldegeneration models were tested: the rd10 mouse, which has a point mutation inthe gene encoding the beta subunit of rod phosphodiesterase, and light inducedretinal damage (LIRD). For LIRD studies, albino Balb/C adult mice weresubcutaneously injected with TUDCA (500 mg/kg body weight) or vehicle (0.15 MNaHCO(3)). Sixteen h later, each mouse received repeat injections. Half of eachtreatment group was then placed in bright light (10,000 lux) or dim light (200 lux) for seven h. At the end of exposure, animals were transferred to their regular housing.Electroretinograms (ERGs) were assessed 24 h later, mice sacrificed, eyesembedded in paraffin and sectioned, and retina sections assayed for morphologyand apoptosis by TUNEL and anti-active caspase-3 immunoreactivity viafluorescent confocal microscopy. A subset of mice were sacrificed 8 and 15 daysafter exposure and retina sections analyzed for morphology and apoptosis. For rd10studies, mice were injected subcutaneously with TUDCA or vehicle at postnatal (P)days 6, 9, 12, and 15. At p18, ERGs were recorded, mice were euthanized andeyes were harvested, fixed, and processed. Retinal sections were stained (toluidineblue), and retinal cell layers morphometrically analyzed by light microscopy.Consecutive sections were analyzed for apopotosis as above. RESULTS: By everymeasure, TUDCA greatly slowed retinal degeneration in LIRD and rd10 mice. ERGa-wave and b-wave amplitudes were greater in mice treated with TUDCA comparedto those treated with vehicle. Retinas of TUDCA-treated mice had thicker outer nuclear layers, more photoreceptor cells, and more fully-developed photoreceptor outer segments. Finally, TUDCA treatments dramatically suppressed signs of apoptosis in both models. CONCLUSIONS: Systemic injection of TUDCA, a primaryconstituent of bear bile, profoundly suppressed apoptosis and preserved functionand morphology of photoreceptor cells in two disparate mouse models of retinaldegeneration. It may be that bear bile has endured so long in Asian pharmacopeiasdue to efficacy resulting from this anti-apoptotic and neuroprotective activity of TUDCA. These results also indicate that a systematic, clinical assessment of

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviTUDCA may be warranted.Schlagwörter Animals; Apoptosisdrug effects; Bilechemistry; Blindnessetiologyprevention &control; Cyclic Nucleotide Phosphodiesterases, Type 6; Disease Models, Animal;Electroretinography; Injections, Subcutaneous; Light; Medicine, East AsianTraditional; Mice; Mice, Mutant Strains; Phosphoric Diester Hydrolasesgenetics;Photoreceptor Cells, Vertebratedrug effectspathology; RetinalDegenerationcomplicationsetiologygeneticsphysiopathology;Taurochenodeoxycholic Acidadministration & dosagechemicalsynthesispharmacology; UrsidaeBöhm, F.; Drygalla, F.; Charlesworth, P.; Böhm, K.; Truscott, T. G.; Jokiel, K. (1996): Bilirubin phototoxicity tohuman cells by green light phototherapy in vitro. In: Photochemistry and photobiology, Jg. 62, H. 6, S. 980–983. AbstractPhototherapy of newborn infants with blue or green light is the most commontreatment of neonatal hyperbilirubinemia. Using bilirubin bound to human lymphoidand basal skin cells we obtained the green light dose dependency of the bilirubinphototoxicity to these cell types. Cells (3-5 x 10(6)/mL) were incubated with bilirubincomplexed to human serum albumin (final concentrations 340 microM bilirubin, 150microM albumin). Under these conditions all cells showed maximum binding of bilirubin. Irradiation with broadband green light (lambda max = 512 nm) over 24 hled to a light dose-dependent population of cells, which contained no bilirubin on thecell membrane as determined by Nomarski interference microscopy. The light-induced mechanism of the disappearance of bilirubin caused lethal membranedamage to the cells (trypan blue exclusion test). The cell kill rate increased with theirradiation dose and with the fraction of cells with no bilirubin. When 90% of lymphoid cells were bilirubin free, 46% of them were dead (using 480 J cm-1 greenlight). Similar results were obtained with basal skin cells. In addition, bilirubin-induced damage of cell membrane and nuclear membrane was also shown bytransmission electron microscopy. Bilirubin (340 microM) in the dark led to 5% of the cells being killed. Basal skin cells bind 2.5 times more bilirubin molecules thanlymphoid cells and showed a different bilirubin disappearance. Irradiation of bilirubinin carbon tetrachloride with 514.5 nm laser light showed generation of singletoxygen via its luminescence at 1270 nm. These results demonstrate that green lightphototherapy of hyperbilirubinemia may cause both skin and immune systemdamage.Schlagwörter Bilirubinmetabolismradiation effects; Cell Deathradiation effects; Cells, Cultured;Humans; Light; Lymphocytescytologymetabolismradiation effects;Phototherapyadverse effects; Skincytologymetabolismradiation effects;SpectrophotometryBynoe, L. A.; Del Priore, L. V.; Hornbeck, R. (1998): Photosensitization of retinal pigment epithelium byprotoporphyrin IX. In: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv für klinische und experimentelle Ophthalmologie, Jg. 236, H. 3, S. 230–233. AbstractBACKGROUND: Clinical evidence of injury to the retinal pigment epithelium is animportant feature of age-related macular degeneration, but the mechanism of thisinjury is unknown. Blue-light-dependent activation of the blood-bornephotosensitizer protoporphyrin IX is known to produce free radicals which maydamage cells and tissues. This study was undertaken to determine the effect of blue light and protoporphyrin IX on retinal pigment epithelial cells in vitro.METHODS: Third-passage porcine retinal pigment epithelial cells were plated insix-well culture plates at 100,000 cells/well and grown to confluence. Retinalpigment epithelial cells were then incubated in culture media with and without 35micrograms/dl protoporphyrin IX and exposed to low intensity (118 microW/cm2)blue, blue-free, or full-spectrum white light in an irradiating incubator for 16 h on/8 hoff cycles for 7 days. Some of the wells were shielded from light (dark controls).Retinal pigment epithelial cells were examined by light microscopy and weretrypsinized and counted after 7 days. RESULTS: White light with and without

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citaviprotoporphyrin IX and protoporphyrin IX in dark conditions did not decrease theretinal pigment epithelial cell count significantly. Blue light alone and blue light withprotoporphyrin IX decreased the cell count by 22 +/- 4% and 35 +/- 3% compared tothe controls, respectively. CONCLUSION: Blue wavelength light without exogenousprotoporphyrin IX has a cytotoxic effect on confluent cultures of retinal pigmentepithelium, suggesting that endogenous photosensitizers may be present in retinalpigment epithelial cells. Protoporphyrin IX has an additive cytotoxic effect in thepresence of blue light, suggesting that this photosensitizer is capable of mediatingblue-light-induced retinal pigment epithelial damage. Since protoporphyrin IX ispresent in blood and tissue fluids, and the retina is chronically exposed to light,protoporphyrin IX-mediated free radical formation may occur in vivo and may play arole in retinal pigment epithelial changes that occur early in the pathogenesis of age-related macular degeneration.Schlagwörter Animals; Cell Count; Cells, Cultured; Light; Photosensitizing Agentspharmacology;Pigment Epithelium of Eyecytologydrug effects; Protoporphyrinspharmacology;SwineCai, Shan-jun; Yan, Mi; Mao, Yong-qui; Zhou, Yan; Liu, Guan-jian (2007): [Relationship between blue light-induced apoptosis and mitochondrial membrane potential and cytochrome C in cultured human retinal pigmentepithelium cells]. In: [Zhonghua yan ke za zhi] Chinese journal of ophthalmology, Jg. 42, H. 12, S. 1095–1102. AbstractOBJECTIVE: To investigate the effect of blue light on apoptosis and mitochondrialpermeability transition (MPT) of cultured human retinal pigment epithelium (RPE)cells in vitro. METHODS: Human RPE cells were exposed to blue light (wave length470 -490 nm). The present study consisted of three parts. Part one studied theeffect of various intensities of blue light on the RPE cells. Cells were irradiated with(500+/-100) lx (group 1) , (2000+/-500) lx (group 2) and (3000+/-500)lx ( group 3)blue light, and followed by 24 hours observation. Part two studied the effect of various duration of blue light at identical intensity on the RPE cells. For the study onvarious subtypes of RPE cells, cells were irradiated by blue light at (2000+/-500) xfor 6, 12, and 24 hours. For the study of mitochondrial membrane potential, cellswere irradiated for 3, 6, and 12 hours. Part three studied cells irradiated with bluelight at identical intensity and duration, but with various prolongation of post-exposure culture. The prolongation of post-exposure culture was 6, 12, 24, and 36hours. Phototoxicity was quantified at various periods after exposure by staining of the nuclei of membrane-compromised cells, by TdT-dUTP terminal nick-endlabeling (TUNEL) of apoptotic cells and by Annexin V labeling for phosphatidylserine exposure. Transmission electronmicroscopy was used todetermine the ultrastructure changes of RPE cells. Mitochondrial membranepotential ( deltaPsim ) was measured by rhodamine 123 staining and subsequentflow cytometry. Cytochrome C activity was assayed by ELISA. Caspase-3 wasdetected by colorimetric assay. RESULTS: TUNEL-positive labeling cells in firstgroup of part two study showed cell shrinkage, membrane blebbing, apoptotic body,condensation and fragmentation of chromatin. Mitochondrial swelling, extinction of inner mitochondrial membrane ridge, dilation of rough endoplasmic reticulum andincrease of the lysosome were also observed in transmission electronmicroscopy.Blue light at (500 +/- 100) x intensity did not induce damage to RPE cells, butdecrease of delta Psim was observed. A significant increase of apoptotic, apoptoticnecrotic and necrotic percentages, as well as significant decrease of deltaPsimwere observed at higher light intensity in part one study. Increase of apoptoticpercentage was the main response to shorter exposure of blue light. Increase of apoptotic necrotic and necrotic percentage and pronounced decrease of deltaPsimoccurred in cells irradiated by longer exposure in part two study. In part 3 study,apoptotic response was increased gradually during 6 and 12 hours prolongation of post-exposure culture, more apoptotic necrosis or necrosis were found after post-exposure 24 hours. Decrease of deltaPsim was observed in 6 hours prolongation of post-exposure culture and lasting for 48 hours. The concentration of cytochrome C