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Cindy M.l. Hutnik - One of the best experts on this subject based on the ideXlab platform.
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Comparison of the in vitro toxicity of indocyanine green to that of trypan blue in human retinal pigment Epithelium Cell cultures.
American journal of ophthalmology, 2004Co-Authors: Jeffrey S. Gale, Alain A. Proulx, John R. Gonder, Alexander Mao, Cindy M.l. HutnikAbstract:Abstract Purpose To compare the in vitro toxicity of indocyanine green (ICG) to that of trypan blue (TB) in human retinal pigment Epithelium Cell cultures. The use of ICG and TB in macular hole surgery is discussed. Design In vitro Cell biology experimental study. Methods The ICG dye and TB were applied to ARPE-19, a commercially available human retinal pigment Epithelium Cell line. Cultures were established and maintained according to supplier protocols. The ICG dye, TB or Hank's balanced salt solution (controls) were then applied to the Cells at varying concentrations and over various exposure periods. Fiberoptic light was also applied to Cells to assess for the possibility of a potentiating phototoxic effect. Cell viability fractions were determined using a well-studied mitochondrial dehydrogenase assay. Results The TB was not toxic to the retinal pigment Epithelium Cell cultures at any concentration or over any period of exposure, whereas ICG dye demonstrated dose-dependent and exposure-dependent toxicity. The ICG dye was found to be toxic to the Cells at all tested concentrations between 5.0 mg/ml (stock concentration, 26.1% Cell survival) and 0.5 mg/ml (92.8% Cell survival) over a 3-minute exposure. No toxicity to TB was seen at the stock concentration of 1.5 mg/mL. Addition of light to the cultures did not significantly alter Cell viability with either dye. Long periods of exposure, 2 hours, 24 hours, and 72 hours, to minute concentrations of either dye did not produce significant Cell death. Conclusions Indocyanine green demonstrates more toxicity than TB to human retinal pigment Epithelium Cell cultures. This is independent of any phototoxic potentiating effect of fiberoptic light or solvent toxicity. A clinically useful concentration of 0.5-mg/ml ICG causes low cytotoxicity at 3 minutes' exposure (Cell survival 92.8%) and shows no detectable toxicity at 1-minute exposure (Cell survival 102%).
R Birngruber - One of the best experts on this subject based on the ideXlab platform.
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origin of retinal pigment Epithelium Cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen
Lasers in Surgery and Medicine, 2000Co-Authors: Ralf Brinkmann, Gereon Huttmann, Jan Rogener, Johann Roider, R BirngruberAbstract:Background and Objective: Selective photodamage of the retinal pigment Epithelium (RPE) is a new technique to treat a variety of retinal diseases without causing adverse effects to surrounding tissues such as the neural retina including the photoreceptors and the choroid. In this study, the mechanism of Cell damage after laser irradiation was investigated. Study Design/Materials and Methods: Single porcine RPE-melanosomes and RPE Cells were irradiated with a Nd:YLF laser (wavelength l = 527 nm, adjustable pulse duration t = 250 nsec-3 msec) and a Nd:YAG laser (l = 532 nm, t = 8 nsec). Fast flash photography was applied to observe vaporization at melanosomes in suspension. A fluorescence viability assay was used to probe the Cells vitality. Results: The threshold radiant exposures for vaporization around individual melanosomes and for ED50 Cell damage are similar at 8-nsec pulse duration. Both thresholds increase with pulse duration; however, the ED50 Cell damage radiant exposure is 40% lower at 3msec. Temperature calculations to model the onset of vaporization around the melanosomes are in good agreement with the experimental results when assuming a surface temperature of 150°C to initiate vaporization and a homogeneous melanosome absorption coefficient of 8,000 cm ˛1 . Increasing the number of pulses delivered to RPE Cells at a repetition rate of 500 Hz, the ED50 value decreases for all pulse durations. However, the behavior does not obey scaling laws such as the N 1/4 equation. Conclusion: The origin of RPE Cell damage for single pulse irradiation up to pulse durations of 3 msec can be described by a damage mechanism in which microbubbles around the melanosomes cause a rupture of the Cell structure. The threshold radiant exposure for RPE damage decreases with increasing number of pulses applied. Lasers Surg. Med. 27:451‐464, 2000. © 2000 Wiley-Liss, Inc.
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origin of retinal pigment Epithelium Cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen
Lasers in Surgery and Medicine, 2000Co-Authors: Ralf Brinkmann, Gereon Huttmann, Jan Rogener, Johann Roider, R Birngruber, Charles P LinAbstract:Background and Objective: Selective photodamage of the retinal pigment Epithelium (RPE) is a new technique to treat a variety of retinal diseases without causing adverse effects to surrounding tissues such as the neural retina including the photoreceptors and the choroid. In this study, the mechanism of Cell damage after laser irradiation was investigated. Study Design/Materials and Methods: Single porcine RPE-melanosomes and RPE Cells were irradiated with a Nd:YLF laser (wavelength l = 527 nm, adjustable pulse duration t = 250 nsec-3 msec) and a Nd:YAG laser (l = 532 nm, t = 8 nsec). Fast flash photography was applied to observe vaporization at melanosomes in suspension. A fluorescence viability assay was used to probe the Cells vitality. Results: The threshold radiant exposures for vaporization around individual melanosomes and for ED50 Cell damage are similar at 8-nsec pulse duration. Both thresholds increase with pulse duration; however, the ED50 Cell damage radiant exposure is 40% lower at 3msec. Temperature calculations to model the onset of vaporization around the melanosomes are in good agreement with the experimental results when assuming a surface temperature of 150°C to initiate vaporization and a homogeneous melanosome absorption coefficient of 8,000 cm ˛1 . Increasing the number of pulses delivered to RPE Cells at a repetition rate of 500 Hz, the ED50 value decreases for all pulse durations. However, the behavior does not obey scaling laws such as the N 1/4 equation. Conclusion: The origin of RPE Cell damage for single pulse irradiation up to pulse durations of 3 msec can be described by a damage mechanism in which microbubbles around the melanosomes cause a rupture of the Cell structure. The threshold radiant exposure for RPE damage decreases with increasing number of pulses applied. Lasers Surg. Med. 27:451‐464, 2000. © 2000 Wiley-Liss, Inc.
Ralf Brinkmann - One of the best experts on this subject based on the ideXlab platform.
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origin of retinal pigment Epithelium Cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen
Lasers in Surgery and Medicine, 2000Co-Authors: Ralf Brinkmann, Gereon Huttmann, Jan Rogener, Johann Roider, R BirngruberAbstract:Background and Objective: Selective photodamage of the retinal pigment Epithelium (RPE) is a new technique to treat a variety of retinal diseases without causing adverse effects to surrounding tissues such as the neural retina including the photoreceptors and the choroid. In this study, the mechanism of Cell damage after laser irradiation was investigated. Study Design/Materials and Methods: Single porcine RPE-melanosomes and RPE Cells were irradiated with a Nd:YLF laser (wavelength l = 527 nm, adjustable pulse duration t = 250 nsec-3 msec) and a Nd:YAG laser (l = 532 nm, t = 8 nsec). Fast flash photography was applied to observe vaporization at melanosomes in suspension. A fluorescence viability assay was used to probe the Cells vitality. Results: The threshold radiant exposures for vaporization around individual melanosomes and for ED50 Cell damage are similar at 8-nsec pulse duration. Both thresholds increase with pulse duration; however, the ED50 Cell damage radiant exposure is 40% lower at 3msec. Temperature calculations to model the onset of vaporization around the melanosomes are in good agreement with the experimental results when assuming a surface temperature of 150°C to initiate vaporization and a homogeneous melanosome absorption coefficient of 8,000 cm ˛1 . Increasing the number of pulses delivered to RPE Cells at a repetition rate of 500 Hz, the ED50 value decreases for all pulse durations. However, the behavior does not obey scaling laws such as the N 1/4 equation. Conclusion: The origin of RPE Cell damage for single pulse irradiation up to pulse durations of 3 msec can be described by a damage mechanism in which microbubbles around the melanosomes cause a rupture of the Cell structure. The threshold radiant exposure for RPE damage decreases with increasing number of pulses applied. Lasers Surg. Med. 27:451‐464, 2000. © 2000 Wiley-Liss, Inc.
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origin of retinal pigment Epithelium Cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen
Lasers in Surgery and Medicine, 2000Co-Authors: Ralf Brinkmann, Gereon Huttmann, Jan Rogener, Johann Roider, R Birngruber, Charles P LinAbstract:Background and Objective: Selective photodamage of the retinal pigment Epithelium (RPE) is a new technique to treat a variety of retinal diseases without causing adverse effects to surrounding tissues such as the neural retina including the photoreceptors and the choroid. In this study, the mechanism of Cell damage after laser irradiation was investigated. Study Design/Materials and Methods: Single porcine RPE-melanosomes and RPE Cells were irradiated with a Nd:YLF laser (wavelength l = 527 nm, adjustable pulse duration t = 250 nsec-3 msec) and a Nd:YAG laser (l = 532 nm, t = 8 nsec). Fast flash photography was applied to observe vaporization at melanosomes in suspension. A fluorescence viability assay was used to probe the Cells vitality. Results: The threshold radiant exposures for vaporization around individual melanosomes and for ED50 Cell damage are similar at 8-nsec pulse duration. Both thresholds increase with pulse duration; however, the ED50 Cell damage radiant exposure is 40% lower at 3msec. Temperature calculations to model the onset of vaporization around the melanosomes are in good agreement with the experimental results when assuming a surface temperature of 150°C to initiate vaporization and a homogeneous melanosome absorption coefficient of 8,000 cm ˛1 . Increasing the number of pulses delivered to RPE Cells at a repetition rate of 500 Hz, the ED50 value decreases for all pulse durations. However, the behavior does not obey scaling laws such as the N 1/4 equation. Conclusion: The origin of RPE Cell damage for single pulse irradiation up to pulse durations of 3 msec can be described by a damage mechanism in which microbubbles around the melanosomes cause a rupture of the Cell structure. The threshold radiant exposure for RPE damage decreases with increasing number of pulses applied. Lasers Surg. Med. 27:451‐464, 2000. © 2000 Wiley-Liss, Inc.
Chang Patricia Chuentsuei - One of the best experts on this subject based on the ideXlab platform.
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plasma induced graft copolymerization of hema onto silicone rubber and tpx film improving rabbit corneal epithelial Cell attachment and growth
Biomaterials, 1994Co-Authors: Hsiue Gingho, Lee Shyhdar, Wang Cheechan, Shiue Michael Hungi, Chang Patricia ChuentsueiAbstract:Abstract A poly(2-hydroxyethyl methacrylate) (pHEMA)-grafted polymer film was prepared by plasma-induced graft copolymerization onto an elastic material, silicone rubber, and a plastic material, poly(4-methyl-1-pentene) (TPX). The control, Ar plasma-treated and pHEMA-grafted silicone rubber and TPX surfaces were characterized by ESCA, FTIR-ATR, SEM and contact angle techniques. ESCA verified the respective chemical shift of control and Ar plasma-treated films. The presence of the grafted pHEMA was also verified by ESCA. The introduction of pHEMA onto a hydrophobic support provided an adequate surface for rabbit corneal Epithelium Cell attachment and growth. Cell attachment and growth onto these surfaces were examined by light microscopy. Cell attachment onto the control and Ar plasma-treated surfaces was negligible, while improved attachment and growth of rabbit corneal Epithelium Cells was demonstrated on the pHEMA-grafted polymeric surface. At 72 h, the pHEMA-grafted silicone rubber surface attached and grew more Cells as compared with those on a pHEMA-grafted TPX surface. The pHEMA-grafted silicone rubber surface demonstrated a confluent Cell layer after 72 h.
Masayo Takahashi - One of the best experts on this subject based on the ideXlab platform.
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characterization of human induced pluripotent stem Cell derived retinal pigment Epithelium Cell sheets aiming for clinical application
Stem cell reports, 2014Co-Authors: Hiroyuki Kamao, Michiko Mandai, Satoshi Okamoto, Noriko Sakai, Akiko Suga, Sunao Sugita, Junichi Kiryu, Masayo TakahashiAbstract:Age-related macular degeneration (AMD) causes severe visual impairment due in part to age-dependent impairment of retinal pigment Epithelium (RPE). It has been suggested that autologous human induced pluripotent stem Cells (hiPSCs) may represent a useful Cell source for the generation of graft RPE. We generated hiPSC-derived RPE (hiPSC-RPE) Cell sheets optimized to meet clinical use requirements, including quality, quantity, consistency, and safety. These Cell sheets are generated as a monolayer of Cells without any artificial scaffolds, express typical RPE markers, form tight junctions that exhibit polarized secretion of growth factors, and show phagocytotic ability and gene-expression patterns similar to those of native RPE. Additionally, upon transplantation, autologous nonhuman primate iPSC-RPE Cell sheets showed no immune rejection or tumor formation. These results suggest that autologous hiPSC-RPE Cell sheets may serve as a useful form of graft for use in tissue replacement therapy for AMD.