• 한국가시화정보학회:학술대회논문집
• /
• 2002.04a
• /
• pp.51-78
• /
• 2002

A number of research groups worldwide are studying electronic implants that can be mounted on retinal optic nerve/visual cortex to restore vision of patients suffering from retinal degeneration. The implants consist of a neural interface made of biocompatible materials, one or more integrated circuits for stimuli generation, a camera, an image processor, and a telemetric channel. The realization of these classes of neural prosthetic devices is largely due to the explosive development of micro- and nano-electronics technologies in the late $20^{th}$ century and biotechnologies more recently. Animal experiments showed promise and some human experiments are in progress to indicate that recognition of images can be obtained and improved over time. We, at NBS-ERC of SNU, have started our own retinal implant project in 2000. We have selected polyimide as the biomaterial for an epi-retinal stimulator. In-vitro and in-vivo biocompatibility studies have been performed on the electrode arrays. We have obtained good affinity to retinal pigment epithelial cells and no harmful effect. The implant also showed very good stability and safety in rabbit eye for 12 weeks. We have also demonstrated that through proper stimulation of inner retina, meaning vision can be obtained.

• Parasites, Hosts and Diseases
• /
• v.57 no.2
• /
• pp.83-92
• /
• 2019

Based on the reactive oxygen species (ROS) regulatory properties of diphenyleneiodonium (DPI), we investigated the effects of DPI on host-infected T. gondii proliferation and determined specific concentration that inhibit the intracellular parasite growth but without severe toxic effect on human retinal pigment epithelial (ARPE-19) cells. As a result, it is observed that host superoxide, mitochondria superoxide and $H_2O_2$ levels can be increased by DPI, significantly, followed by suppression of T. gondii infection and proliferation. The involvement of ROS in anti-parasitic effect of DPI was confirmed by finding that DPI effect on T. gondii can be reversed by ROS scavengers, N-acetyl-L-cysteine and ascorbic acid. These results suggest that, in ARPE-19 cell, DPI can enhance host ROS generation to prevent T. gondii growth. Our study showed DPI is capable of suppressing T. gondii growth in host cells while minimizing the un-favorite side-effect to host cell. These results imply that DPI as a promising candidate material for novel drug development that can ameliorate toxoplasmosis based on ROS regulation.

• Journal of Life Science
• /
• v.17 no.9 s.89
• /
• pp.1204-1210
• /
• 2007

The topoisomerase II inhibitor etoposide causes an accumulation of DNA double strand breaks within the nuclei of cells. In this study, we investigated the effect of etoposide on the cell growth and apoptosis of human RPE cells. Etoposide evoked a significant inhibition of cell growth, and also induced DNA fragmentation in ARPE-19 cells. In addition, etoposide significantly up-regulated the expression of heme oxygenase-1 (HO-1), which is a stress-responsive protein and is known to play a protective role against the oxidative injury. And, etoposide-induced HO-1 expression was affected by the ROS scavenger N-acetyl cysteine. We also used oligonucleotides interfering with HO-1 mRNA (siRNA) for the inhibition of HO-1 expression. Interestingly, knock-down of the HO-1 gene significantly increased the level of DNA fragmentation in etoposide-treated ARPE-19 cells. In conclusion, these results suggest that up-regulated HO-1 plays as an anti-apoptotic factor in the process of apoptosis of ARPE-19 cells stimulated by etoposide.

• Journal of Korean Ophthalmic Optics Society
• /
• v.17 no.1
• /
• pp.91-97
• /
• 2012

Purpose: This purpose of study is to investigate the effect of UV-A-blocking or brown-tinted ophthalmic lens against A2E photooxidation which known as one of the etiologies of AMD(Age-related macular degenaration). Methods: The photooxidation of A2E, synthetic product of two molecules of all-trans-retinal and ethanolamine, was induced by the exposure to blue light (420~470 nm, $94mW/cm^2$) for 3 minutes. The inhibitory effect of UVblocking or brown-tinted ophthalmic lens against A2E photooxidation was evaluated by UV absorbance and HPLC analysis of remained A2E after the exposure to blue light. Results: UV-blocking ophthalmic lens could not inhibit A2E photooxidation induced by blue light irradiation. There was no difference in A2E photooxidation in the presence of brown-tinted ophthalmic lens to block 15% of visible ray, however, those lenses blocking 55% or 86% of visible ray showed the inhibitory effect of A2E photooxidation as 9.98% and 16.55%, respectively. By HPLC analysis, the amount of residual A2E which was not blocked by any lens was $199.29{\pm}26.53{\mu}M$, however, the inhibitory effect against A2E photooxidation was shown in the presence of brown-tinted lens. The remained A2Es were $264.58{\pm}31.91{\mu}M$ and $402.93{\pm}28.68{\mu}M$ in brown-tinted lenses of 55% and 86% blocking visible ray, respectively. However, there was no inhibitory effect against A2E photooxidation in the case of UV-blocking lens by HPLC analysis. Conclusions: In this study, brown-tinted ophthalmic lens was confirmed to have the inhibitory effect against the photooxidation of A2E, a causing substance of AMD onset.