• Bulletin of the Korean Chemical Society
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• v.28 no.12
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• pp.2315-2318
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• 2007

Epinephrine was determined using a lab-made chemiluminescence (CL) system with air pump. Luminolsodium IO4? chemiluminescence system was employed to produce the luminescence of epinephrine. In the reaction, epinephrine was oxidized to produce superoxide or singlet oxygen by periodate in alkaline solution, which enhanced CL of luminol. For optimization, various buffers, such as phosphate, borate, and tris, were studied in this experiment. Compared to NaOH, the phosphate and borate buffer showed better reproducibility with similar sensitivity. Small amount of sample, 22 μL, was required for a measurement. The limit of quantification for epinephrine was obtained to be ~10?9 g/mL after optimization.

• Analytical Science and Technology
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• v.12 no.2
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• pp.99-104
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• 1999

A stepwise gradient elution with two wavelengths detection was performed for the separation and determination of some anions in saline water. The eight anions such as iodate, bromate, nitrite, bromide, nitrate, chromate, iodide and thiocyanate were successfully separated using AS-7 column and sodium chloride/sodium phosphate buffer solution as an eluant within 40 min. The separation behaviors of anions were studied at various sodium chloride concentrations. The peak shapes of anions of bromate, nitrite, bromide and nitrate gradually broadened as the concentration of sodium chloride increased until 1.0 M in the sample solutions. However, no effect was observed in the peak shapes of chromate, iodide and thiocynate. A good linearity was obtained at the range of ppm(mg/L). The detection limit was proved to be $10-720{\mu}g/L$ for the eight anions with $50{\mu}L$ injection volume. This method was applied to the determination of $Br^-$, ${NO_3}^-$ and $I^-$ in sea water.

• Nuclear Engineering and Technology
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• v.3 no.3
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• pp.141-147
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• 1971

In iodine-131 labelling of iodocompounds such as tetrachloro-P-tetraiodo R-fluorescein, sodium orthoiodohippurate and a non-iodocompound, human serum albumin (HSA), the labelling rates and yields are accurately compared with each other. The reaction systems conducted for each compounds were different conditions: sodium iodide-$^{131}$ I containing reducing agent, sodium iodide-$^{131}$ I free from reducing agent, and sodium iodide-$^{131}$ I free from reducing agent but containing considerable amount of iodide-$^{131}$ I etc. The labelling yields were generally poor; 10% in the case of using sodium iodide-$^{131}$ I containing redoing agent, and 50~60% in the case of using sodium iodide-$^{131}$ I free from reducing agent but containing considerable amount of iodide-$^{131}$ I. However, fair yields were obtained in the case of using sodium iodide-$^{131}$ I free from reducing agent and mostly in the form of iodide-$^{131}$ I. The reaction entities involved in these reactions are also briefly discussed.

• Clinical and Experimental Reproductive Medicine
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• v.38 no.4
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• pp.216-221
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• 2011

Objective: To differentiate the human embryonic stem cells (hESCs) into the retinal pigment epithelium (RPE) in the defined culture condition and determine its therapeutic potential for the treatment of retinal degenerative diseases. Methods: The embryoid bodies were formed from hESCs and attached on the matrigel coated culture dishes. The neural structures consisting neural precursors were selected and expanded to form rosette structures. The mechanically isolated neural rosettes were differentiated into pigmented cells in the media comprised of N2 and B27. Expression profiles of markers related to RPE development were analyzed by reverse transcription-polymerase chain reaction and immunostaining. Dissociated putative RPE cells ($10^5$ cells/5 ${\mu}L$) were transplanted into the subretinal space of rat retinal degeneration model induced by intravenous sodium iodate injection. Animals were sacrificed at 1, 2, and 4 weeks after transplantation, and immnohistochemistry study was performed to verify the survival of the transplanted cells. Results: The putative RPE cells derived from hESC showed characteristics of the human RPE cells morphologically and expressed molecular markers and associated with RPE fate. Grafted RPE cells were found to survive in the subretinal space up to 4 weeks after transplantation, and the expression of RPE markers was confirmed with immunohistochemistry. Conclusion: Transplanted RPE cells derived from hESC in the defined culture condition successfully survived and migrated within subretinal space of rat retinal degeneration model. These results support the feasibility of the hESC derived RPE cells for cell-based therapies for retinal degenerative disease.

• Molecules and Cells
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• v.43 no.7
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• pp.632-644
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• 2020

The molecular mechanism underlying autophagy impairment in the retinal pigment epithelium (RPE) in dry age-related macular degeneration (AMD) is not yet clear. Based on the causative role of poly(ADP-ribose) polymerase 1 (PARP1) in RPE necrosis, this study examined whether PARP1 is involved in the autophagy impairment observed during dry AMD pathogenesis. We found that autophagy was downregulated following H₂O₂-induced PARP1 activation in ARPE-19 cells and olaparib, PARP1 inhibitor, preserved the autophagy process upon H₂O₂ exposure in ARPE-19 cells. These findings imply that PARP1 participates in the autophagy impairment upon oxidative stress in ARPE-19 cells. Furthermore, PARP1 inhibited autolysosome formation but did not affect autophagosome formation in H₂O₂-exposed ARPE-19 cells, demonstrating that PARP1 is responsible for impairment of late-stage autophagy in particular. Because PARP1 consumes NAD⁺ while exerting its catalytic activity, we investigated whether PARP1 impedes autophagy mediated by sirtuin1 (SIRT1), which uses NAD⁺ as its cofactor. A NAD⁺ precursor restored autophagy and protected mitochondria in ARPE-19 cells by preserving SIRT1 activity upon H₂O₂. Moreover, olaparib failed to restore autophagy in SIRT1-depleted ARPE-19 cells, indicating that PARP1 inhibits autophagy through SIRT1 inhibition. Next, we further examined whether PARP1-induced autophagy impairment occurs in the retinas of dry AMD model mice. Histological analyses revealed that olaparib treatment protected mouse retinas against sodium iodate (SI) insult, but not in retinas cotreated with SI and wortmannin, an autophagy inhibitor. Collectively, our data demonstrate that PARP1-dependent inhibition of SIRT1 activity impedes autophagic survival of RPE cells, leading to retinal degeneration during dry AMD pathogenesis.