• The Journal of the Petrological Society of Korea
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• v.25 no.3
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• pp.241-252
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• 2016

In this paper, in order to test the possibility of applying K feldspar $pIR-IRSL_{290}$ signal(read out at $290^{\circ}C$) to date old terrace sediments(up to ~ 200 ka, MIS 7) in Korea, we investigated luminescence properties of $pIR-IRSL_{290}$ signals in K feldspar extracts from 27 marine and fluvial terrace sediment samples, and these were compared with those of quartz OSL and conventional K feldspar $IRSL_{50}$ (readout at $50^{\circ}C$) signals. The averaged $2D_0$ value of K feldspar $pIR-IRSL_{290}$ growth curves was ~ 700 Gy, which is consistent with that of $IRSL_{50}$ signal, and this is 3 times higher than that for quartz OSL (~ 250 Gy) on average. Where possible, K feldspar $pIR-IRSL_{290}$ ages were compared with quartz OSL and conventional $IRSL_{50}$ ages. Our preliminary K feldspar $pIR-IRSL_{290}$ ages were older than quartz OSL ages by about 200%, while fading rate-corrected conventional $IRSL_{50}$ ages are in good agreement with those based on quartz OSL. This seems to indicate the possibility of K-feldspar $pIR-IRSL_{290}$ age overestimation due to the presence of unbleachable $pIR-IRSL_{290}$ signals, even with a prolonged exposure to sunlight. Both quartz OSL and K-feldspar $pIR-IRSL_{290}$ signals for the samples from Noeum fluvial terrace and Gusan fault site were all in dose saturation level, thus unable to estimate the formation ages of the sediments. However, $2D_0$ values derived from the dose response growth curves strongly indicate that the Noeum fluvial terrace sediments have formed before 109-140 ka, while the fluvial sediments from Gusan fault were desposited before 100-105 ka. Further, this seems to suggest that the previous quartz OSL ages of ~40-50 ka for Gusan fault sediments should be the underestimated ones due to dose saturation problem.

• Journal of Nutrition and Health
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• v.51 no.6
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• pp.498-506
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• 2018

Purpose: Lycopene, a carotenoid with anti-oxidant properties, occurs naturally in tomatoes and pink grapefruit. Although the beneficial effects of lycopene on various disorders have been established, little attention has been paid to the possible anti-diabetic effects of lycopene focusing on ${\beta}$-cells. Therefore, this study investigated the potential of lycopene to protect ${\beta}$-cells against apoptosis induced by a cytokine mixture. Methods: For toxicity experiments, the cells were treated with 0.1 ~ 10 nM of lycopene, and the cell viability in INS-1 cells (a rat ${\beta}$-cell line) was measured using a MTT assay. To induce cytokine toxicity, the cells were treated with a cytokine mixture (20 ng/mL of $TNF{\alpha}$ + 20 ng/mL of IL-$1{\beta}$) for 24 h, and the effects of lycopene (0.1 nM) on the cytokine toxicity were measured using the MTT assay. The expression levels of the apoptotic proteins were analyzed by Western blotting, and the level of intracellular reactive oxidative stress (ROS) was monitored using a DCFDA fluorescent probe. The intracellular ATP levels were determined using a luminescence kit, and mRNA expression of the genes coding for anti-oxidative stress response and mitochondrial function were analyzed by quantitative reverse-transcriptase PCR. Results: Exposure of INS-1 cells to 0.1 nM of lycopene increased the cell viability significantly, and protected the cells from cytokine-induced death. Lycopene upregulated the mRNA and protein expression of B-cell lymphoma-2 (Bcl-2) and reduced the expression of the Bcl-2 associated X (Bax) protein. Lycopene inhibited apoptotic signaling via a reduction of the ROS, and this effect correlated with the upregulation of anti-oxidative stress response genes, such as GCLC, NQO1, and HO-1. Lycopene increased the mRNA expression of mitochondrial function-related genes and increased the cellular ATP level. Conclusion: These results suggest that lycopene reduces the level of oxidative stress and improves the mitochondrial function, contributing to the prevention of cytokine-induced ${\beta}$-cell apoptosis. Therefore, lycopene could potentially serve as a preventive and therapeutic agent for the treatment of type 2 diabetes.