Chonbuk National University

About: Chonbuk National University is a education organization based out in Jeonju, South Korea. It is known for research contribution in the topics: Apoptosis & Nanofiber. The organization has 14820 authors who have published 28884 publications receiving 554131 citations.

Generalized Precoding-Aided Quadrature Spatial Modulation

Abstract: In this paper, we propose a novel scheme, which is called generalized precoding-aided quadrature spatial modulation (GPQSM), that extends the conventional quadrature spatial modulation to the receiver side. In GPQSM, spatial modulation works in both the in-phase and quadrature parts of the received signals, thus conveying additional information bits compared with conventional generalized precoding-aided spatial modulation (GPSM). The proposed scheme is general and can degenerate into the conventional multiple-input multiple-output (MIMO) scheme. A closed-form upper bound on the average bit error probability of GPQSM is derived. Simulation results verify the theoretical analysis and show that GPQSM outperforms the conventional GPSM scheme and the MIMO scheme under the same spectral efficiency.

A Study on the Effect of Financial Inclusion on the Relationship Between Income Inequality and Economic Growth

Abstract: In this article, we attempt to estimate whether financial inclusion, expressed as financial accessibility, has a positive effect on reducing income inequality. Furthermore, we estimate the effect of such financial inclusion on economic growth by reducing income inequality. From the results of our empirical analysis, we can draw the following three conclusions. First, income inequality has a very negative effect on GDP growth. The negative relationship between income inequality and GDP growth is strong in low-income countries. In addition, income inequality has a stronger effect on reducing economic growth in high-fragility countries. Second, progressivity is not a major factor in reducing income inequality in low-income countries or in high-fragility countries. Finally, financial inclusion improves the relationship between income inequality and economic growth. The reduction in income inequality through financial inclusion changes the negative relationship between income inequality and economic gr...

SIRT1 activation by resveratrol ameliorates cisplatin-induced renal injury through deacetylation of p53

Abstract: Nephrotoxicity is one of the important dose-limiting factors during cisplatin treatment. There is a growing body of evidence that activation of p53 has a critical role in cisplatin-induced renal apoptotic injury. The nicotinamide adenine dinucleotide-dependent protein deacetylase SIRT1 decreases apoptosis through deacetylating of p53, and resveratrol is known as an activator of SIRT1. To study the role of SIRT1 in cisplatin-induced renal injury through interaction with p53, mouse proximal tubular cells (MPT) were treated with cisplatin and examined the expression level of SIRT1, acetylation of p53, PUMA-α, Bax, the cytosolic/mitochondrial cytochrome c ratio, and active caspase-3. The expression of SIRT1 was decreased by cisplatin. Resveratrol, a SIRT1 activator, ameliorated cisplatin-induced acetylation of p53, apoptosis, and cytotoxicity in MPT cells. In addition, resveratrol remarkably blocked cisplatin-induced decrease of Bcl-xL in MPT cells. Further specific SIRT1 inhibition with EX 527 or small interference RNA specific to SIRT1 reversed the effect of resveratrol on cisplatin-induced toxicity. Inhibition of p53 by pifithrin-α reversed the effect of EX527 in protein expression of PUMA-α, Bcl-xL, and caspase-3 and cytotoxicity in MPT cells. SIRT1 protein expression after cisplatin treatment was significantly decreased in the kidney. SIRT1 activation by resveratrol decreased cisplatin-induced apoptosis while improving the glomerular filtration rate. Taken together, our findings suggest that the modulation of p53 by SIRT1 could be a possible target to attenuate cisplatin-induced kidney injury.

ER Stress and Autophagy

Abstract: Eukaryotic cells respond to various types of stresses caused by changes in the extracellular environment. Intracellular factors, such as the accumulation of misfolded proteins in the endoplasmic reticulum (ER), also cause stress and activate the unfolded protein response (UPR), which induces the expression of chaperones and proteins involved in the recovery process. However, if the stress is excessive or sustained, and ER function cannot be restored, the UPR triggers apoptosis, thereby removing the affected cell. It is now apparent that ER stress is also a potent trigger for autophagy, a self-degradative process that has an adaptive function. This review surveys the intersection of ER stress and autophagy and highlights the potential therapeutic implications thereof.