In Situ Growth of FeCo-selenide on Ni Foam as High-Performance Electrode for Electrochemical Energy Storage Devices

An Ye,Jiqiu Qi,Yanwei Sui,Fei Yang,Fuxiang Wei,Yezeng He,Qingkun Meng,Zhi Sun 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2018 NANO Vol.13 No.7

A solid-state energy storage device has been fabricated using FeCo-selenide nanosheet arrays as positive electrode and Fe2O3 nanorod as negative electrode. As an electrode material, the ternary FeCo-selenide nanosheet arrays supported by Ni foam show a highest specific capacitance of 978 F/g (specific capacity of 163 mAh/g) at 1 A/g and a superior cycle behavior of 81.2% are obtained after 5000 cycles at current density of 4 A/g. The asymmetric supercapacitor achieves the maximum energy density of 34.6Wh/kg at the power density of 759.6 W/kg. Furthermore, the superior cycling stability with 83% retention of initial capacitance after 5000 cycles further verify the practical applications of FeCo-selenide//Fe2O3 asymmetric supercapacitor. Meanwhile, the LED bulb and the light board of "CUMT" are lighted by connecting several capacitors to form a series circuit.

siRNA-mediated Silencing of Notch-1 Enhances Docetaxel Induced Mitotic Arrest and Apoptosis in PCa Cells

Ye, Qi-Fa,Zhang, Yi-Chuan,Peng, Xiao-Qing,Long, Zhi,Ming, Ying-Zi,He, Le-Ye Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.6

Purpose: Notch is an important signaling pathway that regulates cell fate, stem cell maintenance and the initiation of differentiation in many tissues. It has been reported that activation of Notch-1 contributes to tumorigenesis. However, whether Notch signaling might have a role in chemoresistance of prostate cancer is unclear. This study aimed to investigate the effects of Notch-1 silencing on the sensitivity of prostate cancer cells to docetaxel treatment. Methods: siRNA against Notch-1 was transfected into PC-3 prostate cancer cells. Proliferation, apoptosis and cell cycle distribution were examined in the presence or absence of docetaxel by MTT and flow cytometry. Expression of $p21^{waf1/cip1}$ and Akt as well as activation of Akt in PC-3 cells were detected by Western blot and Real-time PCR. Results: Silencing of Notch-1 promoted docetaxel induced cell growth inhibition, apoptosis and cell cycle arrest in PC-3 cells. In addition, these effects were associated with increased $p21^{waf1/cip1}$ expression and decreased Akt expression and activation in PC-3 cells. Conclusion: Notch-1 promotes chemoresistance of prostate cancer and could be a potential therapeutic target.

Loss of Hfe Function Reverses Impaired Recognition Memory Caused by Olfactory Manganese Exposure in Mice

Qi Ye,Jonghan Kim 한국독성학회 2015 Toxicological Research Vol.31 No.1

Excessive manganese (Mn) in the brain promotes a variety of abnormal behaviors, including memory deficits, decreased motor skills and psychotic behavior resembling Parkinson’s disease. Hereditary hemochromatosis (HH) is a prevalent genetic iron overload disorder worldwide. Dysfunction in HFE gene is the major cause of HH. Our previous study has demonstrated that olfactory Mn uptake is altered by HFE deficiency, suggesting that loss of HFE function could alter manganese-associated neurotoxicity. To test this hypothesis, Hfe-knockout (Hfe<SUP>?/?</SUP>) and wild-type (Hfe<SUP>+/+</SUP>) mice were intranasally-instilled with manganese chloride (MnCl₂ 5 ㎎/㎏) or water daily for 3 weeks and examined for memory function. Olfactory Mn diminished both short-term recognition and spatial memory in Hfe<SUP>+/+</SUP> mice, as examined by novel object recognition task and Barnes maze test, respectively. Interestingly, Hfe<SUP>?/?</SUP> mice did not show impaired recognition memory caused by Mn exposure, suggesting a potential protective effect of Hfe deficiency against Mn-induced memory deficits. Since many of the neurotoxic effects of manganese are thought to result from increased oxidative stress, we quantified activities of anti-oxidant enzymes in the prefrontal cortex (PFC). Mn instillation decreased superoxide dismutase 1 (SOD1) activity in Hfe<SUP>+/+</SUP> mice, but not in Hfe<SUP>?/?</SUP> mice. In addition, Hfe deficiency up-regulated SOD1 and glutathione peroxidase activities. These results suggest a beneficial role of Hfe deficiency in attenuating Mn-induced oxidative stress in the PFC. Furthermore, Mn exposure reduced nicotinic acetylcholine receptor levels in the PFC, indicating that blunted acetylcholine signaling could contribute to impaired memory associated with intranasal manganese. Together, our model suggests that disrupted cholinergic system in the brain is involved in airborne Mn-induced memory deficits and loss of HFE function could in part prevent memory loss via a potential up-regulation of anti-oxidant enzymes in the PFC.

Loss of Hfe Function Reverses Impaired Recognition Memory Caused by Olfactory Manganese Exposure in Mice

Ye, Qi,Kim, Jonghan Korean Society of ToxicologyKorea Environmental Mu 2015 Toxicological Research Vol.31 No.1

Excessive manganese (Mn) in the brain promotes a variety of abnormal behaviors, including memory deficits, decreased motor skills and psychotic behavior resembling Parkinson's disease. Hereditary hemochromatosis (HH) is a prevalent genetic iron overload disorder worldwide. Dysfunction in HFE gene is the major cause of HH. Our previous study has demonstrated that olfactory Mn uptake is altered by HFE deficiency, suggesting that loss of HFE function could alter manganese-associated neurotoxicity. To test this hypothesis, Hfe-knockout ($Hfe^{-/-}$) and wild-type ($Hfe^{+/+}$) mice were intranasally-instilled with manganese chloride ($MnCl_2$ 5 mg/kg) or water daily for 3 weeks and examined for memory function. Olfactory Mn diminished both short-term recognition and spatial memory in $Hfe^{+/+}$ mice, as examined by novel object recognition task and Barnes maze test, respectively. Interestingly, $Hfe^{-/-}$ mice did not show impaired recognition memory caused by Mn exposure, suggesting a potential protective effect of Hfe deficiency against Mn-induced memory deficits. Since many of the neurotoxic effects of manganese are thought to result from increased oxidative stress, we quantified activities of anti-oxidant enzymes in the prefrontal cortex (PFC). Mn instillation decreased superoxide dismutase 1 (SOD1) activity in $Hfe^{+/+}$ mice, but not in $Hfe^{-/-}$ mice. In addition, Hfe deficiency up-regulated SOD1 and glutathione peroxidase activities. These results suggest a beneficial role of Hfe deficiency in attenuating Mn-induced oxidative stress in the PFC. Furthermore, Mn exposure reduced nicotinic acetylcholine receptor levels in the PFC, indicating that blunted acetylcholine signaling could contribute to impaired memory associated with intranasal manganese. Together, our model suggests that disrupted cholinergic system in the brain is involved in airborne Mn-induced memory deficits and loss of HFE function could in part prevent memory loss via a potential up-regulation of anti-oxidant enzymes in the PFC.

에너지효율성과 재생 에너지 정책 설계

Ye Qi,김민철(번역자),최은영(번역자) 강원대학교 비교법학연구소 2013 환경법과 정책 Vol.11 No.-

이 논문은 멕시코와 중국의 GHG 방출량의 감축(mitigation)에 관한 국가전략 비교 연구이다. 국제적인 약조, 광범위한 경제의 행위자의 내부이해관계의 처분, 정책결정과 기관의 대대로 내려오는 전통 사이의 상호작용의 중요성을 특히 경제발전과 중앙-지방정부 사이의 관계속에서 주-중심(State-centered)으로 분석한다. 이 연구는 기후 변화 정책을 분석을 위하여 효율성에 의하여 집단을 분류하지는 않았으나 개발도상국의 기후 변화 정책 결정을 위해 제반환경과 여건에 대해 연구하였고, 국제 제안 속에서 일반적인 최적 정책 선택, 다른 국가 케이스에 존재할 수 있는 어떤 정치적이고 경제적인 단체의 관련성을 분석하였다. 본 연구는 자유화와 정부조치에서 대대로 내려오는 전통 관습이 경제 행위자의 결정과 관리에 효과적으로 연계될 국가의 능력을 저해시킬 수 있음을 지적한다. 이러한 규칙적인 연관성은 국가간의 잘 맞는 부분을 잘 되지 못하게끔 만들어 경제적으로 효율적인 해답들을 추구하는 것을 저해한다. 중앙 정부에 의해 채택된 안건에 장착되는 지방자치단체를 위한 유인 시스템과의 관련성은 자연스러운 현상이다. This essay compares national strategies on mitigation of GHG emissions for Mexico and China. This state-centered analysis stresses the importance of the interaction between international commitments, the disposition of internal interest of economy-wide actors, and the legacies of policy making and institutions, particularly in relation to economic development and central ? local government relations. This research does not attempt to classify institutions according to their effectives to foster climate change policies, but rather explores specific circumstances for climate change policy making on developing countries. Contrary to international proposal to find a generic optimal policy choice, the research explored the relevance of certain political and economic institutions that can be present in other national cases. It shows that the legacies on liberalization and state retreat undermine the state ability to effectively engage with the economic actors on decisions and management. Likewise regular engagement with them undermines the state affinity towards pursuing economic efficient solutions. The relevance of adequate system of incentives for local government to engage in an agenda that is, by nature, adopted by the central government.

A virtual-sample technology based artificial-neural-network for a complex data analysis in a glass-ceramic system

Wen Qi-Ye,Zhang Huai-Wu,Yang Qing-Hui,Zhang Pei-Xin 한양대학교 세라믹연구소 2008 Journal of Ceramic Processing Research Vol.9 No.4

Artificial neural network has becoming a mainstream technology in the domain of complex materials data analysis. Based on a slag glass-ceramic system we brought forward a virtual sample technology to increase the training samples by fluctuating the content of main compositions in a proper small amplitude. Simulation results proved that a good virtual sample set can not only improve the network’s prediction ability considerably, but can also suppress the “overtraining” phenomenon. Therefore a virtual sample improved neural network model can learn the relationship from a small size experimental data set and give an accurate and stable prediction for the test samples. This is more helpful to the material data analysis and can facilitate the design and development for new materials. Artificial neural network has becoming a mainstream technology in the domain of complex materials data analysis. Based on a slag glass-ceramic system we brought forward a virtual sample technology to increase the training samples by fluctuating the content of main compositions in a proper small amplitude. Simulation results proved that a good virtual sample set can not only improve the network’s prediction ability considerably, but can also suppress the “overtraining” phenomenon. Therefore a virtual sample improved neural network model can learn the relationship from a small size experimental data set and give an accurate and stable prediction for the test samples. This is more helpful to the material data analysis and can facilitate the design and development for new materials.

日本人駐在員妻の海外生活における育兒ネットワ-ク -上海日本人集住マンションを事例に-

( You Qi Ye ) 동서대학교 일본연구센터 2014 次世代 人文社會硏究 Vol.10 No.-

Evaluation of Protective Immune Response Induced by a DNA Vaccine Encoding GRA8 against Acute Toxoplasmosis in a Murine Model

Jia-Qi Chu,Shuai Huang,Xuan-Yan Fan,Wei Ye,Rui Huang,Shi-Cai Ye,Cai-Yuan Yu,Wei-Yun Wu,Yu Zhou,Wei Zhou,Young-Ha Lee,Juan-Hua Quan 대한기생충학열대의학회 2018 The Korean Journal of Parasitology Vol.56 No.4

Lentivirus-Mediated Short-Hairpin RNA Targeting Protein Phosphatase 4 Regulatory Subunit 1 Inhibits Growth in Breast Cancer

Yuying Qi,Tinghui Hu,Kai Li,Renqing Ye,Zuodong Ye 한국유방암학회 2015 Journal of breast cancer Vol.18 No.3

Purpose: Protein phosphatase 4 regulatory subunit 1 (PP4R1), as an interaction partner of the catalytic serine/threonine-protein phosphatase 4 catalytic subunit has been shown to involve in cellular processes and nuclear factor κB signaling. However, the functions of PP4R1 in human breast cancers remain unclear. This study is designed to explore the effect of PP4R1 knockdown on the biological characteristics of breast cancer cells. Methods: A lentivirus-mediated short hairpin RNA (shRNA) was designed to knockdown the expression of PP4R1 in ZR-75-30 breast cancer cells. The efficiency of lentivirus-mediated shRNA infection was determined using fluorescence microscopy to observe lentivirus-mediated green fluorescent protein expression and confirmed to be over 80%. PP4R1 expression in infected ZR-75-30 cells was detected by quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation and colony formation ability were measured by 3-(4,5-dimethyl- 2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony formation assay, respectively. Flow cytometry was used to measure cell cycle progression and cell apoptosis. In addition, apoptosis makers, including poly-ADP-ribose polymerase (PARP) and Caspase-3, were investigated in PP4R1- silenced ZR-75-30 cells by western blot assay. Results: We successfully constructed lentivirus-mediated shRNA to target PP4R1 in ZR-75-30 cells. MTT assay and colony formation assay showed the loss of PP4R1 suppressed the proliferation of ZR-75-30 cells. Flow cytometry analysis indicated cell cycle arrest and increased cell apoptosis in PP4R1 knockdown cells. Further, the apoptosis response in cells depleted of PP4R1 was illustrated by downregulation of PARP and upregulation of Caspase- 3. Conclusion: Our results suggest that PP4R1 could promote breast cancer cell proliferation and might play a vital role in breast cancer occurrence.

Roles of E-Cadherin (CDH1) Genetic Variations in Cancer Risk: a Meta-analysis

Deng, Qi-Wen,He, Bang-Shun,Pan, Yu-Qin,Sun, Hui-Ling,Xu, Ye-Qiong,Gao, Tian-Yi,Li, Rui,Song, Guo-Qi,Wang, Shu-Kui Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8

E-Cadherin (CDH1) genetic variations may be involved in invasion and metastasis of various cancers by altering gene transcriptional activity of epithelial cells. However, published studies on the association of CDH1 gene polymorphisms and cancer risk remain contradictory, owing to differences in living habits and genetic backgrounds. To derive a more better and comprehensive conclusion, the present meta-analysis was performed including 57 eligible studies of the association between polymorphisms of CDH1 gene promoter -160 C>A, -347 G>GA and 3'-UTR +54 C>T and cancer risk. Results showed that these three polymorphisms of CDH1 were significantly associated with cancer risk. For -160 C>A polymorphism, -160A allele carriers (CA and CA+AA) had an increased risk of cancer compared with the homozygotes (CC), and the similar result was discovered for the -160A allele in the overall analyses. In the subgroup analyses, obvious elevated risk was found with -160A allele carriers (AA, CA, CA+AA and A allele) for prostate cancer, while a decreased colorectal cancer risk was shown with the AA genotype. For the -347 G>GA polymorphism, the GAGA genotype was associated with increased cancer risk in the overall analysis with homozygous and recessive models. In addition, results of subgroup analysis indicated that the elevated risks were observed in colorectal cancer and Asian descendants. For +54 C>T polymorphism, a decreased risk of cancer was found in heterozygous, dominant and allele models. Moreover, +54T allele carriers (CT, CT+TT genotype and T allele) showed a potential protective factor in gastric cancer and Asian descendants.