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Shin, Hyun Joo,Jeon, Byeong Tak,Kim, Jungmee,Jeong, Eun Ae,Kim, Myeung Ju,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Springer 2012 Journal of neural transmission Vol.119 No.6
<P>Calcineurin (CaN)-mediated excitotoxicity impairs 관-aminobutyric acid (GABA) transmission and induces neuronal apoptosis. Ca(2+)-dependent K(+)-Cl(-) cotransporter 2 (KCC2) participates in GABAergic inhibitory transmission. However, the mechanism by which CaN mediates GABA receptor-mediated KCC2 in seizures is not fully understood. In the present study, we investigated the altered expression of KCC2 and the effects of the CaN inhibitor FK506 on KCC2 expression in the mouse hippocampus following kainic acid (KA) treatment. FK506 was injected twice 24 h and 30 min before KA treatment and then mice were treated with KA and killed 2 days later. FK506 had anticonvulsant effect on KA-induced seizure activities. CaN cleavage was evident in the hippocampus 24 h after KA treatment. FK506 pretreatment blocked the truncation of CaN in the KA-treated hippocampus. Cresyl violet and TUNEL staining showed that FK506 prevented KA-induced hippocampal cell death. In particular, Western blot analysis showed that KCC2 expression was time dependent, with a peak at 6 h and a return to decreased levels at 48 h, whereas FK506 pretreatment inhibited the KA-induced decrease in KCC2 expression in the hippocampus. Immunofluorescence showed that FK506 pretreatment protected the loss of inhibitory GABAergic KCC2-expressing neurons following KA treatment. Taken together, these results provide evidence that altered KCC2 expression may be associated with Ca(2+)-mediated seizure activity and indicate that neuron-specific KCC2 may be involved in neuroprotection after seizures.</P>
Effects of Multidisciplinary Health Promotion Program Among Children in Community Childcare Center
Yerin Kim,Gyeong Seob Shin,Jungwon Park,Minji Kang,Kumhee Son,Yoon Myung Kim,Park Kyung-Hee,Hyunjung Lim 한국임상영양학회 2024 Clinical Nutrition Research Vol.13 No.1
In this study, the effects of a 12-month multidisciplinary education program on the health status, dietary quality, and eating habits of children and adolescents attending community childcare centers were investigated. A total of 88 participants aged 7 to 17 years from 7 community childcare centers in Gyeonggi-do were enrolled. The intervention consisted of 12 multidisciplinary education sessions covering topics such as nutrition, exercise, and psychological education. All participants received the same education, and the effectiveness of the program was evaluated by categorizing them into a high participation group (HPG) and a low participation group (LPG) based on their participation rates. After intervention, in physical activities, moderate-intensity exercise was significantly reduced in the LPG, and there was no significant difference in psychological parameters. However, notable differences were observed in nutritional data. After intervention, intakes of calorie, carbohydrate, protein, and fat were significantly increased in both groups, and in particular, the change was found to be greater in HPG. Additionally, dietary fiber intake compared to the 2015 Korean Dietary Reference Intakes was increased in both groups. Daily food intake also increased dietary fiber intake in HPG, and meat and fruit intake was increased in LPG. In the nutrition quotient, there was a significant difference in HPG’s pre- and post-scores in the diversity category, and in nutrient adequacy ratio (NAR), the NAR of phosphorus was increased in both groups. The findings of this study suggest that multidisciplinary education implemented at community childcare centers primarily enhanced nutrition-related factors rather than physical activity or psychological aspects.
Yi, Chin-Ok,Jeon, Byeong Tak,Shin, Hyun Joo,Jeong, Eun Ae,Chang, Ki Churl,Lee, Jung Eun,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Korean Association of Anatomists 2011 Anatomy & Cell Biology Vol.44 No.3
<P>AMP-activated protein kinase (AMPK), an enzyme involved in energy homeostasis, regulates inflammatory responses, but its precise mechanisms are not fully understood. Recent evidence has shown that resveratrol (RES), an AMPK activator, reduces prostaglandin E<SUB>2</SUB> production in lipopolysaccharide (LPS)-treated microglia. Here, we examined the effect of RES on nuclear factor kappa B (NF-κB) dependent cyclooxygenase (COX)-2 activation in LPS-treated RWA 264.7 macrophages. We found that treatment with RES increased AMPK activation. AMPK and acetyl CoA carboxylase phosphorylation were attenuated in cells treated with LPS+RES, compared to cells treated with LPS alone. RES inhibited tumor necrosis factor (TNF)-α and TNF receptor 1 in LPS-treated cells. Finally, RES inhibited LPS-induced NF-κB translocation into the nucleus and COX-2 expression. Moreover, the effects of 5-aminoimidazole-4-carboxamide ribose and compound C were consistent with the effects of RES in LPS-treated cells. Taken together, these results suggest that the anti-inflammatory action of RES in RAW 264.7 macrophages is dependent on AMPK activation and is associated with inhibition of the LPS-stimulated NF-κB-dependent COX-2 signaling pathway.</P>
김주한 ( Kim Joo Han ),신윤미 ( Shin Yoon Mi ),엄경섭 ( Eom Gyeong Seob ) 한국정보처리학회 2017 한국정보처리학회 학술대회논문집 Vol.24 No.2
본 연구의 목적은 각양각색으로 증가하고 있는 현대인들의 개인 소지품들로 인해 비례적으로 증가되고 있는 물품 분실의 위험에서 착안하여, 기존의 어플리케이션 기반의 물품 분실 방지 및 분실 물품 추적 시스템에서 벗어나 스마트폰 분실 시에도 대처하기 위한 것이다. 본 시스템은 비콘을 활용한 실내 측위 시스템은 RSSI(Received Signal Strength Indicator) 측정값으로 대상과의 실제 거리를 추정하는 방식을 활용한다. 이를 통해 대상과의 추정 거리가 일정 값 이상이 될 경우 분실로 판단 하고, 분실 처리를 통해 대상을 찾을 수 있다. 본 논문은 2017 년 한이음 ICT 멘토링 프로젝트의 결과물입니다.
Lee, Ji Yeong,Jeon, Beong Tak,Shin, Hyun Joo,Lee, Dong Hoon,Han, Jae Yoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Springer 2009 JOURNAL OF NEURAL TRANSMISSION Vol.116 No.1
<P>Kainic acid (KA)-induced seizure induces the hippocampal cell death. There are reports that AMP-activated protein kinase (AMPK), which is an important regulator of energy homeostasis of cells, has been proposed as apoptotic molecule. In this study, we investigated the altered expression of AMPK cascade in the hippocampus of mice during KA-induced hippocampal cell death. Mice were killed at 2, 6, 24 or 48 h after KA (30 mg/kg) injection. Histological evaluation of KA-treated hippocampus revealed hippocampal cell death first at 6 h and appearing prominently by 48 h after KA injection. Immunoreactivity of Ca(2+)/calmodulin-dependent protein kinase kinasebeta (CaMKKbeta) was increased after KA treatment. In Western blot analysis, AMPK activation was increased 2 h after KA treatment. The proteins of downstream AMPK, including those of glucose transporter1 (GLUT1) and phosphorylation of Acetyl CoA Carboxylase (ACC) were increased in the hippocampus after KA treatment. These results indicate that sustained AMPK activation might be a mechanism by which KA-induced seizure causes hippocampal cell death of mice.</P>
Park, Jeongsook,Park, So Yun,Shin, Eunkyung,Lee, Sun Hee,Kim, Yoon Sook,Lee, Dong Hoon,Roh, Gu Seob,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Jeong, Bo-Young,Kim, Hwajin,Choi, Wan Sung Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.2
Differential transcription of the clusterin (CLU) gene yields two CLU isoforms, a nuclear form (nCLU) and a secretory form (sCLU), which play crucial roles in prostate tumorigenesis. Pro-apoptotic nCLU and anti-apoptotic sCLU have opposite effects and are differentially expressed in normal and cancer cells; however, their regulatory mechanisms at the transcriptional level are not yet known. Here, we examined the transcriptional regulation of nCLU in response to hypoxia. We identified three putative hypoxia response elements (HREs) in the human CLU promoter between positions -806 and +51 bp. Using a luciferase reporter, electrophoretic gel mobility shift, and chromatin immunoprecipitation assays, we further showed that hypoxia-inducible factor-$1{\alpha}$ (HIF-$1{\alpha}$) bound directly to these sites and activated transcription. Exposure to the hypoxia-mimetic compound $CoCl_2$, incubation under 1% $O_2$ conditions, or overexpression of HIF-$1{\alpha}$ enhanced nCLU expression and induced apoptosis in human prostate cancer PC3M cells. However, LNCaP prostate cancer cells were resistant to hypoxia-induced cell death. Methylation-specific PCR analysis revealed that the CLU promoter in PC3M cells was not methylated; in contrast, the CLU promoter in LNCap cells was methylated. Co-treatment of LNCaP cells with $CoCl_2$ and a demethylating agent promoted apoptotic cell death through the induction of nCLU. We conclude that nCLU expression is regulated by direct binding of HIF-$1{\alpha}$ to HRE sites and is epigenetically controlled by methylation of its promoter region.
Jeong, Eun Ae,Jeon, Byeong Tak,Shin, Hyun Joo,Kim, Nayoung,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Elsevier 2011 Experimental neurology Vol.232 No.2
<P><B>Abstract</B></P><P>Similar to fasting, the ketogenic diet (KD) has anti-inflammatory effects and protects against excitotoxicity-mediated neuronal cell death. Recent studies have shown that peroxisome proliferator-activated receptor (PPAR)γ has anti-inflammatory effects in seizure animal models. However, the exact mechanisms underlying the anti-inflammatory effects of the KD have not been determined for seizures. Here we investigated the effect of the KD and acetoacetate (AA) on neuroinflammation in a seizure animal model and glutamate-treated HT22 cells, respectively. Mice were fed the KD for 4weeks and sacrificed 2 or 6h after KA injection. The KD reduced hippocampal tumor necrosis factor alpha (TNF-α) levels and nuclear factor (NF)-κB translocation into the nucleus 2h after KA treatment. KD-induced PPARγ activation was decreased by KA in neurons as assessed by western blotting and immunofluorescence. Finally, the KD inhibited cyclooxygenase (COX)-2 and microsomal prostaglandin E<SUB>2</SUB> synthase-1 (mPGES-1) expression in the hippocampus 6h after KA treatment. AA treatment also protected against glutamate-induced cell death in HT22 cells by reducing TNF-α and PPARγ-mediated COX-2 expression. Thus, the KD may inhibit neuroinflammation by suppressing a COX-2-dependent pathway via activation of PPARγ by the KD or AA.</P> <P><B>Highlights</B></P><P>► Ketogenic diet (KD) attenuated neuroinflammation in the kainic acid (KA)-induced seizure mice. ► KD induces activation of PPARγ expression in the mouse hippocampus. ► KD inhibits NF-κB-mediated COX-2 expression in the KA-treated hippocampus.</P>