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Amyloid β‐induced elevation of O‐GlcNAcylated c‐Fos promotes neuronal cell death
Choi, Heesun,Kim, Chaeyoung,Song, Hyundong,Cha, Moonx2010,Yong,Cho, Hyun Jin,Son, Sung Min,Kim, Haeng Jun,Mook‐,Jung, Inhee BLACKWELL PUBLISHING 2019 Aging Cell Vol.18 No.1
<P><B>Abstract</B></P><P>Alzheimer's disease (AD) is an age‐related neurodegenerative disease characterized by progressive memory loss resulting from cumulative neuronal cell death. O‐linked β‐N‐acetyl glucosamine (O‐GlcNAc) modification of the proteins reflecting glucose metabolism is altered in the brains of patients with AD. However, the link between altered O‐GlcNAc modification and neuronal cell death in AD is poorly understood. Here, we examined the regulation of O‐GlcNAcylation of c‐Fos and the effects of O‐GlcNAcylated c‐Fos on neuronal cell death during AD pathogenesis. We found that amyloid beta (Aβ)‐induced O‐GlcNAcylation on serine‐56 and 57 of c‐Fos was resulted from decreased interaction between c‐Fos and O‐GlcNAcase and promoted neuronal cell death. O‐GlcNAcylated c‐Fos increased its stability and potentiated the transcriptional activity through higher interaction with c‐Jun, resulting in induction of Bim expression leading to neuronal cell death. Taken together, Aβ‐induced O‐GlcNAcylation of c‐Fos plays an important role in neuronal cell death during the pathogenesis of AD.</P>
Lee, Kwangx2010,Ho,Kim, Sangx2010,Mook,Jeong, Huisu,Pak, Yusin,Song, Hui,Park, Jeongpil,Lim, Keonx2010,Hee,Kim, Jaex2010,Hoon,Kim, Youn Sang,Ko, Heung Cho,Kwon, Il Keun,Jung, Gunx2010,Young WILEY‐VCH Verlag 2013 ADVANCED MATERIALS Vol.25 No.23
<P><B>All‐solution‐processed transparent thin film transistors (TTFTs)</B> are demonstrated with silver grid source/drain electrodes, which are fabricated by printing and subsequent silver nanoparticles solution coating, which allows continuous processing without using high vacuum systems. The silver grid electrode shows a reasonable transmittance in visible range, moderate electrical conductance and mechanical strength. The TTFTs are employed to drive liquid crystal cells and demonstrate a successful switching operation.</P>
Transfer‐Free Growth of Few‐Layer Graphene by Self‐Assembled Monolayers
Shin, Hyeonx2010,Jin,Choi, Won Mook,Yoon, Seonx2010,Mi,Han, Gang Hee,Woo, Yun Sung,Kim, Eun Sung,Chae, Seung Jin,Li, Xiangx2010,Shu,Benayad, Anass,Loc, Duong Dinh,Gunes, Fethullah,Lee, Young Hee WILEY‐VCH Verlag 2011 Advanced Materials Vol.23 No.38
<P><B>Graphene layers are directly synthesized</B> <B>on an oxide substrate</B> without transfer. The catalytic structure aids graphene formation without the vaporization of a self‐assembled monolayer (SAM) material and induces direct growth of graphene on the substrate. Film uniformity and the number of graphene layers are modulated. The catalytic structure and growth process provide a robust method for transfer‐free graphene growth with uniform thickness. </P>
SIRT3 deregulation is linked to mitochondrial dysfunction in Alzheimer's disease
Lee, Junghee,Kim, Yunha,Liu, Tian,Hwang, Yu Jin,Hyeon, Seung Jae,Im, Hyeonjoo,Lee, Kyungeun,Alvarez, Victor E.,McKee, Ann C.,Um, Soox2010,Jong,Hur, Manwook,Mook‐,Jung, Inhee,Kowall, Neil W.,Ry John Wiley and Sons Inc. 2018 Aging cell Vol.17 No.1
<P><B>Summary</B></P><P>Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Sirtuins (SIRT, silent mating type information regulation 2 homolog in yeast) are NAD‐dependent histone deacetylases involved in aging and longevity. The objective of this study was to investigate the relationship between SIRT3 and mitochondrial function and neuronal activity in AD. SIRT3 mRNA and protein levels were significantly decreased in AD cerebral cortex, and Ac‐p53 K320 was significantly increased in AD mitochondria. SIRT3 prevented p53‐induced mitochondrial dysfunction and neuronal damage in a deacetylase activity‐dependent manner. Notably, mitochondrially targeted p53 (mito‐p53) directly reduced mitochondria DNA‐encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. ND2 and ND4 gene expressions were significantly decreased in patients with AD. p53‐ChIP analysis verified the presence of p53‐binding elements in the human mitochondrial genome and increased p53 occupancy of mitochondrial DNA in AD. SIRT3 overexpression restored the expression of ND2 and ND4 and improved mitochondrial oxygen consumption by repressing mito‐p53 activity. Our results indicate that SIRT3 dysfunction leads to p53‐mediated mitochondrial and neuronal damage in AD. Therapeutic modulation of SIRT3 activity may ameliorate mitochondrial pathology and neurodegeneration in AD.</P>
Kim, Yonghyun,Kang, Eun Seok,Jang, Hak Chul,Kim, Dong Jun,Oh, Taekeun,Kim, Eun Sook,Kim, Nanx2010,Hee,Choi, Kyung Mook,Kim, Sungx2010,Rae,You, JiYoung,Kim, Sex2010,Jin,Lee, Moonx2010,Kyu Blackwell Publishing Ltd 2019 Diabetes, obesity & metabolism Vol.21 No.3
<P><B>Aim</B></P><P>To assess the efficacy and safety of add‐on therapy with the dipeptidyl peptidase‐4 inhibitor teneligliptin compared with sitagliptin in patients with type 2 diabetes (T2DM) inadequately controlled with metformin and glimepiride.</P><P><B>Materials and Methods</B></P><P>This was a phase 3, randomized, double‐blind, non‐inferiority study of adult Korean subjects with T2DM (n = 201), with HbA1c ranging from 7.0% to 11.0%, on stable doses of metformin plus glimepiride. Subjects were randomized in a 1:1 fashion to receive either oral teneligliptin 20 mg or sitagliptin 100 mg for 24 weeks. The primary endpoint was change from baseline in HbA1c.</P><P><B>Results</B></P><P>At baseline, mean age was 60.56 ± 9.41 years, body mass index was 25.23 ± 2.85 kg/m<SUP>2</SUP> and HbA1c was 8.11% ± 0.79%. At 24 weeks, both groups achieved significant reductions from baseline in HbA1c (teneligliptin, −1.03% ± 0.10% [<I>P</I> < 0.0001]; sitagliptin, −1.02% ± 0.10% [<I>P</I> < 0.0001]). The inter‐group difference was −0.01% (95% confidence interval [CI]: −0.28, 0.26; <I>P</I> = 0.9497); the upper limit of the 95% CI was within the preset limit for non‐inferiority (0.4%). There were no significant differences between groups in the proportion of patients achieving HbA1c targets, or changes from baseline in fasting plasma glucose, body weight or lipid levels at 24 weeks. Rates of adverse events (teneligliptin, n = 63 [61.76%]; sitagliptin, n = 61 [62.24%]; <I>P</I> = 0.9442) and hypoglycaemia (teneligliptin, n = 32 [31.37%]; sitagliptin, n = 28 [28.57%]; <I>P</I> = 0.6656) were similar.</P><P><B>Conclusion</B></P><P>Teneligliptin was non‐inferior to sitagliptin in the context of triple therapy for T2DM and is an important option in this setting.</P>
A cell‐free extract from human adipose stem cells protects mice against epilepsy
Jeon, Daejong,Chu, Kon,Lee, Soonx2010,Tae,Jung, Keunx2010,Hwa,Kang, Kyungx2010,Mook,Ban, Jaex2010,Joon,Kim, Soyun,Seo, Jin Soo,Won, Chongx2010,Hyun,Kim, Manho,Lee, Sang Kun,Roh, Jaex2010,K Blackwell Publishing Ltd 2011 Epilepsia Vol.52 No.9
<P><B>Summary</B></P><P><B>Purpose: </B> Stem cell–based therapies are being considered for various neurologic diseases, such as epilepsy. Recent studies have suggested that some effects of transplanted stem cells are due to bystander effects that modulate the host environment, rather than direct effects of cell replacement. The extract from human adipose stem cells (ASCs) that secrete multiple growth factors including cytokines and chemokines may be a potential source of bystander effects for the treatment of epilepsy, in which inflammation is thought to play an important role. Here, we investigated the effects of a cytosolic extract of human ASCs (ASCs‐E) in a mouse model of epilepsy.</P><P><B>Methods: </B> Human ASCs‐E, boiled ASCs‐E, or fibroblast‐extract (fibroblast‐E) was intraperitoneally administrated to C57BL/6 mice 15 min before pilocarpine‐induced status epilepticus (SE) or during chronic epileptic stage. Blood–brain barrier (BBB) leakage was evaluated by measuring Evans blue dye extravasation. Spontaneous recurrent seizure (SRS) was investigated by long‐term video–electroencephalography (EEG) monitoring. The mice performed elevated plus maze, open‐field, light/dark transition, and novel object recognition tasks.</P><P><B>Key Findings: </B> Acute application of human ASCs‐E before SE led to earlier attenuation of seizure spike activities after treatment with diazepam, reduction of BBB leakage, and inhibition of the development of epilepsy. Human ASCs‐E treatment (for 7 days) during the chronic epileptic stage suppressed SRS and reduced abnormal epileptic behavioral phenotypes. However, neither boiled ASCs‐E nor fibroblast‐E had any effects in the experimental epilepsy model.</P><P><B>Significance: </B> Our results demonstrate that human ASCs‐E prevents or inhibits epileptogenesis and SRS in mice. They also suggest a stem cell–based, noninvasive therapy for the treatment of epilepsy.</P>
Tailored Materials for High‐Performance MgB<sub>2</sub> Wire
Kim, Jung Ho,Oh, Sangjun,Kumakura, Hiroaki,Matsumoto, Akiyoshi,Heo, Yoonx2010,Uk,Song, Kyeongx2010,Se,Kang, Yongx2010,Mook,Maeda, Minoru,Rindfleisch, Matt,Tomsic, Mike,Choi, Seyong,Dou, Shi Xue WILEY‐VCH Verlag 2011 Advanced Materials Vol.23 No.42
<P><B>Carbon‐encapsulated crystalline boron nanopowder</B> and coarse magnesium powder are used as inexpensive tailored starting materials for the fabrication of high‐performance MgB<SUB>2</SUB> superconducting wire. A low sintering temperature leads to a high critical current density, as a result of nanometer‐sized boron powder, surface oxidation preclusion by carbon encapsulation, and grain alignment by elongated magnesium coarse powder.</P>
Kim, Ki Seok,Song, Hui,Nam, Sang Hoon,Kim, Sangx2010,Mook,Jeong, Huisu,Kim, Won Bae,Jung, Gun Young WILEY‐VCH Verlag 2012 Advanced Materials Vol.24 No.6
<P><B>A periodically aligned submicron ZnO hemispheres array was embedded into a TiO<SUB>2</SUB> nanoparticulate thin film</B> (thickness; ca. 12 μm) as a photoanode for dye‐sensitized solar cells (DSSCs). The ZnO hemisphere array provided light scattering centers that excited more dyes and direct electron pathways to the electrodes, which is beneficial for high efficiency DSSCs.</P>
Prediction Model for Transmembrane Pressure in a Submerged Hollow‐Fiber Microfiltration Membrane
Lee, Hwanx2010,Mook,Lee, Chungx2010,Hak,Chung, Kun,Lee, Sangho Taylor Francis 2005 Separation science and technology Vol.39 No.8
<P>In this study, a model equation was derived for a submerged, hollow‐fiber microfiltration (MF) membrane under constant flux. The validity of model equation was examined in two aspects: different feed water concentration and membrane pore size. When the concentration of starch solution (feed water) was varied from 1.5 to 9.0 g/L, the model equation predicted transmembrane pressure (TMP) variation at the precision of 99% within that range of concentration. In the cases of a different nominal membrane pore size (0.1 and 0.4 µm), it was capable of predicting TMP variation in a good manner. From experimental TMP data, it was ascertained that different pore sizes of membrane hardly affected filtration time. At the same time, TMP, flux, and total resistance distributions along the membrane length, which cannot be measured directly, could be calculated using the model equation.</P>
ERK1/2 is an endogenous negative regulator of the γsecretase activity
Kim, Sux2010,Kyoung,Park, Hyunx2010,Jung,Hong, Hyun Seok,Baik, Eun Joo,Jung, Min Whan,Mook‐,Jung, Inhee Federation of American Society for Experimental Bi 2006 The FASEB Journal Vol.20 No.1
<P>As an essential protease in the generation of amyloid beta, gamma-secretase is believed to play an important role in the pathogenesis of Alzheimer's disease. Although a great deal of progress has been made in identifying the components of gamma-secretase complex, the endogenous regulatory mechanism of gamma-secretase is unknown. Here we show that gamma-secretase is endogenously regulated via extracellular signal regulated MAP kinase (ERK) 1/2-dependent mitogen-activated protein kinase (MAPK) pathway. The inhibition of ERK1/2 activity, either by a treatment with a MEK inhibitor or an ERK knockdown transfection, dramatically increased gamma-secretase activity in several different cell types. JNK or p38 kinase inhibitors had little effect, indicating that the effect is specific to ERK1/2-dependent MAPK pathway. Conversely, increased ERK1/2 activity, by adding purified active ERK1/2 or EGF-induced activation of ERK1/2, significantly reduced gamma-secretase activity, demonstrating down-regulation of gamma-secretase activity by ERK1/2. Whereas gamma-secretase expression was not affected by ERK1/2, its activity was enhanced by phosphatase treatment, indicating that ERK1/2 regulates gamma-secretase activity by altering the pattern of phophorylation. Among the components of isolated gamma-secretase complex, only nicastrin was phosphorylated by ERK1/2, and it precipitated with ERK1/2 in a co-immunoprecipitation assay, which suggests binding between ERK1/2 and nicastrin. Our results show that ERK1/2 is an endogenous regulator of gamma-secretase, which raises the possibility that ERK1/2 down-regulates gamma-secretase activity by directly phosphorylating nicastrin.</P>