http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Identification of differentially-expressed genes by DNA methylation in cervical cancer
LEE, HEUN-SIK,YUN, JUN HO,JUNG, JUNGHEE,YANG, YOUNG,KIM, BONG-JO,LEE, SUNG-JONG,YOON, JOO HEE,MOON, YONG,KIM, JEONG-MIN,KWON, YONG-IL D.A. Spandidos 2015 Oncology letters Vol.9 No.4
<P>To identify novel cervical cancer-related genes that are regulated by DNA methylation, integrated analyses of genome-wide DNA methylation and RNA expression profiles were performed using the normal and tumor regions of tissues from four patients; two with cervical cancer and two with pre-invasive cancer. The present study identified 19 novel cervical cancer-related genes showing differential RNA expression by DNA methylation. A number of the identified genes were novel cervical cancer-related genes and their differential expression was confirmed in a publicly available database. Among the candidate genes, the epigenetic regulation and expression of three genes, <I>CAMK2N1</I>, <I>ALDH1A3</I> and <I>PPP1R3C</I>, was validated in HeLa cells treated with a demethylating reagent using methylation-specific polymerase chain reaction (PCR) and quantitative PCR, respectively. From these results, the expression of the <I>CAMK2N1</I>, <I>ALDH1A3</I> and <I>PPP1R3C</I> genes are were shown to be suppressed in cervical cancers by DNA methylation. These genes may be involved in the progression or initiation of cervical cancer.</P>
Lee, Seong Hyuk,Sim, Hyung Sub,Lee, Junghee,Kim, Jong Min,Shin, Young Eui The Japan Institute of Metals 2006 MATERIALS TRANSACTIONS Vol.47 No.11
<P>This article investigates numerically carrier-phonon interaction and nonequilibrium energy transfer in direct and indirect bandgap semiconductors during sub-picosecond pulse laser irradiation and also examines the recombination effects on energy transport from the microscopic viewpoint. In addition, the influence of laser fluence and pulse duration is studied by using the self-consistent three-temperature model, which involves carriers, longitudinal optical phonons, and acoustic phonons. It is found that a substantial non-equilibrium state exists between carriers and phonons during short pulse laser irradiation because of time scale difference between the relaxation time and the pulse duration. It is clear that the two-peak structure in carrier temperature exists and it depends mainly on laser pulses, fluences, and recombination processes. During laser irradiation, in particular, the Auger recombination for Si becomes dominant due to the increase in the carrier number density, whereas for GaAs, the Auger recombination process can be ignored due to an abrupt increase in SRH recombination rates at the initial stages of laser exposure.</P>
Lee, Junghee,Kannagi, Mari,Ferrante, Robert J.,Kowall, Neil W.,Ryu, Hoon Federation of American Society for Experimental Bi 2009 The FASEB Journal Vol.23 No.6
<P>Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by selective degeneration of motor neurons and glial activation. Cell-specific transcriptional regulation induced by oxidative stress may contribute to the survival and activation of astrocytes in the face of motor neuron death. In the present study, we demonstrate an age-dependent increase in Bcl-xL and Ets-2 immunoreactivity that correlates with an increase of glial fibrillary acidic protein (GFAP)-positive cells in the ventral horn of the spinal cord in both ALS transgenic mice [mutant SOD1 (G93A)] and affected humans. Chromatin immunoprecipitation (ChIP) analysis verified that Ets-2 preferentially occupies the Ets-2 binding element in the promoter of Bcl-xL in primary astrocytes under oxidative stress conditions as well as in G93A spinal cords. Ets-2 small-interfering RNA down-regulated the transcriptional activity of Bcl-xL. In primary glial cultures, Bcl-xL overexpression and mutant SOD1 (G93A) both conferred resistance to oxidative stress-induced cell death. Our findings suggest that Ets-2 transcription factor activation of Bcl-xL gene may protect glia from constitutive oxidative stress that is thought to be a key mechanism contributing to the pathogenesis of ALS. This survival pathway may contribute to the glial survival and activation seen in the spinal cord of ALS patients.</P>
Lee, Junghee,Hwang, Yu Jin,Kim, Yunha,Lee, Min Young,Hyeon, Seung Jae,Lee, Soojin,Kim, Dong Hyun,Jang, Sung Jae,Im, Hyoenjoo,Min, Sun-Joon,Choo, Hyunah,Pae, Ae Nim,Kim, Dong Jin,Cho, Kyung Sang,Kowall Springer Verlag 2017 Acta neuropathologica Vol.134 No.5
<P>Huntington's disease (HD) is an autosomal-dominant inherited neurological disorder caused by expanded CAG repeats in exon 1 of the Huntingtin (HTT) gene. Altered histone modifications and epigenetic mechanisms are closely associated with HD suggesting that transcriptional repression may play a pathogenic role. Epigenetic compounds have significant therapeutic effects in cellular and animal models of HD, but they have not been successful in clinical trials. Herein, we report that dSETDB1/ESET, a histone methyltransferase (HMT), is a mediator of mutant HTT-induced degeneration in a fly HD model. We found that nogalamycin, an anthracycline antibiotic and a chromatin remodeling drug, reduces trimethylated histone H3K9 (H3K9me3) levels and pericentromeric heterochromatin condensation by reducing the expression of Setdb1/Eset. H3K9me3-specific ChIP-on-ChIP analysis identified that the H3K9me3-enriched epigenome signatures of multiple neuronal pathways including Egr1, Fos, Ezh1, and Arc are deregulated in HD transgenic (R6/2) mice. Nogalamycin modulated the expression of the H3K9me3-landscaped epigenome in medium spiny neurons and reduced mutant HTT nuclear inclusion formation. Moreover, nogalamycin slowed neuropathological progression, preserved motor function, and extended the life span of R6/2 mice. Together, our results indicate that modulation of SETDB1/ESET and H3K9me3-dependent heterochromatin plasticity is responsible for the neuroprotective effects of nogalamycin in HD and that small compounds targeting dysfunctional histone modification and epigenetic modification by SETDB1/ESET may be a rational therapeutic strategy in HD.</P>
<small>FeSSD</small>: A Fast Encrypted SSD Employing On-Chip Access-Control Memory
Lee, Junghee,Ganesh, Kalidas,Lee, Hyuk-Jun,Kim, Youngjae IEEE 2017 IEEE computer architecture letters Vol.16 No.2
<P>Cryptography is one of the most popular methods for protecting data stored in storage devices such as solid-state drives (SSDs). To maintain integrity of data, one of the popular techniques is that all incoming data are encrypted before they are stored, however, in this technique, the encryption overhead is non-negligible and it can increase I/O service time. In order to mitigate the negative performance impact caused by the data encryption, a write buffer can be used to hide the long latency by encryption. Using the write buffer, incoming unencrypted data can be immediately returned as soon as they are written in the buffer. They will get encrypted and synchronized with flash memory. However, if the write buffer itself is not encrypted, unencrypted secret data might leak through this insecure write buffer. On the other hand, if the entire write buffer is fully encrypted, it incurs significant performance overhead. To address this problem, we propose an on-chip access control memory (ACM) and presents a fast encrypted SSD, called <SMALL>FeSSD</SMALL> that implements a secure write buffering mechanism using the ACM. The ACM does not require a memory-level full encryption mechanism, thus not only solving the unencrypted data leaking problem, but also offering relatively fast I/O service. Our simulation results show that the I/O response time of <SMALL>FeSSD</SMALL> can be improved by up to 56 percent over a baseline where encrypted data are stored in the normal write buffer.</P>
Lee, Hye‐,Mi,Kang, Junghee,Lee, Sung Joong,Jo, Eun‐,Kyeong Wiley Subscription Services, Inc., A Wiley Company 2013 GLIA Vol.61 No.3
<P><B>Abstract</B></P><P>The inflammasome is a multimolecular complex that orchestrates the activation of proinflammatory caspases and interleukin (IL)‐1β, which is generally increased in the cerebrospinal fluids of patients with tuberculous meningitis. However, it has not been clarified whether mycobacteria can activate the inflammasome and induce IL‐1β maturation in microglia. In this study, we found that the priming of primary murine microglial cells with conditioned media from cultures of macrophages infected with <I>Mycobacterium tuberculosis</I> (Mtb) led to robust activation of caspase‐1 and IL‐1β secretion after Mtb stimulation. Potassium efflux and the lysosomal proteases cathepsin B and cathepsin L were required for the Mtb‐induced caspase‐1 activation and maturation of IL‐1β production in primed microglia. Mtb‐induced IL‐1β maturation was also found to depend on the nucleotide binding and oligomerization of domain‐like receptor family pyrin domain containing 3 protein (NLRP3) and apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC), as well as the generation of mitochondrial reactive oxygen species (ROS). Notably, the priming of microglia with tumor necrosis factor‐α or oncostatin M resulted in caspase‐1 cleavage and IL‐1β secretion in response to Mtb. Moreover, dexamethasone, as an adjunctive therapy for patients of tuberculous meningitis, significantly reduced the Mtb‐induced maturation of IL‐1β through inhibition of mitochondrial ROS generation. Collectively, these data suggest that Mtb stimulation induces activation of the microglial NLRP3 inflammasome (composed of NLRP3, ASC, and cysteine protease caspase‐1) through microglia–leukocyte interactions as a priming signal, and that dexamethasone decreases inflammasome activation through inhibition of ROS of mitochondrial origin. © 2012 Wiley Periodicals, Inc.</P>
MST1 functions as a key modulator of neurodegeneration in a mouse model of ALS
Lee, Jae Keun,Shin, Jin Hee,Hwang, Sang Gil,Gwag, Byoung Joo,McKee, Ann C.,Lee, Junghee,Kowall, Neil W.,Ryu, Hoon,Lim, Dae-Sik,Choi, Eui-Ju National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.29
<P>Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder characterized by loss of motor neurons. Dominant mutations in the gene for superoxide dismutase 1 (SOD1) give rise to familial ALS by an unknown mechanism. Here we show that genetic deficiency of mammalian sterile 20-like kinase 1 (MST1) delays disease onset and extends survival in mice expressing the ALS-associated G93A mutant of human SOD1. SOD1(G93A) induces dissociation of MST1 from a redox protein thioredoxin-1 and promotes MST1 activation in spinal cord neurons in a reactive oxygen species–dependent manner. Moreover, MST1 was found to mediate SOD1(G93A)-induced activation of p38 mitogen-activated protein kinase and caspases as well as impairment of autophagy in spinal cord motoneurons of SOD1(G93A) mice. Our findings implicate MST1 as a key determinant of neurodegeneration in ALS.</P>