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Han, HyukSu,Lee, Jae Seok,Ryu, Jeong Ho,Kim, Kang Min,Jones, Jacob L.,Lim, Jiun,Guillemet-Fritsch, Sophie,Lee, Han Chan,Mhin, Sungwook American Chemical Society 2016 The Journal of Physical Chemistry Part C Vol.120 No.25
<P>Hopping motions in cobalt manganese spinel oxides with high cobalt concentration (CoxMn3-xO4, 2.3 <= x <= 2.7) are investigated in order to clarify the origin of unusual electrical behaviors as negative temperature coefficient (NTC) thermistors. Based on the resistance versus temperature (R-T) characteristics, hopping conduction mechanisms in MCO compounds (x = 2.3 and 2.5) are attributed to variable range hopping (VRH) motion with a parabolic distribution of the density of states (DOS) near the Fermi level. However, when Co content increases up to 2.7, transition in the hopping motion occurs from VRH to the nearest neighboring hopping (NNH) motion, which can be responsible for a huge increase of the resistance accompanied by decrease of the factor of thermal sensitivity (B value) in MCO compounds (x = 2.7). Also, hopping distance and activation energies for MCO (x = 2.3 and 2.5) compounds following VRH conduction are calculated as a function of temperature, indicating that higher B value observed in MCO (x = 2.5) compound is due to the larger hopping distance compared to that of MCO (x = 2.3) compound.</P>
Han, Sungwook,Lee, Hosuk,Lee, Andrew J.,Kim, Seung-Kyoon,Jung, Inkyung,Koh, Gou Young,Kim, Tae-Kyung,Lee, Daeyoup Korean Society for Molecular and Cellular Biology 2021 Molecules and cells Vol.44 No.11
CCCTC-binding factor (CTCF) critically contributes to 3D chromatin organization by determining topologically associated domain (TAD) borders. Although CTCF primarily binds at TAD borders, there also exist putative CTCF-binding sites within TADs, which are spread throughout the genome by retrotransposition. However, the detailed mechanism responsible for masking the putative CTCF-binding sites remains largely elusive. Here, we show that the ATP-dependent chromatin remodeler, chromodomain helicase DNA-binding 4 (CHD4), regulates chromatin accessibility to conceal aberrant CTCF-binding sites embedded in H3K9me3-enriched heterochromatic B2 short interspersed nuclear elements (SINEs) in mouse embryonic stem cells (mESCs). Upon CHD4 depletion, these aberrant CTCF-binding sites become accessible and aberrant CTCF recruitment occurs within TADs, resulting in disorganization of local TADs. RNA-binding intrinsically disordered domains (IDRs) of CHD4 are required to prevent this aberrant CTCF binding, and CHD4 is critical for the repression of B2 SINE transcripts. These results collectively reveal that a CHD4-mediated mechanism ensures appropriate CTCF binding and associated TAD organization in mESCs.
Han, Sang Won,Kim, Yong-Jae,Ahn, Seong Hwan,Seo, Woo-Keun,Yu, Sungwook,Oh, Seung-Hun,Nam, Hyo Suk,Choi, Hye-Yeon,Yoon, Sung Sang,Kim, Seo Hyun,Lee, Jong Yun,Lee, Jun Hong,Hwang, Yang-Ha,Lee, Kee Ook,J Korean Stroke Society 2017 Journal of stroke Vol.19 No.3
<P><B>Background and Purpose</B></P><P> To compare the efficacy and safety of antiplatelet agents for the secondary prevention of ischemic stroke based on cytochrome P450 2C19 (CYP2C19) polymorphisms. </P><P><B>Methods</B></P><P> This study was a prospective, multicenter, randomized, parallel-group, open-label, blind genotype trial. First time non-cardiogenic ischemic stroke patients were enrolled and screened within 30 days. Participants were randomized to receive either triflusal or clopidogrel for secondary stroke prevention. The primary outcome was the time from randomization to first recurrent ischemic stroke or hemorrhagic stroke. </P><P><B>Results</B></P><P> The required sample size was 1,080 but only 784 (73%) participants were recruited. In patients with a poor CYP2C19 genotype for clopidogrel metabolism (n=484), the risk of recurrent stroke among those who received triflusal treatment was 2.9% per year, which was not significantly different from those who received clopidogrel treatment (2.2% per year; hazard ratio [HR], 1.23; 95% confidence interval [CI], 0.60–2.53). In the clopidogrel treatment group (n=393), 38% had good genotypes and 62% poor genotypes for clopidogrel metabolism. The risk of recurrent stroke in patients with a good CYP2C19 genotype was 1.6% per year, which was not significantly different from those with a poor genotype (2.2% per year; HR, 0.69; 95% CI, 0.26–1.79). </P><P><B>Conclusions</B></P><P> Whilst there were no significant differences between the treatment groups in the rates of stroke recurrence, major vascular events, or coronary revascularization, the efficacy of antiplatelet agents for the secondary prevention of stroke according to CYP2C19 genotype status remains unclear.</P>
Isorhamnetin Protects Human Keratinocytes against Ultraviolet B-Induced Cell Damage
Han, Xia,Piao, Mei Jing,Kim, Ki Cheon,Hewage, Susara Ruwan Kumara Madduma,Yoo, Eun Sook,Koh, Young Sang,Kang, Hee Kyoung,Shin, Jennifer H,Park, Yeunsoo,Yoo, Suk Jae,Chae, Sungwook,Hyun, Jin Won The Korean Society of Applied Pharmacology 2015 Biomolecules & Therapeutics(구 응용약물학회지) Vol.23 No.4
Isorhamnetin (3-methylquercetin) is a flavonoid derived from the fruits of certain medicinal plants. This study investigated the photoprotective properties of isorhamnetin against cell damage and apoptosis resulting from excessive ultraviolet (UV) B exposure in human HaCaT keratinocytes. Isorhamnetin eliminated UVB-induced intracellular reactive oxygen species (ROS) and attenuated the oxidative modification of DNA, lipids, and proteins in response to UVB radiation. Moreover, isorhamnetin repressed UVB-facilitated programmed cell death in the keratinocytes, as evidenced by a reduction in apoptotic body formation, and nuclear fragmentation. Additionally, isorhamnetin suppressed the ability of UVB light to trigger mitochondrial dysfunction. Taken together, these results indicate that isorhamnetin has the potential to protect human keratinocytes against UVB-induced cell damage and death.