http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Shin, Sangyun,Kwon, Yeo-Jung,Ye, Dong-Jin,Baek, Hyoung-Seok,Kwon, Tae-Uk,Kim, Donghak,Chun, Young-Jin Elsevier/North Holland [etc.] 2019 Biochimica et biophysica acta Vol.1865 No.9
<P><B>Abstract</B></P> <P>Human steroid sulfatase (STS) has been linked with poor prognosis in steroid-associated tumors and represents an important clinical target in cancers, yet the mechanism of STS-induced carcinogenesis remains unclear. To correlate STS with cancer metabolism, we determined the effects of STS on aerobic glycolysis. STS overexpression increased cellular levels of lactic acid, the final product of aerobic glycolysis. Moreover, STS suppressed the oxygen consumption rate (OCR), which represents mitochondrial respiration. Inhibition of STS by the specific inhibitor STX064 recovered STS-induced OCR repression and lactic acid over-production. DHEA, but not DHEA-S, suppressed the OCR level and enhanced lactic acid production. To understand the molecular mechanism of STS-induced cancer metabolism, we measured the expression of glycolytic enzymes hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2), which was highly upregulated by STS and DHEA at both protein and mRNA levels. HIF1α is a key mediator of aerobic glycolysis, and STS enhanced HIF1α promoter activity, mRNA expression, and protein expression. Down-regulation of HIF1α by siRNA suppressed the HK2 and PKM2 expression induced by both STS and DHEA. HIF1α siRNA also recovered the OCR repression and lactic acid over-production induced by both STS and DHEA. To explore the mechanism <I>in vivo</I>, we produced transgenic mice overexpressing STS and found that STS expression was particularly enhanced in the lung. Consistent with our <I>in vitro</I> results, the expression of HIF1α, HK2, and PKM2 was also increased in mouse lung tissues. In conclusion, we suggest that STS may induce aerobic glycolysis through enhancing HIF1α expression.</P> <P><B>Highlights</B></P> <P> <UL> <LI> STS and its metabolite DHEA increase lactic acid production and suppress oxygen consumption in HeLa cells. </LI> <LI> STS induces expression of glycolytic enzymes both <I>in vivo</I> and <I>in vitro</I>. </LI> <LI> STS and DHEA triggers HIF1α induction. </LI> <LI> HIF1α is a crucial mediator of STS-induced aerobic glycolysis. </LI> </UL> </P>
( Yeon-sang Ryu ),( Sangyun Shin ),( Hong-gyu An ),( Tae-uk Kwon ),( Hyoung-seok Baek ),( Yeo-jung Kwon ),( Young-jin Chun ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.5
Axl receptor tyrosine kinase has been implicated in cancer progression, invasion, and metastasis in various cancer types. Axl overexpression has been observed in many cancers, and selective inhibitors of Axl, including R428, may be promising therapeutic agents for several human cancers, such as breast, lung, and pancreatic cancers. Here, we examined the cell growth inhibition mediated by R428 and auranofin individually as well as in combination in the human breast cancer cell lines MCF-7 and MDAMB- 231 to identify new advanced combination treatments for human breast cancer. Our data showed that combination therapy with R428 and auranofin markedly inhibited cancer cell proliferation. Isobologram analyses of these cells indicated a clear synergism between R428 and auranofin with a combination index value of 0.73. The combination treatment promoted apoptosis as indicated by caspase 3 activation and poly (ADP-ribose) polymerase cleavage. Cancer cell migration was also significantly inhibited by this combination treatment. Moreover, we found that combination therapy significantly increased the expression level of Bax, a mitochondrial proapoptotic factor, but decreased that of the X-linked inhibitor of apoptosis protein. Furthermore, the suppression of cell viability and induction of Bax expression by the combination treatment were recovered by treatment with N-acetylcysteine. In conclusion, our data demonstrated that combined treatment with R428 and auranofin synergistically induced apoptosis in human breast cancer cells and may thus serve as a novel and valuable approach for cancer therapy.
김정은,백민재,한문구,양동원,김상윤 대한치매학회 2003 Dementia and Neurocognitive Disorders Vol.2 No.2
Background: Anterior thalamic lesion is to produce various cognitive impairments. However, these findings are based on case studies rather than group studies. We analyzed the clinical & neuropsychological characteristics of the patients with the left anterior thalamic infarction to investigate the patterns of memory impairment and other cognitive dysfunction of the patients. Methods: We selected 7 patients with acute left anterior thalamic infarction who had been admitted to two referral hospitals. All patients underwent MRI, a careful medical history, physical and neurologic examination, and detailed neuropsychological tests within a week after stroke. Their lesions were confirmed to be located in the anterior nucleus lesion of left thalamus by lesion analysis of brain MRI. Results: All patients showed severe verbal and visual anterograde amnesia and also anomic aphasia and frontal executive dysfunction. The characteristics of the amnesia in these patients were that they showed encoding deficits as well as retrieval deficits. Five patients also had visuospatial dysfunction. Conclusion: Retrieval deficit in memory impairment and executive dysfunctions are suggestive of the unctional involvement of the frontal lobe Multiple cognitive deficits including anomia and visuospatial dysfunction other than memory disturbance also suggest that the anterior nucleus of left thalamus had multiple connections with diffuse fronto-temporo-parietal areas, although the exact circuit or mechanism explaining the pathophysiologic relations between the anterior nucleus of left thalamus and the multiple cortical areas has not been elucidated.
충분 조건을 이용한 안정적인 힘 제한 햅틱 상호 작용 방법
김종필(Jong-Phil Kim),백상윤(Sangyun Baek),류제하(Jeha Ryu) 대한기계학회 2011 대한기계학회 춘추학술대회 Vol.2011 No.5
Stability is a major requirement in haptic interaction since unstable behavior impairs realism and may injure the human operator. In this paper, we propose a force bounding approach by which a robustly stable haptic interaction is made possible for a linear virtual environment. Based on the passivity condition for sampled-data haptic systems, a sufficient condition for the force that can be passively displayed is derived.
Multiple Subarea Pose Models based Top-view People Detection for Smart Home System
Sungmok Hwang(황석목),Taeyup Song(송태엽),Sangyun Kim(김상윤),Seungmyun Baek(백승면),Dubok Park(박두복),Hanseok Ko(고한석) 대한전자공학회 2017 대한전자공학회 학술대회 Vol.2017 No.6
본 논문에서는 평면 시점에서 촬영된 영상에서 효과적인 사람 검출을 위한 다중 영역 자세 모델을 이용한 사람 검출 기술을 제안한다. 제안된 기술은 3가지 단계로 첫 번째로 밝기 변화에 대응하기 위해 히스토그램의 상/하한 문턱값 및 감마 보정을 통한 밝기 보정 기술, 다음으로 다중 영역별 자세 모델을 이용한 사람 검출기술, 마지막으로 카오스 이론 기반의 움직임 측정을 통한 검출결과 정련 기술로 구성된다. 실험 결과를 통해 제안된 방법은 단일 자세 모델기반의 사람 검출 기술에 비해 향상된 성능을 보이는 것을 확인할 수 있다.
Induction of Integrin Signaling by Steroid Sulfatase in Human Cervical Cancer Cells
( Dong-jin Ye ),( Yeo-jung Kwon ),( Sangyun Shin ),( Hyoung-seok Baek ),( Dong-won Shin ),( Young-jin Chun ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
Steroid sulfatase (STS) is an enzyme responsible for the hydrolysis of aryl and alkyl sulfates. STS plays a pivotal role in the regulation of estrogens and androgens that promote the growth of hormone-dependent tumors, such as those of breast or prostate cancer. However, the molecular function of STS in tumor growth is still not clear. To elucidate the role of STS in cancer cell proliferation, we investigated whether STS is able to regulate the integrin signaling pathway. We found that overexpression of STS in HeLa cells increases the protein and mRNA levels of integrin β1 and fibronectin, a ligand of integrin α5β1. Dehydroepiandrosterone (DHEA), one of the main metabolites of STS, also increases mRNA and protein expression of integrin β1 and fibronectin. Further, STS expression and DHEA treatment enhanced phosphorylation of focal adhesion kinase (FAK) at the Tyr 925 residue. Moreover, increased phosphorylation of ERK at Thr 202 and Tyr 204 residues by STS indicates that STS activates the MAPK/ ERK pathway. In conclusion, these results suggest that STS expression and DHEA treatment may enhance MAPK/ERK signaling through up-regulation of integrin β1 and activation of FAK.
Induction of Integrin Signaling by Steroid Sulfatase in Human Cervical Cancer Cells
Ye, Dong-Jin,Kwon, Yeo-Jung,Shin, Sangyun,Baek, Hyoung-Seok,Shin, Dong-Won,Chun, Young-Jin The Korean Society of Applied Pharmacology 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
Steroid sulfatase (STS) is an enzyme responsible for the hydrolysis of aryl and alkyl sulfates. STS plays a pivotal role in the regulation of estrogens and androgens that promote the growth of hormone-dependent tumors, such as those of breast or prostate cancer. However, the molecular function of STS in tumor growth is still not clear. To elucidate the role of STS in cancer cell proliferation, we investigated whether STS is able to regulate the integrin signaling pathway. We found that overexpression of STS in HeLa cells increases the protein and mRNA levels of integrin ${\beta}1$ and fibronectin, a ligand of integrin ${\alpha}5{\beta}1$. Dehydroepiandrosterone (DHEA), one of the main metabolites of STS, also increases mRNA and protein expression of integrin ${\beta}1$ and fibronectin. Further, STS expression and DHEA treatment enhanced phosphorylation of focal adhesion kinase (FAK) at the Tyr 925 residue. Moreover, increased phosphorylation of ERK at Thr 202 and Tyr 204 residues by STS indicates that STS activates the MAPK/ERK pathway. In conclusion, these results suggest that STS expression and DHEA treatment may enhance MAPK/ERK signaling through up-regulation of integrin ${\beta}1$ and activation of FAK.
Cortical Hubs and Subcortical Cholinergic Pathways as Neural Substrates of Poststroke Dementia
Lim, Jae-Sung,Kim, Nayoung,Jang, Min Uk,Han, Moon-Ku,Kim, SangYun,Baek, Min Jae,Jang, Myung Suk,Ban, Byeolnim,Kang, Yeonwook,Kim, Dong-Eog,Lee, Ji Sung,Lee, Juneyoung,Lee, Byung-Chul,Yu, Kyung-Ho,Blac American Heart Association, Inc. 2014 Stroke Vol.45 No.4
<P><B>Background and Purpose—</B></P><P>A role of neural networks in the development of poststroke dementia has not been clearly established. We hypothesized that stroke-mediated disruption of subcortical cholinergic pathway or large-scale neural networks contributes to poststroke dementia.</P><P><B>Methods—</B></P><P>A matched case–control study was conducted in a predetermined cohort with acute ischemic stroke. Cases were defined as newly developed dementia diagnosed >3 months after stroke using the Korean Vascular Cognitive Impairment Harmonization Standards. Each case was matched to 2 controls for age, education, and initial stroke severity. The Cholinergic Pathways HyperIntensities Scale was applied with some modifications to characterize disruption of cholinergic pathways by acute stroke lesions. Involvement of major cortical hub locations of the default mode network, central executive network, and salience network was also investigated.</P><P><B>Results—</B></P><P>After matching, 38 cases and 66 matched controls were included. Cholinergic Pathways HyperIntensities Scale scores were significantly higher in cases than in controls (2.2±2.9 versus 0.9±1.4). Acute ischemic lesions affecting the default mode and central executive networks were more frequently observed in cases compared with controls (36.8% versus 7.6% and 26.3% versus 6.1%, respectively). These findings remained significant in the multiple logistic regression models adjusted for various sets of potential confounders. Lesion location analysis revealed that cases were more likely to have acute lesions in the left corona radiata, hippocampal formation, and posterior parietal cortex.</P><P><B>Conclusions—</B></P><P>Disruption of cholinergic pathways and major hubs of large-scale neural networks might contribute to newly developed dementia after acute ischemic stroke.</P>