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한규량,이상배,김연희 忠州大學校 2008 한국교통대학교 논문집 Vol.43 No.-
Local self-sufficiency promotion center began to operate with the enforcement of the law for the securing of the least life of the people from October, 2000. It was made for the support of self-sufficiency of the poor who could work. As of December, 2006, 242 local self-sufficiency promotion centers are operating nationally. Their main business is to look after the patient, to repair the house, to clean, and to reuse the food. But now besides of these business, it widened its range from farming, eating out, helping mother who deliver a baby, and assisting the education of the disabled, to taking care of the old. The achievement of self-sufficiency business have inspired the will of life of the workers who took part in the self-sufficiency business and have promoted the vitality of them as components of the society by accepting their joining the social life in their community. This study has grasped the present condition of Chungbuk Association of Self-Sufficiency Promotion Center for the last 7 years and estimated its achievement and discussed the plan for the development of it.
좌측 전대뇌동맥 영역의 뇌경색 후 발생한 초피질성 혼합 실어증 1예
심미섭,이연수,김은희,이인숙,한설희 대한치매학회 2003 Dementia and Neurocognitive Disorders Vol.2 No.1
We present a case of transcortical mixed aphasia (TMA) presumably caused by left anterior cerebral artery infarction. A 53-year-old, right-handed woman suddenly developed speech disturbance and abnormal behavior. Her spontaneous speech was remarkably reduced to almost mutistic state and objective naming, comprehension, reading and writing were severely impaired. However, repetition of phonemes and sentences were fully preserved. She showed echolalia and completion phenomenon, which prompted us to make a diagnosis of TMA. Although the lesion was confined to extrasylvian area on MRI, SPECT demonstrated diminished blood flow left perisylvian cortices suggestive of functional isolation of speech area. In spite of her echolalic repetition, she couldn't repeat affective prosody, presumably, because of the left anterior corpus callosal lesion. Treatment with bromocriptine, a dopamine agonist helped her recovery of behavioral changes, namely abulia or akinetic mutism consisitent with mesial frontal syndrome.
[PB-0073] 무(Raphanus sativus L.) 품종의 표현형적 특성과 heterozygosity 간의 상관관계 분석
Hui Yeon Hong(Hui Yeon Hong),Jun Ho Lee(Jun Ho Lee),Yoon Ah Jang(Yoon Ah Jang),Jin Hee Kim(Jin Hee Kim),Ji Won Kim(Ji Won Kim),Ji Hyeon Lim(Ji Hyeon Lim),Hye Won Yu(Hye Won Yu),Won Byoung Chae(Won Byo 한국육종학회 2022 한국육종학회 공동학술발표집 Vol.2022 No.-
[PB-0071] GBS 분석을 통한 국내 무(Raphanus sativus L.) 품종의 유전적 유연관계 분석
Hui Yeon Hong(Hui Yeon Hong),Jun Ho Lee(Jun Ho Lee),Yoon Ah Jang(Yoon Ah Jang),Jin Hee Kim(Jin Hee Kim),Ji Won Kim(Ji Won Kim),Ji Hyeon Lim(Ji Hyeon Lim),Hye Won Yu(Hye Won Yu),Won Byoung Chae(Won Byo 한국육종학회 2022 한국육종학회 공동학술발표집 Vol.2022 No.-
Hui-yeon Kim 미래사회통합연구센터 2020 Journal of Conflict and Integration Vol.4 No.2
Low-skilled Cambodian workers are not concerned by “multicultural programs” in South Korea. In this context, they deal with this situation through the help of religious institutions, such as the Onnuri Presbyterian Church, by recreating a sort of ethnonational community. Labour migration permits Cambodian workers to weave different kinds of social links between them, with Koreans of the peninsula, and also with Koreans in Cambodia. This article examines the singular form of integration or exclusion of these migrant workers in South Korea, and tries to demonstrate its impact on their life upon their return home.
( Yeon Hui Jeong ),( Jin Sun Park ),( Dong Hyun Kim ),( Hee Sun Kim ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.6
In the present study, we found that the natural compound arctigenin inhibited hydrogen peroxide-induced reactive oxygen species (ROS) production in rat primary astrocytes. Since hemeoxygenase-1 (HO-1) plays a critical role as an antioxidant defense factor in the brain, we examined the effect of arctigenin on HO-1 expression in rat primary astrocytes. We found that arctigenin increased HO-1 mRNA and protein levels. Arctigenin also increases the nuclear translocation and DNA binding of Nrf2/c-Jun to the antioxidant response element (ARE) on HO-1 promoter. In addition, arctigenin increased ARE-mediated transcriptional activities in rat primary astrocytes. Further mechanistic studies revealed that arctigenin increased the phosphorylation of AKT, a downstream substrate of phosphatidylinositol 3-kinase (PI3K). Treatment of cells with a PI3K-specific inhibitor, LY294002, suppressed the HO-1 expression, Nrf2 DNA binding and ARE-mediated transcriptional activities in arctigenin-treated astrocyte cells. The results collectively suggest that PI3K/AKT signaling pathway is at least partly involved in HO-1 expression by arctigenin via modulation of Nrf2/ARE axis in rat primary astrocytes.
PPARδ Reprograms Glutamine Metabolism in Sorafenib-Resistant HCC
Kim, Mi-Jin,Choi, Yeon-Kyung,Park, Soo Young,Jang, Se Young,Lee, Jung Yi,Ham, Hye Jin,Kim, Byung-Gyu,Jeon, Hui-Jeon,Kim, Ji-Hyun,Kim, Jung-Guk,Lee, In-Kyu,Park, Keun-Gyu American Association for Cancer Research 2017 Molecular cancer research Vol.15 No.9
<P>The tyrosine kinase inhibitor sorafenib is the only therapeutic agent approved for the treatment of advanced hepatocellular carcinoma (HCC), but acquired resistance to sorafenib is high. Here, we report metabolic reprogramming in sorafenib-resistant HCC and identify a regulatory molecule, peroxisome proliferator-activated receptor-delta (PPAR delta), as a potential therapeutic target. Sorafenib-resistant HCC cells showed markedly higher glutamine metabolism and reductive glutamine carboxylation, which was accompanied by increased glucose-derived pentose phosphate pathway and glutamine-derived lipid biosynthetic pathways and resistance to oxidative stress. These glutamine-dependent metabolic alterations were attributed to PPAR delta, which was upregulated in sorafenibresistant HCC cells and human HCC tissues. Furthermore, PPAR delta contributed to increased proliferative capacity and redox homeostasis in sorafenib-resistant HCC cells. Accordingly, inhibiting PPAR delta activity reversed compensatory metabolic reprogramming in sorafenib-resistant HCC cells and sensitized them to sorafenib. Therefore, targeting compensatory metabolic reprogramming of glutamine metabolism in sorafenib-resistant HCC by inhibiting PPAR delta constitutes a potential therapeutic strategy for overcoming sorafenib-resistance in HCC. (C) 2017 AACR.</P>
Kim, Ji Hoon,Sohn, Bo Hwa,Lee, Hyun-Sung,Kim, Sang-Bae,Yoo, Jeong Eun,Park, Yun-Yong,Jeong, Woojin,Lee, Sung Sook,Park, Eun Sung,Kaseb, Ahmed,Kim, Baek Hui,Kim, Wan Bae,Yeon, Jong Eun,Byun, Kwan Soo,C Public Library of Science 2014 PLoS medicine Vol.11 No.12
<▼1><P>In this study, Lee and colleagues develop a genomic predictor that can identify patients at high risk for late recurrence of hepatocellular carcinoma (HCC) and provided new biomarkers for risk stratification.</P></▼1><▼2><P><B>Background</B></P><P>Typically observed at 2 y after surgical resection, late recurrence is a major challenge in the management of hepatocellular carcinoma (HCC). We aimed to develop a genomic predictor that can identify patients at high risk for late recurrence and assess its clinical implications.</P><P><B>Methods and Findings</B></P><P>Systematic analysis of gene expression data from human liver undergoing hepatic injury and regeneration revealed a 233-gene signature that was significantly associated with late recurrence of HCC. Using this signature, we developed a prognostic predictor that can identify patients at high risk of late recurrence, and tested and validated the robustness of the predictor in patients (<I>n = </I>396) who underwent surgery between 1990 and 2011 at four centers (210 recurrences during a median of 3.7 y of follow-up). In multivariate analysis, this signature was the strongest risk factor for late recurrence (hazard ratio, 2.2; 95% confidence interval, 1.3–3.7; <I>p</I> = 0.002). In contrast, our previously developed tumor-derived 65-gene risk score was significantly associated with early recurrence (<I>p</I> = 0.005) but not with late recurrence (<I>p</I> = 0.7). In multivariate analysis, the 65-gene risk score was the strongest risk factor for very early recurrence (<1 y after surgical resection) (hazard ratio, 1.7; 95% confidence interval, 1.1–2.6; <I>p</I> = 0.01). The potential significance of <I>STAT3</I> activation in late recurrence was predicted by gene network analysis and validated later. We also developed and validated 4- and 20-gene predictors from the full 233-gene predictor. The main limitation of the study is that most of the patients in our study were hepatitis B virus–positive. Further investigations are needed to test our prediction models in patients with different etiologies of HCC, such as hepatitis C virus.</P><P><B>Conclusions</B></P><P>Two independently developed predictors reflected well the differences between early and late recurrence of HCC at the molecular level and provided new biomarkers for risk stratification.</P><P><I>Please see later in the article for the Editors' Summary</I></P></▼2><▼3><P><B>Editors' Summary</B></P><P><B>Background</B></P><P>Primary liver cancer—a tumor that starts when a liver cell acquires genetic changes that allow it to grow uncontrollably—is the second-leading cause of cancer-related deaths worldwide, killing more than 600,000 people annually. If hepatocellular cancer (HCC; the most common type of liver cancer) is diagnosed in its early stages, it can be treated by surgically removing part of the liver (resection), by liver transplantation, or by local ablation, which uses an electric current to destroy the cancer cells. Unfortunately, the symptoms of HCC, which include weight loss, tiredness, and jaundice (yellowing of the skin and eyes), are vague and rarely appear until the cancer has spread throughout the liver. Consequently, HCC is rarely diagnosed before the cancer is advanced and untreatable, and has a poor prognosis (likely outcome)—fewer than 5% of patients survive for five or more years after diagnosis. The exact cause of HCC is unclear, but chronic liver (hepatic) injury and inflammation (caused, for example, by infection with hepatitis B virus [HBV] or by alcohol abuse) promote tumor development.</P><P><B>Why Was This Study Done?</B></P><P>Even when it is diagnosed early, HCC has a poor prognosis because it often recurs. Patients treated for HCC can experience two distinct types of tumor recurrence. Early recurrence, which usually happens within the first two years after surg
( Yeon Hui Jeong ),( Jin Won Hyun ),( Tien Kim Van Le ),( Dong Hyun Kim ),( Hee Sun Kim ) 한국응용약물학회 2013 Biomolecules & Therapeutics(구 응용약물학회지) Vol.21 No.5
Microglial activation plays an important role in the development and progression of various neurological disorders such as cerebral ischemia, multiple sclerosis, and Alzheimer`s disease. Thus, controlling microglial activation can serve as a promising therapeutic strategy for such brain diseases. In the present study, we showed that kalopanaxsaponin A, a triterpenoid saponin isolated from Kalopanax pictus, inhibited inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated microglia, while kalopanaxsaponin A increased anti-infl ammatory cytokine interleukin (IL)-10 expression. Subsequent mechanistic studies revealed that kalopanaxsaponin A inhibited LPS-induced DNA binding activities of NF-κB and AP-1, and the phosphorylation of JNK without affecting other MAP kinases. Furthermore, kalopanaxsaponin A inhibited the intracellular ROS production with upregulation of anti-infl ammatory hemeoxygenase-1 (HO-1) expression. Based on the previous reports that JNK pathway is largely involved in iNOS and proinfl ammatory cytokine gene expression via modulating NF-κB/AP-1 and ROS, our data collectively suggest that inhibition of JNK pathway plays a key role in anti-infl ammatory effects of kalopanaxsaponin A in LPS-stimulated microglia.