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대구지역 금호강 및 주요 지천 퇴적물의 시·공간적 독성변화
정홍배,문성환,정진애,김재현,박정규,배철한,황인영 한국환경독성학회 2001 환경독성보건학회지 Vol.16 No.4
1. 사전에 선정된 공통 조사 정점들 가운데 KㆍH4(금호대교)이후의 퇴적물 독성이 상부의 것보다 크게 나타났다. 즉, 정점 KH3과 KH4, 그리고 KH4와 KH5 사이에 독성물질 유입원이 있는 것으로 판단되었다. 2. 하천 퇴적물의 독성 수준에 영향을 주고 있는 물질의 종류와 배출원 파악이 필요하였다. 이러한 내용을 향후 계속적 연구 및 조사를 통하여 수행되어야 하는 과제라 사료된다. 3. 퇴적물 시료의 채취 시점에 따라서 동일 정점의 독성 변화가 심하였다. 유해화학물질에 의한 오염 수준과 하천 생태계의 영향을 예측하기 위해서는 하천 퇴적물을 대상으로 경시적으로 독성의 변화를 계속 관측하는 것이 필요하다고 판단되었다. In aqueous ecosystems, the level of toxicity is highly responsive dependant to multiple variables, including rainfall, sunlight, pH, adhesion, etc. Because Korea has particularly distinct wet and dry seasons, the toxicity of pollutants in rivers or streams is dependant on the sampling season and time. In order to examine the effects of rainfall on toxicity, sediment samples were collected from five sites along the Keumho river. It was found that Microlox toxicity levels were generally higher during the dry season than the wet season. It indicated that river pollutants are carried off more quickly by the water during the wet season. As a result, it was recommended that the point sources of pollutants of the Keumho river would be placed between KH3 (Paldalgyo) and KH4 (Keumhogyo), KH4 (Keumhogyo) and KH5 (Dasa).
국내 하천 퇴적물 건강성평가를 위한 Microtox 독성시험 조건확립 연구
정홍배,박정규,문성환,류태권,김소정,배철한,황인영 한국환경독성학회 2001 환경독성보건학회지 Vol.16 No.4
1. 하천 퇴적물 공극수, 증류수 추출용액 및 유기용매 추출액을 pH6.0~6.5 범위로 조절한 후 Microtox 독성을 측정하는 것이 퇴적물내의 암모니아 독성이 배제된, 유해화학물질 오염에 의한 퇴적물 독성을 평가하는 방안임을 확인하였다. 2. 퇴적물에 대해 공극수, 증류수 추출물, 유기용매 추출물 구분하여 Microtox 독성을 구하는 것이 퇴적물 내 유해화학물질의 독성발현 특성을 예측할 수 있는 기법이라고 사료된다. 3. 조사정점 내 시료 채취 지점간 독성에 편차로 인하여, 동일 정점의 반경 50~100m 내에서 최소 4지점 이상의 퇴적물을 확보하는 것이 해당 정점의 독성 대표값을 산출할 수 있는 방안이 된다고 판단된다. 4. 한강수계인 남한강 지천인 복하천과 양화천, 금강수계인 청주 미호천, 대전 갑천, 낙동강수계인 대구 금호강, 영산강수계인 황룡강 그리고 익산 만경강을 대상으로 한 예비 조사한 결과, 집중연구대상 하천으로의 조건은 금호강이 가장 우수하였다. 5. 하천 퇴적물의 증류수 추출액과 유기용매 추출액의 Microtox 독성값 간의 상호 상관성이 높았다. 그러나, 농축 과정이 용이하므로 정점간 비교를 위한 독성 측정시 유기용매 추출액을 사용하는 것이 바람직하다고 사료되었다. Six rivers were selected as preliminary screening sites to determine the test conditions of Microtox in assessing the toxicity of the sediment. In addition, a pH range of 6.0--6.5 was established in testing pore water, aqueous extracts and organic extracts. Each extractable fraction of sediment showed different toxicities. Therefore, in order to properly examine the toxicity in the sediment, all extractable fractions of sediment samples needed to be tested with Microtox. Thus, sediment samples were additionally collected from at least 4 secondary sites within 50~100 m area of the primary sampling site to reduce any variation or deviation in toxicity assessment. From all sediment toxicity data that was collected from this study, it was concluded that the Keumho river was the most polluted with the highest sediment toxicity of all the rivers analyzed and needed further detailed research on its pollution problem.
양승부,최교창,이상진,정영진,임한혁,한효상,황인철,조환성 순천향의학연구소 2005 Journal of Soonchunhyang Medical Science Vol.11 No.1
Objective : Our purpose of this study is to evaluate the effectiveness of the transcatheter arterial embolization for the management of abnormal uterine bleeding. Materials and Methods : 14 patients with massive or recurrent uterine bleeding underwent percutaneous transcatheter arterial embolization between February 2003 and September 2004. We reviewed 14 cases of uterine artery or internal iliac artery embolization using gelfoam or PVA particles. Results : Good management of uterine bleeding was achieved in 13 of 14(93%) cases. The cause of abnormal uterine bleeding was myoma(5 case), post D & E bleeding(3), acquired vascular malformation(3), pseudoaneurysm(1), adenomyosis(1), and endometrial hyperplasia(1). Conclusion : Transcatheter artery embolization is an effective and life-saving procedure in massive or recurrent uterine bleeding. Early diagnosis and prompt transcatheter arterial embolization is a useful mangement of uterine bleeding.
( Chul Ju Hwang ),( Hyung Mun Yun ),( Kyung Ran Park ),( Ju Kyung Song ),( Hyun Ok Seo ),( Byung Kook Hyun ),( Dong Young Choi ),( Hwan Soo Yoo ),( Ki Wan Oh ),( Dae Yeun Hwang ),( Sang Bae Han ),( Ji 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-
Estrogen has been known to reduce the development of Alzheimer’s disease (AD). However, exact mechanisms are not clear. We investigated whether estrogen can increase amyloid-beta (Aβ) degradation and affects Aβ- induced memory impairment in an estrogen deficiency model. Estrogen receptor alpha (ERα) knockout mice and wild-type mice were intracerebroventricular (ICV) infused with Aβ (300 pmol) for 2 weeks. Cognitive function was then assessed by the Morris water maze test and passive avoidance test. In addition, Western blot analysis, immunostaining, immunofluorescence staining, ELISA, and enzyme activity assays were used to examine the degree of Aβ deposition in the brains of ERα knockout mice. In our present study, Aβ was accumulated more in the ERα knockout mice brain and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. These results suggest that estrogen may protect memory impairment by stimulating the degradation of Aβ and down-regulate neurogenic inflammation as well as amyloidogenesis.
Leukocyte-specific protein 1 regulates T-cell migration in rheumatoid arthritis
Hwang, Seong-Hye,Jung, Seung-Hyun,Lee, Saseong,Choi, Susanna,Yoo, Seung-Ah,Park, Ji-Hwan,Hwang, Daehee,Shim, Seung Cheol,Sabbagh, Laurent,Kim, Ki-Jo,Park, Sung Hwan,Cho, Chul-Soo,Kim, Bong-Sung,Leng, National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.47
<P><B>Significance</B></P><P>We screened rheumatoid arthritis (RA)-associated copy number variations (CNVs) across the whole genome and identified significant deletion variants encompassing leukocyte-specific protein 1 (LSP1) gene. Functional assays revealed that LSP1, induced by T-cell receptor activation, negatively regulates T-cell migration. Loss of <I>Lsp1</I> promotes T-cell migration into antigen-instilled tissues and draining lymph nodes in mice with T-cell–dependent chronic inflammation. Moreover, patients with RA show diminished expression of LSP1 in peripheral T cells with increased migratory capacity. To our knowledge, our work is the first to demonstrate how CNVs result in immune dysfunction and a disease phenotype, highlighting the importance of <I>LSP1</I> CNVs and LSP1 insufficiency in the pathogenesis of RA.</P><P>Copy number variations (CNVs) have been implicated in human diseases. However, it remains unclear how they affect immune dysfunction and autoimmune diseases, including rheumatoid arthritis (RA). Here, we identified a novel leukocyte-specific protein 1 (<I>LSP1</I>) deletion variant for RA susceptibility located in 11p15.5. We replicated that the copy number of LSP1 gene is significantly lower in patients with RA, which correlates positively with LSP1 protein expression levels. Differentially expressed genes in <I>Lsp1-</I>deficient primary T cells represent cell motility and immune and cytokine responses. Functional assays demonstrated that LSP1, induced by T-cell receptor activation, negatively regulates T-cell migration by reducing ERK activation in vitro. In mice with T-cell–dependent chronic inflammation, loss of <I>Lsp1</I> promotes migration of T cells into the target tissues as well as draining lymph nodes, exacerbating disease severity. Moreover, patients with RA show diminished expression of LSP1 in peripheral T cells with increased migratory capacity, suggesting that the defect in LSP1 signaling lowers the threshold for T-cell activation. To our knowledge, our work is the first to demonstrate how CNVs result in immune dysfunction and a disease phenotype. Particularly, our data highlight the importance of <I>LSP1</I> CNVs and LSP1 insufficiency in the pathogenesis of RA and provide previously unidentified insights into the mechanisms underlying T-cell migration toward the inflamed synovium in RA.</P>
Hwang, Ki Eun,Park, Chul,Seol, Chang Hwan,Hwang, Yu Ri,Hwang, June Seong,Jung, Jae Wan,Choi, Keum Ha,Jeong, Eun Taik,Kim, Hak Ryul The Korean Academy of Tuberculosis and Respiratory 2013 Tuberculosis and Respiratory Diseases Vol.75 No.2
Background: This study was conducted in order to elucidate the effects of docetaxel on the growth of peroxiredoxin 1 (Prx1) knockdown A549 xenograft tumors and further tested the role of Prx1 as a predictor for how a patient would respond to docetaxel treatment. Methods: Effects of docetaxel on the growth of scrambled- and shPrx1-infected A549 xenograft tumors in nude mice were measured. Moreover, immunohistochemical expression of Prx1 was evaluated in paraffin-embedded tissues from 24 non-small cell lung cancer patients who had received docetaxel-cisplatin regimens as a first-line treatment. Results: Docetaxel treatment in Prx1 knockdown xenograft tumor resulted in reduced tumors growth compared with other groups. Prx1 knockdown increased the production of cleaved caspases-8 and -9 in the control itself compared to scramble tumors. Moreover, docetaxel treatment in Prx1 knockdown tissue led to an increased protein band. Phosphorylated Akt was found in Prx1 scramble tissues. Phosphorylated FOXO1 was detected in the docetaxel treatment group. On the other hand, Prx1 knockdown completely suppressed the Akt-FOXO1 axis. The median progression-free survival (PFS) of patients with low Prx1 expression was 7 months (95% confidence interval [CI], 6.0-7.7), whereas the median progression-free survival of patients with high Prx1 expression was 4 months (95% CI, 4.0-5.0). However, high Prx1 expression was not associated with decreased PFS (p=0.114). Conclusion: Our findings suggest that elevated Prx1 provides resistance to docetaxel treatment through suppression of FOXO1-induced apoptosis in A549 xenograft tumors, but may not be related with the predictive significance for response to docetaxel treatment.
Memory Impairment in Estrogen Receptor α Knockout Mice Through Accumulation of Amyloid-β Peptides
Hwang, Chul Ju,Yun, Hyung-Mun,Park, Kyung-Ran,Song, Ju Kyung,Seo, Hyun Ok,Hyun, Byung Kook,Choi, Dong Young,Yoo, Hwan-Soo,Oh, Ki-Wan,Hwang, Dae Yeun,Han, Sang-Bae,Hong, Jin Tae Springer US 2015 Molecular Neurobiology Vol.52 No.1
<P>Estrogen has been known to reduce the development of Alzheimer’s disease (AD). However, exact mechanisms are not clear. We investigated whether estrogen can increase amyloid-beta (Aβ) degradation and affects Aβ-induced memory impairment in an estrogen deficiency model. Estrogen receptor alpha (ERα) knockout mice and wild-type mice were intracerebroventricular (ICV) infused with Aβ (300 pmol) for 2 weeks. Cognitive function was then assessed by the Morris water maze test and passive avoidance test. In addition, Western blot analysis, immunostaining, immunofluorescence staining, ELISA, and enzyme activity assays were used to examine the degree of Aβ deposition in the brains of ERα knockout mice. In our present study, Aβ was accumulated more in the ERα knockout mice brain and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. These results suggest that estrogen may protect memory impairment by stimulating the degradation of Aβ and down-regulate neurogenic inflammation as well as amyloidogenesis.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1007/s12035-014-8853-z) contains supplementary material, which is available to authorized users.</P>