http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Lee, Kang-Yo,Oh, Sehee,Choi, You-Jin,Oh, Seon-Hee,Yang, Young-Su,Yang, Mi-Jin,Lee, Kyuhong,Lee, Byung-Hoon Oxford University Press 2013 Toxicological sciences Vol.136 No.1
<P>Amiodarone, bi-iodinated benzofuran derivative, is one of the most frequently prescribed and efficacious antiarrhythmic drugs. Despite its low incidence, amiodarone-induced pulmonary toxicity is of great concern and the leading cause of discontinuation. Autophagy is an essential homeostatic process that mediates continuous recycling of intracellular materials when nutrients are scarce. It either leads to a survival advantage or initiates death processes in cells under stress. In the present study, we investigated the role of autophagy in amiodarone-induced pulmonary toxicity. Amiodarone treatment–induced autophagy in H460 human lung epithelial cells and BEAS-2B normal human bronchial epithelial cells was demonstrated by increased LC3-II conversion, <I>Atg7</I> upregulation, and autophagosome formation. Autophagic flux, as determined by the lysosomal inhibitor bafilomycin A1, was also increased following amiodarone treatment. To determine the role of autophagy in amiodarone toxicity, amiodarone-induced cell death was evaluated in the presence of 3-methyladenine or by knocking down the autophagy-related genes <I>Atg7</I>. Inhibition of autophagy decreased cellular viability and significantly increased apoptosis. Intratracheal instillation of amiodarone in rats increased the number of inflammatory cells recovered from bronchoalveolar lavage fluid, and periodic acid-Schiff-positive staining in bronchiolar epithelial cells. However, induction of autophagy by rapamycin treatment inhibited amiodarone-induced pulmonary toxicity. In conclusion, amiodarone treatment induced autophagy, which is involved in protection against cell death and pulmonary toxicity.</P>
Genotype distribution of infectious haematopoietic necrosis virus (IHNV) in Korea
( Seung Joo Cha ),( Yo Han Jung ),( Hyun Young Lee ),( Ji Yoon Jung ),( Hee Jung Cho ),( Mi Seon Park ) 한국어병학회 2012 한국어병학회지 Vol.25 No.3
Infectious haematopoietic necrosis virus (IHNV) is an important fish pathogen that infects both wild and cultured salmonids. Since the first isolation of IHNV from rainbow trout and masu salmon in 1991, a series of IHN disease outbreak has been reported in Korea. In 2011, we isolated two IHNV isolates from rainbow trout cultured in Korea. The full open-reading frame (ORF) encoding the glycoprotein (G) of them were sequenced and the amino acid sequences were phylogenetically analyzed. Phylogenetic analysis of the G revealed that both IHNV isolates were grouped into an Asian genogroup containing Korean IHNV isolates and Japanese IHNV isolates. However, based on their sequence variation, they were divided into different subgroup. While one isolate was similar to other Korean isolates, the other isolate showed a high level of similarity with Japanese isolates, suggesting the possibility of influx of new IHNV strain into Korea.
Genotype distribution of infectious haematopoietic necrosis virus (IHNV) in Korea
Cha, Seung Joo,Jung, Yo Han,Lee, Hyun Young,Jung, Ji Yoon,Cho, Hee Jung,Park, Mi Seon The Korean Society of Fish Pathology 2012 한국어병학회지 Vol.25 No.3
Infectious haematopoietic necrosis virus (IHNV) is an important fish pathogen that infects both wild and cultured salmonids. Since the first isolation of IHNV from rainbow trout and masu salmon in 1991, a series of IHN disease outbreak has been reported in Korea. In 2011, we isolated two IHNV isolates from rainbow trout cultured in Korea. The full open-reading frame (ORF) encoding the glycoprotein (G) of them were sequenced and the amino acid sequences were phylogenetically analyzed. Phylogenetic analysis of the G revealed that both IHNV isolates were grouped into an Asian genogroup containing Korean IHNV isolates and Japanese IHNV isolates. However, based on their sequence variation, they were divided into different subgroup. While one isolate was similar to other Korean isolates, the other isolate showed a high level of similarity with Japanese isolates, suggesting the possibility of influx of new IHNV strain into Korea.
Kim, Joon Mee,Sohn, Jin Hee,Cho, Mee-Yon,Kim, Woo Ho,Chang, Hee Kyung,Jung, Eun Sun,Kook, Myeong-Cherl,Jin, So-Young,Chae, Yang Seok,Park, Young Soo,Kang, Mi Seon,Kim, Hyunki,Lee, Jae Hyuk,Park, Do Yo Springer Japan 2016 GASTRIC CANCER Vol.19 No.4
<P><B>Background</B></P><P>Discrepancies in the clinicopathologic parameters pre- and post-endoscopic submucosal dissection (ESD) sometimes necessitate additional surgical resection. The aim of this study was to assess such discrepancies in clinicopathologic parameters before and after ESD in the context of reducing the risk of failure of curative ESD.</P><P><B>Methods</B></P><P>Data on 712 early gastric cancer patients were prospectively collected from 12 university hospitals nationwide. The inclusion criteria were differentiated carcinoma <3 cm in size, no ulceration, submucosal invasion <500 μm, and no metastasis. Clinicopathologic factors were compared retrospectively.</P><P><B>Results</B></P><P>The discrepancy rate was 20.1 % (148/737) and the most common cause of discrepancy was tumor size (64 cases, 8.7 %). Ulceration, undifferentiated histology, and SM2 invasion were found in 34 (4.6 %), 18 (2.4 %), and 51 cases (6.9 %), respectively. Lymphovascular invasion (LVI) was observed in 34 cases (4.6 %). Cases with lesions exceeding 3 cm in size showed more frequent submucosal invasion, an elevated gross morphology, and upper and middle locations (<I>p</I> < 0.05). In the cases with ulceration, depth of invasion (DOI) was deeper than in the cases without ulceration (<I>p</I> = 0.005). Differentiation was correlated with DOI and LVI (<I>p</I> = 0.021 and 0.007). DOI was correlated with tumor size, ulceration, differentiation, LVI, gross type, and location. There were statistically significant differences between mucosal cancer cases and submucosal cancer cases in tumor size, differentiation, ulceration, LVI, and location.</P><P><B>Conclusions</B></P><P>The overall discrepancy rate was 20.1 %. To reduce this rate, it is necessary to evaluate the DOI very cautiously, because it is correlated with other parameters. In particular, careful checking for SM-invasive cancer is required due to the high incidence of LVI irrespective of the depth of submucosal invasion.</P>
Kim, Hyoung Kyu,Jeon, Jouhyun,Song, In-Sung,Heo, Hae Jin,Jeong, Seung Hun,Long, Le Thanh,Thu, Vu Thi,Ko, Tae Hee,Kim, Min,Kim, Nari,Lee, Sung Ryul,Yang, Jae-Seong,Kang, Mi Seon,Ahn, Jung-Mo,Cho, Je-Yo Elsevier 2019 Biochimica et biophysica acta Vol.1865 No.11
<P><B>Abstract</B></P> <P>Tetrahydrobiopterin (BH4) shows therapeutic potential as an endogenous target in cardiovascular diseases. Although it is involved in cardiovascular metabolism and mitochondrial biology, its mechanisms of action are unclear. We investigated how BH4 regulates cardiovascular metabolism using an unbiased multiple proteomics approach with a sepiapterin reductase knock-out (<I>Spr</I> <SUP>−/−</SUP>) mouse as a model of BH4 deficiency. <I>Spr</I> <SUP>−/−</SUP> mice exhibited a shortened life span, cardiac contractile dysfunction, and morphological changes. Multiple proteomics and systems-based data-integrative analyses showed that BH4 deficiency altered cardiac mitochondrial oxidative phosphorylation. Along with decreased transcription of major mitochondrial biogenesis regulatory genes, including <I>Ppargc1a</I>, <I>Ppara</I>, <I>Esrra</I>, and <I>Tfam</I>, <I>Spr</I> <SUP>−/−</SUP> mice exhibited lower mitochondrial mass and severe oxidative phosphorylation defects. Exogenous BH4 supplementation, but not nitric oxide supplementation or inhibition, rescued these cardiac and mitochondrial defects. BH4 supplementation also recovered mRNA and protein levels of PGC1α and its target proteins involved in mitochondrial biogenesis (mtTFA and ERRα), antioxidation (Prx3 and SOD2), and fatty acid utilization (CD36 and CPTI-M) in <I>Spr</I> <SUP>−/−</SUP> hearts. These results indicate that BH4-activated transcription of PGC1α regulates cardiac energy metabolism independently of nitric oxide and suggests that BH4 has therapeutic potential for cardiovascular diseases involving mitochondrial dysfunction.</P> <P><B>Highlights</B></P> <P> <UL> <LI> BH4 deficiency impairs mitochondrial and cardiac function. </LI> <LI> BH4 regulates PGC1α, ERRα, and mtTFA transcription. </LI> <LI> BH4 regulates proteins related to mitochondrial antioxidation and fatty acid utilization. </LI> <LI> BH4 is essential for mitochondrial biogenesis and oxidative phosphorylation. </LI> <LI> BH4 has therapeutic potential for cardiovascular diseases involving mitochondrial dysfunction. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>