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김기식,주선종,윤향식,김민아,박성규,김태수 한국식품저장유통학회 ( 구 한국농산물저장유통학회 ) 2003 한국식품저장유통학회지 Vol.10 No.3
본 연구는 검은비늘버섯((CBPM-6호)의 선도유지 효과를 알아보기 위해 포장재(Wrap, PE, PP, AF) 및 저장온도(1℃, 3℃, 6℃)을 달리하여 18일간 결과를 다음과 같다. 저장기간 중 포장재별 중량 감모율은 랩 포장시 1℃에서 18일 후 3.17%이었으나, AF필름에서는 1.08%의 낮은 중량 감모율을 나타내었다. 색도는 저장기간이 연장될수록 명도와 황색도는 약간 증가하는 반면 랩 표장에서는 감소하는 경향을 나타내었다. 버섯 저장 전 색깔은 랩 포장에서는 3일, PE, PP, AF포장지에서는 18일까지 유지되었다. 경도는 저장온도가 높을수록 낮아지는 경향이었으며 1℃에서 저장할 때 AF 밀봉 저장이 경도의 변화가 가장 적은 것으로 나타났다. 신선도는 1℃ 저장시 신선도 8을 기준으로 랩 포장은 3일, PE 밀봉은 6일, PP 밀봉은 9일, AF 밀봉으로 15일간 저장시 상품성을 유지할 수 있다. This study was carried out to develop storage method for the keeping freshness with various packing film(Wrap, PE, PP and AF and storage temperature(1, 3 and 6℃) of Pholiota adiposa(CBPM-no6) mushroom. The rate of weight loss packed with Wrap film was 3.17%, but AF film was 1.08% after 18days. As the storage periods, lightness and yellowness of mushroom packed with PE, PP and AF were slighty increased, while Wrap film was decreased. The color of original raw mushroom preserved 3days using Wrap film and 18 dyas using PE, PP and AF. As storage temperature high, the rigidity of mushroom decreased. Rigidity of mushroom packed with AF film was less change compared with the other film. Freshness degree of mushroom(refer to Minamide method) could preserve for 3days using Wrap, 6 days using PE, 9 days using PP and 15days using AF film at 1℃.
Kim, Bu-Yeo,Suh, Kyung-Suk,Lee, Je-Geun,Woo, Seon Rang,Park, In-Chul,Park, Sun-Hoo,Han, Chul Ju,Kim, Sang-Bum,Jeong, Sook-Hyang,Yeom, Young Il,Yang, Suk-Jin,Kim, Chang-Min,Cho, Su Jin,Yoo, Young Do,Ch Raven Press 2012 Annals of Surgical Oncology Vol.19 No.suppl3
<P>The tissue environment in the region of hepatocellular carcinoma (HCC) influences both vascular invasion and recurrence. Thus, HCC patient prognosis depends on the characteristics not only of the tumor but also those of adjacent surrounding liver tissue.</P>
KIM, Seon-Hyang,ZHAO, Ming-Hui,LIANG, Shuang,CUI, Xiang-Shun,KIM, Nam-Hyung 家畜繁殖硏究所 2015 Journal of Reproduction and Development Vol.61 No.4
<P> Cathepsin B, a lysosomal cysteine protease of the papain family, has recently been implicated in the quality and developmental competence of bovine preimplantation embryos. In this study, to determine whether inhibition of cathepsin B activity can improve porcine oocyte maturation and early embryo developmental competence, we supplemented <I>in vitro</I> maturation or embryo culture media with E-64, a cathepsin B inhibitor. Cathepsin B activity was high in poor quality germinal vesicle stage oocytes, but no differences in mRNA expression or protein localization were observed between good and poor quality oocytes, which were categorized based on morphology. Following treatment with 1 μM E-64, cathepsin B activity sharply decreased in 4-cell and blastocyst stage embryos. E-64 had no effect on cell number but significantly (P < 0.05) increased blastocyst formation and decreased the number of apoptotic cells in blastocysts. It also significantly (P < 0.05) enhanced mitochondrial membrane potential in blastocysts, reducing the release of cytochrome <I>c</I> and resulting in decreased expression of <I>Caspase-3</I> and <I>Caspase-9</I>. In conclusion, inhibition of cathepsin B activity in porcine parthenotes using 1 μM E-64 resulted in attenuation of apoptosis via a reduction in the release of cytochrome <I>c</I> from mitochondria.</P>
Novel mechanism of conjoined gene formation in the human genome.
Kim, Ryong Nam,Kim, Aeri,Choi, Sang-Haeng,Kim, Dae-Soo,Nam, Seong-Hyeuk,Kim, Dae-Won,Kim, Dong-Wook,Kang, Aram,Kim, Min-Young,Park, Kun-Hyang,Yoon, Byoung-Ha,Lee, Kang Seon,Park, Hong-Seog Springer 2012 Functional & integrative genomics Vol.12 No.1
<P>Recently, conjoined genes (CGs) have emerged as important genetic factors necessary for understanding the human genome. However, their formation mechanism and precise structures have remained mysterious. Based on a detailed structural analysis of 57 human CG transcript variants (CGTVs, discovered in this study) and all (833) known CGs in the human genome, we discovered that the poly(A) signal site from the upstream parent gene region is completely removed via the skipping or truncation of the final exon; consequently, CG transcription is terminated at the poly(A) signal site of the downstream parent gene. This result led us to propose a novel mechanism of CG formation: the complete removal of the poly(A) signal site from the upstream parent gene is a prerequisite for the CG transcriptional machinery to continue transcribing uninterrupted into the intergenic region and downstream parent gene. The removal of the poly(A) signal sequence from the upstream gene region appears to be caused by a deletion or truncation mutation in the human genome rather than post-transcriptional trans-splicing events. With respect to the characteristics of CG sequence structures, we found that intergenic regions are hot spots for novel exon creation during CGTV formation and that exons farther from the intergenic regions are more highly conserved in the CGTVs. Interestingly, many novel exons newly created within the intergenic and intragenic regions originated from transposable element sequences. Additionally, the CGTVs showed tumor tissue-biased expression. In conclusion, our study provides novel insights into the CG formation mechanism and expands the present concepts of the genetic structural landscape, gene regulation, and gene formation mechanisms in the human genome.</P>
Kim, Mirang,Lee, Kyung-Tae,Jang, Hay-Ran,Kim, Jeong-Hwan,Noh, Seung-Moo,Song, Kyu-Sang,Cho, June-Sik,Jeong, Hyun-Yong,Kim, Seon-Young,Yoo, Hyang-Sook,Kim, Yong Sung American Association for Cancer Research 2008 Molecular cancer research Vol.6 No.2
<P>The promoter region of Discoidin, CUB and LCCL domain containing 2 (DCBLD2) was found to be aberrantly methylated in gastric cancer cell lines and in primary gastric cancers, as determined by restriction landmark genomic scanning. DCBLD2 expression was inversely correlated with DCBLD2 methylation in gastric cancer cell lines. Treatment with 5-aza-2'-deoxycytidine and trichostatin A partially reversed DCBLD2 methylation and restored gene expression in DCBLD2-silenced cell lines. In an independent series of 82 paired gastric cancers and adjacent normal tissues, DCBLD2 expression was down-regulated in 79% of gastric cancers as compared with normal tissues as measured by real-time reverse transcription-PCR. Pyrosequencing analysis of the DCBLD2 promoter region revealed abnormal hypermethylation in gastric cancers, and this hypermethylation was significantly correlated with down-regulation of DCBLD2 expression. Furthermore, ectopic expression of DCBLD2 in gastric cancer cell lines inhibited colony formation in both anchorage-dependent and anchorage-independent cultures and also inhibited invasion through the collagen matrix. These data suggest that down-regulation of DCBLD2, often associated with promoter hypermethylation, is a frequent event that may be related to the development of gastric cancer.</P>
Meta- and gene set analysis of stomach cancer gene expression data.
Kim, Seon-Young,Kim, Jeong-Hwan,Lee, Heun-Sik,Noh, Seung-Moo,Song, Kyu-Sang,Cho, June-Sik,Jeong, Hyun-Yong,Kim, Woo Ho,Yeom, Young-Il,Kim, Nam-Soon,Kim, Sangsoo,Yoo, Hyang-Sook,Kim, Yong Sung Korean Society for Molecular Biology 2007 Molecules and cells Vol.24 No.2
<P>We generated gene expression data from the tissues of 50 gastric cancer patients, and applied meta-analysis and gene set analysis to this data and three other stomach cancer gene expression data sets to define the gene expression changes in gastric tumors. By meta-analysis we identified genes consistently changed in gastric carcinomas, while gene set analysis revealed consistently changed biological themes. Genes and gene sets involved in digestion, fatty acid metabolism, and ion transport were consistently down-regulated in gastric carcinomas, while those involved in cellular proliferation, cell cycle, and DNA replication were consistently up-regulated. We also found significant differences between the genes and gene sets expressed in diffuse and intestinal type gastric carcinoma. By gene set analysis of cytogenetic bands, we identified many chromosomal regions with possible gross chromosomal changes (amplifications or deletions). Similar analysis of transcription factor binding sites (TFBSs), revealed transcription factors that may have caused the observed gene expression changes in gastric carcinomas, and we confirmed the overexpression of one of these, E2F1, in many gastric carcinomas by tissue array and immunohistochemistry. We have incorporated the results of our meta- and gene set analyses into a web accessible database (http://human-genome.kribb.re.kr/stomach/).</P>