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A novel prognostic factor for hepatocellular carcinoma: protein disulfide isomerase
Yu, Su Jong,Won, Jae-Kyung,Ryu, Han Suk,Choi, Won-Mook,Cho, Hyeki,Cho, Eun-Ju,Lee, Jeong-Hoon,Kim, Yoon Jun,Suh, Kyung-Suk,Jang, Ja-June,Kim, Chung Yong,Lee, Hyo-Suk,Yoon, Jung-Hwan,Cho, Kwang-Hyun The Korean Association of Internal Medicine 2014 The Korean Journal of Internal Medicine Vol.29 No.5
<P><B>Background/Aims</B></P><P>Protein disulfide isomerase (PDI) has been implicated in the survival and progression of some cancer cells, by compensating for endoplasmic reticulum stress by upregulating the protein-folding capacity. However, its prognostic role in patients with hepatocellular carcinoma (HCC) has not been investigated.</P><P><B>Methods</B></P><P>We collected HCC tissues from 83 HCC patients who underwent surgical resection for an immunohistochemical study of PDI. Overall survival (OS) was measured from the date of surgical resection until the date of death from any cause. Radiological progression was evaluated using the modified Response Evaluation Criteria in Solid Tumors in an independent radiological assessment.</P><P><B>Results</B></P><P>PDI expression was found to be increased in human HCC compared to adjacent nontumor tissues. Increased immunopositivity for PDI was associated with a high Edmondson-Steiner grade (<I>p</I> = 0.028). Univariate analysis of patients who had undergone surgical resection for HCC showed that tumor PDI upregulation is a significant risk factor for poor OS (<I>p</I> = 0.016; hazard ratio [HR], 1.980) and time to progression (TTP; <I>p</I> = 0.007; HR, 1.971). Multivariate analyses revealed that high PDI expression was an independent predictor of a shorter TTP (<I>p</I> = 0.015; HR, 1.865) and poor OS (<I>p</I> = 0.012; HR, 2.069).</P><P><B>Conclusions</B></P><P>Upregulated PDI expression is associated with aggressive clinicopathological features of HCC; thus, PDI might serve as an independent prognostic factor and a potential therapeutic target for HCC patients.</P>
Notes : Proteomes Induced by S-Adenosyl-L-Methionine in Streptomyces coelicolor A3(2)
( Kwang Pyo Kim ),( Choon Shik Shin ),( Soo Jae Lee ),( Ji Hye Kim ),( Jung Mo Young ),( Yu Kyung Lee ),( Joong Hoon Ahn ),( Joo Won Suh ),( Yoong Ho Lim ) 한국미생물 · 생명공학회 2006 Journal of microbiology and biotechnology Vol.16 No.5
Won, Tae Joon,Kim, Bongjoon,Oh, Eun Seul,Bang, Joon Seok,Lee, Yoon Jeong,Yoo, Jong-Sun,Yu, Hyunmin,Yoon, Joowon,Hyung, Kyeong Eun,Park, So-Young,Hwang, Kwang Woo Canadian Science Publishing 2011 Canadian journal of physiology and pharmacology Vol.89 No.6
<P> Four Lactobacillus strains - Lactobacillus plantarum CJLP133, L. plantarum CJLP243, L. plantarum CJNR26, and Lactobacillus gasseri CJMF3 - were isolated from Korean fermented food or healthy infant feces, and their capacity to modulate cellular and humoral immune responses was studied. Feeding of the tested lactobacilli for 8 weeks did not alter the weight of and cell numbers in the spleen of mice. However, CJLP133 and CJLP243 strains increased the T lymphocyte population in the spleen of mice, while CJNR26 and CJMF3 increased the B lymphocyte population. In splenocytes treated with concanavalin A, ingestion of CJLP133 and CJLP243 promoted T lymphocyte proliferation and secretion of T cell cytokines, whereas feeding of the CJNR26 and CJMF3 strains enhanced B lymphocyte proliferation in splenocytes treated with lipopolysaccharide and plaque formation. These results suggest that CJLP133 and CJLP243 have immunostimulating activity through the enhancement of T cell activation, while CJNR26 and CJMF3 exhibit immunopotentiation through the increment of B cell activation. </P>
HBV : PE-023 ; Lower quantitative HBsAg level in patients with HCC than in patients without HCC
( Yu Jin Kim ),( Yong Han Paik ),( Yang Won Min ),( Geum Youn Gwak ),( Moon Seok Choi ),( Joon Hyeok Lee ),( Kwang Cheol Koh ),( Seung Woon Paik ),( Byung Chul Yoo ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background: Recently, quantitative hepatitis B surface antigen (qHBsAg) levels in chronic hepatitis B (CHB) have been described. However, data on qHBsAg levels according to the presence of hepatocellular carcinoma (HCC) is insufficient. We aimed to describe and compare qHBsAg levels in CHB patients with or without HCC. Methods: We retrospectively enrolled 739 treatment naive CHB patients from January 2009 to December 2010. We reviewed their medical record collected data including qHBsAg level, hepatitis B virus (HBV) DNA, and disease status when HBsAg level was quantified. Presence of HCC was defined as described in KASL guideline. qHBsAg levels were compared using student`s t- test or ANOVA between HCC and non-HCC patients. Results: Two hundred eighteen patients (29.5%) had HCC. Mean value of qHBsAg (log IU/mL) level was 2.53 ± 1.17 in patients with HCC and 3.03 ± 1.32 in non-HCC patients (p<0.000) and HBV DNA (log IU/m) level was 4.13 ±2.25 and 4.3 ± 2.71 (p=0.419), respectively. qHBsAg level was compared in patients with HCC vs without HCC according to each phase of CHB: 3.20 ± 0.58 (n=36) vs 4.10 ± 0.68 (n=146) in HBeAg positive hepatitis (p<0.000), 2.26 ± 1.13(n=60) vs 2.66 ± 1.27 (n=277) in HBeAg negative hepatitis (p=0.027), 3.30 ± 0.35 (n=12) vs 3.49 ± 0.77 (n=28) in HBeAg positive hepatitis with liver cirrhosis (LC) (p=0.059), and 2.37 ± 1.27 (n=110) vs 2.09 ± 1.29 (n=70) in HBeAg negative hepatitis with LC. In 218 patients with HCC, qHBsAg level was 2.46 ± 1.24 in patients with LC (n=122) and 2.61 ± 1.06 without LC (p=0.346). Conclusions: In this study, qHBsAg level was not higher in patients with HCC than in patients without HCC. This tendency was observed regardless of the phase of CHB.
Kwang-Won Yu,Jong-Hyun Hwang 한국식품영양과학회 2001 Preventive Nutrition and Food Science Vol.6 No.3
Bone marrow cell proliferating arabinogalactan-like polysaccharide (ALR-3Ha-l-l) has been purified from rhizomes of Atractylodes lancea DC. In order to characterize the essential structure of ALR-3Ha-l-l for expression of the activity, sequential enzymatic digestion using exo-α-L-arabinofuranosidase (AFase) and exo-β-D- (1→3)-galactanase (GNase) was employed. After ALR-3Ha-l-l was digested with the AFase, the GNase digestion cleaved only 10% and 23% of 3-linked and 3,6-branched galactose, respectively, from arabinose-trimmed ALR-3Ha-1-1 (AT-ALR- 3Ha-1-1), and gave small amounts of intermediate size (AT-G-2) and shorter oligosaccharides (AT-G-3) fractions in addition to a large amount of the GNase resistant fraction (AT-G-1). When AT-G-1 was redigested gradually with the AFase and GNase, it released trace amounts of oligosaccharides in addition to a large amount of the resistant fraction. When the final enzyme-resistant fraction from AT-G-1 was digested simultaneously with both AFase and GNase, the resistant fraction was significantly degraded into two long fragments (3AT-3G-l and 2). The mixture of digestion products from the first GNase digestion of AT-ALR-3Ha-1-1 showed a significantly decreased bone marrow cell proliferation activity to about 30% of the activity of ALR-3Ha-1-1, but the GNase resistant fraction (AT-G-1) still had significant activity. Although the second gradual enzymatic digestion of AT-G-l showed a marginal decrease in activity, the resulting fragments (3AT-3G-1 and 2) by the final simultaneous enzymatic digestion lost most of the activity. Component sugar, methylation and FAB-MS analyses indicated that the digestion products (AT-G-2, AT-G-3, 2AT-2G-2 and 2AT-2G-3) released from AT-ALR-3Ha-1-1 by the sequential enzymatic digestion contained galactose-containing oligosaccharides mainly comprising 6-linked galactose, that some of which were partially arabinosylated, and these oligosaccharides were attached to β-D-(1→3)-galactan backbone in its non-reducing terminal side as side chains.
Yu, Kwang-Won,Hwang, Jong-Hyun The Korean Society of Food Science and Nutrition 2001 Preventive Nutrition and Food Science Vol.6 No.3
Bone marrow cell proliferating arabinogalactan-like polysaccharide (ALR-3IIa-1-1) has been purified from rhizomes of Atractylodes lancea DC. In order to characterize the essential structure of ALR-3IIa-1-1 for expression of the activity, sequential enzymatic digestion using ego-$\alpha$-L-arabinofurasidase (AFase) and ego-$\beta$-D-(1longrightarrow3)-galactanase (GNase) was employed. After ALR-3IIa-1-1 was digested with the AFase, the GNase digestion cleaved only 10% and 23% of 3-linked and 3,6-branched galactose, respectively, from arabinose-trimmed ALR-3IIa-1-1 (AT-ALR-3IIa-1-1), and gave small amounts of intermediate size (AT-G-2) and shorter oligosaccharides (AT-G-3) fractions in addition to a large amount of the GNase resistant fraction (AT-G-1). When AT-G-1 was redigested gradually with the AFase and GNase, it released trace amounts of oligosaccharides in addition to a large amount of the resistant fraction. When the final enzyme-resistant fraction from AT-G-1 was digested simultaneously with both AFase and GNase, the resistant fraction was significantly degraded into two long fragments (3AT-3G-1 and 2). The mixture of digestion products from the first GNase digestion of AT-ALR-3IIa-1-1 showed a significantly decreased bone marrow cell proliferation activity to about 30% of the activity of ALR-3IIa-1-1, but the GNase resistant fraction (AT-7-1) still had significant activity. Although the second gradual enzymatic digestion of AT-G-1 showed a marginal decrease in activity, the resulting fragments (3AT-3G-1 and 2) by the final simultaneous enzymatic digestion lost most of the activity. Component sugar, methylation and FAB-MS analyses indicated that the digestion products (AT-G-21 AT-G-31 2AT-2G-2 and 2AT-2G-3) released from AT-ALR-3IIa-1-1 by the sequential enzymatic digestion contained galactose-containing oligosaccharides mainly comprising 6-linked galactose, that some of which were partially arabinosylated, and these oligosaccharides were attached to $\beta$-D-(1longrightarrow3)-galactan backbone in its non-reducing terminal side as side chains.