1.Expression of MUC3, MUC5AC, MUC6 and Epidermal Growth Factor Receptor in Gallbladder Epithelium according to Gallstone Composition.
Hyo Jung KIM ; Jae Seon KIM ; Kyoung Oh KIM ; Ki Ho PARK ; Hyung Joon YIM ; Jin Yong KIM ; Jong Eun YEON ; Jong Jae PARK ; Jae Jeong SHIM ; Kwan Soo BYUN ; Young Tae BAK ; Chang Hong LEE
The Korean Journal of Gastroenterology 2003;42(4):330-336
BACKGROUND/AIMS: Gallbladder (GB) mucin is one of the key factors in the gallstone formation. However, there is little information about the diversity of mucin secretion according to the stone composition. Epidermal growth factor receptor (EGFR) functions in proliferation including mucin secreting goblet cell hyperplasia. We compared the expressions of MUC3, MUC5AC, MUC6 and EGFR in the GB epithelium with cholesterol gallstones (GB-chol) group and pigment gallstones (GB-pig group). METHODS: GBs from elective laparoscopic cholecystectomy for the gallstone disease were studied. Stone composition was analyzed by the spectrophotometer. Immunohistochemical stain was performed using each monoclonal antibody. The percentage of stained proportion was scored by the NIH image program and the results were compared between both groups. RESULTS: Total 20 patients were enrolled (10 patients with cholesterol gallstones, 10 patients with pigment gallstones). The percentages of stained proportion for MUC3, MUC5AC, and MUC6 were 42+/-27%, 31+/-15%, and 17+/-9%, respectively in GB-chol group and 32+/-22%, 33+/-23%, and 15+/-10%, respectively in GB-pig group (p>0.05). The expression of EGFR was 50% (5/10) in the GB-chol group and 80% (8/10) in the GB-pig group respectively. CONCLUSIONS: There was no difference in the expressions of MUC3, MUC5AC, and MUC6 between the two groups. Further studies are needed to elucidate the role of EGFR in the gallstore formation.
Bile Pigments/analysis
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Cholelithiasis/chemistry/*metabolism
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Cholesterol/analysis
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Epithelium/metabolism
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Gallbladder/*metabolism
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Humans
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Immunohistochemistry
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Mucin 5AC
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Mucin-3
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Mucin-6
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Mucins/*analysis
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Receptor, Epidermal Growth Factor/*analysis
3.Bile Acid Analysis in Biliary Tract Canacer.
Jeong Youp PARK ; Byung Kyu PARK ; Jun Sang KO ; Seungmin BANG ; Si Young SONG ; Jae Bock CHUNG
Yonsei Medical Journal 2006;47(6):817-825
The etiology of biliary tract cancer is obscure, but there are evidences that bile acid plays a role in carcinogenesis. To find the association between biliary tract cancer and bile acid, this study compared the bile acid concentration and composition among patients with biliary cancer, biliary tract stones, and no biliary disease. Bile was compared among patients with biliary tract cancer (n = 26), biliary tract stones (n = 29), and disease free controls (n = 9). Samples were obtained by percutaneous transhepatic biliary drainage, endoscopic nasobiliary drainage, or gallbladder puncture, and analyzed for cholic, deoxycholic, chenodeoxycholic, lithocholic, and ursodeoxycholic acid composition. Total bile acid concentration was lower in the cancer group than the biliary stone and control groups; the proportions of deoxycholic (2.2% vs. 10.2% and 23.6%, p < 0.001 and p < 0.001, respectively) and lithocholic acid (0.3% vs. 0.6% and 1.0%, p = 0.065 and p < 0.001, respectively) were also lower. This result was similar when disease site was limited to bile duct or gallbladder. Analysis of cases with bilirubin < or = 2.0 mg/dL also showed lower total bile acid concentration and deoxycholic acid composition in the cancer group compared to controls (5.7% vs. 23.6%, p = 0.003). Although the presence of bile duct obstruction explains some of the difference in total concentration and composition of bile acid, there are other contributing mechanisms. We suspect the alteration of bile acid transport might decrease bile acid excretion and cause the accumulation of carcinogenic bile acid in bile duct epithelium.
Tumor Markers, Biological/analysis
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Middle Aged
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Male
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Humans
;
Gallbladder Neoplasms/metabolism
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Female
;
Cholic Acids/*analysis/metabolism
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Cholelithiasis/metabolism
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Biliary Tract Neoplasms/*chemistry/metabolism
;
Aged, 80 and over
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Aged
;
Adult
;
Adolescent
4.Bile Acid Analysis in Biliary Tract Canacer.
Jeong Youp PARK ; Byung Kyu PARK ; Jun Sang KO ; Seungmin BANG ; Si Young SONG ; Jae Bock CHUNG
Yonsei Medical Journal 2006;47(6):817-825
The etiology of biliary tract cancer is obscure, but there are evidences that bile acid plays a role in carcinogenesis. To find the association between biliary tract cancer and bile acid, this study compared the bile acid concentration and composition among patients with biliary cancer, biliary tract stones, and no biliary disease. Bile was compared among patients with biliary tract cancer (n = 26), biliary tract stones (n = 29), and disease free controls (n = 9). Samples were obtained by percutaneous transhepatic biliary drainage, endoscopic nasobiliary drainage, or gallbladder puncture, and analyzed for cholic, deoxycholic, chenodeoxycholic, lithocholic, and ursodeoxycholic acid composition. Total bile acid concentration was lower in the cancer group than the biliary stone and control groups; the proportions of deoxycholic (2.2% vs. 10.2% and 23.6%, p < 0.001 and p < 0.001, respectively) and lithocholic acid (0.3% vs. 0.6% and 1.0%, p = 0.065 and p < 0.001, respectively) were also lower. This result was similar when disease site was limited to bile duct or gallbladder. Analysis of cases with bilirubin < or = 2.0 mg/dL also showed lower total bile acid concentration and deoxycholic acid composition in the cancer group compared to controls (5.7% vs. 23.6%, p = 0.003). Although the presence of bile duct obstruction explains some of the difference in total concentration and composition of bile acid, there are other contributing mechanisms. We suspect the alteration of bile acid transport might decrease bile acid excretion and cause the accumulation of carcinogenic bile acid in bile duct epithelium.
Tumor Markers, Biological/analysis
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Middle Aged
;
Male
;
Humans
;
Gallbladder Neoplasms/metabolism
;
Female
;
Cholic Acids/*analysis/metabolism
;
Cholelithiasis/metabolism
;
Biliary Tract Neoplasms/*chemistry/metabolism
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Aged, 80 and over
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Aged
;
Adult
;
Adolescent
5.Regulation of calculus bovis on the function of mice oral fibroblasts.
Jianping DAI ; Jun CHEN ; Bangxing HAN ; Yufei BEI ; Xiaokun ZHOU
Chinese Journal of Biotechnology 2009;25(3):448-451
To explore the influence of calculus bovis on the function of primary cultured mice oral fibroblasts, we determined the effects of calculus bovis on the fibroblast proliferation, collagen production, matrix metalloproteinases-2, -9 activities and tissue inhibitor of metalloproteinase-1 production by MTT assay, chloramine T method, gelatin zymography and enzyme-linked immunosorbent assays respectively. The results showed that calculus bovis could significantly inhibit the proliferation of fibroblasts and collagen synthesis in a concentration dependent manner, could significantly (P<0.05) suppress matrix metalloproteinases-2 activity and very significantly (P<0.01) inhibit the production of tissue inhibitor of metalloproteinase-1. In conclusion, the major function of calculus bovis in the process of ulcer healing is not to promote tissue regeneration, the mechanism that calculus bovis inhibits collagen synthesis may be partly due to its ability to very significantly (P<0.01) suppress the production of tissue inhibitor of metalloproteinase-1.
Animals
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Cattle
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Cell Proliferation
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drug effects
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Cells, Cultured
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Cholelithiasis
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chemistry
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veterinary
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Collagen
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drug effects
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metabolism
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Fibroblasts
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cytology
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physiology
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Materia Medica
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pharmacology
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Mice
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Mice, Inbred BALB C
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Mouth Mucosa
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cytology
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Tissue Inhibitor of Metalloproteinase-1
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drug effects
;
metabolism