- Detection of HBV DNA in Needle Biopsied Paraffin Embedded Liver Tissues of Chronic Hepatitis B Patients by PCR: Comparison with Serological and Immunohistochemical Studies.
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Hye Soo Lee, Kahng Yeul Oh, Joo Heon Kim, Yoon Jeong Kim, Sam Im Choi, Dong Geun Lee, Sang Ho Kim
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Korean J Pathol. 1996;30(6):495-504.
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 Abstract
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- In this study, the prevalence of Hepatitis B virus(HBV) DNA in the needle biopsied paraffin embedded liver tissues of chronic hepatitis B patients by rapid nested PCR was examined. DNA was extracted by NaOH with boiling, and amplified by rapid air thermocycler with glass capillary tubes and nested PCR with two primer sets specific for the surface and the core genes of HBV. The PCR results were compared to that of serum HBeAg, serum HBV DNA by dot blot hybridization with a radioactive DNA probe, and tissue immunohistochemical (HBsAg/ HBcAg) studies. Among 44 patients with chronic hepatitis with serum HBsAg positivity, HBV DNA could be detected by PCR in 43 liver tissues (98%).
This results were comparable to the positive rates of 94%(31/33) for serum HBV DNA, 80%(35/44) for serum HBeAg, and 59%(26/44) and 75%(33/44) for tissue HBsAg and HBcAg, respectively. The accordance rate between tissue PCR and serum DNA probe testing was 91%. The results indicate that HBV DNA detection by rapid nested PCR of paraffin embedded liver tissues by needle biopsy is a more sensitive method to detect the HBV DNA carrier than the serum HBeAg or tissue HBsAg/HBcAg status, and is well correlated with the result of serum HBV DNA probe testing. Therefore this method is a practical indicator for the diagnosis and replication status in retrospective analysis.
- An Experimental Study of Pathogenesis of Duodenal Ulceration Produced by Mepirizole.
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Myung Jae Kang, Jae Ryong Jung, Hye Soo Lee, Sang Ho Kim
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Korean J Pathol. 1988;22(4):383-392.
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Abstract
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- To investigate the pathogenesis of the duodenal ulceration produced by mepirizole (1-(4-methoxy-6-methyl-2-pyrimidinyl)-3-methyl-5-methoxypyrazole) in rat, the effects of various concentraion and sorts of antiulcer drugs and truncal vagotomy on the mepirizole (200 mg/kg of body weight) induced duodenal ulcers were observed morphologically, and after mepirizole administration (200 mg/kg), amount and acidity of gastric jucie were measured sequently. The results were as follows: 1) In the control group of fasting for 24 hours after mepirizole administration only, duodenal ulcers were developed in all animals with 21.5+/-5.8 mm2 of ulcer index, perforation rate was 15%, and mortality rate was 0%. But lesions of the stomach were hemorrhagic and erosive with erosion index of 3.8+/-1.6 mm2. 2) The antiulcer drugs were significantly inhibited duodenal ulceration and gastric erosion produced by mepirizole although the inhibition effects were different. 3) After truncal vagotomy, duodenal ulcer and gastric erosion induced by mepirizole were also significantly inhibited. 4) On the gastric analysis, decrease of amount, increase of acidity, and decrease of concentration of gastric juice were observed after administration of mepirizole compared with nontreated normal group. Above findings suggest that the pathogenesis of the duodenal ulceration by mepirizole is the action of gastric acid on the duodenal mucosa with breakdown of defence mechanisms of the duodenum.
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