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Myung Jae Kang 2 Articles
An Experimental Study of DMBA (9,10-Dimethyl-1,2-Benzanthracene) Induced Knee Joint Tumors in the Rats.
Myung Jae Kang, Dong Geun Lee, Sam Im Choi, Sang Ho Kim
Korean J Pathol. 1988;22(4):424-434.
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AbstractAbstract PDF
For the morphological analysis of DMBA (9,10-diemethyl-1,2-benzanthracene) induced tumor, thirty Sprague-Dawley rats were received 0.1 ml of a 2% paraffin solution of DMBA into the knee joint cavity, which was repeated three times at an interval of 4 weeks. The induced tumor masses were removed at the 12th week after the first injection. Histological and histochemical examinations (H & E, PAS, alcian blue, Van Gieson, prussian blue, reticulin, PTAH stain) and enzyme histochemical examinations (acid phosphatase, alkaline phosphatase, alpha-naphthyl acetate esterase) were performed. The results were as follows: 1) By the 12th week after the first injection of DMBA, the tumor incidence rate was 20 percent. 2) On histological and histochemical examination, most of the induced tumor disclosed the features of the fibrous histiocytoma originating from mesenchymal cells, and the remains sweat gland adenoma and adenocarcinoma originating from epithelial cells. 3) On enzyme histochemical examination, most of the mesenchymal cell-derived tumor cells showed positive reactions for acid phosphatase and alpha-naphthyl acetate esterase, which were similar characteristic features of enzyme stains as shown in the component cells of fibrous histiocytoma.
An Experimental Study of Pathogenesis of Duodenal Ulceration Produced by Mepirizole.
Myung Jae Kang, Jae Ryong Jung, Hye Soo Lee, Sang Ho Kim
Korean J Pathol. 1988;22(4):383-392.
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AbstractAbstract PDF
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.

J Pathol Transl Med : Journal of Pathology and Translational Medicine