No abstract available.

The authors have made a CD-ROM titled 'Atlas of Pathology (AP)' for medical students to understand histopathologic findings with ease. We used a 35 mm film scanner to convert an existing file into digital images. A pathologist and two professional programmers collaborated to create the program 'AtlasMaster 1.0' based on (IBM) PC for organization of previously captured digital images. Minimum system requirement for the 'AP' was Pentium II 166 MHz, 32 MB RAM, Windows 95 or 98, 800 600 resolution, 16-bit color, 20 speed CD-ROM drive. The 'AP' was composed of a execution file (Pathology_Atlas.exe), a DB file (pathology.mdb), and reference files (*.bmp, *.jpg, *.txt). The DB file contained fields for chapter, section, disease entity, and information for location of reference files. About 1,000 color images for various kinds of gross and microscopic pictures were stored in the CD-ROM and those were classified according to the chapters, sections, and disease entities. The 'AP' was easy to manipulate, and had advantages of self-learning for students. It could be applied to other fields in which many images were dealt with, such as histology, radiology, endoscopy, dermatology, and plastic surgery. The 'AP' was handy and very useful for medical students to study pathology and it would be a powerful self-learning tool.
CD-ROM* ; Dermatology ; Endoscopy ; Humans ; Pathology ; Students, Medical* ; Surgery, Plastic

BACKGROUND: Cardiac hypertrophy is the compensatory response of the myocadium to increased workload. Compensatory mechanisms come into play when the hypertrophied heart can no longer accommodate the increased demand or persistent stimuli. Although it has been reported that the molecular changes in hypertrophied hearts that initially mediate enhanced function may contribute to the development of heart failure, the structural/biochemical/molecular basis for myocardial contractile failure is still obscure. This study was aimed to clarify the structural basis for relation between hypertrophy and failure. METHOD: Nine pairs of rabbits were sacrificed at 8,12,24,48 hours and 1,2,4,6,8 weeks after experiment aortic constriction. There hearts were studied with routine histopathology. Each heart was weighed and compared with total body weight. Multiple sections were embedded in paraffin, sectioned at 5um, and stained with hematoxylin and cosin and Masson's trichrome and analysed. RESULTS: The heart weight to body weight ratio(g/Kg) increased progressively with time after aortic banding. Banding of the aorta in the rabbit resulted in multifocal areas of myofiber degeneration, necrosis and fibrosis through the wall of the left ventricle, in the papillary muscles of the left ventricle and in the left ventricular portions of the interventricular septum in rabbit of 6 and 8 weeks after aortic banding. By 4 weeks after banding, the foci of necrosis were not observed. CONCLUSION: There findings suggest that the increased necrosis, fibrosis in animals with cardiac hypertrophy induced by banding the aorta may play a role in progression to heart failure.
Animals ; Aorta ; Body Weight ; Cardiomegaly ; Constriction ; Fibrosis ; Heart Failure ; Heart Ventricles ; Heart* ; Hematoxylin ; Hypertrophy ; Necrosis* ; Papillary Muscles ; Paraffin ; Rabbits

No abstract available.
Humans ; Oligochaeta* ; Prospective Studies*

No abstract available.
Constriction, Pathologic*

We experienced the 17 hands of 11 patients with Dupuytren disease, which was known as relatively rare in orientals. Retrospectively, we analyse it and the results were followings; l. Among 11 patients, 10 patients were male and average age was 62.5 years (49 to 77 years) 2. Most (15 hands, 88%) of patients had symptoms of flexion contracture, nodule and contracted cord, simultaneously. 3. Occupation of patients was agricultural laborer in 9 patients (82%). 4. In 9 patients(82%); individual habit of alcoholic drinking, more than 3 times per week, and smoking, 1 package per day, over 20 years more, was observed. 5. In 15 hands (88%), ulnar side of fingers (4th+5th, 5th only or 3rd+4th+5th)was involved. 6. Surgical treatment was performed in 9 hands of 7 patients, with results of excellent in 6 hands (67%) and no recurrence, in average follow up 2.6 years (1.5 year to 3.7 year)
Alcoholics ; Clinical Study ; Contracture ; Drinking ; Dupuytren Contracture ; Fingers ; Follow-Up Studies ; Hand ; Humans ; Male ; Occupations ; Recurrence ; Retrospective Studies ; Smoke ; Smoking

No abstract available.
Cough* ; Humans ; Sarcoidosis* ; Skin*

No abstract available.
Caroli Disease*

No abstract available.
Ileum*

PURPOSE: Bile acids (especially deoxycholate) was known to be toxic and mutagenic on colon epithelium. They proposed at least four mechanisms for the bile acid toxicity. It is the one of these mechanisms that bile acid inhibits the xenobiotic metabolizing enzyme activity (esp glutathione S-transferase, GST). So we measured the cytosolic GST level of colon carcinoma cell lines after deoxycholate exposure whether or not the deoxycholate lowered the cytosolic GST activity. METHODS: Three colon cancer cell lines (LoVo, SW480, HT29) were used for this study. We calculated the cellular toxicity by MTS method. And cytosolic GST activity was measured according to the method as Habig described. For total GST activity, 2.5 mM 1-chloro-2,4-dinitrobenzene was used for substrate, and measured as absorbance in 340 nm. RESULTS: Basal cytosolic GST level for LoVo, SW480, HT29 cell line was 514.59+/-27.01, 291.63+/-38.44 and 344.58+/-47.92 nmol/min/mg cytosol protein. GST level did not changed significantly after 5 days culture without DCA. But GST level was decreased significantly to 128.63+/-21.35, 134.33+/-41.76 and 163.10+/-22.73 nmol/min/mg cytosol protein each cell line after 5 days deoxycholate exposure (p<0.005). CONCLUSION: Cytosolic GST level was lowered significantly after deoxycholate exposure for 5 days. One of the mechanisms of bile acid toxicity for colon cancer cell is proposed to inhibit cytosolic GST activity.
Bile ; Bile Acids and Salts ; Cell Line* ; Colon* ; Colonic Neoplasms* ; Cytosol* ; Deoxycholic Acid* ; Dinitrochlorobenzene ; Epithelium ; Glutathione Transferase* ; Glutathione* ; HT29 Cells ; Humans