Studies on echinococcosis. XXI. Electron microscopical observations on general structure of larval tissue of multilocular Echinococcus.
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Biomedical subjects
Publications and source records attributed to M Sugimura.
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OBJECTIVE: Our purpose was to compare the morphological changes in renal veins during normal pregnancy and pregnancy involving preeclampsia. METHODS: We used ultrasonography to measure maximum diameters of the right and left renal veins, and the diameter of the left renal vein where it crosses the abdominal aorta in normal pregnancy and preeclampsia. RESULTS: In women with normal pregnancy, the maximum diameter of the left renal vein was 5.5 +/- 1.9 mm in the 1st trimester, 5.8 +/- 1.6 mm in the 2nd trimester, and 6.4 +/- 1.4 mm in the 3rd trimester. The diameter of the left renal vein where it crosses the abdominal aorta was 3.3 +/- 1.1 mm in the 1st trimester, 4.1 +/- 1.3 mm in the 2nd trimester, and 4.0 +/- 0.9 mm in the 3rd trimester. In contrast, the maximum diameter of the left renal vein in women that had preeclampsia with onset in the 2nd trimester was 9.8 +/- 2.4 mm and that in women whose preeclampsia began in the 3rd trimester was 8.7 +/- 1.6 mm. The diameter of the left renal vein in preeclampsia was significantly larger than that in normal pregnancy (P < 0.05). There were no significant differences between normal pregnancy and preeclampsia in the maximum diameter of the right renal vein or that of the left renal vein where it crosses the abdominal aorta. CONCLUSIONS: In preeclamptic women, a dilatation of the left renal vein was observed. This suggests that the relative constriction and congestion of the left renal vein takes part in the pathophysiology of preeclampsia. Measurement of the diameter of the left renal vein would provide a simple, cost-effective tool for the diagnosis of preeclampsia.
Forty oral squamous cell carcinomas and 20 leukoplakias were examined for expression of p53 oncoprotein using an immunohistochemical technique with BP53-12 monoclonal antibody. Positive staining was found in 21/40 (52%) of the carcinomas and 2/20 (10%) of the leukoplakias. Furthermore, comparison of p53 expression with binding of PC10 monoclonal antibody to proliferating cell nuclear antigen (PCNA) and degree of histological malignancy in terms of invasion and histological differentiation of carcinomas demonstrated a positive correlation in both cases.
The purpose of this study was to evaluate the immediate loading of Brånemark System implants following placement with a screw-retained provisional prosthesis in edentulous patients. Twelve mandibular and 5 maxillary arches were treated from December 1997, including 3 bimaxillary patients. The provisional prosthesis, made of heat-polymerizing resin, had an inner casting of cobalt-chromium alloy to provide rigidity. The implants whose placement torque was more than 40 Ncm were immediately loaded. Implants that were placed with placement torque of less than 40 Ncm or that were associated with bone grafting were submerged. Following abutment connection, temporary cylinders were incorporated into the provisional prosthesis intraorally with autopolymerizing resin. After the provisional prosthesis was completed extraorally, it was screw-retained. After a 4- to 6-month healing period, a definitive prosthesis was fabricated and placed. Of the 140 immediately loaded implants, 136 osseointegrated during an 8- to 24-month follow-up period (97.2%). All 17 submerged implants osseointegrated. The results suggest that immediate loading of Brånemark System implants at the time of placement in edentulous patients can be a valuable adjunct to therapy and as predictable as delayed loading, in both mandibular and maxillary arches.
We have previously produced transgenic mice carrying the human renin gene, whose expression is regulated in a tissue-specific manner. In the present study, we further characterized expression of the transgene. Northern blot analysis showed that the human renin gene is expressed in the kidney but not in the liver of two lines of transgenic mice with 10 and 50 copies of the transgene, suggesting that the integrated copy number of the human renin gene does not influence the dominant-renal expression pattern. Immunohistochemical study using a monoclonal antibody specific for human renin demonstrated that expression of human renin in the transgenic mouse kidney is confined to the epithelioid juxtaglomerular cells. Transfection experiments indicated that the chloramphenicol acetyltransferase fusion gene containing the 3-kb upstream sequences of the renin gene is activated only in human epithelioid embryonic 293 cells derived from kidney but not in human HepG2 cells from liver. These findings suggest that transfer of the cloned renin gene into mice and in vitro cultured cell lines can give rise to cell type-specific expression.
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