[Treatment of the newborn in asphyxia: resuscitation].
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Biomedical subjects
Publications and source records attributed to H Sawa.
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PURPOSE: To determine the site of rebleeding into the vitreous after vitrectomy in patients with diabetic retinopathy. METHODS: We studied in detail 4 eyes of 4 patients in whom rebleeding into the vitreous followed successful vitrectomy for proliferative diabetic retinopathy. In addition, the fibrous membrane removed at surgery was studied by light and electron microscopy. RESULTS: In these 4 eyes, the second operation revealed that the source of the vitreous rebleeding was from a fibrovascular proliferation around the scleral wounds of the initial surgery, and no other neovascularization and/or reproliferation were observed in the whole retina. Rebleeding in these 4 eyes developed at an average of 9 weeks after initial surgery. The proliferative membrane was oval in shape and expanded from the residual vitreous that had been incarcerated in the scleral wound. The proliferative membrane removed during vitrectomy was poor in cellular components and contained extracellular matrix. Blood vessels of various sizes were also present. Electron microscopy showed the membrane was rich in extracellular components and contained high and low electron density cells. These cells often had microvilli and seemed to be of epithelial origin. CONCLUSIONS: These findings show that vitreous rebleeding may develop from fibrovascular proliferation from the scleral wound created during initial surgery. The proliferated membrane showed histological similarities with the fibrovascular proliferation usually seen in the diabetic retina and may represent a type of anterior proliferation secondary to retinal ischemia.
Three eyes of 3 patients were operated on for severe proliferative diabetic retinopathy with tractional and/or rhegmatogenous retinal detachment using perfluoro-n-octane as temporary tamponade. The perfluorocarbon was removed at the end of the procedure. Intraocular tamponade was provided by a long-acting gas in all eyes. The intraoperative use of perfluorocarbon effectively facilitated retinal flattening and endophotocoagulation. Anatomical success was obtained in all 3 cases, with a minimum follow-up of 10 months. Visual acuity improved in all eyes. The main advantages of perfluorocarbon are that it enables easy flattening of the posterior retinal folds and effective endophotocoagulation with good visual conditions.
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Neuronal and glial specific proteins were studied in 35 cases of medulloblastomas, using immunohistochemical methods and antibodies to neurofilament triplet proteins (NF68Kd, NF160Kd, NF210Kd), gamma-enolase, GFAP, S-100 protein, and myelin basic protein. NF160Kd positive cells were observed in 12 of the 35 cases. NF160Kd positive cells were noted in 2, but NF210Kd positive cells were not detected. Gamma-enolase positive cells were observed in 23 cases. GFAP and S-100 protein positive cells were seen in 25 and 28 cases respectively; many of these cells were reactive astrocytes. The myelin basic protein positive cells could not be identified. The expression of neuronal and glial proteins had no relation to the postoperative survival of patients with medulloblastoma, but gamma-enolase may be one factor for evaluating prognosis.
We have previously described how mouse monoclonal antibody Mab S-11E10 specifically stained ruffling membranes and filopodia of cultured human glioma cells. We found that this antibody stains ruffling membranes, not only of human astrocytes and glioma cells, but also of rat astrocytes and rat C6 glioma cells. In addition, we newly prepared rabbit polyclonal antibody for the antigens, which were eluted by Mab S-11E10 affigel 10 (Bio Rad) affinity column chromatography from cultured rat C6 glioma cells. The polyclonal antibody detects 65KDa, 57KDa, 46KDa, 43KDa bands in Western blotting analysis and specifically stained ruffling membranes of human glioma cells on cell spreading. Using the polyclonal antibody, we studied the change of the distribution of the antigens during cell spreading and in fully spread cells. At the beginning of cell spreading, ruffling membranes were specifically stained, but 72 hours after plating the immunofluorescence was localized in membranes of supranuclear regions and small protuberances. Furthermore, we semi-quantitatively measured the contents of the antigens detected by the polyclonal antibody, using dot blotting immunoassay. The contents of the antigens rapidly increased at the beginning of cell spreading and thereafter gradually reduced. The change of the contents seemed to be time--and cell density--dependent and to relate to the extent of cell spreading. These results suggest that the antigens may play an important role in cell spreading of glial cells.
Seven resected medulloblastomas were inoculated into hereditary athymic (nude) and asplenic athymic (Lasat) mice. From these, only one transplantable tumor line was obtained, in nude mice. We studied the transplanted medulloblastoma immunohistochemically and by electron microscope. In addition, using enzyme immunoassay, the gamma-enolase contents of the transplanted medulloblastomas were measured and the results were compared with those of transplanted glioblastomas. Neurofilament proteins (NF68Kd, NF160Kd) and gamma-enolase positive cells were maintained in the successful transplants of medulloblastomas, but the GFAP positive cells were lost. Under the electron microscope, a few cells with ten nanometer intermediate filaments and microtubules were observed in the transplanted tumor. The medulloblastoma possesses some of the neuronal characteristics which are maintained in the transplants in nude mice.
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BACKGROUND: The expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and class II major histocompatibility complex antigens was studied in control lung tissue and preserved human donor lungs. The three controls were represented by wedge biopsy specimens taken from non-neoplastic lung surrounding bronchogenic carcinomas. METHODS: Nine lungs were harvested from six brain-dead donors, flushed with Euro-Collins solution or low potassium-dextran-glucose solution, and stored at 1 degree C or 10 degrees C. Samples of the latter organs were taken at the time of surgical harvest (baseline) and after 2, 12, 24, and 48 hours of preservation time. Immunostains with monoclonal antibodies against intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and class II major histocompatibility complex molecules were performed on all samples, and the relative presence of these determinants was evaluated. RESULTS: In both the controls and preserved lungs, intercellular adhesion molecule-1 expression was intense in the septal capillary endothelium and alveolar pneumocytes, but essentially absent in bronchial epithelium. Vascular cell adhesion molecule-1 was moderately to strongly labeled in the endothelia of large and small blood vessels of all types, and it was not seen in other cell types. Class II major histocompatibility complex antigens were variably observed in pulmonary epithelial cells, but they were not expressed by endothelia. There appeared to be no significant difference in the immunohistologic density of intercellular adhesion molecule-1 or vascular cell adhesion molecule-1 immunostaining in allografts at the specified time points of preservation; this conclusion was confirmed by Western blot analysis. Similar findings pertained to staining results for human leukocyte DR antigens. There was likewise no significant difference in the expression of the three analytes when donor lungs perfused with Euro-Collins solution versus low potassium-dextran-glucose solution were compared; this was also true of organs preserved at 1 degree C versus 10 degrees C. CONCLUSIONS: These results suggest that, in the immediate post-harvest period, modulations in the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, or class II major histocompatibility complex antigens in pulmonary allografts are not attributable to the influences of preservation conditions.