Morphology of retinal ganglion cells that regenerated axons along peripheral nerve graft in cats.
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Biomedical subjects
Publications and source records attributed to Y Fukuda.
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The effect of portal arterialization was examined in 20 heterotopic auxiliary rat livers. Portal blood was supplied from recipient iliac artery (0.58 mm in diameter) connected to the donor portal vein using the cuff technique. Portal hypertension caused by arterial blood pressure resulted in the immediate operative death by bleeding in four of the rats (20%) from the spontaneous rupture of the graft capsule. Severe graft congestion was noticed at autopsy 3-14 days after transplantation in 13 rats. Massive portal and sinusoidal congestion and focal hemorrhagic necrosis were confirmed by pathological examination. The results of our study demonstrate that the portal arterialization used in the auxiliary rat liver transplantation would not be applicable unless the optimal hemodynamic condition is warranted.
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The gastric epithelia of the rat after administrated with the minimal mixed bile acids and lysozyme for 9-weeks were studied using morphometric analysis and anti-Bromodeoxyuridine staining immunohistochemistry. Our results show that the atrophic changes and increased anti-BrdU antibody staining positive and mitotic cells of the pyloric glands area in the group administration only bile acids. Lysozyme inhibited bile acids activation on these changes of this area.
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The important processes in fetal pulmonary development are devoted to gain large surfaces for gas exchange and surfactant production. Basement membrane components, collagen fibers and elastic fibers are formed immediately around the epithelium in the early stage of lung development. Primordia of alveolar septa composed of elastic fibers and smooth muscle cells, develop in the glandular stage and form alveolar septa by protruding into the glandular lumina in later stages. The differentiation of alveolar walls, including the appearance of surfactant-producing cells, begins earlier in the proximal portion than in the distal portion of primitive alveoli. The process of fibrosis and regeneration in lung fibrosis defectively mimics the embryogenesis of the lung. Pulmonary structural remodeling occurs when the epithelial basement membrane, a scaffold for regenerating epithelial cells, is lost because of intra-alveolar fibrosis. In panacinar emphysema, simple and dilated air spaces are formed by the degradation of elastic fibers in alveolar septa, and this process may be reverse to the formation of alveolar septa in developing lung.
Fifty audiologically normal young adults, 25 men and 25 women, were submitted to the auditory brainstem response (ABR) test. The mean latencies of the waves I, II, III, IV and V and the interpeak latencies (IPLs) I-III, I-V and III-V were calculated and compared to the normative values published by other groups. We have observed a great similarity among these values, specially in the interpeak latencies. The latencies of the principal ABR parameters were compared between the sexes showing significant differences in all the waves, particularly in the wave V. No significant correlations were found among the values when the head size and the ABR principal components latencies were confronted.
The authors reports on a case of pulsatile tinnitus, where otoscopy revealed a retrotympanic mass. The initial tympanic diagnosis was confirmed by a CT-scan. However, surgical exploration revealed a large artery situated on the promontory. Post-operatory arteriography confirmed that this artery in the tympanic cavity was in fact the internal carotid artery.
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Two murine monoclonal antibodies, 2A3D2 and 2D11E2 (both IgM), which are directed to the gangliosides and sialoglycoproteins related to a rare blood group antigen, Cad, were obtained by using a ganglioside mixture prepared from human hepatocellular carcinoma cells (PLC/PRF/5) as the immunogen. These two monoclonal antibodies detected multiple ganglioside antigens present in the PLC/PRF/5 cells, and the major antigenic ganglioside was characterized as IV4GalNAc beta-GD1a, which has the carbohydrate structure GalNAc beta 1----4(NeuAc alpha 2----3)Gal beta 1----3GalNAc beta 1---- 4(NeuAc alpha 2----3)Gal beta 1----Cer. The two antibodies also reacted with GM2 (GalNAc beta 1----4[NeuAc alpha 2----3]Gal beta 1----4Glc beta 1----Cer) and a Cad-active lactoseries ganglioside (IV4GalNAc beta-sialosylparagloboside, GalNAc beta 1----4[NeuAc alpha 2----3]Gal beta 1----4GlcNAc beta 1---- 3Gal beta 1----4Glc beta 1----Cer), which have carbohydrate structures related to IV4GalNAc beta-GD1a. Beside gangliosides, both antibodies recognized the carbohydrate determinant carried by glycophorin A on very rare Cad-positive human RBC; the structure of which is GalNAc beta 1----4(NeuAc alpha 2----3)Gal beta 1----3(NeuAc alpha 2---- 6)GalNAc alpha 1----Ser/Thr. From these findings, it is clear that monoclonal antibodies 2A3D2 and 2D11E2 both recognize the nonreduced carbohydrate terminus composed of three sugar residues, GalNac beta 1----4(NeuAc alpha 2----3)Gal beta 1----R, and are useful for detecting the Cad-related antigen in cells and tissues. By using these monoclonal antibodies, it was revealed that many cultured human hepatocellular carcinoma cell lines and cancer tissues taken from patients with hepatocellular carcinoma contain both Cad-active glycoprotein antigens and related gangliosides, while normal liver tissues contain no appreciable amount of either species of antigen. The Cad-active glycoprotein antigens in cultured human hepatocellular carcinoma cells appeared as triplet bands having molecular weights of 92,000, 75,000, and 61,000, under either reducing or nonreducing conditions in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Essentially the same triplet proteins were observed in as many as 4 of 9 cases (44%) of cancer tissue from patients with hepatocellular carcinoma, but not in neighboring cirrhotic tissues or normal livers tissues. These results suggest that the rare blood group antigen Cad is associated with human cancers, especially hepatocellular carcinoma.
Gene expression of liver facilitated glucose transporter was rapidly induced during the liver regenerating process in rats. It reached maximum of 2.7 times at 8 hr of the regenerating course and returned to normal by 48 hr. The protein synthesis inhibitor, cycloheximide, did not interfere with the increased gene expression of liver facilitated glucose transporter. By contrast, erythrocyte/brain-type glucose transporter mRNA could not be detected in the livers of partially hepatectomized rats and sham-operated rats. The plasma glucose levels were transiently increased within 2 hr of the regenerative course and then decreased to a nadir at 4 hr. These results suggest that the increased gene expression of liver facilitated glucose transporter contributes to the decrease in plasma glucose levels.
An accumulation of sulfated and very complex, highly acidic glycolipids was observed in cultured human hepatocellular carcinoma cells. Among the cells tested, PLC/PRF/5 cells contained a significant amount of very complex sulfated acidic glycolipids, and HepG2 cells were characterized as having a large amount of relatively simple sulfated glycolipids. Several monoclonal antibodies (all IgM) directed to these sulfated and highly acidic glycolipids were established. Among them, 49-D6 and 7-E10 were both directed to SM3 (LacCer-II3-sulfate), a relatively simple sulfated glycolipid, and 34-A4 was directed to SD1a (GgOse4Cer II3,IV3-disulfate) and more complex sulfated glycolipids. The other four antibodies, 26-A10, 34-B9, 79-C8, and 16-E10, reacted with unknown highly acidic glycolipids, which were eluted in 0.9-2.7 M ammonium acetate in DEAE chromatography, indicating that these antigenic glycolipids were far more acidic than the usual glycolipids described until now. Analysis of the glycolipids extracted from the hepatocellular carcinoma tissues and cirrhotic livers of patients and from a normal liver with these monoclonal antibodies revealed that sulfated glycolipids having simple carbohydrate structures such as SM3 accumulated significantly in the cirrhotic liver (2 of 4 cases) as well as hepatocellular carcinoma tissue (15 of 17 cases, 88%), and more complex sulfated glycolipids and highly acidic glycolipids were much more specific to hepatocellular carcinoma tissues (10 of 17 cases, 59%) compared to the cirrhotic liver (0 of 4 cases).
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To determine whether a mitochondrial mRNA deficiency exists in mitochondrial myopathies, muscle biopsies from a patient with chronic progressive external ophthalmoplegia (CPEO) and a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) were studied using in situ hybridization. Histochemistry and immunohistochemistry were performed along with hybridization. Hybridization reactions were widely distributed over the sarcoplasm of all muscle fibers in the patient with MELAS. In the patient with CPEO, 80% of the fibers showed a marked decrease in density of autoradiographic grains. This marked decrease corresponded to the histochemical and immunohistochemical findings of a very weak staining of cytochrome c oxidase (CCO). The isotope-labeled cDNA probe used in in situ hybridization in this study complements a part of subunit I of CCO and a part of subunit II of complex I in the mitochondrial gene. Our results suggest a defect in the mRNA in this CPEO patient.
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