Biomedical subjects
Publications and source records attributed to T Shimamura.
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Previous work has shown that normal mice respond to the intravenous injection of sheep erythrocytes (SRBC) with a transient increase in splenic cyclic AMP peaking after 2 minutes, and this cyclic AMP response has been shown to be due to prostaglandins (PGs) released from antigen-specific cells. In the present study, the cell type responsible for PG production in response to antigen was determined using a fluorescence-activated cell sorter (FACS) and an electron microscope. C57Bl/6 mice injected with SRBC showed a 2% increase of PGE-producing spleen cells relative to controls. In control mice injected with phosphate-buffered saline (PBS), 19% of the spleen cells produced PGE. An electron microscopic study of PGE-producing cells sorted on FACS showed that they were small lymphocytes and plasma cells. In addition, nude mice also increased the number of PGE-producing spleen cells in response to antigen. These findings suggest that lymphocytes involving at least B-cells respond to antigen with an increase in PGE production.
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The inner medulla and the cortex of the rat kidney were surgically traumatized or threaded with a silk suture, and the sequence of morphologic events occurring in these two topographic locations were studied by light microscopy on Days 7, 14, and 28. On Days 7, 14, and 28 following the infliction of the surgical trauma, such cellular reactions as mononuclear cell infiltration and fibroblastic proliferation were less intense in the injured site of the inner medulla than in the cortex. Numerous foreign body type giant cells appeared about the suture material in the cortex as early as Day 7 and were persistently present on Days 14 and 28. A similar type of foreign body giant cells did not appear about the suture material within the inner medulla throughout the experiment. Our results suggest that there is a difference in cellular reaction to injury or to a foreign body between the inner medulla and the cortex of rat kidneys.
Little is known about hepatic structural alterations induced by administration of the aromatic amine, N,N'-diacetylbenzidine. Therefore, we injected adult rats with this chemical at a dose of approximately 1 g/kg of body weight. Light and electron microscopy of liver specimens revealed hepatocellular degeneration and prominent changes in bile canaliculi, including dilation, disappearance of microvilli, and an apparent loss of structural integrity of the cell membrane. These findings were seen in the peripheral part of the hepatic lobules. Cirrhotic changes eventually developed. We concluded that N,N'-diacetylbenzidine injected intraperitoneally is capable of inflicting structural damage to the liver in rats.
Effects of inflammatory mediators such as serotonin, histamine, and bradykinin upon glomerular localization of i.v. administered ferritins have been investigated. These mediators appear to enhance accumulation of the i.v. injected ferritins in the glomerular capillary walls of rats.
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Twenty-seven of 37 non-toxigenic, urease-negative strains originally identified as Clostridium bifermentans that were isolated in the Antarctic are reidentified as C. sordellii by the tests for DNA-DNA homology, by the absence of mannose in the cell wall, and by growth inhibition of mannose. The test for cell wall sugar components of urease-negative and -positive strains of C. sordellii revealed that glucose, mannose, and rhamnose could not be detected in any of eight urease-negative strains used by galactose was detectable in seven of the eight strains and that glucose or galactose or both of the two sugars were present in the urease-positive strains tested.
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Rats were exposed to repeated episodes of hydropenia for periods of 5 and 16 weeks, and structural alterations of renal medulla were investigated by light and electron microscopy. The hydropenia induced, within the inner medulla, focally severe structural changes in the tubular and endothelia and loss of interstitial cells. The findings present evidence that repeated episodes of hydropenia are capable of inducing cellular alterations of the renal medulla, particularly in the interstitial cells.
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Renal papillary necrosis was produced in rats by administration of 2-bromoethylamine hydrobromide. The rats drank either 0.9 per cent sodium chloride solution or distilled water, and structural restoration of renal papilla and effect on urine-concentrating ability were examined. All rats drinking distilled water had no evidence of structural restoration of the injured papilla and no significant improvement of urine-concentrating ability. When rats started drinking 0.9 per cent sodium chloride solution shortly after indution of the necrosis, enhanced cellular reconstitution of the necrosed papillary tissue and partial restoration of urine-concentrating ability occurred in a significant number of rats. The most successful structural reparation was the collecting tubules, followed by the thin loops of Henle and the capillaries. Repopulation of the interstitial cells was the least successful. In conclusion, repair of necrosed renal papilla was enhanced when rats drank 0.9 per cent sodium chloride solution starting shortly after injection of renal papilla-necrotizing dose of 2-bromoethylamine hydrobromide.
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