A cilium in the human mesangial cell.
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Biomedical subjects
Publications and source records attributed to T Shimamura.
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Between January 1986 and March 1988, 35 cases with primary liver cancer were treated by arterial infusion therapy using implanted reservoir. Twenty-one of these cases were treated by the repeated infusion of ADM and CDDP. Results were as follows. 1) Three of 7 non-curatively resected cases died, with a mean survival time of 11 months. Four cases survival for at most 14 months. 2) The response rate (PR) of whole unresectable cases was 29.2%. The cumulative survival rate after treatment was 52.5% at one year. 3) The response rate (PR) of the unresectable cases which were treated with ADM CDDP intraarterial infusion was 33.3%. The cumulative survival rate after treatment was 63.5% at one year. 4) Severe side effects and complications were not seen. We suggested that this form of therapy could prolong the survival time of unresectable hepatoma.
Vesical foreign bodies readily lead to urolith formation but not in Brattleboro rats with diabetes insipidus. This experiment was designed to examine the roles of vesical foreign bodies, urine osmolality, and vesical infection in the formation of uroliths and associated reactive urothelial hyperplasia. ADH-deficient Brattleboro rats received surgical insertion of a silk suture in the bladder. Their bladders were infected with intravesical injection of urease positive P. vulgaris, while controls were similarly injected with sterile Ringer's sol. They received daily injections of either pitressin tannate in oil (1 U/kg body weight) or peanut oil. Urine flow rate, urine osmolality, urine culture, and gross and light microscopic examinations of the bladders were carried out at the end of 4th week. The results indicated that uroliths readily formed in the presence of all three factors; vesical foreign bodies, high urine osmolality, and infection, but not as readily in the presence of two or less of these three factors. The urothelial hyperplasia was prominent in infected bladders followed by non-infected bladder with high osmolar and low osmolar urine in this order.
Dietary phosphate has recently been recognized as a factor which might influence the rate of progression of a chronic renal disease. In order to examine the role of dietary phosphate, 1&3/4 partially nephrectomized rats (Nx) were fed Purina rat chow supplemented with either 15 g % dihydroxyaluminum aminoacetate (DHAAA), chelator of intestinal phosphate absorption, or 15 g % of half and half mixture of glycine and gum arabic. At the end of the 7th week, renal functional parameters, blood pressure, plasma electrolytes, parathyroid glands, and renal morphology were examined. Nx with chelator demonstrated a statistically lower value of BUN, plasma creatinine, plasma phosphate, systolic blood pressure, renal weight, glomerulosclerosis index, and 24 hours' urinary protein output than Nx without chelator. Nx without chelator showed larger parathyroid glands than Nx with chelator. Under the experimental condition, the inhibition of intestinal phosphate absorption in rats with subtotal nephrectomy delayed the progression of glomerulosclerosis, preserved the renal function, and prevented the enlargement of parathyroid glands.
Glomerulosclerosis and vascular lesions occurring in rats receiving 11-deoxycorticosterone and salt-loading have been studied in order to examine their relationship. The glomerular lesion started as focal segmental sclerosis. The globally sclerosed glomeruli were enlarged in size, demonstrating that these showed no evidence of ischemic atrophy. Advanced glomerulosclerosis occurred independent of preglomerular arteriolar pathologic lesion. No meaningful structural changes were observed in the arterial system. In conclusion, DOC-salt-induced glomerulosclerosis started as segmental lesion, occurred independent of structural alterations in the preglomerular arterioles, and took place without evidence of intrarenal arterial stenosis. Further studies are necessary to clarify about the role of hemodynamic stress-related injury to glomerular microcirculatory system as a major cause for DOC-Salt-induced glomerulosclerosis.
Foreign bodies in the urinary tract induce uroliths. This study examined reactions to vesical foreign bodies in Brattleboro rats manifesting diabetes insipidus and Sprague-Dawley rats. A silk suture was placed in the bladder of these rats and the occurrence of vesical uroliths, stone composition, and mucosal morphology were examined. Sprague-Dawley rats readily formed bladder stones in addition to a urolith formed over the suture, but there was little evidence that Brattleboro rats developed similar stones. Stone composition was primarily ammonium magnesium phosphate. The mucosal reactive hyperplasia was pronounced in the Sprague-Dawley, but was negligible in the Brattleboro rats. In conclusion, vesical foreign bodies readily induced uroliths in Sprague-Dawley rats, but there was no similar evidence in Brattleboro rats. It is suggested that the excessive diuresis of the latter may play a major role for this resistance to form stones, but the precise mechanisms of it are complex and remain to be explored.
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A silk suture in the urinary bladder of rats induces tumorous growths of urothelia. Whether these tumorous growths are due to initiation or due to promotion by the suture remains unknown. A 3-O silk suture was therefore placed in the bladders of rats for 4 or 8 weeks. After removal of the suture and a period of recovery, the bladders of these and sham-operated control rats were exposed to N-methyl-N-nitrosourea (MNU) in order to examine whether the effects of the suture were reversible following its removal from the bladder. In addition, the bladder mucosa was exposed to either MNU or Ringer's solution followed by placement of the silk suture in the bladder wall in order to examine promotor activity of the suture. The tumor incidence induced by MNU was little influenced by the prior temporary placement of the suture in the bladder wall, thus indicating a reversibility of the effects of the suture. The placement of the silk suture in the bladder wall that had a prior exposure to MNU resulted in a significant incidence of invasive tumors. All these results are consistent with the fact that a silk suture in the bladder acts as a promoter but not as an initiator.
As reported in a previous paper by the authors (J. Biochem. 99, 227-235, 1986), the Fab' of a monoclonal antibody, VIA2 IgG1, prepared by fusion of splenic cells of a mouse immunized with guinea-pig peritoneal macrophages with a myeloma cells line, completely inhibits the binding of ovalbumin (OA)-complexed IgG1 antibody to macrophages, but only partially the binding of OA-complexed IgG2 antibody. Based on these results, it was proposed that the cells have at least two types of Fc receptor (FcR) for homologous IgG isotypes: FcR2 for IgG2 and FcR1.2 for both IgG2 and IgG1, and also that VIA2 IgG1 is anti-FcR1.2 antibody. Thereafter, complete inhibition of the binding of OA-complexed IgG2 antibody to macrophages occurred when the Fab' of another monoclonal antibody, VIIA1 IgG1 was added to the Fab' of VIA2 IgG1, whereas the former did not affect the binding of OA-complexed IgG1 antibody. This effect of the Fab' of VIIA1 IgG1 indicates that VIIA1 IgG1 is a monoclonal antibody capable of selectively blocking the binding of OA-complexed IgG2 antibody to FcR2. When the antigen of VIIA1 IgG1 was isolated by affinity chromatography on the F(ab')2 of the antibody coupled to Sepharose, it gave a single band with a mol. wt of 52,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. It moved slightly faster than the FcR1.2 with a mol. wt of 55,000, which was isolated by the use of VIA2 IgG1, and corresponded to the fast moving portion of the broad band of FcRs isolated with OA-complexed IgG2 antibody. These results strongly suggest that VIIA1 IgG1 is a monoclonal antibody to FcR2.
Ovalbumin (OA)-complexed guinea-pig IgG1 and IgG2 antibodies were found to bind to homologous polymorphonuclear leukocytes (PMNs). As these bindings are assumed to be mediated by certain Fc receptors (FcRs) for IgG1 and IgG2, the variety and properties of the FcRs on the cells were investigated by the use of two monoclonal antibodies to guinea-pig macrophage FcRs which were prepared by Shimamura T. et al., 1987 (Molec. Immun. 24, 67-74): VI A2 IgG1 to the FcR for IgG1 and IgG2 (FcR1,2) and VII A1 IgG1 to the FcR for IgG2 (FcR2). PMNs were shown to bind the Fab' of VI A2 IgG1 (VI A2 Fab') by flow cytofluorometry, suggesting that the cells possess a certain FcR which cross-reacts antigenically with macrophage FcR1,2. In fact, VI A2 Fab' inhibited completely the binding of OA-complexed IgG1 antibody to the cells. When the FcR was isolated by affinity chromatography on the F(ab')2 of VI A2 IgG1 coupled to Sepharose, it gave a 55,000 mol. wt band on sodium dodecylsulfate-polyacrylamide gel electrophoresis, as in the case of macrophage FcR1,2. The number of the FcR molecules per PMN cell was estimated to be 2 X 10(4) by measuring the binding of 125I-VI A2 Fab'. The binding of OA-complexed IgG2 antibody to PMNs was also inhibited with VI A2 Fab', but partially. This finding indicates that the FcR bound by VI A2 Fab' may be an FcR1,2 which is able to bind both OA-complexed IgG1 and IgG2 antibodies, and also that PMNs possess another FcR, namely FcR2 which binds IgG2 antibody alone. The Fab' of VII A1 IgG1 (VII A1 Fab'), on the other hand, did not exhibit any inhibitory activity on the bindings of OA-complexed IgG1 and IgG2 antibodies to PMNs. Since no evidence indicating the binding of VII A1 Fab' to PMN cells was obtained by flow cytofluorometry, the FcR2 of PMNs may be antigenically different from its macrophage counterpart. In conclusion, these results indicate that two distinct types of FcR for IgG isotypes exist on guinea-pig PMN cells: FcR1,2 similar to macrophage FcR1,2, and FcR2 distinct from macrophage FcR2.
We examined the effect of arsenic (As) on the immune response of mice to sheep erythrocytes, assaying the spleen for plaque-forming cells (PFC). The effect of As on the PFC response to sheep erythrocytes was dose-dependent. At high doses of As the PFC response was erythrocytes was dose-dependent. At high doses of As the PFC response was suppressed, whereas it enhanced the response at low doses. The suppression was due to the cytotoxic action of As against lymphocytes generally. On the other hand, enhancement was seen on the addition of As at the start of the culture or as a result of pretreatment of normal spleen cells with As. Even low doses of As were cytotoxic, to both B and T cells. They differed, however, in their susceptibility to As. When normal spleen cells were added to the culture of As-treated spleen cells, the enhancement of the PFC response was reversed. Suppressor-inducer B cells, in the normal spleen cells, could not induce suppressor T cells from As-treated spleen cells. And As did not affect suppressor T cells. These findings indicate that As deletes the precursors of suppressor T cells from normal spleen cells, and thus enhances the immune response.
This study is to describe the reaction of urothelial cells to a silk suture placed surgically in the urinary bladder. Experimental rats have a single silk suture transmurally inserted in the wall and lumen of the bladder. The controls received sham operations. At various time intervals up to the 54th week, the sequence of morphologic events which took place in the bladder wall has been studied by gross and by light and electron microscopic examinations. The mucosal hyperplasia was the major finding for those sacrificed at weeks 2, 4, and 8. A single growth or multiple polypoid growths composed of well differentiated urothelial cells were found at weeks 16, 24, and 54. None of these growths were invasive. They exhibited little evidence of progressive morphologic change with time. Ultrastructurally, the tumor cells essentially showed characteristics of urothelial cells. None of the controls developed a similar urothelial growth. In conclusion, presence of a silk suture in the urinary bladder resulted in mucosal hyperplasia followed by noninvasive tumorous growth of well differentiated transitional cells. Exact mechanisms of this growth promotion by a silk suture and the potential of the growths becoming invasive neoplasms remain to be determined.
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Tryptophan, its metabolites and related enzyme activity in synovial fluid, blood and urine in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) were measured. The levels of tryptophan, kynurenine and anthranilic acid in the synovial fluid higher in RA were than in OA, whereas the xanthurenic acid level was equal in RA and OA. Indoleamine 2, 3-dioxygenase activity in the synovial membrane was higher in RA than in OA. 5-Hydroxytryptamine (5-HT) levels in the synovial fluid and the blood and the 5-hydroxyindole acetic acid (5-HIAA) level in the synovial fluid were essentially the same for both diseases. However, the 5-HIAA level in the serum of RA patients was higher than in those with OA, and the 5-HIAA level in the urine of RA patients was lower than in those with OA. In addition, monoamine oxidase-A and B activity in the synovial fluid of RA patients was decreased than in those with OA. These findings suggest that metabolism of tryptophan is altered in patients with RA.
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The variety and properties of Fc receptors (FcR's) for homologous IgG on guinea pig peritoneal macrophages were investigated with the use of a mouse monoclonal antibody, VIA2 IgG1, prepared by fusion of splenic cells of a mouse immunized with guinea pig macrophages with a mouse myeloma cell line. VIA2 IgG1 completely inhibited the formation of macrophage rosettes with IgG1 antibody-sensitized erythrocytes, but not that with IgG2 antibody-sensitized erythrocytes. The Fab' of VIA2 IgG1 also completely inhibited the bindings of both monomeric and ovalbumin-bound IgG1 antibodies to macrophages. On the other hand, the Fab' did not affect the binding of monomeric IgG2 antibody to macrophages, although it partially inhibited that of ovalbumin-bound IgG2 antibody. These results show that at least two distinct types of FcR are present on guinea pig macrophages; one (FcR1,2) binds monomeric IgG1 antibody and also antigen-bound IgG1 and IgG2 antibodies, and the other (FcR2) binds monomeric and antigen-bound IgG2 antibodies alone, and also that VIA2 IgG1 binds specifically to FcR1,2. When FcR1,2 was isolated by affinity chromatography on F(ab')2 of VIA2 IgG1 coupled to Sepharose, it gave a main band with a molecular weight of 55,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, which was indistinguishable from the main band isolated with the IgG1 immune complex. The number of FcR1,2 per macrophage cell was estimated to be 2 X 10(5) by measuring the binding of 125I-Fab' of VIA2 IgG1.
We found that thiols reduced the amount of cholera toxin produced by Vibrio cholerae 569B in vitro. A sulfhydryl group at least was necessary for the reduction of cholera toxin production by thiols.