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Biomedical subjects

H Inage

Publications and source records attributed to H Inage.

At least 19 recordsLinked to original sources
PubMed1987

Studies on platelet function in patients with prostatic cancer. Preliminary report.

Platelet function was evaluated as an index of the thromboembolic tendency in patients with untreated, advanced prostatic cancer. Patients with benign prostatic hypertrophy (BPH) and similar age distribution served as a comparison group. Platelet aggregations were elevated in both groups, but not significantly different from each other. Platelet serotonin level in patients with prostatic cancer was lower than in patients with BPH (p less than 0.01), whereas plasma serotonin level in patients with prostatic cancer (within normal ranges in our series) was lower than in patients with BPH (p less than 0.001). Levels of 2 intraplatelet proteins, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) in the two groups of patients were similar. However, levels of beta-TG were elevated significantly in both groups of patients compared with those of healthy individuals. These studies revealed that the platelet serotonin levels in advanced prostatic cancer patients differed significantly from those in patients with BPH. The platelet serotonin level thus may provide an index of platelet activation in patients with prostatic cancer.

Aged↗
PubMed1986

Abnormal expression of complement receptor (CR1) in IgA nephritis: increase in erythrocytes and loss on glomeruli in patients with impaired renal function.

The number of complement receptor for C3b (CR1) molecules in erythrocytes from patients with renal diseases was measured by an immunoradiometric assay using monoclonal antibodies against CR1. IgA nephritis patients with high serum creatinine value (Scr) showed markedly elevated levels of CR1, whereas patients with normal Scr had normal CR1 levels. A similar increase in CR1 number was observed in membranoproliferative glomerular nephritis with high Scr. CR1 of these patients functioned normally as a cofactor of C3b inactivator in cleaving immune complex-bound C3b. In contrast, a high frequency (5/6) of negative staining of glomerular CR1 was observed in IgA nephritis patients with high Scr by immunofluorescence study. We postulate that the disease-associated, acquired factors at least in part contribute to the abnormal expression of CR1: elevated levels in erythrocytes and defective expression on glomeruli.

Anticoagulants↗
PubMed1986

Effect of chemical cationization of antigen on glomerular localization of immune complexes in active models of serum sickness nephritis in rabbits.

The effect of chemical cationization of antigen on the glomerular localization and formation of immune complexes (IC) was investigated utilizing the models of acute accelerated and chronic serum sickness nephritis in rabbits. In acute accelerated serum sickness, neither antibody nor antigen was detected in the glomerulus before the second injection of antigen. At 15 min after the challenge, rabbits given cationized BSA developed IC deposition along the peripheral capillary walls, whereas no IC deposition was found in rabbits given native BSA. In chronic serum sickness, rabbits injected with a high dose (5 mg/rabbit/day), but not a low dose (500 micrograms/rabbit/day) of cationized BSA developed membranous nephropathy with severe proteinuria. In the group given cationized BSA, the levels and avidity of antibodies were lower than in the group given native BSA. Sucrose density gradient analysis of the complexes composed of 125I-cationized BSA showed that IC formed in vivo were slightly larger than 7S. These antibody characteristics, i.e. low precipitation and low avidity, continued from early on to the late period of immunization. These results suggest that chemical cationization altered the immunogenicity of the antigen and resulted in the formation of antibody of low precipitability and low avidity, even during long-term immunization.

Animals↗
PubMed1986

Effect of chemical modification of antigen on characteristics of immune complexes and their glomerular localization in the murine renal tissues.

In order to investigate the effect of chemical cationization of antigen on the glomerular localization of immune complexes (IC), the glomerular localization was studied in passive serum sickness nephritis of mice using IC composed of antigens with various pI values and antibody raised against the unmodified antigen. The chemical cationization of antigen altered the interaction between antigen and antibody: as the pI of the antigen became higher, the precipitating efficiency of antigen-antibody complexes became lower or zero. This phenomenon was due to a decrease in valence of the antigen and a decrease in avidity between the cationized antigen and antibody directed against unmodified antigen. Therefore, the size of IC composed of the antigens with higher pI became smaller. However, the IC appeared not to dissociate in vivo and in vitro where the pI of antigen was between 9.15 and 10.25. The pI of the IC made with cationic antigen was also above 9.5. In the animals given IC composed of the antigens with higher pI values, peripheral glomerular localization of IC was increased. In contrast, in the animals given IC composed of unmodified antigen, focal mesangial deposition of IC was seen.

Animals↗
PubMed1986

Role of antigenic charge and antibody avidity on the glomerular immune complex localization in serum sickness of mice.

Passive injection of mice with preformed immune complexes (IC) made from cationized bovine serum albumin (BSA) and anti-native BSA antibody gave immune deposits along the glomerular capillary walls at predominantly subepithelial sites, while similar quantities of complexes made with native, anionized BSA did not deposit. Peripheral localization could be obtained also using low avidity antibody and a great excess of native BSA. Ultracentrifugation analysis showed that the size of IC in the animals given complexes containing cationized BSA was a little larger than 7 S, whereas those formed with the native or anionized BSA were around 19 S. The anti-native BSA antibody had a low avidity for cationized BSA in vitro, and thus all the IC which could deposit peripheral capillary walls were small and contained low avidity antibody. Chemical cationization of BSA alters the precipitability of the antibody and also the size and stability of the complexes formed. In an active model, injection of cationized BSA into mice preimmunized with cationized BSA caused localization of the BSA and its antibody in the peripheral capillary walls. Analysis of the circulating IC formed in this model also revealed low avidity of antibody and small-sized IC. From these results, it is clear that chemical cationization of antigen changes the characteristics of the antigen-antibody interaction, e.g. low precipitating efficiency and the formation of small-sized IC. Therefore, in addition to interaction of cationized IC with the polyanion layer of the glomerular basement membrane (GBM), the properties of antigen-antibody interaction play an important role in the deposition of IC along the peripheral capillary walls in a model of membranous glomerulonephritis.

Animals↗
PubMed1985

A new method of evaluating the degree of stenosis using a multisensor catheter. Application of the pressure loss coefficient.

A new method of evaluating the degree of stenosis using the pressure loss coefficient is presented here. The pressure loss coefficient was obtained in patients with pulmonary or aortic stenosis by measuring the pressure and velocity of the blood simultaneously with a multisensor catheter. Although the pressure gradient across the stenosis was augmented by increasing the blood velocity with pharmacological loading, the pressure loss coefficient remained nearly constant. This confirmed that the pressure loss coefficient is more appropriate for evaluating the degree of stenosis than the pressure gradient, which depends on the blood velocity. The pressure loss coefficients obtained from the preoperative and postoperative catheterization data were compared to evaluate the effects of the surgical operation. A pressure loss coefficient of 15 was proposed as the critical value for the indication of operation.

Adolescent↗
PubMed1985

Circulating immune complexes and immunosuppressive acidic protein in patients with renal cell carcinoma.

Sera from 23 patients with renal cell carcinoma were tested for circulating immune complexes by Clq binding assay and immunosuppressive acidic protein by single radial immunodiffusion. The mean values of circulating immune complexes and immunosuppressive acidic protein in the patients were significantly higher than those of normal controls, and over-all positive rates were 52 and 35 per cent, respectively. There was a significant correlation between immunosuppressive acidic protein levels and the extent of tumor invasion. Immunosuppressive acidic protein may be a more useful marker than circulating immune complexes. However, presently synthetic evaluations of patients with various nonspecific markers, including these 2 factors, will be necessary.

Adult↗
PubMed1985

Platelet involvement in the nephritis of acute serum sickness in rabbits: protection by dipyridamole and FUT-175.

In the acute serum sickness model in rabbits, we investigated platelet release of 5-HT, platelet surface immunoglobulins, and platelet aggregation in response to ADP, together with the effect of dipyridamole and the Clr antagonist FUT-175. The immune release of 5-HT from platelets occurred between 4 and 6 days after injection of bovine serum albumin (BSA), before immune elimination and proteinuria, but coincident with the appearance of immune complexed BSA in the circulation. Nevertheless, platelet turnovers were not detectably accelerated. Treatment with dipyridamole 50 mg/kg/24 h prevented the release of 5-HT and inhibited proteinuria, glomerular hypercellularity and immune complexes in the glomeruli. Using the Clr antagonist FUT-175, similar abrogation of the disease was obtained. We conclude that in the nephritis of acute serum sickness in rabbits, some of the immune release from platelets may be the result of immune complex binding to the platelet, perhaps through the receptor for C3b.

Adenosine Diphosphate↗