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Biomedical subjects

Y Nomoto

Publications and source records attributed to Y Nomoto.

At least 217 records · Page 12Linked to original sources

Impaired solubilization of glomerular immune deposits by sera from patients with IgA nephropathy.

A study of the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy and other glomerular diseases. These specimens were incubated with fresh and heated sera from the same patients and healthy adults at 37 degrees C for one hour in plastic tubes. The sections were stained with fluorescein isothiocyanate (FITC)-labeled heavy chain specific anti-human IgA antiserum and then examined with a fluorescent microscope. It was shown that the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy was significantly less than that by sera from healthy adults. It is possible that impaired solubilization of immune complexes in vivo could lead to the accumulation of glomerular immune deposits in patients with IgA nephropathy.

Antigen-Antibody Complex↗

Increase of peripheral blood B cells with Fc receptor for IgA in patients with IgA nephropathy.

A B-cell subset with Fc receptors for IgA (B alpha cells) has been observed in human peripheral blood. To investigate aberrations of B cells in a diseased state, the percentages of B alpha cells were enumerated in peripheral blood from patients with IgA nephropathy, which is characterized by preponderant deposition of IgA-dominant immune complexes in the glomerular mesangial area. The present study showed a significant increase in B alpha cells in peripheral blood from patients with IgA nephropathy but not in those with chronic proliferative glomerulonephritis without mesangial IgA deposition. Most Fc alpha R-bearing cells were observed in surface IgA bearing lymphocytes. No linear correlation was observed between the levels of serum IgA and the percentages of B alpha cells. The addition of aggregated IgA to cultures did not induce Fc alpha R-bearing B cells in vitro. It is postulated that B alpha cells might have some pathogenetic role in the development of IgA nephropathy and that some antigenic stimuli might play a role in the increase of peripheral blood B alpha cells in patients with IgA nephropathy.

B-Lymphocytes↗

Immunopathological similarities between IgA nephropathy and Henoch-Schoenlein purpura (HSP) nephritis.

A study on the immunopathological similarities between IgA nephropathy and Henoch-Schoenlein purpura (HSP) nephritis is described. Various examinations were performed as follows. (1) Pathological studies: light microscopic findings and immunofluorescent staining; (2) Measurement of the levels of IgA in pharyngeal washings and sera, and those of IgA quantitated by radial immunodiffusion; (3) Elution studies: renal biopsy specimens obtained from patients with IgA nephropathy and HSP nephritis were treated with citrate buffer (pH 3.2) and the "eluate" was neutralized by sodium hydroxide. The "eluate" was then applied to the acid-treated sections obtained from the same and other patients with IgA nephropathy as well as sections from patients with HSP nephritis and other glomerular diseases. The sections were stained with FITC-conjugated heavy chain specific antihuman IgA antisera and then examined with a fluorescent microscope. There were no differences in pathological findings of IgA nephropathy and HSP nephritis in the light microscopic and immunofluorescent examinations. The levels of IgA in pharyngeal washings and sera were significantly increased in patients with both diseases. IgA antibodies deposited in kidneys from patients with HSP nephritis crossreacted with kidneys from some patients with IgA nephropathy, and vice versa. However, antibodies from patients with IgA nephropathy and HSP nephritis did not react with normal glomeruli or other nephritic glomeruli. It is concluded that there are some immunopathological similarities between IgA nephropathy and HSP nephritis.

Adolescent↗

Mesangial deposition of J chain-linked polymeric IgA in IgA nephropathy.

Renal biopsy specimens from 8 patients with IgA nephropathy (Berger's disease) were examined immunocytochemically at the light and electron microscopic levels with peroxidase-labeled antibodies to IgA, IgM, J chain and secretory component. In 2 of the 8 specimens heavy deposits of IgA, but no IgM, were found in the mesangium. After acid-urea treatment of these tissue sections, J chain, a subunit of polymeric immunoglobulins, was identified in a distribution similar to that of IgA. In the remaining 6 specimens, small amounts of IgM in addition to denser deposits of IgA and J chains were found. We conclude that the IgA deposits in at least some patients with Berger's disease consist of IgA polymers linked by J chain.

Animals↗

Metabolic deterioration in shock state and its modulation.

The initial cellular reaction against the deleterious effects of shock-inducing stimuli apparently elevates the energy-producing capacity so that the cell is able to sustain its normal function. Several endocrine events are fundamentally important as triggering factors for this kind of reaction. As the shock state advances, cellular metabolism deteriorates progressively and cellular energy is exhausted. Depression of intracellular cAMP may induce cellular metabolic unresponsiveness to hormonal stimuli. Consistent degradation of high-energy substances, extreme deviation of the redox state in the NAD+-NADH system, and decrease of endogenous key substances such as L-carnitine ultimately may lead to a standstill of cellular enzymatic reactions (Fig. 13). Methods intended to sustain cellular membrane and enzymatic systems may offer the best contribution to the improvement of shock therapy.

Adenine Nucleotides↗

A case of Fabry's disease.

A case of Fabry's disease in a 22-year-old male patient who had mild proteinuria and dark-red eruptions is reported. He had been treated as a case of a so-called "chronic glomerulonephritis" for one year. However, histopathological findings of the renal biopsy specimens showed the presence of numerous vacuolated cells in the glomeruli. These vacuolated cells contained numerous electron dense bodies observed by electron microscopy. Skin lesions of this patient were consistent with those of angiokeratoma corporis. The levels of serum alpha-galactosidase were significantly lower than those of healthy controls. The mother of this patient also showed decreased levels of serum alpha-galactosidase. The pedigree of this patient showed a familial history of various types of renal diseases. It was postulated that Fabry's disease occurring in older patients has a worse clinical course. it is concluded that early detection of this disease through biopsy and the assay of serum alpha-galactosidase levels is important in managing the future course of patients with Fabry's disease.

Adult↗

Enzyme histo-cytochemical studies in human adrenocortical adenomas. [II] Cushing's syndrome.

Enzyme histo-cytochemical staining was performed for 3 beta-hydroxysteroid dehydrogenase, alkaline phosphatase and acid phosphatase in the compact and clear cells of the adrenocortical adenomas associated with Cushing's syndrome (Cushing's adenomas). In the compact cells, enzymatic activities of 3 beta-hydroxysteroid dehydrogenase and alkaline phosphatase were stronger than those in the clear cells. Electron microscopic localization of alkaline phosphatase was mostly present on well developed microvilli, while, acid phosphatase was observed in lysosomes near the well developed smooth endoplasmic reticula. On the other hand, in the clear cells, cytochemical localization of alkaline phosphatase was mainly present on the intercellular plasma membrane, while acid phosphatase was mostly observed near the lipid droplets. Based on these data, functional aspects of the compact and clear cells in Cushing's adenomas are discussed.

3-Hydroxysteroid Dehydrogenases↗

Hepatic glomerulosclerosis with IgA deposition. Report of three cases.

Hepatic glomerulosclerosis is characterized by depositions of IgA in mesangial areas of glomeruli similar to those found in primary IgA nephropathy. The mechanism of IgA deposition is presently obscure. We have attempted to elucidate histopathological changes of IgA deposition in such patients. Three cirrhotic patients who had abnormal urinalysis underwent renal biopsy in Tokai University Hospital. Renal biopsy specimens obtained from these three patients showed IgA measangial deposition on immunofluorescence staining, and various histopathological changes on light microscopy. It is suggested that these variable renal changes in patients with hepatic cirrhosis may be related to the alteration of the handling of immune complexes in injured liver.

Biopsy↗

Immunogenetical study in patients with chronic glomerulonephritis.

HLA-A, B and DR typing was performed on a total of 236 patients with chronic glomerulonephritis (CGN) which were diagnosed by renal biopsies evaluated by light microscopy, direct immunofluorescent staining and whenever indicated electron microscopy. The interrelationship between the HLA system and the histopathologic classification of CGN was examined. There were 20 patients with benign recurrent hematuria (BRH), 82 with IgA nephropathy (IgA-N), 24 with proliferative glomerulonephritis (PGN), 47 with minimal change nephrotic syndrome (MCNS), 4 with membranous nephropathy (MN), 43 with membranoproliferative glomerulonephritis (MPGN) and 16 with focal glomerulosclerosis (FGS). The following results were obtained: 1) Antigens from different loci were associated with different subgroups of CGN. There were three types of associations; a) HLA-A locus associated as found in PGN, b) HLA-B locus associated as found in BRH and c) HLA-DR locus associated as found in MCNS. IgA-N, MPGN and FGS seemed to be included in this group. 2) The association of HLA-A locus antigens with MCNS could be subdivided by age o onset suggesting that in MCNS HLA-A antigens are linked to disease expression. 3) A heterogeneity in IgA-N is suggested by its association with different HLA antigens; a) a HLA-B37 associated group, b) a HLA-DR4 or DYT associated group and c) a HLA-DEn (Dw 6.1) or B12 associated group. These data suggest differences in the mechanisms of HLA and disease association in each histopathologic subtype of CGN.

Adolescent↗

Enzyme histocytochemical studies in human adrenocortical adenomas. [I]. Primary aldosteronism.

Enzyme histocytochemical staining including alkaline phosphatase, acid phosphatase, 3 beta hydroxysteroid dehydrogenase and 11 beta hydroxysteroid dehydrogenase was studied in human adrenocortical adenomas associated with primary aldosteronism. Histochemically, these enzyme activities were weaker in clear cell type adenomas than in the normal human adrenal cortex. While compact cell type adenomas showed stronger enzyme activities than the clear cell type adenomas. Electron microscopic localization of alkaline phosphatase was mainly observed in plasma membrane at the intercellular sites. Occasionally, this enzyme activity was also observed in the mitochondrial outer membrane, mainly in compact cells. The significance of these enzymes in the adenoma cells is discussed.

3-Hydroxysteroid Dehydrogenases↗

A case of granulomatous renal sarcoidosis with a dramatic response to corticosteroid and urokinase therapy.

A case of renal granulomatous sarcoidosis that presented with chronic renal failure (CRF) is described. Renal biopsy specimens revealed typical features of sarcoidosis in light microscopy and immunofluorescence microscopy examinations. The absence of bilateral hilar lymphadenopathy (BHL) was a distinctly unusual feature of sarcoidosis although uveitis and rectal granuloma were observed during the clinical course. A dramatic response occurred on corticosteroid and urokinase therapy, characterized by a fall of serum creatinine levels.

Adult↗

Ultrastructural and biochemical studies in human adrenocortical adenomas associated with primary aldosteronism.

Correlation between ultrastructural features and adrenal steroid hormone contents was studied in two human adrenocortical adenomas associated with primary aldosteronism. In two adrenocortical adenoma cells, large numbers of lipid droplets were characteristically observed in the cytoplasm, these lipid droplets were closely related to the endoplasmic reticula or mitochondria. On the other hand, biochemically, in two adrenocortical adenomas, aldosterone and progesterone were higher than those in the normal parts of the same adrenal glands. Whereas, dehydroepiandrosterone was less than that in the normal parts of the same adrenal glands. From these data, the functional aspects in adrenocortical adenomas associated with primary aldosteronism are discussed.

Adenoma↗

Cross-reactivity of IgA antibodies between renal mesangial areas and nuclei of tonsillar cells in patients with IgA nephropathy.

A study on autoradiographical analysis of antigenic sites in patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy. These specimens were treated with citrate buffer (pH 3.2) and the 'eluate' was neutralized by sodium hydroxide. The 'eluate' was labelled with 125iodine by the chloramine-T method. 125I-labelled eluate was then applied to the tonsillar cells obtained from the same and other patients with IgA nephropathy as well as to those with other glomerular diseases. The tonsillar cells were dipped into the emulsion (NBT-2) and then examined with a light microscope. It was demonstrated that the antibodies eluted from renal tissues of patients with IgA nephropathy specificially bound with the nuclear regions of tonsillar cells. The binding of eluted antibodies and tonsillar cells was completely inhibited by the addition of anti-human IgA antisera, but not inhibited by human IgA myeloma proteins. The eluted antibodies bound with tonsillar cells from the same patients, but only 10% of them bound with the tonsillar cells obtained from other patients with IgA nephropathy. It is concluded that IgA antibodies deposited in glomeruli specifically bind with tonsillar cells obtained from patients with IgA nephropathy and these antibodies show some heterogeneity among those patients.

Adult↗

Specificity of eluted antibody from renal tissues of patients with IgA nephropathy.

A study on the specificity of antibodies eluted from renal biopsy specimens in patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy and other glomerular diseases. These specimens were treated with citrate buffer (pH 3.2) and the "eluate" was neutralized by sodium hydroxide. The "eluate" was then applied to the acid-treated sections obtained from the same and other patients with IgA nephropathy as well as to those with other glomerular diseases. The sections were stained with FITC-labeled heavy-chain-specific anti-human IgA antisera and examined with a fluorescent microscope. It was demonstrated that the antibodies obtained from patients with IgA nephropathy specifically recombined with the glomerular mesangial areas in such patients, while these antibodies did not combine with renal tissues obtained from patients with out IgA nephropathy. The eluted antibodies combined with autologous tissues, but only one-third of them combined with allogeneic renal specimens with IgA nephropathy. It is concluded that IgA antibodies deposited in glomeruli are specific to mesangial areas of patients with IgA nephropathy and that these antibodies show some heterogeneity among patients with this disorder.

Adolescent↗

Double immunofluorescence studies of immunoglobulins, complement components and their control proteins in patients with IgA nephropathy.

A study on double immunofluorescent staining of immunoglobulins, complement components, and their control proteins in renal tissues from patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy. These biopsy specimens were stained with anti sera to human C1q, C4-binding protein, and beta 1H globulin by indirect immunofluorescent staining. These samples were then stained with rhodamine-conjugated anti human IgG, IgM, and IgA. Although C1q and C4-binding protein do not combine with IgA, they ubiquitously combine with IgG and/or IgM. beta 1H globulin also combine with IgG, IgM and/or IgA. It was demonstrated that the complement system activated in IgA nephropathy was via both alternative and classical pathways. The presence of C4-binding protein in glomeruli appeared to be a more sensitive indicator of classical pathway activation than the presence of C4.

Carrier Proteins↗

Increase of IgA specific helper T alpha cells in patients with IgA nephropathy.

Patients with IgA nephropathy show an emergence of IgA dominant circulating immune complexes (CIC) as well as increased levels of serum IgA and/or IgA bearing peripheral blood lymphocytes. In order to elucidate immunological aberrations responsible for the increased IgA synthesis in such patients, quantitative and qualitative analysis was performed on T alpha cells which have been recently identified as possessing IgA specific helper activity on human B cells. Three different methods were employed to quantitate T alpha cells. These methods included a rosette formation of T cells with either bovine red cells coated with the IgA fraction of anti-bovine red cell antiserum or those coated with TNP and anti-TNP IgA antibody, and an analysis of T cells combined with fluorescein conjugated human IgA myeloma protein. T alpha cells were sorted by a fluorescence activated cell sorter and co-cultured with a B cell rich fraction to evaluate whether there is a qualitative difference in IgA specific helper activity between patients and healthy adults. T alpha cells were significantly increased in patients with IgA nephropathy while there were no significant changes in patients with chronic proliferative glomerulonephritis without mesangial deposition of IgA. There was no qualitative difference in IgA specific helper activity of T alpha cells between patients and healthy adults. It is suggested that increased levels of T alpha cells in patients with IgA nephropathy may be responsible for increased synthesis of IgA in such patients.

Adult↗