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Biomedical subjects

I Nakabayashi

Publications and source records attributed to I Nakabayashi.

12 recordsLinked to original sources
PubMed2001

Crystallization process of transparent conductive oxides Zn(k)In2O(k+3).

Crystallization process of the homologous compounds Zn(k)In2O(k+3) from the coprecipitants was examined by XAFS spectroscopy and X ray diffractometry. Interesting crystallization behavior could be observed. Though zinc oxide already crystallized as the wurtzite-type ZnO at 573K, indium oxide remained amorphous. Subsequently bixbyite-type In2O3 appeared at 873K for k=5 and 7 and at below 773K for the other k-members, respectively. The InO distance in the amorphous In2O3 was a little shorted than that in the bixbyite-type In2O3 by 0.06-7A. The distance remained constant but abruptly increased to that observed in the bixbyite-type In2O3 in accordance with the progress of crystallization. Then the distance gradually decreased and converged to ca. 2.12A at the temperature range of 1173-1373K, due to the reaction between In2O3 and ZnO to form the homologous compound.

Journal Article↗
PubMed2000

Up-regulation of galectin-3 in acute renal failure of the rat.

Galectin-3, a multifunctional beta-galactoside-binding lectin, is known to participate in development, oncogenesis, cell-to-cell attachment, and inflammation. We studied to determine whether galectin-3 is associated with cell injury and regeneration in two types of acute renal failure (ARF), namely ischemic and toxic ARF. In ischemia/reperfusion renal injury in rats (bilateral renal pedicles clamped for 40 minutes), galectin-3 mRNA began to increase at 2 hours and extended by 6.2-fold at 48 hours (P: < 0.01 versus normal control rats), and then decreased by 28 days after injury. In addition, a significant negative correlation between galectin-3 mRNA expression and serum reciprocal creatinine was shown at 48 hours after injury (n = 13, r = -0.94, P: < 0.0001). In folic acid-induced ARF, galectin-3 mRNA was found to be up-regulated at 2 hours after injury and increased levels continued until at least 7 days post-injury. In immunohistochemistry, at 2 hours following reperfusion, galectin-3 began to develop in proximal convoluted tubules. From 6 hours up to 48 hours, galectin-3 was also found in proximal straight tubules, distal tubules, thick ascending limbs, and collecting ducts. In later stages of regeneration, galectin-3 expressions were found in macrophages. In conclusion, we demonstrated that galectin-3 expressions were markedly up-regulated in both ischemic and toxic types of ARF. Galectin-3 may play an important role in acute tubular injury and the following regeneration stage.

Acute Kidney Injury↗
PubMed1999

Juxtaglomerular cell tumor with retroperitoneal fibrosis and secondary immune-complex glomerulonephritis: a possible contribution of the renin angiotensin system to renal fibrosis.

We present a case of a 25-year-old woman with a renin-secreting juxtaglomerular cell tumor, retroperitoneal fibrosis associated with glomerular hypertrophy, glomerulonephritis, and marked tubulointerstitial alterations. Myofibroblasts, as shown by positive immunostaining for alpha-smooth muscle actin, were found along with transforming growth factor-beta (TGF-beta) in the interstitium of the tumor-free kidney. Regarding the pathogenesis of renal fibrosis and glomerular hypertrophy, this case may provide evidence not only experimentally but also clinically that the renin-angiotensin system plays an important role because angiotensin II is known to induce renal fibrosis associated with increased TGF-beta and the appearance of myofibroblasts.

Actins↗
PubMed1997

Glomerular proliferating cell kinetics in acute post-streptococcal glomerulonephritis (APSGN).

To investigate the time sequence of glomerular cell proliferation in acute human glomerulonephritis, renal biopsy tissues were examined from 15 acute post-streptococcal glomerulonephritis (APSGN) patients (who were biopsied 1-31 days after onset), using an immunoperoxidase technique with monoclonal antibodies against proliferating cell nuclear antigen (PCNA) and various cell surface markers. Few, if any, PCNA+ cells were observed in normal glomeruli, but many cells were positive for PCNA in the acute phase of APSGN. Glomerular PCNA+ cells were observed either within glomerular tufts, or lining Bowman's capsule (parietal epithelial cells); the number of positive cells tended to decrease exponentially as the disease duration increased (r = -0.91, P < 0.0001). PCNA+ cells within glomerular tufts were further identified by double immunostaining. PCNA was not found in PMN or T cells, but a small proportion of macrophages were PCNA+. Most of the remaining PCNA+ cells were resident glomerular cells; the proportion of PCNA+ endothelial cells (CD31+) was over 80 per cent in the early phase, but as the disease continued the proportion of mesangial cells (alpha-smooth muscle actin+) increased to about half of the total PCNA+ cells within the tuft. These data indicate that the hypercellular glomeruli in APSGN are due not only to immune cell infiltration, but also to resident glomerular cell proliferation, probably induced by locally produced growth factors.

Acute Disease↗
PubMed1997

Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen.

FITC-labelled IgG obtained from patients convalescing from acute poststreptococcal glomerulonephritis (APSGN) stains glomeruli of patients with early APSGN. We previously reported a streptococcal antigen (preabsorbing antigen (PA-Ag)) that preabsorbed the stain out of sera from the convalescent patients and thus prevented glomerular staining. To confirm the nephritogenicity of PA-Ag, we administered up to 40 mg of this antigen to rabbits for 8 days and observed them for up to 9 weeks. Immunohistological analysis showed diffuse and global glomerular staining for C3 without notable staining for gamma-globulin. Light microscopic examinations revealed slight to moderate proliferative glomerulonephritis with exudative change. Control rabbits, which received similar doses of bovine serum albumin, did not show significant staining for C3. A transient and significant decrease in CH50 was observed from weeks 3 to 7 (9.7 +/- 0.3 U/ml at week 3; normal range 12.9 +/- 0.6 U/ml). This experimental model showed a resemblance to immunological and immunohistological features of APSGN in humans. Although the precise mechanisms are yet to be determined, complement activation by PA-Ag seems to hold a key position in this model and in the human disease.

Acute Disease↗
PubMed1996

Asymptomatic acute poststreptococcal glomerulonephritis following upper respiratory tract infections caused by Group A streptococci.

During an observation period of 1-2 years in 2 different districts in Japan, 104 patients were found to have upper respiratory infections caused by group A streptococci. Fourty-nine of these patients were followed prospectively to determine if renal involvement would occur. Twelve patients developed transient serum complement (CH50) depression and urinary abnormality, and 2 of these developed mild hypertension. The latent period was from 1-8 weeks after the streptococcal infection. Renal biopsies of the 12 patients with "asymptomatic" of "subclinical" acute poststreptococcal glomerulonephritis (APSGN) were examined by light, immunofluorescent and electron microscopy. Glomerular lesions ranged from mild proliferative changes to the classical pathology seen in APSGN. The 12 patients were followed for 10 years. Two of them developed persistent or intermittent hematuria, and renal biopsies obtained 4 years after the initial infection revealed mesangial proliferative glomerulonephritis without IgA deposits. The remaining patients showed no abnormal findings after the acute episode. These findings suggested that glomerular involvement after group A streptococcal infection is frequent and mesangial proliferative glomerulonephritis, which was found to develop in some, may rank with IgA nephropathy as a major cause of unexplained microscopic hematuria.

Acute Disease↗
PubMed1995

[Identification and analysis of immune cells infiltrating into the glomerulus and interstitium in lupus nephritis].

This study was performed to investigate the role of cell-mediated immunity in lupus nephritis (LN). Frozen sections from 38 patients with LN were examined by indirect immunoalkaline-phosphatase labeling using monoclonal antibodies to identify the immune cells infiltrating into the interstitium and glomerulus. 14 patients showed minor glomerular abnormality (MGA), 9 had mesangial LN (MesLN), 12 had diffuse proliferative LN (DPLN) and 3 had membranous LN (MLN). Monocyte/macrophage and helper/inducer T cells infiltrated in the interstitium predominantly, but intraglomerular infiltration of these cells was rare. Monocyte/macrophage and suppressor/cytotoxic T cell levels were significantly higher (p < 0.05) in the interstitium in DPLN patients and monocyte/macrophage level was significantly higher (p < 0.05) in MesLN patients than in MGA patients. In the interstitium, serum creatinine level was highly correlated with infiltrations of suppressor/cytotoxic T cell, monocyte/macrophage (p < 0.01), pan T cell and total leucocyte (p < 0.05). Clinical activity score was correlated with suppressor/cytotoxic T cell (p < 0.001), monocyte/macrophage and pan T cell (p < 0.01). These results suggest that suppressor/cytotoxic T cell and and monocyte/macrophage may play an important role in the progression of lupus nephritis.

Antibodies, Monoclonal↗
PubMed1995

A case report of mixed P- and C-ANCA positive patients with pauci-immune crescentic glomerulonephritis.

We describe 2 patients with pauci-immune crescentic glomerulonephritis and elevated titers of perinuclear and cytoplasmic anti-neutrophil cytoplasmic antibody (P-ANCA and C-ANCA) which were associated with both 29 and 59 kD bands on Western blots. The presence of C-ANCA corresponds with a clinical and/or histological diagnosis of Wegener's granulomatosis, but although both patients suffered from pulmonary complications there was no clinical nor histological evidence of granulomatosis. Transbronchial lung biopsy showed only interstitial pneumonia and old hemorrhage. Therefore, the patients' conditions were interpreted as microscopic polyarteritis nodosa or hitherto undefined vasculitis associated with ANCA.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1994

Hemolytic uremic syndrome without hemolytic anemia: a case report.

Hemolytic uremic syndrome (HUS) is characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. Most cases of HUS are caused by E. coli O157:H7 verotoxin. In the case reported here, diarrhea continued for twenty days after an E. coli 0157:H7 infection and was followed by acute renal failure and thrombocytopenia. Examination of percutaneous renal biopsy tissue showed typical HUS findings, e.g., mesangiolysis in glomeruli and thickening of capillary walls with prominent double outlines, but there was no indication of hemolytic anemia. LDH and haptoglobin, indications of hemolytic anemia, were in the normal range throughout the patient's clinical course. The patient's red blood cells had P1 antigen, which reportedly provides protection by adsorption of toxin into the red blood cells thereby preventing or limiting toxic damage to other organs. Therefore, we assumed that because of the expression of P1 antigen in this patient, the kidneys were not severely damaged and microangiopathic hemolytic anemia was thereby avoided.

Acute Kidney Injury↗
PubMed1993

ANCA associated vasculitis allergica cutis (VAC) and mild proliferative necrotizing glomerulonephritis.

We report here the case of a 69-year-old male with vasculitis allergica cutis (VAC) accompanied by a nephrotic syndrome associated with serum perinuclear-staining anti-neutrophil cytoplasmic antibody (P-ANCA). Renal biopsy specimens showed mild proliferative glomerulonephritis with crescentic and necrotizing lesion in the glomeruli, while lesional skin biopsy specimens showed leukocytoclastic vasculitis in the deep dermis. Pauci-immune deposits were evident (deposits of immunoglobulins and complements were absent) by immunofluorescence microscopy in both tissues. The appearance of weakly positive P-ANCA associated with skin lesions and renal dysfunction occurred twice in this patient. Following corticosteroid administration, renal dysfunction was remarkably diminished and proteinuria decreased. P-ANCA titer were decreased, reaching the normal level. ANCA associated glomerulonephritis complicated by VAC has not been reported previously. In the present case, the vasculitis cutis and glomerulonephritis is assumed to be associated with the appearance of weakly positive P-ANCA.

Aged↗