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N Aya

Publications and source records attributed to N Aya.

15 recordsLinked to original sources
PubMed2001

Morphological control of laser-synthesized silicon nanoparticles.

Size and crystallinity controlled silicon nanoparticles were prepared by a laser ablation, in situ annealing and mobility size-selection with a differential mobility analyzer (DMA). The shape and crystal structure of generated particles were observed by a transmission electron microscopy (TEM). Both densification of agglomerates and crystal growth of the particles were observed. The size of silicon primary particle was increased by the annealing, and the uniformity of the particle classified at 10 nm was improved as a result.

Crystallization↗
PubMed1994

Cellular localization of inflammatory cytokines in human glomerulonephritis.

We evaluated the expression of inflammatory cytokines in renal tissues obtained from 45 patients with several types of glomerulonephritis. Immunofluorescence studies with specific antibodies to interleukin (IL)-1 alpha, IL-1 beta, IL-6, tumour necrosis factor (TNF)-alpha, and TNF-beta showed intense cytoplasmic staining in the glomeruli and interstitium. Cells positive for these cytokines were found frequently in tissue from patients with lupus nephritis (WHO Class IV) and membranoproliferative glomerulonephritis, and, to a lesser extent, in tissue from patients with mesangial proliferative glomerulonephritis, Henoch-Schönlein purpura nephritis, and minimal change nephrotic syndrome. Most of these cells were dual-stained with a monoclonal antibody to monocytes-macrophages. In situ hybridization for cytokine mRNA, combined with immunoperoxidase staining for monocytes-macrophages, detected IL-1 alpha, IL-6, and TNF-alpha mRNA in monocytes-macrophages infiltrating the glomeruli and interstitium. Occasionally, there was weak or moderate immunostaining for IL-1 alpha, IL-6, and TNF-alpha in the glomerular mesangial and epithelial cells, but in situ hybridization signals were rarely found in these loci. These findings suggest that infiltrating monocytes-macrophages, rather than resident glomerular cells, are the major source of inflammatory cytokines in human glomerulonephritis.

Glomerulonephritis↗
PubMed1994

The target antigen of anti-tubular basement membrane antibody-mediated interstitial nephritis.

Our previous studies showed that 54 kD and 48 kD tubular basement membrane (TBM) proteins were the major form of the target antigen involved in anti-TBM antibody-mediated tubulo-interstitial nephritis in humans. In those studies, we isolated the 54 kD glycoprotein (named gp54) from collagenase-digested bovine TBM. NH2-terminal amino acid sequencing indicated that gp54 represented a newly defined glycoprotein. In this study, we further characterized the target antigen, using mouse monoclonal antibodies to gp54 and polyclonal anti-gp54 peptide antibody. Two monoclonal antibodies (H79 and H80) were established, and they reacted, by immunofluorescence, predominantly with the proximal TBM of humans, rabbits, and Wistar, Sprague-Dawley, and Brown-Norway rats, but not with that of Lewis rats. They were also fixed by blotting intensely to the 54 kD component and weakly to the 48 kD component of collagenase-digested human TBM. In vivo transfer of H79 to Wistar rats showed extensive linear binding of mouse IgG to the TBM and the basal membrane of the small intestine; however, no pathologic changes were seen by light microscopy. The anti-gp54 peptide antibody reacted with both the 54 kD and 48 kD TBM components of human TBM. mRNA was prepared from rabbit kidneys, and fractionated to enrich mRNA encoding the 54 kD and 48 kD peptides. On in vitro translation experiments with the mRNA fraction, the 54 kD and 48 kD peptides were immunoprecipitated with anti-gp54 antibodies. These findings indicate that the 54 kD and 48 kD components are encoded with different mRNA, but that they share the same antigenic epitope.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Combined therapy in children and adolescents with IgA nephropathy.

We retrospectively evaluated renal outcome in a total of 38 children and adolescents with IgA nephropathy who were selected for 6-month therapy for clinical (proteinuria > 1 g/m2/24 hour) and pathologic (mesangial proliferation, crescent formation, and tubulo-interstitial changes) features suggestive of progressive renal failure. Seventeen patients (group A) were treated with a combination of prednisolone, cyclophosphamide and dipyridamole, and the remaining patients (21; group B) were treated with the same drugs plus warfarin. All the patients were followed-up for more than 2 years (range 2-10 years, mean 4.8). In both groups, the mean urinary protein excretion value was significantly reduced after the therapy, compared with that at entry into the therapy. The significant reduction continued for up to 6 years in group A and up to 5 years in group B. Creatinine clearance was stable until 5-6 years after the trial in both groups, but 4 patients progressed to end-stage renal failure after that period. Post-therapy biopsy was performed in 14 patients, and was compared with the pre-therapy biopsy. The activity score had improved in both groups, but the chronicity score did not. These results indicate that there was a temporary effect and limited benefit with this treatment of combined drugs for children and adolescents with IgA nephropathy. The additive effect of warfarin was not substantiated.

Adolescent↗
PubMed1993

Immunohistochemical localization of C3d fragment of complement and S-protein (vitronectin) in normal and diseased human kidneys: association with the C5b-9 complex and vitronectin receptor.

The localization of C3d, a fragment produced by C3 activation and S-protein (vitronectin), a regulatory factor of C5b-9, was studied immunohistochemically in normal human kidney and renal biopsies from patients with several types of glomerulonephritis. Immunofluorescent staining of the normal kidneys showed that C3d was present along the glomerular basement membrane (GBM), tubular basement membrane (TBM) and arterioles, and that S-protein was present in the GBM, mesangium, TBM, and arterioles. Immunoelectron microscopy of isolated basement membranes showed that C3d was localized exclusively on the epithelial side of the GBM, and that S-protein was present along both the epithelial and endothelial sides. In nephritic tissues, glomerular staining of C3d, C5b-9, and S-protein was increased when compared with that in normal tissues. S-protein, frequently co-localized with C3d and C5b-9 neoantigen, was intensely positive in the immune deposits of glomerular capillaries and the mesangial area, overlapping the background staining of GBM and mesangial matrix. S-protein and its receptor were occasionally co-localized in the glomeruli. These findings indicate that C3d and S-protein are normally present in the glomeruli. Co-staining of C3d, C5b-9 neoantigen, and S-protein within the immune deposits of nephritic kidneys suggests in situ binding of S-protein to locally-formed C5b-9 complex, or merely co-distribution of S-protein with the complex, rather than trapping of large molecular SC5b-9 complex from the circulation.

Complement C3d↗
PubMed1993

Apolipoproteins and lipoprotein receptors in glomeruli in human kidney diseases.

This study offers morphological evidence of the involvement of lipid abnormalities in human glomerular injury. Renal biopsy tissues from patients with several types of glomerular diseases were immunocytochemically examined using antibodies to apolipoproteins (apo) A-I, B-100, and E, and antibodies to low density lipoprotein (LDL) receptors and scavenger receptors. Immunofluorescent staining showed the predominant deposition of apo B and apo E in the mesangial area in mesangial proliferative types of glomerulonephritis; the distribution and staining intensity of these apolipoproteins correlated with the grade of mesangial proliferation and proteinuria, but were independent of plasma lipid levels. Immunoelectron microscopy revealed that apo B and apo E were distributed in droplets within glomerular epithelial and mesangial cells or in a granular pattern in the expanded mesangial matrix. Apo A-I was mainly localized in the visceral epithelial cells of normal human kidneys. Staining for apo A-I was increased in the glomerular epithelial cells of nephritic kidneys, compared to the pattern in normal human kidneys, and was decreased in the sclerosed areas of glomeruli. An immunogold technique revealed the expression of LDL receptors on the surface membranes of glomerular mesangial and epithelial cells. Dual immunofluorescent staining showed that apo B and LDL receptors were occasionally co-localized in nephritic glomeruli. Scavenger receptor was detected on the plasma membranes of mesangial and visceral epithelial cells. The glomerular expression of scavenger receptor was increased in glomeruli with marked mesangial proliferation. In addition, the expression of this receptor was intense in monocytes/macrophages occasionally infiltrating the glomeruli. Our present findings indicate that in human nephritic kidneys, glomerular epithelial and mesangial cells express both LDL receptors and scavenger receptors. The accumulation of apolipoproteins, whether receptor-mediated or mediated by other mechanisms, can occur independently of plasma lipid levels, and may be associated with mesangial expansion and proteinuria.

Apolipoproteins↗
PubMed1992

Tissue-type plasminogen activator and its inhibitor in human glomerulonephritis.

We carried out an immunohistochemical study of tissue-type plasminogen activator (PA) and urokinase-type PA, and their inhibitors, PA inhibitor-1 and PA inhibitor-2, using renal biopsy specimens obtained from 86 patients with various forms of glomerulonephritis. The controls were four normal renal tissue specimens. On immunofluorescent observation, granular staining for tissue-type PA was found to be distributed along the glomerular capillary walls. The fluorescence was weak in the normal renal tissue and occasionally intense in the tissues of patients with IgA nephritis, minimal change nephrotic syndrome, and lupus nephritis. PA inhibitor-1 was abundant in the glomerular epithelial cells and scarce in the mesangial area and glomerular capillary lumens of the normal renal tissues. This was confirmed by immunoelectron microscopy using gold staining. The fluorescence of PA inhibitor-1 was weaker in some specimens of nephritic tissues than in the normal renal tissues. Urokinase-type PA and PA inhibitor-2 were negative within the glomeruli in all the specimens. In the glomerulonephritic tissues which were fibrin deposition-positive, tissue-type PA expression in the glomeruli tended to be strong. An association between fibrin deposition and PA inhibitor-1 staining was not clear. These data suggest that expression of tissue-type PA in the glomeruli increases in association with fibrin deposition.

Fibrin↗
PubMed1990

Identification and localization of epidermal growth factor and its receptor in the human glomerulus.

Radioimmunoassay for epidermal growth factor (EGF) was performed using the homogenates of glomeruli and tubular preparations obtained from normal human kidneys. EGF-immunoreactive material was 3- to 5-fold higher in the glomerular fractions than in the tubular fraction. By indirect immunofluorescence with a monoclonal antibody, EGF was positive in three of five normal human kidney tissues and in tissues of 24 of 33 patients with proliferative and nonproliferative types of glomerular diseases. Acid-urea treatment of tissue sections to unmask a hidden epitope of the EGF molecule disclosed EGF immunoreactivity in four more kidney specimens. EGF was localized along the glomerular capillary walls and was also present in the arterioles and small arteries. Staining with three monoclonal antibodies recognizing two different epitopes of EGF receptor (EGF-R) was positive in tissues of 2 normal subjects and 15 patients with glomerular diseases. EGF-R was found along the glomerular capillary walls, in peritubular capillaries, and within the epithelial cells of distal tubules and collecting ducts. Immunoelectron microscopy with colloidal gold staining showed that EGF and EGF-R were localized in the plasma membrane of glomerular endothelial cells. Immunofluorescence with or without acid-urea denaturation showed coexpression of EGF and EGF-R in glomeruli of 1 normal subject and 12 patients. This study demonstrated the presence of EGF and EGF-R in human glomeruli. There was no obvious difference in EGF and EGF-R expression in glomeruli derived from normal or diseased state.

Antibodies, Monoclonal↗
PubMed1989

Immunoelectron microscopic localization of membrane attack complex and hepatitis B e antigen in membranous nephropathy.

Immunoelectron microscopy was used to localize membrane attack complex (MAC) and hepatitis B e (HBe) antigen in renal tissue specimens from a total of 9 patients with membranous nephropathy (MN); 6 with MN associated with a hepatitis B virus (HBV) infection, 2 with idiopathic MN, and 1 with lupus nephritis. All the patients were proteinuric, and 2 patients were classified as stage I-II, 6 as stage II, and 1 as stage IV. MAC, along with IgG and C3, was distributed within the subepithelial electron dense deposits in all the stages. MAC was also stained in the striated membranous structures within the glomerular basement membrane and mesangial matrix of some patients. In HBV-associated MN, HBe antigen was localized in the subepithelial electron dense deposits of 5 patients, while it was absent from the subepithelial deposits in a patient that was sero-positive for hepatitis B s antigen but negative for HBe antigen. This patient also lacked MAC deposition in these loci. These results suggest that MAC is associated with the formation of subepithelial deposits and proteinuria in MN. In HBV-associated MN, HBe antigen-antibody immune complex makes up the subepithelial deposits and is likely to activate the terminal components of complement in situ.

Complement Membrane Attack Complex↗
PubMed1989

[Two brothers with reflux nephropathy].

This paper reports two brothers with reflux nephropathy. Patients who were 10-year-old and 12-year-old were referred to our hospital due to proteinuria and deterioration of renal function. Diagnosis of reflux nephropathy was made on drip infusion pyelography (DIP), voiding cystogram (VCG), and renal biopsy findings. The following findings were observed in renal tissues; focal and segmental sclerosis by light microscopy, IgM deposition by immunofluorescent microscopy, and glomerular basement membrane alterations and detachment of podocytes by electron microscopy. The HLA typing and analysis showed that both brothers and their mother possessed HLA-A9, which is reported to be closely associated with progression of primary reflux nephropathy to end-stage renal disease.

Child↗
PubMed1989

Monocyte infiltration and cross-linked fibrin deposition in IgA nephritis and Henoch-Schoenlein purpura nephritis.

To clarify the role of immune cell infiltration and fibrin deposition in glomerular injury, renal biopsy specimens taken from patients with primary IgA nephritis and Henoch-Schönlein purpura nephritis (HSPN) were evaluated using monoclonal antibodies specific to mononuclear cell surfaces and cross-linked fibrin (XFb). Monocytes/macrophages were the predominant cell type infiltrating glomeruli in IgA nephritis and HSPN. The intraglomerular monocyte population in both diseases was significantly higher than that in normals, mesangial proliferative (non-IgA) glomerulonephritis or minimal change nephrotic syndrome. In IgA nephritis, there was a clear correlation between glomerular monocyte accumulation and the degree of proteinuria. Although the monocyte influx tended to decline with time in HSPN, it remained unchanged in IgA nephritis. XFb deposition was found in the glomeruli of 27 out of 48 patients with IgA nephritis, and in 15 out of 20 with HSPN. The degree of XFb deposition in IgA nephritis correlated significantly with the degree of mesangial proliferation. These findings indicate a close relationship of monocyte/macrophage infiltration and XFb deposition with glomerular injury in IgA nephritis.

Adolescent↗
PubMed1986

Studies on drug absorption from oral cavity: physicochemical factors affecting absorption from hamster cheek pouch.

A new experimental method using a hamster cheek pouch in vivo for studying absorption processes across the keratinized oral mucous membrane was developed and some characteristics of the oral-mucosal absorption were clarified. A positive correlation between the absorption rate and the lipophilicity was observed in 18 aromatic compounds examined. The absorption of ionizable compounds was poor in the ionized form. These results suggest that the absorption from the keratinized hamster cheek pouch is due to a passive diffusion mechanism and obeys pH-partition hypothesis. The systemic transfer of salicylic acid after intra-cheek-pouch administration could be approximated by the first-order absorption model including a lag time process and the plasma levels found were consistent with this model.

Absorption↗