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Biomedical subjects

N Negoro

Publications and source records attributed to N Negoro.

At least 37 records · Page 2Linked to original sources
PubMed1994

[A case of adult T cell leukemia complicated with strongyloidiasis and amplification of pneumocystis carinii DNA in bronchoalveolar lavage fluid].

The patient was a 75-year-old male, who simultaneously showed symptoms of bacterial meningitis during steroid treatment for erythroderma and symptoms of respiratory failure. Based on ground-glass shadows in both lungs on chest X ray, bronchoalveolar lavage (BAL) was carried out and strongyloides was detected. In addition to strongyloidiasis, the patient was shown to have the complication of pneumocystis carinii (PC) pneumonia after PC DNA was detected in BAL fluid using a PCR assay. When other causes for immunodeficiency affecting the incidence of opportunistic infection were investigated, the ATL virus was detected in peripheral blood cells and monoclonal amplification was indicated, though the presence of anti-ATL antibody was negative. According to the results, this patient was found to have early stage adult T cell leukemia. In conclusion, we treated this adult T cell leukemia patient who had strongyloidiasis and amplification of PC DNA in BAL and for which the PCR assay, a new technology used for diagnosing PC pneumonia, was considered to be effective.

Aged↗
PubMed1993

Significance of enzyme linked immunosorbent assay (ELISA) for antibodies to double stranded and single stranded DNA in patients with lupus nephritis: correlation with severity of renal histology.

The correlation between renal histology and class specific (IgG and IgM) antibodies to double stranded DNA (dsDNA) and single stranded DNA (ssDNA) was studied by enzyme linked immunosorbent assay (ELISA) in 40 untreated patients with systemic lupus erythematosus (SLE). The levels of IgG antibodies to dsDNA were significantly higher in patients with World Health Organisation class IV nephritis than in those with class I, class II, or class III nephritis. IgG antibodies to ssDNA were higher in patients with class IV than in those with class II nephritis. IgG antibodies to dsDNA showed a close correlation with the histological activity score and the amount of electron dense deposit. IgG antibodies to ssDNA showed only a weak correlation with the renal histological activity score. IgM antibodies to dsDNA and IgM antibodies to ssDNA were not correlated with renal histological features. Patients with moderate to severe nephritis had a lower ratio of IgM antibodies to dsDNA to IgG antibodies to dsDNA than those with mild nephritis. These results indicate that the measurement of IgG antibodies to dsDNA is predictive in evaluating renal histological activity in patients with SLE.

Antibodies, Antinuclear↗
PubMed1992

Increased Na+/H+ exchange activity in vascular smooth muscle cells of spontaneously hypertensive rats and possible involvement of protein kinase C.

1. Na+ influx into cultured vascular smooth muscle cells (VSMC) obtained from spontaneously hypertensive rats (SHR) and from Wistar-Kyoto rats (WKY) was measured. Na+ influx via the Na+/H+ exchange system was measured as the rate of 22Na+ influx into cultured VSMC sensitive to ethylisopropylamiloride (EIPA), a specific inhibitor of the exchange system. 2. The total 22Na+ influx rate in SHR was significantly higher than in WKY (6.08 +/- 0.16 vs 4.13 +/- 0.09 nmol/min per mg protein; P less than 0.001; n = 14). The EIPA (1 X 10(-4) mol/L)-sensitive 22Na+ influx rate in SHR was significantly higher than that in WKY (4.32 +/- 0.27 vs 2.17 +/- 0.14 nmol/min per mg protein; P less than 0.001; n = 14). There was no difference in EIPA-insensitive 22Na+ influx between SHR and WKY. The EIPA-sensitive 22Na+ influx rate into VSMC was significantly decreased in SHR but not in WKY by the addition of 1 X 10(-4) mol/L 1-(5-isoquinoline-sulfonyl)-methylpiperazine (H-7), an inhibitor of protein kinase C (PK-C). 3. These results suggest that the increase in Na+ influx in SHR may be due to elevation of the Na+/H+ exchange activity, and possible involvement of PK-C in the increased Na+/H+ exchange activity in VSMC from SHR.

Amiloride↗
PubMed1992

Platelet-derived growth factor gene expression in the kidney of malignant hypertension.

To examine the pathogenetic role of platelet-derived growth factor (PDGF) in hypertensive kidney damage, we studied the gene expression of PDGF A-chain and B-chain in an animal model of malignant hypertension. Experimental malignant hypertension induced by unilateral nephrectomy combined with deoxycorticosterone and salt loading in the spontaneously hypertensive rat resulted in severely elevated blood pressure and renal histological damage, characterized by necrotizing vasculitis. Using reverse transcription-polymerase chain reaction analysis followed by Southern blot analysis, we observed that PDGF B-chain gene expression was increased in the kidney of experimental malignant hypertension and was correlated with the severity of glomerular damage, while PDGF A-chain gene expression was unaffected. Antihypertensive treatment with manidipine reduced glomerular damage and a decreased gene expression of PDGF B-chain. These results suggest that PDGF B-chain may have a role in mediating hypertensive kidney damage.

Animals↗
PubMed1991

Angiotensin II induced biphasic inositol 1,4,5-triphosphate response in rat vascular smooth muscle cells.

We examined angiotensin II induced changes of inositol 1,4,5-triphosphate (Ins(1,4,5)P3) in cultured vascular smooth muscle cells from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) using a specific protein binding assay system. We observed a rapid biphasic Ins(1,4,5)P3 response, which peaked at 5 s and at 30 s after angiotensin II stimulation. At every period of time the Ins(1,4,5)P3 level of SHR was 2- to 5-fold higher than that of WKY. Thus, the Ins(1,4,5)P3 specific assay revealed a complex Ins(1,4,5)P3 response after angiotensin II stimulation and suggested the need for further investigation of the Ins(1,4,5)P3 metabolism following agonist stimulation in vascular smooth muscle cells.

Angiotensin II↗
PubMed1990

Corticosteroid- and furosemide-induced increase in proteinuria in nephrosis.

A corticosteroid- and furosemide-induced excessive increase in proteinuria developed in a 34-year-old nephrotic patient with focal glomerulosclerosis. The concentration of urinary protein increased almost in parallel with that of urinary glucose. This finding indicates that corticosteroids and/or furosemide can promote the disturbance of the tubular reabsorption mechanism together with increases in glomerular permeability and glomerular filtration rate.

Adult↗
PubMed1989

The clinical significance of iC3b neoantigen expression in plasma from patients with systemic lupus erythematosus.

We studied the expression of an iC3b neoantigen (iC3b-NEO) in plasma from patients with systemic lupus erythematosus (SLE), by using a monoclonal antibody specific for iC3b/C3dg/C3d, to investigate the activation of the third component of complement in SLE. The plasma iC3b-NEO level in 40 untreated patients with active SLE was significantly higher than that in 36 normal subjects (mean +/- SD 31.5 +/- 13.9 micrograms/ml versus 12.3 +/- 3.3 micrograms/ml; P less than 0.001). The plasma iC3b-NEO level was highly correlated with clinical disease activity (tau = 0.62, P less than 0.0001), and it was the parameter most closely correlated with renal histologic activity in lupus nephritis (tau = 0.52, P less than 0.0001). Also, patients with diffuse proliferative lupus nephritis had the highest levels of plasma iC3b-NEO among all World Health Organization classes of lupus nephritis (P less than 0.01). We conclude that the plasma iC3b-NEO level is strongly associated with clinical disease activity and renal histologic activity in patients with SLE, and that plasma iC3b-NEO may be a sensitive and useful measure of complement activation in SLE.

Antibodies, Monoclonal↗
PubMed1989

Plasminogen activation in plasma of patients with systemic lupus erythematosus.

We measured alpha 2-plasmin inhibitor-plasmin complexes (PI-PC) in plasma of patients with systemic lupus erythematosus (SLE) to examine the plasminogen activation in SLE. The plasma PI-PC level in 23 patients with SLE was significantly higher than that in 18 normal subjects (P less than 0.001) and the SLE patients with nephrotic syndrome had higher plasma PI-PC levels than those without nephrotic syndrome (P less than 0.01). In addition, the plasma PI-PC level was significantly correlated with the level of plasma C3 breakdown products (iC3b/C3dg) in the patients with SLE (r = 0.53, P less than 0.01). These results suggest that plasminogen is activated in plasma of patients with SLE and that the plasminogen activation may be associated with the activation of complement in SLE.

Adult↗
PubMed1989

Possible involvement of interferon alfa in the pathogenesis of fever in systemic lupus erythematosus.

Serum concentrations of interferon alfa, interleukin 1, and tumour necrosis factor alpha were measured in 25 untreated patients with systemic lupus erythematosus (SLE). A close correlation was found between serum concentrations of interferon alfa and the degree of fever, while no significant correlations were found between fever and interleukin 1 or tumour necrosis factor alpha. These results suggest the possible involvement of interferon alfa in the pathogenesis of fever in SLE.

Fever↗
PubMed1989

Clinical significance of antibodies to histones in systemic lupus erythematosus.

IgG antibodies to whole histones and to individual histones H1, H2A+H4, H2B and H3 were measured by enzyme linked immunosorbent assay in serum samples from 46 untreated patients with systemic lupus erythematosus (SLE) who had undergone renal biopsy. Patients with the WHO Class IV lupus nephritis had significantly higher levels of antibodies to histones (except H1) than those with milder forms of nephritis. Among antibodies to individual histones, the levels of antibodies to H2B histones best correlated with the renal histologic and the clinical activity of disease (rs = 0.759, rs = 0.577, p less than 0.001, respectively).

Antibodies, Antinuclear↗
PubMed1988

Expression of c-myc proto-oncogene in hearts and cultured smooth muscle cells of spontaneously hypertensive rats.

We studied the expression of c-myc proto-oncogene in hearts and cultured aortic smooth muscle cells of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), in order to investigate the association of the c-myc gene with cardiac hypertrophy and atherosclerosis in SHR. Transcription of the c-myc gene in hearts of SHR was higher than that of WKY at 10 weeks of age, when cardiac hypertrophy had developed in SHR. The c-myc gene expression in cultured aortic smooth muscle cells of SHR, after the addition of serum to the serum-deprived cultures, was higher than that of WKY. These results suggest that the enhanced expression of the c-myc gene in the hearts and cultured aortic smooth muscle cells of SHR may be associated with the growth control of these cells, and may play a role in the development of cardiac hypertrophy and atherosclerotic lesions in SHR.

Animals↗
PubMed1987

Nuclear ribonucleoprotein immune complexes in pericardial fluid of a patient with mixed connective tissue disease.

We performed immunopathologic studies of the pericarditis present in a patient with mixed connective tissue disease. A large number of nuclear RNP (nRNP) immune complexes (ICs) were found in the pericardial fluid, but not in the serum. The pericardial small vessels had no deposits of IgG. These results suggest that locally formed nRNP ICs were closely associated with the pathogenesis of pericarditis in this patient.

Adult↗
PubMed1987

Clinical significance of U1-RNP immune complexes in mixed connective tissue disease and systemic lupus erythematosus.

We measured U1-RNP: anti-U1-RNP immune complexes (U1-RNP ICs) in patients with mixed connective tissue disease (MCTD) and systemic lupus erythematosus (SLE) to examine the clinical significance of circulating U1-RNP ICs. The level of U1-RNP ICs in 11 patients with MCTD was significantly higher than that in 22 normal subjects and there was a close correlation between the level of U1-RNP ICs and the clinical disease activity index of MCTD. In contrast, the level of U1-RNP ICs in 31 patients with SLE was not significantly higher than that in normal subjects and that was not correlated with the clinical disease activity index of SLE or the renal histologic activity index of lupus nephritis. We conclude that U1-RNP ICs are present in sera of patients with MCTD and SLE, and that the level of U1-RNP ICs may be closely associated with clinical disease activity in patients with MCTD.

Adult↗
PubMed1987

Complement activation in IgA nephropathy.

Activation of alternative complement pathway is presumed to be important pathogenically in IgA nephropathy since renal biopsies usually exhibit glomerular deposition of C3 and P (properdin). Surprisingly, little is known about plasma complement activation in this disease, and the plasma C3 and C4 concentrations are usually normal or increased. We quantitated C3 activation in 202 plasmas from 81 patients with IgA nephropathy using a sensitive new assay that detects a neoantigen [iC3b-C3d neoantigen) which appears when C3b is inactivated to iC3b, C3dg, or C3d. This assay accurately quantitates small amounts of in vivo C3 activation. The concentration of iC3b-C3d neoantigen in plasma was significantly increased, indicating C3 activation in 37% of the pediatric and 57% of the adult plasmas assayed. When data from serial determinations in the patients were analyzed, 75% of the adult and 57% of the pediatric patients had C3 activation on at least one occasion. Classical pathway activation, quantitated by C4 activation was found in 20% of the adult and 5% of the pediatric plasmas. No association was found between elevated iC3b-C3d neoantigen concentration and history of macroscopic hematuria, chronic renal insufficiency or degree of proteinuria. These studies show that complement activation can frequently be detected in the plasma of IgA nephropathy patients. However, the pathophysiologic significance of this complement activation remains to be determined.

Adult↗
PubMed1987

Serum levels of interferons in patients with systemic lupus erythematosus.

Serum levels of alpha (alpha) and gamma (gamma)-interferons (IFN) were measured in 30 patients with untreated systemic lupus erythematosus (SLE) with a solid-phase, sandwich immunoradiometric assay using specific monoclonal antibodies. The serum levels of alpha-IFN were higher in patients with SLE than in normal subjects, and correlated with the clinical activity index (rs = 0.60, P less than 0.01), but not with renal histological activity. The serum level of alpha-IFN correlated with the serum level of immune complexes (r = 0.46, P less than 0.01) and the number of peripheral lymphocytes inversely (r = -0.49, P less than 0.01). Serum gamma-IFN levels were also higher in patients with SLE than in control subjects but no correlations were found between it and either clinical activity, renal histological activity or various laboratory parameters. Serum levels of both alpha-IFN and gamma-IFN were higher in SLE patients with erythema than in those without. These results suggested that serum levels of alpha-IFN were more closely related to clinical activity of SLE than were those of gamma-IFN, and that peripheral lymphocytes were probably not the source of the elevated serum IFN-alpha concentration.

Antibodies, Monoclonal↗