Search PubMed⌕ Search

Biomedical subjects

O Sakai

Publications and source records attributed to O Sakai.

At least 55 records · Page 3Linked to original sources
PubMed1997

Massive uncomplicated vascular immune complex deposits in the kidney of a patient with systemic lupus erythematosus.

The case of a patient with systemic lupus erythematosus (SLE) is reported which was accompanied by renal dysfunction and massive vascular immune deposits in the kidney without active glomerular lesions. The renal biopsy showed arterioles and small arteries with circumferential periodic acid-Schiff (PAS) and Masson trichrome-positive homogenous material in the subendothelial area in the absence of thrombotic, necrotizing or inflammatory lesions. Immunofluorescence and electron microscopy examination demonstrated immune deposits in the vascular walls. Glomeruli showed only minor abnormalities with a trend to collapse. There was no improvement in renal dysfunction over a 4-year period until the patient's death, despite steroid therapy producing a decrease in disease activity. The autopsy showed similar vascular changes to those seen in the biopsy, however; glomeruli were either sclerotic or showed a trend to collapse. Massive uncomplicated vascular immune complex deposition without active glomerular lesions is rare. The present case indicates that this type of lupus vasculopathy may be a prognostic factor for the loss of renal function in SLE mediated by hemodynamic glomerular injury.

Aged↗
PubMed1996

Stimulation by corticotropin-releasing factor of atrial natriuretic peptide and brain natriuretic peptide secretions from cultured neonatal rat cardiomyocytes.

The new functional role of corticotropin-releasing factor (CRF) in the regulation of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) release was investigated using cultured neonatal rat cardiomyocytes. Treatment with CRF (10(-10)-10(-6) M) resulted in dose- and time-dependent increase in ANP and BNP secretion, up to 2.5-fold and 1.8-fold above control values, respectively. The effect was significant at 6 hr and persisted for at least 36 hr. The effect of CRF (10(-7) M) was partially blocked by alpha-helical CRF(9-41) (10(-7) M), a specific CRF receptor antagonist. The effect of CRF (10(-7) M) was not only blunted by cAMP-dependent protein kinase A (PKA) inhibitor, H-89 (10(-5) M), but also by protein kinase C inhibitors, H-7 (50 microM) and Calphostin C (10(-6) M). H-7 (50 microM) and Calphostin C (10(-6) M) alone lowered basal ANP and BNP levels. Furthermore, CRF (10(-7) M) stimulates protein synthesis up to 1.2-fold. These results indicate that CRF stimulates ANP and BNP secretions through the CRF receptor and, at least in part, via PKA activation during cardiac hypertrophy.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

Effects of a hepato-protective agent and a hepato-secreting chelator on cadmium-induced nephrotoxicity in Syrian hamsters.

Cadmium (Cd)-induced nephropathy in male Syrian hamsters was treated with D/L-penicillamine (D/L-p) or neomynophagen C (NMC). The subcutaneous injection of CdCl(2), 3 mg/kg, three times a week led to marked renal damage, ie., increased proteinuria and the excretion of urinary N-acetyl-beta-D-glucosaminidase (NAG) as compared with the saline-injected controls. Cd-treated hamsters that were injected intraperitoneally with D/L-p, 0.1 mg/kg, five times a week, showed less renal damage, including a reduction in urinary protein from 3.60 + or - 0.42 to 1.77 + or - 0.7 mg/d. NMC-treated hamsters showed a reduced excretion of NAG (from 1.47 +/ - 0.34 to 0.91 + or - 0.68 u/d). The concentration of Cd in renal cortical tissue was reduced slightly (from 2.78 + or - 0.08 to 2.34 + or - 0.3 mg/g.prot) by NMC treatment, but not by D/L-p. The elevated malondialdehyde (MDA) in renal cortical tissue was unaffected by administering D/L-p or NMC. The concentration of glutathione (CSH) in the renal cortex was not elevated after administering Cd, but the ratio of the reduced to the oxidized GSH was elevated. The Cd induced liver dysfunction, as compared with untreated controls. The dysfunction was improved slightly by NMC administration, but not by that of D/L-p. Changes in renal morphology induced by Cd involving marked degeneration and necrosis of tubules as shown by light microscopy, were unaffected by treatment with D/L-p or NMC. We thus demonstrated the efficacy of D/L-p of NMC in treating the nephropathy induced by Cd in hamsters. The mechanism of therapeutic effect is not known.

Acetylglucosaminidase↗
PubMed1996

The influence of aging on renal response to cadmium in Syrian hamsters.

To determine the renal effects of cadmium (Cd) in older animals, we administered subcutaneously a single dose of cadmium, 3.0 mg/kg/BW, to Syrian hamsters aged 16 wk ("young") and 60 wk ("old"). Marked morphologic changes in the kidney and renal dysfunction were observed, especially in the older animals. The concentration of MDA in the renal cortex was significantly increased only in young hamsters treated with cadmium. Concentrations of glutathione (GSH) in the renal cortex were increased in the old hamsters on d 6. Increased levels of renal MDA after cadmium treatment may induce the production of GSH in the kidney thus preventing renal damage. Aging can increase the susceptibility to the renal effects of cadmium.

Acetylglucosaminidase↗
PubMed1996

Acinic cell Carcinoma of the parotid gland: CT and MRI.

We report CT and MRI bindings in two cases of acinic cell carcinoma of the parotid glands which behaved differently on T2-weighted images. Differences in signal intensities were considered to reflect the histology of the lesion, although a histological diagnosis could not be made on imaging grounds alone.

Adult↗
PubMed1996

Evidence for amelioration of endothelial cell dysfunction by erythropoietin therapy in predialysis patients.

Evidence for the involvement of endothelial cells in the pathogenesis or erythropoietin-induced hypertension, and for endothelial cell damage in patients with chronic renal failure, has emerged and appears to be of major concern. We, therefore, investigated the effect of recombinant human erythropoietin (rHuEPO) therapy on endothelium-derived hormones in predialysis patients with progressive renal anemia. At the entry to the trial, the serum thrombomodulin concentration (Tm) and plasma endothelin-1 concentration (ET-1) in the predialysis patients were significantly higher than those in age- and sex-matched normal subjects. Following a 16 week period of treatment with 6000IU rHuEPO given intravenously once a week, patients' hematocrit increased from 27.1 +/- 2.6% to 34.6 +/- 3.2% (n = 16, P < .001). A positive correlation was found between Tm and serum creatinine concentration (Cr) (r = 0.61, P < .05 (n = 16), but no correlation was found between ET-1 and Cr. Tm and Tm/Cr significantly decreased from 7.9 +/- 2.8 ng/mL to 6.6 +/- 2.4 ng/mL (P < .01, n = 16), and from 2.1 +/- 0.7 (x10(-10) to 1.6 +/- 0.7 (x10(-10), P < .01, n = 16), respectively. However, there was no change in ET-1 as a result of the rHuEPO therapy. Creatinine clearance (Ccr), Cr, total amount of daily Tm excretion, Tm clearance/Ccr, daily urinary protein and albumin excretion, and blood pressure also remained unchanged throughout the trail. The present study indicates that correcting anemia by rHuEPO therapy reduces an abnormally elevated Tm in predialysis patients while blood pressure and renal function remain unchanged, suggesting that rHuEPO has a beneficial effect on endothelial cell dysfunction in chronic renal failure patients. This effect may be mediated via an improved oxygen supply to the endothelial cells due to the amelioration of anemia by rHuEPO.

Adult↗
PubMed1996

Development of nephrotic syndrome in a patient with acute myeloblastic leukemia after treatment with macrophage-colony-stimulating factor.

We describe a patient with acute myeloblastic leukemia (AML) who developed nephrotic syndrome after receiving several courses of chemotherapy, including macrophage-colony-stimulating factor (M-CSF). At the onset of nephrotic syndrome, the patient remained in a hematological remission. A renal biopsy showed diffuse mesangial proliferation with marked glomerular infiltration of macrophages and massive subendothelial and mesangial deposits. After the institution of the combined therapy with corticosteroid, anticoagulant, and dipyridamole, urinary protein excretion was attenuated to less than 1.0 g/day. It should be emphasized that the recurrence of nephrotic syndrome was observed after the following chemotherapy, including M-CSF, whereas the bone marrow still remained completely remitted. In contrast, after the last course of chemotherapy, which did not include M-CSF, urinary protein excretion was not enhanced. Of note is that the renal histology at autopsy showed a remarkable improvement of mesangial hypercellularity with concomitant reduction in the number of glomerular macrophages. These evolutional changes in both proteinuria and glomerular histology suggest a close linkage between the M-CSF treatment and macrophage-related glomerular injury. The possibility can be raised that M-CSF accelerated the underlying renal disease in this case through enhancing macrophage accumulation into the glomerulus, leading to the development of nephrotic syndrome.

Antineoplastic Combined Chemotherapy Protocols↗