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Biomedical subjects

H Inariba

Publications and source records attributed to H Inariba.

12 recordsLinked to original sources
PubMed1993

Multicenter study with recombinant human erythropoietin.

A multicenter study with recombinant human erythropoietin (rh-EPO) was carried out. Of 172 hemodialysis patients with anemia selected for the study from 20 hospitals and clinics, 77 were males and 95 females (mean age 53.9 years). A starting dose of 1,500 U of rh-EPO (Epoetin beta) was administered intravenously at the end of every dialysis session. If the efficacy was not acceptable, the dose was increased to 3,000 U. When the target hematocrit was achieved (30%), the total dose was decreased. The results of the study were excellent relative to those of other multicenter studies with regard to efficacy, safety, and changes in laboratory data. The incidence of hypertension was lower in our study compared with other reports because we used a low initial dose. The efficacy of rh-EPO therapy was determined earlier and more reliably by reticulocytes than by hematocrit or hemoglobin. Prompt iron supplement therapy is recommended with careful observation of serum iron and ferritin.

Anemia↗
PubMed1993

EPO test in hemodialysis patients.

It is well known that red blood cell (RBC) and reticulocyte counts increase when anemic hemodialysis patients receive repeated administrations of recombinant human erythropoietin(rh-EPO). However, the early response of reticulocyte has not been reported precisely. In this study, reticulocyte counts and its fractions were observed in 8 maintenance hemodialysis patients after a single intravenous administration of 60 u/Kg of rh-EPO. The peripheral blood cells taken from the patients were stained with auramine 0, which bound to RNA and caused fluorescence. R-1000 (Sysmex, Kobe, Japan) analyzed the reticulocytes and classified the stained cells into three groups by the intensity of fluorescence. The number of highly fluorescent reticulocyte, which was young and large, increased and reached its highest level on day 4 after a single administration of rh-EPO. The reticulocyte counts paralleled these changes, but RBC counts did not change after administrations of rh-EPO. These data suggest that the observation of reticulocytes and its fractions in hemodialysis patients after a single administration of rh-EPO could tell us whether reticulocytes are responsive to rh-EPO or not, and this could be called as EPO test.

Adult↗
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↗
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↗
PubMed1990

Chronic antihypertensive drug treatment decreases protein kinase C activity in platelets from SHR.

There is evidence that protein kinase C activity in platelets from adult SHR is significantly higher than this activity in age-matched WKY. In the present study, protein kinase C activity in the SHR was measured following antihypertensive drug treatment. Chronic administration of enalapril to SHR for 2 weeks decreased both systolic blood pressure and protein kinase C activity to the levels seen in the WKY. Similar results were obtained in case of chronic treatment of SHR with hydralazine or nifedipine. These results suggest that enhanced protein kinase C activity of SHR can be suppressed by lowering blood pressure by antihypertensive drugs.

Animals↗
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↗
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↗
PubMed1988

Intracellular pH in platelets from spontaneously hypertensive rats and Wistar-Kyoto rats.

Intracellular pH in platelets from spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) was measured using a pH-sensitive fluorescent dye, 2',7'-bis(carboxyethyl)carboxyfluorescein tetraacetoxy methyl ester (BCECF). Intracellular pH in platelets was significantly higher in SHR than in WKY (7.12 +/- 0.04 versus 7.06 +/- 0.02, P less than 0.01; n = 10). There was a close correlation between intracellular pH and systolic blood pressure (r = 0.66, P less than 0.01). Addition to platelets of 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (H-7), a specific inhibitor of protein kinase C, produced a significantly larger decrease in intracellular pH in SHR than in WKY (0.06 +/- 0.02 versus 0.03 +/- 0.00, P less than 0.01, n = 5). These results suggest that protein kinase C may play an important role in the increased intracellular pH in SHR.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1983

Morphological studies on proliferation and desquamation of the alveolar lining epithelium in carrageenan-induced experimental pneumonia.

An experimental model of carrageenan-induced pneumonia in rabbits was used to study the proliferation and desquamation of alveolar lining epithelium, light and electron microscopically. Observation at 5 hr after intrapulmonary injection of 0.5% lambda carrageenan solution revealed epithelial cell (predominantly type 1 pneumocyte) injury, exposing the basement membrane of the alveolar wall, and that at 40 hr demonstrated an appearance of many large pneumocytes among the alveolar lining epithelium as a reparative reaction. This proliferative response of immature type 2 pneumocytes reached to the maximum in 60 and 72 hr followed by an intense desquamative response of the excessive alveolar epithelium in 5 and 6 days. The sloughed off epithelial cells were demonstrated as cell sheets or as clusters of epithelial cells. Inflammatory infiltrates in alveolar and interstitial spaces consisted of neutrophils and monocytes (or macrophages) at early stages, and mononuclear cells or macrophages at latter stages. Observation in 2nd and 3rd week showed accumulation of macrophages with many osmiophilic lamellar bodies in the alveolar spaces. The alveolar wall lining epithelium was still cuboidal or elliptical in shape in some alveoli and membranous in the others. Thickened alveolar septa at this stage were also noted. Thus this animal model appears to be a valuable tool for further understanding of the events leading to proliferation and desquamation of the alveolar lining epithelium.

Animals↗