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Biomedical subjects

F Marumo

Publications and source records attributed to F Marumo.

At least 523 records · Page 29Linked to original sources
PubMed1991

The 'oral 1,25-dihydroxyvitamin D3 pulse therapy' in hemodialysis patients with severe secondary hyperparathyroidism.

Many hemodialysis patients are still suffering from secondary hyperparathyroidism although 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) has been used to treat renal osteodystrophy for the last two decades. The main reason for its failure to correct the secondary hyperparathyroidism is that in patients, hypercalcemia occurs before adequate parathyroid hormone (PTH) suppression is obtained when a large daily dose of 1,25(OH)2D3 is started. In this study, the oral dose of 1,25(OH)2D3 (4.0 micrograms) was administered only twice a week at the end of hemodialysis ('oral 1,25(OH)2D3 pulse therapy'), in 19 patients with severe secondary hyperparathyroidism. Serum immunoreactive PTH started to decrease after 6 weeks of therapy, and the original level of 41.2 +/- 7.24 was reduced to 24.4 +/- 6.12 ng/ml by the end of the 6-month therapy (p less than 0.001). Serum alkaline phosphatase also was reduced by 64.4%. Three out of 19 patients suffered from hypercalcemia during the 4th month of therapy. Calcium supplement given to 6 other patients with severe secondary hyperparathyroidism did not lower serum PTH levels significantly after 6 weeks of therapy, although serum calcium levels increased and were sustained above 10 mg/dl for the last 5 weeks. These findings strongly suggest that the suppressive effect of the oral 1,25(OH)2D3 pulse therapy was attained by a direct action of 1,25(OH)2D3 on the parathyroid gland rather than by its ability to elevate serum calcium levels. In conclusion, the oral 1,25(OH)2D3 pulse therapy effectively lowered PTH levels in hemodialysis patients who cannot tolerate large daily doses of 1,25(OH)2D3.

Administration, Oral↗
PubMed1991

Endothelin-1-like immunoreactivity in human urine.

By using a radioimmunoassay specific for endothelin-1 (ET-1), we studied whether ET-1-like immunoreactivity (LI) is present in human urine. Significant amounts of ET-1-LI were present in human urine, and the daily urinary excretion of ET-1-LI in 30 normal subjects was 67.6 +/- 35.5 ng/day. The mean urinary excretion of ET-1-LI determined in spot urine was 82.8 +/- 38.2 pg/mg creatinine (n = 30), while the mean plasma concentrations of ET-1-LI in the same individuals were 1.1 +/- 0.5 pg/ml. There was no significant correlation between urinary ET-1-LI excretion and its plasma levels. Reverse-phase high-pressure liquid chromatography of human urine extract revealed a major ET-1-LI component coeluting with standard ET-1. The present study demonstrates the presence of ET-1-LI excreted in human urine, although its exact source and physiological significance in renal tissues remain to be determined.

Adult↗
PubMed1991

Angiotensin-converting enzyme activity as a prognostic factor in acute renal failure.

We evaluated serum angiotensin-converting enzyme (ACE) activity and thyroid function to determine the importance as prognostic factors in acute renal failure (ARF). Among 37 ARF patients, 24 survived (recovered group) and 13 died (lethal group). Both serum thyroxine (T4) level and ACE activity were lower in ARF as a whole group (n = 37) than normal control group (n = 27, p less than 0.01). Both serum T4 level and ACE activity in lethal group (n = 13) were significantly lower than those of the recovered group (n = 24, p less than 0.01). Serum ACE activity but not serum T4 level was significantly related to the prognosis of ARF (p less than 0.02, Mantel-Haenszel analysis). This suggests that lowered serum T4 levels are not a specific indicator of ARF, but lowered ACE activity is significantly related to the prognosis of the patient in ARF. Serum ACE activity seems to be one of several clinically useful prognostic indicators in ARF.

Acute Kidney Injury↗
PubMed1991

Cellular mechanism of endothelin-1 release by angiotensin and vasopressin.

Release of endothelin-1, a novel potent vasoconstrictor peptide originally isolated from endothelial cells, from cultured bovine endothelial cells has been shown to be stimulated by arginine vasopressin and angiotensin II. To elucidate the cellular mechanism by which endothelin-1 is released by these vasoconstrictors, we tested the effects of several compounds on the agonist-induced endothelin-1 release and studied the changes of cytosolic free Ca2+ concentrations and phosphoinositide breakdown by these agonists in cultured bovine endothelial cells. Protein kinase C inhibitors (H-7, staurosporine), an intracellular Ca2+ chelator, and an inhibitor of phospholipase C (neomycin), all abolished the agonist-induced endothelin-1 release, whereas the Ca2+ channel blocker nicardipine was ineffective. Although synthetic 1,2-diglyceride (diolein) dose dependently stimulated endothelin-1 release, downregulation of protein kinase C after pretreatment with phorbol ester resulted in decreased effects to increase endothelin-1 release by the agonists. Both arginine vasopressin and angiotensin II induced immediate and transient increases in intracellular Ca2+ levels of fura-2-loaded endothelial cells as well as formation of inositol trisphosphate; the agonist-induced intracellular Ca2+ increases were not affected either by nicardipine or by chelating extracellular Ca2+. The arginine vasopressin- and angiotensin II-induced intracellular Ca2+ increases, inositol trisphosphate formation, and endothelin-1 release were completely abolished by V1-receptor antagonist and saralasin, respectively. It is concluded that arginine vasopressin and angiotensin II stimulate the release of endothelin-1 by a common mechanism, involving receptor-mediated mobilization of intracellular Ca2+ and activation of protein kinase C in endothelial cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Endothelin-1 induces hypertrophy with enhanced expression of muscle-specific genes in cultured neonatal rat cardiomyocytes.

To determine whether endothelin-1 (ET-1) induces hypertrophy of cardiomyocytes, the effects of ET-1 on the expression of muscle-specific genes and a proto-oncogene, c-fos, in cultured neonatal rat cardiomyocytes were examined by Northern blot analysis. ET-1 (10(-7) M) induced about twofold to fourfold increases in the gene expression of myosin light chain 2, alpha-actin, and troponin I after 6 hours, which continued up to 24 hours. The ET-1-induced increases in mRNA levels for these muscle-specific genes were dose dependent (10(-9) to 10(-7) M). Run-on transcriptional assay showed that the changes in mRNA level for three muscle-specific genes were regulated, at least in part, at the transcriptional level. 12-O-Tetradecanoylphorbol 13-acetate (TPA), a potent protein kinase C activator, and the Ca2+ ionophore ionomycin also increased mRNA levels of three muscle-specific genes. ET-1, TPA, and ionomycin similarly induced the expression of c-fos after 30 minutes, which returned to an undetectable level after 6 hours. ET-1 remarkably and dose-dependently stimulated accumulation of total inositol phosphates in cardiomyocytes. Morphometrical evaluation showed that ET-1 significantly increased surface area of cardiomyocytes without cell proliferation. ET-1 also dose-dependently stimulated the synthesis of protein and DNA, which was unaffected by the L-type calcium channel blocker nicardipine. These data suggest that ET-1 induces hypertrophy of cardiomyocytes associated with the induction of muscle-specific gene transcripts through the possible involvement of protein kinase C activation or intracellular Ca2+ mobilization.

Animals↗
PubMed1991

Endothelin-1 is an autocrine/paracrine growth factor for human cancer cell lines.

We studied whether a novel vasoconstrictor peptide, endothelin-1 (ET-1), is synthesized by and released from human carcinoma cell lines, and whether ET-1 stimulates proliferation of these tumor cells. ET-1-like immunoreactivity was released from both HeLa and HEp-2 cells as a function of time. Reverse-phase HPLC of the conditioned media from HeLa cells revealed a major peak coeluting with standard ET-1. Northern blot analysis demonstrated the expression of mRNA for ET-1 precursor in both tumor cell lines. Both cell lines contained a single class of specific binding sites for ET-1. ET-1 dose-dependently induced increases in cytosolic free Ca2+ concentration in fura-2-loaded tumor cells, whose effect was completely abolished by chelating extracellular Ca2+ or by Ca(2+)-channel blocker. ET-1 stimulated proliferation of the quiescent cell lines in a dose-dependent manner, whose effect was inhibited by Ca(2+)-channel blocker. Polyclonal antibody for ET-1 inhibited proliferation of these cell lines, whereas nonimmune serum had no effect. These results demonstrate that ET-1 is synthesized by and released from human epithelial carcinoma cell lines, and that exogenous and endogenous ET-1 stimulates proliferation of the cells possibly through Ca2+ influx, suggesting its role as an autocrine/paracrine growth factor for certain tumor cells.

Calcium↗
PubMed1991

Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

The regulation of osmotic water permeability (Pf) by vasopressin (VP) in kidney collecting tubule involves the exocytic-endocytic trafficking of vesicles containing water channels between an intracellular compartment and apical plasma membrane. To examine effects of transcellular water flow on vesicle movement, Pf was measured with 1-s time resolution in the isolated perfused rabbit cortical collecting tubule in response to addition and removal of VP (250 microU/ml) in the presence of bath greater than lumen (B greater than L), lumen greater than bath (L greater than B), and lumen = bath (L = B) osmolalities. With VP addition, Pf increased from 12 to 240-270 x 10(-4) cm/s (37 degrees C) in 10 min. At 1 min, Pf was approximately 70 x 10(-4) cm/s for B greater than L, L greater than B, and L = B conditions. At later times, Pf increased fastest for L greater than B and slowest for B greater than L osmolalities; at 5 min, Pf was 250 x 10(-4) cm/s (L greater than B) and 158 x 10(-4) cm/s (B greater than L). With VP removal, Pf returned to pre-VP levels at the fastest rate for B greater than L and the slowest rate for L greater than B osmolalities; at 30 min, Pf was 65 x 10(-4) cm/s (B greater than L) and 183 x 10(-4) cm/s (L greater than B). For a series of osmotic gradients of different magnitudes and directions, the rates of Pf increase and decrease were dependent upon the magnitude of transcellular volume flow; control studies showed that paracellular water flux, asymmetric transcellular water pathways, or changes in cell volume could not account for the data. VP-dependent endocytosis was measured by apical uptake of rhodamine-dextran; in paired studies where the same tubule was used for + and - gradients, B greater than L and L greater than B osmolalities gave 168% and 82% of uptake measured with no gradient. In contrast, endocytosis in proximal tubule was not dependent on gradient direction. These data provide evidence that transcellular volume flow modulates the vasopressin-dependent cycling of vesicles containing water channels, suggesting a novel driving mechanism to aid or oppose the targeted, hormonally directed movement of subcellular membranes.

Animals↗
PubMed1991

Reduced high harmonic power spectra in patients with old myocardial infarction.

Acceleration of blood flow ejected from the ventricle into the aorta and the hydraulic power state of blood flow in the aorta may be affected by asynchronous or locally depressed contraction of the left ventricle as well as by arterial impedance. In order to evaluate the effect of an infarcted heart on the hydraulic power state of blood flow, the aortic input impedance spectrum and the hydraulic power spectrum were calculated from simultaneous recordings of pulsatile aortic pressure and flow velocity at the aortic root in 6 normal controls (group 1), 6 patients with old myocardial infarction (OMI) without aneurysm (group 2), and 6 patients of OMI with aneurysm (group 3). The ratios (Rh) of power in high harmonics to that of fundamental harmonics, that is, Rh = (E2 + E3 + ...E10)/E1, where E represents hydraulic power and the numbers represent harmonic numbers, were 0.64 +/- 0.17, 0.23 +/- 0.09, and 0.22 +/- 0.10 in groups 1, 2, and respectively (p less than 0.001 between groups 1 and 2; p less than 0.001, between groups 1 and 3). As the acceleration of ejecting flow of blood by the left ventricle is inversely related with arterial impedance, Rh will be also inversely related with arterial impedance. Then, the product of Rh and the characteristic impedance (Zc) would be an indicator of the left ventricular contractility. In fact, the products were 64 +/- 15, 32 +/- 14, and 31 +/- 13 dyne.sec.cm-5 in groups 1, 2, and 3 respectively (p less than 0.005, between groups 1 and 2; p less than 0.005, between groups 1 and 3). These results suggest that asynchronous or locally depressed contractions of the left ventricular wall are closely related to depressed Rh and further to depressed values of the products of Rh and Zc. It is concluded that analysis of the power spectrum of blood flow in the root of the aorta provides information of the left ventricular contractility in connection with arterial impedance.

Blood Flow Velocity↗
PubMed1991

Hemodynamic mechanism of the elevation in blood pressure following the improvement of anemia with recombinant human erythropoietin.

Following the administration of recombinant human erythropoietin (rHuEPO) to 18 patients undergoing hemodialysis, the hematocrit (Ht) increased from 19.7 +/- 1.8 to 31.0 +/- 2.0%. The incidence of hypertension according to the criteria of WHO was 11.1%. The systolic blood pressure (SBP) increased significantly from 120 +/- 21 to 129 +/- 26 mmHg (p less than 0.01) and diastolic blood pressure (DBP) increased from 67 +/- 14 to 73 +/- 12 mmHg (p less than 0.05). The cardiac index (CI) decreased significantly from 4.07 +/- 1.13 to 3.56 +/- 0.88 L/min/m2 (p less than 0.05). Total peripheral resistance index (TPRI) and blood volume (BV) increased significantly from 1,725 +/- 406 to 2,170 +/- 643 dynes/sec/cm-5/m2 (p less than 0.001) and from 78.9 +/- 11.2 to 87.8 +/- 14.8 ml/kg (p less than 0.005) respectively. Pulse rate (PR) decreased significantly from 73.0 +/- 10.7 to 65.9 +/- 7.8 beats/min (p less than 0.01). Patients who developed a blood pressure (BP) elevation of 10% or more for the mean blood pressure (MBP) showed a slight and insignificant decrease in CI from 3.65 +/- 1.12 to 3.49 +/- 1.06 L/min/m2, which clearly contrasted to that in another group of patients who showed a reduced increase in MBP and a significant reduction in CI from 4.50 +/- 1.03 to 3.63 +/- 0.72 L/min/m2 (p less than 0.05). Stroke volume index (SVI) was unchanged in both groups but PR decrease significantly in the latter group. A significant increase in TPRI or BV was observed equally in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Appearance of beta-human atrial natriuretic peptide in collagen disease.

To elucidate the circulating forms of human atrial natriuretic peptide (hANP) in collagen disease, we analysed plasma samples obtained from 21 patients with systemic lupus erythematosus, rheumatoid arthritis or progressive systemic sclerosis with no clinical evidence of cardiac involvement. The findings were compared with those obtained from 21 healthy control subjects. Plasma hANP-like immunoreactivity was normal in all but three of the controls and in two patients with the nephrotic syndrome due to lupus nephritis. Reverse-phase high-performance liquid chromatography, gel permeation chromatography and subsequent radioimmunoassay for hANP revealed that the circulating hANP consisted of alpha-hANP, beta-hANP and gamma-hANP in the patients with collagen disease whereas alpha-hANP predominated in the control group. beta-hANP appeared in 18 of the 21 patients but was not observed in the controls. These data suggest that beta-hANP circulates in the plasma of patients with collagen disease even when no myocardial involvement is apparent and that the appearance of beta-hANP is not always associated with an increase in total plasma hANP-like immunoreactivity. Thus the appearance of beta-hANP in plasma is not a phenomenon specific to congestive heart failure.

Adult↗
PubMed1991

[Right ventricular infarction following acute inferior myocardial infarction confirmed by dual isotope single photon emission computed tomography (SPECT) of [99mTc] pyrophosphate and [201Tl] chloride].

A 56-year-old man, complaining of severe substernal chest pain, was admitted. In this patient, right ventricular infarction following by acute inferior myocardial infarction was suggested by serial enzymes, electrocardiogram, echocardiogram, and hemodynamic data, but it was not confirmed. A dual isotope SPECT with 99mTc-pyrophosphate and 201Tl-Cl was performed and color-coded tomograms were obtained. It showed a characteristic image of right ventricular infarction, especially in the short axis view right ventricular infarction looked like shape of a tongue which protruded from left ventricle. We concluded that though the diagnosis of right ventricular infarction is difficult, a dual isotope SPECT is a useful method because it shows a characteristic image.

Diphosphates↗
PubMed1991

[Diffuse panbronchiolitis in two brothers with different clinical courses].

Diffuse panbronchiolitis in two brothers is reported. The elder brother aged 46, was admitted in May 1983 due to severe dyspnea and productive cough, which had gradually worsened over several years. He had severe hypoxemia and hypercapnia. He died at age 47 of respiratory failure due to pseudomonas infection despite antibiotic therapy. The younger brother, at age 41, was admitted in March 1983 due to fever, productive cough, and abnormal shadows on chest X-ray films. He showed mild hypoxemia and his symptoms improved with antibiotic treatment. Since then he has been followed as an outpatient for over 7 years while taking 400 mg of Erythromycin per day, and he has had no exacerbation. These two cases had different clinical courses despite the facts that both had similar conditions of chronic sinusitis and appeared to be exposed to no special environmental or occupational hazards. These facts suggest that not only intrinsic factors, such as defenselessness of airways, but extrinsic factors such as viral, mycoplasmal, or bacterial infection may act together on the mechanisms of the onset and progression of diffuse panbronchiolitis.

Adult↗
PubMed1991

[Interleukin-2 (IL-2) in active pulmonary tuberculosis].

To clarify the precise of cellular immunity mechanism in pulmonary tuberculosis, we investigated the amount of IL-2 in patients with untreated active pulmonary tuberculosis. When serum adenosine deaminase (ADA) activity was examined using enzyme assay, an abnormally high level was observed in all patients (29.0 + 11.6 IU/ml, mean + SD; 4.5-17.8, normal range). Likewise, the level of serum-soluble interleukin-2 receptor (IL-2R) measured by ELISA showed abnormal high level in all patients (844.3 + 584.8 IU/ml; 80-300, normal range). When stimulated using PHA, the peripheral lymphocyte's ability to produce IL-2 revealed no difference between control subjects and patients. It was, however, noted that the lymphocytes of the patients significantly suppressed IL-2 responsiveness when compared to the control subjects (P less than 0.05). The serum IL-2 concentration measured using RIA could not be detected in any of the patients as was the same for control subject. All of the above mentioned results suggest that T-cell activation which caused increment in serum ADA activity and soluble IL-2R occurred in active pulmonary tuberculosis. The suppressed IL-2 responsiveness in the peripheral lymphocytes of patients proposes the possibility of soluble IL-2R reduction by the negative feedback mechanism in IL-2-sensitive lymphocytes.

Adenosine Deaminase↗