Search PubMed⌕ Search

Biomedical subjects

S Morimoto

Publications and source records attributed to S Morimoto.

At least 559 records · Page 31Linked to original sources
PubMed1988

[Adrenal incidentaloma: report of eight cases].

Since 1983, eight cases of adrenal incidentaloma were experienced at the Department of Urology, Wakayama Medical College and affiliated hospitals. Six adrenal masses were incidentally detected by computed tomography, and two were first noted by either ultrasonography or intravenous pyelography. Surgical exploration was performed in all cases as the final diagnostic measure. Of them, three had adrenocortical adenomas, three had adrenal cysts, one had adrenal metastasis and one had pheochromocytoma. Preoperative evaluation revealed that all patients except one with pheochromocytoma had no endocrinological abnormality. The management of the adrenal incidentaloma, which will be discovered more frequently accompanied with the increasing use of computed tomography, was discussed with special references to its precise indication of surgical treatment.

Adenoma↗
PubMed1988

Immunological identification of rat urinary inactive kallikrein as a proform of tissue kallikrein.

Antibody was raised against a synthetic undecapeptide (PS 11) which corresponds to the prosegment of the rat tissue kallikrein precursor. The potential to recognize rat urinary active or inactive kallikrein was assessed by an enzyme immunoassay method for PS 11, using beta-D-galactosidase as the labeling enzyme. The active kallikrein failed to compete with the enzyme-labeled PS 11 in binding to the antibody. The inactive kallikrein displaced the enzyme-labeled PS 11 in this enzyme immunoassay, and the displacement curve was in parallel with that of PS 11. These results indicate that rat urinary inactive kallikrein contains a prosequence recognized by the antibody to PS 11. This inactive kallikrein is probably a proform of tissue kallikrein.

Animals↗
PubMed1987

[Radioimmunoassay of the calcitonin gene-related peptide and its measurement in the plasma of patients with medullary thyroid carcinoma and in the cerebrospinal fluid of normal subjects].

Calcitonin gene-related peptide (CGRP) is a peptide recently found by recombinant DNA and molecular biological techniques in rat medullary thyroid carcinoma cells, but its physiological role(s) is unknown. We established a radioimmunoassay for this peptide using human-CGRP (1-37) as a standard, 125I-human-CGRP (1-37) as a tracer, and anti-rat-CGRP (28-37) serum as a first antibody. Aprotinin, an inhibitor of proteolytic enzymes in the plasma, was also added to the assay system, because in its absence the tracer was degraded during incubation with plasma samples. The sensitivity of the assay was 60 pg/ml and the intra- and inter-assay coefficients of variation were 6.0% and 8.5%, respectively. The recovery was 105 +/- 17%. The plasma levels of CGRP in 17 normal subjects (mean +/- S.D. age, 45 +/- 12 years) were all below 300 pg/ml, the mean level being 132 +/- 77 pg/ml. The levels were also below 300 pg/ml in 20 of 21 patients with medullary thyroid carcinoma, but one patient who had a high level of 942 pg/ml (mean value, 142 +/- 193 pg/ml). There was no significant difference between the mean plasma levels of CGRP in normal subjects and patients with medullary thyroid carcinoma. The mean plasma levels of CGRP in 5 patients with medullary thyroid carcinoma did not increase in response to infusion of either 4.3 mg/kg of calcium in 10 minutes or 4 micrograms/kg of tetragastrin in 5 minutes, although the plasma levels of calcitonin in these patients increased markedly during these provocation tests. The levels of CGRP in the cerebrospinal fluid of 16 normal volunteers were all below the detectable limit (less than 60 pg/ml). These findings suggest that fewer patients with medullary thyroid carcinoma than reported previously have high plasma levels of CGRP, either in the basal state or in response to calcium or gastrin, and that the levels of CGRP in the cerebrospinal fluid of normal subjects are very low.

Adolescent↗
PubMed1987

Renin release in anesthetized rats is enhanced by the calmodulin antagonist W-7.

In foregoing work, we found that the release of renin from rat kidney cortical slices was stimulated by the calmodulin antagonist W-7. The present work was done to determine whether W-7 would stimulate renin release in vivo. W-7 and its control agent, W-5 were directly infused into the renal artery of anesthetized rats. W-7 and W-5, at 50 micrograms/kg/min, produced no significant effects on renin release. Infusion of W-7 at 100 micrograms/kg/min resulted in a marked stimulation of renin release, but there was no significant alteration in the release when the same dose of W-5 was infused. Both compounds elicited a slight decrease in renal blood flow. The alterations in renin release and renal blood flow seen with W-7 were not affected by pretreatment with phentolamine or propranolol. As W-7 stimulates renin release in vivo, the hypothesis that Ca2+-calmodulin plays an inhibitory role in renin release from the kidney is given added support.

Animals↗
PubMed1987

Effects of nitrates and calcium channel blockers on Ca2+-ATPase in the microsomal fraction of porcine coronary artery smooth muscle cells.

The effects of the antianginal drugs nitroglycerin, nicorandil, diltiazem, verapamil and nicardipine on the activity of calcium-stimulated magnesium-dependent ATPase (Ca2+-ATPase) were investigated in the microsomal fraction from porcine coronary artery smooth muscle cells. Two discrete Ca2+-dependent ATPase components were observed: [1] a high affinity component, which was a specific Ca2+-ATPase, [with a half saturation constant for Ca2+ (Km) of 0.44 microM, and maximum velocity (Vmax) of 124.3 pmol of phosphate (Pi) released/micrograms of protein/30 min]: [2] a low affinity component in which Ca2+ could be replaced by Mg2+ without loss of its activity. Nitroglycerin and nicorandil (1 microM and 10 microM) both stimulated the activity of the Ca2+-ATPase significantly [142 +/- 12 (mean +/- standard error), and 137 +/- 10% of the control with nitroglycerin, and 152 +/- 17 and 135 +/- 20% with nicorandil] at a Ca2+ concentration of 0.3 microM. Diltiazem, verapamil and nicardipine did not cause significant stimulation. Nitroglycerin and nicorandil (1 microM), significantly decreased the Km for Ca2+ from the control value of 0.44 +/- 0.06 microM to 0.26 +/- 0.03 and 0.22 +/- 0.03 microM, respectively. Nitroglycerin and nicorandil may dilate coronary arteries by stimulating this Ca2+ extrusion pump enzyme through reduction of intracellular Ca2+ in smooth muscle cells.

Animals↗
PubMed1987

Ca2+- and Sr2+-sensitivity of the ATPase activity of rabbit skeletal myofibrils: effect of the complete substitution of troponin C with cardiac troponin C, calmodulin, and parvalbumins.

The Ca2+-sensitive ATPase activity of rabbit skeletal myofibrils disappeared completely after treatment with a solution containing CDTA, a strong divalent cation chelator, at a low ionic strength. A gel electrophoretic study revealed that all troponin C and about half of myosin light chain 2 were removed from the myofibrils by the CDTA treatment. The CDTA-treated myofibrils, when reconstituted with skeletal troponin C, showed almost exactly the same Ca2+- or Sr2+-sensitive ATPase activity as that of intact myofibrils. The CDTA-treated myofibrils reconstituted with porcine cardiac troponin C showed the same Ca2+- or Sr2+-sensitivity of the ATPase as that of porcine cardiac myofibrils; Sr2+-sensitivity relative to Ca2+-sensitivity was about ten times higher than, and the maximal slope of the activation curve was about half that of skeletal myofibrils. These findings indicate that these characteristic features of divalent cation regulation in the contraction of skeletal and cardiac muscles are determined solely by the species of troponin C. Bovine brain calmodulin hardly activated the ATPase activity of the CDTA-treated myofibrils even in the presence of Ca2+. Excess calmodulin, however, was found to give Ca2+- or Sr2+-sensitivity to the ATPase activity of the CDTA-treated myofibrils. Frog skeletal parvalbumins 1 and 2, even in excess, did not affect the ATPase activity of the CDTA-treated myofibrils.

Adenosine Triphosphatases↗
PubMed1987

Mediastinal distortions from focal masses: a CT and radiographic study.

Fifty-seven mediastinal masses were studied by computed tomography (CT) and chest radiographs to determine how their specific site of origin affected their direction of expansion and the distortion of contiguous structures. Forty-four masses arose anterior to the heart and great vessels (precardiovascular compartment). When these masses arose on the right, they extended posteriorly only as far as the coronal plane of the trachea. Left-sided masses were not similarly limited in their posterior extension. Thirteen masses arose around the trachea and esophagus or in the subcarinal space (tracheoesophageal compartment). Masses in the upper part of this compartment caused tracheal and great-vessel displacement. The mobile superior vena cava (SVC) was more often distorted than was the aortic arch. Subcarinal masses always expanded to the right, displacing the right lower lobe. The heart and great arteries were more resistant to displacement and distortion than were the systemic veins. The trachea and mediastinal bronchi were intermediate in their displacement. The hila were effective barriers to the expansion of mediastinal masses.

Adolescent↗
PubMed1987

High-performance liquid chromatographic separation of corticosteroids in plasma of rats. Its application to the determination of the circadian rhythm of 18-hydroxycorticosterone related to aldosterone and corticosterone.

An efficient separation of corticosteroids in plasma of rats was obtained by reversed-phase high-performance liquid chromatography (HPLC). Plasma corticosteroid assays with HPLC separation were used to determine the circadian rhythm of 18-hydroxycorticosterone (18-OHB) and its possible relationship to aldosterone or corticosterone in conscious rats under standard conditions (regular diet; 12-hour light and 12-hour dark cycle). Significant circadian rhythms of plasma corticosterone, 18-OHB and aldosterone were observed with peak values at 20.00 h and nadir values at 08.00 h. The mean ratio of plasma 18-OHB to aldosterone during 24 h was 2.4. The circadian rhythm of 18-OHB was also correlated with that of plasma aldosterone or corticosterone.

18-Hydroxycorticosterone↗
PubMed1987

Effect of dietary calcium and magnesium on experimental renal tubular deposition of calcium oxalate crystal induced by ethylene glycol administration and its prevention with phytin and citrate.

Oral administration of ethylene glycol to rats, and the resultant intratubular depositions of microcrystals of calcium oxalate were studied investigating the influences of dietary calcium or magnesium and assessing the protective efficacies against the crystallizations by treatment with phytin and sodium citrate. With increase of calcium intake and consequent increase of urinary calcium excretion there was a marked increase in the amount of tubular deposit of calcium oxalate crystal and in the calcium content of renal tissue. Although magnesium deficiency accelerated renal tubular calcium oxalate deposition, the protection against the crystal formation was not observed with excessive dietary magnesium. When rats were fed a high-calcium diet supplemented with phytin, a significant inhibition of the intratubular crystallization was observed. It appeared obvious that a hypocalciuric action of phytin was attributed to the effect of the prevention. There was vigorous protection of crystal formation by treatment with sodium citrate, which correlated with the level of citrate concentration in the drinking water.

Animals↗
PubMed1987

Mechanism of luminal enlargement in PTCA and restenosis: a histopathological study of necropsied coronary arteries collected from various centers in Japan.

Necropsy studies of coronary arteries were made in 14 patients who died after percutaneous transluminal coronary angioplasty (PTCA). Eight patients died shortly after PTCA, while the other six patients died some considerable time later. A total of 9,920 serial step sections of necropsied coronary arteries at the site of PTCA were prepared and examined histopathologically by light microscope to determine the mechanism of luminal enlargement in PTCA, as well as the occurrence of restenosis. Of the eight patients who died shortly after PTCA, two had disruption of the intima and the media in the arterial wall located opposite the site that had atheroma, in spite of the fact that the former wall is more normal than the latter. Dissection of the media was camed out in four patients and intimal desquamation performed in six. All the patients revealed fresh thrombus formation. Of the six patients who survived for a long time after PTCA was performed, two had disruption of the intima and the media located opposite the site with atheroma. In one, the media was dissected and in another, intimal desquamation was camed out. In one patient, release of atheroma into the lumen was suspected. Proliferation of intimal cells was revealed in three patients indicating that restenosis had occurred. No compression of the atheroma was observed in any of the 14 patients. The above findings led to the conclusion that the mechanisms of luminal enlargement in PTCA are: 1) intimal and medial disruption in the arterial wall located opposite the atheroma; 2) medial dissection; 3) intimal desquamation; 4) release of atheroma into the lumen; and 5) any combination of 1) -4).

Adult↗
PubMed1987

Effect of atrial natriuretic factor on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from spontaneously hypertensive rats.

The effect of alpha-human atrial natriuretic factor (alpha-hANP, 10(-6) M- 10(-8) M) on basal, and maximum angiotensin II (AII, 4.8 X 10(-8) M)-, ACTH (4.3 X 10(-9) M)-, and potassium (8mM)-stimulated levels of corticosterone, 18-hydroxycorticosterone (18-OHB) and aldosterone production were studied in adrenal glomerulosa cells from spontaneously hypertensive rats (SHR) at 14 weeks of age as compared to those in the age-matched Wistar-Kyoto rats (WKY) on a normal sodium diet. Plasma corticosterone, 18-OHB and aldosterone levels and the aldosterone response in vitro to the graded doses of AII were similar in SHR and WKY. Basal, and maximum AII-, ACTH-, and potassium-stimulated levels of corticosterone, 18-OHB and aldosterone also were similar in the cells from SHR and WKY. alpha-hANP similarly inhibited basal and stimulated levels of these corticosteroids in the cells from SHR and WKY. These results indicate that the inhibitory effect of alpha-hANP on aldosteronogenesis is unaltered in SHR at 14 weeks of age on a normal sodium diet.

18-Hydroxycorticosterone↗
PubMed1987

Inhibitory effects of calcium channel agonists on renin release from rat kidney cortical slices.

Inhibitory effects of calcium channel agonists such as Bay K 8644 [methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)- pyridine-5-carboxylate] and CGP 28392 [ethyl-4-(2-difluoromethoxyphenyl)-1,4,5,7-tetrahydro-2-methyl- 5-oxofuro-(3,4-b)-pyridine-3-carboxylate] on renin release were investigated, using rat kidney cortical slices. Bay K 8644 or CGP 28392 alone had no effect on renin release from the slices, whereas both compounds produced a concentration-dependent inhibition of the release in the presence of 15 mM potassium. The Bay K 8644-induced inhibitory action was more effective and potent than that seen with CGP 28392. Bay K 8644 caused a leftward shift of the dose-response curve of the potassium-induced decrease in renin release. In contrast, the dose-response relationships of the release to norepinephrine and methoxamine were not affected by Bay K 8644. The combination of the maximum effective doses of calcium channel agonists and norepinephrine exerted an apparent additive effect on the release of renin. The inhibitory effects of Bay K 8644 and CGP 28392 were attenuated in the presence of decreased extracellular calcium concentrations. Nifedipine and verapamil elicited a blocking action on the inhibition of renin release by Bay K 8644 or CGP 28392, in a concentration-dependent manner. Calmodulin antagonists, such as trifluoperazine and calmidazolium suppressed significantly the decreasing effect of Bay K 8644 or CGP 28392 on renin release from the slices.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Effect of nicorandil on the cytosolic free calcium concentration and microsomal (Ca2+ + Mg2+)-ATPase activity of vascular smooth muscle cells.

The influence of nicorandil, a potent antianginal drug, on cellular calcium in vascular smooth muscle cells (VSMC) was investigated by studying its effects on the cytosolic free calcium concentration ([Ca2+]i) and calcium-stimulated magnesium-dependent ATPase [(Ca2+ + Mg2+)-ATPase] in the cells. VSMC were prepared from rat aorta, and their [Ca2+]i level was determined by measuring the fluorescence of the free calcium indicator, fura 2. Preincubation with nicorandil for 5 min significantly decreased the rise in [Ca2+]i evoked by addition of either angiotensin II in control solution or prostaglandin F2 alpha, the latter in either the presence or absence of extracellular calcium. The effect of nicorandil on (Ca2+ + Mg2+)-ATPase activity in the microsomal fraction of porcine coronary artery smooth muscle, which is rich in plasma membranes and sarcoplasmic reticulum, was also investigated. Nicorandil at concentrations of 10(-6) and 10(-5) M increased the activity of (Ca2+ + Mg2+)-ATPase significantly at a free calcium concentration of 0.3 microM. At 10(-6) M, nicorandil significantly decreased the Kd for calcium of this enzyme without significantly changing its Vmax. These data suggest that nicorandil suppressed increase of [Ca2+]i, possibly by stimulating (Ca2+ + Mg2+)-ATPase, thereby inhibiting contraction of vascular smooth muscle.

Angiotensin II↗
PubMed1987

[Adenomatous polyps with prostatic type epithelium: a report of two cases].

Two cases of adenomatous polyps with prostatic type epithelium are reported. The first case was of a 62-year-old male suffering from asymptomatic hematuria. Cystoscopic findings showed an urethral tumor in the prostatic urethra. He was treated by transurethral resection of the prostate. The second case was of a 47-year-old male with complaints of hematuria and doubtful findings in urinary cytology. Cystoscopic findings showed that he had an urethral tumor in the prostatic urethra as well as bladder tumor. Both were resected transurethrally. Histological examination revealed that both urethral tumors were papillary adenoma of the prostatic urethra, corresponding to the adenomatous polyps with prostatic type epithelium in the classification of AFIP. The peroxidase-antiperoxidase complex method was performed using the anti-prostatic acid phosphatase antibody and anti-prostatic-specific antigen antibody, and positive reactions were obtained which confirmed that the tumors originated in the prostatic tissue. Benign urethral tumor in males is not common and description of adenomatous polyps with prostatic type epithelium is very rare. We could find only 11 cases in the Japanese literature.

Humans↗