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S Morimoto

Publications and source records attributed to S Morimoto.

At least 361 records · Page 20Linked to original sources
PubMed1991

[Chest radiograph of foreign bodies in the tracheobronchial tree].

Chest radiographs in 14 children with foreign bodies in the tracheobronchial trees were evaluated retrospectively. The most common causative materials were nuts, and both main bronchi were most commonly involved. The initial chest radiographs that were used for analysis were obtained one hour to 50 days after aspiration or onset of symptoms. Of the nine cases in which chest radiographs were taken within 7 hours after aspiration, six showed hyperlucency with (three cases) or without overinflation (three cases) in the affected lungs, and the other three showed normal chest radiographs. Two patients had indeterminate diagnoses on chest radiographs at inspiration: one patient underwent chest radiographs at expiration and the other underwent fluoroscopy. Air-trapping was demonstrated in both patients. Of another five cases in which chest radiographs were taken 18 hours after aspiration of a foreign body, three cases showed atelectasis or consolidation and the other two showed hyperlucent lung. From these observations, hyperlucent lung indicates an early stage of the disorder while atelectasis or consolidation indicates a fairly advanced stage. In patients with clinically suspected foreign bodies, we advocate that additional examinations be performed to establish a final diagnosis, even when chest radiographs are normal or indeterminate.

Bronchi↗
PubMed1991

[HLA-antigens in thyrotoxic patients with overt diabetes mellitus].

The incidence of thyrotoxicosis accompanied by overt diabetes has been reported to be 2 to 3%. Several workers have suggested the possible role of immunological and inherited factors in the occurrence of thyrotoxic patients with overt diabetes. We investigated, therefore, the clinical characteristics, backgrounds, and HLA antigens in thyrotoxic patients with overt diabetes. In nine thyrotoxic patients with overt diabetes (group DM) (3 men and 6 females, average age of 45.8 +/- 2.9 yr), mean levels of free-triiodothyronine (FT3) and free thyroxine (FT4) were 8.2 +/- 0.8 pg/ml and 4.9 +/- 0.4 ng/dl, respectively. Although these levels were extremely high, they were significantly lower than those levels in forty thyrotoxic patients without overt diabetes (group ND) (8 men and 32 females, average age 35.1 +/- 4.5 yr). Mean levels of both thyrotrophin receptor-antibody (TR-Ab) and thyroid simulating antibody (TS-Ab) in group DM were relatively lower than those in group ND. Mean titers of both antithyroid antibody (TGHA) and antimicrosomal antibody (MCHA) in group DM were also relatively lower than those in group ND, respectively. Regarding the clinical features in thyrotoxic patients with overt diabetes, mean duration of diabetes mellitus was 4.1 +/- 2.5 years with mean levels of fasting plasma glucose (FPG), HbA1c, and serum fructosamine 208.1 +/- 34.0 mg/dl, 10.6 +/- 0.6%, and 3.9 +/- 0.9 mmol/L, respectively. Seven patients in group DM frequently had ketosis or ketoacidosis in their histories, and they had been treated with insulin injection. However, the diabetic complications in group DM were moderate or severe.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Conversion of big endothelin-1 to endothelin-1 by two-types of metalloproteinases of cultured porcine vascular smooth muscle cells.

Incubation of big endothelin-1 (big ET-1, 1-39) with the membrane fraction obtained from cultured vascular smooth muscle cells (VSMCs) resulted in an increase in immunoreactive-ET (IR-ET), which was inhibited by EDTA but not by phosphoramidon, a metalloproteinase inhibitor. When the incubation was performed in the presence of N-ethylmaleimide (NEM), the generation of IR-ET was markedly augmented and this augmentation was abolished by phosphoramidon. The pH profile for IR-ET generation in the presence of NEM was apparently distinct from that observed in the absence of NEM. Reverse-phase HPLC of the incubation mixture with or without NEM revealed one major IR-ET component corresponding to the elution position of synthetic ET-1 (1-21). When the cultured VSMCs were incubated with big ET-1, a conversion to the mature ET-1 was observed. This ET-1 generation from exogenously applied big ET-1 was markedly inhibited by the addition of phosphoramidon, although the inhibitor did not influence the basal secretion of ET-1-like materials. These results suggest the presence of two types of metalloproteinases, which can generate ET-1, in VSMCs. The possibility that ET-1 functions in an autocrine manner to control the cardiovascular system warrants further attention.

Animals↗
PubMed1991

N-ethylmaleimide differentiates endothelin converting activity by two types of metalloproteinases derived from vascular endothelial cells.

We have recently found that cultured vascular endothelial cells (ECs) contain two types of metalloproteinases which convert big endothelin-1 (big ET-1) to endothelin-1 (ET-1) via a single cleavage between Trp21 and Val22. In the present study, two enzymes were clearly differentiated by using sulfhydryl blocking reagents and anion-exchange HPLC. As reported, the converting activity of the membrane fraction of ECs was specifically inhibited by phosphoramidon. N-ethylmaleimide (NEM) markedly enhanced the apparent converting activity of the membrane fraction. This enhancement was not due to the direct action on the converting enzyme, but rather to inhibition of the degradation of big ET-1 and/or ET-1. In contrast, the converting activity of the cytosolic fraction was abolished by NEM treatment. Effects of phosphoramidon and NEM on converting activities of both fractions were confirmed after anion-exchange HPLC of each fraction, using a COSMOGEL QA column. Our results provide new information on two types of metalloproteinases which convert big ET-1 to ET-1, in vascular ECs.

Animals↗
PubMed1991

Phosphoramidon inhibits the conversion of intracisternally administered big endothelin-1 to endothelin-1.

It is suggested that endothelin-1 (ET-1), a potent vasoconstrictor peptide, is involved in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). We examined the effects of intracisternal administration of big ET-1 on the cerebral arteries in the absence or presence of pretreatment with phosphoramidon, an inhibitor of ET converting enzyme, in anesthetized dogs. After intracisternal administration of big ET-1 (10 micrograms/dog), the caliber of the basilar artery on the angiogram was decreased to about 59% of the control. This was accompanied by a marked increase in immunoreactive ET in the cerebrospinal fluid. Systemic arterial pressure was markedly elevated following big ET-1 injection. All changes induced by big ET-1 were effectively prevented with phosphoramidon. These data suggest that intracisternally administered big ET-1 is converted to ET-1 and that the generated ET-1 produces cerebral vasospasm and hypertension. A phosphoramidon-sensitive metalloproteinase appears to contribute to this conversion.

Animals↗
PubMed1991

Evidence for phosphoramidon-sensitive conversion of big endothelin-1 to endothelin-1 in isolated rat mesenteric artery.

The effect of phosphoramidon, a metalloproteinase inhibitor, on the pressor response to big endothelin-1 (big ET-1) in the isolated perfused rat mesenteric artery was examined. Big ET-1 (10(-9)-10(-7) M) caused a concentration-dependent increase in the perfusion pressure. The pressor response was markedly suppressed by phosphoramidon (10(-5) M). The inhibitor did not influence the ET-1 (5 X 10(-11)-10(-8) M)-induced pressor action. Big ET-1 (5 X 10(-8) M)-induced pressor action was accompanied by an increase in immunoreactive (IR)-ET in the perfusate, and this increase was suppressed by the addition of phosphoramidon. IR-ET in the perfusate was confirmed to be ET-1, as determined by reverse-phase HPLC. These findings strongly suggest that phosphoramidon-sensitive metalloproteinase contributes to the conversion of big ET-1 to ET-1, in vivo.

Animals↗
PubMed1991

Pulmonary artery morphology and hemodynamics in pulmonic valve atresia with ventricular septal defect before and after repair.

Cardiac catheterization and angiography were performed in 22 patients with pulmonic valve atresia and ventricular septal defect to evaluate pulmonary morphology and hemodynamics before and after repair. In 12 of the 22, pulmonic valve atresia and ventricular septal defect were associated with major aortopulmonary collateral arteries, which were ligated in most. Mean postoperative pulmonary artery pressure (PAP) ranged from 9 to 92 mm Hg (mean 28 +/- 19) and pulmonary vascular resistance ranged from 1.1 to 35.2 U.m2 (mean 6.4 +/- 8.0). These data correlated (r = 0.89, p less than 0.001). The number of pulmonary artery subsegments connected to the central pulmonary arteries was 22 to 42 (mean 38 +/- 6). Univariate analysis revealed that the mean postoperative PAP correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = -0.81, p less than 0.001), with mean postoperative PAP (r = 0.79, p less than 0.001), with the postoperative pulmonary artery area index of the right and left pulmonary arteries at prebranching (r = -0.76, p less than 0.001), and with the sum of the pulmonary artery areas after branching (r = -0.69, p less than 0.005). Pulmonary vascular resistance correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = -0.85, p less than 0.001), with the mean preoperative PAP (r = 0.79, p less than 0.001), with the sum of the pulmonary artery areas after branching (r = -0.73, p less than 0.001), and with the postoperative pulmonary artery area index (r = -0.70, p less than 0.001). The incidence of pulmonary vascular resistance being less than 3 U.m2 was significantly higher in patients with greater than 36 pulmonary artery subsegments connected to the central pulmonary arteries and with a preoperative pulmonary artery area index greater than 0.5 (88%) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

The effect of Mg2+ on the Ca2+ binding to troponin C in rabbit fast skeletal myofibrils.

The effect of Mg2+ on the Ca2+ binding to rabbit fast skeletal troponin C and the CA2+ dependence of myofibrillar ATPase activity was studied in the physiological state where troponin C was incorporated into myofibrils. The Ca2+ binding to troponin C in myofibrils was measured directly by 45Ca using the CDTA-treated myofibrils as previously reported (Morimoto, S. and Ohtsuki, I. (1989) J. Biochem. 105, 435-439). It was found that the Ca2+ binding to the low and high affinity sites of troponin C in myofibrils was affected by Mg2+ competitively and the Ca2(+)- and Mg2(+)-binding constants were 6.20 x 10(6) and 1.94 x 10(2) M-1, respectively, for the low affinity sites, and 1.58 x 10(8) and 1.33 x 10(3) M-1, respectively, for the high affinity sites. The Ca2+ dependence of myofibrillar ATPase was also affected by Mg2+, with the apparent Ca2(+)- and Mg2(+)-binding constants of 1.46 x 10(6) and 276 x 10(2) M-1, respectively, suggesting that the myofibrillar ATPase was modulated through a competitive action of Mg2+ on Ca2+ binding to the low affinity sites, though the Ca2+ binding to the low affinity sites was not simply related to the myofibrillar ATPase.

Adenosine Triphosphatases↗
PubMed1991

Effect of synthetic prostaglandin E1 analog (ornoprostil) on gastric emptying and pancreatic polypeptide release after solid-meal ingestion in man.

The effect of orally administered ornoprostil, 17S,20-dimethyl-6-oxoprostaglandin E1 methyl ester, on gastric emptying and on pancreatic polypeptide (PP) release after solid meal ingestion, was investigated in man. A radionuclide technique was used to measure gastric emptying of eight healthy volunteers. In addition, four parameters [SI (starting index): the lag time in the start of emptying; K value: the emptying rate; T1/2: the half emptying time; 120 min RR: the percent retention at 120 min] were determined for evaluation. Also, the PP response was analyzed according to two parameters: IPPRSI the integrated PP response for periods up to SI, and IPPR120, the integrated PP response for 120 min. The results demonstrated that 5 micrograms of orally administered ornoprostil significantly reduced the gastric emptying rate of solid meal (T1/2 and 120 min RR, P less than 0.05). However, ornoprostil affected neither the basal PP concentrations nor the cephalic phase of PP secretion which was determined as IPPRSI. This thus suggests that ornoprostil affects the gastric motor function without interfering with the vagal-cholinergic pathway to the stomach.

Adult↗
PubMed1991

Studies on the role of platelet-activating factor in blood pressure regulation.

Circulating levels of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (C16PAF) in human subjects were measured by gas chromatography/mass spectrometry using negative ion chemical ionization. The mean (+/- S.D.) circulating C16PAF levels in patients with essential hypertension (18.1 +/- 5.3 pg/mL, n = 16) were not significantly different from those in normotensive subjects (17.2 +/- 7.2 pg/mL, n = 14). During a salt balance study, high salt intake (20 g/day) significantly increased the circulating level of C16PAF, and changes in circulating C16PAF significantly and positively correlated with changes in mean arterial blood pressure (r = 0.47, p less than 0.05). Changes in C16PAF also correlated with changes in creatinine clearance (r = 0.55, p less than 0.05), but did not correlate with changes in plasma sodium concentration, plasma chloride concentration and plasma volume. An intravenous injection of 50 micrograms of human atrial natriuretic peptide (hANP) decreased circulating C16PAF levels from 20.0 +/- 2.7 to 13.9 +/- 2.4 pg/mL of blood (n = 10, p less than 0.01) in healthy subjects. The data appear to indicate that C16PAF levels are changed by salt intake-induced mild increase in blood pressure, and that hANP may be an endogenous factor which lowers circulating C16PAF.

Atrial Natriuretic Factor↗
PubMed1991

Phosphoramidon prevents cerebral vasospasm following subarachnoid hemorrhage in dogs: the relationship to endothelin-1 levels in the cerebrospinal fluid.

There is increasing evidence that the conversion of big endothelin-1 (big ET-1) to endothelin-1 (ET-1) is specifically inhibited by the metalloproteinase inhibitor phosphoramidon. We investigated the effect of phosphoramidon on delayed cerebral vasospasm from subarachnoid hemorrhage (SAH) using a two-hemorrhage canine model. The magnitude of the vasospasm and the drug effect were determined angiographically. On SAH Day 7, diameter of the basilar artery decreased to about 55% of the control value obtained before SAH (on Day 0). Immunoreactive ET (IR-ET) in the cerebrospinal fluid (CSF) significantly increased after SAH (on Day 7). The intracisternal pretreatment of phosphoramidon potently suppressed the decrease in diameter of the basilar artery after SAH, i.e., observed decrease was only about 20%, compared with the value before SAH. In the phosphoramidon group, IR-ET in CSF markedly increased (on SAH Day 2), but the increased levels of IR-ET significantly declined on SAH Day 7. These results clearly indicate that phosphoramidon effectively prevents delayed cerebral vasospasm. Whether the prevention is due to the inhibition of conversion of big ET-1 to ET-1 is now under study.

Animals↗
PubMed1991

Clinical study on urothelial tumors of dye workers in Wakayama City.

Between January 1951 and December 31, 1990 urothelial tumors were detected in 112 of 1,085 male dye workers (10.3%) in Wakayama City who were formerly engaged in manufacturing of benzidine and/or beta-naphthylamine. The period from exposure to the chemicals to development of the tumor was a mean of 24.1 +/- 9.4 years. A peak incidence of urothelial tumors was observed also approximately 25 years after the peak period of manufacturing these intermediate products of dyes. The mean period from exposure to such carcinogenic chemicals to the onset of the disease was estimated to be 25 years. Of the 78 patients with primary bladder cancer diagnosed since 1969, 43 (55.1%) had tumors diagnosed mostly as a result of a positive urinary cytology test obtained as part of a screening program and 35 (44.9%) had tumors diagnosed as the result of symptoms. Ten patients (24.4%) in the screened group had been treated with total cystectomy by the last followup examination compared with 17 (50.0%) in the symptomatic group. The 10-year cumulative survival rates were significantly (p less than 0.05) higher in the screened patients (75.1%) than in the symptomatic patients (55.1%). Our results indicate that screening of high risk populations with urinary cytology tests is effective for early diagnosis and treatment of urothelial tumors, and it improves patient prognosis. Furthermore, the biological behavior of occupational urothelial tumors may be different from that of urothelial tumors in the general population.

2-Naphthylamine↗
PubMed1991

Effect of myosin cross-bridge interaction with actin on the Ca2(+)-binding properties of troponin C in fast skeletal myofibrils.

Ca2+ binding to fast skeletal muscle troponin C reincorporated into troponin C-depleted (CDTA-treated) myofibrils has been measured directly by using 45Ca and indirectly by using a fluorescent probe. Direct Ca2(+)-binding measurements have shown that the Ca2+ affinity of the low-affinity sites is enhanced in the absence of ATP and conversely reduced when myosin is selectively extracted from myofibrils, compared to the Ca2+ affinity in the presence of ATP. Fluorescence intensity changes of a dansylaziridine label at the Met-25 residue of troponin C have shown the same Ca2(+)-sensitivity whether or not ATP is present, while much lower Ca2(+)-sensitivity is seen in the myosin-extracted myofibrils. Since the Met-25 residue is in the amino terminal side alpha-helix of Ca2(+)-binding site I and far from Ca2(+)-binding site II in the primary structure, Ca2+ binding to site II has been evaluated by assuming that the fluorescence change monitors Ca2+ binding to site I alone. Ca2+ binding to site II thus estimated has shown high positive cooperativity only in the presence of ATP and has been found to be nearly proportional to the activation of myofibrillar ATPase, suggesting that Ca2(+)-binding site II is directly involved in the activation of myofibrillar ATPase activity. On the other hand, Ca2(+)-binding site I has been suggested to regulate the interaction of weakly binding cross-bridges with the thin filament, since the fluorescence change in the presence of ATP is saturated at the free Ca2+ concentration required for the activation of myofibrillar ATPase.

Actins↗
PubMed1991

Conversion of big endothelin-1 to endothelin-1 by phosphoramidon-sensitive metalloproteinase derived from aortic endothelial cells.

When big endothelin-1 (big ET-1, 1-39) was incubated with the membrane fraction obtained from cultured endothelial cells (ECs) at pH 7.0 for 6 h, the immunoreactive (ir) ET in the reaction mixture was markedly increased. Phosphoramidon, a metalloproteinase inhibitor, as well as metal chelators specifically suppressed the above increase. Using reverse-phase high-performance liquid chromatography, ir-ET was confirmed to be ET-1[1-21]. In addition, we noted that the alterations in ET-1 correlated with those in the C-terminal fragment (CTF, 22-39) of big ET-1. When cultured ECs were incubated with phosphoramidon, time-dependent secretion of ET-1 and CTF from the cells was markedly suppressed. In contrast, the secretion of big ET-1 was increased by phosphoramidon. Thiorphan, a specific inhibitor of neutral endopeptidase 24.11, was without effect on the secretion of ET-related peptides. Moreover, phosphoramidon potently inhibited the hypertensive effect of big ET-1 without affecting the ET-1-induced hypertension in anesthetized rats. From these findings, it seems reasonable to consider that phosphoramidon-sensitive and membrane-bound metalloproteinase, which is not a neutral endopeptidase 24.11, is the most plausible candidate for big ET-1-converting enzyme in vivo.

Animals↗
PubMed1991

Mode of cleavage of porcine big endothelin-1 by aspartic proteinases.

Cleavage sites of porcine big endothelin-1 (big ET-1, 1-39) by cathepsin D were examined and compared with those by other aspartic proteinases including pepsin. Cathepsin D cleaved not only the Trp21-Val22 bond, but also the Asp18-Ile19 bond of big ET-1[1-39]. The mature ET-1[1-21], generated by the cleavage between Trp21 and Val22, was subsequently degraded by removal of the C-terminal tripeptide (Ile19-Ile20-Trp21). On the other hand, pepsin cleaved the Trp21-Val22 bond of big ET-1[1-39] to produce ET-1[1-21], but did not degrade the generated ET-1[1-21]. These results indicate that aspartic proteinases such as cathepsin D and pepsin are capable of converting big ET-1[1-39] to ET-1[1-21], whereas the former proteinase is by no means specific for the Trp21-Val22 bond of big ET-1[1-39].

Amino Acid Sequence↗
PubMed1991

The role of endogenous angiotensin II in antidiuresis and norepinephrine overflow induced by stimulation of renal nerves in anesthetized dogs.

We examined the possible involvement of endogenous angiotensin II (ANG II) in norepinephrine (NE) overflow and antidiuresis induced by renal nerve stimulation (RNS). RNS at a frequency of 0.5-2.0 Hz, which did not influence renal hemodynamics, produced significant reductions in urine flow and urinary excretion of sodium, and elevations in NE secretion rate (NESR) and renin secretion rate (RSR). Intrarenal arterial (i.r.a.) infusion of phentolamine (10 micrograms/kg/min) abolished the RNS-induced antidiuresis. In dogs receiving captopril (15 micrograms/kg/min i.v.), RNS-induced antidiuresis and increase in NESR were significantly attenuated. The i.r.a. administration of propranolol at 5 micrograms/kg/min, a dose that inhibited completely the RNS-induced increase in RSR, did not influence the alterations in NESR and urine formation in response to RNS. During ANG II infusion (1 ng/kg/min i.r.a.), RNS produced a reduction in urine formation and an increase in NESR, at a magnitude similar to that seen without ANG II infusion. These results suggest that RNS at a low frequency increased the NESR and RSR without affecting renal hemodynamics and that the antidiuretic effect was probably produced via the activation of postsynaptic alpha-adrenoceptors, but not via the ANG II receptor, located on the renal tubules. The release of NE appears to be modulated by ANG II through the activation of a facilitatory prejunctional mechanism, which is maximally stimulated by endogenously and locally generated basal levels of ANG II.

Anesthesia↗
PubMed1991

Interleukin-6 stimulates proliferation of cultured vascular smooth muscle cells independently of interleukin-1 beta.

The effects of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) on proliferation of cultured vascular smooth muscle cells (VSMCs) were investigated. Treatment with IL-6 caused a rapid increase in the c-myc mRNA level, and resulted in increases in DNA synthesis and cell number. IL-1 beta stimulated the DNA synthesis of the cells. EGF showed synergistic and PDGF or IL-1 beta showed additive effects with IL-6 on the DNA synthesis. These results suggest that IL-6, independently of IL-1 beta, may be important in the proliferation of VSMCs.

Animals↗