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J Masuda

Publications and source records attributed to J Masuda.

At least 91 records · Page 5Linked to original sources
PubMed1993

Human neonatal and adult vascular smooth muscle cells in culture.

Neonatal vascular smooth muscle cells (SMC) in culture have been demonstrated to be quite different from adult SMC and to be similar to intimal SMC in animal models. To characterize human neonatal vascular SMC in culture, cultures of arterial SMC were prepared by an explant method from the subclavian arteries of autopsied patients (10 adults and 6 neonates). The morphology and growth characteristics of these cells were compared. All cells were positively immunostained with HHF 35, a monoclonal antibody specific for muscle actin. Electron microscopically, both adult and neonatal SMC were of synthetic phenotype. SMC from neonates had a short population doubling time (PDT, 28.6 +/- 7.5 hr) and high saturation density (SD, 37.5 +/- 11.9 x 10(4) cells/cm2). They did not show hill and valley growth patterns. Among the SMC cultured from adult media, two subtypes were distinguished, based on their growth characteristics. Classical adult SMC (7 of 10 cases) grew in hill and valley patterns with long PDT and low SD values (61.7 +/- 28.8 hr, 6.5 +/- 1.9 x 10(4) cells/cm2, respectively). The second subtype (3 of 10 cases), neonatal-type adult SMC, had PDT and SD values (22.9 +/- 4.0 hr, 31.3 +/- 14.7 x 10(4) cells/cm2, respectively) similar to those of neonatal SMC. Intimal SMC became senescent in early phases of subculture. To test for the possible participation of autocrine growth factors in the heterogeneity of the growth patterns, Northern blot analysis was conducted for PDGF-A, TGF-beta, c-myc, and c-fos mRNA in three types of SMC. There was no significant difference in these mRNA levels between the SMC. We demonstrated that human neonatal vascular SMC in culture are quite different in their growth characteristics from classical adult SMC in culture and that neonatal-type SMC can be isolated from adult media.

Adult↗
PubMed1993

Smooth muscle cell proliferation and localization of macrophages and T cells in the occlusive intracranial major arteries in moyamoya disease.

BACKGROUND AND PURPOSE: Stenosis or occlusion due to fibrocellular intimal thickening in the intracranial major arteries is thought to be the primary lesion in moyamoya disease, but its etiology and pathogenesis are unknown. The present study was designed to analyze cellular components of the lesions and their pathological process. METHODS: Stenotic or occlusive intracranial arterial lesions were collected from six autopsied patients who died of moyamoya disease. The cellular components were analyzed by immunohistochemical staining using cell-type-specific monoclonal antibodies. The sections were also immunostained for proliferating cell nuclear antigen (PCNA) to detect proliferating cells and for two different types of intermediate filaments, desmin and vimentin, to evaluate phenotypes of the intimal smooth muscle cells. RESULTS: The thickened intima was composed predominantly of smooth muscle cells with an admixture of some macrophages and T cells. Macrophages and T cells were scattered in the superficial layer of the intimal thickening, and these were occasionally associated with organization of fibrin thrombi. Proliferating smooth muscle cells, indicated by PCNA-positive nuclei and muscle actin-positive cytoplasm, were found in the thickened intima in four patients. Immunohistochemical staining for intermediate filaments revealed intimal smooth muscle cells showing positive staining for vimentin and negative staining for desmin, compatible with the phenotype of synthetic smooth muscle cells. CONCLUSIONS: The present study provides evidence that smooth muscle cells are proliferating in the occlusive lesions in intracranial major arteries in moyamoya disease. The colocalization of inflammatory cells and PCNA-positive cells suggests that inflammatory stimuli may induce proliferative response of smooth muscle and contribute to the formation of the intracranial occlusive lesions in moyamoya disease.

Adolescent↗
PubMed1992

Prostaglandins A and J arrest the cell cycle of cultured vascular smooth muscle cells without suppression of c-myc expression.

The effects of prostaglandins (PGs) A and J, which are anti-tumor eicosanoids, on the proliferation of cultured vascular smooth muscle cells were investigated. Serum-stimulated DNA synthesis was potently inhibited by PGA1, PGA2, PGJ2, and delta 12-PGJ2 in similar dose-dependent fashions. The effects of PGA1 and PGA2 were reversible when they were removed from the culture media, whereas recoveries were only partial in the cells treated with PGJ2 and delta 12-PGJ2. PGs were effective even if they were added immediately before entry into S phase. Inhibition of DNA synthesis was sustained when hydroxyurea, which blocks cell cycle at the G1/S border, was added after the removal of PGA2, and vice versa; PGs blocked DNA synthesis when they were added after the removal of hydroxyurea. Levels of c-myc mRNA formed two peaks during the G1 phase, at 1-2 h and at 8-12 h. The PGs did not affect the first elevation, but enhanced the second and sustained it up to 18-24 h, whereas in controls, c-myc mRNA decreased quickly after entry into S phase. The rate of degradation of c-myc mRNA was much smaller in PG-treated cells than in nontreated cells. We conclude, therefore, that PGA and PGJ inhibit a crucial event(s) in the cell cycle occurring at the G1/S border, but that this inhibition is not accompanied by the reduction in c-myc gene expression in contrast with some types of tumor cells treated with PGs.

Animals↗
PubMed1992

Interferon-gamma suppresses PDGF production from THP-1 cells and blood monocyte-derived macrophages.

Involvement of the immunological mechanisms in atherogenesis has recently been suggested by immunohistological detection of macrophages and T lymphocytes in atherosclerotic lesions. In the present study, we have investigated the regulatory effect of interferon-gamma (IFN-gamma), a cytokine secreted by activated T cells, on the production and secretion of platelet-derived growth factor (PDGF) from macrophages in culture. The human monocytic leukemia cell line, THP-1, was treated with phorbol 12-myristate 13-acetate (PMA) for 24 h to induce macrophage differentiation and PDGF production, and then various doses of recombinant human IFN-gamma (0-1000 I.U./ml) were added to the culture. After 48 h, the conditioned medium and the cells were harvested and analyzed for PDGF production. PDGF-dependent mitogenic activity in the conditioned medium, estimated by neutralization of mitogenic activity with anti-PDGF antibody, was suppressed by IFN-gamma treatment. Radioimmunoassays for PDGF also revealed a decrease in both PDGF-AA and -BB in the conditioned medium with IFN-gamma treatment, whereas neither total cell DNA as an indication of cell number nor overall protein synthesis based on [3H]leucine incorporation were decreased. Northern analysis of total RNA extracted from the cells demonstrated that IFN-gamma suppressed the level of PDGF mRNA. Analysis of mRNA degradation in the presence of actinomycin D demonstrated that the decrease in PDGF mRNA was not due to enhanced degradation of mRNA. A similar inhibitory effect of IFN-gamma on PDGF mRNA levels was also found in monocyte-derived macrophages cultured in the presence of granulocyte-macrophage colony stimulating factor. These results suggest that IFN-gamma modulates production and secretion of PDGF from macrophages and that the functions of macrophages in atherogenesis may be regulated by the cellular interactions between T cells and macrophages through the action of cytokines such as IFN-gamma.

Animals↗
PubMed1992

Mitogenic activity of interferon gamma on growth-arrested human vascular smooth muscle cells.

Interferon gamma (IFN-gamma) is a multifunctional lymphokine secreted by activated T lymphocytes, which are found in atherosclerotic lesions. IFN-gamma has been reported to suppress the proliferation of vascular smooth muscle cells (SMCs). However, as we report in this paper, IFN-gamma is mitogenic for vascular SMCs under certain circumstances. Recombinant human IFN-gamma (1-100 units/ml), in a dose-dependent fashion, stimulated cell multiplication and [3H]thymidine and 5-bromo-2'-deoxyuridine incorporation into DNA by cultured arterial SMCs that had been growth arrested by culturing in 1% plasma-derived serum for 5 days. IFN-gamma also accentuated the mitogenic activity of platelet-derived growth factor (PDGF)-BB. A time-course study revealed that there was a time lag of 4-6 hours between the G1-->S transition of quiescent SMCs stimulated by IFN-gamma and that of SMCs stimulated by PDGF-BB. A synergistic effect of IFN-gamma on the mitogenicity of PDGF became apparent after a similar time lag, suggesting that the IFN-gamma-related mitogenicity is mediated by a substance(s) secreted by IFN-gamma-treated SMCs. In fact, conditioned medium of IFN-gamma-treated SMCs was mitogenic for SMCs. Mitogenic activity in the conditioned medium was also detected by an assay using Swiss 3T3 cells, which originate from mice and, therefore, are not responsive to human IFN-gamma. The production of the mitogenic factor was blocked by anti-IFN-gamma antibody. Mitogenicity of the conditioned medium was not eliminated by addition of neutralizing antibody against PDGF, indicating that any autocrine growth factor(s) secreted by IFN-gamma-treated SMCs was not PDGF.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1992

Histopathological analysis of the mechanisms of intracranial hemorrhage complicating infective endocarditis.

BACKGROUND AND PURPOSE: We conducted the present study to elucidate the pathological mechanisms leading to intracranial hemorrhage complicating infective endocarditis. METHODS: Neurological, neuroradiological, and histopathological analyses were performed in 16 patients (one surgical and 15 autopsy cases), 12 men and four women 26-68 years of age, who had demonstrated central nervous system complications during the course of infective endocarditis. RESULTS: Intracranial hemorrhage was found in all cases; parenchymal hematomas were found in 12 cases, hemorrhagic infarcts in four cases, and primary subarachnoid hemorrhages in two cases. Chronological analysis of neurological examination and computed tomographic scan of the brain confirmed that antecedent cerebral ischemic events had occurred in five of 12 patients showing parenchymal hematomas at autopsy. Hemorrhagic infarct, indicated by petechial or diffuse hemorrhages within the infarct, was seen in another four patients, so that hemorrhagic transformation of the ischemic infarct was confirmed in nine patients. Although mycotic aneurysms were found in five patients, only three of these were ruptured; the other two were occluded with septic emboli. Pyogenic arteritis without aneurysm was found to be distributed in the small cortical arterial branches located in the spaces of cortical sulci, with rupture occurring in five patients. CONCLUSIONS: These results suggest that hemorrhagic transformation of the ischemic infarct due to septic emboli is the most frequent mechanism leading to intracerebral hemorrhage encountered in patients dying of infective endocarditis and that rupture of pyogenic arteritis may be responsible for such hemorrhage in many cases, with ruptures of mycotic aneurysms as an alternative mechanism.

Adult↗
PubMed1991

De novo interstitial deletion of 4q[46,XX,del(4)(q27q28.2)] with intact blood group-MN locus, confining its locus to 4q28.2-4q31.1.

We report a malformed female infant with de novo interstitial deletion of 4q[46,XX,del(4)(q27q28.2)]. The MN blood type analysis of the family members showed that the patient had an intact blood group-MN locus. The locus of the gene responsible for the MN antigen activity is confined to a 4q28.2-4q31.1 segment on the basis of the result of this patient and the previous mapping data.

Abnormalities, Multiple↗
PubMed1991

[Does methylprednisolone potentiate the effects of dobutamine during thoracic epidural analgesia?].

The cardiovascular effects of dobutamine (DOB) combined with methylprednisolone (MP) were studied during thoracic epidural analgesia (TEA) in 59 patients undergoing operations on upper abdomen. To establish TEA, 8-10 ml of lidocaine 20 mg.ml-1 was injected into the epidural space through the T8-T9 interspace. The patients was intubated after fentanyl 0.2 mg, thiopental 3 mg.kg-1 and vecuronium 0.2 mg.kg-1. Anesthesia was maintained with 67% N2O, 33% O2 and 0.6% enflurane and DOB was infused at a rate of 5 micrograms.kg-1.min-1 during the surgical operation. Systolic blood pressure and urinary output after TEA did not decrease in the two groups, pretreated with MP 5 mg.kg-1 one hour or immediately before TEA, but decreased in the control group without MP injection. Heart rate showed no significant changes after TEA in all groups. We conclude that MP may potentiate the cardiovascular effects of DOB during TEA.

Anesthesia, Epidural↗
PubMed1991

[Does pulmonary air embolism affect the pulsatility of pulmonary capillary blood flow in dogs?].

The difference in the uptake rate through the lungs between nitrous oxide and oxygen has been shown to represent the pulmonary capillary blood flow (Qc). The pulsatility of Qc, defined as the ratio of maximum Qc and mean Qc (Qc max/Qc), the ratio of Qc max and stroke volume (Qc max/SV), and the ratio of systolic Qc and SV (Vsyst/SV), has been also shown to indicate the pulmonary vasodilation as well as vasoconstriction. We measured Qc by means of body plethysmography in dogs with pulmonary air embolism, in order to evaluate its effect on the pulmonary vasculature. Ten adult dogs were anesthetized with pentobarbital and pancuronium, and were mechanically ventilated. A volume of air (0.5 ml/kg) was injected into the central vein. Although there was no significant change in systemic blood pressure, cardiac output, heart rate, and airway pressure after the injection of air, pulmonary arterial pressure and pulmonary vascular resistance increased significantly. Qc, Qc max, Qc max/Qc, and Qc max/SV decreased significantly after the air injection. Since these findings suggest that the pulmonary air embolism provoked pulmonary vasoconstriction, and attenuated the pulsatility of Qc, optimal pulmonary vasodilation therapy would be recommended to improve the pulmonary hypertension secondary to pulmonary air embolism.

Animals↗
PubMed1990

Localization of PDGF-B protein in macrophages in all phases of atherogenesis.

Lesions of atherosclerosis occur in the innermost layer of the artery wall and consist primarily of proliferated smooth muscle cells surrounded by large amounts of connective tissue, numerous lipid-laden macrophages, and varying numbers of lymphocytes. Growth-regulatory molecules may be involved in intimal accumulation and proliferation of smooth muscle cells responsible for the occlusive lesions of atherosclerosis. Platelet-derived growth factor (PDGF) B-chain protein was found within macrophages in all stages of lesion development in both human and nonhuman primate atherosclerosis. Thus macrophages may play a critical role in the disease by providing PDGF, a potent chemotactic and growth-stimulatory molecule, to the intimal smooth muscle cells.

Animals↗
PubMed1990

Rupture of atheromatous plaque as a cause of thrombotic occlusion of stenotic internal carotid artery.

We analyzed the clinical profiles and autopsy findings of five patients who died shortly after developing cerebral infarction following thrombotic occlusion of the internal carotid artery. In all five cases, thrombotic occlusion was caused by rupture of the fibrous lining over the gruel of atheroma at the origin of the internal carotid artery showing tight stenosis of the lumen. The mean +/- SD shorter diameter of the lumen at the site of occlusion was 1.5 +/- 0.4 mm. Our results show that an internal carotid artery with tight stenosis of the lumen by atheroma containing gruel harbors a risk of thrombotic occlusion, which may give rise to cerebral infarction by artery-to-artery embolism or by reduced cerebral perfusion.

Aged↗
PubMed1990

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion.

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.

Animals↗
PubMed1989

[Effect of sevoflurane on respiratory impedance measured by the forced oscillation method with random noise input].

This study was performed to investigate the effect of sevoflurane, a new inhalation anesthetic, on the respiratory impedance measured by forced oscillation method with random noise input. Random noise (1 to approximately 25Hz) oscillated by a loudspeaker was imposed on the respiratory system of dogs through a tracheostomy and the oscillatory pressure wave and flow wave were monitored at the same point with a pressure transducer and a pneumotachograph. This procedure was repeated during inhalation of 100%-oxygen, 2.0%-then 4.0%-sevoflurane-oxygen mixture, respectively. Impedance was calculated with fast Fourier transform by spectrum analyzer and a personal computer. During inhalation of 4.0%-sevoflurane-oxygen mixture, respiratory impedance especially respiratory resistance decreased at the high frequency area (6to approximately 20Hz), but 2.0%-sevoflurane-oxygen mixture did not cause a significant change of respiratory impedance. This study suggests that inhalation of an anesthetic concentration of sevoflurane produces weak bronchodilation compared with halothane or enflurane.

Anesthetics↗