Biomedical subjects

A Mishima

Publications and source records attributed to A Mishima.

At least 55 records · Page 3Linked to original sources

PubMed1994

[Cooley operation for hypertrophic obstructive cardiomyopathy associated with Noonan Syndrome following Morrow operation--a case report].

A 21-year-old female underwent ventricular septoplasty (Cooley operation) for severe left ventricular outflow tract obstruction (LVOTO), which had developed after performance of a Morrow operation at the age of 14. Diagnosis of Noonan syndrome and hypertrophic obstructive cardiomyopathy had been already established by clinical manifestations and a myocardial biopsy. The septoplasty technique and valve replacement could be successfully used to repair the residual LVOTO and aortic regurgitation. We found that this approach was one of the most convenient and provided effective management of LVOTO. Post-operative course has been uneventful and the patient remains completely well as of the 18th months after surgery.

Adult↗

PubMed1993

Zinc protection against cadmium-induced destruction of the monolayer of cultured vascular endothelial cells.

The effect of zinc on the destruction of vascular endothelial cell monolayer caused by cadmium was investigated using bovine aortic endothelial cells in a culture system. It was histologically revealed that cadmium-induced de-endothelialized area formation was markedly prevented by zinc. Zinc prevented cadmium-induced detachment of [3H]thymidine-labeled endothelial cells from the monolayer. Although cadmium increased the activity of lactate dehydrogenase in the medium, a marker of nonspecific cell damage, zinc markedly suppressed it. On the other hand, zinc significantly prevented cadmium-induced decrease in the incorporation of [3H]thymidine into the acid-insoluble fraction of the growing cells. From these results, it was suggested that impairment of the endothelial cell monolayer caused by cadmium is protected by zinc; this protection was postulated to be due to both a reduction of the cell detachment caused by cadmium-induced nonspecific cell damage and a decrease in cadmium inhibition of the cell proliferation which would help the repair of de-endothelialized areas.

Analysis of Variance↗

PubMed1993

[Lipid peroxide and free radical scavengers in congenital heart disease with pulmonary hypertension].

There is a strong possibility that lipid peroxide (LPO) exerts a great influence on the persistence of pulmonary vascular obstruction (PVO) after radical operation of congenital heart disease with pulmonary hypertension (PH). We investigated the relationship between LOP and PVO, and discussed the effects of scavengers. Fourteen cases of infantile open heart surgery were investigated. LPO, superoxide dismutase SOD and reduced glutathione (GSH) were measured in blood and lung tissue. In the cases of PH group, the levels of lung tissue and plasma LPO showed significantly higher than those of PS group (p < 0.05) before and after radical operation. The levels of Pp/Ps and pulmonary vascular resistance (PVR) of PH cases showed still higher than those of PS group (p < 0.05) even after radical operation. In addition, the levels of plasma and lung tissue SOD, lung tissue GSH of PH cases were lower than those of PG group. These suggest that LPO plays an important role as the cause of PVO before operation and which remains unchanged even after operation. It is to be expected that increase of the free radical scavengers will be effective to suppress the generation of LPO and at last to reduce the level of PVR after operation.

Free Radical Scavengers↗

PubMed1993

[A histochemical study on the testes from patients with idiopathic male infertility: identification of acidic glycoconjugates in the seminiferous tubular walls].

Acidic glycoconjugates in the seminiferous tubular walls in the testes from patients with idiopathic male infertility was identified light microscopically with the sensitized high iron diamine method in combination with digestions with chondroitinase ABC, chondroitinase B or testicular hyaluronidase. Tissue specimens were obtained by testicular biopsy from 37 patients with idiopathic male infertility and 9 fertile adult males. Chondroitin sulfate A, B and C were identified in the tubular walls of oligozoospermic patients with idiopathic male infertility irrespective of the thickness of the walls. Similar results were obtained in the tubular walls of the testes from normal males. On the other hand, chondroitin sulfate B was a main acidic glycoconjugate in the tubular walls of the testes from azoospermic patients with idiopathic male infertility irrespective of the thickness of the walls. These findings suggest that the etiological factors of the impaired spermatogenesis in patients with idiopathic male infertility are not only the disturbance of nutritional transport across the seminiferous tubular walls due to peritubular thickening but the functional alterations of the tubular walls associated with changes in components of acidic glycoconjugates in the tubular walls. The pathogenesis of oligozoospermia does not seem to be similar to that of azoosspermia since components of acidic glycoconjugates in the peritubular tissues between the two types of disorders are quite different.

Adult↗

PubMed1992

Possible mechanism for zinc protection against cadmium cytotoxicity in cultured vascular endothelial cells.

We investigated the effect of zinc on cadmium cytotoxicity in vascular endothelial cells in a culture system. The cytotoxicity was evaluated by [3H]adenine release assay. Cadmium at 2 microM concentration and above significantly increased the [3H]adenine release, but zinc at 80 microM and below did not induce such a response after a 24-h incubation. Metallothionein was induced by cadmium at 0.1 microM and above but not by zinc at 300 microM and below; however, zinc at 10 microM and above significantly decreased cadmium-(2 and 5 microM) induced cytotoxicity. Zinc protection against cadmium cytotoxicity was also observed in the presence of 1 microM cycloheximide. Zinc caused significantly less accumulation of cadmium in the cell layer accompanied with a significant accumulation of zinc. The distribution (%) of cadmium in the particulate fraction of the cells was significantly decreased by zinc. In contrast, cadmium in the cytosol fraction was increased in the cells treated with both cadmium and zinc. Gel filtration chromatography of the cytosol showed that cadmium was capable of being bound to high-molecular-weight proteins and metallothionein. The metallothionein-bound cadmium was not increased by zinc; however, the relative distribution of cadmium in the high-molecular-weight fraction in the cytosol was decreased in cadmium plus zinc-treated cells. From these results, it was suggested that the mechanism by which zinc protects endothelial cells from cadmium cytotoxicity was decreased accumulation of cadmium in the particulate fraction and in the high-molecular-weight fraction in the cytosol of the cells. This alteration is postulated to be caused by both zinc-induced decrease in the intracellular cadmium accumulation and the sequestration of cadmium by cadmium-induced metallothionein.

Adenine↗

PubMed1992

Plasmin stimulates the release of dermatan sulfate from vascular smooth muscle cells in culture.

We investigated the effect of plasmin on the release of sulfated glycosaminoglycans (GAG) from cultured vascular smooth muscle cells. Confluent cultures of vascular smooth muscle cells from bovine aorta were labelled with [35S]sulfate and incubated at 37 degrees C for principally 60 min in a serum-free medium in the presence of plasmin. Plasmin at 10 mU/ml (approximately 2.7 micrograms/ml) and above significantly increased the release of [35S]sulfate-labeled GAG (35S-GAG) from the cell layer after a 60 min incubation. A time course study showed that plasmin at 10 mU/ml significantly increased the 35S-GAG release after 20 min and longer. However, plasminogen at 100 mU/ml and below did not cause a significant change of the 35S-GAG release after a 90 min incubation. A characterization of 35S-GAG revealed that plasmin increased both dermatan sulfate and the other 35S-GAG in the medium. Plasmin at 100 mU/ml enhanced the cell detachment significantly but only slightly. From these results, it was suggested that a endogenous thrombin inhibitor heparin cofactor II may be activated in the liquid phase by dermatan sulfate released from plasmin-stimulated vascular smooth muscle cells when the vascular is disrupted and plasma is exposed to extravessel.

Animals↗

PubMed1992

Effect of cadmium on the monolayer maintenance of vascular endothelial cells in culture.

We investigated the effect of cadmium on the maintenance of the monolayer of vascular endothelial cells to clarify a possible involvement of endothelium injury in cadmium-induced vascular disorders. Endothelial cells from bovine aorta were cultured with cadmium chloride (0.5, 1.0, 2.0 or 5.0 microM) for 24 or 72 h. A histological observation revealed that a de-endothelialized space was formed in the monolayer by cadmium treatment; the number of endothelial cells was significantly decreased by the metal. Cadmium significantly decreased the number of growing endothelial cells with a significant decrease in the [3H]thymidine incorporation, suggesting that cadmium inhibited the cell proliferation. On the other hand, cadmium significantly increased the detachment of [3H]thymidine-labeled endothelial cells from the monolayer with a parallel increase in the lactate dehydrogenase activity in the medium. From these results, it was suggested that cadmium impairs the endothelial cell monolayer; the de-endothelialized space was formed by both an increase in the cell detachment by cadmium cytotoxicity and a retardation of the repair of the space which was due to an inhibition of the cell proliferation caused by the metal.

Animals↗

PubMed1992

Protective effect of copper against cadmium cytotoxicity on cultured vascular endothelial cells.

We investigated the effect of copper on cadmium-induced cytotoxicity on vascular endothelial cells from bovine aorta in a culture system. Cytotoxicity was evaluated by the [3H]adenine release assay and the histological observation. After a 24-h incubation, cadmium exhibited a significant cytotoxicity on confluent cultures of endothelial cells in a dose-dependent manner, while copper only slightly did after a 24-h incubation. It was found that copper (5 microM) significantly decreased cadmium (1 and 2 microM) cytotoxicity; histologically, formation of de-endothelialized areas in the cell layer caused by cadmium was reduced by copper. The accumulation of cadmium in the cell layer was significantly decreased by copper; however, that of copper was unaffected by cadmium. It was therefore suggested that copper significantly protects cadmium-induced cytotoxicity on cultured endothelial cells primarily through decreasing the cellular cadmium accumulation.

Animals↗

PubMed1991

Inhibitory effects of clonidine and tizanidine on release of substance P from slices of rat spinal cord and antagonism by alpha-adrenergic receptor antagonists.

Effects of clonidine and tizanidine, which have antinociceptive and alpha 2-agonistic actions, were studied on the release of substance P from slices of spinal cord from the rat. Veratridine-evoked depolarization induced a 2-3-fold increase in the release of substance P from the slices of spinal cord. Exposure of the cord tissue to 10 microM clonidine and tizanidine significantly reduced the release of substance P. The inhibitory effects of clonidine and tizanidine were attenuated by pre-exposure of the tissue to 10 microM piperoxane, which has alpha 2-antagonistic activity and the inhibitory effect of clonidine was attenuated by 10 microM yohimbine. Moreover, the inhibitory effects of clonidine and tizanidine were also blocked by a small dose of prazosin, an antagonist for alpha 1- and alpha 2B-receptors. None of the antagonists had any effect on release of substance P, when given alone. These results suggest that alpha 2B-adrenoceptors are involved in the inhibitory effects of clonidine and tizanidine on the release of substance P.

Adrenergic alpha-Antagonists↗

PubMed1991

[A case of graft-versus-host disease following irradiated fresh blood transfusion].

We reported a case of a fatal graft-versus-host disease (GVHD) which developed in a 65-year-old, male patient which was considered to have been induced by irradiated fresh blood donated by his son after a coronary bypass surgery. Fresh blood was obtained from his relatives, and a 15 Gy irradiation was performed before transfusion. The diagnosis of acute GVHD was made by clinical symptoms and histological examinations of the skin and the bone marrow. He died of sepsis on the 19th post-operative day. The HLA typing of the lymphocytes, revealed that the patient had A 2, A 24, Bw 52, Bw 62, Cw 4, DR 2, and his son had A 24, Bw 52, DR 2. A 24 and Bw 52 were homogeneous making his son histocompatible with one of the patient's haplotype. This might well be attributable to the occurrence of GVHD in this case, meaning that 15 Gy irradiation was not sufficient for the prevention of this disease.

Aged↗

PubMed1990

Inhibition of forskolin-induced neurite outgrowth and protein phosphorylation by a newly synthesized selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), of PC12D pheochromocytoma cells.

A newly synthesized isoquinolinesulfonamide, H-89 (N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide), was shown to have a potent and selective inhibitory action against cyclic AMP-dependent protein kinase (protein kinase A), with an inhibition constant of 0.048 +/- 0.008 microM. H-89 exhibited weak inhibitory action against other kinases and Ki values of the compound for these kinases, including cGMP-dependent protein kinase (protein kinase G), Ca2+/phospholipid-dependent protein kinase (protein kinase C), casein kinase I and II, myosin light chain kinase, and Ca2+/calmodulin-dependent protein kinase II were 0.48 +/- 0.13, 31.7 +/- 15.9, 38.3 +/- 6.0, 136.7 +/- 17.0, 28.3 +/- 17.5, and 29.7 +/- 8.1 microM, respectively. Kinetic analysis indicated that H-89 inhibits protein kinase A, in competitive fashion against ATP. To examine the role of protein kinase A in neurite outgrowth of PC12 cells, H-89 was applied along with nerve growth factor (NGF), forskolin, or dibutyryl cAMP. Pretreatment with H-89 led to a dose-dependent inhibition of the forskolin-induced protein phosphorylation, with no decrease in intracellular cyclic AMP levels in PC12D cells, and the NGF-induced protein phosphorylation was not not inhibited. H-89 also significantly inhibited the forskolin-induced neurite outgrowth from PC12D cells. This inhibition also occurred when H-89 was added before the addition of dibutyryl cAMP. Pretreatment of PC12D cells with H-89 (30 microM) inhibited significantly cAMP-dependent histone IIb phosphorylation activity in cell lysates but did not affect other protein phosphorylation activity such as cGMP-dependent histone IIb phosphorylation activity, Ca2+/phospholipid-dependent histone IIIs phosphorylation activity, Ca2+/calmodulin-dependent myosin light chain phosphorylation activity, and alpha-casein phosphorylation activity. However, this protein kinase A inhibitor did not inhibit the NGF-induced neurite outgrowth from PC12D cells. Thus, the forskolin- and dibutyryl cAMP-induced neurite outgrowth is apparently mediated by protein kinase A while the NGF-induced neurite outgrowth is mediated by a protein kinase A-independent pathway.

Adrenal Gland Neoplasms↗

PubMed1990

[Effects of ulinastatin on plasma polymorphonuclear leukocyte elastase activity and respiratory function in patients undergoing cardiopulmonary bypass].

Plasma polymorphonuclear leukocyte elastase (PMNE) activity is known to increase during cardiopulmonary bypass (CPB), and is considered to mediate pulmonary tissue damage causing postoperative respiratory failure. We made a clinical study in order to clarify the effects of ulinastatin (Miraclid), a proteolytic enzyme inhibitor, on plasma PMNE activity and respiratory function. Twenty adult patients undergoing coronary artery bypass grafting were divided into 2 groups; 10 to group U and 10 to group C. The patients in group U received 500 U/kg body weight of ulinastatin intravenously before and after CPB, and the patients in group C not receiving the dose served as controls. Arterial blood samples were obtained before the operation, 1 hour after CPB, 3 hours, 1 day and 4 days after the operation. The leukocyte count was significantly lower in group U 1 hour after CPB and 3 hours after the operation compared to group C (p less than 0.01). The plasma PMNE activity rose rapidly after starting CPB and the peak level appeared 1 hour after CPB; 1165 +/- 560 micrograms/l in group U and 1981 +/- 562 micrograms/l in group C (p less than 0.02). There was a significant correlation between the leukocyte reduction and the rate of increase of beta-glucuronidase activity were diminished in group U compared to preoperative values (p less than 0.05). The recovery of the oxygenation index (PaO2/F1O2), which was used for evaluation of the respiratory function, was worse in group C (p less than 0.01). These results suggest that the administration of ulinastatin in patients undergoing CPB is useful for the prevention of the deleterious effects of PMNE on the lung.

Aged↗

PubMed1989