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M Sakamoto

Publications and source records attributed to M Sakamoto.

At least 541 records · Page 30Linked to original sources
PubMed1992

[A cross-sectional study of lipid peroxide levels (plasma TBA levels) in a mass health examination].

Differences in plasma thiobarbituric acid (TBA) levels were studied by sex and age in 1,178 adults (471 males and 707 females) participating in a mass health examination conducted in a town of Kumamoto Prefecture in 1989. The relationships between plasma TBA levels and obesity, the consumption of cigarettes, alcohol, and fish, and various indices for health status derived from the data of physiological examinations were analyzed in age-groups 40-59 and 60-79 for both sexes. The prevalence of abnormal physiological findings by plasma TBA levels were further investigated. The results were as follows; 1. The highest plasma TBA levels for males were observed in the group aged 40-49, with levels gradually decreasing with age thereafter. The plasma TBA levels for females increased with age and the highest levels were obtained at age 60-69. The plasma TBA levels for males were significantly higher than for females at aged 40-49. 2. Plasma TBA levels for both sexes increased with obesity and the amount of fish consumed. 3. Plasma TBA levels in all examined groups had significant and strong positive correlations with serum total cholesterol levels and atherogenic indices, and had significant positive correlations with serum calcium and gamma-GTP levels. 4. A stepwise multiple regression analysis showed that plasma TBA levels for males were associated with serum total cholesterol, gamma-GTP, fish consumption and serum HDL-cholesterol in that order. The levels for female were associated with serum total cholesterol, body mass index, serum HDL-cholesterol and serum calcium in that order. The relationship with serum HDL-cholesterol was a negative correlation. 5. Prevalence of abnormal values of serum total cholesterol, atherogenic index and body mass index were significantly higher in the high-plasma TBA level group than in the group with median-plasma TBA level. These results suggest that plasma TBA levels may be useful as an index of undesirable lipid metabolism. Further studies should be performed to establish the significance of the relation of plasma TBA levels to fish consumption.

Adult↗
PubMed1992

[Studies of emergency cardiopulmonary bypass (ECPB) for cardiopulmonary-cerebral resuscitation; (1) Introduction of a portable-percutaneous ECPB system].

The authors have developed an ECPB system, which can be applied quickly, safely and easily under an emergency condition requiring cardiac massage and artificial ventilation. Fundamentally, the ECPB system consists of 3 parts; a portable ECPB apparatus, a pair of percutaneous cannulae and a short circuit connecting an oxygenator with the cannulae. The ECPB apparatus is assembled with commercially available components (i.e., a centrifugal pump, a battery pack, a temperature controller, a compact membrane oxygenator with a heat exchanger, etc) and they are placed on a mobile cart. The circuit is primed with 300 ml of lactated Ringer solution. The priming can be done within 15 minutes via a reservoir. It is also possible to keep the primed circuit to be ready for emergency use at least for a week. The cannulae are placed intravascularly through the femoral artery and vein by using the Seldinger's percutaneous method. In an emergency situation, the arterial and venous cannulations are carried out separately on the both inguinal regions to save time. The tip of the venous cannula is adjusted to be placed near the right atrium under fluoroscopy. Initiation of ECPB via the femoro-femoral V-A cannulae assures instant and stable supply of oxygenated blood to all of the vital organs. At the present time, nothing is more important than a quick supply of oxygenated blood to the brain to ameliorate the post-ischemic brain damage.

Cardiopulmonary Bypass↗
PubMed1991

Inhibitory effect of heparin cofactor II on thrombin-stimulated prostacyclin production by cultured vascular smooth muscle cells.

We investigated the effect of heparin cofactor II (HCII) on thrombin-induced prostacyclin (PGI2) production by A10 cells, an established cell line of vascular smooth muscle cells from murine aorta. Confluent monolayers of A10 cells were incubated with 0.1 NIH U/ml of thrombin for 30 min in the presence of antithrombin III (ATIII) or HCII, and PGI2 production by the cells was measured by radioimmunoassay as 6-keto-prostaglandin F1a, the stable metabolite of PGI2. ATIII at 40 mInh.U/ml and more significantly inhibited thrombin-induced PGI2 production by A10 cells, but HCII at the same doses did only slightly. However, when A10 cells were preincubated with HCII for 30 min before exposure to thrombin, the PGI2 production was markedly inhibited. The medium conditioned by A10 cells for 30 min did not enhance the inhibitory effect of HCII on thrombin-induced PGI2 production by the cells. On the other hand, A10 cells synthesized both dermatan sulfate and heparan sulfate which are capable of activating HCII. From these results, it was suggested that HCII would be activated by glycosaminoglycans (GAGs) such as dermatan sulfate of the cell layers and could inhibit thrombin-induced PGI2 production. HCII may be a modulator of thrombin on the physiological functions of vascular smooth muscle cells, reacting to the cell surface GAGs.

Antithrombin III↗
PubMed1991

Collagenase synthesis by cloned rabbit pulp cells--molecular and immunological identity of pulp cell and fibroblast enzyme.

Cultures of cloned rabbit pulp (RP) cells without stimulation produced collagenase of a concentration as high as reference rabbit skin fibroblast cultures which were stimulated with phorbol myristate acetate (PMA, 100 ng/ml). The RP cell collagenase was compared with reference fibroblast collagenase in Western blot analysis using monoclonal antibodies prepared against RP cell collagenase and a polyclonal antibody prepared against rabbit fibroblast collagenase. Both enzyme preparations revealed, with either antibody, identical bands of approximate molecular masses 57,000, 52,500, and 45,000. These antibody preparations variously inhibited RP cell collagenase activity. Intracellular collagenase in RP cells in culture was demonstrated by the indirect immunofluorescence antibody technique using polyclonal anti-fibroblast collagenase antibody. RNA samples from RP cells hybridized with rabbit fibroblast collagenase cDNA (clone H9) and showed a distinct band at 2.7 kb. Both control and PMA-stimulated RP cells and PMA-stimulated reference skin fibroblasts demonstrated strong cytoplasmic hybridization between H9 and collagenase mRNA. The results indicate that RP cell collagenase is identical to rabbit fibroblast collagenase, and that the RP cell line provides a useful in vitro reference system for the study of collagenolysis in the rabbit model.

Animals↗
PubMed1991

Expression of a monocot LHCP promoter in transgenic rice.

The beta-glucuronidase (GUS) gene linked to the promoter of rice light harvesting chlorophyll a/b-binding protein of photosystem II (LHCPII) was introduced into rice by electroporation. Expression of the GUS gene with the LHCP promoter in transformed protoplasts and callus was much lower than with the cauliflower mosaic virus (CaMV) 35S promoter. In green organs, however, LHCP-GUS activity with the LHCP promoter was 10-fold higher than that with the CaMV 35S promoter. Expression of the LHCP-GUS gene was detected in leaves, stems and floral organs but not in roots. Histochemical analysis of leaves showed that the GUS gene was expressed specifically in green tissues. In selfed seeds of the transformants, GUS gene expression was detectable only in the germinated embryos after greening. Northern blot analysis revealed that transcription of the GUS gene with the LHCP promoter was not detectable in dark-grown seedlings of transformants but was induced by exposure to light. These results show that regulation of the introduced chimeric gene in transgenic plants was characteristic of the LHCP gene itself.

Blotting, Southern↗
PubMed1991

Micro-mainframe-like personal clinical research system.

We constructed a micro-mainframe-link clinical research system for personal use (Personal Clinical Research System). This system was developed with both a mainframe computer and a personal computer (PC). The prepared programs included a database manager (on the mainframe computer), a user interface program (on the PC), and a communication control program that connected the mainframe computer with the PC. The database on the mainframe computer was constructed by two methods. The first method was to transmit data from the PC to the mainframe computer. The second method was to extract data from the patient information database. Using this system, a physician is able to construct a personal research database that contains interesting data for the physician. In addition, the physician is able to accumulate data on a special field using this system. A discharge summary system is now in operation as an example of this system.

Computers, Mainframe↗
PubMed1991

A random allocation system with the minimization method for multi-institutional clinical trials.

This paper describes the random allocation system used to perform precise and rapid treatment assignments in multi-institutional clinical trials. This system is based on sophisticated randomization procedures, according to Pocock and Simon's minimization method and Zelen's method for institution balancing. The major advantage of randomized treatment assignments with this system is to balance treatment numbers for each level of various prognostic factors over the entire trial and at the same time balance the allocation of treatments within an institution. Therefore, the randomized treatment assignments by this system can prevent degrading of the statistical power of a particular treatment factor. This system is designed to run on a small-sized notebook computer and therefore can be set up beside a telephone for registration, without occupying a large space. At present, this system is conveniently being used in two clinical trials.

Algorithms↗
PubMed1991

Schistosoma mansoni: possible involvement of protein kinase C in linoleic acid-induced proteolytic enzyme release from cercariae.

The possible involvement of protein kinase C and Ca2+ metabolism in the proteolytic enzyme release from schistosome cercariae was studied. Cercariae were placed in dechlorinated tap water containing 0.37 mM calcium in the small glass petri dish and exposed to the stimuli (linoleic acid, phorbol esters, and Ca2+ ionophore) with or without inhibitors of protein kinase C or Ca2+ metabolism. The proteolytic activity of incubation medium of cercariae thus treated was measured by the azocoll assay. The penetration response of cercariae induced by linoleic acid, a physiological stimulus, was mimicked by phorbol esters. When exposed to phorbol esters, 0.02 to 2 microM of 12-O-tetradecanoylphorbol-13-acetate (TPA) and 0.2 to 2 microM of phorbol-12,13-dibutyrate (PDBu), cercariae ceased the swimming movement, began a rhythmic thrusting of the anterior tip of the parasite, and released the proteolytic enzyme, but they did not shed the tails. Lowering Ca2+ in water by addition of 5 mM ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA), phorbol ester-induced release of enzyme was completely inhibited. Phorbol ester-induced release of enzyme was partially inhibited by 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, at a concentration of 100 microM. H-7 alone, at a concentration of 100 microM, did not affect the swimming movement of cercariae. The cercariae were stimulated to release the enzyme by high concentrations (10 and 100 microM) of the Ca2+ ionophore, A23187, but enzyme was not released by low concentrations (0.5 and 1 microM) of this drug. Cercariae exposed to A23187 behaved differently from those exposed to phorbol esters. They ceased swimming, showed strong muscle contraction, and shed their tail. A23187 stimulated cercariae to release the enzyme in the water containing 5 mM EGTA. A23187-induced enzyme release was not inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin antagonist, trifluoperazine (TFP), a better calmodulin antagonist on schistosome, or by verapamil, a Ca2+ channel blocker. Linoleic acid-induced release of enzyme was partially inhibited by 0.5 and 5 mM of EGTA and by 1 to 100 microM of H-7. While it was not inhibited by N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide (H-8) and N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004), inhibitors of cyclic nucleotide-dependent protein kinase which were used as negative controls of H-7, W-7, TFP, 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8), an intracellular Ca2+ antagonist, and verapamil.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Rhodamine B inhibition of glycosaminoglycan production by cultured human lip fibroblasts.

Rhodamine B (Rh B) is a dye which is used in cosmetics such as lipsticks. We investigated the effect of the dye on the metabolism of [3H]glucosamine-labeled glycosaminoglycans ([3H]-GAG) in confluent cultures of human lip fibroblast KD cells. It was found that Rh B at 10 micrograms/ml and above significantly decreased the accumulation of [3H]-GAG in both the cell layer and the medium after a 24-hr culture. This Rh B (50 micrograms/ml) effect was recognized in the cell layer and the medium after 8 and 24 hr, respectively, and longer. The Rh B at the 25 micrograms/ml-induced decrease in the [3H]-GAG accumulation was reversible in both the cell layer and the medium. On the other hand, the release of [3H]-GAG from the cell layer was unaffected by Rh B. A characterization of [3H]-GAG revealed that all components of the GAG including hyaluronic acid, heparan sulfate, chondroitin 4- and/or 6-sulfate, and dermatan sulfate were significantly decreased by 50 micrograms/ml Rh B in both the cell layer and the medium. Rh B significantly decreased the accumulation of [3H]-GAG in the presence of either 10 microM cycloheximide or 1 mM p-nitrophenyl-beta-D-xyloside, suggesting that Rh B inhibited the sugar chain formation rather than core protein synthesis. Although the number of confluent KD cells was significantly decreased by Rh B at 10 micrograms/ml and above, this Rh B effect was much weaker than that on the [3H]-GAG accumulation. The release of lactate dehydrogenase from the cell layer was significantly increased by 100 micrograms/ml Rh B but not by the dye at 75 micrograms/ml and below. From these results, it was suggested that Rh B decreases the GAG content of human lip fibroblasts through a functional suppression of polysaccharide chain formation in the process of the GAG production.

Cell Count↗
PubMed1991

Vitamin A deficiency and the induction of cutaneous toxicity in murine skin by TCDD.

The mechanisms involved in the induction of toxicity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a prototype for a group of toxic polyhalogenated aromatic hydrocarbons, are largely unknown. To test the hypothesis that TCDD-induced toxicity involves the reduction of vitamin A levels, we investigated the role of vitamin A deficiency in modulating the cutaneous response of congenic haired (+/+) and hairless (hr/hr) mice to TCDD. Hairless mice are recognized as sensitive models for expression of TCDD-induced cutaneous toxicity. Haired mice normally do not develop a cutaneous response to TCDD. Mice raised on a vitamin A-deficient diet, and age- and sex-matched controls raised on standard chow, were treated topically with TCDD and their cutaneous responses monitored histologically. Body weights and thymus gland weights were monitored as additional parameters of toxicity. Liver and skin vitamin A levels were determined by HPLC. Vitamin A depletion by itself had no effect on the normal cutaneous histology of the haired phenotype, nor were any changes in cutaneous morphology attributable to TCDD toxicity observed in haired, TCDD-treated animals even when they were severely vitamin A depleted. On the other hand, in hairless mice, vitamin A deficiency caused a distinct increase in keratinization of dermal epithelial cysts, and an increase in the sensitivity of these cysts to TCDD-induced hyperkeratinization. TCDD-induced body weight loss and atrophy of the thymus gland were not affected by the vitamin A status of either the haired or hairless animals. Analysis of vitamin A levels in skin and liver, following topical treatment of mice with TCDD, indicated that TCDD exposure did not affect cutaneous levels, but did significantly lower liver levels of vitamin A. These experiments suggest that although systemic vitamin A deficiency may potentiate the expression of TCDD-induced toxicity in skin of hairless mice, expression of TCDD-induced toxicity probably involves more complex mechanisms than a reduction in vitamin A levels.

Administration, Topical↗
PubMed1991

Early stages of multistep hepatocarcinogenesis: adenomatous hyperplasia and early hepatocellular carcinoma.

From a series of 320 heptocellular carcinoma (HCC) cases treated surgically, we selected small nodular lesions that had not destroyed the preexisting liver structure grossly. After excluding metastases and large regenerative nodules, 58 lesions from 41 cases were chosen. All the lesions were hypercellular. Among them, 33 lesions showing histologic features of very well-differentiated HCC (Edmondson grade I), that is, small hepatocytes with little cellular atypia but with structural atypia, such as a thin trabecular structure of acinar formation in some areas, were classified as early HCC (eHCC). In seven eHCCs, areas of overt carcinoma, classified as Edmondson grade II, were found in the background of Edmondson grade I carcinoma. The remaining 25 lesions lacked structural atypia and were classified as adenomatous hyperplasia (AH). Among the AHs, 10 nodules with a very focal abnormal structure were subclassified as atypical adenomatous hyperplasia (AAH). There was a tendency for the size and cellularity of the atypical lesions to increase in order from AH to AAH to eHCC. All nodules larger than 1.5 cm were eHCC. A degree of cellularity more than twice that of a regenerative nodular was suggested to be an indicator of HCC. All small nodular lesions were associated with chronic liver disease. These histologic observations appear to explain the stepwise development of overt HCC from very well-differentiated eHCC, and of eHCC from AH probably through AAH, at least in cases of HCC associated with chronic liver disease.

Adenoma↗
PubMed1991

Present mercury levels in red blood cells of nearby inhabitants about 30 years after the outbreak of Minamata disease.

Samples of red blood cells (RBCs) from 1178 inhabitants, consisting of 546 males and 795 females (over 40 years old), of a coastal town near Minamata City were analyzed for total mercury. The mercury concentrations in the RBCs showed lognormal distributions for both sexes with higher values in males than in females. The geometric mean of the mercury concentrations in the RBCs was 27.5 ng/g (ranging from 8.0 to 69.1 ng/g) for males and 20.4 ng/g (ranging from 7.0 to 63.7 ng/g) for females. The mercury concentrations in the RBCs decreased with advancing age. A significant regression between the geometric mean of the mercury concentrations in the RBCs and age was obtained for both sexes. The mercury concentrations in the RBCs from male inhabitants of the coastland area were significantly higher than those from male inhabitants of the inland area. In terms of occupation, the highest mercury concentrations were observed in the RBCs from fisherman. No significant difference in the present mercury concentrations in the RBCs was observed between the cases with Minamata disease and the controls.

Aged↗
PubMed1991

Inhibitory effect of rhodamine B on the proliferation of human lip fibroblasts in culture.

The effect of the cosmetic dye rhodamine B on the proliferation of human lip fibroblasts (KD cells) was investigated in a culture system. Rhodamine B at 25 micrograms/ml and above significantly decreased the number of the cells after a 72 h culture. A time course study revealed that 50 micrograms/ml of rhodamine B-induced decrease in the cell number occurred after 48 h and longer, suggesting that the dye inhibited cell proliferation without a decrease in cell attachment. The detachment of [3H]thymidine-labeled cells from the monolayer was unaffected by rhodamine B at 100 micrograms/ml and below. The incorporation of [3H]thymidine and [14C]leucine into the acid-insoluble fraction of the cell layer was significantly inhibited by 50 micrograms/ml rhodamine B treatment. Histologically, the damage of KD cells was not marked, however, a degenerative change of nuclei and an irregular shape of the cells as well as a decrease in the cell number were caused by 50 micrograms/ml rhodamine B. Rhodamine 6G caused a severe damage of the cells, and rhodamine B significantly decreased the cell number; rhodamine 123 had no significant effect; rhodamine 116 significantly increased the cell number. Furthermore, rhodamine B decreased the number of both vascular endothelial cells from bovine aorta and vascular smooth muscle cells from murine aorta after a 72 h culture. It is concluded that rhodamine B inhibits the proliferation of human lip fibroblasts. This rhodamine B effect may be a warning sign for the dye toxicity.

Cell Division↗
PubMed1991

Effect of lead on the glycosaminoglycans metabolism of bovine aortic endothelial cells in culture.

We investigated the effect of lead nitrate (0.1, 1.0, 10 or 20 microM) on the metabolism of glycosaminoglycans (GAG) in confluent cultures of bovine aortic endothelial cells. It was found that lead at 10 and 20 microM significantly decreased the accumulation of [35S]sulfate-labeled GAG ([35S]GAG) both in the cell layer and the medium after a 24-h culture. A time course study showed that 10 microM lead decreased the accumulation of [3H]glucosamine-labeled GAG both in the cell layer and the medium after 24 h and longer. The release of [35S]GAG from the cell layer during the last 3 h of a 24 h culture was not changed by lead. The detachment of [3H]thymidine-labeled cells from the monolayer was unaffected by lead. It was shown that lead at 10 microM decreased both heparan sulfate and the other GAG in the cell layer; the former was more sensitive to lead treatment. Lead at 20 microM and below failed to increase the release of lactate dehydrogenase, suggesting that non-specific cell damage was not caused by lead. From these results, it was suggested that lead decreases endothelial cell heparan sulfate content through a decrease in the GAG production without a non-specific cell damage. Lead may be a risk factor of vascular disorders.

Animals↗
PubMed1991

Stimulation of heparan sulphate release from cultured endothelial cells by plasmin.

We investigated the effect of plasmin on the release of glycosaminoglycans (GAG) from bovine aortic endothelial cells in culture. Plasmin significantly increased the release of [35S]sulphate-labelled GAG (35S-GAG) from the cell layer, although plasminogen did not show such a stimulatory effect. The percentage of heparan sulphate in the released 35S-GAG (about 80%) was not changed by plasmin. Plasmin enhanced the detachment of endothelial cells from the monolayer only slightly. From these results, it was suggested that the local anticoagulant activity on endothelium mediated by the anticoagulant heparan sulphate will be increased by plasmin; the conversion of plasminogen to plasmin may be mediated by plasminogen activators released from thrombin-stimulated endothelial cells.

Animals↗