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Biomedical subjects

T Matsubara

Publications and source records attributed to T Matsubara.

At least 487 records · Page 27Linked to original sources
PubMed1984

[Abnormalities in the ventricular configuration and movement of the interventricular septum].

We discussed the left ventricular deformity in atrial septal defect (ASD) using two-dimensional echocardiography and elucidated the mechanism responsible for the production of mitral valve prolapse (MVP) associated with ASD. Two-dimensional echocardiography was performed for 78 cases with ASD, ranging in age from three to 64 years. The diagnosis was made by cardiac catheterization in all patients and was verified by surgical intervention in 66 cases. Two-dimensional images were obtained using an electronic sector scanning system of Toshiba (SSH-11A). The recording was made with 8 mm cinematography and an ordinary 35 mm camera. The major diameter/the minor diameter of the short-axis cross-section of the left ventricle was defined as the left ventricular distortion ratio (LVDR). The LVDR in early diastole was significantly larger than those in end-diastole and end-systole (p less than 0.001, n = 33). Furthermore, in end-diastole, the left ventricle showed a greater distortion ratio than that in end-systole (p less than 0.001, n = 33). The left ventricular short-axis area (LVSAA) corrected for the body surface area (BSA) was significantly greater both in early diastole and end-diastole than that in end-systole (p less than 0.001, n = 33). In early diastole, there was a poor correlation between the LVDR and the pulmonic to systemic flow ratio (Qp/Qs) (r = 0.44, p less than 0.05, n = 33). Similarly, the LVDR was poorly related with the right ventricular dimension (RVD) in early diastole (r = 0.43, p less than 0.05, n = 30).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

A possible role of protein kinase C in signal-induced lysosomal enzyme release.

In platelets, activation of protein kinase C and mobilization of Ca2+ were selectively induced by the addition of 1-oleoyl-2-acetyl-glycerol and a low concentration of A23187, respectively (Kaibuchi, K., Takai, Y., Sawamura, M., Hoshijima, M., Fujikura, T. and Nishizuka, Y. (1983) J. Biol. Chem. 258, 6701-6704). Using this procedure evidence was obtained suggesting that the protein phosphorylation and Ca2+ mobilization were both essential and synergistically effective to cause release of lysosomal acid hydrolases such as N-acetylglucosaminidase. A similar observation was made for the lysosomal enzyme release from rat neutrophils.

Animals↗
PubMed1983

The thickening of basement membrane in synovial capillaries in rheumatoid arthritis.

Synovial tissues from seven rheumatoid arthritis (RA) patients were used for the ultrastructural investigation of capillary cellular components and basement membranes (BM). Attention has been specially paid to the mechanism of BM thickening of the capillaries in the inflammatory sites. The capillary BM were multilamellated in the inflammatory sites. The multilamellation was characteristic not only in the BM surrounding the endothelial cells and pericytes but also in the BM between these two types of cells. Cell debris was frequently encountered between the multilamellated BM. The hyperplasia and various stages of degeneration of the endothelial cells were observed in these regions. Some endothelial cells were activated and occasionally located in capillaries containing degenerated endothelial cells. The high incidence of these findings indicates the following hypotheses. The accelerated rate of death and replenishment of capillary cellular components may play a role in BM thickening in the inflammatory sites of RA synovium. These cells may not only produce one layer of BM in their life-time but may also be activated to produce excessive amounts of BM components to make several layers.

Adult↗
PubMed1983

The ultrastructural localization of fibronectin in the lining layer of rheumatoid arthritis synovium: the synthesis of fibronectin by type B lining cells.

The distribution of fibronectin in the lining layer of inflamed rheumatoid arthritis (RA) synovium has been ultrastructurally investigated using an anti-human plasma fibronectin antibody. The hyperplasia of lining cells was prominent in the lining layer of the inflamed RA synovium. A high level of fibronectin was localized in this region. Ultrastructurally the fibronectin was observed on the surface of both type A (type M) and type B (type F) cells, and in the extracellular fibrin-like material. This glycoprotein was detectable in rough endoplasmic reticulum (RER), some Golgi apparatus, and peripheral vesicles of type B cells. On the other hand, RER and Golgi apparatus of type A cells failed to be immunostained with the antibody. Type A cells occasionally contacted each other with interdigitation of cytoplasmic processes, and a high amount of fibronectin was localized in this region. These findings indicate that fibronectin is synthesized along the classic secretory pathway through RER and Golgi apparatus of type B cells. On the contrary, type A cells seem not to be associated with the local synthesis of the glycoprotein. Fibronectin may play a structural role in organizing these proliferated lining cells by promoting cell adhesion. The synthesis of fibronectin by proliferated type B cells may be responsible in part for the local increase of this glycoprotein in the lining layer of RA synovium.

Adult↗
PubMed1983

Inhibition of concanavalin A-induced phosphatidylinositol turnover and lysosomal enzyme release by cyclic AMP-elevating agents in rat peritoneal macrophages.

When rat peritoneal macrophages were stimulated with concanavalin A (Con A), phosphatidylinositol (PI) turnover was rapidly induced and concomitantly N-acetylglucosaminidase was released. These two reactions were markedly inhibited by prostaglandin E1, which elevated the cellular cyclic AMp levels. This effect was mimicked by dibutyryl cyclic AMP. These results suggest that the elevation of the cellular cyclic AMP levels might play a role in the inhibition of the early stages of Con A-induced activation of macrophages through the inhibition of PI turnover.

Acetylglucosaminidase↗
PubMed1983

The localization of fibronectin in rheumatoid arthritis synovium by light and electron microscopic immunohistochemistry.

The distribution of fibronectin in rheumatoid arthritis (RA) synovium has been investigated by light and electron microscopic immunohistochemistry using an antihuman fibronectin antibody. Heavy accumulation of fibronectin was observed in the lining layer and the areas of proliferation of fibroblasts. Rough endoplasmic reticulum (RER) and peripheral vesicles of proliferated type B lining cells and fibroblasts contained large amounts of fibronectin. Thus these cells seem to participate actively in the local synthesis and secretion of this glycoprotein. Type A lining cells and migrated mononuclear phagocytes contained many phagolysosomes in some of which dense accumulation of fibronectin was observed. Some of the materials in the phagolysosomes, with dense accumulation of fibronectin, resembled the fibrinous material-fibronectin complexes frequently seen in the pericellular spaces. Accordingly fibronectin seems to play a role in the clearance of fibrinous materials by these phagocytes. The proliferated capillaries and small vessels possessed multilamellated basement membranes with heavy accumulation of fibronectin. However, RER or Golgi apparatus of the endothelial cells contained no detectable amounts of fibronectin. This indicates that these cells do not actively participate in the synthesis of fibronectin and that the majority of this glycoprotein in the basement membranes originates in fibronectin from blood vessel exudate. Fibrinous material-fibronectin complexes were frequently seen on the endothelial cell surfaces. Circulating platelets and mononuclear cells occasionally came in contact with these complexes, suggesting an association of fibronectin with the formation and clearance of thrombi in the vascular lumina at the inflammatory sites of RA synovium.

Arthritis, Rheumatoid↗
PubMed1983

Results of microsurgical management of ruptured intracranial aneurysms.

The authors report the results of microsurgical management of 209 cases of ruptured intracranial aneurysms. The outcome of the surgery is discussed from the point of view of operative timing, preoperative grade, age and the effect of vasospasm. The operative results at the time of discharge were as follows: 137 excellent cases, 18 good, 31 fair, 8 poor and 15 deaths. The overall mortality rate was 7% and those patients designated as excellent and good who returned to work fully accounted for 74%. The result was achieved even though 65% of the patients were operated on within 2 weeks after the onset, and 44% of the patients were categorized as grade III, IV and V in Hunt's classification. In the morbidity and mortality, over half of the patients categorized as fair, poor and death were complicated by vasospasm, and the result was attributed mainly to the vasospasm. Therefore, we strongly believe that radical surgery is recommended to prevent rebleeding in the waiting period, there should be a greater understanding of "vasospasm" in order to improve overall morbidity and mortality.

Adolescent↗
PubMed1983

The role of phosphatidylinositol turnover in initiation of prostaglandin biosynthesis in concanavalin A-induced activation of rat peritoneal macrophages.

When macrophages were stimulated by concanavalin A (50 micrograms/ml) in the presence of 32Pi and 3H-arachidonic acid (AA), rapid incorporation of these radiolabeled substances into phosphatidylinositol (PI) and phosphatidic acid (PA) were induced within 10 min. The pool of PI and PA incorporating 3H-AA was the same as that of PI and PA which incorporated 32P. However, significant increase in incorporation of 32P and 3H-AA did not occur in phosphatidylcholine, phosphatidylethanolamine or phosphatidylserine within this time interval as compared with control levels. These results indicate that PI turnover might play a role in the initiation of prostaglandin biosynthesis in the early stages of macrophage activation induced by concanavalin A.

Animals↗
PubMed1983

Possible antidotes in severe intoxication with fenitrothion in rats.

We investigated antidotal effects of nine drugs against acute fenitrothion poisoning in rats. The antidotal effects were evaluated by a relief from toxic signs, an increased survival ratio and a prolonged surviving time. In the poisoning with approximate LD50 fenitrothion (500 mg/kg), oximes such as 2-PAM (2-pyridine aldoxime methiodide) and TPMM (1-(methyl morphorinium)-3-(4-hydroxyiminomethylpyridinium) propane dibromide), diphenhydramine and parasympatholytics such as atropine, scopolamine and biperiden significantly increased survival ratio and/or prolonged surviving time. These effective drugs did not sufficiently depress the toxic signs, except that the parasympatholytics markedly blocked salivation, miosis and motor ataxia. In contrast, reduced glutathione and central depressants such as diazepam and phenobarbital made the poisoning serious. In the poisoning with 100% lethal dose of fenitrothion (800 mg/kg), the parasympatholytics were more effective than 2-PAM and diphenhydramine, and they elevated the survival ratio up to 20-40%. The best therapy against the severe poisoning with 100% lethal dose of fenitrothion was confirmed to be the repeated and combined treatment with atropine and 2-PAM as established in parathion poisoning, resulting in 90% survival ratio and considerable alleviation from the toxic signs.

Animals↗
PubMed1983

Liver microsomal cytochrome P-450-dependent O-dealkylation reaction in various animals.

Liver microsomal O-dealkylation activity was determined using O-methyl, O-ethyl and O-propyl derivatives of p-nitrophenol, 7-hydroxycoumarin (umbelliferon) and 7-hydroxyphenoxazone (resorufin) as substrates. Microsomal O-dealkylation activities of p-nitrophenol and 7-hydroxycoumarin O-alkyl derivatives were of similar levels, but the activities of 7-hydroxyphenoxazone O-alkyl derivatives were very low compared with those of other substrates. Pretreatment of rats with beta-naphthoflavone resulted in the preferential increase of O-deethylation and O-depropylation activities regardless of the ring structure of the substrates, and the ratio of O-deethylation and O-depropylation activities to that of O-demethylation increased markedly. On the other hand, the O-dealkylase activity of all substrates increased generally upon pretreatment of the rats with phenobarbital, but the ratio of O-deethylase or O-depropylase activity to that of O-demethylase in the pretreated rats was not very different from that of the untreated animals. Hexobarbital inhibited competitively the O-dealkylation activity in control and phenobarbital-pretreated rat microsomes. On the other hand, the O-dealkylase activity in microsomes obtained from beta-naphthoflavone-pretreated rats was inhibited remarkably by alpha-naphthoflavone, but not in microsomes prepared from untreated and phenobarbital-pretreated rats. Based on these results, this report discusses the relationship between the alteration of O-dealkylation activity and the composition change of cytochrome P-450 in microsomal membrane. Species differences in the substrate specificity of the O-dealkylation reaction and in the responsiveness of the animals to typical inducers were also observed using liver microsomes obtained from several animals under various conditions.

Animals↗
PubMed1983

Biotransformation of coumarin derivatives. (2). Oxidative metabolism of 7-alkoxycoumarin by microsomal enzymes and a simple assay procedure for 7-alkoxycoumarin O-dealkylase.

The in vitro biotransformation of 7-alkoxycoumarin by rat liver microsomes was studied to develop a simple and accurate assay procedure for 7-alkoxycoumarin O-dealkylase. 7-Alkoxycoumarin was converted to the O-dealkylated metabolite, 7-hydroxycoumarin, by aerobic incubation of the parent compound with microsomes and NADPH, but the decreased amount of 7-alkoxycoumarin in the reaction mixture was several times higher than that of the 7-hydroxycoumarin produced during the incubation. The thin-layer chromatogram of the ether extractable metabolites in the reaction mixture showed the existence of several fluorescent metabolites including 7-hydroxycoumarin. Fluorescent properties of the parent compound, 7-alkoxycoumarin, and most of the metabolites differed from that of 7-hydroxycoumarin, but the reaction cofactor, NADPH, showed similar properties. Treatment of the reaction mixture with perchloric acid resulted in conversion of NADPH to the non-fluorescent form without any effect upon the fluorescent properties of 7-hydroxycoumarin and its related compounds. Based on these properties, an improved and simple in vitro fluorometric assay of the O-dealkylation of 7-alkoxycoumarin was developed. The method is applicable to routine determination of O-dealkylase activity in both isolated microsomes and whole homogenate. Species differences in the substrate specificity of the O-dealkylation reaction and in the responsiveness of animals to the inducer were observed even with use of the liver homogenate obtained from untreated and phenobarbital- or beta-naphthoflavone-pretreated animals, similar to what was observed with the microsomal system.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1983

Carbon tetrachloride-induced hepatotoxicity in rats: evidence for different susceptibilities of rat liver lobes.

The hepatotoxic effect of carbon tetrachloride (CCl4), reflected by augmented blood aspartate aminotransferase and alanine aminotransferase activities and the extent of histological liver damage, was observed following oral administration of CCl4 to rats. A marked increase of blood transaminase activities and severe degeneration of hepatocytes in the centrilobular region were detected 1-2 days after the administration, while the cytochrome P-450 content and the drug metabolizing activity in livers were depressed immediately after the administration. Based on these results, the effect of CCl4 on hepatic cytochrome P-450 and the histological pattern of liver cells was observed using tissue samples obtained from various liver lobes of rats given CCl4 24 hr previously. Dose-dependent inactivation of cytochrome P-450 by the administration of CCl4 was observed throughout the liver, with the most extensive decrease in the cytochrome content in the median lobe. The extent of liver damage (hydropic swelling degeneration and central necrosis in lobule) was also greater in the median and right liver lobes than in the left lobe. When a small amount of CCl4 was administered, degeneration of liver cells was detected only in the median and right lobes with only slight degeneration in the left lobe. These results indicate different susceptibilities of rat liver lobes to CCl4.

Alanine Transaminase↗
PubMed1983

Mucociliary clearance in chronic sinusitis: related human nasal clearance and in vitro bullfrog palate clearance.

Nasal mucociliary clearance was measured in both healthy subjects and patients with chronic sinusitis using saccharin granule technique. Nasal mucociliary transit time (ST) was significantly slower in the patients with chronic sinusitis compared with that in controls (p less than 0.005). Nasal mucus collected from each nasal cavity was used for in vitro bullfrog palate clearance studies and compared to the in vivo nasal ST. Mucociliary clearance rate (MTR) on frog palate was 12.5 +/- 2.5 mm/min in the mucus from control subjects, 6.1 +/- 1.5 mm/min in the mucus from the patients. The difference was statistically significant (p less than 0.005). The MTR on frog palate in the patients whose nasal ST was within normal range was significantly slower than that in controls (p less than 0.005), but not significantly different from that in the patients whose nasal ST was over the normal range. These results suggest that the nasal mucous properties which decreased the mucociliary clearance on frog palate did not contribute to the mucociliary clearance of the patients who had a normal one. No significant correlation existed between MTR on frog palate and nasal ST in both control and chronic sinusitis. In chronic sinusitis patients, decelerated nasal ST was recovered significantly by normal saline nebulization compared with the value before the nebulization (p less than 0.01). None of the significant change of ST was observed in control before and after the nebulization.

Adolescent↗