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R Kuribayashi

Publications and source records attributed to R Kuribayashi.

At least 19 recordsLinked to original sources
PubMed2000

Requirement for lysine-19 of the yeast mitochondrial ATPase inhibitor for the stability of the inactivated inhibitor-F1Fo complex at higher pH.

The ATPase inhibitor is a regulatory subunit of mitochondrial ATP synthase. In this study, the role of Lys19 of the yeast ATPase inhibitor was examined by site-directed mutagenesis. Two amino acids (Gln and Glu) were substituted for the Lys19. The purified mutant inhibitor (Lys19-->Gln) had similar ATPase inhibitory activity to that of the wild-type inhibitor at pH 6.5, but was less active at pH 7.4. ATP synthesis in mutant mitochondria was normally activated by the addition of ADP and succinate, but the inactivated ATPase complex in the mutant mitochondria was activated more readily than that in control cells by raising pH. These results show that Lys19 of the yeast ATPase inhibitor is not essential for ATPase inhibitory activity, but increases the stability of the inhibitor-F1Fo complex at higher pH.

Adenosine Triphosphate↗
PubMed1999

Heparin coupling in inhibition of calcification of vascular bioprostheses.

Inhibitory effect of heparin coupling on calcification of bioprosthetic vascular grafts of different origin was studied. Heparin-bonded (Hep) and 0.625% glutaraldehyde-cross-linked (GA) segments of porcine thoracic aorta (AO), pulmonary artery (PA), jugular vein (JV) and rabbit aorta (RA) were implanted subcutaneously in weanling rats for 5 months. Heparin bonding is ineffective in prevention of calcification of JV (Hep: Ca, 159 +/- 32.26 mg g-1; GA: Ca, 193.55 +/- 17.81; p = 0.075) and RA (Hep: Ca, 150.17 +/- 14.78; GA: Ca, 192.12 +/- 26.61; p = 0.015). Calcium content of heparin-coupled PA and AO was significantly less when compared with their GA-treated counterparts. Calcification inhibition was achieved to a greater extent in heparin-bonded PA (Hep: Ca = 22.62 +/- 5.72, GA: Ca = 115.99 +/- 21.91, p < 0.0001) than in the AO coupled to heparin (Hep: Ca = 63.77 +/- 22.75, GA: Ca = 150.40 +/- 35.21, p < 0.0001). Elastin fibers were the predominant site of calcification in all explanted vascular grafts. Heparin-bonded porcine pulmonary artery is seemed to be the best among all vascular bioprostheses in this study.

Animals↗
PubMed1998

Inhibitory effect of photooxidation on intimal and medial thickening of saphenous vein.

BACKGROUND: The inhibitory effect of short-term photooxidation on medial and neointimal proliferation of human saphenous vein was investigated. METHODS: Culture medium-filled surgically prepared saphenous vein segments were photooxidized in 0.01% methylene blue solution for 5 minutes. Photooxidized and nonphotooxidized saphenous veins were checked for viability of endothelial cells by culturing vein segments for 21 days followed by histologic and immunohistochemical studies. RESULTS: Endothelial cells of saphenous vein segments remained unaffected after photooxidation. Both the intima and media of nonphotooxidized veins became highly cellular and thickened because of the proliferation and migration of smooth muscle cells. Like precultured fresh saphenous vein, intimal (0.031+/-0.017 mm; p=0.0067) and medial thicknesses (0.702+/-0.123 mm; p < 0.0001) and proliferating cell nuclear antigen-positive cell count (14+/-8/mm2; p=0.0005) of cultured photooxidized veins were significantly less than those of cultured nonphotooxidized veins (intimal thickness, 0.059+/-0.041 mm; medial thickness, 0.997+/-0.228 mm; proliferating cell nuclear antigen positive cell count, 34+/-16/mm2. CONCLUSIONS: Methylene blue-induced short-term photooxidation is effective in inhibition of intimal and medial thickening of saphenous vein.

Aged↗
PubMed1998

In vitro and in vivo calcification of vascular bioprostheses.

Efficacy of different chemical treatments on calcification of vascular graft in vitro and in vivo was studied. Culture medium-filled rat aortas were separately treated in 0.2% glutaraldehyde and epoxy compound, and photooxidized in 0.01% methylene blue for a shorter period (group 1). Another group of rat aortas were separately treated in the same chemicals for a longer period (group 2). All fresh and treated aortas of both groups were cultured for 21 days in an organ culture medium and implanted (except for group 1) in weanling rats for five months. Histology and immunohistochemistry revealed that differently treated aortas of group 1 grow and calcify, and the smooth muscle cells between elastin fibers are the primary site of calcium deposition. In contrast, differently treated aortas of group 2 neither grew, nor did calcify in the medium except the epoxy compound cross-linked aorta of group 2 which did not grow but did calcify. Untreated aorta did not calcify. All fresh and differently treated aortic homografts calcified severely in rats. Our whole arterial segment-calcification system would be useful for analyzing the molecular and cellular mechanisms of both bioprosthetic and atherosclerotic calcification of vascular graft. New anticalcification technique is the only hope for better outcome of future vascular bioprostheses.

Animals↗
PubMed1997

Prevention of calcification in glutaraldehyde-treated porcine aortic and pulmonary valves.

BACKGROUND: The problem of calcification in porcine aortic (AVs) and pulmonary (PVs) valves and its relationship to glutaraldehyde (GA) is of current interest. We proposed an anticalcification treatment to develop noncalcifying porcine AVs and PVs. METHODS: Porcine AVs and PVs were cross-linked in GA. Partially degraded heparin was coupled to the GA-treated AVs and PVs through intermediate surface-bound substrate containing amino groups. Control AVs and PVs were cross-linked in 0.625% GA but had no heparin coupling. All specimens were implanted subdermally in 3-week-old rats for 5 months for calcification studies. RESULTS: Control AVs (Ca, 233.69 +/- 42.61 mg/g) and PVs (Ca, 181.48 +/- 4.06 mg/g) were severely calcified. Coupling of partially degraded heparin revealed complete prevention of calcification in GA-treated AVs (Ca, 0.73 +/- 0.27) and PVs (Ca, 1.125 +/- 0.22 mg/g) implanted subcutaneously in weanling rats for 5 months. CONCLUSIONS: The proposed anticalcification treatment is effective in preventing calcification of GA-treated AVs and PVs implanted subcutaneously in weanling rats for 5 months.

Animals↗
PubMed1997

New-generation valved conduit: an experimental study.

OBJECTIVE: An ideal valved conduit to repair complex congenital heart defects is yet to be developed. In this study we have evaluated the merits of our newly developed calcification-free biologic valve incorporated in a compatible conduit of biologic origin in an animal model. METHODS: Porcine aortic valves and main pulmonary arteries were cross-linked in glutaraldehyde, followed by coupling to partially degraded heparin through an intermediate surface-bound substrate containing amino groups. Because commercially available valves are treated only with glutaraldehyde, control aortic valves and main pulmonary arteries were cross-linked in 0.625% glutaraldehyde. Valved conduits were fabricated from main pulmonary arteries, which were sewn to the aortic and ventricular ends of aortic valves. Valved conduits were examined for calcification and other pathologic changes after being implanted in the descending thoracic aorta in juvenile sheep for 5 months. RESULTS: Severe calcification was noticed in all layers of cusps (calcium, 231.86 +/- 17.90 mg/gm) and aortic wall (calcium, 123.24 +/- 24.72 mg/gm) of aortic valves and main pulmonary arteries (calcium, 135.43 +/- 26.63 mg/gm) of valved conduits treated with 0.625% glutaraldehyde. Cusps (calcium, 1.28 +/- 0.22 mg/gm) of the aortic valve of heparin-bonded conduits did not calcify at all. Only sparse calcific deposits were noticed in the medial layer of the aortic wall (calcium, 25.90 +/- 22.79 mg/gm) of aortic valves and main pulmonary arteries (calcium, 9.64 +/- 10.79 mg/gm) of the valved conduits coupled to heparin. CONCLUSION: Heparin coupling is effective in preventing calcification of glutaraldehyde cross-linked valved conduits implanted in the systemic circulation of juvenile sheep.

Animals↗
PubMed1997

Heparin in calcification prevention of porcine pericardial bioprostheses.

Calcific degeneration is the main cause of failure of glutaraldehyde-treated xenograft heart valve substitutes implanted in humans. Coupling of heparin through an intermediate surface-bound substrate containing amino groups showed complete prevention of calcification of glutaraldehyde-treated porcine pericardium implanted subdermally in weanling rats for 5 months (heparin bonded pericardium: calcium, 0.625 +/- 0.24 mg g(-1); glutaraldehyde-only-treated pericardium: calcium, 228.32 +/- 37.39 mg g(-1); P < 0.0001). Conceivably, inactivation of unpaired aldehyde moieties present in bioprostheses after exposure to glutaraldehyde by amino compounds followed by blocking the potential binding sites of the graft with a surface modifying agent like heparin would be the key steps in the prevention of calcification and degeneration of glutaraldehyde-treated biological tissue grafts.

Animals↗
PubMed1997

Valved conduit in the descending thoracic aorta in juvenile sheep: a useful, cost-effective model for accelerated calcification study in systemic circulation.

To evaluate the efficacy of any new anticalcificant in bioprostheses, a cost-effective and easy circulatory model is proposed. Calcification of 0.625% glutaraldehyde-treated porcine aortic valved conduits implanted in the descending thoracic aorta in 11 juvenile sheep for 5 months was compared with that of leaflets of glutaraldehyde-treated porcine aortic valve implanted subcutaneously in 3-week-old male Wistar rats for the same period. Cusps of valved conduits (Ca, 205.41 +/- 16.24 mg g(-1)) in sheep and aortic valve leaflets in rats (Ca, 235.21 +/- 45.25 mg g(-1)) (P = 0.0299) were severely calcified. Morphological characteristics of calcification of all explants were virtually identical. This model provides a model for testing calcification that lies between the subcutaneous weanling rat model and orthotopic whole valve replacement on the left side of the heart. It is less costly and easier to perform than the latter, but does provide exposure to the bloodstream under pressure, which the rat model does not.

Animals↗