| 1. |
- Matsui, S, et al.
(författare)
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Beneficial effect of angiotensin-converting enzyme inhibitor on dilated cardiomyopathy induced by autoimmune mechanism against beta1-adrenoceptor.
- 2000
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Ingår i: Journal of cardiovascular pharmacology. - 0160-2446. ; 36 Suppl 2
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Tidskriftsartikel (refereegranskat)abstract
- We have shown that a peptide corresponding to the sequence of the second extracellular loop of the human beta1-adrenoceptor (beta1-peptide) was able to induce an autoimmune cardiomyopathy in rabbits. In this study, we examined the effect of angiotensin-converting enzyme inhibitor (ACEI) on beta1-peptide-induced cardiomyopathy. Rabbits were divided into four groups: (1) control group (n= 6) receiving saline injection; (2) beta1-peptide group (n = 8) immunized with beta1-peptide; (3) ACEI group (n = 6), lisinopril (3 mg/day) given orally and receiving saline injection; and (4) ACEI + beta1-peptide group (n = 7), lisinopril (3 mg/day) given orally and immunized with beta1-peptide. Our results showed that, after 1 year, all rabbits in the beta1-peptide group had an increase in heart weight, wall thinning and dilatations of both ventricles as compared with rabbits in the ACEI + beta1-peptide group that had normal heart weight and shape. All rabbits in the beta1-peptide group exhibited multifocal degeneration and necrosis of myocardial cells with moderate infiltration of inflammatory cells. In the ACEI + beta1-peptide group, three rabbits showed focal degeneration and necrosis of myocardial cells accompanied by mononuclear cells. The lesions in this group were apparently less marked than those in the beta1-peptide group. In conclusion, ACEI protects the myocardium from injury induced by an autoimmune mechanism against beta1-adrenoceptor.
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| 2. |
- Matsui, S, et al.
(författare)
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Protective effect of bisoprolol on beta-1 adrenoceptor peptide-induced autoimmune myocardial damage in rabbits.
- 2000
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Ingår i: Herz. - 0340-9937. ; 25:3, s. 267-70
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Tidskriftsartikel (refereegranskat)abstract
- Idiopathic dilated cardiomyopathy is a severe disease of unknown etiology. Accumulating evidence suggests that agonist-like autoantibodies against the beta 1 adrenoceptor in the circulation of dilated cardiomyopathy may play an important role. The aim of this study was to evaluate the effects of the selective beta 1-adrenoceptor blocker, bisoprolol, on beta 1-adrenoceptor peptide induced autoimmune myocardial damage. In the animal model of autoimmune cardiomyopathy induced by active immunization of rabbits with beta 1-adrenoceptor peptide, bisoprolol was given at a dose of 3 mg/day throughout the study period. Our results showed high titer of anti-beta 1-adrenoceptor antibody in the immunized group throughout the study but not in the group receiving only bisoprolol. Cross-reactivity to beta 2 adrenoceptors was observed in some of the immunized rabbits, but disappeared almost entirely after 6 months. As compared to the beta 1-adrenoceptor peptide immunized group without bisoprolol treatment, bisoprolol treated beta 1-receptor peptide immunized group showed increase in the wall thickness and decreases in cavity dimension in anatomical measurements and only mild alterations in macro- and microscopic examinations. Thus, our study clearly demonstrated a beneficial effect of bisoprolol in rabbits who have developed autoimmune myocardial damage.
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| 3. |
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| 4. |
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| 5. |
- Fu, Y, et al.
(författare)
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Formation and charge control of a quantum dot by etched trenches and multiple gates
- 2002
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Ingår i: Applied Physics A. - : Springer Science Business Media. - 0947-8396 .- 1432-0630. ; 74:6, s. 741-745
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Tidskriftsartikel (refereegranskat)abstract
- We have fabricated a GaAs/InGaAs/AlGaAs-based single-electron transistor (SET) formed by etched trenches and multiple gates. Clear Coulomb-blockade oscillations have been observed when the gate biases are scanned. By self-consistently solving three-dimensional Schrodinger and Poisson equations, we have studied the energy-band structure and the carrier distribution of our SET. General agreement between numerical simulation results and measurement data has been obtained, thus indicating the effectiveness of our SET-device design as well as the necessity of a complete three-dimensional quantum-mechanical simulation.
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| 6. |
- Matsui, S, et al.
(författare)
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Beneficial effect of muscarinic-2 antagonist on dilated cardiomyopathy induced by autoimmune mechanism against muscarinic-2 receptor.
- 2001
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Ingår i: Journal of cardiovascular pharmacology. - 0160-2446. ; 38 Suppl 1
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Tidskriftsartikel (refereegranskat)abstract
- We have previously shown that a peptide corresponding to the sequence of the second extracellular loop of the human muscarinic-2 (M2) receptor (M2-peptide) was able to induce an autoimmune cardiomyopathy in rabbits. In this study, we investigated the effect of M2-antagonist (otenzepad) on M2-peptide-induced cardiomyopathy in rabbits. New Zealand White rabbits were divided into four groups: 1) control group, saline injection; 2) M2-peptide group, M2-peptide injection; 3) M2-antagonist group, otenzepad (30 mg/day) orally and saline injection; and (4) M2-antagonist + M2-peptide group, otenzepad (30 mg/day) orally and M2-peptide injection. The study duration was 1 year. Saline or peptide was injected once a month. All rabbits in both the M2-peptide group and the M2-antagonist + M2-peptide group had high titers of anti-M2-autoantibodies in their sera. Rabbits in the M2-peptide group showed an increase in heart weight, wall thinning and dilatation of the right ventricle. On the contrary, rabbits in the M2-antagonist + M2-peptide group had normal heart weight and shape. All rabbits in the M2-peptide group showed multifocal degeneration and necrosis of myocardial cells with moderate infiltration of inflammatory cells, while four rabbits in the M2-antagonist + M2-peptide group showed slight infiltration of inflammatory cells with normal myocardial cells and interstitium, and another three showed no histological changes in the hearts. In conclusion, M2-antagonist protects the myocardium from injury induced by autoimmune mechanism against M2-muscarinic receptor.
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