| 1. |
- 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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| 2. |
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| 3. |
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| 4. |
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| 5. |
- Li, Z-F, et al.
(författare)
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Determination of carrier-transfer length from side-wall quantum well to quantum wire by micro-photoluminescence scanning
- 2003
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Ingår i: Journal of Electronic Materials. - : Springer Science Business Media. - 0361-5235 .- 1543-186X. ; 32:8, s. 913-916
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Tidskriftsartikel (refereegranskat)abstract
- Micro-photoluminescence (mu-PL) line scanning across a single V-groove, GaAs/AlGaAs quantum wire (QWR) has been performed at room temperature, revealing a clear spatial-dependence of the PL. After fitting each PL spectrum by multi-Gaussian line shapes, intensity profiles of each PL component from confined structures have been obtained as functions of the scanning position. The PL quenching of a side-wall quantum well (SQWL) has been recognized in a certain area in the vicinity of the QWR and is interpreted by carrier transfer into the QWR within effective transfer length. By simulating the carrier-transfer process from SQWL to QWR as a convolution of a step function for carrier distribution and a Gaussian function for exciting laser irradiance, the effective transfer length of about 1.8+/-0.3 mum has, therefore, been concluded.
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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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| 7. |
- Song, B C, et al.
(författare)
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Methimazole interferes with the progression of experimental autoimmune myocarditis in rats.
- 2001
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Ingår i: Autoimmunity. - 0891-6934. ; 34:4, s. 265-74
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Tidskriftsartikel (refereegranskat)abstract
- In order to ascertain whether methimazole, a drug commonly used for the treatment of hyperthyroidism, interferes with the progression of autoimmune-mediated myocardial injury, we investigated the effect of methimazole on experimental autoimmune myocarditis (EAM) in rats. EAM was induced by immunization with porcine cardiac myosin. Methimazole administration markedly slowed the body weight growth in both normal and EAM rats, but did not induce morphologic change of cardiac tissue in normal rats. In EAM rats, macroscopic examination revealed discoloration of the cardiac surface, and histopathological examination by light microscopy showed extensive myocardial necrosis, infiltration by inflammatory cells and myocardial fibrosis. In the EAM rats treated with methimazole, the discolored areas on the cardiac surface were markedly diminished in size, and the myocardial necrosis, cellular infiltration and fibrosis were significantly less severe. To identify the mechanism responsible of this effect, we investigated the change of regulatory lymphocyte subsets in peripheral blood using an immunofluorescence technique with a flow cytometer. A decrease in the helper/suppressor T cell ratio as a result of the increased proportion of suppressor T cells and a decrease in the proportion of B cells were observed in normal rats after methimazole administration, and similar findings were made in the EAM rats treated with methimazole. These results indicate that methimazole interferes with the progression of EAM, and immunosuppression may, at least in part, be involved in the inhibitory effect of methimazole on EAM in rats.
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| 8. |
- Zong, Z P, et al.
(författare)
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Growth hormone interferes with the progression of myocarditis in rats.
- 2001
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Ingår i: European journal of pharmacology. - 0014-2999. ; 415:1, s. 51-60
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Tidskriftsartikel (refereegranskat)abstract
- In this study, we investigated whether recombinant human growth hormone (rhGH) influences the progression of myocarditis. We induced experimental autoimmune myocarditis in F344 rats by subcutaneous injection of cardiac myosin, and divided the rats into three groups: (1) control group, saline injection; (2) pre-treated group, subcutaneous injection of rhGH (100 mIU/rat/day for 10 days) before induction of experimental autoimmune myocarditis; and (3) post-treated group, subcutaneous injection of rhGH (100 mIU/rat/day for 10 days) after induction of experimental autoimmune myocarditis. On the 35th day after induction of experimental autoimmune myocarditis, all rats were sacrificed and the hearts were examined. The increase in body weight was smaller in the control group than the pre-treated group and the rate of heart weight/body weight was larger in the control group than in the two treated groups. Histopathologically, rats in the control group showed multifocal infiltration by inflammatory cells, mainly neutrophils, lymphocytes and macrophages, extensive fibrosis, and a higher proportion of mast cells in the inflamed region. In contrast, rats in the two treated groups showed only minor changes. We found that rhGH did not influence the distribution of lymphocytes in peripheral blood in the three groups, and that rhGH induced G1 checkpoint dysfunction, thereby arresting the cell cycle in G1 and inhibiting the proliferation of mast cells in vitro. These findings suggest a possible role for mast cells in the progression of myocarditis and the rhGH may be a candidate for use as a new tool to treat myocarditis.
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| 10. |
- Carolipio, E. M., et al.
(författare)
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The toroidicity-induced Alfven eigenmode structure in DIII-D : Implications of soft x-ray and beam-ion loss data
- 2001
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Ingår i: Physics of Plasmas. - : AIP Publishing. - 1070-664X .- 1089-7674. ; 8:7, s. 3391-3401
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Tidskriftsartikel (refereegranskat)abstract
- The internal structure of the toroidicity-induced Alfven eigenmode (TAE) is studied by comparing soft x-ray profile and beam ion loss data taken during TAE activity in the DIII-D tokamak [W. W. Heidbrink , Nucl. Fusion 37, 1411 (1997)] with predictions from theories based on ideal magnetohydrodynamic (MHD), gyrofluid, and gyrokinetic models. The soft x-ray measurements indicate a centrally peaked eigenfunction, a feature which is closest to the gyrokinetic model's prediction. The beam ion losses are simulated using a guiding center code. In the simulations, the TAE eigenfunction calculated using the ideal MHD model acts as a perturbation to the equilibrium field. The predicted beam ion losses are an order of magnitude less than the observed similar to6%-8% losses at the peak experimental amplitude of deltaB(r)/B(0)similar or equal to2-5x10(-4).
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