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- Fu, Ying, 1964, et al.
(författare)
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Photoluminescence spectra of doped GaAs films
- 2004
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Ingår i: Applied Physics A. - : Springer Science Business Media. - 0947-8396 .- 1432-0630. ; 79:3, s. 619-623
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Tidskriftsartikel (refereegranskat)abstract
- We have studied the dependence of the photoluminescence (PL) spectrum on the doping level and the film thickness of n-GaAs thin films, both experimentally and theoretically. It has been shown theoretically that modification of the PL spectrum of p-type material by p-type doping is very small due to the large valence-band hole effective mass. The PL spectrum of n-type material is affected by two factors: (1) the electron concentration which determines the Fermi level in the material; (2) the thickness of the film due to re-absorption of the PL signal. For the n-type GaAs thin films under current investigation, the doping level as well as the film thickness can be very well calibrated by the PL spectrum when the doping level is less than 2 x 10(18) cm(-3) and the film thickness is in the range of the penetration length of the PL excitation laser.
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- Larsson, Lisa, 1976, et al.
(författare)
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Beneficial effect on cardiac function by intravenous immunoglobulin treatment in patients with dilated cardiomyopathy is not due to neutralization of anti-receptor autoantibody
- 2004
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Ingår i: Autoimmunity. - 0891-6934. ; 37:6-7, s. 489-493
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Tidskriftsartikel (refereegranskat)abstract
- Anti-beta1-adrenoceptor (beta1AR) autoantibodies have been shown to be pathophysiologically important in idiopathic dilated cardiomyopathy (DCM). Treatment with intravenous immunoglobulin (IVIG) has shown beneficial effects in both DCM and ischemic cardiomyopathy. However, the underlying mechanism has not been clarified. In the present study, we therefore examined whether the improvement of cardiac function was due to neutralization of functional beta1AR autoantibodies by anti-idiotypic antibodies. Autoantibodies against the beta1AR was analysed in sera from patients with DCM and coronary artery disease (CAD) treated with IVIG or placebo before, 6 and 12 months. Six month after treatment, DCM patients showed increase in beta1AR autoantibodies, mostly in IgG1 and IgG2, whereas in CAD patients mostly in IgG2. No changes in beta1AR autoantibodies after 12 months were detected. In summary, our results indicate that improvement of cardiac function by IVIG is not due to neutralization of beta1AR autoantibodies.
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- 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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