| 1. |
|
|
| 2. |
- Hallin, Caroline, et al.
(författare)
-
De värsta konsekvenserna av Babet ligger framför oss
- 2024
-
Ingår i: Sydsvenskan. - 1652-814X.
-
Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Debattartikel om kustskydd och brister i framförhållningen inför kommande stormar under Aktuella frågor i Sydsvenskan.
|
|
| 3. |
- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
-
Voluntary chronic exercise augments in vivo natural immunity in rats.
- 1996
-
Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - 8750-7587. ; 80:5, s. 1799-803
-
Tidskriftsartikel (refereegranskat)abstract
- The effect of chronic voluntary exercise on the immune response was studied in spontaneously hypertensive rats. Exercise consisted of voluntary running in wheels for 5 wk, and the mean running distance was 4.2 km/24 h. In vivo cytotoxicity was measured as clearance of injected 51Cr-labeled YAC-1 lymphoma cells from the lungs. The clearance of YAC-1 cells in vivo was significantly increased in runners compared with sedentary controls (P < 0.001). The total number of mononuclear cells in the spleen was significantly decreased in runners compared with controls. Analysis of splenic lymphocyte phenotypes revealed a significantly increased fraction of OX52+/CD5- natural killer cells in runners compared with sedentary controls. In contrast to changes in natural immunity, immunoglobulins G and M levels in serum, the antibody response to antigen in vivo, and the proliferation of splenic T cells in vitro were unchanged. Our data suggest that chronic voluntary exercise augments natural cytotoxicity mechanisms in vivo, whereas splenic T-cell proliferation and the antibody-mediated immune response remain unchanged.
|
|
| 4. |
- Pontén, Annica, et al.
(författare)
-
Transgenic overexpression of platelet-derived growth factor-C in the mouse heart induces cardiac fibrosis, hypertrophy, and dilated cardiomyopathy
- 2003
-
Ingår i: American Journal of Pathology. - 0002-9440 .- 1525-2191. ; 163:2, s. 673-682
-
Tidskriftsartikel (refereegranskat)abstract
- The platelet-derived growth factors are implicated in development of fibrotic reactions and disease in several organs. We have overexpressed platelet-derived growth factor-C in the heart using the alpha-myosin heavy chain promoter and created a transgenic mouse that exhibits cardiac fibrosis followed by hypertrophy with sex-dependent phenotypes. The transgenic mice developed several pathological changes including cardiac fibroblast proliferation and deposition of collagen, hypertrophy, vascular defects, and the presence of Anitschkow cells in the adult myocardium. Male mice developed a hypertrophic phenotype, whereas female mice were more severely affected and developed dilated cardiomyopathy, leading to heart failure and sudden death. The vascular defects initially included dilation of microvessels and vascular leakage. Subsequently, a marked loss of microvessels, formation of large vascular sac-like structures, and an increased density of smooth muscle-coated vessels were observed in the myocardium. In part, the observed vascular changes may be because of an up-regulation of vascular endothelial growth factor in cardiac fibroblasts of the transgenic hearts. This unique animal model reveals that a potent mitogen for cardiac fibroblasts result in an expansion of the interstitium that induce a secondary sex-dependent hypertrophic response in the cardiomyocytes.
|
|
