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- Hansson, A C, et al.
(författare)
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Corticosterone actions on the hippocampal brain-derived neurotrophic factor expression are mediated by exon IV promoter.
- 2006
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Ingår i: Journal of neuroendocrinology (Print). - : Wiley. - 0953-8194 .- 1365-2826. ; 18:2, s. 104-114
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Tidskriftsartikel (refereegranskat)abstract
- Brain-derived neurotrophic factor (BDNF) expression is strongly regulated by adrenocorticosteroids via activated gluco- and mineralocorticoid receptors. Four separate promoters are located upstream of the BDNF noncoding exons I to IV and may thus be involved in adrenocorticosteroid-mediated gene regulation. In adrenalectomised rats, corticosterone (10 mg/kg s.c.) induces a robust down-regulation of both BDNF mRNA and protein levels in the hippocampus peaking at 2-8 h. To study the role of the individual promoters in the corticosterone response, we employed exon-specific riboprobe in situ hybridisation as well as real-time polymerase chain reaction (PCR) in the dentate gyrus. We found a down-regulation, mainly of exon IV and the protein-coding exon V, in nearby all hippocampal subregions, but exon II was only down-regulated in the dentate gyrus. Exon I and exon III transcripts were not affected by corticosterone treatment. The results could be confirmed with real-time PCR in the dentate gyrus. It appears as if the exon IV promoter is the major target for corticosterone-mediated transcriptional regulation of BDNF in the hippocampus.
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- Holzapfel, Gerhard A., et al.
(författare)
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Layer-specific 3D residual deformations of human aortas with non-atherosclerotic intimal thickening
- 2007
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Ingår i: Annals of Biomedical Engineering. - : Springer Science and Business Media LLC. - 0090-6964 .- 1573-9686. ; 35:4, s. 530-545
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Tidskriftsartikel (refereegranskat)abstract
- Data relating to residual deformations in human arteries are scarce. In this paper we investigate three-dimensional residual deformations for intact strips and for their separate layers from human aortas in their passive state. From 11 abdominal aortas with identified anamnesis, 16 pairs of rings and axial strips were harvested, and the rings cut open. After 16 h images of the resulting geometries were recorded, and the strips were separated into their three layers; after another 6 h images were again recorded. Image processing and analysis was then used to quantify residual stretches and curvatures. For each specimen histological analysis established that the intima, media and adventitia were clearly separated, and the separation was atraumatic. Axial in situ stretches were determined to be 1.196 +/- 0.084. On separation, the strips from the adventitia and media shortened (between 4.03 and 8.76% on average), while the intimal strips elongated on average by 3.84% (circumferential) and 4.28% (axial) relative to the associated intact strips. After separation, the adventitia from the ring sprang open by about 180 degrees on average, becoming flat, the intima opened only slightly, but the media sprang open by more than 180 degrees (as did the intact strip). The adventitia and intima from the axial strips remained flat, while the media (and the intact strip) bent away from the vessel axis. This study has shown that residual deformations are three dimensional and cannot be described by a single parameter such as 'the' opening angle. Their quantification and modeling therefore require consideration of both stretching and bending, which are highly layer-specific and axially dependent.
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- Wurdak, H, et al.
(författare)
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Inactivation of TGF beta signaling in neural crest stem cells leads to multiple defects reminiscent of DiGeorge syndrome
- 2005
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Ingår i: Genes & Development. - : Cold Spring Harbor Laboratory. - 1549-5477 .- 0890-9369. ; 19:5, s. 530-535
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Tidskriftsartikel (refereegranskat)abstract
- Specific inactivation of TGFbeta signaling in neural crest stem cells (NCSCs) results in cardiovascular defects and thymic, parathyroid, and craniofacial anomalies. All these malformations characterize DiGeorge syndrome, the most common microdeletion syndrome in humans. Consistent with a role of TGFbeta in promoting non-neural lineages in NCSCs, mutant neural crest cells migrate into the pharyngeal apparatus but are unable to acquire non-neural cell fates. Moreover, in neural crest cells, TGFbeta signaling is both sufficient and required for phosphorylation of CrkL, a signal adaptor protein implicated in the development of DiGeorge syndrome. Thus, TGFbeta signal modulation in neural crest differentiation might play a crucial role in the etiology of DiGeorge syndrome.
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