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- Horsch, S, et al.
(författare)
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Late germinal matrix hemorrhage-like lesions in very preterm infants
- 2010
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Ingår i: Journal of child neurology. - : SAGE Publications. - 1708-8283 .- 0883-0738. ; 25:7, s. 809-814
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Tidskriftsartikel (refereegranskat)abstract
- In preterm infants, the germinal matrix is a common origin of hemorrhages during the first 7 days of life. Sonographically, germinal matrix hemorrhages present as subventricular echodensities evolving into pseudocysts. Similar lesions have been reported as incidental findings also beyond 7 days of life. They may result from vasculitis and ischemic infarction, rather than hemorrhage. To assess the occurrence, time course, and significance for neurodevelopment of such late germinal matrix hemorrhage-like lesions, we reviewed serial cerebral ultrasound examinations obtained in 86 sequentially admitted infants (gestational age <32 weeks or birth weight <1500 g). Neurodevelopment was assessed at 3 years (Bayley Scales of Infant Development). Nine infants had late isolated germinal matrix hemorrhage-like lesions. Their Psychomotor Development Index scores were significantly lower than that in infants without hemorrhage. Our results suggest that late isolated germinal matrix hemorrhage-like lesions are of clinical significance because of their notable incidence and association with neurodevelopmental outcome.
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- Saarikangas, J, et al.
(författare)
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Missing-in-metastasis MIM/MTSS1 promotes actin assembly at intercellular junctions and is required for integrity of kidney epithelia
- 2011
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Ingår i: Journal of cell science. - : The Company of Biologists. - 1477-9137 .- 0021-9533. ; 124:8Pt 8, s. 1245-1255
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Tidskriftsartikel (refereegranskat)abstract
- MIM/MTSS1 is a tissue-specific regulator of plasma membrane dynamics, whose altered expression levels have been linked to cancer metastasis. MIM deforms phosphoinositide-rich membranes through its I-BAR domain and interacts with actin monomers through its WH2 domain. Recent work proposed that MIM also potentiates Sonic hedgehog (Shh)-induced gene expression. Here, we generated MIM mutant mice and found that full-length MIM protein is dispensable for embryonic development. However, MIM-deficient mice displayed a severe urinary concentration defect caused by compromised integrity of kidney epithelia intercellular junctions, which led to bone abnormalities and end-stage renal failure. In cultured kidney epithelial (MDCK) cells, MIM displayed dynamic localization to adherens junctions, where it promoted Arp2/3-mediated actin filament assembly. This activity was dependent on the ability of MIM to interact with both membranes and actin monomers. Furthermore, results from the mouse model and cell culture experiments suggest that full-length MIM is not crucial for Shh signaling, at least during embryogenesis. Collectively, these data demonstrate that MIM modulates interplay between the actin cytoskeleton and plasma membrane to promote the maintenance of intercellular contacts in kidney epithelia.
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