Neonatal disorders of germinal matrix
The germinal matrix (GM) is a richly vascularized, transient layer near the ventricles. It produces neurons and glial cells, and is present in the foetal brain between 8 and 36 weeks of gestation. At 25 weeks, it reaches its maximum volume and subsequently withers. The GM is vulnerable to haemorrhage in preterm infants. This selective vulnerability is explained by limited astrocyte end-feet coverage of microvessels, reduced expression of fibronectin and immature tight junctions. Focal lesions in the neonatal period include haemorrhage, germinolysis and stroke. Such lesions in transient layers interrupt normal brain maturation and induce neurodevelopmental sequelae.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2015 |
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Erschienen: |
2015 |
Enthalten in: |
Zur Gesamtaufnahme - volume:28 Suppl 1 |
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Enthalten in: |
The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians - 28 Suppl 1(2015) vom: 24. Nov., Seite 2286-90 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Raets, M M A [VerfasserIn] |
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Links: |
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Themen: |
Fibronectins |
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Anmerkungen: |
Date Completed 23.08.2016 Date Revised 10.11.2015 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.3109/14767058.2013.796169 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM230245153 |
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520 | |a The germinal matrix (GM) is a richly vascularized, transient layer near the ventricles. It produces neurons and glial cells, and is present in the foetal brain between 8 and 36 weeks of gestation. At 25 weeks, it reaches its maximum volume and subsequently withers. The GM is vulnerable to haemorrhage in preterm infants. This selective vulnerability is explained by limited astrocyte end-feet coverage of microvessels, reduced expression of fibronectin and immature tight junctions. Focal lesions in the neonatal period include haemorrhage, germinolysis and stroke. Such lesions in transient layers interrupt normal brain maturation and induce neurodevelopmental sequelae | ||
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