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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Cetin, I; Foidart, JM; Miozzo, M; Raun, T; Jansson, T; Tsatsaris, V; Reik, W; Cross, J; Hauguel-de-Mouzon, S; Illsley, N; Kingdom, J; Huppertz, B.
Fetal growth restriction: a workshop report.
PLACENTA 2004 25: 753-757. Doi: 10.1016/j.placenta.2004.02.004 [OPEN ACCESS]
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Co-Autor*innen der Med Uni Graz
Huppertz Berthold
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Abstract:
Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious, can influence fetal growth by damaging the placenta, leading to IUGR as a result of many possible fetal, placental and maternal disorders. Strict definitions of IUGR and of its severity are needed in order to eventually distinguish among different phenotypes, such as gestational age at onset, degree of growth restriction and presence of hypoxia. This report explores and reviews some of the most recent developments in both clinical and basic research on intrauterine growth restriction, by seeking mechanisms that involve genetic factors, utero-placental nutrient availability and vascular growth factors. New exciting findings on the genomic imprinting defects potentially associated with IUGR, and the placental anomalies associated with the decreased nutrient transport are summarized. Moreover, recent data on angiogenic growth factors as well as new information arising from application of gene chip technologies are discussed.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Angiogenesis Inducing Agents - metabolism
Female - metabolism
Fetal Growth Retardation - etiology
Genomic Imprinting - etiology
Humans - etiology
International Cooperation - etiology
Placenta - metabolism
Pregnancy - metabolism

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