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10.1097/mop.0b013e328326773b http://scihub22266oqcxt.onion/10.1097/mop.0b013e328326773b 19663040!2726974!19663040     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\19663040.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Pediatr 2009 ; 21 (2): 230-4 Nephropedia Template TP {{tp|p=19663040|t=2009. The developmental origins of adult disease |pdf=|usr=}}{{19663040}} gab.com Text The developmental origins of adult disease JO: Curr Opin Pediatr http://www.kidney.de/pget.php?&tw=1&pmid=19663040 #FOAvip PURPOSE OF REVIEW: Intrauterine growth restriction (IUGR) is associated with an increased propensity to develop adult-onset disease and is described by the developmental origins of adult disease hypothesis. Sequelae of fetal growth restriction include metabolic disease as well as nonmetabolic disorders. Although it has become clear that the morbidities associated with IUGR are complex and result from disruptions to multiple pathways and multiple organs, the mechanisms driving the long-term effects are only just beginning to be understood. RECENT FINDINGS: IUGR affects most organ systems by either interrupting developmental processes such as apoptosis or producing lasting changes to levels of key regulatory factors. Both of these are associated with an often persistent change in gene expression. Epigenetic modulation of transcription is a mechanism that is at least partially responsible for this. IUGR is accompanied by changes in the quantity and activity of enzymes responsible for making modifications to chromatin as well as global and gene-specific modifications of chromatin. SUMMARY: The subtle adjustments needed to ensure developmental plasticity in IUGR are provided by epigenetic modulation of critical genes. Translating the messages of the epigenetic profile and identifying the players that mediate the effects remains one of the major challenges in the field. An understanding of the mechanisms driving the epigenetic changes will facilitate identification of dietary and pharmaceutical approaches that can be applied in the postnatal period. Twit Text FOAVip The developmental origins of adult disease ????Curr Opin Pediatr http://www.kidney.de/pget.php?&tw=1&pmid=19663040 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19663040 #FOAvip English Wikipedia <ref>{{Cite pmid|19663040}}</ref> The developmental origins of adult disease #MMPMID19663040 Joss-Moore LA; Lane RH Curr Opin Pediatr 2009[Apr]; 21 (2): 230-4 PMID19663040show ga PURPOSE OF REVIEW: Intrauterine growth restriction (IUGR) is associated with an increased propensity to develop adult-onset disease and is described by the developmental origins of adult disease hypothesis. Sequelae of fetal growth restriction include metabolic disease as well as nonmetabolic disorders. Although it has become clear that the morbidities associated with IUGR are complex and result from disruptions to multiple pathways and multiple organs, the mechanisms driving the long-term effects are only just beginning to be understood. RECENT FINDINGS: IUGR affects most organ systems by either interrupting developmental processes such as apoptosis or producing lasting changes to levels of key regulatory factors. Both of these are associated with an often persistent change in gene expression. Epigenetic modulation of transcription is a mechanism that is at least partially responsible for this. IUGR is accompanied by changes in the quantity and activity of enzymes responsible for making modifications to chromatin as well as global and gene-specific modifications of chromatin. SUMMARY: The subtle adjustments needed to ensure developmental plasticity in IUGR are provided by epigenetic modulation of critical genes. Translating the messages of the epigenetic profile and identifying the players that mediate the effects remains one of the major challenges in the field. An understanding of the mechanisms driving the epigenetic changes will facilitate identification of dietary and pharmaceutical approaches that can be applied in the postnatal period. |*Fetal Growth Retardation[MESH] |Adult[MESH] |Animals[MESH] |Apoptosis/genetics[MESH] |Chronic Disease[MESH] |Disease Progression[MESH] |Epigenesis, Genetic[MESH] |Fetal Development/genetics[MESH] |Gene Expression Regulation, Developmental[MESH] |Humans[MESH] |Metabolic Diseases/*embryology/genetics[MESH] |Obesity/*embryology/genetics[MESH]The developmental origins of adult disease (epmc).pdf DeepDyve Pubget Overpricing