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In the present study, we examine whether selected genetic polymorphisms cont ribute to the development of cerebral palsy (CP) in very preterm infants. Subjec ts were 96 singleton infants with later- diagnosed CP and 119 control children, white non- Hispanic (n for CP = 74, controls = 88) or white Hispanic (CP = 22, controls = 31), born < 32 wk gestation. Presence of CP was identified through state service agencies, with review of medical records. DNA extracted from archi ved neonatal blood was genotyped using multi- locus polymerase chain reaction a mplification and immobilized sequence- specific oligonucleotide probes. Single nucleotide polymorphisms (SNPs) showing evidence of association with development of CP were endothelial nitric oxide synthase (eNOS) A(- 922)G, factor 7 (F7) a rg353gln and del(- 323)10bp- ins, and lymphotoxin A (LTA) thr26asn. In white n on- Hispanic children, beta- 2 adrenergic receptor gln27glu was associated wit h CP risk; in Hispanic children, plasminogen activator inhibitor- 1 (PAI- 1)- 4G(- 675)5G and G11053T were associated with risk of CP. In a logistic regress ion considering these SNPs simultaneously in non- Hispanics, an association wit h CP was observed for heterozygotes of eNOS - 922 (OR 3.0, CI 1.4- 6.4), F7 (O R 2.7, CI 1.1- 6.5), LTA (OR 2.1, CI 1.0- 4.6), and PAI- 1 (OR 3.2, CI 1.2- 8.7). Factor 5, Factor 2, methylene tetrahydrofolate reductase, tumor necrosis f actor- alpha, and other SNPs tested were not significantly associated with CP r isk. We conclude that further study of genetic factors that may influence suscep tibility to CP in very preterm infants is warranted.
In the present study, we examine whether selected genetic polymorphisms cont ribute to the development of cerebral palsy (CP) in very preterm infants. Subjec ts were 96 singleton infants with later-diagnosed CP and 119 control children, white non- Hispanic (n for CP = 74, controls = 88) or white Hispanic (CP = 22, controls = 31), born <32 wk gestation. Presence of CP was identified through state service agencies, with review of medical records. DNA extracted from archi ved neonatal blood was genotyped using multi- locus polymerase chain reaction a mplification and immobilized sequence-specific oligonucleotide probes. Single nucleotide polymorphisms (SNPs) showing evidence of association with development with CP were endothelial nitric oxide synthase (eNOS) A (-922) G, factor 7 (F7) a rg353gln and del (- 323) 10bp-ins, and lymphotoxin A (LTA) thr26asn. In white n on- Hispanic children, beta- 2 adrenergic receptor gln27glu was associated wit h CP risk; in Hispanic children, plasminogen ac Tivator inhibitor-1 (PAI-1) - 4G (- 675) 5G and G11053T were associated with risk of CP. In a logistic regress ion considering these SNPs simultaneously in non- Hispanics, an association wit h CP was observed for heterozygotes of eNOS - 922 (OR 3.0, CI 1.4- 6.4), F7 (OR 2.7, CI 1.1- 6.5), LTA (OR 2.1, CI 1.0- 4.6), and PAI- 1 , Factor 2, methylene tetrahydrofolate reductase, tumor necrosis f actor-alpha, and other SNPs tested were not significantly associated with CP r isk. We conclude that further study of genetic factors that may influence suscep tibility to CP in very preterm infants is warranted.