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Richard H. Finnell

Researcher at Baylor College of Medicine

Publications -  441
Citations -  19138

Richard H. Finnell is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Neural tube & Population. The author has an hindex of 70, co-authored 423 publications receiving 17470 citations. Previous affiliations of Richard H. Finnell include UPRRP College of Natural Sciences & Texas A&M University System.

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Analysis of gene expression in single live neurons.

TL;DR: Electrophysiological analysis coupled with molecular biology within the same cell will facilitate a better understanding of how changes at the molecular level are manifested in functional properties.
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Neural tube defects and folate: case far from closed

TL;DR: Biochemical, genetic and epidemiological observations have led to the development of the methylation hypothesis, which suggests that folic acid prevents neural tube defects by stimulating cellular methylation reactions.
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The Continuing Challenge of Understanding, Preventing, and Treating Neural Tube Defects

TL;DR: The process of neural tube development and how defects in this process lead to NTDs are reviewed and it is suggested that discovering the genetic risk factors for these serious birth defects could provide ways to prevent and treat neural tube defects.
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Practice parameter update: management issues for women with epilepsy - focus on pregnancy (an evidence-based review): teratogenesis and perinatal outcomes. Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society

TL;DR: Reassessment of evidence for management issues related to the care of women with epilepsy (WWE) during pregnancy finds it highly probable that intrauterine first-trimester valproate (VPA) exposure has higher risk of major congenital malformations (MCMs) compared to carbamazepine and possible compared to phenytoin or lamotrigine.
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Mice lacking the folic acid-binding protein Folbp1 are defective in early embryonic development.

TL;DR: The results suggest that Folbp1 has a critical role in folate homeostasis during development, and that functional defects in the human homologue (FOLR1) of FolBP1 may contribute to similar defects in humans.