Maya Barsky
Baylor College of Medicine
13 Papers
27 Citations
Maya Barsky is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Medicine & Polycystic ovary. The author has an hindex of 3, co-authored 12 publications. Previous affiliations of Maya Barsky include Baystate Medical Center & Boston Children's Hospital.
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Papers
Embryo cryopreservation and preeclampsia risk
Cynthia K. Sites,Donna Wilson,Maya Barsky,Dana Bernson,Ira M. Bernstein,Sheree L. Boulet,Yujia Zhang +6 more
TL;DR: Among ART pregnancies conceived using autologous eggs resulting in live births, those involving transfer of cryopreserved-warmed embryos, as compared with fresh ETs, had increased risk for preeclampsia with severe features and preterm delivery.
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Are perinatal outcomes affected by blastocyst vitrification and warming
TL;DR: In this paper, the authors examined the effect of blastocyst vitrification and warming on perinatal outcomes, including preeclampsia rate, birthweight, percentage of low birthweight and preterm delivery rate.
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Iconographies supplémentaires de l'article : Are perinatal outcomes affected by blastocyst vitrification and warming?
Maya Barsky,Peter St. Marie,Tayyab Rahil,Glenn Markenson,Cynthia K. Sites +4 more
- 26 Oct 2016
TL;DR: It is concluded that embryo vitrification with warming may affect some perinatal outcomes since preeclampsia is increased compared to fresh blastocyst transfer, however, other per inatal outcomes such as low birthweight and preterm delivery rate are not affected.
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Fetal programming of polycystic ovary syndrome: Effects of androgen exposure on prenatal ovarian development.
Maya Barsky,Jamie Merkison,Pardis Hosseinzadeh,L. Yang,Janet Bruno-Gaston,Jay Dunn,William Gibbons,Chellakkan S. Blesson,Chellakkan S. Blesson +8 more
TL;DR: In this paper, the role of excessive prenatal androgens in ovarian development was investigated by identifying how hyperandrogenemia affects gene expression and mitochondria in neonatal ovary, and DHT exposure altered mitochondrial ultrastructure and function by increasing mitochondrial oxygen consumption and decreasing mitochondrial efficiency.
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