Publications by authors named "Eugene Galdones"

Background: The maturation of the female germ cell, the oocyte, requires the synthesis and storing of all the necessary metabolites to support multiple divisions after fertilization. Oocyte maturation is only possible in the presence of surrounding, diverse, and changing layers of somatic cells. Our understanding of metabolic interactions between the oocyte and somatic cells has been limited due to dynamic nature of ovarian follicle development, thus warranting a systems approach.

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In vitro follicle growth has emerged as a technology that can provide new information about folliculogenesis and serve as part of a suite of methods currently under development to assist women whose fertility is threatened by cancer treatments. Though it has been shown that in vitro-grown follicles secrete peptide and steroid hormones, much of the follicular transcriptome remains unknown. Thus, microarray analysis was performed to characterize the transcriptome and secretome of in vitro-grown follicles.

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Context: A previous genome-wide association study in Chinese women with polycystic ovary syndrome (PCOS) identified a region on chromosome 2p16.3 encoding the LH/choriogonadotropin receptor (LHCGR) and FSH receptor (FSHR) genes as a reproducible PCOS susceptibility locus.

Objective: The objective of the study was to determine the role of the LHCGR and/or FSHR gene in the etiology of PCOS in women of European ancestry.

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Vitamin A derivatives modulate gene expression through retinoic acid and rexinoid receptor (RAR/RXR) heterodimers and are indispensable for limb development. Of particular interest, RARgamma is highly expressed in cartilage, a target affected following retinoid-induced limb insult. The goal of this study was to examine how selective activation of RARgamma affects limb development.

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Background: Derivatives of retinol (vitamin A), commonly referred to as retinoids, signal through retinoic acid and retinoid X receptors (RARs/RXRs) and are essential for normal limb formation. Retinoid imbalances or perturbations in receptor function result in aberrant limb development. To examine the mechanisms underlying retinol-induced limb defects, we determined the responsiveness of limbs from RARalpha1-/-gamma mice to excess retinol in vitro.

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