4 Papers
136 Citations
V. Mais is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Luteal phase & Follicular phase. The author has an hindex of 4, co-authored 4 publications. Previous affiliations of V. Mais include Salk Institute for Biological Studies.
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Papers
The dependency of folliculogenesis and corpus luteum function on pulsatile gonadotropin secretion in cycling women using a gonadotropin-releasing hormone antagonist as a probe.
V. Mais,V. Mais,Ralph R. Kazer,Ralph R. Kazer,Nancy S. Cetel,Nancy S. Cetel,J. Rivier,J. Rivier,W. Vale,W. Vale,S. C C Yen,S. C C Yen +11 more
TL;DR: It is inferred that the functional integrity of ovarian cyclicity is remarkably sensitive to brief (3 days) and partial reduction in pulsatile gonadotropin secretion, which disrupts folliculogenic processes and induces the demise of the corpus luteum.
119
The Dependency of Folliculogenesis and Corpus Luteum Function on Pulsatile Gonadotropin Secretion in Cycling Women Using a Gonadotropin-Releasing Hormone Antagonist as a Probe
V. Mais,V. Mais,Ralph R. Kazer,Ralph R. Kazer,Nancy S. Cetel,Nancy S. Cetel,J. Rivier,J. Rivier,W. Vale,W. Vale,S. C C Yen,S. C C Yen +11 more
TL;DR: It is inferred that the functional integrity of ovarian cyclicity is remarkably sensitive to brief (3 days) and partial reduction in pulsatile gonadotropin secretion, which disrupts folliculogenic processes and induces the demise of the corpus luteum.
59
Prolactin-releasing action of gonadotropin-releasing hormone in hypogonadal women.
V. Mais,S. S. C. Yen +1 more
TL;DR: It is demonstrated that in these two hypogonadal models, the PRL response to exogenous GnRH corresponds to the FSH response and suggests that GnRH-stimulated PRL release may be mediated by a paracrine effect between FSH-enriched gonadotrophs and lactOTrophs.
27
Hormonal Dynamics During Luteal-Follicular Transition
TL;DR: The findings indicate that the initiation of folliculogenesis for the ensuing cycle occurs during the late luteal phase by a process of selective augmentation in FSH secretion independent of hypothalamic GnRH secretion.