The UCSD Training Program in Reproductive Sciences takes a multidisciplinary approach to the training of postdoctoral scholars as physician-scientists and basic scientists in the field of neuroendocrine and endocrine control of reproductive processes. Three fellows are supported in two categories: those seeking advanced basic research experience after the Ph.D. or M.D. degree, and those seeking clinical and research training with the aim of becoming board-certified in Reproductive Endocrinology after residency in ob/gyn or in endocrinology after residency in medicine. A cohesive group of faculty members from the Division of Reproductive Endocrinology in the Department of Reproductive Medicine and the Division of Endocrinology in the Department of Medicine at UCSD with common interests and complimentary backgrounds provides basic and clinical training and fosters the careers of the trainees. Many of the faculty members are members of the UCSD NICHD Specialized Cooperative Centers Program in Reproductive Research and many of the senior faculty members are mentors in the NICHD Women's Reproductive Health Research Program for the training of junior faculty members in research careers. Thus, this Training Program is integrated with both NICHD Centers, allowing the teaching staff and fellows to interact at many levels, creating an atmosphere of cooperation, collaboration, and career support. Our research activities range from molecular to patient-oriented research utilizing models from in vitro analysis and cell culture, to whole animal and clinical research. Major foci of investigation include: pituitary and hypothalamic development, ovarian physiology, polycystic ovary disease, signal transduction, GnRH and gonadotropin gene expression and secretion, metabolic impact on reproductive function, activin and growth factors in reproduction, and estrogen replacement therapies. The Program of training for the fellows includes group meetings and presentations, journal clubs, clinical activity and training, laboratory training and independent research, seminars, national meetings, and course work in molecular biology, neuroendocrinology, biostatistics, and ethics.
Our aim i s to prepare physician-scientists and basic scientists to become the future leaders in academic reproductive research. The urgency and importance of producing critically needed basic, translational, and clinical scientists in the area of women's health is well recognized by the leadership of NIH, the scientific community, the national government, and the society as a whole.
|Glidewell-Kenney, Christine A; Trang, Crystal; Shao, Paul P et al. (2014) Neurokinin B induces c-fos transcription via protein kinase C and activation of serum response factor and Elk-1 in immortalized GnRH neurons. Endocrinology 155:3909-19|
|Shayya, Rana F; Rosencrantz, Marcus A; Chuan, Sandy S et al. (2014) Decreased inhibin B responses following recombinant human chorionic gonadotropin administration in normal women and women with polycystic ovary syndrome. Fertil Steril 101:275-9|
|Ahow, Maryse; Min, Le; Pampillo, Macarena et al. (2014) KISS1R signals independently of G?q/11 and triggers LH secretion via the ?-arrestin pathway in the male mouse. Endocrinology 155:4433-46|
|Tolson, Kristen P; Garcia, Christian; Yen, Stephanie et al. (2014) Impaired kisspeptin signaling decreases metabolism and promotes glucose intolerance and obesity. J Clin Invest 124:3075-9|
|Do, Minh-Ha T; Kim, Taeshin; He, Feng et al. (2014) Polyribosome and ribonucleoprotein complex redistribution of mRNA induced by GnRH involves both EIF2AK3 and MAPK signaling. Mol Cell Endocrinol 382:346-57|
|Kim, Taeshin; Do, Minh-Ha T; Lawson, Mark A (2014) Translational control of gene expression in the gonadotrope. Mol Cell Endocrinol 385:78-87|
|Terasaka, Tomohiro; Otsuka, Fumio; Tsukamoto, Naoko et al. (2013) Mutual interaction of kisspeptin, estrogen and bone morphogenetic protein-4 activity in GnRH regulation by GT1-7 cells. Mol Cell Endocrinol 381:8-15|
|Skarra, Danalea V; Arriola, David J; Benson, Courtney A et al. (2013) Forkhead box O1 is a repressor of basal and GnRH-induced Fshb transcription in gonadotropes. Mol Endocrinol 27:1825-39|
|Kim, Joshua; Tolson, Kristen P; Dhamija, Sangeeta et al. (2013) Developmental GnRH signaling is not required for sexual differentiation of kisspeptin neurons but is needed for maximal Kiss1 gene expression in adult females. Endocrinology 154:3273-83|
|Glidewell-Kenney, Christine A; Shao, Paul P; Iyer, Anita K et al. (2013) Neurokinin B causes acute GnRH secretion and repression of GnRH transcription in GT1-7 GnRH neurons. Mol Endocrinol 27:437-54|
Showing the most recent 10 out of 46 publications