The urgency and importance of producing critically needed basic, translational, and clinical scientists in the area of women's health and reproduction is well recognized by the leadership of NIH, the scientific community, the national government, and the society as a whole. The UCSD T32 Training Program in Reproductive Sciences takes a unique multidisciplinary approach to the training of postdoctoral scholars as physician- scientists and reproductive biologists in the field of neuroendocrine and endocrine control of reproductive processes. The combination of clinical, physiological, and molecular approaches to reproductive biology and medicine creates an exceptional opportunity for the training of physician-scientists and basic scientists, as well- rounded reproductive endocrinologists who become extraordinarily qualified for academic careers. The program supports both fellows seeking advanced basic/translational research experience after the Ph.D. and/or M.D. degree, and those seeking clinical and research training with the aim of becoming board-certified in Reproductive Endocrinology and Infertility and continuing in academic clinical research. We have an outstanding 30-year track record as recognized by an NIH MENTOR AWARD that extended the program for 10 years from 2003-2012. A cohesive group of NIH-funded faculty 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, shared grants, joint publications, and complimentary backgrounds, provides basic, translational, and clinical training and fosters the success and careers of the trainees. All faculty are members of the UCSD NICHD U54 Specialized Cooperative Centers Program in Reproductive and Infertility Research and all of the senior faculty members are mentors in the UCSD NICHD K12 Women's Reproductive Health Research Program for the training of OB/GYN junior faculty in research careers. Thus, this training program is integrated with both NICHD Centers, allowing the faculty and fellows to interact at many levels, creating an atmosphere of cooperation, collaboration, mentoring, 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: gonadal, pituitary and hypothalamic development, ovarian physiology, polycystic ovary disease, signal transduction, Kisspeptin, NeurokininB, GnRH, and gonadotropin gene expression and secretion, metabolic impact on reproductive function, and activin and growth factors in reproduction. The program of training for the fellows includes group meetings and presentations, journal clubs, seminars, national meetings, clinical activity and training, laboratory training, independent research, grantsmanship training, and coursework in molecular biology, neuroendocrinology, bio- statistics, and ethics, and an innovative "Thesis Committee" mentoring structure.
Our aim i s to prepare outstanding physician-scientists and basic scientists to become the future leaders in academic reproductive research.
The UCSD Training Program in Reproductive Sciences takes a multidisciplinary approach to prepare physician-scientists and reproductive biologists to become the future leaders in academic reproductive research. Postdoctoral scholars with Ph.D. and/or M.D. degrees are trained in the fields of reproductive neuroendocrine and gonadal physiology and development through advanced basic research experiences or engaging in clinical investigation of reproductive endocrine disorders. A cohesive, highly interactive group of faculty mentors from the Division of Reproductive Endocrinology in the Department of Reproductive Medicine and the Division of Endocrinology in the Department of Medicine with common interests, shared grants, co- authored publications, and complimentary backgrounds, provides intensive basic and clinical research training and fosters the careers of outstanding postdoctoral trainees within the environment of the Center for Reproductive Science and Medicine at UCSD.
|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|
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