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.
|Stephens, Shannon B Z; Chahal, Navdeep; Munaganuru, Nagambika et al. (2016) Estrogen Stimulation of Kiss1 Expression in the Medial Amygdala Involves Estrogen Receptor-Î± But Not Estrogen Receptor-Î². Endocrinology 157:4021-4031|
|Mora-Castilla, Sergio; To, Cuong; Vaezeslami, Soheila et al. (2016) Miniaturization Technologies for Efficient Single-Cell Library Preparation for Next-Generation Sequencing. J Lab Autom 21:557-67|
|Kelley, Scott T; Skarra, Danalea V; Rivera, Alissa J et al. (2016) The Gut Microbiome Is Altered in a Letrozole-Induced Mouse Model of Polycystic Ovary Syndrome. PLoS One 11:e0146509|
|Schoeller, Erica L; Clark, Daniel D; Dey, Sandeepa et al. (2016) Bmal1 Is Required for Normal Reproductive Behaviors in Male Mice. Endocrinology 157:4914-4929|
|Huang, Polly P; Brusman, Liza E; Iyer, Anita K et al. (2016) A Novel Gonadotropin-Releasing Hormone 1 (Gnrh1) Enhancer-Derived Noncoding RNA Regulates Gnrh1 Gene Expression in GnRH Neuronal Cell Models. PLoS One 11:e0158597|
|De Bond, Julie-Ann P; Tolson, Kristen P; Nasamran, Chanond et al. (2016) Unaltered Hypothalamic Metabolic Gene Expression in Kiss1r Knockout Mice Despite Obesity and Reduced Energy Expenditure. J Neuroendocrinol 28:|
|Maas, Kevin H; Chuan, Sandy; Harrison, Evan et al. (2016) Androgen responses to adrenocorticotropic hormone infusion among individual women with polycystic ovary syndrome. Fertil Steril 106:1252-1257|
|Luo, Elena; Stephens, Shannon B Z; Chaing, Sharon et al. (2016) Corticosterone Blocks Ovarian Cyclicity and the LH Surge via Decreased Kisspeptin Neuron Activation in Female Mice. Endocrinology 157:1187-99|
|Lu, JingWei; Plank, Terra-Dawn; Su, Fang et al. (2016) The nonsense-mediated RNA decay pathway is disrupted in inflammatory myofibroblastic tumors. J Clin Invest 126:3058-62|
|Shum, Eleen Y; Jones, Samantha H; Shao, Ada et al. (2016) The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay. Cell 165:382-95|
Showing the most recent 10 out of 89 publications