This training program provides basic and clinical-translational research training for Neonatology and Maternal- Fetal Medicine physicians (board eligible or certified in their primary specialty) and Basic Scientists who have completed a PhD degree. The research training includes concepts and techniques in perinatal/developmental physiology, biochemistry, and cell and molecular biology. Training is for 2-3 years in preparation for academic careers in reproductive medicine within departments of Pediatrics and Obstetrics &-Gynecology or in basic science departments with direct links to the clinical departments. Trainees will be appointed after demonstrating research commitment and accomplishment during their 1st 2 years of fellowship/postdoctoral training, which will be balanced by 4th and/or 5th years of training as Fellow/Instructors but with Assistant Professor salaries. During the first year in the T32 program, trainees work with faculty advisors to select basic research projects and mentors. Research mentors, projects, and labs are selected among current T32 faculty, but include the breadth of faculty and research opportunities and facilities on the UCD Medical Campus. Each area includes clinical- translational, whole animal, organ, cell, and molecular research so that a trainee can participate at any one or several levels of biological investigation. Trainees attend seminars that review intrauterine development and fetal, maternal, and neonatal physiology. Courses in the graduate school dealing with cell culture, genetics, developmental biology, cell and molecular biology, isotope applications, biostatistics, data processing and informatics, statistics, graphics and imaging, bioethics, and ethical conduct of research are included. Seminar programs in research design and abstract and manuscript preparation are provided. The 2nd and 3rd years are devoted to the completion of the research projects begun in the 1st year and expansion into new areas of research and new research techniques. Each trainee develops institutional animal and clinical research protocols to address technical and ethical issues involved in human and animal research. Trainees plan and conduct their research projects as independently as they can, but with full faculty mentoring. This program provides multidisciplinary training in basic and clinical-translational biological investigation, integrating state-of-the-art research techniques with important questions in perinatal medicine and biology. This approach equips the trainees with the capacity to move independently and successfully into academic careers in either basic or clinical-translational science. Over many years, graduates of this training program have achieved high academic positions nationally and internationally and have had major impact on developing and supporting research training programs. Such ultimate research/academic leadership is a major aim of this program.

Public Health Relevance

The primary purpose of this Training Program is to develop academic leaders among Neonatologists, Maternal- Fetal Medicine (MFM) Specialists, and Basic Scientists who know how to work together collaboratively and who have the capacity, based on personal meritorious accomplishment in research, to identify, understand, and solve important problems in reproductive (perinatal) biology and medicine. Research accomplishment and academic achievement are intimately intertwined goals and are fundamental and inseparable for achieving academic and research success. Through top academic leadership positions, our graduates have made major national impact on research program development and support.

National Institute of Health (NIH)
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Institutional National Research Service Award (T32)
Project #
Application #
Study Section
Developmental Biology Subcommittee (CHHD)
Program Officer
Raju, Tonse N
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Colorado Denver
Schools of Medicine
United States
Zip Code
Soto, Susan M; Blake, Amy C; Wesolowski, Stephanie R et al. (2017) Myoblast replication is reduced in the IUGR fetus despite maintained proliferative capacity in vitro. J Endocrinol 232:475-491
Deng, Guiying; Orfila, James E; Dietz, Robert M et al. (2017) Autonomous CaMKII Activity as a Drug Target for Histological and Functional Neuroprotection after Resuscitation from Cardiac Arrest. Cell Rep 18:1109-1117
Qiao, Liping; Wattez, Jean-Sebastien; Lee, Samuel et al. (2017) Adiponectin Deficiency Impairs Maternal Metabolic Adaptation to Pregnancy in Mice. Diabetes 66:1126-1135
Rudolph, M C; Young, B E; Lemas, D J et al. (2017) Early infant adipose deposition is positively associated with the n-6 to n-3 fatty acid ratio in human milk independent of maternal BMI. Int J Obes (Lond) 41:510-517
Checkley, L Allyson; Rudolph, Michael C; Wellberg, Elizabeth A et al. (2017) Metformin Accumulation Correlates with Organic Cation Transporter 2 Protein Expression and Predicts Mammary Tumor Regression In Vivo. Cancer Prev Res (Phila) 10:198-207
Barry, James S; Rozance, Paul J; Brown, Laura D et al. (2016) Increased fetal myocardial sensitivity to insulin-stimulated glucose metabolism during ovine fetal growth restriction. Exp Biol Med (Maywood) 241:839-47
Rudolph, Michael C; Young, Bridget E; Jackson, Kristina Harris et al. (2016) Human Milk Fatty Acid Composition: Comparison of Novel Dried Milk Spot Versus Standard Liquid Extraction Methods. J Mammary Gland Biol Neoplasia 21:131-138
Wesolowski, Stephanie R; Hay Jr, William W (2016) Role of placental insufficiency and intrauterine growth restriction on the activation of fetal hepatic glucose production. Mol Cell Endocrinol 435:61-68
Lemas, Dominick J; Young, Bridget E; Baker 2nd, Peter R et al. (2016) Alterations in human milk leptin and insulin are associated with early changes in the infant intestinal microbiome. Am J Clin Nutr 103:1291-300
Heinz, Richard E; Rudolph, Michael C; Ramanathan, Palani et al. (2016) Constitutive expression of microRNA-150 in mammary epithelium suppresses secretory activation and impairs de novo lipogenesis. Development 143:4236-4248

Showing the most recent 10 out of 50 publications