The goal of this doctoral and postdoctoral training program is to educate scientists who will provide fundamental insights into the causes and prevention of birth defects and functional abnormalities of prenatal origin. Predoctorates are selected from among interested Molecular and Developmental Biology (MDB) Program graduate students who all take classes in developmental biology, molecular genetics, cell biology and biochemistry as their core curriculum;teratology students take these classes and courses in teratology, biostatistics (new requirement), and toxicology (optional). Neuroteratology students take the aforementioned courses and courses in neuroscience. Postdoctorates also take the teratology course and all pre- and postdoctorates take an ethics in research course. Postdoctorates enter the training program through the Cincinnati Children's Research Foundation (CCRF) Office of Postdoctoral Affairs (new). All of the training faculty operate active, extramurally funded laboratories and all have experience training graduate students and postdoctorates. As a result, trainees show high research productivity, attend national meetings, and secure good positions upon completion. A high percentage of past trainees remain in science, most in teratology, thereby helping to fill the national need for scientists in this specialty. Accordingly, four predoctoral and three postdoctoral positions are requested (as before). During the current funding period, the program had its first URM trainee;in addition, several curriculum changes have been made that strengthen training in developmental genetics, and a new research building and new core facilities are being built that will add to the current research environment. Faculty membership continues to evolve with new faculty added during this period and faculty research shifting toward more investigations involving environmental agents and their effects on development. This program fills a unique niche as the only NIEHS training grant dedicated to training in teratology. This is important because teratology is not a field with its own academic home because it spans disciplines ranging from developmental biology to genetics, and toxicology to neurobiology. This renewal represents a continuation of the strengths of the program from the past and adds new initiatives that will move teratology training to the next level in understanding the mechanisms of abnormal development. BACKGROUND This NIEHS training program was established in 1977. Since the last competing renewal several mentors resigned from the program due to retirement, or because they are no longer accepting trainees or they are shifting focus away from areas directly relevant to the NIEHS mission. Conversely, the training program added five new faculty members (Drs. Campbell, Karp, Kuan, Wells, and Williams) who have research programs relevant to the training program. The training program has also retained seven continuing faculty members (Drs. Daston, Ma, Nebert, Potter, Scott, Vorhees, and Yutzey) from the previous funding cycle. Several curriculum changes have been made that have strengthen the training in developmental genetics, and a new research building and new Core facilities are being built that will add to the current research environment. This application represents a continuation of the strengths of the program from the past and adds new initiatives that will move teratology training to the next level in understanding the mechanisms of abnormal development

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Institutional National Research Service Award (T32)
Project #
5T32ES007051-35
Application #
8101140
Study Section
Environmental Health Sciences Review Committee (EHS)
Program Officer
Shreffler, Carol K
Project Start
1977-07-01
Project End
2012-06-30
Budget Start
2011-07-01
Budget End
2012-06-30
Support Year
35
Fiscal Year
2011
Total Cost
$167,236
Indirect Cost
Name
Cincinnati Children's Hospital Medical Center
Department
Type
DUNS #
071284913
City
Cincinnati
State
OH
Country
United States
Zip Code
45229
Millington, Grethel; Elliott, Kelsey H; Chang, Ya-Ting et al. (2017) Cilia-dependent GLI processing in neural crest cells is required for tongue development. Dev Biol 424:124-137
Jablonski, Sarah A; Graham, Devon L; Vorhees, Charles V et al. (2017) Effects of Neonatal Methamphetamine and Stress on Brain Monoamines and Corticosterone in Preweanling Rats. Neurotox Res 31:269-282
Hufgard, J R; Williams, M T; Vorhees, C V (2017) Phosphodiesterase-1b deletion confers depression-like behavioral resistance separate from stress-related effects in mice. Genes Brain Behav 16:756-767
Amos-Kroohs, Robyn M; Davenport, Laurie L; Atanasova, Nina et al. (2017) Developmental manganese neurotoxicity in rats: Cognitive deficits in allocentric and egocentric learning and memory. Neurotoxicol Teratol 59:16-26
Rowley, Shane; Sun, Xiaofei; Lima, Isabel V et al. (2017) Cannabinoid receptor 1/2 double-knockout mice develop epilepsy. Epilepsia 58:e162-e166
Amos-Kroohs, Robyn M; Graham, Devon L; Grace, Curtis E et al. (2016) Developmental stress and lead (Pb): Effects of maternal separation and/or Pb on corticosterone, monoamines, and blood Pb in rats. Neurotoxicology 54:22-33
Vorhees, Charles V; Williams, Michael T (2016) Cincinnati water maze: A review of the development, methods, and evidence as a test of egocentric learning and memory. Neurotoxicol Teratol 57:1-19
Braun, Amanda A; Amos-Kroohs, Robyn M; Gutierrez, Arnold et al. (2016) 6-Hydroxydopamine-Induced Dopamine Reductions in the Nucleus Accumbens, but not the Medial Prefrontal Cortex, Impair Cincinnati Water Maze Egocentric and Morris Water Maze Allocentric Navigation in Male Sprague-Dawley Rats. Neurotox Res 30:199-212
Amos-Kroohs, Robyn M; Davenport, Laurie L; Gutierrez, Arnold et al. (2016) Developmental manganese exposure in combination with developmental stress and iron deficiency: Effects on behavior and monoamines. Neurotoxicol Teratol 56:55-67
Perna, Marla K; Kokenge, Amanda N; Miles, Keila N et al. (2016) Creatine transporter deficiency leads to increased whole body and cellular metabolism. Amino Acids 48:2057-65

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