To provide resources and facilitate the transfer of knowledge gained through studies in clinical applications of basic science methodologies, a cohort of established Pediatric investigators and established investigators in basic science departments at Vanderbilt whose research address issues of normal and perturbed ontogeny will pool their experience, talents and resources to establish a Child Health Research Center that provides shared CORE Laboratories and training for Junior Pediatric faculty. The theme of the Vanderbilt CHRC, molecular regulation of growth and development, was chosen to intensify and expand studies of the mechanisms that control normal growth and function at a molecular level. Perturbation of molecular regulation by genetic or environmental factors potentially contributes to all disease processes, particularly those affecting children. Furthermore, better understanding of molecular regulation will provide insights to our understanding, diagnosis and treatment of diseases that affect children. Our overall goal is to contribute to the understanding of the molecular mechanisms that regulate cell and tissue growth and function in normal and deranged development. To achieve this goal we plan the following specific aims: 1) develop an administrative and organizational structure to support the Vanderbilt CHRC, 2, enhance the quality and productivity of all CHRC investigators by facilitating access to current concepts and techniques applicable to studies of the molecular bases of disease pathogenesis, (3) support research initiatives by Junior Pediatric faculty in studying diseases of childhood that perturb normal growth and development at a molecular level, 4) support new initiatives in research by Junior Pediatric faculty through provision and access to New Project Development Awards, and 5) recruit and foster the development of research skills of Pediatric oriented medical students, residents, follows and Junior faculty. Realization of these specific aims will increase the understanding of normal growth and development as well as disease processes by Junior Pediatric faculty and enhance their development as independent investigators. The technology and concepts involved in molecular analysis apply to a majority of Pediatric disciplines where molecular, physiological, cell biology and biochemical studies are needed to gain complete insight to regulation in normal and pathologic processes.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Center Core Grants (P30)
Project #
5P30HD028819-05
Application #
2201328
Study Section
Special Emphasis Panel (SRC (04))
Project Start
1991-09-30
Project End
1997-08-31
Budget Start
1995-09-01
Budget End
1997-08-31
Support Year
5
Fiscal Year
1995
Total Cost
Indirect Cost
Name
Vanderbilt University Medical Center
Department
Pediatrics
Type
Schools of Medicine
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212
Dasouki, M; Jurecic, V; Phillips 3rd, J A et al. (1997) DiGeorge anomaly and chromosome 10p deletions: one or two loci? Am J Med Genet 73:72-5
Williams, J B; Rexer, B; Sirripurapu, S et al. (1997) The human HNP36 gene is localized to chromosome 11q13 and produces alternative transcripts that are not mutated in multiple endocrine neoplasia, type 1 (MEN I) syndrome. Genomics 42:325-30
Raskin, S; Philips 3rd, J A; Krishnamani, M R et al. (1997) Regional distribution of cystic fibrosis-linked DNA haplotypes in Brazil: multicenter study. Hum Biol 69:75-88
Repaske, D R; Medlej, R; Gultekin, E K et al. (1997) Heterogeneity in clinical manifestation of autosomal dominant neurohypophyseal diabetes insipidus caused by a mutation encoding Ala-1-->Val in the signal peptide of the arginine vasopressin/neurophysin II/copeptin precursor. J Clin Endocrinol Metab 82:51-6
Raskin, S; Cogan, J D; Summar, M L et al. (1996) Genetic mapping of the human pituitary-specific transcriptional factor gene and its analysis in familial panhypopituitary dwarfism. Hum Genet 98:703-5
Spearman, P; Ratner, L (1996) Human immunodeficiency virus type 1 capsid formation in reticulocyte lysates. J Virol 70:8187-94
Martincic, D; Whitlock, J A (1996) Improved detection of p53 point mutations by dideoxyfingerprinting (ddF). Oncogene 13:2039-44
Cogan, J D; Ramel, B; Lehto, M et al. (1995) A recurring dominant negative mutation causes autosomal dominant growth hormone deficiency--a clinical research center study. J Clin Endocrinol Metab 80:3591-5
Summar, M L; Dasouki, M J; Schofield, P J et al. (1995) Physical and linkage mapping of human carbamyl phosphate synthetase I (CPS1) and reassignment from 2p to 2q35. Cytogenet Cell Genet 71:266-7
Campbell 3rd, P W; Phillips 3rd, J A; Heidecker, G J et al. (1995) Detection of Pseudomonas (Burkholderia) cepacia using PCR. Pediatr Pulmonol 20:44-9

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