No description available.

No description available.

The purpose of this secondary analysis of data was to investigate the relationship between family factors and obesity in Mexican American and Anglo preschool children. The purposive sample consisted of 341 mothers and their children, of which 180 were Mexican Americans and 161 were Anglos. Demographic characteristics indicated that Mexican American children: were heavier; living in single parent families more frequently; had more body fat; had mothers with higher body mass index (BMI); had larger family size; were less likely to be first born or only children; had less educated parents with lower level occupations and lower family income; and had mothers who used control in feeding practices more often than their Anglo counterparts. Results identify areas for prevention of childhood obesity.

The purpose of this research was to investigate the relationship between specific infant and maternal characteristics with the developmental outcome of low birth weight infants. Birth weight was statistically significant in relation to the Mental Developmental Index (p =.001) and the Psychomotor Developmental Index for chronologic age (p =.023). Birth weight predicted 25% of the variance in infant cognitive development and 24% in infant motor development. There was no statistically significant positive correlation between maternal education and infant cognitive developmental outcome. There was a statistically significant correlation between: number of hospital days (MDI, P =.006; PDI P =.010); number of days on oxygen (MDI, p =.006; PDI p =.037); gestational age (MDI p =.006); and infants with bronchopulmonary dysplasia (MDI p =.020; PDI, p =.020) in relation to developmental outcome. These findings support the premise that co-morbidity of infants appears to increase the risk of developmental delay.

Source: Dissertation Abstracts International, Volume: 35-02, Section: B, page: 0906. / Thesis (Ph.D.)--The Florida State University, 1974.

In addition to its classical role as a guardian of the genome, p53 functions as a developmental regulator. In the embryonic mouse kidney, p53 prevents ectopic budding from the nephric duct by antagonizing GDNF-Ret signaling. Moreover, p53 regulates expression of a subset of renal function genes (RFG) via direct binding to the target promoters. Cellular p53 levels are normally kept low via proteosomal degradation mediated by interactions with the E3 ubiquitin ligase, mdm2. Upon cellular stress (e.g., DNA damage), p53 is activated via post-translational modifications, which induce dissociation and caspase-mediated cleavage of Mdm2. The mechanisms mediating p53 stabilization and activation in the embryonic kidney are unknown. Utilizing a panel of p53 antibodies directed against phosphorylated serine/threonine or acetylated lysines, we demonstrate that embryonic kidney p53 is phosphorylated on serines S6, S9, S15, S20 and S392 and acetylated on lysines K373, K382, and K386. Site-directed mutagenesis demonstrated that some modifications are necessary, e.g., Ser15, Ser 20, Thr18, whereas others are dispensable, e.g., Ser392, K373, K382, K386, for p53 stability. Moreover, in vitro transfection experiments revealed that p53 modifications exert differential transcriptional effects on target renal differentiation genes. Chromatin Immunoprecipitation assays indicate that onset of nephron differentiation is accompanied by enhanced p53 binding to RFGs promoters. In vivo, selected p53 modifications tend to be associated with cell type-specific expression pattern; for example, p-p53S392 is enriched in differentiating proximal tubules, whereas ac-p53K373,K382/K386 is expressed in nephron progenitors and collecting ducts. In addition, embryonic p53 exists mostly in a mono-ubiquitinated form, whereas, in postnatal kidney, p53 is polyubiquitinated. This finding correlates with the developmental switch from cleaved to intact Mdm2. We conclude that factors within the embryonic microenvironment promote enhanced p53 stability via post-translational modifications / acase@tulane.edu

Epigenetic mechanisms play a key role in the control of gene expression and cell fate decisions. Histone deacetylases (HDACs) are a conserved group of epigenetic regulators and chromatin remodelers. While the critical role of HDACs in cancer and immune disorders is increasingly recognized, their role in organogenesis remains largely unknown. The present study investigates the developmental biology of Hdacs in the mouse metanephric kidney. We demonstrate that Class I Hdac genes are highly expressed during nephrogenesis and ureteric bud branching morphogenesis, and are downregulated postnatally. Whereas Class I Hdacs are enriched in the epithelial and mesenchyme cell lineages, Class II Hdacs are predominantly vascular. Utilizing distinct classes of HDAC inhibitors, we demonstrate that Hdacs regulate the master developmental programs of metanephric development. The Hdac-regulated transcriptome encompasses regulators of the cell cycle, Wnt/beta-catenin, TGF-beta/Smad and PI3K-Akt pathways. In the metanephric mesenchyme, the Osr1/Eya1/Pax2/Hox11/WT1 regulatory network is a primary target of Hdac activity. In the ureteric bud lineage, Wnt9b, Spry1 and Emx2 are among the Hdac-target genes. Consistent with these findings, expression of c-Myc, Cnd1, Axin2, Fgf8, Pax8, Wnt4, and Lhx1 genes is highly dependent on Hdac activity. Persistent inhibition of metanephric Hdac activity culminates in irreversible growth arrest and apoptosis. Gene knockdown in the metanephric mesenchyme cell line MK4 confirmed a cell-autonomous role for Hdac1 and Hdac2 in regulation of Pax2, Pax8, Sfrp1, and Wnt4 gene expression. Collectively, these data demonstrate that Hdacs are critical epigenetic regulators of metanephric gene expression, cell proliferation, and survival / acase@tulane.edu

No description available.

No description available.

Epithelial to mesenchymal cell transformation (EMT) in the atrioventricular canal (AV canal) produces a population of fibroblast cells that contribute to the mitral and tricuspid valves of the fully formed heart. Formation of these cells is critical for normal heart development and disruption of this process leads to congenital heart disease. This study describes the role of the homeodomain containing transcription factor Mox-1 during this cell transformation process. Mox-1 protein and mRNA expression were detected during cell transformation in the cardiac cushions. This expression corresponded in time to stages of EMT characterized by cell shape change and invasion of the extracellular matrix. Antisense oligonucleotides to Mox-1 inhibited cell transformation in cultured AV canal explants. Previous reports indicated that the TGFβ3 signaling pathway also regulates cell transformation at similar stages. Experiments inhibiting the TGFβ3 pathway also inhibit Mox-1 expression. A 2kb portion of the Mox-1 promoter was cloned and a portion of this construct demonstrated a capacity to initiate transcription in AV canal cultures. The active fragment of the Mox-1 promoter was responsive to TGFβ3 signaling. This study indicates that Mox-1 is necessary but not sufficient for cell transformation in the AV canal cushions and is regulated by an important signaling pathway involved in this process.