Title from title page of PDF (University of Missouri--St. Louis, viewed March 3, 2010). Includes bibliographical references (p. 86-99).

The Atlanta Beltline is an urban redevelopment project that was designed to increase access to trails, parks, and greenspace in Atlanta, Georgia. Thirty-three miles of new trail will be developed, providing a place for the community to engage in purposeful physical activity and active transport around the city of Atlanta. Because physical activity is associated with improvements in birth outcomes and under the assumption that close proximity to the Atlanta Beltline encourages physical activity, I hypothesize that women residing within 0.5 mile of the Atlanta Beltline will show improvements in birth outcomes, as compared to women residing 1-1.5 miles away from the Beltline. Birth outcomes were measured as rates for low birth weight, premature live birth, and fetal mortality rates. Census tract data for birth outcomes for the time period “pre-Beltline,” 2002 - 2007, and “post-Beltline,” 2008 - 2012, was obtained from Georgia Department of Public Health. 18 census tracks in three areas along the Beltline (Northside, Eastside, West End) were identified as exposed and 17 in the same areas were unexposed. We found the following mean rates (SDs) of the outcomes in the exposed census tracks during the pre-Beltline period: 119.22 (48.39) low birth weight, 154.94 (55.80) premature birth, and 16.17(15.81) fetal death, all per 1,000 live birth. During the post-Beltline period in the exposed area, these measurements were: 107.55 (39.66) low births weight, 131.06 (48.92) premature birth, and 12.28 (13.51) fetal death, all per 1000 live birth. In the unexposed census tracks during the pre-Beltline period, mean rates (SDs) of the outcomes were 110.82 (42.81) low births weight, 144.88 (46.49) premature birth, and 19.94 (35.45) fetal death, all per 1000 live birth. During the post-Beltline period, these measurements in the unexposed area were: 100.88 (40.76) low births, 134.17 (47.85) premature birth, and 8.06 (6.89) fetal death, all per 1000 live birth. Overall in both the exposed and unexposed areas, the time trends for the examined measurements of birth outcomes were towards improvement; however, only a decrease in premature live birth in the exposed area (p=0.2) and fetal mortality in the unexposed area (p=0.1) were of statistically marginal significance. We conclude that currently no significant improvements in birth outcomes, associated with close proximity to the Atlanta Beltline have been detected.

Analysis of the genomic sequences of Streptococcus mutans UA159 and Group B Streptococcus (GBS) strains Streptococcus agalactiae NEM316 and S. agalactiae 2603V/R indicated the presence of two putative collagenase genes in each organism. smcol1 from S. mutans was previously cloned and analyzed and the results indicated that the enzyme belonged to the U32 family of collagenases/peptidases. This enzyme shares homology with the prtC of Porphyromonas gingivalis, one of the principal examples of the U32 family of peptidases. Considering the potential role of these enzymes in the pathogenicity of P. gingivalis (periodontitis or gum disease), GBS (premature rupture of the amniochorionic membrane) and S. mutans (dental root decay), it is necessary to study these enzymes and establish their role in the virulence of these organisms. Toward this goal the present study has focused on cloning collagenase 2 (smcol2) from S. mutans and cloning collagenase 1 (gbscol1), and collagenase 2 (gbscol2), from GBS. The information obtained will contribute to a further understanding of the U32 peptidase family.

Skeletal muscle (SkM) possesses an impressive ability to regenerate in response to injury or chronic disease. This regenerative capacity is attributed to its resident mononuclear myogenic progenitors. Previous studies have identified several types of myogenic progenitors within SkM, some of which are isolated by fluorescence activated cell sorting (FACS) using cell surface markers. Studies in our laboratory have identified melanoma cell adhesion molecule (MCAM) as a cell surface marker expressed by myogenic progenitors in human fetal SkM. However, the relationship between MCAM expression and the degree of myogenic commitment of distinct MCAM+ populations has not been elucidated. In the present study, subpopulations of MCAM+ cells were purified by FACS on the basis of Hoechst 33342 dye uptake. Specifically, MCAM+ side population (SP) was isolated by Hoechst exclusion and MCAM+ main population (MP) on Hoechst incorporation. Sorted populations were first optimized for growth in vitro since SkM SP cells are difficult to maintain in culture. In particular, Invitrogen’s StemPro® MSC SFM medium was found to support propagation of human fetal SkM SP cells with minimal differentiation. Following this optimization, sorted populations were assessed for expression of myogenic markers before and after propagation and then for fusion potential in vitro and engraftment potential in vivo. The MCAM+ subpopulations were found to express myogenic markers to a significantly greater extent than MCAM- subpopulations. Furthermore, the MCAM+ subpopulations fused robustly into myotubes in vitro whereas the MCAM- subpopulations did not. Interestingly, the MCAM+ SP population exhibited the highest fusion potential in vitro and was the only MCAM+ subpopulation to engraft into dystrophic muscle in vivo following propagation. These results indicate that MCAM is associated with myogenicity and can be used to prospectively isolate a pure myogenic fraction from human fetal SkM tissue. Moreover, the MCAM+ SP retain its myogenic potential to a greater extent than MCAM+ MP after propagation. This suggests that the MCAM+ SP fraction contains a higher percentage of early myogenic progenitors compared to the MCAM+ MP fraction. Additional studies on MCAM-expressing populations in human fetal SkM may elucidate a potent population for use in cell-based therapeutic strategies for treating muscle diseases.

Together with the advancements in animal cloning, the ability to efficiently target specific genes in somatic cells would greatly enhance several areas of research. While it has been possible for quite some time to target specific genes in the germ cells of mice, the advancements in somatic cell gene targeting has been slowed for two main reasons. First, the finite lifespan of somatic cells, due mainly to the inability of the somatic cells to regenerate or maintain their telomeres, poses a major problem given the lengthy selection process needed to identify a targeting event. The second problem is the overall inefficiency of homologous recombination. A double strand break or introduction of foreign DNA into a cell can be processed either through the homologous recombination or non-homologous end joining pathways. Of these two, non-homologous end joining is dominant in somatic cells. A two plasmid recombination system was used to study the effects of the manipulation of several non-homologous end joining and homologous recombination pathway molecules on the rates of homologous recombination in porcine fetal fibroblasts. In addition, the effect of telomerase expression, cell synchrony, and DNA nuclear delivery was examined. Results indicate a strong positive relationship between inactivation of p53, cell synchronization, and efficient DNA nuclear delivery in enhancing the rate of homologous recombination. These findings were then applied to an actual locus in the pig, the α1,3 galactosyltransferase gene. Results from these transfections are compared to published accounts of successful targeting at this locus and possibilities for the differences found are discussed.

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Intrauterine growth restriction (IUGR) reduces bone mass by 10-30% and impairs arachidonic (AA) and docosahexaenoic (DHA) acid status in infants. Because AA and DHA enhance neonatal bone mass, the aim of this study was to determine the effects of dietary 0.5% AA and 0.2% DHA (w/w) prior to weaning on bone and growth. 40 guinea pigs were randomized to either a control (C) or low-protein diet (LP) during pregnancy and the C diet or the C diet with AA+DHA during lactation. Measurements included bone mass, metabolism, and strength, and erythrocyte lipid of sows and offspring from birth to 16 wk post-partum. The LP diet induced IUGR, while the AA+DHA increased bone mass by 5-20% in sows and offspring and corrected growth and bone mass in IUGR pups. Thus, AA+DHA provided in lactation rescues the growth trajectory in an IUGR state and is beneficial to maternal and neonatal bone mass.