Thesis (M.Orth.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves [102]-122) Also available in print.

During early embryonic development, endodermal cells leave the inner cell mass (ICM) and migrate over an extracellular matrix (ECM), located on the blastocoelic side of the trophectoderm, to form a continuous layer of extraembryonic endoderm. Cell migration events depend on a family of cell surface proteins known as integrins that bind specific ECM proteins. In an effort to understand the mechanisms involved in bovine endodermal cell migration, two experiments were conducted. In the first experiment, expression of the ECM proteins fibronectin, laminin and vitronectin was evaluated by immunofluorescent staining in in vivo and in vitro developing embryos during Day 6-10 and Day 7-10, respectively (Day 0=onset of estrus). Fibronectin was detected in all stages of in vivo and in vitro embryos, however no difference (P>0.10) was observed due to day or developmental stage. Laminin staining was moderately expressed in all stages of in vivo embryos, with an increase (P<0.05) in Day 10 in vivo embryos. Laminin staining in Day 9 in vitro embryos was less intense (P<0.05) than Day 7 and 8 in vitro embryos. Higher (P<0.05) expression of laminin was observed in Day l0 in vivo embryos as compared to Day 10 in vitro. Vitronectin staining was expressed throughout all stages of development. Day 6 in vivo embryos exhibited more intense (P<0.05) staining compared to Day 8 in vivo embryos. Day 10 in vivo embryos expressed more (P<0.05) vitronectin than Day 10 in vitro embryos. In the second experiment, the effects of ECM-type and inhibitors of integrin binding on bovine endodermal cell outgrowth from the ICM were evaluated. Day 7 embryos were nonsurgically collected and cultured for 96 h on either fibronectin-layered microdrops containing 0 (control), 0.5 or 1.0 mg/ml RGD and/or EILDV peptides or vitronectin-layered microdrops containing 0, 0.5 or 1.0 mg/ml RGD peptides. At 24-h intervals, ICM were photographed and the numbers of cells leaving the ICM were counted. Areas of cellular outgrowth were calculated from the photomicrographs. Compared to the control, addition of 0.5 or 1.0 mg/ml RGD, EILDV or RGD and EILDV did not (P>0.10) reduce the areas of cellular outgrowth from the ICM on matrices of fibronectin. Numbers of cells in outgrowths were greater (P<0.05) in control ICM compared to 0.5 mg/ml RGD, but this effect was eliminated (P>0.10) when the inhibitor concentration was increased to 1.0 mg/ml. Addition of 0.5 or 1.0 mg/ml RGD did not reduce (P>0.10) the area of cellular outgrowth from the ICM on vitronectin and had no effect (P>0.10) on numbers of cells in the outgrowths. Detection of fibronectin, laminin and vitronectin by immunofluorescence suggests these proteins are present in the developing bovine embryo to support endodermal cell migration and stabilization in extraembryonic endoderm formation. Because cell migration over fibronectin and vitronectin was not inhibited by the RGD and EILDV peptides, endodermal cells must use either an integrin that recognizes alternative binding sites in fibronectin and vitronectin or an alternative cell adhesion system. / Graduation date: 2003

Graduation date: 1997

Thesis (Ph. D.)--University of Hong Kong, 2006.

Marfan syndrome, affecting approximately one out of every 5,000 people, is characterized by abnormal bone growth, ectopia lentis, and often-fatal aortic dilation and dissection. The root cause is a faulty extracellular matrix protein, fibrillin-1, which associates with elastin in many tissues. Common carotids from wild-type controls and mice heterozygous for the mgR mutation, the most commonly used mouse model of Marfan syndrome, were studied in a biaxial testing device. Mechanical data in the form of pressure-diameter and force-stretch tests in both the active and passive states were collected, as well data on the functional responses to phenylephrine, carbamylcholine chloride, and sodium nitroprusside. Although little significant difference was found between the heterozygous and wild-type groups in general, the in vivo stretch for both groups was significantly different from previously studied mouse vessels. Although the two groups do not exhibit significant differences, this study comprises a control group for future work with mice homozygous for mgR, which do exhibit Marfan-like symptoms. As treatment of Marfan syndrome improves, more Marfan patients will survive and age, increasing the likelihood that they will develop many of the vascular complications affecting the normal population, including hypertension and atherosclerosis. Therefore, it is imperative to gather biomechanical data from the Marfan vasculature so that clinicians may predict the effects of vascular complications in Marfan patients and develop appropriate methods of treatment.

Nature encourages diversity in life forms (morphologies). The study of morphogenesis deals with understanding those processes that arise during the embryonic development of an organism. These processes control the organized spatial distribution of cells, which in turn gives rise to the characteristic form for the organism. Morphogenesis is a multi-scale modeling problem that can be studied at the molecular, cellular, and tissue levels. Here, we study the problem of morphogenesis at the cellular level by introducing an integrated biomechanical model of cells embedded in the extracellular matrix. The fundamental aspects of mechanobiology essential for studying morphogenesis at the cellular level are the cytoskeleton, extracellular matrix (ECM), and cell adhesion. Cells are modeled using tensegrity architecture. Our simulations demonstrate cellular events, such as differentiation, migration, and division using an extended tensegrity architecture that supports dynamic polymerization of the micro-filaments of the cell. Thus, our simulations add further support to the cellular tensegrity model. Viscoelastic behavior of extracellular matrix is modeled by extending one-dimensional mechanical models (by Maxwell and by Voigt) to three dimensions using finite element methods. The cell adhesion is modeled as a general Velcro-type model. We integrated the mechanics and dynamics of cell, ECM, and cell adhesion with a geometric model to create an integrated biomechanical model. In addition, the thesis discusses various computational issues, including generating the finite element mesh, mesh refinement, re-meshing, and solution mapping. As is known from a molecular level perspective, the genetic regulatory network of the organism controls this spatial distribution of cells along with some environmental factors modulating the process. The integrated biomechanical model presented here, besides generating interesting morphologies, can serve as a mesoscopic-scale platform upon which future work can correlate with the underlying genetic network.

Benthic microalgae (BMA) living within the surface sediment of salt marshes are highly productive organisms that provide a significant proportion of organic carbon inputs into estuarine systems. BMA secrete extracellular carbohydrates in the form of low molecular weight carbohydrates and extracellular polymeric substances (EPS) as they migrate within the sediment. EPS plays an important role in the structure and function of BMA biofilms in shallow-water systems as EPS affects habitat structure, stabilizes the sediment, reduces sediment erosion, and is a carbon source for organisms. This study looked at the effect of nutrients and carbohydrate additions on BMA biomass, bacterial biomass, carbohydrate production, and glycosidase activity in the surface 5 mm of intertidal sediment in a subtropical salt marsh (Galveston Bay, Texas). Nitrogen and phosphorus were added to cores collected from the salt marsh and incubated in the lab over four days. Very little change was seen in the biomass of the benthic microalgae or in the different carbohydrate fractions with the added nutrients. The mean chlorophyll a concentration was 13 +/- 5 ug g-1 sediment, the mean saline extractable carbohydrate concentration was 237 +/- 113 ug g-1 sediment, and the mean EPS concentration was 48 +/- 25 ug g-1 sediment. The chlorophyll a and saline extractable carbohydrate concentrations initially decreased over the first 24 hours, but then increased over the rest of the experiment, indicating a possible species compositional shift in the BMA. With no major response with nutrient additions, it is likely that a different environmental factor is limiting for the growth of the benthic microalgae, and therefore the production of sEPS, in this salt marsh. A series of experiments was conducted in situ by adding glucose, alginic acid, and phosphorus to sediment within experimental plots. Samples were taken periodically over three to seven days to determine the biomass of the microbial community, enzyme activities and kinetics, and changes in the concentrations of several sediment carbohydrate pools. u-glucosidase activities (15 +/- 3 nmol g-1 h-1) were significantly higher than u-xylosidase (6 +/- 2 nmol g-1 h-1) and u-galactosidase (8 +/- 2 nmol g-1 h-1) activities within the sediment, and there was no suppression of u-glucosidase activity measured with the glucose addition. These data represent the first measurement of u- xylosidase and u-galactosidase activity in intertidal sediment dominated by BMA. Although preliminary experiments suggested a possible phosphorus limitation within the sediment, there was little change in the bacteria abundance or the benthic microalgae biomass when phosphorus was added in situ. This study begins to illustrate the dynamics of carbohydrate production and loss in this salt marsh, and the ability for the microbial community in the salt marshes of Galveston Bay to adjust to the nutrient and carbohydrate treatments.

Thesis (Ph. D.)--University of Chicago, Dept. of Chemistry, June 2001. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph.D.)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Biomedical Engineering. Title from resource description page. Includes bibliographical references.

Thesis (M.Sc.)--York University, 2007. Graduate Programme in Biology. / Typescript. Includes bibliographical references (leaves 119-133). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR38842