Hepatoma-derived growth factor (HDGF) is a nucleus-targeting mitogen for various types of cells. Besides, HDGF overexpression is associated with tumor progression and poor survival outcome in patients with hepatocellular carcinoma (HCC) and lung cancer. HDGF is capable of promoting the proliferation and migration in various types of cells. HDGF is composed of 240 amino acids and contains 2 putative bipartite nuclear localization signals (NLSs). By dividing HDGF into two deletion domains: PWWP (residues 1-100) and C140 (residues 101-240), we found that both PWWP and C140 domains are capable of promoting nuclear localization, However, only C140 domain promoted cell proliferation and migration as HDGF. Mutation in NLS domains abrogated the nuclear localization and growth-promoting function, but not the migratory potential of HDGF. Beside, Ser165 was predicted as putative cdc2 phosphorylation site. In vitro kinase assay indicated that Ser165 of HDGF is the phosphorylated site of cdc2 kinase. We also demonstrated that mutations in cdc2 phoshprylation site did not affect the nuclear localization, proliferation-stimulating activities of HDGF but enhance migration-stimulating abilities of HDGF. Recently, the HDGF domain containing residues 81 to 100 is shown to be responsible for binding to membrane receptor in NIH3T3 cells. Besides, Lys96 plays a pivotal role for receptor binding. By generation of HDGF Lys96A mutant protein, we found that mutation of Lys96 indeed caused a prominent reduction in cellular binding affinity of HDGF to NIH3T3 cells and affect cell migration. In summary, the NLSs are essential for the mitogenic effect of HDGF, but not required for migration. And the cdc2 phoshorylation site is important for NIH3T3 migration. The Lys96 of HDGF play an important role of membrane receptor binding and cell migration.

In response to the presence of portable devices and the change in usage patterns, mobility support for computer networking has received increasing attentions in recent years. There has been wide variety of established works focusing on the shortening of the handover delay. Most of them had tried their best in maintaining the connections to their peer nodes as mobile nodes moving across different network domains. This might not be a best policy in certain applications, such as homogeneous content distribution systems. A new handover scheme incorporating anycasting and service migration is developed and presented in this thesis. In the proposed approach, anycast is used to locate a new nearest server as a mobile node entering a new domain, and an ongoing service will be dynamically migrated from a distant server to a new server with shorter weighted network distance to the client. As a result, the individual service connection, as well as the global network environment, will benefit from the service migration, in terms of improved service quality and bandwidth utilization.

Hepatocyte growth factor (HGF) is a multifunctional mitogen, stimulating cell proliferation, motility, angiogenesis and morphogenesis via activating its receptor, c-Met tyrosine kinase. Overexpression of HGF and c-Met has been shown as a characteristic of cancer transformation and metastasis. Inhibition of HGF/c-Met signaling may abrogate the malignant and metastatic states of cancer cells and offer a useful therapeutic approach for treating cancers. Thus with the aim of creating inhibitors to HGF-cMet signaling, we constructed plasmids containing truncated N-terminus of HGF, NK1, NK2, NK3 and NK4, respectively, and transfected into MDA MB 435S cells by electroporation. After selection with antibiotics, stable transfectants were obtained. Proliferation assay showed that the truncated NKs significantly inhibited the growth of the cells. Moreover, wound healing assay showed that migration of the NK-transfected cells were also significantly inhibited in comparison with GFP-transfected and nontransfected cells. These results therefore suggest that truncated NKs may be good inhibitors to HGF/c-Met signaling in the proliferation and migration of human breast cancer cells in vitro. In the future, the in vivo animal model is needed to be carried out to further clarify the clinical values of truncated NKs for application to cancer therapy.

This dissertation proposes a new, synthesized perspective for explaining the “Nonmetropolitan Turnaround” in the 1970s and 1990s. By studying the definition of urbanization carefully, using the human ecological perspective, many processes happening during the “Nonmetropolitan Turnaround” in the 1970s and 1990s, such as suburbanization, deconcentration, and counterurbanization, can be understood as different forms of the urbanization processes. When the majority of the population was rural, the dominant pattern of urbanization was rural-urban migration. When the majority of the population became urban, the dominant urbanization pattern reversed to urbanrural migration because urban centers had reached beyond their optimal density and processes operated to reduce their density. This paper hypothesizes that the two “turnarounds” were simply the result of different aspects of urbanization complicated by metropolitan status reclassifications. The perspectives of suburbanization, counterurbanization and deconcentration are integrated into the urbanization perspective. Using migration flow data compiled by the Census Bureau from 1975 to 1980 and from 1995 to 2000, the summary analyses confirmed that the net migration due to the three forms of urbanization largely accounted for all of the net migrant flows. This dissertation further tested the validity of optimal density theory with net migration data and confirmed the utility of this perspective in predicting the direction of net migration.

Lung cancer is the leading cause of death in Taiwan cancer patients. The cancer cells are capable of spreading by metastasis and invasion. When tumors spread to distant parts of the body, it is difficult to treat by surgery. In this study, we discovered the novel anti-invasion drugs DMHMPC and DE-DMPC that can inhibit the metastasis and invasion of human lung cancer cell A549. From screening of a chemical library of 420 small molecule compounds using Boyden chamber and MTT assay, the compound DMHMPC and DE-DMPC showed the inhibitory activity toward the invasiveness but not proliferation in human lung cancer cell A549. The results of wound healing assay also showed that DMHMPC and DE-DMPC inhibited the motility of A549 in a dose dependent manner. Moreover, the results of growth curve assay and colony formation assay also showed that DMHMPC and DE-DMPC are not effect proliferation in A549. Together, these results suggested that DMHMPC and DE-DMPC could be the potential drugs to inhibit the invasion of cancer cells that may lead to the new avenue of the cancer prevention therapy.

Texte remanié: Th. doct.--Géogr.--Paris 10, 1996. Titre de soutenance : Migrants et pionniers en Indonésie occidentale. / CRET = Centre de recherche sur les espaces tropicaux.

Zugl.: Trier, Univ., Diss., 2008

Zugl.: Münster (Westfalen), Univ., Diss., 2008

Thesis (Ph. D.)--University of California, San Diego, 2002. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references. Available also from UMI Company.