This study critically analyzed the current body of published research on microblogging in education (MIE) to build a deep and comprehensive understanding of this increasingly popular phenomenon. Twenty-one studies on MIE in 2008-2011 were selected based on the selection criteria and analyzed to answer the following questions: (a) What types of research have been published on MIE? (b) How was microblogging used for teaching and learning in these studies? (c) What educational benefits did microblogging have on teaching and learning? and (d) What suggestions and implications did the current research have for future MIE research and practices? The analysis suggested that microblogging has a potential to encourage participation, engagement, reflective thinking as well as collaborative learning under different learning settings. The quality of research, however, varies greatly, suggesting a need for rigorous research on MIE. The analysis has implications for MIE practices as well as research and development efforts.

c-Met is a well-characterized receptor tyrosine kinase for hepatocyte growth factor (HGF). Compelling evidence from studies in human tumors and both cellular and animal tumor models indicates that signaling through the HGF/c-Met pathway mediates a plethora of normal cellular activities, including proliferation, survival, migration, and invasion, that are at the root of cancer cell dysregulation, tumorigenesis, and tumor metastasis. Inhibiting HGF-mediated signaling may provide a novel therapeutic approach for treating patients with a broad spectrum of human tumors. Toward this goal, we generated and characterized five different fully human monoclonal antibodies that bound to and neutralized human HGF. Antibodies with subnanomolar affinities for HGF blocked binding of human HGF to c-Met and inhibited HGF-mediated c-Met phosphorylation, cell proliferation, survival, and invasion. Using a series of human-mouse chimeric HGF proteins, we showed that the neutralizing antibodies bind to a unique epitope in the B-chain of human HGF. Importantly, these antibodies inhibited HGF-dependent autocrine-driven tumor growth and caused significant regression of established U-87 MG tumor xenografts. Treatment with anti-HGF antibody rapidly inhibited tumor cell proliferation and significantly increased the proportion of apoptotic U-87 MG tumor cells in vivo. These results suggest that an antibody to an epitope in the B-chain of HGF has potential as a novel therapeutic agent for treating patients with HGF-dependent tumors.

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