A Decentralized Method for Joint Admission Control and Beamforming in Coordinated Multicell Downlink

In cellular networks, admission control and beamforming optimization are intertwined problems. While beamforming optimization aims at satisfying users' quality-of-service (QoS) requirements or improving the QoS levels, admission control looks at how a subset of users should be selected so that the beamforming optimization problem can yield a reasonable solution in terms of the QoS levels provided. However, in order to simplify the design, the two problems are usually seen as separate problems. This paper considers joint admission control and beamforming (JACoB) under a coordinated multicell MISO downlink scenario. We formulate JACoB as a user number maximization problem, where selected users are guaranteed to receive the QoS levels they requested. The formulated problem is combinatorial and hard, and we derive a convex approximation to the problem. A merit of our convex approximation formulation is that it can be easily decomposed for per-base-station decentralized optimization, namely, via block coordinate decent. The efficacy of the proposed decentralized method is demonstrated by simulation results.Comment: 2012 IEEE Asilomar Conference on Signals, Systems, and Computer

Bridgewater Normal School and Isawa Shuji’s Reforms of Modern Teacher Education in Meiji Japan

Shuji Isawa was sent by the Ministry of Education in Japan to study at Bridgewater Normal School in Massachusetts from 1875 to 1877 and at Harvard University from 1877 to 1878. He was one of the famous intellectuals who tested the telephone with Alexander Graham Bell and translated ideas of evolution into Japan. Through his studies with Boston public school music teacher Luther Whiting Mason, Isawa was instrumental in introducing new curriculum for the teaching of music, physical education, and special education for elementary schools in Meiji Japan. Isawa’s life highlights the complex process in the negotiation between traditional and modern or East and West in his quest for learning. His writings in the 1880s demonstrate his efforts of integrating Japanese and western educational curriculum, while his later studies of Chinese language and culture show his ambivalence towards East Asia especially as an educational offi cial in colonial Taiwan in 1895. Through studies of Isawa’s records at Bridgewater State College, a recent visit to his birth house in Ina, Nagano and attendance at the Isawa music festival in October 2007, as well as meeting with a fourth-generation descendant of Isawa in Tokyo, this paper is a preliminary study of the relationship between history and memory in Isawa’s legacy in both Japan and the United States

Molecular Mechanisms of Cell Migration Inhibition by Synthetic Triterpenoids

Cell migration is an important mediator of cancer metastasis and invasion, which is responsible for 90% of cancer-related premature deaths in Canada. Synthetic triterpenoids are a class of promising anti-cancer compounds that have shown considerable efficacy in targeting various cellular functions including apoptosis, growth, inflammation and cytoprotection in both cell culture and animal tumor models. However, their effect on cell migration, an important event in metastasis, remains poorly understood. This thesis focuses on deciphering the molecular mechanisms whereby the synthetic triterpenoids affect cell migration. I observed that the imidazolide and methyl ester derivatives of the synthetic triterpenoid, 2-cyano-3,12-dioxooleana-1,9-dien-28-oic aic acid (CDDO-Im and CDDO-Me), inhibit cell migration by disrupting microtubule dynamics. In addition, I found that these triterpenoids disrupt cell polarity by displacing proteins at the leading edge of migrating cells. Furthermore, using a two-pronged proteomic approach involving protein arrays and mass spectrometry, I identified numerous triterpenoid-binding targets involved in actin polymerization and focal adhesion maintenance. My data further revealed that triterpenoids inhibit branched actin polymerization by targeting Arp3 in the Arp2/3 complex and target GSK3b activity to alter focal adhesion sizes. Collectively, my studies provided novel insights on the underlying molecular mechanisms by which triterpenoids act to affect cell migration. This knowledge will be important for developing a more efficacious and specific therapeutic triterpenoid compound that targets cancer metastasis

The regulation of Fibronectin matrix assembly by Tenascin-C

Fibronectin (FN) is a ubiquitous component of the extracellular matrix (ECM). Its assembly into 3D fibrillar matrices is essential during development and tissue repair to maintain tissue architecture and provide environmental signals to cells. However, FN deposition must be tightly regulated as excessive assembly is a major hallmark of fibrotic diseases and cancer. Tenascin-C (TN-C) is a large, multi-domain ECM glycoprotein that co-localizes with newly synthesized FN fibrils in vivo during development, wound repair and tumorigenesis. However, it is not known precisely how FN and TN-C interact within the ECM, or whether their interaction has any functional relevance. I have demonstrated that distinct domains of TN-C inhibit FN matrix assembly by fibroblasts, whereas full length TN-C has no effect. I have identified regions within TN-C domains that are essential for binding to fibrillar FN, but not to soluble FN, and mapped where they interact within the FN molecule. I have found that domains containing these regions interfere with inter-molecular FN-FN interactions during fibrillogenesis. I also identified other TN-C domains that interfered with FN matrix assembly by FNindependent mechanisms. I demonstrated that one of these TN-C domains was internalized by fibroblasts causing morphological changes that may interfere with cytoskeleton organization or cell surface receptor availability to prevent the maintenance of a fibrillar FN matrix at the cell surface. Recently emerging evidence indicates that deposition of FN by epithelial and endothelial cells is absolutely vital for tubulogenesis and the formation of new blood vessels. Without this scaffold, the cells fail to generate sufficient tensional force required for the morphogenesis and migration essential for tubule formation. I have shown that specific domains of TN-C can inhibit tubulogenesis by epithelial cells within a 3D collagen matrix and may also affect angiogenesis of endothelial cells within a 3D collagen matrix environment. These data suggest that proteolysis of TN-C during tissue remodelling may create fragments that act to limit FN matrix assembly. Persistent TN-C expression during fibrosis and tumour growth may contribute to uncontrolled FN deposition and angiogenesis during disease progression