ITC/USA 2006 Conference Proceedings / The Forty-Second Annual International Telemetering Conference and Technical Exhibition / October 23-26, 2006 / Town and Country Resort & Convention Center, San Diego, California / Wireless communication systems may use training signals for the receiver to learn the fading coefficients of the channel. Obtaining channel state information (CSI) at the receiver is often times necessary for the receiver to correctly detect and demodulate transmitted symbols. The type of training signal, the length of time to spend training, and the frequency of training are all important parameters in these types of systems. In this work, we derive an analytic expression for calculating the optimal training parameters for continuously fading channels. We also provide simulation results showing why this training scheme is considered optimal.

Thesis (PhD)--Stellenbosch University, 2003. / ENGLISH ABSTRACT: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Current knowledge suggests that MS is associated with autoimmunity and that infectious agents and hereditary factors may be involved. The demonstration of a higher recurrence risk of MS in families (4-5%) compared with the general population (0.1%) provides strong evidence for a genetic basis. Extensive analyses of the entire human genome to identify new genes that may underlie MS have indicated that several genes may contribute to disease susceptibility, but these remain largely unidentified. In this study candidate genes involved in iron metabolism and immunology have been analysed for the first time within the context of both autoimmune and infectious disease susceptibility, in order to investigate the role of genetic and viral factors implicated in the pathogenesis of MS. The Z-DNA forming repeat polymorphism in the promoter region of the solute carrier family 11 (proton-coupled divalent ion transporters) member 1 (SLC11A1) gene was found to be significantly associated with MS (P<0.01) in the genetically homogeneous Afrikaner population of South Africa, but not in the German and French populations using a case-control study and transmission linkage disequilibrium approach, respectively. However, significant differences were observed in genotype distribution between German MS patients with a primary- and secondary progressive disease course (P<0.05), and between the German patients with relapsing remitting and primary progressive MS (P<0.05). These findings provide further evidence that the SLC11A1 gene is associated with MS, most likely due to its role in iron homeostasis. In order to investigate the influence of viruses in the apparent multi-step aetiology of MS, serum and peripheral blood mononuclear cells (PBMCs) of MS patients, close relatives and unrelated controls were screened for the presence of MS-associated retrovirus (MSRV) and two herpes virus (HHV-6 and EBV) sequences. Detection of the pol gene expression of MSRV in the serum RNA of 69% of South African MS patients and in 70% of their unaffected close relatives, whilst absent in the serum of 39 unrelated healthy control individuals (P<0.001), indicated that virus infections affect the population risk but not the familial risk in MS. HHV-6 sequences were also present at a significantly lower frequency (P<0.04) in the PBMCs of unrelated controls (5%) compared to MS patients (22.5%). A point mutation (77C^G) in the gene encoding protein-tyrosine phosphatase, receptortype C (PTPRC), which is essential for activation of T and B cells, was found to be associated with MS in the German population. Analysis of the Afrikaner and German study populations included in our study did not indicate a causative role for the PTPRC gene in MS. However, it seems likely that this mutation may contribute to disease expression, since in one of the South African families with two MS affected sibs, the most severely affected sister was heterozygous for the 77C-»G mutation. The PTPRC mutation may therefore be of significance in disease prognosis. The multidisciplinary study approach has led to a stepwise accumulation of scientific information, which forever changed our understanding of the disease process underlying MS. / AFRIKAANSE OPSOMMING: Veelvoudige sklerose (VS) is ‘n kroniese inflammatoriese siekte van die sentrale senuweestelsel. Oor die algemeen word aanvaar dat VS geassosieerd is met outoimmuniteit en dat infektiewe agente en oorerflike faktore ’n rol speel. Die hoër herhalingsrisiko van VS in families (4-5%) in vergelyking met die voorkoms in die algemene populasie (0.1%) dui op 'n genetiese basis. Alhoewel volledige analise van die mensgenoom om gene onderliggend aan VS te identifiseer aangedui het dat verskeie gene waarskynlik bydra tot vatbaarheid vir die siekte, is die aard van die gene wat betrokke is grootliks onbekend. In hierdie studie is kandidaatgene betrokke by ystermetabolisme en immunulogie vir die eerste keer geanaliseer binne die konteks van beide outoimmuun en infektiewe siekte vatbaarheid, ten einde die rol van genetiese en virale faktore in die patogenese van VS te ondersoek. Die Z-DNS herhalingsvolgorde polimorfisme in die promotor area van die SLC11A1 geen was betekenisvol geassosieerd met VS (P<0.01) in die geneties homogene Afrikaner populasie van Suid-Afrika. ’n Soortgelyke assosiasie kon egter nie aangetoon word in die Duitse en Franse populasies deur gebruik te maak van onderskeidelik ‘n gevalle-kontrole studie en transmissie-koppelings-disekwilibrium benadering nie. Betekenisvolle verskille in die genotipe verspreiding is egter tussen Duitse VS pasiente met ‘n sekonder- en primer progressiewe verloop van die siekte (P<0.05), en tussen die Duitse pasiente met terugvallende en primere progressiewe VS aangetoon (P<0.05). Hierdie bevinding verskaf verdere bewyse dat die SLC11A1 geen geassosieerd is met VS, heel waarskynlik weens die rol van die geen in yster-homeostase. Ten einde die invloed van virusse in die etiologie van VS te ondersoek is serum en witbloedselle van VS pasiente, naby-verwante familielede en nie-verwante kontroles getoets vir die teenwoordigheid van die VS-geassosieerde retrovirus (MSRV) en twee herpesvirus (HHV-6 en EBV) geenvolgordes. Die pol geen uitdrukking van MSRV was teenwoordig in die serum RNA van 69% van die Suid-Afrikaanse VS pasiente en in 70% van hul ongeaffekteerde naby-verwante familielede, terwyl dit afwesig was in 39 nieverwante kontrole individue (P<0.001). Dit dui daarop dat virusse waarskynlik die risiko vir VS meer in die populasie verhoog as in families. HHV-6 was ook teenwoordig teen ‘n beduidende laer frekwensie (P<0.04) in nie-verwante kontroles (5%) in vergeleke met VS pasiente. ‘n Puntmutasie (77C-G) in die geen wat kodeer vir die proteien tirosien fosfatase reseptor tipe C (PTPRC), wat belangrik is vir aktivering van T- en B-helperselle, is vroeer gevind om geassosieerd te wees met VS in die Duitse populasie. Analise van die Afrikaner en Duitse populasies in ons studie het egter geen bewyse gelewer dat die PTPRC geen ‘n rol speel in VS nie. Dit egter is moontlik dat hierdie mutasie bydra tot die uitdrukking van VS, aangesien die mees geaffekteerde VS pasient in een van die Suid- Afrikaanse families met twee geaffekteerde susters positief getoets het vir die mutasie. Die mutasie mag dus van belang wees in die prognose van VS. Die multidissiplinere studie-benadering en stapsgewyse insameling van wetenskaplike inligting het gelei tot ’n nuwe perspektief ten opsigte van die siekteproses onderliggend aan VS.

ITC/USA 2011 Conference Proceedings / The Forty-Seventh Annual International Telemetering Conference and Technical Exhibition / October 24-27, 2011 / Bally's Las Vegas, Las Vegas, Nevada / This paper describes the design of an inexpensive and scalable transmitter for a Multiple-Input Multiple-Output (MIMO) communication system. The transmitter is intended to be used in aerospace applications, especially in spin stabilized vehicles. A field programmable gate array (FPGA) in the modulator will implement a modified Alamouti space time block code which will take advantage of the cyclostationary nature of the channel to increase the system data rate.

Multiple-Input Multiple-Output (MIMO) communication uses multiple transmit and receive antennas to improve the throughput in wireless channels. In cellular networks, self-interference greatly degrades MIMO's potential gain, especially in multiuser MIMO systems where multiple users in each cell share the spatial channel in order to maximize the total throughput. In a multiuser MIMO downlink, the two main causes of this self-interference are residual inter-user interference due to imperfect spatial separation between the users and other-cell interference due to cochannel transmissions in other cells. This dissertation develops adaptive transmission strategies to deal with both residual inter-user interference and other-cell interference in cellular MIMO networks. For the residual inter-user interference caused by imperfect channel state information at the transmitter, we explicitly characterize the impact of channel quantization and feedback delay. Achievable ergodic rates for both single-user and multiuser MIMO systems with different channel state information are derived. Adaptive switching between single-user and multiuser MIMO modes is proposed to improve the throughput, based on the accuracy of the available channel information. It is then extended to a multi-mode transmission strategy which adaptively adjusts the number of active users to control residual interference and provide additional array gain. To adaptively minimize the other-cell interference, two practical base station coordination strategies are proposed. The first is a cluster based coordination algorithm with different coordination strategies for cluster interior and cluster edge users. It performs full intra-cluster coordination for enhancing the sum throughput and limited inter-cluster coordination for reducing the interference for cluster edge users. A multi-cell linear precoder is designed to perform the coordination. The second is an adaptive intercell interference cancellation strategy, where multiple base stations jointly select transmission techniques based on user locations to maximize the sum throughput. Spatial interference cancellation is applied to suppress other-cell interference. Closed-form expressions are derived for the achievable throughput, and the proposed adaptive strategy is shown to provide significant average and edge throughput gain. The feedback design to assist the interference cancellation is also discussed. / text

When hostile missile raids are launched, protecting allied assets requires that many targets be tracked simultaneously. In these raids, it is possible that the number of missiles could outnumber the sensors available to measure them. In these situations, communication between sensors can be utilized along with dynamic task planning to increase the amount of knowledge available concerning these missiles. Since any allied decisions must depend on the knowledge available from the sensors, it follows that improving the overall knowledge will improve the ability of allies to protect their assets through improved decision making. The goal of the this research effort is to create a Sensor Resource Management (SRM) algorithm to optimize the information available during these missile raids, as well as strengthening the simulation framework required to evaluate the performance of the SRM. The SRM must be capable of near-real-time run time so that it could potentially be deployed in a real-world system. The SRM must be capable of providing time-varying assignments to sensors, allowing more than one target to be observed by a single sensor. The SRM must predict measurements based on sensor models to assess the potential information gain by each assignment. Using these predictions, an optimal allocation of all sensors must be constructed. The initial simulation, upon which this work was built, was capable of simulating a set number of missiles launched simultaneously, providing appropriate charts to display the accuracy of knowledge on each target as well as their predicted impact locations. Communication delays are implemented within the simulation, and sensor models are refined. In refining the sensor models, they are given geometric limitations such as range and viewing angles. Additionally, simulated measurements incorporate geometric considerations to provide more realistic values. The SRM is also improved to account for the details added to the simulation. These improvements include creating assignment schedules and allowing a time-varying numbers of targets. The resulting simulation and SRM are presented, and potential future work is discussed. / text

Multiple-input multiple-output (MIMO) radar has been receiving increasing attention in recent years due to the dramatic advantages offered by MIMO systems in communications. The amount of energy reflected from a common radar target varies considerably with the observation angle, and these scintillations may cause signal fading which severely degrades the performance of conventional radars. MIMO radar with widely spaced antennas is able to view several aspects of a target simultaneously, which realizes a spatial diversity gain to overcome the target scintillation problem, leading to significantly enhanced system performance. Building on the initial studies presented in the literature, MIMO radar is investigated in detail in this thesis. First of all, a finite scatterers model is proposed, based on which the target detection performance of a MIMO radar system with arbitrary array-target configurations is evaluated and analyzed. A MIMO radar involving a realistic target is also set up, whose simulation results corroborate the conclusions drawn based on theoretical target models, validating in a practical setting the improvements in detection performance brought in by the MIMO radar configuration. Next, a hybrid bistatic radar is introduced, which combines the phased-array and MIMO radar configurations to take advantage of both coherent processing gain and spatial diversity gain simultaneously. The target detection performance is first assessed, followed by the evaluation of the direction finding performance, i.e., performance of estimating angle of arrival as well as angel of departure. The presented theoretical expressions can be used to select the best architecture for a radar system, particularly when the total number of antennas is fixed. Finally, a novel two phase radar scheme involving signal retransmission is studied. It is based on the time-reversal (TR) detection and is investigated to improve the detection performance of a wideband MIMO radar or sonar system. Three detectors demanding various amounts of a priori information are developed, whose performance is evaluated and compared. Three schemes are proposed to design the retransmitted waveform with constraints on the transmitted signal power, further enhancing the detection performance with respect to the TR approach.

by Nellie Yuk Fei Chung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 111-120). / Abstract also in Chinese. / Abstract --- p.i / List of Abbreviations --- p.iii / Acknowledgements --- p.iv / Publication of this study --- p.vi / Table of Contents --- p.vii / Chapter Chapter1: --- Introduction --- p.1 / Chapter 1.1 --- Multiple Myeloma --- p.2 / Chapter 1.2 --- The Problem --- p.2 / Chapter Chapter2: --- Literature Review --- p.5 / Chapter 2.1 --- Molecular Genetics of Multiple Myeloma --- p.6 / Chapter 2.1.1 --- Cytogenetics --- p.6 / Chapter 2.2 --- Alterations of Proto-Oncogenes --- p.9 / Chapter 2.2.1 --- c-myc --- p.9 / Chapter 2.2.2 --- Ras --- p.10 / Chapter 2.2.3 --- Bcl-2 and Related Protein --- p.10 / Chapter 2.3 --- Alteration of Tumor-Suppressor genes --- p.11 / Chapter 2.3.1 --- p53 Gene Mutations --- p.11 / Chapter 2.3.2 --- Retinoblastoma (Rb) Gene --- p.11 / Chapter 2.3.3 --- p16 and p15 Genes --- p.13 / Chapter Chapter3: --- DNA Methylation and Cancers --- p.14 / Chapter 3.1 --- Role of DNA Methylation --- p.15 / Chapter 3.2 --- CpG Islands --- p.15 / Chapter 3.3 --- Abnormalities of DNA Methylation in Neoplasia --- p.16 / Chapter 3.3.1 --- DNA Hypomethylation in Cancer --- p.16 / Chapter 3.3.2 --- DNA Methyltransferase Activity in Cancer --- p.17 / Chapter 3.4 --- Regional DNA Hypermethylation in Cancer --- p.17 / Chapter 3.4.1 --- p16 and p15 Genes in Solid Tumors --- p.18 / Chapter 3.4.2 --- The p16 and p15 Genes in Leukemia and other Hematopoietic Malignancies --- p.19 / Chapter 3.4.3 --- Retinoblastoma Gene --- p.20 / Chapter 3.5 --- Mechanism Underlying the DNA Methylation Changes --- p.21 / Chapter Chapter4: --- Background of Study --- p.23 / Chapter 4.1 --- Background of Study --- p.24 / Chapter 4.2 --- Project Objectives --- p.27 / Chapter Chapter5: --- Materials and Methods --- p.29 / Chapter 5.1 --- Patients Samples --- p.30 / Chapter 5.2 --- Normal Controls --- p.30 / Chapter 5.3 --- Storage of the Samples --- p.32 / Chapter 5.4 --- Materials --- p.32 / Chapter 5.4.1 --- Chemicals --- p.32 / Chapter 5.4.2 --- Primers --- p.33 / Chapter 5.4.3 --- Enzymes --- p.35 / Chapter 5.5 --- Methods --- p.35 / Chapter 5.5.1 --- Cloning of p16 and p15 Exon 1 Probes for Southern Analysis --- p.35 / Chapter 5.5.1.1 --- PCR Amplification of p16 and p15 exon1 Probes from Normal Blood DNA --- p.35 / Chapter 5.5.1.2 --- Recovery and Purification of p16 and p15 Exon 1 DNA Fragment --- p.36 / Chapter 5.5.1.3 --- Ligation --- p.37 / Chapter 5.5.1.4 --- Transformation --- p.37 / Chapter 5.5.1.5 --- Plating --- p.38 / Chapter 5.5.1.6 --- Screening of Recombinant Plasmid --- p.38 / Chapter 5.5.1.7 --- Confirmation of Cloned DNA by Sequencing --- p.42 / Chapter 5.5.2 --- DNA Extraction and Purification --- p.45 / Chapter 5.5.2.1 --- DNA Extraction from Bone Marrow Aspirate and Peripheral Blood --- p.45 / Chapter 5.5.2.2 --- Isolation of Plasmid DNA from Transformant Cutures --- p.46 / Chapter 5.5.2.3 --- Qualification and Quantification of DNA --- p.49 / Chapter 5.5.3 --- Detection of Hypermethylation by Southern Analysis --- p.50 / Chapter 5.5.3.1 --- Restriction Enzyme Digestion --- p.50 / Chapter 5.5.3.2 --- Agarose Gel Electrophoresis --- p.51 / Chapter 5.5.3.3 --- Southern Transfer --- p.51 / Chapter 5.5.3.4 --- Membrane Fixation --- p.51 / Chapter 5.5.3.5 --- Recovery and Purification of p16 and p15 Exon 1 Probes from Plasmid --- p.52 / Chapter 5.5.3.6 --- Probe Labeling --- p.54 / Chapter 5.5.3.7 --- Purification of Radioactive labeled DNA --- p.54 / Chapter 5.5.3.8 --- Southern Hybridization --- p.55 / Chapter 5.5.3.9 --- Post Hybridization --- p.55 / Chapter 5.5.3.10 --- Autoradiography --- p.56 / Chapter 5.5.4 --- Polymerase Chain Reaction-Single Strand Conformational Polymorphism Analysis (PCR-SSCP) --- p.56 / Chapter 5.5.4.1 --- 5'- end Radioactive Labeling of Primer --- p.56 / Chapter 5.5.4.2 --- Amplification of Target Sequence by PCR --- p.57 / Chapter 5.5.4.3 --- Non-denaturing Polyacrylamide Gel Electrophresis --- p.57 / Chapter 5.5.4.4 --- Direct DNA Sequence of PCR Products --- p.58 / Chapter 5.5.5 --- Prevention of Overall Contamination in PCR --- p.60 / Chapter 5.5.6 --- "Sensitivity, Specificity Controls" --- p.62 / Chapter Chapter6: --- Results --- p.64 / Chapter 6.1 --- Patient Characteristics --- p.65 / Chapter 6.1.1 --- General Patient Characteristics --- p.65 / Chapter 6.1.2 --- Clinical and Laboratory Features --- p.65 / Chapter 6.2 --- Southern Blot Analysis of p16/p15 and Rb --- p.79 / Chapter 6.2.1 --- Absence of Deletions or hypermethylationin Normal Controls --- p.79 / Chapter 6.2.2 --- Absence of Homozygous Deletions or Mutationsin p16/15 and Rb among all MM Patients --- p.79 / Chapter 6.2.3 --- Hypermethylation of p16 --- p.89 / Chapter 6.2.4 --- Hypermethylation of p15 --- p.92 / Chapter 6.3 --- Hypermethylation of p16/p15 and Clinico-pathologic Correlation --- p.94 / Chapter Chapter7: --- Discussion --- p.97 / Chapter 7.1 --- "Absence of Homozygous Deletions, Gene Rearrangements and Mutations in p16/p15 and Rb" --- p.98 / Chapter 7.2 --- Hypermethylation of p16/p15-An Alternative Way for Gene Inactivation --- p.100 / Chapter 7.2.1 --- Methylation of p15 Gene --- p.101 / Chapter 7.2.2 --- Methylation of 5'-CpG Island of p16/p15 and Lack of Gene Expression --- p.102 / Chapter 7.2.3 --- Comparison of Methylation Status of Primary Samples and Cell Lines in MM --- p.103 / Chapter 7.2.4 --- Progressive Gene Inactivation by Random Methylation Errors --- p.104 / Chapter 7.2.5 --- The Lack of Correlation of Tumor Contents Revealed by the Southern Analysis and Morphologic Assessment --- p.105 / Chapter 7.3 --- Knudson's Two-hit Model of Tumorigenesis --- p.106 / Chapter 7.4 --- Inverse Relationship of p16 and Rb --- p.107 / Chapter 7.5 --- Implications of Our Findings --- p.109 / Chapter 7.6 --- Future Studies --- p.109 / References --- p.111

Leung Sau Ching. / Thesis submitted in: October 2003. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 142-165). / Abstracts in English and Chinese. / Acknowledgments --- p.ii / Abstract (English Version) --- p.iii / Abstract (Chinese Version) --- p.vi / Table of Contents --- p.viii / List of Tables --- p.xii / List of Figures --- p.xiii / List of Abbreviations --- p.xv / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Multiple Myeloma (MM) --- p.1 / Chapter 1.1.1 --- Epidemiology --- p.3 / Chapter 1.1.2 --- Clinical and Pathologic Features of MM --- p.3 / Chapter 1.1.3 --- Diagnosis and Staging --- p.4 / Chapter 1.1.4 --- Prognosis --- p.6 / Chapter 1.1.5 --- Treatment --- p.7 / Chapter 1.2 --- Molecular Abnormalities of MM --- p.8 / Chapter 1.2.1 --- Genetic Alterations: Chromosomal Aberrations --- p.8 / Chapter 1.2.2 --- Genetic Alterations: Ras Mutations --- p.11 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.12 / Chapter 2.1 --- Epigenetic Alterations: DNA Methylation --- p.12 / Chapter 2.1.1 --- Characteristics of CpG Island --- p.14 / Chapter 2.1.2 --- Mechanism of Methylation-Related Gene Silencing --- p.14 / Chapter 2.1.3 --- DNA Methylation Is Important for Normal Cellular Functions --- p.17 / Chapter 2.1.4 --- DNA Methylation Changes in Cancer Cells --- p.17 / Chapter 2.1.5 --- Global DNA Hypomethylation --- p.18 / Chapter 2.1.6 --- Regional DNA Hypermethylation --- p.20 / Chapter 2.1.6.1 --- De Novo Methylation --- p.21 / Chapter 2.1.6.2 --- DNA Hypermethylation Acts as a Third Pathway to Loss of Function in Carcinogenesis --- p.21 / Chapter 2.1.6.3 --- DNA Hypermethylation Contributes to Tumorigenesis --- p.25 / Chapter 2.1.6.4 --- Methodologies in the Study of DNA Hypermethylation --- p.26 / Chapter 2.1.6.5 --- Single Gene Hypermethylation --- p.28 / Chapter 2.1.6.6 --- Multiple Gene Hypermethylation --- p.30 / Chapter 2.1.6.7 --- Potential Clinical Applications of DNA Hypermethylation --- p.36 / Chapter 2.1.6.7.1 --- Tumor Cells Detection by 5'CpG Island Hypermethylation --- p.37 / Chapter 2.1.6.7.2 --- Prognostic and Predictive Significances of DNA Hypermethylation --- p.39 / Chapter 2.1.6.7.3 --- Therapeutic Intervention of CpG island Hypermethylation --- p.40 / Chapter 2.2 --- DNA Hypermethylation in MM and MGUS --- p.43 / Chapter 2.3 --- Six-Genes Panel for the Hypermethylation Study --- p.45 / Chapter 2.3.1 --- Apoptotic Pathway: DAP-kinase --- p.45 / Chapter 2.3.2 --- Retinoid Signaling Pathway: RARβ --- p.50 / Chapter 2.3.3 --- Angiogenic Pathway: THBS-1 --- p.52 / Chapter 2.3.4 --- Cell cycle Regulatory Pathway: pl6 and p15 --- p.57 / Chapter 2.3.5 --- Ras Signaling Pathway: RASSF1A --- p.62 / Chapter CHAPTER 3 --- BACKGROUND OF STUDY --- p.67 / Chapter 3.1 --- Rationale --- p.67 / Chapter 3.2 --- Hypothesis --- p.69 / Chapter 3.3 --- The Objectives of Study --- p.70 / Chapter CHAPTER 4 --- MATERIALS AND METHODS --- p.71 / Chapter 4.1 --- Culture of Human Multiple Myeloma (MM)-derived Cell Lines --- p.71 / Chapter 4.2 --- Demethylation Treatment --- p.72 / Chapter 4.3 --- Patient and Control Samples --- p.72 / Chapter 4.4 --- DNA Extraction --- p.73 / Chapter 4.5 --- MS-PCR --- p.73 / Chapter 4.6 --- Plasma Cell Isolation --- p.77 / Chapter 4.7 --- RNA Extraction and RT-PCR --- p.78 / Chapter 4.8 --- Statistics --- p.82 / Chapter CHAPTER 5 --- RESULTS --- p.84 / Chapter 5.1 --- Patient Characteristics --- p.84 / Chapter 5.2 --- Single Gene Hypermethylation --- p.87 / Chapter 5.2.1 --- Normal PB Did Not Show Methylation --- p.87 / Chapter 5.2.2 --- DNA Hypermethylation in Human MM-derived Cell Lines --- p.87 / Chapter 5.2.3 --- DNA Hypermethylation in Primary MM --- p.89 / Chapter 5.3 --- Demethylation Treatment --- p.93 / Chapter 5.4 --- Concurrent Hypermethylation --- p.96 / Chapter 5.5 --- Statistical Analyses of Primary MM --- p.101 / Chapter 5.5.1 --- Statistical Analyses Between Single Gene Hypermethylation and Clinical Parameters (Categorical) --- p.101 / Chapter 5.5.2 --- Statistical Analyses Between Single Gene Hypermethylation and Clinical Parameters (Non-Categorical) --- p.101 / Chapter 5.5.3 --- Survival Analyses of Single Gene Hypermethylation --- p.105 / Chapter 5.5.4 --- Correlation Analyses of Concurrent Hypermethylation --- p.107 / Chapter 5.5.5 --- Correlation Analyses Between Concurrent Hypermethylation and Clinical Parameters --- p.107 / Chapter CHAPTER 6 --- DISCUSSION --- p.110 / Chapter 6.1 --- Involvement of Cellular Pathways by Hypermethylation --- p.111 / Chapter 6.1.1 --- Apoptotic Pathway: DAP-kinase and RARβ --- p.111 / Chapter 6.1.2 --- "Cell Cycle Regulatory Pathway: p16, p15 and RASSF1A" --- p.113 / Chapter 6.1.3 --- Angiogenic Pathway: THBS-1 --- p.117 / Chapter 6.2 --- Hypermethylation-Associated Gene Silencing --- p.119 / Chapter 6.3 --- Hypermethylation in Cell Lines and Primary MM --- p.120 / Chapter 6.4 --- Concurrent Hypermethylation --- p.122 / Chapter 6.4.1 --- DNA Hypermethylation is Common in MM --- p.122 / Chapter 6.4.2 --- Extent of Hypermethylation --- p.123 / Chapter 6.4.3 --- Involvement of Cellular Pathways by DNA Hypermethylation --- p.124 / Chapter 6.4.4 --- Concurrent p16 and DAP-kinase Hypermethylation --- p.126 / Chapter 6.5 --- Clinical Applications of DNA Hypermethylation --- p.129 / Chapter 6.5.1 --- Methylation As Tumor Markers for MM --- p.129 / Chapter 6.5.2 --- Prognostic Implications of DNA Hypermethylation in MM --- p.130 / Chapter 6.5.3 --- Correlations Between DNA Hypermethylation and Clinical Parameters --- p.131 / Chapter 6.6 --- MS-PCR --- p.136 / Chapter CHAPTER 7 --- CONCLUSION --- p.137 / Chapter CHAPTER 8 --- FURTHER STUDIES --- p.140 / References --- p.142

Tese de doutoramento. Engenharia Electrotécnica e de Computadores. Faculdade de Engenharia. Universidade do Porto. 2009

Thesis (M.Ed.)--University of Hong Kong, 1984. / Includes bibliographical references (leaf 68-74). Also available in print.