Browsing by Author "Kumar, Atul"
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Item Differential Chaos Shift Keying Modulation for Cooperative and Spatial Diversity Communication Systems(2015) Kumar, AtulChaotic signals are unstable and aperiodic, making them naturally harder to identify and predict. It has wideband characteristic, it is resistant against multipath fading and it offers a cheaper solution to traditional spread spectrum systems. In this thesis, the performance of differential chaos shift keying (DCSK) modulation is analyzed in different wireless communication scenarios. First, a relay selection based DCSK cooperative diversity scheme, namely DCSK selection relaying (DCSK-SR) scheme is proposed. The relay which maximizes the total received signal-to-noise ratio (SNR) at the destination is selected from a multiple multiple-input multiple-output (multiple MIMO) relay cluster to cooperate with the source node. Mathematical expression for the probability density function (PDF) of SNR for each hop and end-to-end bit error rate (BER) is derived. Secondly, a spectrum and energy efficient DCSK bidirectional relaying (DCSK-BDR) scheme is proposed in which two source nodes exchange their information through a relay node. The end-to-end BER expression for the DCSK-BDR scheme is derived. Thirdly, DCSK modulation based transmit antenna selection (TAS) schemes are proposed to reduce the effect of signal fading with less hardware complexity at the receiver. Based on receiver structure/specifications, DCSK-TAS, DCSK-joint antenna selection (DCSK-JAS) and DCSK-transmit antenna selection/equal gain combining (DCSK-TAS/EGC) schemes are proposed. BER and throughput of the proposed schemes are derived and evaluated over Nakagami-m fading channels. Finally, a high-data-rate DCSK scheme based on spatial modulation (SM), spatially modulated DCSK (SM-DCSK) is proposed. Analytical expression for the symbol error rate (SER) of the SM-DCSK scheme is derived. All the expressions derived in the thesis are validated by Monte Carlo simulation results...Item Study of microenvironment mediated chemoresistance in Chronic Myeloid Leukemia(2016) Kumar, AtulChronic Myeloid Leukemia (CML) is a myelo proliferative disorder in which the leukemic stem cells (LSC) give rise to abnormally high number of myeloid cells. CML is initiated by BCRABL fusion (9;22) (q34;q11) which is the result of reciprocal translocation between chromosome 9 and chromosome 22. BCR-ABL fusion gene codes for Bcr-Abl fusion protein which is a constitutively active tyrosine kinase. Tyrosine kinase inhibitors (TKIs) such as Imatinib mesylate (IM) is the mainline drug used for the treatment of CML. CML responds to IM treatment efficiently, especially in the chronic phase. However, in several patients, CML relapses even after few years of remission, mainly upon discontinuation of IM intake. Mutations in the BCRABL kinase domain have been reported to be the main cause of IM resistance. However, persistent leukemic cells in the BM in spite of IM treatment play a major role in causing relapse in CML patients. BM stromal microenvironment has been implicated to be the major cause of this persistence, where mesenchymal stromal cells (MSC) and their derivatives provide chemoprotection to CML cells through secreted factors as well as direct cell-cell contact.