Adaptive wireless multimedia communication systems

In recent years, due to the rapid convergence of multimedia services, Internet and wireless communications, there has been a growing trend of heterogeneity (in terms of channel bandwidths, mobility levels of terminals, end-user quality-of-service (QoS) requirements) for emerging integrated wired/wireless networks. Moreover, in nowadays systems, a multitude of users coexists within the same network, each of them with his own QoS requirement and bandwidth availability. In this framework, embedded source coding allowing partial decoding at various resolution is an appealing technique for multimedia transmissions. This dissertation includes my PhD research, mainly devoted to the study of embedded multimedia bitstreams in heterogenous networks, developed at the University of Bologna, advised by Prof. O. Andrisano and Prof. A. Conti, and at the University of California, San Diego (UCSD), where I spent eighteen months as a visiting scholar, advised by Prof. L. B. Milstein and Prof. P. C. Cosman. In order to improve the multimedia transmission quality over wireless channels, joint source and channel coding optimization is investigated in a 2D time-frequency resource block for an OFDM system. We show that knowing the order of diversity in time and/or frequency domain can assist image (video) coding in selecting optimal channel code rates (source and channel code rates). Then, adaptive modulation techniques, aimed at maximizing the spectral efficiency, are investigated as another possible solution for improving multimedia transmissions. For both slow and fast adaptive modulations, the effects of imperfect channel estimation errors are evaluated, showing that the fast technique, optimal in ideal systems, might be outperformed by the slow adaptive modulation, when a real test case is considered. Finally, the effects of co-channel interference and approximated bit error probability (BEP) are evaluated in adaptive modulation techniques, providing new decision regions concepts, and showing how the widely used BEP approximations lead to a substantial loss in the overall performance.

Reconstruction and analysis of the NF-kB pathway interactome: a systems biology approach

Background. One of the phenomena observed in human aging is the progressive increase of a systemic inflammatory state, a condition referred to as “inflammaging”, negatively correlated with longevity. A prominent mediator of inflammation is the transcription factor NF-kB, that acts as key transcriptional regulator of many genes coding for pro-inflammatory cytokines. Many different signaling pathways activated by very diverse stimuli converge on NF-kB, resulting in a regulatory network characterized by high complexity. NF-kB signaling has been proposed to be responsible of inflammaging. Scope of this analysis is to provide a wider, systemic picture of such intricate signaling and interaction network: the NF-kB pathway interactome. Methods. The study has been carried out following a workflow for gathering information from literature as well as from several pathway and protein interactions databases, and for integrating and analyzing existing data and the relative reconstructed representations by using the available computational tools. Strong manual intervention has been necessarily used to integrate data from multiple sources into mathematically analyzable networks. The reconstruction of the NF-kB interactome pursued with this approach provides a starting point for a general view of the architecture and for a deeper analysis and understanding of this complex regulatory system. Results. A “core” and a “wider” NF-kB pathway interactome, consisting of 140 and 3146 proteins respectively, were reconstructed and analyzed through a mathematical, graph-theoretical approach. Among other interesting features, the topological characterization of the interactomes shows that a relevant number of interacting proteins are in turn products of genes that are controlled and regulated in their expression exactly by NF-kB transcription factors. These “feedback loops”, not always well-known, deserve deeper investigation since they may have a role in tuning the response and the output consequent to NF-kB pathway initiation, in regulating the intensity of the response, or its homeostasis and balance in order to make the functioning of such critical system more robust and reliable. This integrated view allows to shed light on the functional structure and on some of the crucial nodes of thet NF-kB transcription factors interactome. Conclusion. Framing structure and dynamics of the NF-kB interactome into a wider, systemic picture would be a significant step toward a better understanding of how NF-kB globally regulates diverse gene programs and phenotypes. This study represents a step towards a more complete and integrated view of the NF-kB signaling system.