D3M: multicast listener mobility support mechanisms over distributed mobility anchoring architectures

The explosion in mobile data traffic is a driver for future network operator technologies, given its large potential to affect both network performance and generated revenue. The concept of distributed mobility management (DMM) has emerged in order to overcome efficiency-wise limitations in centralized mobility approaches, proposing not only the distribution of anchoring functions but also dynamic mobility activation sensitive to the applications needs. Nevertheless, there is not an acceptable solution for IP multicast in DMM environments, as the first proposals based on MLD Proxy are prone to tunnel replication problem or service disruption. We propose the application of PIM-SM in mobility entities as an alternative solution for multicast support in DMM, and introduce an architecture enabling mobile multicast listeners support over distributed anchoring frameworks in a network-efficient way. The architecture aims at providing operators with flexible options to provide multicast mobility, supporting three modes: the first one introduces basic IP multicast support in DMM; the second improves subscription time through extensions to the mobility protocol, obliterating the dependence on MLD protocol; and the third enables fast listener mobility by avoiding potentially slow multicast tree convergence latency in larger infrastructures, by benefiting from mobility tunnels. The different modes were evaluated by mathematical analysis regarding disruption time and packet loss during handoff against several parameters, total and tunneling packet delivery cost, and regarding packet and signaling overhead.

Optimization of a multielectrode array (MEA)-based approach to study the impact of Aβ on the SH-SY5Y cell line

The human brain stores, integrates, and transmits information recurring to millions of neurons, interconnected by countless synapses. Though neurons communicate through chemical signaling, information is coded and conducted in the form of electrical signals. Neuroelectrophysiology focus on the study of this type of signaling. Both intra and extracellular approaches are used in research, but none holds as much potential in high-throughput screening and drug discovery, as extracellular recordings using multielectrode arrays (MEAs). MEAs measure neuronal activity, both in vitro and in vivo. Their key advantage is the capability to record electrical activity at multiple sites simultaneously. Alzheimer’s disease (AD) is the most common neurodegenerative disease and one of the leading causes of death worldwide. It is characterized by neurofibrillar tangles and aggregates of amyloid-β (Aβ) peptides, which lead to the loss of synapses and ultimately neuronal death. Currently, there is no cure and the drugs available can only delay its progression. In vitro MEA assays enable rapid screening of neuroprotective and neuroharming compounds. Therefore, MEA recordings are of great use in both AD basic and clinical research. The main aim of this thesis was to optimize the formation of SH-SY5Y neuronal networks on MEAs. These can be extremely useful for facilities that do not have access to primary neuronal cultures, but can also save resources and facilitate obtaining faster high-throughput results to those that do. Adhesion-mediating compounds proved to impact cell morphology, viability and exhibition of spontaneous electrical activity. Moreover, SH-SY5Y cells were successfully differentiated and demonstrated acute effects on neuronal function after Aβ addition. This effect on electrical signaling was dependent on Aβ oligomers concentration. The results here presented allow us to conclude that the SH-SY5Y cell line can be successfully differentiated in properly coated MEAs and be used for assessing acute Aβ effects on neuronal signaling.