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Abstract: Piezoelectric Energy Harvesters (PEHs) can be used to supply power to small electronic devices as the Wireless Sensor Nodes (WSNs). However, the harvested energy from the harvesters are usually little and needs to be stored into storage elements. A high-efficiency electrical interface with minimum power losses is required to bridge between the PEHs and the storage device. In this thesis, a novel self-powered high-efficiency Negative Voltage Converter – Parallel Synchronized Switch Harvesting on Inductor (NVC-PSSHI) AC/DC interface circuit is designed to rectify the output AC voltage from the PEH to DC voltage. The NVC-PSSHI interface, built with discrete components, targets low voltage (2 Vpp to 7 Vpp) and low power applications (in the microwatt power range). Analytical, simulation and experimental work with a single PEH have been provided to prove and validate the NVC-PSSHI interface circuit. The output power from a single PEH might not be enough to power the electrical interface. Therefore, analyzing the output power from an array of PEHs against several operating conditions is of great importance, to determine the conditions of maximum output power from the PEH array. An analytical model is derived to calculate the output power from an array of PEH against the voltage magnitude and phase angle mismatch between the PEHs in the array, the number and connections (series and parallel) of the PEHs in the array, and the loading resistance connected to the PEH array. Experimental work with 4 PEHs is provided to compare with the analytical results.iii In order to charge a Lithium-Polymer (LiPo) battery at 4.2 V, a battery management (BM) circuit is needed. The designed high efficiency NVC-PSSHI interface circuit is validated with a selected battery management (BM) circuit for low power applications. The two-stage NVC-PSSHI BM interface is powered by an optimized array of PEHs to maximize the overall efficiency from the energy harvesting system. The maximum efficiency of the novel self-powered high efficiency NVC-PSSHI interface reaches 82.1% when powered by a single PEH and loaded with 15 kΩ resistance. Compared to the conventional PSSHI interface, the designed NVCPSSHI improves the efficiency by up to 23.4% at 3 Vpp and 100 Hz frequency. Considering an array of 2 PEHs, a higher reduction of output power occurs when the voltage mismatch from the 2 PEHs is 1 Vpp (35%), while only 25% of the output power is reduced when the phase angle mismatch is ±60°. The experimental output power deviation of 2 PEHs from the analytical results reaches a maximum of 16.5% for the series connection and 19.5% for the parallel connection. The maximum efficiency of the NVC-PSSHI BM interface reaches 77% at 100 kΩ loading resistance. The two-stage energy harvester interface can charge a 1 mF super capacitor to 4.2 V in around 7 minutes, and a LiPo battery from 3.8 V to 4.1 V in 14 days with charging current at 50 μA.

Acute myocardial infarction (AMI) triggers the mobilization of stem/progenitor cells from bone marrow (BMSPCs) into peripheral blood (PB). The underlying mechanisms orchestrating this mobilization and subsequent homing of BMSPCs to the myocardium are poorly understood. While the role of traditional chemokines in the mobilization and homing of hematopoietic stem cell (HSCs) to BM niches is undisputed, their role in directing BMSPCs to the highly proteolytic environment of the ischemic myocardium is debatable and other redundant mechanism may exist. Based on our observation that bioactive lipids, such as sphingosine-1 phosphate (S1P) and ceramide-1 phosphate (C1P), play an important role in regulating trafficking of HSCs; we explored if they also direct trafficking of BMSPCs in the setting of myocardial ischemia. While BMSPCs expressed S1P receptors regardless of the source, the expression of S1P receptor 1 (S1PR1) and receptor 3 (S1PR3), which are responsible for migration and chemotaxis, was elevated in BMSPCs in naïve BM cells and was reduced following mobilization. This expression correlated to differential response of BMSPCs to S1P in chemotaxis assays. By employing flow cytometry analyses, we observed an increase in circulating PB CD34+, CD133+ and CXCR4+ lineage negative (Lin-)/CD45- cells that are enriched in non-HSCs (P < 0.05 vs. controls). This corroborated our mass spectrometry studies showing a temporal increase in S1P and C1P plasma levels. At the same time, plasma obtained in the early phases following AMI strongly chemoattracted human BM-derived CD34+/Lin- and CXCR4+/Lin- cells in Transwell chemotaxis assays in an S1P dependent fashion. We examined other mechanisms that may contribute to the homing of BMSPCs to the infarcted myocardium due to the reduction of S1PRs upon mobilization. We observed that hypoxia induced higher expression of cathelicidins in cardiac tissues. Indeed, PB cells isolated from patients with AMI migrated more efficiently to low, yet physiological, gradient of SDF-1 in Transwell migration assays compared to SDF-1 alone. Together, these observations suggest that while elevated S1P plasma levels early in the course of AMI may trigger mobilization of non-HSCs into PB, cathelicidins appear to play an important role in their homing to ischemic and damaged myocardium.