Energy harvesting embedded wireless sensor system for building environment applications

For many wireless sensor networks applications, indoor light energy is the only ambient energy source commonly available. Many advantages and constraints co-exist in this technology. However, relatively few indoor light powered harvesters have been presented and much research remains to be carried out on a variety of related design considerations and trade-offs. This work presents a solution using the Tyndall mote and an indoor light powered wireless sensor node. It analyses design considerations on several issues such as indoor light characteristics, solar panel component choice, maximum power point tracking, energy storage elements and the trade-offs and choices between them.

Statistical method of modeling and optimization for wireless sensor nodes with different interconnect technologies and substrates

A comparison study was carried out between a wireless sensor node with a bare die flip-chip mounted and its reference board with a BGA packaged transceiver chip. The main focus is the return loss (S parameter S11) at the antenna connector, which was highly depended on the impedance mismatch. Modeling including the different interconnect technologies, substrate properties and passive components, was performed to simulate the system in Ansoft Designer software. Statistical methods, such as the use of standard derivation and regression, were applied to the RF performance analysis, to see the impacts of the different parameters on the return loss. Extreme value search, following on the previous analysis, can provide the parameters' values for the minimum return loss. Measurements fit the analysis and simulation well and showed a great improvement of the return loss from -5dB to -25dB for the target wireless sensor node.

Design and implementation of the embedded capacitance layers for decoupling of wireless sensor nodes

In this paper, the embedded capacitance material (ECM) is fabricated between the power and ground layers of the wireless sensor nodes, forming an integrated capacitance to replace the large amount of decoupling capacitors on the board. The ECM material, whose dielectric constant is 16, has the same size of the wireless sensor nodes of 3cm*3cm, with a thickness of only 14μm. Though the capacitance of a single ECM layer being only around 8nF, there are two reasons the ECM layers can still replace the high frequency decoupling capacitors (100nF in our case) on the board. The first reason is: the parasitic inductance of the ECM layer is much lower than the surface mount capacitors'. A smaller capacitance value of the ECM layer could achieve the same resonant frequency of the surface mount decoupling capacitors. Simulation and measurement fit this assumption well. The second reason is: more than one layer of ECM material are utilized during the design step to get a parallel connection of the several ECM capacitance layers, finally leading to a larger value of the capacitance and smaller value of parasitic. Characterization of the ECM is carried out by the LCR meter. To evaluate the behaviors of the ECM layer, time and frequency domain measurements are performed on the power-bus decoupling of the wireless sensor nodes. Comparison with the measurements of bare PCB board and decoupling capacitors solution are provided to show the improvement of the ECM layer. Measurements show that the implementation of the ECM layer can not only save the space of the surface mount decoupling capacitors, but also provide better power-bus decoupling to the nodes.

Multi-sensor classification of tennis strokes

In this work, we investigate tennis stroke recognition using a single inertial measuring unit attached to a player’s forearm during a competitive match. This paper evaluates the best approach for stroke detection using either accelerometers, gyroscopes or magnetometers, which are embedded into the inertial measuring unit. This work concludes what is the optimal training data set for stroke classification and proves that classifiers can perform well when tested on players who were not used to train the classifier. This work provides a significant step forward for our overall goal, which is to develop next generation sports coaching tools using both inertial and visual sensors in an instrumented indoor sporting environment.

The s-mote: a versatile heterogeneous multi-radio platform for wireless sensor networks applications

This paper presents a novel architecture and its implementation for a versatile, miniaturised mote which can communicate concurrently using a variety of combinations of ISM bands, has increased processing capability, and interoperability with mainstream GSM technology. All these features are integrated in a small form factor platform. The platform can have many configurations which could satisfy a variety of applications’ constraints. To the best of our knowledge, it is the first integrated platform of this type reported in the literature. The proposed platform opens the way for enhanced levels of Quality of Service (QoS), with respect to reliability, availability and latency, in addition to facilitating interoperability and power reduction compared to existing platforms. The small form factor also allows potential of integration with other mobile platforms including smart phones.

Towards persistent structural health monitoring through sustainable wireless sensor networks

This paper documents the design, implementation and characterisation of a wireless sensor node (GENESI Node v1.0), applicable to long-term structural health monitoring. Presented is a three layer abstraction of the hardware platform; consisting of a Sensor Layer, a Main Layer and a Power Layer. Extended operational lifetime is one of the primary design goals, necessitating the inclusion of supplemental energy sources, energy awareness, and the implementation of optimal components (microcontroller(s), RF transceiver, etc.) to achieve lowest-possible power consumption, whilst ensuring that the functional requirements of the intended application area are satisfied. A novel Smart Power Unit has been developed; including intelligence, ambient available energy harvesting (EH), storage, electrochemical fuel cell integration, and recharging capability, which acts as the Power Layer for the node. The functional node has been prototyped, demonstrated and characterised in a variety of operational modes. It is demonstrable via simulation that, under normal operating conditions within a structural health monitoring application, the node may operate perpetually.

Development and characterization of novel transgenic techniques for the study of neuronal circuitry

Modern neuroscience relies heavily on sophisticated tools that allow us to visualize and manipulate cells with precise spatial and temporal control. Transgenic mouse models, for example, can be used to manipulate cellular activity in order to draw conclusions about the molecular events responsible for the development, maintenance and refinement of healthy and/or diseased neuronal circuits. Although it is fairly well established that circuits respond to activity-dependent competition between neurons, we have yet to understand either the mechanisms underlying these events or the higher-order plasticity that synchronizes entire circuits. In this thesis we aimed to develop and characterize transgenic mouse models that can be used to directly address these outstanding biological questions in different ways. We present SLICK-H, a Cre-expressing mouse line that can achieve drug-inducible, widespread, neuron-specific manipulations in vivo. This model is a clear improvement over existing models because of its particularly strong, widespread, and even distribution pattern that can be tightly controlled in the absence of drug induction. We also present SLICK-V::Ptox, a mouse line that, through expression of the tetanus toxin light chain, allows long-term inhibition of neurotransmission in a small subset (<1%) of fluorescently labeled pyramidal cells. This model, which can be used to study how a silenced cell performs in a wildtype environment, greatly facilitates the in vivo study of activity-dependent competition in the mammalian brain. As an initial application we used this model to show that tetanus toxin-expressing CA1 neurons experience a 15% - 19% decrease in apical dendritic spine density. Finally, we also describe the attempt to create additional Cre-driven mouse lines that would allow conditional alteration of neuronal activity either by hyperpolarization or inhibition of neurotransmission. Overall, the models characterized in this thesis expand upon the wealth of tools available that aim to dissect neuronal circuitry by genetically manipulating neurons in vivo.

Hollow core photonic crystal fibre as a viscosity and Raman sensor

This PhD thesis investigates the application of hollow core photonic crystal fibre for use as an optical fibre nano litre liquid sensor. The use of hollow core photonic crystal fibre for optical fibre sensing is influenced by the vast wealth of knowledge, and years of research that has been conducted for optical waveguides. Hollow core photonic crystal fibres have the potential for use as a simple, rapid and continuous sensor for a wide range of applications. In this thesis, the velocity of a liquid flowing through the core of the fibre (driven by capillary forces) is used for the determination of the viscosity of a liquid. The structure of the hollow core photonic crystal fibre is harnessed to collect Raman scatter from the sample liquid. These two methods are integrated to investigate the range of applications the hollow core photonic crystal fibre can be utilised for as an optical liquid sensor. Understanding the guidance properties of hollow core photonic crystal fibre is forefront in dynamically monitoring the liquid filling. When liquid is inserted fully or selectively to the capillaries, the propagation properties change from photonic bandgap guidance when empty, to index guidance when the core only is filled and finally to a shifted photonic bandgap effect, when the capillaries are fully filled. The alterations to the guidance are exploited for all viscosity and Raman scattering measurements. The concept of the optical fibre viscosity sensor was tested for a wide range of samples, from aqueous solutions of propan-1-ol to solutions of mono-saccharides in phosphate buffer saline. The samples chosen to test the concept were selected after careful consideration of the importance of the liquid in medical and industrial applications. The Raman scattering of a wide range of biological important fluids, such as creatinine, glucose and lactate were investigated, some for the first time with hollow core photonic crystal fibre.

The role of mitogen activated protein kinase phosphatase-1 in neurotoxic and inflammatory-induced changes in the development of midbrain dopaminergic neurons: relevance to Parkinson’s disease

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterised by the loss of midbrain dopaminergic neurons from the substantia nigra pars compacta(SNpc), which results in motor, cognitive and psychiatric symptoms. Evidence supports a role for the mitogen-activated protein kinase p38 in the demise of dopaminergic neurons, while mitogen-activated protein kinase phosphatase-1 (MKP-1), which negatively regulates p38 activity, has not yet been investigated in this context. Inflammation may also be associated with the neuropathology of PD due to evidence of increased levels of proinflammatory cytokines such as interleukin-1β (IL-1β) within the SNpc. Because of the specific loss of dopaminergic neurons in a discreet region of the brain, PD is considered a suitable candidate for cell replacement therapy but challenges remain to optimise dopaminergic cell survival and morphological development. The present thesis examined the role of MKP-1 in neurotoxic and inflammatory-induced changes in the development of midbrain dopaminergic neurons. We show that MKP-1 is expressed in dopaminergic neurons cultured from embryonic day (E) 14 rat ventral mesencephalon (VM). Inhibition of dopaminergic neurite growth induced by treatment of rat VM neurons with the dopaminergic neurotoxin 6- hydroxydopamine (6-OHDA) is mediated by p38, and is concomitant with a significant and selective decrease in MKP-1 expression in these neurons. Dopaminergic neurons transfected to overexpress MKP-1 displayed a more complex morphology and contributed to neuroprotection against the effects of 6-OHDA. Therefore, MKP-1 expression can promote the growth and elaboration of dopaminergic neuronal processes and can help protect them from the neurotoxic effects of 6-OHDA. Neural precursor cells (NPCs) have emerged as promising alternative candidates to fetal VM for cell replacement strategies in PD. Here we show that phosphorylated (and thus activated) p38 and MKP-1 are expressed at basal levels in untreated E14 rat VM NPCs (nestin, DCX, GFAP and DAT-positive cells) following proliferation as well as in their differentiated progeny (DCX, DAT, GFAP and βIII-tubulin) in vitro. Challenge with 6-OHDA or IL-1β changed the expression of endogenous phospho-p38 and MKP-1 in these cells in a time-dependent manner, and so the dynamic balance in expression may mediate the detrimental effects of neurotoxicity and inflammation in proliferating and differentiating NPCs. We demonstrate that there was an up-regulation in MKP-1 mRNA expression in adult rat midbrain tissue 4 days post lesion in two rat models of PD; the 6-OHDA medial forebrain bundle (MFB) model and the four-site 6-OHDA striatal lesion model. This was concomitant with a decrease in tyrosine hydroxylase (TH) mRNA expression at 4 and 10 days post-lesion in the MFB model and 10 and 28 days post-lesion in the striatal lesion model. There was no change in mRNA expression of the pro-apoptotic gene, bax and the anti-apoptotic gene, bcl-2 in the midbrain and striatum. These data suggest that the early and transient upregulation of MKP-1 mRNA in the midbrain at 4 days post-6-OHDA administration may be indicative of an attempt by dopaminergic neurons in the midbrain to protect against the neurotoxic effects of 6-OHDA at later time points. Collectively, these findings show that MKP-1 is expressed by developing and adult dopaminergic neurons in the midbrain, and can promote their morphological development. MKP-1 also exerts neuroprotective effects against dopaminergic neurotoxins in vitro, and its expression in dopaminergic neurons can be modulated by inflammatory and neurotoxic insults both in vitro and in vivo. Thus, these data contribute to the information needed to develop therapeutic strategies for protecting midbrain dopaminergic neurons in the context of PD.

Characterisation of the role of canonical BMP-Smad 1/5/8 signalling in the development of ventral midbrain dopaminergic neurons

Ventral midbrain (VM) dopaminergic (DA) neurons, which project to the dorsal striatum via the nigrostriatal pathway, are progressively degenerated in Parkinson’s disease (PD). The identification of the instructive factors that regulate midbrain DA neuron development, and the subsequent elucidation of the molecular bases of their effects, is vital. Such an understanding would facilitate the generation of transplantable DA neurons from stem cells and the identification of developmentally-relevant neurotrophic factors, the two most promising therapeutic approaches for PD. Two related members of the bone morphogenetic protein (BMP) family, BMP2 and growth/differentiation factor (GDF) 5, which signal via a canonical Smad 1/5/8 signalling pathway, have been shown to have neurotrophic effects on midbrain DA neurons both in vitro and in vivo, and may function to regulate VM DA neuronal development. However, the molecular (signalling pathway(s)) and cellular (direct neuronal or indirect via glial cells) mechanisms of their effects remain to be elucidated. The present thesis hypothesised that canonical Smad signalling mediates the direct effects of BMP2 and GDF5 on the development of VM DA neurons. By activating, modulating and/or inhibiting various components of the BMP-Smad signalling pathway, this research demonstrated that GDF5- and BMP2-induced neurite outgrowth from midbrain DA neurons is dependent on BMP type I receptor activation of the Smad signalling pathway. The role of glial cell-line derived neurotrophic factor (GDNF)-signalling, dynamin-dependent endocytosis and Smad interacting protein-1 (Sip1) regulation, in the neurotrophic effects of BMP2 and GDF5 were determined. Finally, the in vitro development of VM neural stem cells (NSCs) was characterised, and the ability of GDF5 and BMP2 to induce these VM NSCs towards DA neuronal differentiation was investigated. Taken together, these experiments identify GDF5 and BMP2 as novel regulators of midbrain DA neuronal induction and differentiation, and demonstrate that their effects on DA neurons are mediated by canonical BMPR-Smad signalling.

Fabrication, characterisation and electroanalysis at 1-dimensional nanostructures

Integrated nanowire electrodes that permit direct, sensitive and rapid electrochemical based detection of chemical and biological species are a powerful emerging class of sensor devices. As critical dimensions of the electrodes enter the nanoscale, radial analyte diffusion profiles to the electrode dominate with a corresponding enhancement in mass transport, steady-state sigmoidal voltammograms, low depletion of target molecules and faster analysis. To optimise these sensors it is necessary to fully understand the factors that influence performance limits including: electrode geometry, electrode dimensions, electrode separation distances (within nanowire arrays) and diffusional mass transport. Therefore, in this thesis, theoretical simulations of analyte diffusion occurring at a variety of electrode designs were undertaken using Comsol Multiphysics®. Sensor devices were fabricated and corresponding experiments were performed to challenge simulation results. Two approaches for the fabrication and integration of metal nanowire electrodes are presented: Template Electrodeposition and Electron-Beam Lithography. These approaches allow for the fabrication of nanowires which may be subsequently integrated at silicon chip substrates to form fully functional electrochemical devices. Simulated and experimental results were found to be in excellent agreement validating the simulation model. The electrochemical characteristics exhibited by nanowire electrodes fabricated by electronbeam lithography were directly compared against electrochemical performance of a commercial ultra-microdisc electrode. Steady-state cyclic voltammograms in ferrocenemonocarboxylic acid at single ultra-microdisc electrodes were observed at low to medium scan rates (≤ 500 mV.s-1). At nanowires, steady-state responses were observed at ultra-high scan rates (up to 50,000 mV.s-1), thus allowing for much faster analysis (20 ms). Approaches for elucidating faradaic signal without the requirement for background subtraction were also developed. Furthermore, diffusional process occurring at arrays with increasing inter-electrode distance and increasing number of nanowires were explored. Diffusion profiles existing at nanowire arrays were simulated with Comsol Multiphysics®. A range of scan rates were modelled, and experiments were undertaken at 5,000 mV.s-1 since this allows rapid data capture required for, e.g., biomedical, environmental and pharmaceutical diagnostic applications.

A highly efficient sensor platform using simply manufactured nanodot patterned substrates

Block copolymer (BCP) self-assembly is a low-cost means to nanopattern surfaces. Here, we use these nanopatterns to directly print arrays of nanodots onto a conducting substrate (Indium Tin Oxide (ITO) coated glass) for application as an electrochemical sensor for ethanol (EtOH) and hydrogen peroxide (H

The neuropeptide pituitary adenylate cyclase activating protein stimulates human monocytes by transactivation of the Trk/NGF pathway.

Transactivation is a process whereby stimulation of G-protein-coupled receptors (GPCR) activates signaling from receptors tyrosine kinase (RTK). In neuronal cells, the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) acting through the GPCR VPAC-1 exerts trophic effects by transactivating the RTK TrkA receptor for the nerve growth factor (NGF). Both PACAP and NGF have pro-inflammatory activities on monocytes. We have tested the possibility that in monocytes, PACAP, as reported in neuronal cells, uses NGF/TrkA signaling pathway. In these cells, PACAP increases TrkA tyrosine phosphorylations through a PI-3kinase dependent but phospholipase C independent pathway. K252a, an inhibitor of TrkA decreases PACAP-induced Akt and ERK phosphorylation and calcium mobilisation resulting in decreases in intracellular H2O2 production and membrane upregulation of CD11b expression, both functions being inhibited after anti-NGF or anti-TrkA antibody treatment. K252a also inhibits PACAP-associated NF-KB activity. Monocytes increase in NGF production is seen after micromolar PACAP exposure while nanomolar treatment which desensitizes cells to high dose of PACAP prevents PACAP-induced TrkA phosphorylation, H2O2 production and CD11b expression. Finally, NGF-dependent ERK activation and H2O2 production is pertussis toxin sensitive. Altogether these data indicate that in PACAP-activated monocytes some pro-inflammatory activities occur through transactivation mechanisms involving VPAC-1, NGF and TrkA-associated tyrosine kinase activity.

Novel DNA sensor for guanine content.

The bifunctional complex [Ru(TAP)(2)POQ-Nmet](2+), 1, formed with a [Ru(TAP)(2)Phen](2+) metallic unit linked to a quinoline moiety, and [Ru(TAP)(2)Phen](2+), 2, as reference, have been tested as photoprobes of DNA. Interestingly, 1 exhibits an emission enhancement of a factor of 16-17 upon binding to calf thymus DNA. Moreover, this emission is modulated by the nucleic base content of the polynucleotide. It varies by almost an order of magnitude from a polynucleotide containing 100% of G-C to a guanine-free nucleic acid where the excited-state lifetime reaches about 2 micros. The origins of these interesting properties are analyzed by comparing 1 with reference 2 in the presence of different polynucleotides.

Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease.

Neurodegenerative diseases such as Huntington disease are devastating disorders with no therapeutic approaches to ameliorate the underlying protein misfolding defect inherent to poly-glutamine (polyQ) proteins. Given the mounting evidence that elevated levels of protein chaperones suppress polyQ protein misfolding, the master regulator of protein chaperone gene transcription, HSF1, is an attractive target for small molecule intervention. We describe a humanized yeast-based high-throughput screen to identify small molecule activators of human HSF1. This screen is insensitive to previously characterized activators of the heat shock response that have undesirable proteotoxic activity or that inhibit Hsp90, the central chaperone for cellular signaling and proliferation. A molecule identified in this screen, HSF1A, is structurally distinct from other characterized small molecule human HSF1 activators, activates HSF1 in mammalian and fly cells, elevates protein chaperone expression, ameliorates protein misfolding and cell death in polyQ-expressing neuronal precursor cells and protects against cytotoxicity in a fly model of polyQ-mediated neurodegeneration. In addition, we show that HSF1A interacts with components of the TRiC/CCT complex, suggesting a potentially novel regulatory role for this complex in modulating HSF1 activity. These studies describe a novel approach for the identification of new classes of pharmacological interventions for protein misfolding that underlies devastating neurodegenerative disease.