VictorJuiz/thesis huggingface dataset:
Radiated Electric and Magnetic Fields Caused by Lightning Return Strokes to the Toronto CN Tower
Keywords: Return Stroke
Engineering Model
CN Tower
Five-Section Model
Variable Return Stroke Speed
Electric Field
Magnetic Field
Cartesian Coordinates

In the present PhD work, three sophisticated models based on the "Engineering" modeling approach have been utilized to conveniently describe and thoroughly analyze details of Lightning events at the CN Tower. Both the CN Tower and the Lightning Channel are represented by a number of connected in series Transmission Line sections in order to account for the variations in the shape of the tower and for plasma processes that take place within the Lightning Channel. A sum of two Heidler functions is used to describe the "uncontaminated" Return Stroke current, which is injected at the attachment point between the CN Tower and the Lightning Channel. Reflections and refractions at all points of mismatched impedances are considered until their contribution becomes less than 1% of the originally injected current wave. In the proposed models, the problem with the current discontinuity at the Lightning Channel front, commonly taken care of by introducing a "turn-on" term when computing radiation fields, is uniquely treated by introducing reflected and transmitted components. For the first time, variable speed of propagation of the Return Stroke current front has been considered and its influence upon the predicted current distributions along the whole Lightning Channel path and upon the radiated distant fields analyzed. Furthermore, as another novelty, computation of the electromagnetic field is accomplished in Cartesian Coordinates. This fact permits to relax the requirement on the verticality of the Lightning Channel, normally imposed in Cylindrical Coordinates. Therefore, it becomes possible to study without difficulty the influence of a slanted Lightning Channel upon the surrounding electromagnetic field. Since the proposed sophisticated Five-Section Model has the capability to represent very closely the structure of the CN Tower and to emulate faithfully the shape of, as well as physical processes within the Lightning Channel, it is believed to have the potential of truthfully reproducing observed fields. The developed modeling approach can be easily adapted to study the anticipated radiated fields at tall structures even before construction.
To Live and Learn with Neurological Challeges: Life Histories of Two Teenagers in and Educative Community
Keywords: special education
disability
child development
risk and resiliency
youth at risk
neurological disorders
tourette syndrome
social work

The research, on which this account is based, took place within the context of Blooming Acres, my home, and the learning community that I co-founded with my wife Sherri-Ann. In the first chapters, I tell the story of how I came to home-educate learners with complex special needs at my farm north of Toronto, Canada. I describe the neurological disorders that the children in my care are diagnosed with and map out the main literature that guides how I think about and practice education. The aim of this section is to paint a picture of the context in which the research takes place and describe my role in this community. The second section consists of my research with two of the children who lived and learned at Blooming Acres. This includes their stories as told by them, their parent(s), and the educators at Blooming Acres. As I juxtaposed the life experiences of these learners with each other, and wove together aspects of these stories, significant themes emerged relating to their academic and medical histories, as well as their social, extracurricular, and family life, and finally, their experience at Blooming Acres. I employed a life history methodology; one that honours the meaning and knowledge that exists in the storied lives of individuals. As I applied this methodology and engaged in the storied lives of these learners I learned more about what it is like to live and learn with neurological disorders. Four major themes emerged. The first, Pathology for Support / Support for Pathology, relates to learning issues, referral, assessment, diagnosis, medications and “school battles”. Second, Parent Stress includes behavioural issues, judgment, stressful calls from teachers and principals and school failure. Third, Oasis Teachers / Mentors is an expression of care, support, social competence, self-esteem and relationships. Finally, Strengths and Coping is a culmination of issues such as advocacy for support, strategies for success, identifying and coping with stress, understanding diagnosis and becoming well. These emergent themes are articulated within the context of neurology and school failure (risk) and the context of transformation and getting well (resilience). This work contributes to parenting, education, social work, disabilities, medical and risk / resiliency literature.
The Neural Correlates of Auditory Processing in Adults and Children who Stutter
Keywords: developmental stuttering
speech production
auditory processing
neuroimaging
magnetoencephalography (MEG)
magnetic resonance imaging (MRI)
voxel-based morphometry (VBM)
motor movement

This dissertation is comprised of four studies investigating the hypothesis that adults and children who stutter differ from their same-age fluent peers in the neuroanatomy and neurophysiology underlying auditory speech processing. It has been consistently reported that adults who stutter demonstrate unique functional neural activation patterns during speech production, including reduced auditory activation, relative to nonstutterers. The extent to which these functional differences are accompanied by abnormal morphology of the brain in stutterers is unclear. The first study in this dissertation examined the neuroanatomical differences in speech-related cortex between adults who do and do not stutter using magnetic resonance imaging and voxel-based morphometry analyses. Adults who stutter were found to have localized grey matter volume increases in auditory and motor speech related cortex. The second study extended this line of research to children who stutter, who were found to have localized grey matter volume decreases in motor speech related cortex. Together, these studies suggest an abnormal trajectory of regional grey matter development in motor speech cortex of people who stutter. The last two studies investigated the mechanism underlying the repeated findings of reduced auditory activation during speech in people who stutter in more detail. Magnetoencephalography was used to investigate the hypothesis that people who stutter have increased speech induced suppression of early evoked auditory responses. Adults and children who stutter demonstrated typical levels of speech induced suppression relative to fluent peers. However, adults and children who stutter showed differences from peers in the timing of cortical auditory responses. Taken together, the studies demonstrate structural and functional abnormalities in brain regions related to auditory processing and point to the possibility that people who stutter have difficulty forming the neural representations of speech sounds necessary for fluent speech production.
Dysfunctional AMPA Receptor Trafficking in Traumatic Brain Injury
Keywords: Trauma
Glutamate
AMPA
Injury

Traumatic brain injury (TBI) is a devastating public health problem for patients and their families. The neurodegeneration that follows TBI is complex, but can be broadly subdivided into primary and secondary damage. Though primary damage is irreversible and therefore unsalvageable, extensive literature aimed at understanding the tissue, cellular, inflammatory and subcellular processes following the injury have proven unequivocally that secondary pathophysiological events are delayed and progressive in nature. Understanding these secondary events at the cellular levels is critical in the eventual establishment of targeted therapeutics aimed at limiting progressive injury after an initial trauma. One such secondary event is referred to in the literature as excitotoxicity; a sustained and de-regulated activation of glutamate receptors that leads to rapid cytotoxic edema and calcium overload. Our understanding of excitotoxicity has evolved to include not only a role for elevated extracellular glutamate in mediating neuronal damage, but also post-synaptic receptor modifications that render glutamate profoundly more toxic to injured neurons than healthy tissue. In this thesis, we explored the hypothesis that glutamate excitotoxicity can be perpetuated by trauma-induced post-synaptic modification of the AMPA receptor. Specifically, we used a cortical culture model of TBI as well as the fluid percussion injury device to test the hypothesis that TBI confers a reduction of surface GluR2 protein, an AMPA receptor subunit that limits neuronal calcium permeability. We conjectured that this decrease in the expression of surface GluR2 would increase the expression of calcium-permeable AMPA receptors, thereby rendering neurons vulnerable to secondary excitotoxic injury. We further investigated the subcellular mechanisms responsible for the internalization of surface GluR2, and the phenotypic consequences of GluR2 endocytosis in both models. Our data revealed that both models of TBI resulted in a regulated signaling cascade leading to the phosphorylation and internalization of GluR2. By exogenously interrupting the trafficking of GluR2 protein with an inhibitory peptide, we further observed that GluR2 internalization was mediated by a protein interaction involving protein interacting with C kinase 1 (PICK1) and protein kinase C alpha (PKCα), two PDZ domain-containing proteins that mediate GluR2 trafficking during constitutive synaptic plasticity. We observed that GluR2 endocytosis was NMDA receptor dependent, and resulted in increased neuronal calcium permeability, augmented AMPA receptor-mediated electrophysiological activity and increased susceptibility to delayed cell death. Finally, we demonstrated that the interruption of GluR2 trafficking is cytoprotective, suggesting that sustaining surface GluR2 protein protects neurons against secondary injury. Overall, our findings suggest that experimental TBI promotes the expression of injurious GluR2-lacking AMPA receptors, thereby enhancing cellular vulnerability to secondary excitotoxicity.
Networks Are Not Enough: Urban Governance and Workforce Development in Three Ontario Cities
Keywords: urban governance
workforce development

Cities everywhere are struggling to develop strategic responses to vast and rapid economic changes brought about by globalization while mediating the social impact of economic change. Workforce development is a policy area that straddles the divide between economic development and social welfare imperatives. This thesis examines local networks supporting workforce development activities in three Ontario cities in order to better understand the dynamics of urban governance in Canada. The analysis focuses on the two central questions of whether cities have the political autonomy to develop their own strategic workforce development networks, and if so, do these networks reflect efforts to integrate economic development and social welfare considerations. It engages with three theoretical perspectives that offer different explanations for local governance dynamics: neo-institutionalist theories argue that higher institutional structures shape and constrain local governance efforts; the critique of neo-liberalism argues that local governance dynamics will be dominated by the interests of capital for economic development; and theories of urban governance argue that cities have the autonomy to shape their own governance efforts. Theories of urban governance also focus analytical attention on how the patterns of interaction between local state and non-state actors shape local governance dynamics. The study does find evidence of local workforce development networks, and finds that these networks vary according to the patterns of interaction between local state and non-state actors. From a neo-institutionalist perspective, however, the study also finds that macro-institutional policy frameworks shape and constrain these local governance efforts.
A Composite Polymeric Drug Delivery System for Treatment of Spinal Cord Injury
Keywords: drug delivery
hydrogel
nanoparticle
spinal cord injury

There are no clinically approved drug delivery strategies designed for localized and sustained release to the injured spinal cord, two features which are heavily exploited in pre-clinical demonstrations of efficacy. We have previously shown that injection of drug loaded hydrogels into the intrathecal space is safe, minimally invasive, and drug release localized to the site of injection for up to one day. In the present work we developed a platform for sustained release from 1 to 28 days based on a physical gel of methylcellulose with hyaluronan and poly(lactic-co-glycolic acid) (PLGA) nanoparticles added as gelation agents. These composite hydrogels met the design criteria of injectability, fast gelation, minimal swelling, and 28 day stability. Sustained release of 6 therapeutic molecules from the composite was achieved by encapsulation in the particles or dissolution in the hydrogel. Release of PLGA encapsulated drugs from the composite was linear for 28 days. Drugs dissolved in the hydrogel were released by Fickian diffusion. The HAMC hydrogel/PLGA nanoparticle composite was delivered to uninjured and spinal cord injured rats and the animals monitored for 14 and 28 days respectively. The composite was well tolerated in the intrathecal space with no impact on motor function as determined by the BBB scale and minimal inflammation in both studies. No increase in reactive astrocytes or cavity volume was found in clip compression spinal cord injured rats, indicating that the composite did not affect these aspects of the secondary injury cascade. We then turned to sustained release of anti-NogoA, a promising neuroregenerative molecule typically delivered for 2 - 4 weeks. Formulations of anti-NogoA or a model IgG were prepared and release was demonstrated over 28 days in vitro. Bioactivity was assessed using a novel ELISA which utilized anti-NogoA / NogoA binding to detect only active antibody, advantageous because anti-NogoA release can now be easily optimized prior to in vivo studies of efficacy. The key features of current work are the development of an intrathecal drug delivery platform, demonstration of safety in a rat model, and formulation for use with anti-NogoA.
Late Assyrian Arms and Armour: Art versus Artifact
Keywords: Assyria
weapons
arms
armour
military
Nimrud
art history
Mesopotamia
reliefs
Neo-Assyrian
warfare

The present study was intended as a new approach to the study of the military equipment of the Late Assyrian period which has traditionally relied upon the pictorial representations of the palace reliefs. By examining extant artifacts from the first millennium in their own right, with the reliefs merely serving to contextualize them, a truer understanding of Assyrian arms and armour can be gathered. This is necessary because the artwork only provides us with a filtered view of the real world, the reliefs are as much works of propaganda as of history. The approach taken here is to first examine the existing weapons typologically, and then to evaluate whether such weapon types appear to be accurately represented in contemporary artwork. Textual sources are also used where they can aid in the discussion. Five categories of arms and armour were studied: swords and daggers, spearpoints, shields, armour and helmets. The quality and quantity of the items in these categories varied significantly, providing for a much better representative sample of some items than others. Further questions concerning the possible ritual, rather than military, use of some of the existing artifacts were raised. However, the main conclusions reached were that the reliefs suffer not only from a propagandistic viewpoint which sometimes obscures the reality of Assyrian warfare, but that they also suffer from artistic license and spatial restraints, the difficulties in representing three-dimensional objects in a two-dimensional manner, the possible unfamiliarity of the artists with changing military technology and methods of construction, and finally, our inability to understand artistic short-hand for what were commonplace objects to the contemporary viewer. These have led to misunderstanding both as to the dating and chronological changes in weaponry, and also to the tactics used by the Late Assyrian military. This study of the artifacts themselves reveals a more mundane, utilitarian, and conservative military force which shows both a basic homogeneousness throughout the empire, and the myriad tiny variables of an army on the move drawing weapons and troops from many regions.
Mechanisms Underlying Cardioprotective Effects of Glucagon like Peptide-1 in Ischemia-reperfusion Injury
Keywords: GLP-1
ischemia reperfsuion

Cardioprotective effects of glucagon-like peptide-1 (GLP-1), the GLP-1 receptor (GLP-1R) agonist exendin-4 (Ex-4), and GLP-1(9-36), a cleavage product of GLP-1, were examined in ischemia-reperfusion (I/R) models of both isolated mouse hearts and cultured cardiac myocytes (CMs) using both wild-type (WT) and GLP-1R knockout (Glp1r-/-) mice. In WT hearts, GLP-1 and Ex-4 significantly improved left ventricular functional recovery vs. untreated controls following I/R, whether the drugs were administered prior to ischemia (pre-ischemia) or during reperfusion (post-ischemia). Surprisingly, the cardioprotective effects of pre- and post-ischemia treatments with GLP-1, but not Ex-4, remained evident in Glp1r-/- hearts. Although pre-ischemia infusion of GLP-1(9-36) induced lower functional recovery than untreated controls, post-ishemia infusion of GLP-1(9-36) augmented functional recovery and reduced infarct size to a similar extent to that of GLP-1 and Ex-4 in hearts from both WT and Glp1r-/- mice. Mass spectrometry was used to assay conversion of GLP-1 to GLP-1(9-36) in coronary effluents of isolated mouse hearts. Within 15 min of infusing GLP-1, significant amounts of GLP-1(9-36) were generated by the heart. By 30 min, only trace amounts of intact GLP-1 remained in coronary effluents indicating the heart rapidly converts GLP-1 to GLP-1(9-36). In CMs undergoing simulated I/R injury in vitro, both GLP-1(9-36) and Ex-4 significantly improved cell viability, LDH release and caspase-3 activation. These effects were significantly attenuated by co-treatments with LY294002, PD98059 and Ex(9-39), inhibitors of PI3K, ERK1/2, and GLP-1R respectively. The actions of Ex-4, but not GLP-1(9-36), were lost in CMs isolated from Glp1r-/- mice and only GLP-1(9-36), but not Ex-4, improved the survival of human aortic endothelial cells (HAEC) undergoing simulated I/R injury. Of note, both GLP-1 and GLP-1(9-36) treatments also demonstrated potent vasodilatory effects, as manifested by increased coronary flow rates in isolated hearts and increased diameters of pre-constricted mesenteric arteries isolated from both WT and Glp1r-/- mice. The cardioprotective effects on isolated hearts and vasodilatory effects on isolated mesenteric arteries, induced by GLP-1 was blunted by co-treatment with a dipeptidyl peptidase-4 (DPP-4) enzyme inhibitor known to block conversion of GLP-1 to GLP-1(9-36). Together, these data suggest that the beneficial effects of GLP-1 in I/R injury are mediated in part by GLP(9-36) and support the existence of a GLP-1(9-36) responsive, but Ex(9-39)-sensitive cardioprotective signaling pathway distinct from that associated with the classical GLP-1R.
Maternal-infant Predictors of Attendance at Neonatal Follow-up Programs
Keywords: Mothers of At-Risk Infants
Premature Infants
Predictors
Psychosocial Outcomes
Neonatal Follow-up Programs
Health Disparity
Quantitative
Health Services Use
Neonate
Health Behavioural Research

Attendance at Neonatal Follow-up (NFU) programs is crucial for parents to gain access to timely diagnostic expertise, psychosocial support, and referral to needed services for their infants. Although NFU programs are considered beneficial, up to 50% of parents do not attend these programs with their infants. Non-attending infants have poorer outcomes (e.g., higher rates of disabilities and less access to required services) as compared to attenders. The purpose was to determine factors that predicted attendance at NFU. Naturally occurring attendance was monitored and maternal-infant factors including predisposing, enabling, and needs factors were investigated, guided by the Socio-Behavioral Model of Health Services Use. A prospective two-phase multi-site descriptive cohort study was conducted in 3 Canadian Neonatal Intensive Care Units that refer to 2 NFU programs. In Phase 1, standardized questionnaires were completed by 357 mothers (66% response rate) prior to their infant’s (N= 400 infants) NICU discharge. In Phase 2, attendance patterns at NFU were followed for 12 months. Higher maternal stress at the time of the infant’s NICU hospitalization was predictive of attendance at NFU. Parenting alone, more worry about maternal alcohol or drug use, and greater distance to NFU were predictive of non-attendance at NFU. Attendance at NFU decreased over time from 84% at the first appointment to 74% by 12 months. Two distinct attendance patterns emerged: no or minimal attendance (18.5%) and attendance at all or the majority of scheduled appointments (81.5%). The most frequent point of withdrawal from NFU occurred between NICU discharge and the first scheduled appointment; followed by drop-out following the first NFU appointment. These results provide new insight into patterns of attendance and the maternal-infant factors that characterize attenders/non-attenders at NFU and serve as the critical first step in developing interventions targeted at improving attendance, infant outcomes, and reporting of developmental sequelae.