Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 171-177).

Graphene is widely considered to be a promising candidate for a new generation of electronics, but there are many outstanding fundamental issues that need to be addressed before this promise can be realized. This thesis focuses on the production and properties of graphene grown epitaxially on the carbon terminated face (C-face) of hexagonal silicon carbide leading to the construction of a novel graphene transistor structure. C-face epitaxial graphene multilayers are unique due to their rotational stacking that causes the individual layers to be electronically decoupled from each other. Well-formed C-face epitaxial graphene single layers have exceptionally high mobilities (exceeding 10,000 cm^2/Vs), which are significantly greater than those of Si-face graphene monolayers. This thesis investigates the growth and properties of C-face single layer graphene. A field effect transistor based on single layer graphene was fabricated and characterized for the first time. Aluminum oxide or boron nitride was used for the gate dielectric. Additionally, an all graphene/SiC Schottky barrier transistor on the C-face of SiC composed of 2DEG in SiC/Si2O3 interface and multilayer graphene contacts was demonstrated. A multiple growth scheme was adopted to achieve this unique structure.

Asthma is a chronic disorder highlighted by intermittent airway inflammation and characterized by paroxysmal dyspnea and airway hyperresponsiveness (AHR). A key feature of severe asthma is the development of airway wall remodeling, which is thought to occur through repeated rounds of inflammation and tissue repair. Remodeling includes structural changes such as increased mass of airway smooth muscle (ASM), and excessive collagen deposition. ASM cells contribute to airway remodeling via the expression and secretion of extracellular matrix (ECM) proteins. This is particularly driven by inflammatory processes, which include mediators such as transforming growth factor (TGF)-β1 and damage associated molecular pattern (DAMP) proteins, such as high mobility group box 1 (HMGB1). HMGB1 is ubiquitously expressed as a non-histone DNA-binding protein that can regulate gene expression, but can also be released in response to stress to underpin inflammation and tissue repair. In this study we tested the hypothesis that extracellular HMGB1 induces signaling pathways that control responses linked to progression of airway inflammation, remodeling and hyperresponsiveness in human ASM cells. We used primary cultured ASM cells as well as hTERT-immortalized human ASM cells. With immunoblotting we demonstrate that exogenous HMGB1 (10 ng/mL) can induce rapid and sustained phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK) that is comparable to that induced by a potent mitogen, platelet derived growth factor (PDGF-BB, 10 ng/mL). We also found that TGF-β1 (2.5 ng/mL) promotes the accumulation of secreted HMGB1 in culture medium in a time line concomitant with expression of ECM proteins, collagen and fibronectin, suggesting a role for HMGB1 in pro-fibrotic effects of TGF-β1. By lentiviral delivery, we induced stable expression of short hairpin RNA (shRNA) that silenced expression of endogenous HMGB1 or mammalian diaphanous 1 (mDia1), a cytoplasmic scaffold protein that is required for HMGB1-induced cell responses through one of its receptors, receptor for advanced glycation end products (RAGE). Immunoblot analyses revealed that silencing of mDia1 was associated with markedly decreased induction of p42/p44 MAPK phosphorylation by exogenous HMGB1. In HMGB1-silenced human ASM cells, we observed significantly reduced synthesis and secretion of collagen A1 and fibronectin in response to TGF-β1 (2.5 ng/mL, 0-48 hrs). However, exogenous HMGB1 was not sufficient to rescue ECM synthesis in response to TGF-β1 in HMGB1-silenced cells - this suggests that intracellular, but not necessarily secreted HMGB1, regulates ECM expression and secretion in response to TGF-β1. Consistent with this interpretation, exogenous HMGB1 alone was not sufficient to induce ECM synthesis or secretion in primary cultured ASM cells. In conclusion, we show that though in human ASM cells extracellular HMGB1 alone can activate MAPK signaling, likely via mDia1-dependent pathways involving RAGE. it is not capable of prompting ECM protein expression. Recombinanat exogenous HMGB1 does not appear to directly affect ECM synthesis, rather intracellular (nuclear) HMGB1 likely modulates activity of genes that are affected by TGF-β1. Overall, HMGB1 has potential to regulate tissue repair processes involving ASM through intracellular and extracellular mechanisms, thus our findings support further work to elucidate the role of HMGB1 in pathogenesis of obstructive airway disease.

In today’s electronics, transistors are the main building blocks of the vast majority of electronic devices and integrated circuits. Types of transistors vary depending on the device structure and operation principle. Metal-oxide-based thin film transistors (MO TFTs), in particular, are an emerging technology that has a promising future in many applications, such as large-area display and wearable electronics. It exhibits unique features that make it superior to the existing Si-based technology, such as optical transparency and mechanical flexibility. However, some technical challenges in MO TFTs limit their emplyoment in today’s applications, such as low carrier mobility and high processing temperature. Solution-processed MO TFT based on spray pyrolysis combined with a carefully engineered TFT structure offers a dramatically enhance carrier mobility at low processing temperature. In this work, we are utilizing spray pyrolysis to grow In2O3 and ZnO based TFTs at low processing temperature. The structural effects of the channel layer on the electrical performance is investigated in two parts. The first part highlights the impact of thickness of the channel layer on the device performance of both In2O3 and ZnO, while the second part explores In2O3/ZnO heterojunction-based active layer. The results showed that increasing the channel thickness of both In2O3 and ZnO based TFTs enhanced the carrier mobility due to a reduced surface-roughness scattering effect. In addition, evidence showed that the electron transport mechanism in In2O3/ZnO heterojunction transitioned from trap-limited conduction (TLC) to percolation conduction (PC) process. Thanks to the existence of a 2D-confined electron sheet at the atomically sharp In2O3/ZnO heterointerface, the electron mobility was dramatically enhanced.

Objective: The mechanisms by which lipopolysaccharide (LPS) pretreatment induces cardioprotection following ischaemia/reperfusion (I/R) have not been fully elucidated. We hypothesized that activation of phosphoinositide 3-kinase (PI3K)/Akt and high mobility group box 1 (HMGBx1) signaling plays an important role in LPS-induced cardioprotection. Methods: In in vivo experiments, age- and weight-matched male C57BL/10Sc wild type mice were pretreated with LPS before ligation of the left anterior descending coronary followed by reperfusion. Infarction size was examined by triphenyltetrazolium chloride (TTC) staining. Akt, phospho-Akt, and HMGBx1 were assessed by immunoblotting with appropriate primary antibodies. In situ cardiac myocyte apoptosis was examined by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. In an in vitro study, rat cardiac myoblasts (H9c2) were subdivided into two groups, and only one was pretreated with LPS. After pretreatment, the cells were transferred into a hypoxic chamber under 0.5% O2. Levels of HMGBx1 were assessed by immunoblot. Results: In the in vivo experiment, pretreatment with LPS reduced the at risk infarct size by 70.6% and the left ventricle infarct size by 64.93% respectively. Pretreatment with LPS also reduced cardiac myocytes apoptosis by 39.1% after ischemia and reperfusion. The mechanisms of LPS induced cardioprotection involved increasing PI3K/Akt activity and decreasing expression of HMGBx1. In the in vitro study, pretreatment with LPS reduced the level of HMGBx1 in H9c2 cell cytoplasm following hypoxia. Conclusion: The results suggest that the cardioprotection following I/R induced by LPS pretreatment involves PI3K/Akt and HMGBx1 pathways.

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Graphene is widely considered to be a promising candidate for a new generation of electronics, but there are many outstanding fundamental issues that need to be addressed before this promise can be realized. This thesis focuses on the production and properties of graphene grown epitaxially on the carbon terminated face (C-face) of hexagonal silicon carbide leading to the construction of a novel graphene transistor structure. C-face epitaxial graphene multilayers are unique due to their rotational stacking that causes the individual layers to be electronically decoupled from each other. Well-formed C-face epitaxial graphene single layers have exceptionally high mobilities (exceeding 10,000 cm ²/Vs), which are significantly greater than those of Si-face graphene monolayers. This thesis investigates the growth and properties of C-face single layer graphene. A field effect transistor based on single layer graphene was fabricated and characterized for the first time. Aluminum oxide or boron nitride was used for the gate dielectric. Additionally, an all graphene/SiC Schottky barrier transistor on the C-face of SiC composed of 2DEG in SiC/Si₂O ₃ interface and multilayer graphene contacts was demonstrated. A multiple growth scheme was adopted to achieve this unique structure.

Kou Ying Chuck. / "July 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 186-199). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.