Defective structures in two-dimensional (2D) materials have been proved to have significant influences on the materials' properties. Understanding structural defects in 2D materials at atomic scale is therefore required. With the use of advanced imaging techniques, one of the main approaches applied in this project was aberration-corrected transmission electron microscopy (AC-TEM), the structures are able to be resolved with single-atom sensitivity with the reduction of both spherical aberration and the influence of chromatic aberration. This laid the foundation for the first two experiments, which involve the bond length measurement of each C-C bond within three types of divacancies and Si-C bonds at graphene edges. The former explains the tendency of bond rotations within the divacancies from the perspective of strain inside the defective areas and surrounding lattice; the latter revels the interactions between isolated Si atoms and zigzag/armchair graphene edges. The use of in-situ heating holder in the AC-TEM makes the direct visualization of structures and their dynamics at elevated temperatures possible. The Si-graphene edge interactions, as well as the following two experiments are all designed to study the high-temperature performances for different systems. Gold nanoclusters are introduced to monolayer graphene by thermal evaporation to study the interaction between gold and graphene at elevated temperature. Due to the strong interaction between gold and graphene, gold crystals are able to adapt to planar configurations with two different crystalline forms, and an epitaxial relationship was found for planar gold crystals and graphene. Atomically flat and long line defects and zigzag edges in monolayer molybdenum disulfide (MoS₂) are successfully created by in-situ thermal annealing. The relationship between S vacancy mobility and defect forms are revealed based on the experiment. High-temperature atomic configurations of line defects and edge terminations are resolved in the first time. Their electronic properties are also explored with the support of density functional theory calculations.

Ventral body wall closure (VBW) defects are amongst the most common human congenital anomalies. They represent a wide and heterogeneous group of phenotypic defects that can present in isolation or as a component in a larger syndromic anomaly. In addition, the incidence of associated anomalies is high and reaches 75% of fetuses in some types of VBW closure defects. Nevertheless, the embryonic origin and the underlying cellular and molecular mechanisms between ventral closure defects and their associated congenital anomalies remain poorly characterised. This is in part due to the poor understanding of the physiological mechanisms that regulate the development of ventral organs and the lack of representative transgenic animal models allowing detailed in vivo analysis of defect formation. Transforming growth factor beta (TGF-ÃŽÂ2) signalling is essential for VBW closure and vascular and cardiac development. Yet, its mechanism of action and the responding cell(s) in the body wall remain largely unknown. In addition, in various cells TGF-B can induce the expression of Tagln, encoding for a cytoskeleton associated protein that enhances cell migration. No function has been ascribed to TAGLN in body wall development. I define here a role of TGF-B during a critical time window in embryonic development to fashion the ventral body wall, anterior diaphragm and parts of the circulatory system. I identify a population of TAGLN+ myofibroblasts that respond to a temporally regulated TGF-B signalling originating from the epithelium of the primary body wall. Deletion of TGF-B receptor in TAGLN+ cells leads to failure of ventral body wall closure, anterior diaphragmatic hernia, cardiac and outflow tract anomaly. Nevertheless, the descending aorta and the large aortic branches are spared. By using advanced transgenic methodology, I generated novel transgenic mouse lines that enabled me to fate map the cells that initiate the formation of important mesenchymal tissues. These studies revealed that the origin of aortic vascular smooth muscle cells can be traced back to a group of progenitor cells that reside in the wall of the dorsal aorta before the VBW closure. My studies provide intriguing evidence for spatially restricted role for TGF-B signalling in ascending but not descending aorta morphogenesis. I used a variety of techniques to characterise, analyse and quantify important mechanisms during mesenchymal and vascular development, their response to injury and repair. This thesis has been written in an alternative format, comprising the different areas which have been investigated. Collectively, the results presented here provide new insights into the role of migratory and mechanically stabilising cells in the development and maintenance of critical structures in the body and their common role in the development of concurrent congenital anomalies. A detailed understanding of the molecular signalling pathways and cells that drive VBW closure raises the hope that the related birth defects can in the future be treated by precise gene and cell therapies.

La technologie Flash représente aujourd’hui la mémoire non-volatile de référence dans plusieurs applications électroniques. Néanmoins, le « scaling » des cellules Flash conventionnelles fait aujourd’hui face à plusieurs limitations et un effort d’optimisation accru est nécessaire pour atteindre de meilleures performances, notamment en terme de fiabilité (rétention de données et tenue en endurance). La rétention de l’information stockée a ainsi fait l’objet de nombreuses études dans la littérature, aboutissant à une bonne compréhension et une modélisation précise des phénomènes de Stress Induced Leakage Current (SILC). En revanche, une description précise et microscopique des mécanismes de dégradation de cellules Flash en cours d’endurance Programmation/Effacement (P/E) reste manquante. Notamment dans le cas des technologies Flash de type NOR, dont la nature 2D des mécanismes de dégradation complexifie l’analyse, la compréhension et la modélisation de la perte de performances en cours d’endurance.Cette thèse se propose d’investiguer le vieillissement en endurance de la technologie embarquée NOR Flash 40nm produite à STMicroelectronics. Grâce à un ensemble de caractérisations électriques et de simulations TCAD spécifiquement développées, la thèse fourni une compréhension physique des différents mécanismes de vieillissement impliqués durant l’endurance. En particulier, les rôles respectifs des opérations de Programmation (par porteurs chauds) et d’Effacement (par injection Fowler-Nordheim) sont soulignés et leur impact sur les caractéristiques des cellules mémoires établis. Enfin, grâce à la description microscopique et exhaustive précédemment établie, un modèle physique reproduisant la dégradation de la cellule pendant l’endurance est proposé. L’application de ce modèle permet de définir des conditions de programmation optimales conduisant en une amélioration de la durée de vie des cellules NOR Flash considérées. / Flash technology still represents the preferred storage memory in many portable consumers and computer applications. However, the conventional Flash cell is now facing technological barriers and needs to be optimized pushing its working condition to the intrinsic physical limit. Such an optimization has to be done mainly focusing on reliability concerns, i.e. data retention and endurance, since representing the main limiting factors of technology down-scaling. For this reason, several works dealt with data retention concerns analyzing, characterizing and modeling the Stress Induced Leakage Current (SILC) with the final aim of limiting or control such an issue. However, there is no work which accurately explored the overall cell evolution during Program/Erase (P/E) cycling from a microscopic physical standpoint, especially in NOR technology, whose intrinsic 2D degradation nature makes complex the modeling and the analysis of the combined aging mechanisms.In this thesis, an in-depth investigation of P/E degradation mechanisms in 40nm NOR Flash technology issued from STMicroelectronics is conducted. With the help of advanced electrical characterization and proper TCAD simulation, this thesis provides an accurate understanding, evaluation and modeling of the different aging mechanisms involved during P/E cycling. In particular, the respective roles of Hot Carrier Degradation (HCD) and Fowler-Nordheim Stress (FNS) are pointed out, and their impact on memory cell characteristic drifts and on memory lifetime is assessed. The main challenge is to build a physically-based model which reproduces the Flash cell wear out during P/E cycling. This enables to push the memory lifetime towards its maximum intrinsic performance, as for example by correctly managing the P/E electrical operations. In addition, such an approach allows to assess the limiting physical mechanism factors for memory cell degradation and consequently to take action for some specific process step optimizations.

INTRODUCTION: Currently, patients diagnosed with Congenital Heart Disease (CHD) are living longer lifespans, leading to an increased number of these patients presenting for non-cardiac procedures/surgeries. Little research has been recently done analyzing intraoperative complications/risks for CHD patients undergoing non-cardiac surgeries. This study aims to identify common intraoperative events experienced by CHD patients undergoing non-cardiac surgeries using more recent data, while at the same time analyzing to see if there is any difference in frequency of intraoperative events experienced between different types of CHD diagnoses. METHODS: After receiving IRB approval, patients with CHD presenting for non-cardiac procedures/surgeries between the years 2008 and 2012 were pulled from Boston Children’s Hospital’s Electronic Medical records. 1,024 non-cardiac surgical encounters from 362 patients were analyzed to determine average age, average weight, patient gender, average ASA class, frequency of CHD diagnoses, ventricular function, type of non-cardiac procedure, premedication administration, type of induction and type and frequency of intraoperative events experienced. The 1,024 encounters were divided into two groups: those done in patients diagnosed with single ventricle physiology (n=79) and those done in patients diagnosed with non-single ventricle physiology (n=945). Unpaired Mann-Whitney tests were performed to determine if there was a significant difference in overall and specific intraoperative event occurrence between the single ventricle and non-single ventricle groups. RESULTS: Average age and weight at the time of these surgical encounters was 4.86 years and 20.57 Kg. A majority of the surgical encounters were done in males (59.2%). Atrial septal defect was the most common type of CHD, and most of the patients in these surgical encounters received an ASA class of 3. Intraoperative events occurred in 24.4% of the surgical encounters with cardiovascular events being the most common (44.82% of total events). Other events made up 30.49% of events experienced intraoperatively, with respiratory events making up the remaining 24.70%. There was a significant difference in the occurrence of overall events between the single ventricle and non-single ventricle group (P<0.0001). Additionally, there was a significant difference in the occurrence of cardiovascular events (P<0.0001) and Other events (P=0.0001) between the single ventricle and non-single ventricle groups. There was no significant difference in the occurrence of respiratory events between the two groups (P=0.648). DISCUSSION: The most common type of intraoperative event experienced by CHD patients during a non-cardiac surgery was cardiovascular events. Significantly more overall intraoperative events, including cardiovascular and other events, occurred in surgical encounters performed on CHD patients exhibiting single ventricle physiology than those encounters done on CHD patients with a non-single ventricle physiology. Results of this study suggest that it would be likely for CHD patients to have a cardiovascular event occur during non-cardiac surgery and that this may be more likely in patients with a single ventricle physiology. This study was subjected to the limitations of retrospective chart review, as well as missing and infrequent documentation. Future analysis will look to find correlations between the occurrence of intraoperative events, and demographic and procedure variables analyzed in this study. / 2017-06-16T00:00:00Z

Contents: a. The oxidation of metals by atomic and molecular oxygen -- b. Calculation of the heats of formation of point defects in some transition metal oxides.

Submitted by Maria Medeiros (maria.dilva1@ufcg.edu.br) on 2018-08-29T13:13:33Z No. of bitstreams: 1 IVÂNDERSON OLIVEIRA MOREIRA - DISSERTAÇÃO (PPGF) 2018.pdf: 5107079 bytes, checksum: 1e0912f4ced4ad6d7239469d05856b77 (MD5) / Made available in DSpace on 2018-08-29T13:13:33Z (GMT). No. of bitstreams: 1 IVÂNDERSON OLIVEIRA MOREIRA - DISSERTAÇÃO (PPGF) 2018.pdf: 5107079 bytes, checksum: 1e0912f4ced4ad6d7239469d05856b77 (MD5) Previous issue date: 2018-07-26 / Capes / Defeitos topológicos são soluções de equações diferenciais que conectam configurações distintas de um sistema. Para modelos unidimensionais essas soluções são chamadas de kinks. Com isso, neste trabalho vamos estudar as soluções do tipo torção, denominadas twistons topológicos e também investigaremos o comportamento de fermions na presença de estruturas do tipo kink. Primeiramente estudaremos os twistons topológicos presentes no polietileno cristalino que representam uma torção de 180 na cadeia de CH2 causando também uma contração do comprimento da molécula. Pretendemos então construir um modelo efetivo de dois campos que não contenha degenerescência na energia através da aplicação do chamado Método de Extensão, buscando também obter soluções analíticas desse modelo. Após este estudo, voltaremos nossas investigações para as análises de férmions na presença de kinks com o objetivo de obter um controle da energia de limiar (gap de energia onde residem os estados ligados) usando dois campos escalares. / Topological defects are solutions of differential equations that connect distinct confi gurations of a system. For one-dimensional models these solutions are called kinks. In this work we will study the twist-like solutions, called topological twistons and also investigate the behavior of fermions in the presence of kink-like structures. First we will study the topological twistons present in the crystalline polyethylene which represent a 180 twist in the CH2 chain also causing a contraction of the length of the molecule. We intend to construct an effective model of two elds that does not contain degeneracy in the energy through the application of the so called Extension Method, also seeking to obtain analytical solutions of this model. After this study, we will turn our investigations for fermion analyzes in the presence of kinks in order to control of the threshold energy (energy gap where bound states reside) using two scalar elds.

Os defeitos superficiais são os maiores problemas de qualidade em barras laminadas a quente, representando inúmeros transtornos durante o processo produtivo, pois dependendo de suas características geram elevada rejeição durante o processo de inspeção. Elevada rejeição significa retrabalho e possível sucateamento. Dentre as diversas causas para a ocorrência de defeitos superficiais, estão os defeitos nos tarugos, a temperatura de laminação, conseqüência da temperatura de reaquecimento e ritmo de laminação e a remoção de carepa após o reaquecimento. Definiu-se o aço SAE 1043 para o desenvolvimento deste trabalho devido aos níveis de rejeição superficial e elevados volumes de produção, o que gera grande impacto na produção das linhas de inspeção. Os resultados obtidos a partir dos testes realizados demonstram que a temperatura de laminação até determinado limite não tem influência na rejeição superficial, mas que abaixo deste gera elevado índice de rejeição. O uso do descarepador tem grande influencia nos níveis de defeitos superficiais, e o controle de seus parâmetros principais é fundamental. O condicionamento superficial dos tarugos é o parâmetro que mais apresentou influência positiva sobre a rejeição superficial, demonstrando que defeitos pré-existentes na matéria-prima têm grande impacto no produto final da laminação. / Surface defects are major quality problems in hot rolled bars, representing numerous disturbances during the production process, as depending on their characteristics generate high rejection during the inspection process. High rejection means rework and scrap. Among the various causes for the occurrence of surface defects are defects in the billets, rolling temperature, a consequence of the reheating temperature and rate of roll and removal of scale after reheating. The steel SAE 1043 used in this work was selected due to its level of surface defects and high production volumes, which generates large impact on production inspection process. The results show that the rolling temperature of up to a certain limit does not influence the surface defects, but below this generates a high rate of rejection. The use of descaling has a large influence on the levels of surface defects, and control of its main parameters is essential. The surface conditioning of billets is the parameter that showed a positive influence on the reduction of surface defects, demonstrating that pre-existing defects in materials has large impact on the final rolled product.

Carbon-based materials have attracted great attention over past few years in hydrogen storage applications. In particular, nanofibrous carbon working as support for sodium alanate exhibits great improvement in the kinetics of H2 releasing/uptaking. Herein, we used graphene with various dopants to simulate the carbon materials and performed a periodic density functional theory study on the impact of the modifications on the hydrogen interaction in the supported sodium alanate. Our results showed that the impact of various defects and dopants can be categorized in groups: (i) Pristine graphene and pentagon-heptagon (5-7) pair defective graphene, as well as nitrogen and sulfur doped graphene do not promote H2 formation. (ii) Carbon vacancies, as well as boron and chlorine doped systems, cause instantaneous H2 formation. (iii) Oxygen, phosphor and fluorine doped graphene led to the formation of a meta-stable di-hydrogen state with a H-H distance of ~ 0.96 Å. In addition, we confirmed the importance of van der Waals interaction in our system.

Our research investigated the correlations of five key contaminants in drinking water in the State of Illinois with the incidence rates of three different categories of negative reproductive outcomes: birth defects, adverse pregnancy outcomes and preterm births. The five water contaminants included three agrichemical-based contaminants (atrazine, nitrate and nitrite) and two disinfectant byproducts (total trihalomethanes and haloacetic acids). We obtained nearly 38,000 measurements of the individual concentrations of these five contaminants from the Illinois Environmental Protection Agency (IEPA). These data, spanning over a five-year period (1998-2002), were collected from nearly 1,800 community water supplies (CWS) located in all 102 Illinois counties. The county-specific incidence rate data for the same time period for preterm births, seven groups of birth defects and seven groups of adverse pregnancy outcomes were collected from the Illinois Department of Public Health (IDPH). The traditional approach of establishing correlation of one explanatory variable at a time indicated that nitrate concentration in drinking water was statistically correlated to the incidence rate of only one category of negative reproductive outcome, i.e., birth defects. However, multiple regression analysis, which took into consideration all water contaminant data simultaneously, established statistical significance of the correlation between nitrate and all three categories of negative reproductive outcomes. Total trihalomethanes (TTHM) and haloacetic acids (HAA5) were also found to be the statistically significant explanatory variables for all three types of negative reproductive outcomes. Nitrite was found to be associated with adverse pregnancy outcomes and preterm births only; its correlation with birth defect rates could not be established at 80% confidence level. Atrazine was found to be among the significant explanatory variables for all three negative reproductive outcomes. However, its correlations with birth defect model developed using censored data and preterm birth model developed based on observed data were not statistically significant. Nearly 21.5%, 35.8% and 16.6% of the variabilities in incidence rates of different types of birth defects, adverse pregnancy outcomes and preterm births, respectively, were correlated to average concentrations of above mentioned five contaminants in community drinking water supplies. The monthly average concentrations of two of three agrichemical-based contaminants, i.e., atrazine and nitrate were significantly higher in SW(surface water)-based than GW(ground water)-based community water supplies. On the other hand, concentrations of both disinfectant byproducts and the other agrichemical-based contaminant, i.e., nitrite were significantly higher in GW-based water supplies. Further correlation analysis based on the actual observed concentration (excluding all 0 detections) was conducted utilizing SW-based atrazine and nitrate data and GW-based nitrite, TTHM and HAA5 data. All categories of negative reproductive outcomes were found significantly correlated with at least one type of water contaminants. The overall negative reproductive outcomes were correlated with nitrate, nitrite and atrazine. Birth defects specifically correlated with nitrate and TTHM, whereas adverse pregnancy outcomes were correlated with nitrate, nitrite and HAA5; preterm birth was correlated with the concentrations of nitrite, atrazine and TTHM. Further investigation indicated significant correlations among the explanatory variables (drinking water contaminants data), which is referred as multicollinearity. In such case, multiple linear regression based analysis may not provide reliable results. Partial least squares (PLS) approach of regression analysis was introduced into our study to overcome the multicollinearity problem. As much as 65.5% of the variability in the county-wide average concentrations of five contaminants in public drinking water supplies was explained by the 4 component PLS regression model, whereas only 7.7% of the incidence rates of different types of birth defects, adverse pregnancy outcomes and preterm births in various Illinois counties, were explained by PLS regression. Although, individual negative reproductive outcome model could be generated, the low R2 values indicated the poor reliability of these models. We attempted to corroborate our statistical analysis findings with the physiological effects of various water contaminants reported in the literature. It is well known that excessive exposure to any of the five key water contaminants may cause malfunction of organism or the immune system, reproduction, nervous and endocrine system and others, which may further result in potential risk of developing adverse effects. Nitrate and nitrite in drinking water associate to a certain extent with congenital malformations, such as central nervous system abnormalities, in human offsprings. Excessive exposure to atrazine is known to increase the risk of potential cardiovascular or reproductive system problems. A certain type of TTHM, i.e., BDCM are known to be associated with an increased risk of spontaneous miscarriage in pregnant women. It also may result in an increased risk of reproductive problem, such as fetal growth restriction.

The transcription factor DEAF-1 is the mammalian homologue of a critical Drosophila developmental gene and is essential for neonatal survival in mice. Haploinsufficiency of Deaf-1 in the testis of adult mice was initially thought to cause loss of spermatogenesis and disrupted morphology of the seminiferous tubules, and this heterozygosity was thought to be sufficient to disrupt epigenetic programming in the developing sperm to produce inheritance of testicular defects in both heterozygous and genotypically normal offspring. Although Deaf-1 knockout mice do display disrupted testis structure, infertility at advanced age, hyperproliferation of early germ cells, and abnormal staging of seminiferous tubules, this phenotype was also observed in normal mouse strains that were born in the SIUC vivarium. Mice ordered from a vendor and raised at SIUC did not show testicular defects. This suggests an environmental factor at the SIUC vivarium may act as an endocrine disruptor during embryonic testicular development. Deaf-1-/- mice die soon after birth, often as the result of exencephaly, a gross neural tube defect (NTD). Unlike many mouse models, exencephalic Deaf-1-/- mice do not display a higher incidence of NTDs in females as compared to their male littermates. DEAF-1 promotes Bax-mediated apoptosis; studies using terminal UTP nick-end labeling (TUNEL) suggest a global increase in apoptosis in both exencephalic and normal Deaf-1-/- fetuses during neurulation as compared to their Deaf-1+/+ littermates. This indicates that Deaf-1 is crucial for correct apoptotic patterning during development, which, in turn, is essential for neural tube closure. Finally, cDNA microarray comparison of e14.5 Deaf-1 knockout and wildtype fetuses reveals expression of translation initiation factor 4g3 (Eif4g3) to be downregulated in Deaf-1-/- fetuses. Electrophoretic mobility shift assay using recombinant DEAF-1, and chromatin immunoprecipitation assay of a human cell line confirmed DEAF-1 could bind the eIF4G3 promoter both in vitro and in vivo. Additionally, transcription of the Deaf-1 Antisense Transcript (Das) was found to be significantly downregulated in both e14.5 fetuses and e18.5 fetal brains from Deaf-1-/- mice, suggesting that either lack of Deaf-1 protein or lack of exons 2 through 5 in Deaf-1 knockout mice causes changes in levels of the noncoding RNA that shares Deaf-1's promoter in the mouse.