VictorJuiz/thesis huggingface dataset:
Characterization and modeling of thermal diffusion and aggregation in nanofluids [electronic resource]

Fluids with higher thermal conductivities are sought for fluidic cooling systems in applications including microprocessors and high-power lasers. By adding high thermal conductivity nanoscale metal and metal oxide particles to a fluid the thermal conductivity of the fluid is enhanced. While particle aggregates play a central role in recent models for the thermal conductivity of nanofluids, the effect of particle diffusion in a temperature field on the aggregation and transport has yet to be studied in depth. The present work separates the effects of particle aggregation and diffusion using parallel plate experiments, infrared microscopy, light scattering, Monte Carlo simulations, and rate equations for particle and heat transport in a well dispersed nanofluid. Experimental data show non-uniform temporal increases in thermal conductivity above effective medium theory and can be well described through simulation of the combination of particle aggregation and diffusion. The simulation shows large concentration distributions due to thermal diffusion causing variations in aggregation, thermal conductivity and viscosity. Static light scattering shows aggregates form more quickly at higher concentrations and temperatures. An optimum nanoparticle diameter for these particular fluid properties is calculated to be 130 nm to optimize the fluid stability by reducing settling, thermal diffusion and aggregation.

Keywords: Mechanical Engineering
Advisor: Goodson Kenneth E.
Eaton John K. advisor. Thesis advisor
Santiago Juan G. advisor. Thesis advisor
Characterization of Listeria monocytogenes growth and colonization of the murine gallbladder [electronic resource]

Listeria monocytogenes is a facultative intracellular pathogen that causes severe invasive disease in susceptible populations. Using in vivo bioluminescent imaging, it was recently discovered that this bacterium can colonize the murine gallbladder of otherwise asymptomatic mice. This finding was surprising as L. monocytogenes, after invasion of the intestines, was thought to survive only intracellularly in an infected host and in the gallbladder the bacteria lived extracellularly. It was also surprising that a bacterium could grow and replicate in the pure bile environment of the gallbladder lumen as bile is a potent antimicrobial compound. In this study, we characterized how Listeria monocytogenes is able to reach the gallbladder during infection and examined how this pathogen is able to survive in this environment. Using a mouse adapted L. monocytogenes which expresses a modified InlA capable of binding murine E-cadherin we were able to follow the kinetics of gallbladder colonization after oral infection using in vivo bioluminescent imaging. We then utilized surgical manipulation of the mouse host and repeated the oral infection to determine how L. monocytogenes reaches the gallbladder. Once we had determined the mechanism of gallbladder entry, we then utilized whole genome microarrays to characterize the transcriptome of L. monocytogenes during in vivo growth in the gallbladder and in freshly isolated murine bile. Finally, we attempted to determine what nutrients are utilized by L. monocytogenes during growth in bile and looked at the ability of other bacterial species to grow in this environment. Through these experiments we demonstrated regular asymptomatic gallbladder colonization by L. monocytogenes after oral infection and that L. monocytogenes reaches the gallbladder via the hepatic duct only after first causing systemic infection and escaping the liver. We also demonstrated that the lifestyle in the gallbladder is similar to that in the intestine with the exception of the need for bile resistance genes, and finally that it appears as though simple carbon sources may be utilized during bile growth and that bile may not be as toxic to bacteria as has been thought. Our work suggests that gallbladder colonization may not be exclusive to only L. monocyctogenes and Salmonella Typhi since other bacteria can grow, and in some cases better than L. monocyctogenes, in pure bile.

Keywords: Microbiology and Immunology
Advisor: Contag Christopher H. primary advisor. Thesis advisor
Amieva Manuel advisor. Thesis advisor
Boothroyd John C. advisor. Thesis advisor
Wandless Thomas advisor. Thesis advisor
Characterization of the Chibby family of centrosomal proteins [electronic resource]

The Chibby protein antagonizes Wnt/Beta-Catenin signaling, a prominent regulator pathway of development, via direct interaction with the transcriptional activator domain of Beta-Catenin. Chibby mutant mice have a defect in the formation of motile cilia in the airway epithelium. The centrosome is the major microtubule organizing center of animal cells and includes two centrioles, termed mother and the daughter based on their age and replicative history. The mother harbors subdistal and distal appendages, which, respectively, anchor the interphase microtubule array and are required for ciliation. Several lines of published evidence suggest a link between the primary cilium, a single, non-motile structure found on many cells, and Wnt/Beta-Catenin signaling. Based on this evidence I investigated Chibby, and related members of the Chibby protein family, to determine its role in centrosome and cilium structure and function. I report here that the Chibby family of proteins is associated physically and functionally with the centrioles of the centrosome in mammalian cells. The Chibby family consists of Chibby (Cby1), Nurit/Cby2, and the previously uncharacterized, Chibby3 (Cby3). Fluorescence microscopy revealed that Cby1 localized to the mother centriole of the centrosome, and that this localization was partially shared with Nurit/Cby2 and Cby3. Cby1 colocalizes at the mother centriole with phospho-Beta-Catenin, a modified form of Beta-Catenin that, in some contexts it is targeted for proteasome-mediated degradation. I also found that Cby1 partially colocalized with phospho-Beta-Catenin at a ring-like structure at the midbody during cytokinesis, where they might regulate abscission. The localization of Cby1 to the mother centriole was similar to that described for proteins for the distal appendages of the mother centriole. I found that Cby1 colocalized with, and exhibited cell cycle dynamics similar to, Cep164, a known distal appendage protein that is required for primary cilium formation. Consistent with a role for Cby1 in these centriolar structures, Cby1-/- mouse embryonic fibroblasts exhibited a strong reduction in primary cilium formation that could be complemented by expression of the wild-type Cby1 protein. Remarkably, overexpression of either GFP-tagged Beta-Catenin or GFP-Cby1 in hTERT-RPE1 cells resulted in fewer, but longer, cilia than controls suggesting that both of these proteins are important for structure and function of the primary cilium. In summary, I propose that Cby1 is associated with the distal appendages of the mother centriole, that defects in those structures are the likely cause of the failure of cilium formation in cells lacking Cby1, and that both primary and motile cilia display this requirement for Cby1.

Keywords: Biological Sciences
Advisor: Stearns Tim primary advisor. Thesis advisor
Burkholder William
Frydman Judith advisor. Thesis advisor
Nelson W. J. (W. James) advisor. Thesis advisor
Characterizing and modeling close-proximity exposure to an air pollution source in naturally ventilated residences [electronic resource]

Near an active indoor emission source, air pollutant levels are elevated and highly-variable, due to non-instantaneous mixing -- this causes great uncertainty in estimating a person's exposure level. This research investigated the magnitude and variability of short-term exposures close to an active point source inside 2 homes, under a range of natural ventilation conditions. The findings from a newly-developed monitor signal reconstruction method were applied to measurements from 30-37 real-time monitors to capture the spatial and temporal variations of concentrations over 30-min CO tracer gas releases. For 11 experiments involving 2 houses, with natural ventilation conditions ranging from < 0.2 to > 5 air changes per h, an eddy diffusion model was used to determine the turbulent diffusion coefficients. The air change rate showed a significant positive linear correlation with the air mixing rate, defined as the turbulent diffusion coefficient divided by a squared length scale representing the room size. To predict the magnitude of exposure close to an active source, an indoor dispersion model was formulated, invoking the theory of random walk, and incorporating the physical processes of anisotropic turbulent diffusion, removal of the air pollutant, and air pollutant wall reflection. Then, to capture the variability of concentrations in close proximity to an active source, a new piece-wise random walk algorithm was developed to stochastically simulate the transient directionality of emitted plume. The distribution of different exposure cases generated using this model reasonably covered the range of experimental measurements collected in 2 houses, while preserving ensemble averages satisfying the principle of Fickian diffusion.

Advisor: Hildemann Lynn M. (Lynn Mary) primary advisor. Thesis advisor
Fringer Oliver B. (Oliver Bartlett) advisor. Thesis advisor
Kitanidis P. K. (Peter K.) advisor. Thesis advisor
Characterizing personal exposure in close proximity to indoor air pollution sources [electronic resource]

A total of 68 experiments were conducted in two homes under natural ventilation rates ranging from 0.2 -- 5.4 air exchanges per hour, each involving 12 to 37 real-time carbon monoxide (CO) or particulate matter (PM2.5) monitors placed in proximity (0.25 -- 5.0 m) to a controlled stationary point source. Concentrations measured in close proximity (within 1 m) to the source were highly variable, with 5-min averages that typically varied by > 100-fold. This variability was due to short-duration (< 10 s) pollutant concentration peaks ("microplumes") that were frequently recorded in close proximity to the source -- for PM2.5, these peaks often exceeded 1000 ug/m3. Compared with concentrations predicted assuming uniform, instantaneous mixing within the room, average concentrations measured within 0.25 m of the source were 6 -- 20 times as high. As distance from the active source increased the ratio of measured concentration to the well-mixed prediction decreased. For most cases, ratios approached 1 (well-mixed) at distances of 3 -- 5 m from the source. Air change rate and vertical distance from source to receptor were two factors that affected horizontal concentration profiles. Under natural ventilation conditions, as air change rate increased, the concentrations close to the source became more elevated, magnifying the proximity effect. Mechanical ventilation increased mixing in the room, and resulted in a diminished proximity effect. Vertical mixing of the pollutant was even more hindered, due to temperature stratifications present in the rooms -- the concentrations more than 0.5 m vertically from the height of a nonbuoyant plume rapidly approached the well-mixed prediction. For buoyant stationary plumes, such as emissions from a smoldering cigarette or stick of incense, the height of maximum concentrations was typically 0.5 -- 1 m above the source, due to plume rise. The rise of a buoyant plume was more limited under natural than mechanical ventilation conditions, presumably due to less temperature stratification. For an actual smoker, where both highly buoyant sidestream smoke and less buoyant exhaled mainstream smoke were generated, and where the cigarette was moved around by the smoker, emissions were dispersed over a broader vertical extent. However, for 20 indoor experiments involving 2-4 people sitting in close proximity to an active smoker, the magnitude of the proximity effect within 0.5 -- 1 m was comparable to measurements for the stationary nonbuoyant source experiments.

Advisor: Hildemann Lynn M. (Lynn Mary) primary advisor. Thesis advisor
Boehm Alexandria advisor. Thesis advisor
Leckie Jim
Characterizing the mechanism of continued primer synthesis at stalled replication forks and its contribution to checkpoint activation [electronic resource]

Stalled replication forks activate and are stabilized by the ATR-mediated checkpoint, but ultimately they must also recover from the arrest. While primed ssDNA is sufficient for checkpoint activation, it is still unknown how this signal is generated at a stalled replication fork. Furthermore, it is not clear how recovery and fork restart occur in higher eukaryotes. Using Xenopus egg extracts, we show that DNA replication continues at a stalled fork through the synthesis and elongation of new primers independent of the checkpoint. This synthesis is dependent on the activity of PCNA, Pol[lowercase Delta] and Pol[Epsilon], and it contributes to the phosphorylation of Chk1. We also used defined DNA structures to show that for a fixed amount of ssDNA, increasing the number of primer-template junctions strongly enhances Chk1 phosphorylation. These results suggest that new primers are synthesized at stalled replication forks by the leading and lagging strand polymerases and that accumulation of these primers may contribute to checkpoint activation.

Keywords: Chemical and Systems Biology.
Advisor: Cimprich Karlene primary advisor. Thesis advisor
Chen James Kenneth advisor. Thesis advisor
Straight Aaron
Wang Teresa. Thesis advisor
Characterizing the role of the p53/p63 target gene, Perp, in epidermal homeostasis and cancer [electronic resource]

Desmosomes are multi-protein cell-cell adhesion junctions found throughout stratified squamous epithelia and the myocardium. These specialized adhesion complexes maintain the structural integrity of these tissues, which are continuously exposed to mechanical stress. Perturbations in desmosome structure and function lead to clinical symptoms associated with a variety of human skin and heart disorders. While the molecular basis for these phenotypes is mainly attributable to the role of the desmosome in resisting mechanical stress, emerging roles for this complex in cellular signaling, apoptosis, and tissue morphogenesis are accumulating. Understanding the molecular mechanisms of desmosome function in both normal tissue homeostasis and disease will bring new insights into these complex biological processes. Loss of cellular adhesion junctions is a common feature of epithelial cancer progression. However, the specific contribution of how desmosome function affects this disease has not been looked at in great detail. In the first two chapters, we examined the consequences of desmosome loss to tumor formation using mice deficient for the desmosomal protein Perp. In-depth analyses focusing on Perp's mechanism of action revealed new insights into the role of Perp and the desmosome in adhesion, apoptosis, and inflammation. In the second part of my thesis, we investigated the role of the desmosome in epithelial wound healing and in Ankyloblepharon Ectodermal Dysplasia and Cleft Lip/Palate (AEC), a human skin disease characterized by severe craniofacial abnormalities, skin erosions, and alopecia. We first showed that proper desmosome function is essential for efficient wound healing in vivo. Lastly, we investigated whether some of the clinical symptoms associated with AEC were attributable to defects in Perp function. We identified a subset of AEC derived p63 mutants that were capable of transactiving Perp expression, despite being previously characterized as inactive for other p63 target genes. Analysis of skin biopsies revealed disrupted Perp expression in a subset of AEC patients, further corroborating a role for Perp dysfunction in the pathogenesis of this disease. Together these studies have uncovered important roles for Perp and the desmosome in maintaining proper skin homeostasis and insights into the mechanisms of how Perp loss and desmosome disruption contributes to disease progression in a variety of contexts.

Advisor: Attardi Laura primary advisor. Thesis advisor
Nelson W. J. (W. James) advisor. Thesis advisor
Oro Anthony
Sage Julien advisor. Thesis advisor
Chemerin and IL-17 in inflammation, obesity, and metabolism [electronic resource]

Inflammation is characterized by the influx and activation of leukocytes to sites of tissue damage. Upon recruitment, immune cells become activated and can secrete pro-inflammatory cytokines and chemoattractants that can modulate cellular responses and leukocyte trafficking. However, if inflammation occurs inappropriately, it can lead to unwanted tissue damage to the host or can affect metabolic processes (e.g. glucose metabolism or bone metabolism). Evidence indicates inflammation also occurs in adipose tissue during obesity and that adipose tissue leukocytes secrete cytokines that can contribute to systemic, chronic inflammation. The mechanisms that regulate inflammation and mediate its effects on metabolism are not fully understood. To help clarify what factors mediate inflammation, we sought to determine the role that the chemerin receptor, CMKLR1, may play in mediating immune cell trafficking to inflamed tissue. We found CMKLR1 is expressed by murine peritoneal macrophages, which can migrate to chemerin in vitro. CMKLR1 was upregulated by TGF[Beta] and downregulated by pro-inflammatory cytokines and TLR ligands. Furthermore, we found that CMKLR1 exacerbated the progression of experimental murine autoimmune encephalomyelitis (EAE). Chemerin was expressed in inflamed central nervous system (CNS) tissue, and microglial cells and CNS-associated myeloid dendritic cells expressed CMKLR1 in mice with EAE. Additionally, we discovered CCRL2 as a novel receptor for chemerin and determined it is a non-signaling decoy receptor which may bind and present chemerin to CMKLR1. We found that CCRL2 is expressed by mouse mast cells and can enhance tissue swelling and tissue leukocyte infiltration during mast cell-dependent passive cutaneous anaphylaxis. In an attempt to uncover a role for chemerin/CMKLR1 in obesity development or obesity-related inflammation, we discovered an unexpected role for the pro-inflammatory cytokine, IL-17, in adipocyte metabolism. IL-17 was upregulated in obese adipose tissue by T cells. IL-17 KO mice were more susceptible to diet-induced obesity. IL-17 inhibited adipocyte development and insulin stimulated glucose uptake by adipocytes. Furthermore, young IL-17 deficient mice were more insulin sensitive than their WT counterparts. Overall, our data indicate a role for chemerin and chemerin receptors in leukocyte migration and function in inflammatory diseases, and suggest that IL-17 regulates metabolic responses associated with obesity.

Keywords: Immunology.
Advisor: Butcher Eugene primary advisor. Thesis advisor
Chawla Ajay advisor. Thesis advisor
Jones Patricia advisor. Thesis advisor
Martinez Olivia
Chemical reaction modeling in a subsurface flow simulator with application to in-situ upgrading and CO2 mineralization [electronic resource]

Chemical reactions occur in a number of subsurface flow processes. Numerical modeling is an essential tool for understanding and optimizing complex reactive flows in a variety of application areas. In this work, we propose and implement chemical reaction modeling capabilities in Stanford's General Purpose Research Simulator (GPRS). The formulations developed include a procedure based on species conservation equations and an approach based on element conservation equations. The species-based formulation is suitable for solving reactive flow problems characterized by kinetic reactions only. In the element-based formulation, by contrast, both equilibrium and kinetic reactions can be treated consistently in the fully coupled system. This procedure represents a new treatment for reactive flow modeling. Additionally, in both formulations, a new generic representation of reaction terms is developed, which allows simultaneous modeling of homogeneous and heterogeneous reactions within or among phases (i.e., gas, liquid, water and solid phases). We apply the species-based formulation to model the in-situ upgrading of oil shale. Oil shale is a highly abundant but difficult to produce energy resource. The in-situ upgrading process entails heating the oil shale to about 700 F, at which point the kerogens decompose to gas and liquid hydrocarbons through a series of chemical reactions. After adjusting a few uncertain parameters (within physical ranges), our simulation results show relatively close agreement with available field data. The other application considered in this work is the modeling of carbon storage in deep saline aquifers. Detailed results are presented for a fine-grid model of a benchmark study. For this case, chemical reactions are not considered. Carbon mineralization reactions are then modeled using the element-based reactive flow formulation. Coarse-grid models are used for these simulations. Because the chemistry data relevant to carbon mineralization are, to date, not fully defined, we provide simulation results using available chemistry parameters. We discuss the remaining challenges that must be overcome before mineralization reactions can be simulated on fine-grid models. We note finally that the chemical reaction modeling capabilities in GPRS can be extended to other subsurface reactive flow processes (e.g., enhanced coalbed methane recovery).

Keywords: Energy Resources Engineering
Advisor: Durlofsky Louis primary advisor. Thesis advisor
Tchelepi Hamdi primary advisor. Thesis advisor
Kovscek Anthony R. (Anthony Robert) advisor. Thesis advisor
Choreography in conversation [electronic resource] : the imperial ballet and Russian literature, 1851-1905

In "Choreography in Conversation: The Imperial Ballet and Russian Literature, 1851-1905, " I argue that the simultaneous incorporation of cosmopolitan influences and promotion of national themes in Russian literature and ballet in the second half of the nineteenth century participated in the construction of identity through performance. The emergence of a professional cadre of writers alongside an imperial system of ballet patronage led to a perceived division between the "progressive" realm of realist prose and the "retrograde" world of ballet. Yet I show how, contrary to contemporary criticism and subsequent scholarly interpretations, these two cultural spheres developed along similar artistic lines and in lively conversation, with attention to folkloric sources and concerns about authenticity and in anticipation of modernist experiments with form. Drawing on the historical production of Jules Perrot's 1851 ballet "The Naiad and the Fisherman, " I first consider the fetishization of ballet in the case of Lev Tolstoy and his lifelong polemic with dance: in his early story "The Tale of How Another Girl Named Varenka Quickly Grew Up, " his novels "War and Peace" and "Anna Karenina, " and his aesthetic manifesto "What is Art?." I then examine Arthur Saint-Léon's adaptation of fairytales by Peter Ershov and Alexander Pushkin into "national ballets, " which were popularly lauded as "authentically" Russian yet parodied by the prominent radical writer Mikhail Saltykov-Shchedrin as ballet travesties. I next propose that Nikolai Nekrasov's long poem "Ballet" mirrors Marius Petipa's "Florida" in a poetic pastiche of peasants, pirates, and patrons. Finally, I posit a shared provenance in the fin-de-siècle fugues of Peter Tchaikovsky, Lev Ivanov, and Petipa's "Swan Lake" and Anton Chekhov's "The Seagull." In my dissertation, I offer a new understanding of the relationship between text and spectacle, in which ballet evolved from a space for discourse on Russian identity to an integral part of the Russian national narrative and one of its most celebrated cultural commodities.

Keywords: Slavic Languages and Literatures
Advisor: Safran Gabriella
Freidin Gregory advisor. Thesis advisor
Greenleaf Monika
Scholl Tim