VictorJuiz/thesis huggingface dataset:
Digital fingerprinting in digital cinema systems

Increasing adoption of digital cinema, in theatres has caused the movie industry to seriously consider active measures against piracy. Unfortunately, employing digital watermark (DW) techniques does not deter collusion attacks, which can result in the alterations or removal of forensic marks embedded in the digital movie. To combat colluders, traceability (TA) codes should be employed in addition to DW. In this research, we investigate methods of combining the use of TA codes and DW, analyze their effects and applicability in digital movies, and implement an anti-piracy scheme utilizing both techniques in a digital cinema context. The proposed system is shown to counter collusion and frame replacement attacks in addition to conventional attack methods. We demonstrate experimentally the capabilities of the proposed anti-piracy system and show that it is successful in tracing all colluding members of a coalition of size c = 7 for a 30-minute movie clip.
Structure-function relationships in human [beta]-hexosaminidase

Human β-hexosaminidase (Hex) isozymes are dimeric enzymes composed of α and/or β subunits, i.e. Hex A (αβ), Hex B (ββ) and Hex S (αα). Only Hex A has a unique in vivo function, i.e., hydrolysis of ganglioside GM2. Thus, mutations in the either α or β subunit of Hex A can result in ganglioside storage and two major forms of GM2 gangliosidosis, i.e. Tay-Sachs or Sandhoff diseases, respectively. The goal of this thesis is to study structure-function relationship in human Hex. The first project was to characterize a novel missense mutation (βPro504Ser) associated with the chronic form of Sandhoff disease using both the patients' and transfected cells. Biochemical studies of mutant Hex A demonstrated that this substitution directly affects the ability of Hex A to hydrolyze its natural substrate and also intracellular transport, producing chronic Sandhoff disease. The second project was to examine the validity of the molecular modeling of human Hex based on the X-ray structure of bacterial chitobiase. To achieve this, I first developed a new method for the generation of a C-terminal His6-tagged form of pro-Hex B in transfected cells. Re-examination of βArg21 I Lys using this highly purified form of mutant Hex B indicated that the substitution resulted in an enzyme with a more than 10-fold increase in its apparent Km and over a 1000-fold decrease in its Vmax. Thus βArg211 plays a critical role in substrate binding and in orientating the substrate in the active site. Next I used the same approach to analyze the candidate conserved active acidic residues in human Hex B. The βGlu355GIn substitution reduced Vmax >8000-fold with a slight lowering of the Km, consistent with Glu355 being the catalytic acid group in human Hex. The βAsp354Asn mutant also had an almost normal 0Km but a 6000-fold Vmax decrease, also conforming with Asp354 functioning as a “base” to aid in the proposed substrate-assisted catalysis. βAsp241, along with βAsp240 and βAsp290, is involved in substrate binding; whereas βAspl96 is important in the initial folding or dimer formation of the β-subunits rather than any involvement in its active site. Taken together, I concluded that the chitobiase model is correct in light of the active site residues in human Hex characterized thus far. The studies of these active site residues suggest that human Hex and probably all the Family 20 enzymes have similar structures and a conserved substrate-assisted catalysis mechanism.
Leslie Marmon Silko's "Ceremony": An ecocritical approach for transformative learning

Literary texts can be a powerful pedagogical tool within learning processes, for a story is a key to redirect our way of being and knowing in everyday life and to enhance both personal and social transformation. This thesis makes connections between literary analysis and transformative education. In particular, I demonstrate an ecocritical reading of Leslie Marmon Silko's (1977) Ceremony and examine the main themes, the plot, and the concepts of home, Mother Earth, and wholeness, which will help to create a transformative space and discourse across national and geographical borders. I further discuss the potential of this text in terms of exposing social and environmental injustice and structural and cultural violence. Finally, this thesis suggests transformative learning possibilities through critical reading practice as a way of developing inner reflection as well as intercultural dialogues, thereby exploring the value of a planetary consciousness that deepens our sense of self and place.

Keywords: Transformative learning
Ecocriticism
Environmental protection
On the relationship between osteoconduction and surface texture during peri-implant osteogenesis

In clinical implant dentistry, it is generally held that the texture of an endosseous implant surface has an effect on peri-implant osteogenesis. “Roughened” surfaces promote contact osteogenesis, whereas “smooth” surfaces tend to result in distance osteogenesis. However, the mechanisms by which surface texture influences such phenomena are not fully understood. This work investigates the hypothesis that textured surfaces promote contact osteogenesis by retention of the post-traumatic peri-implant fibrin clot through which osteogenic cells migrate and form bone on the implant surface. In order to test individual aspects of the hypothesis, the following in vitro experiments were conducted. Rat bone marrow cultures and cloned cell populations were maintained under osteogenic conditions, and a previously described interfacial mineralized afibrillar matrix was shown to be an appropriate morphological marker for de novo bone formation. Biochemical analysis of the matrix, produced under scorbutic culture conditions that inhibit the formation of collagenous matrix, identified osteopontin (OPN) as the major glycoprotein constituent. However, cultures from OPN-deficient mice demonstrated that OPN presence was not necessary for the elaboration of this matrix. To verify the proposed mechanism of osteoconduction, fibrin gels were polymerized on top of bone cell cultures, and osteogenic cell migration into the fibrin matrix was observed. This was verified by employing both cloned cell populations and scorbutic culture conditions. Furthermore, the initiation of de novo bone formation within the fibrin scaffolds, as identified by the presence of afibrillar matrix, could be demonstrated. To show that osteogenic cells contract the matrix through which they migrate, rat bone marrow cells were cultured on fibrin gels. The influence of implant surface texture on fibrin matrix retention was also measured. Among several candidate implant surfaces that were verified to have similar surface chemistry, those with a more complex texture showed significantly higher fibrin matrix retention, as proposed by the hypothesis.
Dissolution behavior of cobalt, nickel and iron from smelter slag using aqueous sulphur dioxide

Thermodynamic modeling, applying OLI, was used to study the slag-SO 2 system. The model developed was adequate in describing the dissolution of slag in aqueous SO2. The main species in the system were the metal-S(IV) species: FeSO30, CoSO3 0 and NiSO30. The model suggested that iron could be removed from the system as FeSO3.3H2O with increase of total S(IV). Experimentally by increasing the pH of the leach solution the precipitate FeSO3.3H2O was obtained. As a result the ratio of Co to Fe and Ni to Fe increased significantly. However, coprecipitation of Co and Ni also occurred with Fe. The metal/Fe ratio in solution was sensitive to pH. Lower pH was desirable for high metal to Fe ratio in solution. Smelter slags, an industrial waste product, contain valuable metals such as Co, Ni and Cu in proportions of less than 1 wt% along with about 40wt% of Fe and 15wt% of Si. This research has focused on understanding the dissolution behavior of Co, Ni and Fe from smelter slag applying aqueous SO2, another product of metallurgical industries. Such an understanding would help lay the foundation for developing a scheme for the extraction of the valuable metals from slag using aqueous SO2.
Chx10 is necessary for mammalian neuroretinal cell identity in a pathway with FGF and Mitf

In mammalian retinal development, a neuroectodermal cell undergoes a cell fate decision to become either (1) a presumptive neuroretinal cell (under the influence of FGF) that expresses the homeodomain transcription factor Chx10 or (2) a presumptive retinal pigment epithelium (RPE) cell that expresses the basic helix-loop-helix protein Mitf. Chx10 loss-of-function mutations in human and mouse result in the orthologous phenotype of microphthalmia (small eye) due to defects in neuroretinal progenitor proliferation. In contrast, mutations in Mitf result in a dorsal RPE cell fate change to a neuroretinal phenotype. Unexpectedly, Mitf RNA and protein is ectopically expressed in the neuroretina in Chx10 mutant mice. To determine the role of the ectopic Mitf in the Chx10 mutant phenotype, we misexpressed human MITF in the neuroretina (NR-MITF) and found no major defects, including normal retinal proliferation. To test whether the lack of phenotype in the NR-MITF mice was caused by competition with the Chx10 protein that is also present in these neuroretinal cells, we crossed the NR-MITF mice to the Chx10 mutant mouse. We observed a pigmented monolayer (PML) in place of a neuroretina suggesting a dramatic cell identity change, supportive of a role for Chx10 in maintaining neuroretinal cell identity. In the opposite experiment, expression of human CHX10 in the RPE in conjunction with the loss of one copy of Mitf results in neuroretinal-like structure in the dorsal region. Finally double Chx10;Mitf mutant animals present with an improvement of both the RPE and neuroretina, demonstrating that the two genes interact genetically. Therefore, both Chx10 and Mitf regulate retinal cell identity in an antagonistic and/or dose dependent manner. Importantly, we have also demonstrated that Chx10 is the first gene identified that is necessary for mammalian neuroretinal cell identity. Finally we have shown that Chx10 is downstream of FGF in directing neuroretinal cell identity. Mechanistically, Chx10 functions by repressing Mitf directly or indirectly in eye development, but also through non Mitf-dependent pathways. These findings demonstrate that FGF, Chx10 and Mitf function in a pathway to regulate cell fate identity in the developing mammalian neuroretina.
Mapping the distribution of cell surface molecules by chromophore localization in the transmission electron microscope via low electron energy loss imaging

From cell surface studies involving ruthenium red, trypan blue and two lipophilic PKH dyes, the importance of chromophore preservation during specimen preparation was realized. The stability of the binding of fluorescein conjugated cholera toxin to the sphingolipid, GM1 permitted energy filtered imaging and lipid raft localization in T cells with a spatial resolution that was over 100-fold better than light microscopy. We are using a technique developed in our lab to map the distribution of chromophore-tagged cell surface molecules by electron microscopy. The technique employs the use of our previously modified electron energy filter that permits imaging with an energy resolution of 1 eV. Such an energy filter makes it possible to select electrons that in traversing the specimen, have lost energies of only a few electron volts, corresponding to absorption energies of visible colours. Our approach is aimed at imaging cells that have been stained with conventional dyes that are commonly used in light microscopy but delivering such images with the spatial resolution of the electron microscope.
Influence of genetic polymorphisms in P450 C17[alpha](T27C), catechol-O-methyltransferase (VAL158MET), and activity level of cytochrome P450 1A2 on mammographic density levels and other risk factors for breast cancer

The objective of this thesis was to study the genetic basis of ovarian hormone metabolism and its potential influence on mammographic density levels and other risk factors for breast cancer. Using a cross-sectional design, polymorphisms in 2 genes, P450 c17alpha (CYP17, T27C, A1 and A2 allele, respectively) and catechol-O-methyltransferase (COMT, VAL158MET, COMT*1 and COMT*2 allele, respectively), as well as cytochrome P450 1A2 (CYP1A2) activity were examined in their relationships with mammographic density, sex hormones, the growth hormone-insulin growth factor-I (IGF-1) axis, and anthropometric variables. Each low activity COMT*2 allele was associated with lower levels of percent breast density amongst pre- but not postmenopausal subjects. In premenopausal women the low activity COMT*2 allele was also associated with lower serum levels of IGF-1, higher levels of FSH and progesterone, and with a larger waist-to-hip ratio, body mass index (BMI), and subscapular skinfold. Information was obtained on risk factors, diet, and anthropometric measures. Blood levels of sex hormones, lipids, and growth factors were measured; and, CYP17 and COMT genotypes were determined. In vivo CYP1A2 activity was assessed by measuring caffeine metabolites in urine. Serum and urinary malondialdehyde (MDA), and MDA-deoxyguanosine adducts in DNA were measured. Mammograms were determined using a computer-assisted method. CYP17 genotype was not associated with mammographic density levels. In premenopausal women, the A2 allele was associated with higher levels of dehydroepiandrosterone sulfate, and in postmenopausal women, with higher levels of total estradiol and lower levels of follicle stimulating hormone. Among premenopausal subjects, interactions were observed between CYP17 genotype and endogenous insulin levels as well as various dietary variables. These findings indicate that CYP17 and COMT genotypes, as well as CYP1A2 activity are associated with several risk factors for breast cancer. CYPIA2 activity in post-, but not premenopausal, women was positively associated with breast density levels. In premenopausal women, CYP1A2 activity was associated with serum and urinary MDA levels, age, BMI, smoking status, and levels of sex hormone binding globulin (SHBG), total cholesterol, insulin, triglyceride, and caffeine intake. In postmenopausal subjects, independent associations were observed with smoking status, age at menarche, blood triglycerides, SHBG, and IGF-1 levels.
La representation de la femme dans l'oeuvre romanesque de Margeurite Yourcenar: aAnalyse de la construction narrative du personnage feminin yourcenarien

Notre étude, "La représentation de la femme dans l'oeuvre de Marguerite Yourcenar: Analyse de la construction narrative du personnage féminin yourcenarien", ouvre la voie à une nouvelle lecture du personnage féminin dans l'oeuvre romanesque de Marguerite Yourcenar. Souvent analysé mais rarement défini, ce sujet controversé de la figure féminine yourcenarienne continue à susciter de nombreux débats critiques. Dans cette analyse, nous nous proposons de porter un nouveau regard sur l'étude du personnage féminin en considérant celui-ci comme une composante essentielle du procédé constructif du texte romanesque. Notre approche méthodologique consiste ainsi à analyser "la construction narrative" du personnage féminin en tant qu'élément textuel du système structural du texte yourcenaricn. Pour ce faire, nous examinons les personnages féminins dans Anna, soror ..., Nouvelles orientales, et Denier du rêve selon une perspective solidement ancrée dans les apports de la théorie littéraire, en particulier, ceux de la sémiotique, de la symbolique et de la réflexion sur l'altérité ...
Identification of cellular protein interactions with the EBNA1 protein of Epstein-Barr virus and characterization of the interaction with USP7

Epstein-Barr virus is a gamma herpesvirus that infects human B lymphocytes. The viral protein essential for maintaining latent infection within the host is EBNA1, (Epstein-Barr Nuclear Antigen 1). To better understand how EBNA1 mediates its many functions during viral latency, we set out to identify human cellular proteins that interact with EBNA1 and contribute to its various roles within the cell. By coupling EBNA1 affinity chromatography and EBNA1 TAP-tagging with identification of bound proteins by mass spectrometry, previously unknown interactions of EBNA1 with NAP1, TAF-Ibeta, casein kinase II, PRMT5, and USP7 were observed. The significance of the EBNA1 interaction with USP7, a protein formerly found to associate with the Herpes Simplex protein, ICP0, was further investigated. The USP7 protein was purified, and used to characterize the protein in vitro. The structural organization of USP7 was determined and showed that USP7 is comprised of four structural domains; an N-terminal domain known to bind p53, a catalytic domain, and two C-terminal domains. We showed that the p53 binding domain was also responsible for the EBNA1 interaction, while the ICP0 binding domain mapped to a C-terminal domain between amino acids 599--801. Binding assays indicated that EBNA1 peptide 395--450 bound with 10 fold higher affinity to USP7 than did p53 peptides, suggesting EBNA1 may sequester USP7 in order to moderate p53 levels. EBNA1 was also found to efficiently compete for USP7 from p53 in gel filtration analyses. The region of EBNA1 mediating the interaction with USP7 was mapped. An EBNA1 mutant (Delta395--450) lacking this region was used to investigate the possible role of USP7 interaction on EBNA1 functions. Deletion of the USP7 binding residues from EBNA1 increased the efficiency with which EBNA1 initiated DNA replication, and slightly decreased the transcriptional activation function of EBNA1. Preliminary data suggests that removal of amino acids 395--450 from EBNA1 results in a deregulation of p53 levels, as cells expressing Delta395--450 demonstrate higher steady state levels of p53 as compared to cells expressing wild-type EBNA1. Current evidence also suggests that cells expressing Delta395--450 exhibit a decreased capacity to avoid apoptosis, as compared to cells expressing wild-type EBNA1.
The role of TIMP3 in mammary gland morphogenesis, involution, inflammation, and tumourigenesis

Responsible for producing milk that protects and nourishes the offspring, the mammary gland undergoes cyclical remodeling as dictated by estrous and gestation. The orchestration of mammary gland cell types with local and systemic tissue microenvironment factors can create an epithelial arbor, or differentiate it to secretory units, or even deconstruct the tissue. Ironically, the same remodeling property of the gland renders it susceptible to lesions, including breast cancer. Given the pro-apoptosic and pro-inflammatory roles of TIMP3 loss in involution, its role in mammary tumourigenesis was next investigated. Loss of TIMP3 caused a greater than 90% reduction in tumour burden and metastasis in MMTV-PyMT, an aggressive model of breast cancer. In the non-viral oncogenesis, physiological model, MMTV-Neu, 40% of Timp3 -/- mice were resistant to mammary tumours. Tumours that did emerge in Timp3-/- mice were more malignant. In both models, Timp3 heterozigosity inhibited tumourigenesis. Further, Timp3-null stroma halted the growth of initiated tumours and mammary epithelial cells derived from Timp3-/- tumours were more sensitive to apoptosis compared to controls. Tumourigenesis attenuation was accompanied by increased infiltration of macrophages, CD4+, and CD8+ T-cells. These studies demonstrate the critical role of TIMP3 during mammary gland physiology and tumourigenesis. Importantly, the loss of one or both Timp3 alleles results in mammary tumour suppression, providing an impetus for exploring TIMP3 as a potential therapeutic target against breast cancer. Extracellular proteolysis mediated by the balanced activity of matrix metalloproteinase (MMP) and tissue inhibitors of metalloproteinases (TIMPs) facilitates mammary gland remodeling. In particular, TIMP3 has the capacity to not only control ECM protein turnover, but also regulate the shedding and bioactivity of ligands and cell surface molecules. The role of TIMP3 in signaling mechanisms governing mammary gland biology were investigated using genetically engineered mice. Timp3-/- primary mammary epithelial cells had increased transcriptional activity of the survival factor, beta-catenin, consistent with an acceleration of epithelial ductal morphogenesis. During post-lactational mammary gland involution, TIMP3 deficiency caused accelerated mammary epithelial apoptosis through a concerted fragmentation of E-cadherin and activation of TNF-dependent apoptosis. Concomitantly, an increased infiltration of macrophages and sustained T-cell presence were observed, which were not mitigated in Timp3-/-/Tnf-/- mice.
Evaluation of lung tumour motion surrogates in radiotherapy

A methodology is presented to study the relationship between lung tumour motion and two external surrogate indicators of respiration, abdominal displacement and respiratory volume. Surrogates can be used to guide radiotherapy techniques that aim to minimize planning target volumes and consequently allow for dose escalation. However, few data exist to validate the ability of these surrogates to accurately localize the tumour. A clinical study is described in which time-synchronized x-ray fluoroscopy, spirometry and abdominal motion measurements are performed over multiple days on 11 patients undergoing radiotherapy for lung cancer. Analysis demonstrates a higher and more stable correlation between tumour motion and respiratory volume versus abdominal displacement. Variable tumour-surrogate phase relationships as a result of unstable respiration are observed in all patients. Inter- and intra-fractional changes in these relationships can result in localization errors as great as 25 mm. Suggestions for improving the accuracy of the surrogates are made.