Thèse de doctorat : Stylistique et poétique. Langue française et littérature : Paris 12 : 2005. / Version électronique uniquement consultable au sein de l'Université Paris 12 (Intranet). Titre provenant de l'écran-titre. Bibliogr. : 423 réf. Index.

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Sucrose content is one of the important seed quality traits in soybean, especially for oriental soyfood production. However, little genetic information is available on this quantitative trait yet. A previous study was conducted on seed sucrose content of soybean using a population of F2-derived lines from an interspecific cross between an adapted high-sucrose (8.3%) G. max breeding line (V71-370) and a low sucrose (1.6%) G. soja plant introduction (PI407162). Nineteen marker loci, mapping to seven linkage groups (A1, A2, E, F, L1, I, and M), were significantly associated with seed sucrose content after screening 178 polymorphic genetic markers, including RFLPs, SSRs, RAPDs and morphological markers. The replicated field experiments were planted in 1993 and 1995. The objective of my study was to evaluate QTLs associated with seed sucrose content utilizing an additional 153 F2:3 families from the same cross. DNA samples from the additional families were analyzed with the nineteen genetic markers associated with sucrose in the previous study. Sucrose data were obtained from seeds harvested from a field experiment conducted in 1995. Single factor analysis of variance results for the sucrose data obtained from the 153 F2:3 families were compared to the 1995 data for the 144 F2:3 families of the previous study. Of the nineteen genetic markers significantly associated with seed sucrose content in the previous study, seven were also significantly associated in this study. These genetic markers include sgA458a on linkage group A2, NBS61 on linkage group E, sgB164, R-B4a and sgB162 on linkage group L1, and R-B4b and sgA144 on linkage group I. The percent phenotypic variation explained by significant individual markers varied from 2.9 to 6.8% in the 153 F2:3 families. This study shows that seed sucrose content, a quantitative trait, may be improved using the molecular marker technology. Further research is necessary in different genetic backgrounds of G. max in order to implement these markers in a breeding program for selection. / Master of Science

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Over the last twenty years, fragment-based drug discovery (FBDD) has emerged as a highly successful way to provide lead compounds for subsequent optimisation into drug candidates. Initial hits usually exhibit lower potency than those identified by more traditional techniques, such as High-Throughput Screening (HTS), but the optimisation phase of FBDD is highly efficient, thus providing superior lead-like compounds. The recent application of FBDD in a variety of protein kinase campaigns has successfully led to the identification of novel binding sites and highly efficient chemical ligands. This demonstrates the utility of the FBDD strategy against well-established kinase targets, where selectivity is otherwise challenging due to significant conservation of the ATP-binding site. Protein kinase CK2 is a ubiquitously expressed and constitutively active regulator of cell growth, proliferation and apoptosis. Elevated levels of CK2 protein and activity have historically been involved in human cancer, including lung, cervical and head and neck cancer types, and its overexpression is associated with worse prognosis. A number of CK2 inhibitors are currently available displaying activity against multiple cancers in vitro and in the clinic, however the majority of these candidates target the ATP-binding site and thus display poor selectivity in kinase panel assays. Here we explore the application of FBDD towards the development of potent and selective inhibitors of the catalytic α-subunit of CK2. This project exploits a novel, conserved binding site, named the αD pocket, for the generation of allosteric inhibitor molecules. Following structure-based optimisation of a potent inhibitor series, and characterisation of a previously unreported binding mode, a fragment linking strategy between the lead αD-site fragment and a low-affinity pseudosubstrate peptide is investigated. This work validates the utility of FBDD towards the discovery of new binding modes, presents a first in class CK2α allosteric inhibitor series and provides the first X-ray crystal structure of protein kinase CK2 in complex with a ligand binding in the substrate-binding channel.

In order to realize the advanced graphics rendering algorithms which tends to become more complex and flexible, more and more graphics processor units (GPU) include a micro-processor-like core to support the programmable shading capability. However, since the number of cycles spent in the fragment shader in programmable GPU will vary with different applications, the hardware implementation of the remaining fixed function of the graphics rendering flow becomes not trivial because the suitable target throughput is hard to set. In addition, the data transfer between the shader processor and other hardware fixed-function modules will also represent a big overhead. Therefore, this thesis focuses on realizing the rasterization, which is a very important fixed rendering function, and proposes a pure-software solution that can be executed by the shader processor. The pure-software rasterization requires 98 cycles in setup-stage, and an average of 13 cycles per pixel in interpolation-stage. To further accelerate this rasterization, this thesis also proposes an hardware-software codesign which uses a embedded scan-conversion unit to cooperate with the shader processor. This unit costs about 8.5K gates, which occupies only 1.7% of the entire GPU, but can help reduce more than 30% cycles compared with the pure-software approach in the test-benches used in this thesis. The other contribution of this thesis is to implement the stereoscopic graphic rendering function. To provide stereoscopic effect, the graphic rendering system has to run the entire rendering flow for additional passes to generate the results from different views. However, this thesis will embed an additional code in the fragement shader to adjust the x-coordinate position generated by vertex shader to avoid the additional running pass of the vertex shader.

Reproduction de : Thèse de doctorat : Philosophie : Paris 8 : 2006. / Titre provenant de l'écran-titre. Bibliogr. f. 245-251.

Reproduction de : Thèse de doctorat : Littérature française : Lyon 2 : 2005. / Titre provenant de l'écran-titre. Bibliogr.

The prothrombinase (IIase) complex is an essential component of the coagulation cascade and is composed of a serine protease, Factor Xa (FXa), its non-enzymatic cofactor, Factor Va (FVa), calcium and a phospholipid membrane surface. It activates prothrombin (FII) to thrombin, the principal stimulator of clot formation in vivo. FII activation by IIase is mediated by specific interactions between FII and FVa. Preliminary NMR and peptidyl mimicry studies identified six residues within the FII Fragment 2 (F2) domain (S160, Q177, R181, L182, V184 and T185) that likely mediate an interaction between it and the heavy chain of FVa. Therefore, six recombinant FII derivatives were prepared whereby each of the aforementioned residues was mutated to alanine. FII activation kinetics by FXa in the presence or absence of FVa was measured by DAPA-thrombin complex formation. The results show that FII-S160A, -R181A, -L182A, -V184A and -T185A had no significant effect on the catalytic efficiency of the reaction in the presence of FVa. In the absence of FVa, the catalytic efficiency of FII-R181A, -L182A, -V184A, and -T185A derivatives decreased by 17-27% compared with wildtype, while FII-S160A had no effect. FII-Q177A, however, showed a significant increase of 17% in catalytic efficiency in the presence of FVa but no change in its absence. Two double (FII-Q177A/R181A and FII-R181A/T185A) and one triple (FII-Q177A/R181A/T185) mutants were generated to determine if multiple mutations would have an additive effect. These derivatives were indistinguishable from wildtype in the presence of FVa. In the absence of FVa, however, their catalytic efficiency values decreased 12-25% compared with wildtype. Further comparison of these values showed that FII-R181A and -Q177A/R181A both decreased by 25%, while FII-R181A/T185A and -Q177A/R181A/T185A decreased by 12% and 24% with respect to the wildtype, respectively. Both comparisons, where the only difference was an additional mutation at Q177, suggest that Q177 does not affect the activation kinetics of FII in the absence of FVa. Taken together, our data suggest that Q177 in the F2 domain of FII is likely involved in interacting with IIase through a FVa-dependent mechanism while residues R181, L182, V184 and T185 may be involved through a FVa-independent mechanism. / Thesis (Master, Biochemistry) -- Queen's University, 2012-07-31 11:38:32.262

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