Thesis (Ph. D.)--University of Alberta, 2009. / Title from pdf file main screen (viewed on Nov. 25, 2009). "A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy, Department of Chemistry, University of Alberta." Includes bibliographical references.

Thesis (doctoral)--Swedish University of Agricultural Sciences, 2002. / Thesis documentation sheet inserted. Appendix reprints four papers and manuscripts, three co-authored with others. Includes bibliographical references. Issued also electronically via World Wide Web in PDF format; online version lacks appendix.

Thesis (Ph. D.)--Mechanical Engineering, Georgia Institute of Technology, 2004. / Abdel-Khalik, Said, Committee Chair. Vita. Includes bibliographical references (leaves 376-384).

Thesis (Ph. D.)--Institute of Paper Chemistry, 1959. / Includes bibliographical references (p. 66-69).

published_or_final_version / Civil Engineering / Master / Master of Philosophy

The steady-state structure of a tokamak scrape-off plasma within a divertor chamber is numerically modeled. The simulation code OAKLEAF approximates the relevant atomic and molecular hydrogenic physics within the plasma as well as examining the effects of several wall impact events including charged particle reflection, absorption, and re-emission, secondary electron emission, and the sputtering of wall material by incident particles. Results indicate the presence of a two parameter solution space. With appropriate choices for these parameters the simulation code produces the electrostatic potential and density profiles within the divertor system as well as snapshots of the particle distribution functions at several points in the chamber. Using the distribution function information the model determines the detailed particle fluxes incident to the divertor plate and calculates the resulting sputtering rates. A study of sputtering rates as a function of initial plasma temperature is then presented. The work concludes by reviewing the scope of the thesis and by making recommendations for future work in the area.

Κατά τον αντισεισμικό σχεδιασμό δύσκαμπτων και ογκωδών κατασκευών εδαφικής αντιστήριξης (π.χ. τοίχοι αντιστήριξης από σκυρόδεμα) οι δράσεις που λαμβάνονται υπόψη κατά τις αναλύσεις ευστάθειας περιλαμβάνουν την στατική και δυναμική εδαφική ώθηση καθώς και την αδρανειακή δύναμη του τοίχου. Οι τρέχουσες μέθοδοι σχεδιασμού (ψευδοστατική, μετακινήσεων) θεωρούν ότι οι δύο ανωτέρω δράσεις ενεργούν συγχρονισμένα, δηλαδή οι μέγιστες τιμές τους ασκούνται ταυτόχρονα στην κατασκευή αντιστήριξης. Εν τούτοις αποτελέσματα πρόσφατων πειραματικών και υπολογιστικών διερευνήσεων υποδεικνύουν ότι (τουλάχιστον στην περίπτωση των ευμετακίνητων κατασκευών αντιστήριξης) αναπτύσσεται σημαντική διαφορά φάσης μεταξύ των δύο δράσεων (ασύγχρονη δράση). Αυτό έχει ως αποτέλεσμα να προκύπτει ιδιαίτερα συντηρητικός σχεδιασμός της κατασκευής αντιστήριξης όταν γίνεται δεκτό ότι τα μέγιστα των δύο δράσεων συμπίπτουν χρονικά (σύγχρονη δράση). Στην παρούσα Διατριβή διερευνάται με παραμετρικές αριθμητικές αναλύσεις η ορθότητα της παραδοχής της σύγχρονης δράσης στην περίπτωση των ακλόνητων κατασκευών εδαφικής αντιστήριξης. Χρησιμοποιείται η μέθοδος των πεπερασμένων στοιχείων (χρήση κώδικα πεπερασμένων στοιχείων PLAXIS) για την προσομοίωση ακλόνητων τοίχων αντιστήριξης από σκυρόδεμα που συγκρατούν μη-συνεκτικό επίχωμα με ελαστοπλαστική σχέση τάσεων-παραμορφώσεων (και κριτήριο αστοχίας Mohr-Coulomb) και υποβάλλονται σε οριζόντια ταλάντωση (είτε αρμονική κίνηση είτε καταγεγραμμένη χρονοϊστορία σεισμικών γεγονότων). Οι παραμετρικές αναλύσεις περιλαμβάνουν τη μεταβολή: α) της σχετικής πυκνότητας του επιχώματος (χαλαρή, μετρίως πυκνή και πυκνή κατάσταση), β) της έντασης της επιβαλλόμενης οριζόντιας ταλάντωσης (0.05g έως 0.7g) και γ) του ύψους του τοίχου (4.0m και 7.5m). Τα αποτελέσματα των αναλύσεων χρησιμοποιούνται κατ’ αρχήν για τον προσδιορισμό της στατικής κατανομής και του μεγέθους των εδαφικών ωθήσεων στον τοίχο. Στη συνέχεια υπολογίζεται, η διαφορά φάσης μεταξύ της αδρανειακής δύναμης του τοίχου και της εδαφικής ώθησης, καθώς και του αντίστοιχου ποσοστού της μέγιστης τιμής της δυναμικής εδαφικής ώθησης που ασκείται κατά τη χρονική στιγμή της μεγιστοποίησης της αδρανειακής δύναμης του τοίχου. Οι αναλύσεις υποδεικνύουν ότι η στατική κατανομή των ωθήσεων είναι τριγωνική με τον συντελεστή πλευρικών ωθήσεων να προκύπτει, περίπου, ίσος με Κ0. Κάτω από συνθήκες δυναμικής φόρτισης το ποσοστό της δυναμικής ώθησης προκύπτει πολύ υψηλό (80% έως 90%) – κυρίως για μετρίως πυκνό και πυκνό εδαφικό επίχωμα – ανεξάρτητα από την ένταση της φόρτισης σε αντίθεση με τις πολύ χαμηλές τιμές (δηλαδή ασύγχρονη δράση) που έχουν προκύψει από αντίστοιχη διερεύνηση για την περίπτωση των ευμετακίνητων τοίχων αντιστήριξης. Ιδιαίτερα ενδιαφέρουσα είναι η παρατήρηση ότι για μικρές τιμές της έντασης της δυναμικής φόρτισης (≤ 0.2g) η συμπεριφορά του υψηλού τοίχου (7.5m) προκύπτει διαφοροποιημένη σε σχέση με αυτή του τοίχου των 4.0m: το ποσοστό της σεισμικής ώθησης είναι πολύ μειωμένο (20% έως 40%), ιδιαίτερα στην περίπτωση των πολύ χαλαρών επιχωμάτων. Παρατηρείται επίσης ικανοποιητική συμφωνία της προκύπτουσας τιμής της εδαφικής ώθησης με αυτή από τη σχέση του Wood(1973) και της αναλυτικής λύσης των Kloukinas et al.(2012). Ιδιαίτερο ενδιαφέρον παρουσιάζει η τροποποιημένη κατανομή των εδαφικών ωθήσεων καθ’ ύψος του τοίχου, οι οποίες προκύπτουν αυξημένες στο ανώτερο τμήμα του. Συμπεραίνεται ότι στην περίπτωση του σχεδιασμού των ακλόνητων τοίχων με μετρίως πυκνό και πυκνό επίχωμα η δράση της δυναμικής εδαφικής ώθησης είναι εύλογο και δικαιολογημένο να θεωρείται σύγχρονη με την αδρανειακή δύναμη του τοίχου. / --

The influence of yielding foundations on the mechanical behaviour of reinforced soil walls including wall deformations and loads (strains) in the reinforcement layers is very complex. Based on a review of the literature, there is a need to quantify and isolate the influence of foundation boundary type and magnitude of foundation stiffness on deformations and reinforcement loads in geosynthetic reinforced soil walls. This thesis presents the results of a series of 1/6-scale reinforced soil wall model tests that were carried out to examine the influence of horizontal and vertical toe compliance and vertical foundation compressibility on wall behaviour. The heavily instrumented walls were constructed in a strongbox that was 1.2 m high by 1.6 m wide and retained soil to a distance of 2.3 m behind the facing. The models were uniformly surcharged in stages following construction. The experimental program consisted of three groups of tests. Group 1 tests involved five walls. One wall was constructed with a very stiff horizontal restraint, and three walls were constructed with different horizontal toe stiffness using combinations of coiled springs. The remaining wall in this series was constructed without any horizontal toe restraint. Group 2 was comprised of three walls. One wall was a control wall with a rigid toe. The other two walls were constructed with different vertical toe stiffness support using different combinations of rubber blocks. Group 3 included a control wall with a rigid foundation and a companion wall constructed with a compressible foam and rubber layers below the backfill soil and the wall facing. The results demonstrate that the quantitative behaviour of the models was affected by the type and magnitude of foundation stiffness. For example, as horizontal toe stiffness increased a greater portion of the total horizontal earth load against the wall facing was carried by the toe. The data showed that the shape of facing lateral deformation profiles changed from rotation about the toe for the case of a very stiff horizontal toe to a more uniform profile for the unrestrained toe case. For the case of a rigid vertical footing support below the facing, vertical toe loads were greater than those computed from facing self-weight alone due to down-drag forces developed at the facing–reinforcement connections as the wall facing moved outward. As vertical toe support stiffness decreased with respect to foundation compressibility below the soil backfill, the magnitude of soil down-drag forces diminished resulting in a decrease in vertical toe load. / Thesis (Master, Civil Engineering) -- Queen's University, 2007-10-27 12:15:56.027

The bipolar budding pattern of a/a Saccharomyces cerevisiae cells appears to depend on persistent spatial markers. Genetic analysis reported here indicates that BUD8 and BUD9 potentially encode components of the markers at the distal and proximal poles, respectively. Mutants deleted for BUD8 or BUD9 bud exclusively from the proximal and distal poles, respectively, and the double-mutant phenotype suggests that the bipolar budding pathway has been totally disabled. Moreover, overexpression of these genes can cause either an increased bias for budding at the distal (BUD8) or proximal (BUD9) pole or a randomization of bud position, depending on the level of expression. Both molecules are related plasma membrane glycoproteins that are both N- and O-glycosylated. Each protein was localized predominantly in the expected location, with Bud8p delivered to the presumptive bud site just before bud emergence, and Bud9p delivered to the bud side of the mother-bud neck just before cytokinesisis. Promoter-swap experiments revealed the importance of time of transcription in localization: expression of Bud8p from the BUD9 promoter leads to its localization predominantly in the sites typical for Bud9p, and vice versa. Moreover, expression of Bud8p from the BUD9 promoter fails to rescue the budding-pattern defect of a bud8 mutant but fully rescues that of a bud9 mutant. However, although expression of Bud9p from the BUD8 promoter fails to rescue a bud9 mutant, it also rescues only partially the budding-pattern defect of a bud8 mutant. / Using a collection of mutants individually deleted for almost every yeast gene, I undertook a genome-wide phenotype analysis for altered sensitivity to a yeast antifungal protein, the K1 killer toxin. Mutations in most genes have no effect on toxin sensitivity, with less than 10% having a phenotype. Only 4% of these were previously known to have a toxin phenotype. There is a markedly non-random functional distribution of mutants with a toxin phenotype. Many genes fall into a limited set of functional classes or modules, which define specific areas of cellular function. These include known pathways of cell wall synthesis and signal transduction, and offer new insights into these processes and into cell wall morphogenesis.

CWH41 is required for beta-1,6-glucan biosynthesis and encodes glucosidase I, an enzyme involved in protein N-chain glucose processing. Therefore, the effects of N-chain glucosylation and processing on beta-1,6-glucan biosynthesis were examined, and it was shown that incomplete N-chain glucose processing results in loss of beta-1,6-glucan. To explore the involvement of other N-chain-dependent events with beta-1,6-glucan synthesis, the S. cerevisiae KRE5 and CNE1 genes were investigated, which encode homologs of the 'quality control' components UDP-Glc:glycoprotein glucosyltransferase and calnexin, respectively. The essential activity of Kre5p was found to be separate from its possible role as a UDP-Glc:glycoprotein glucosyltransferase. A ∼30% decrease in beta-1,6-glucan was observed upon disruption of CNE1, a phenotype which is additive with other beta-1,6-glucan synthetic mutants. Analysis of the cell wall anchorage of alpha-agglutinin suggests the existence of two beta-1,6-glucan biosynthetic pathways, one N-chain dependent, the other involving protein glycosylphosphatidylinositol modification. / Fks1p and Fks2p are related proteins thought to be catalytic subunits of the beta-1,3-glucan synthase. The fks1Delta mutant was partial K1 killer toxin resistant and showed a 30% reduction in alkali-soluble beta-1,3-glucan that was accompanied by a modest reduction in beta-1,6-glucan. The gas1Delta mutant lacking a 1,3-beta-glucanosyltransferase displayed a similar reduction in alkali-soluble beta-1,3-glucan but did not share the beta-1,6-glucan defect, indicating that beta-1,6-glucan reduction is not a general phenotype among beta-1,3-glucan biosynthetic mutants. FKS2 overexpression suppressed the killer toxin phenotype of fks1Delta mutants, implicating Fks2p in the biosynthesis of the residual beta-1,6-glucan present in fks1Delta cells. Eight out of twelve fks1tsfks2Delta mutants had altered beta-glucan levels at the permissive temperature: the FKS1F1258Y N1520D allele was severely affected in both polymers and displayed a 55% reduction in beta-1,6-glucan, while the in vitro hyperactive FKS1T6051 M761T allele increased both beta-glucan levels. These beta-1,6-glucan phenotypes may be due to altered availability of, and structural changes in, the beta-1,3-glucan polymer, which might serve as a beta-1,6-glucan acceptor at the cell surface. Alternatively, Fks1p and Fks2p could actively participate in the biosynthesis of both polymers as beta-glucan transporters. beta-1,6-Glucan deficient mutants had reduced in vitro glucan synthase activity and mislocalized Fks1p and Fks2p, possibly contributing to the observed beta-1,6-glucan defects.