Thesis (M.Sc.). / Written for the Dept. of Neurology and Neurosurgery. Title from title page of PDF (viewed 2008/05/14). Includes bibliographical references.

Thesis (doctoral)--Karolinska Institutet, Stockholm, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (doctoral)--Karolinska Institutet, Stockholm, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

No / There is considerable interest, both fundamental and technological, in understanding how additives and impurities influence nucleation, and in being able to modulate nucleation in a predictable way using designer auxiliary molecules. Notable applications involving auxiliaries include the control of nucleation in proteins, inhibition of urinary stone formation, inhibition of ice formation in living tissues during cryoprotection, prevention of blockages in oil and gas pipelines due to wax precipitation, and gas hydrate formation. Despite the immense interest, our understanding of how these molecules exert their effect is still rudimentary, partially because the molecular level processes involved are inaccessible to experiment. We have investigated mechanisms of action of nucleation additives and have derived explicit rules for designing additive molecules for modulating crystal nucleation. The mechanisms of action and the design features have been derived using molecular simulation of simple model systems. Our studies reveal that an effective nucleation inhibitor should have a strong interaction with the solute and have a structure that is able to disrupt the periodicity characterizing the emerging nucleus. Disruption can be achieved by steric effects resulting from structural differences between the additive and solute molecules, the additive possessing extensive degrees of freedom, or via a strong energetic interaction with the solute. Additive molecules that have an amphiphilic character and end up at the solute/solvent interface can inhibit, retard or promote nucleation depending on their specific structure and interactions with the solute and solvent and the given supersaturation, and these specific features and the link with the supersaturation will be discussed. These findings will help to rationalize the mechanisms of action of known nucleation inhibitors and modulators. They will also serve as a framework for rationally identifying or designing additive molecules for either inhibiting or promoting nucleation in specific systems.

Thesis (Ph. D.)--University of Oklahoma. / Bibliography: leaves 153-217.

Resumo: As rotas em que atuam os herbicidas devem ser fundamentais para o crescimento e desenvolvimento vegetal, pois o seu bloqueio deve promover a paralisação do crescimento ou a morte das plantas. De modo análogo, o bloqueio parcial destas rotas, com uso de baixas doses dos herbicidas, também pode ter implicações importantes alterando o balanço de processos metabólicos nas plantas. Sendo assim, foi conduzido no ano agrícola 2006/2007, um experimento em cana soca 2º corte na Fazenda Jurema pertencente ao grupo Cosan, município de Barra Bonita-SP, para verificar os efeitos do glyphosate e do sulfometuron methyl (em sub-doses, maturadores) na fisiologia da cana-de-açúcar. Os tratamentos constituíram-se da aplicação de dois herbicidas: sulfometuron methyl( 480 i.a/Kg) e glyphosate (360 e.a/Kg) em diferentes doses e misturas do produto comercial (Roundap e Curavial), mais a testemunha. As doses utilizadas foram: glyphosate 200 ml do p.c./ha-1; glyphosate 400 ml do p.c./ha-1; glyphosate 200 ml do p.c./ha-1 + 10 g do p.c../ha-1 de sulfometuron methyl; glyphosate 150 ml do p.c./ha-1 + 12 g do p.c../ha-1 de sulfometuron methyl; sulfometuron methyl 20g do p.c../ha-1. O delineamento experimental utilizado foi o de blocos casualizados com quatro repetições. Para verificar os efeitos destes produtos no metabolismo da planta, em pré (15 e 30 Dias Após Aplicação dos produtos) e pós-colheita (30, 60, 90, 120, 150 e 180 Dias Após Colheita), foram avaliados: parâmetros tecnológicos de produção da cana-de-açúcar (POL, TCH, TPH, BRIX, PBU); fatores de crescimento (altura e número de perfilhos); teor de clorofila e carotenóides; dinâmica de macro e micro nutrientes; FDA (fibra em detergente ácido), lignina e celulose; concentração de ácido chiquímico e ácido salicílico. Os resultados... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: The routes in the herbicides that work must be essential to plant growth and development, as its blockade should promote the growth of paralysis or death of plants. Similarly, the partial block of these routes, using low doses of herbicides (maturity), may also have important implications by altering the balance of metabolic processes in plants. Thus, an experiment was conducted in the agricultural year 2006/2007, in ratoon cane cutting 2 at Fazenda Jurema of belonging to the group Cosan. The treatments is the application of two maturity (sulfometuron methyl, and glyphosate) in different doses and mixtures further control (natural aging). The experimental design was a randomized block design with four replications. The objective of this research is to analyze the effects of applying these products in the metabolism of sugar cane in pre-and post-harvest, for both were: parameters of production technology, growth factors (height and number of tillers), content of chlorophyll and carotenoids, dynamics of nutrients, cellulose and lignin, shikmic concentration of acid and salicylic acid. The conclusions: the application of maturity promoted effect on technological parameters, height and number of tiller of culture, the application of glyphosate improved the levels of P and K in the plant and reduced the levels of Fe, Zn and Cu, the contents of chlorophyll and carotenoids influenced with application of glyphosate in the commercial dose, application of methyl sulfometuron increased levels of Mn, higher doses of glyphosate increased the concentration of shikmic; largest concentration of shikmic promoted the higher concentrations of salicylic acid in pre - In post-harvest sampling found... (Complete abstract click electronic access below) / Orientador: Edivaldo Domingues Velini / Coorientador: Fernando Gustavo Tonin / Banca: João Domingos Rodrigues / Banca: Robinson Antonio Pitelli / Banca: Robinson Osipe / Banca: Dionísio Luiz Piza Gazziero / Doutor

Made available in DSpace on 2014-06-11T19:30:24Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-07-02Bitstream added on 2014-06-13T19:19:09Z : No. of bitstreams: 1 meschede_dk_dr_botfca.pdf: 453157 bytes, checksum: 6b9492f4657f3740579e4ee8f73a6dd2 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / As rotas em que atuam os herbicidas devem ser fundamentais para o crescimento e desenvolvimento vegetal, pois o seu bloqueio deve promover a paralisação do crescimento ou a morte das plantas. De modo análogo, o bloqueio parcial destas rotas, com uso de baixas doses dos herbicidas, também pode ter implicações importantes alterando o balanço de processos metabólicos nas plantas. Sendo assim, foi conduzido no ano agrícola 2006/2007, um experimento em cana soca 2º corte na Fazenda Jurema pertencente ao grupo Cosan, município de Barra Bonita-SP, para verificar os efeitos do glyphosate e do sulfometuron methyl (em sub-doses, maturadores) na fisiologia da cana-de-açúcar. Os tratamentos constituíram-se da aplicação de dois herbicidas: sulfometuron methyl( 480 i.a/Kg) e glyphosate (360 e.a/Kg) em diferentes doses e misturas do produto comercial (Roundap e Curavial), mais a testemunha. As doses utilizadas foram: glyphosate 200 ml do p.c./ha-1; glyphosate 400 ml do p.c./ha-1; glyphosate 200 ml do p.c./ha-1 + 10 g do p.c../ha-1 de sulfometuron methyl; glyphosate 150 ml do p.c./ha-1 + 12 g do p.c../ha-1 de sulfometuron methyl; sulfometuron methyl 20g do p.c../ha-1. O delineamento experimental utilizado foi o de blocos casualizados com quatro repetições. Para verificar os efeitos destes produtos no metabolismo da planta, em pré (15 e 30 Dias Após Aplicação dos produtos) e pós-colheita (30, 60, 90, 120, 150 e 180 Dias Após Colheita), foram avaliados: parâmetros tecnológicos de produção da cana-de-açúcar (POL, TCH, TPH, BRIX, PBU); fatores de crescimento (altura e número de perfilhos); teor de clorofila e carotenóides; dinâmica de macro e micro nutrientes; FDA (fibra em detergente ácido), lignina e celulose; concentração de ácido chiquímico e ácido salicílico. Os resultados... / The routes in the herbicides that work must be essential to plant growth and development, as its blockade should promote the growth of paralysis or death of plants. Similarly, the partial block of these routes, using low doses of herbicides (maturity), may also have important implications by altering the balance of metabolic processes in plants. Thus, an experiment was conducted in the agricultural year 2006/2007, in ratoon cane cutting 2 at Fazenda Jurema of belonging to the group Cosan. The treatments is the application of two maturity (sulfometuron methyl, and glyphosate) in different doses and mixtures further control (natural aging). The experimental design was a randomized block design with four replications. The objective of this research is to analyze the effects of applying these products in the metabolism of sugar cane in pre-and post-harvest, for both were: parameters of production technology, growth factors (height and number of tillers), content of chlorophyll and carotenoids, dynamics of nutrients, cellulose and lignin, shikmic concentration of acid and salicylic acid. The conclusions: the application of maturity promoted effect on technological parameters, height and number of tiller of culture, the application of glyphosate improved the levels of P and K in the plant and reduced the levels of Fe, Zn and Cu, the contents of chlorophyll and carotenoids influenced with application of glyphosate in the commercial dose, application of methyl sulfometuron increased levels of Mn, higher doses of glyphosate increased the concentration of shikmic; largest concentration of shikmic promoted the higher concentrations of salicylic acid in pre - In post-harvest sampling found... (Complete abstract click electronic access below)

Tong, Kit Fong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 91-104). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.vi / Table of Contents --- p.vii / List of Figures --- p.x / List of Tables --- p.xii / List of Abbreviations --- p.xiii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Cancer --- p.2 / Chapter 1.1.1 --- Tumor development --- p.2 / Chapter 1.1.2 --- Cell cycle --- p.4 / Chapter 1.1.3 --- Apoptosis --- p.9 / Chapter 1.1.3.1 --- The extrinsic pathway --- p.14 / Chapter 1.1.3.2 --- The intrinsic pathway --- p.16 / Chapter 1.1.3.3 --- The Bcl-2 family proteins --- p.17 / Chapter 1.1.3.4 --- Execution of apoptosis --- p.20 / Chapter 1.1.4 --- Melanoma --- p.22 / Chapter 1.2 --- Polyunsaturated fatty acids (PUFAs) --- p.24 / Chapter 1.2.1 --- "Chemistry, classification, metabolic conversion and sources …" --- p.24 / Chapter 1.2.2 --- Epidemiology studies --- p.27 / Chapter 1.2.3 --- Docosahexaenoic acid (DHA) --- p.28 / Chapter 1.2.3.1 --- Sources --- p.28 / Chapter 1.2.3.2 --- DHA and cancer --- p.29 / Chapter 1.3 --- Objectives --- p.33 / Chapter Chapter 2 --- Materials and Methods --- p.34 / Chapter 2.1 --- In vitro studies of DHA on growth and survival of human cancer cells --- p.34 / Chapter 2.1.1 --- Cell cultures --- p.34 / Chapter 2.1.2 --- Studies of growth inhibition of DHA on human cancer cells --- p.35 / Chapter 2.1.2.1 --- MTT assay --- p.35 / Chapter 2.1.2.2 --- Chemiluminescent-bromodeoxyuridine (Chemi-BrdU) immunoassay --- p.36 / Chapter 2.1.3 --- Studies of growth inhibitory mechanism of DHA on A375 cells. --- p.38 / Chapter 2.1.3.1 --- DNA -flow cytometry analysis --- p.38 / Chapter 2.1.3.2 --- Western blot analysis --- p.39 / Chapter 2.1.3.3 --- Caspase inhibitor studies --- p.42 / Chapter 2.1.3.4 --- Mitochondrial membrane potential analysis --- p.42 / Chapter 2.2 --- In vivo study of the anticancer effect of DHA on A375 cells --- p.44 / Chapter 2.2.1 --- Animals --- p.44 / Chapter 2.2.2 --- Cell inoculation and treatments --- p.44 / Chapter 2.2.3 --- Western blot analysis --- p.45 / Chapter 2.3 --- Statistical analysis --- p.46 / Chapter Chapter 3 --- Results --- p.47 / Chapter 3.1 --- In vitro studies of DHA on growth and survival of human canccr cells --- p.47 / Chapter 3.1.1 --- DHA reduced proliferation and survival of human cancer cells --- p.47 / Chapter 3.1.2 --- DHA modulated cell cycle of A375 cells --- p.52 / Chapter 3.1.3 --- DHA induced apoptosis in A375 cells --- p.55 / Chapter 3.1.4 --- Caspase activations were involved in the DHA-induced apoptosis in A375 cells --- p.59 / Chapter 3.1.5 --- "Caspase 3´ة 6, 8 and 9 were activated in DHA-induced apoptosis of A375 cells" --- p.62 / Chapter 3.1.6 --- DHA dissipated mitochondrial membrane potential in A375 cells --- p.66 / Chapter 3.1.7 --- DHA triggered the mitochondrial pathway of apoptosis --- p.68 / Chapter 3.1.8 --- DHA triggered the death receptor pathway of apoptosis --- p.71 / Chapter 3.2 --- In vivo study of the anticancer effect of DHA on A375 cells --- p.74 / Chapter 3.2.1 --- Effect of DHA on the growth ofA375 xenograft in athymic Bαlb/c mice --- p.74 / Chapter 3.2.2 --- DR4 and TRAIL were upregulated by DHA treatment in A375 solid tumor --- p.77 / Chapter Chapter 4 --- Discussion --- p.79 / References --- p.91

Ho, Tik Shun. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 88-102). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgement --- p.vii / Table of Contents --- p.viii / List of Table --- p.x / List of Figures --- p.xi / List of Abbreviations --- p.xiii / Chapter CHAPTER 1 --- General Introduction --- p.1 / Chapter 1.1 --- Fatty Acid Synthase (FAS) - 7-domain multifunctional enzyme --- p.1 / Chapter 1.1.1 --- Functions --- p.1 / Chapter 1.1.2 --- Structure --- p.2 / Chapter 1.2 --- Fatty Acid biosynthesis reactions --- p.4 / Chapter 1.3 --- Malonyl Coenzyme A - An important mediator in lipogenesis --- p.7 / Chapter 1.4 --- FAS expression in different histotypes --- p.8 / Chapter 1.4.1 --- FAS in normal cells --- p.8 / Chapter 1.4.2 --- FAS in pathological cells --- p.8 / Chapter 1.4.3 --- Tumor-associated FAS (Oncogenic antigen-519) in cancer cells --- p.9 / Chapter 1.5 --- FAS signaling models in breast and prostate cancers --- p.12 / Chapter 1.5.1 --- Association between FAS and PI3K／Akt pathway --- p.12 / Chapter 1.5.2 --- Hypothetical model of FAS hyperactivity in breast and prostate cancer cells --- p.13 / Chapter 1.6 --- FAS inhibition to tackle cancer cell growth --- p.15 / Chapter 1.6.1 --- FAS inhibitors --- p.15 / Chapter 1.6.1.1 --- Cerulenin --- p.16 / Chapter 1.6.1.2 --- C75 --- p.17 / Chapter 1.6.2 --- Small interfering RNA --- p.17 / Chapter 1.7 --- FAS inhibition to enhance chemoresistant cancer cells sensitivity to drugs --- p.19 / Chapter 1.8 --- Hypothesis --- p.20 / Chapter CHAPTER 2 --- Methods and Materials --- p.21 / Chapter 2.1 --- Chemicals and antibodies --- p.21 / Chapter 2.2 --- Cell cultures --- p.21 / Chapter 2.3 --- MTT assay --- p.22 / Chapter 2.4 --- 5-Bromo-2'-deoxyuridine (BrdU)-labeling cell proliferation assay --- p.22 / Chapter 2.5 --- Cytotoxicity detection assay of LDH release --- p.23 / Chapter 2.6 --- DNA flow cytometry --- p.23 / Chapter 2.7 --- Confocal micocropy --- p.24 / Chapter 2.8 --- Immunoblot analysis --- p.24 / Chapter 2.8.1 --- Preparation of protein lysates --- p.24 / Chapter 2.8.2 --- Immunoblotting --- p.25 / Chapter 2.9 --- Caspase inhibitor studies --- p.26 / Chapter 2.10 --- Analysis of mitochondrial membrane potential --- p.26 / Chapter 2.11 --- Determination of caspase activities --- p.27 / Chapter 2.12 --- siRNA transfection --- p.27 / Chapter 2.13 --- Statistical analysis --- p.28 / Chapter CHAPTER 3 --- Results --- p.29 / Chapter 3.1 --- Cytostatic & cytotoxic studies of FAS inhibitors on human cancer cells --- p.29 / Chapter 3.1.1 --- Cerulenin and C75 suppress cell growth of different cancer histotypes --- p.29 / Chapter 3.1.2 --- Cerulenin and C75 suppress cell growth of A-375 dose- and time-dependently --- p.32 / Chapter 3.1.3 --- Cerulenin and C75 exert cytotoxic effect on A-375 but not normal skin HS68 cells --- p.36 / Chapter 3.1.4 --- Cerulenin and C75 arrest cell cycle progression and induce apoptosis with DNA Fragmentation --- p.39 / Chapter 3.2 --- Mechanistic studies of FAS inhibitors in A-375 cells --- p.46 / Chapter 3.2.1 --- Cerulenin and C75 induce caspase-dependent apoptosis --- p.46 / Chapter 3.2.2 --- Cerulenin- and C75-induced apoptosis involve extrinsic death receptor pathway --- p.52 / Chapter 3.2.3 --- Cerulenin- and C75-induced apoptosis involve intrinsic mitochondrial pathway --- p.57 / Chapter 3.2.4 --- Extrinsic death receptor pathway serves as a pioneer and links with intrinsic mitochondrial pathway in cerulenin- and C75-induced apoptosis --- p.65 / Chapter 3.3 --- Small interfering RNA on Fatty Acid Synthase (FAS siRNA) --- p.68 / Chapter 3.3.1 --- FAS siRNA induces PARP cleavage --- p.68 / Chapter 3.3.2 --- FAS siRNA triggers caspase-dependent apoptosis as FAS inhibitors --- p.70 / Chapter CHAPTER 4 --- Discussion --- p.72 / Chapter CHAPTER 5 --- Future Prospect --- p.85 / Chapter CHAPTER 6 --- References --- p.88

This thesis concerns a melanoma-derived growth regulatory factor that inhibited proliferation of several malignant human cell lines, and, in particular, a line designated UCT-BR-1, which was derived from a human breast cancer metastasis. The work is presented in four chapters. Chapter 1 provides a review of the relevant literature at the time of writing; Chapters 2 and 3 describe the experimental work that was done; and in Chapter 4 I discuss the implications of my results for current and future work in growth factors. Experimental results are presented as Charts (which may be Figures or Tables) and the methods and experimental protocols that I used are described in the Chart legends and not in the main text of the thesis. The Appendix contains details of the tissue culture techniques and descriptions of the cell lines that were used. Sources of the various laboratory materials as well as the methods that were employed for the more routine procedures are also described in the appendix.