Proefschrift-Louvain. / At head of title: Katholieke Universiteit te Leuven. Vesalius Instituut. Anatomisch Laboratorium. Without thesis statement. Bibliography: p. [165]-181.

A unique tumor targeted method, which may be able to deliver a molecule to the surface of a tumor cell using the pH gradient between hypoxic tumor cells and normal tissue has recently been developed. Since solid tumors have been found to have a lower extra cellular pH compared to normal tissue (6.5 to 6.9 for tumors verses an average 7.4 for normal tissue), the pH gradient is used as a source of power to activate a strategically designed "molecular engine" capable of delivering a diagnostic or therapeutic agent to tumor cells. To test this hypothesis, a 22- sequence amino acid, which reorganizes to alpha helical form at pH 6.9 causing the molecule to become lipophilic and embed into the plasma membrane of nearby cells was synthesized. The molecule was then attached to 99mTc via a MAG-3 chelating molecule. In-vivo nuclear imaging was performed and showed apparent significant uptake in primary tumors as well as lung and liver in Lewis lung cell model C57blk-J6 mice with confirmed primary tumors at the base of the tail or lungs. This study shows significant promise for early diagnosis and treatment of cancer on a molecular level. / Graduation date: 2006

The structural elucidations of nine new natural products from Thevetia ahouia, Eremocarpus setigerus, Trichilia hispida, Chrysothamus paniculatus, Uvaria acuminata, Wikstroemia monticola, and Uvaria zelanica are discussed in detail. Also included are some known compounds that were found in these plants. Of the new compounds discussed, two are diterpenes (eremone, chrysothame), two are relatively simple triterpenes (hispidols A, B), two are highly oxidized triterpenes (hispidins A, B), one is a fatty acid derivative (uvaricin), one is a shikimate-derived metabolite (1-epizeylenol), and one has both steroidal and carbohydrate features (3'-OMe-evomonoside). ¹H and ¹³C NMR spectral data are given for all the new compounds. Assignments were made by analogy with model compounds, computer simulation, and ¹H-¹H and ¹H-¹³C decoupling where indicated. High resolution mass spectral fragmentations are given for most of the new compounds, and individual structural assignments made for intense peaks. An X-ray analysis (eremone) was done with all pertinent information included. Most of the compounds have been tested for anti-tumor activity, and several exhibit strong cytotoxicity (hispidins A and B, 3'-OMe-evomonoside, huratoxin, uvaricin).

No description available.

Thesis (M.S.)--Brigham Young University. Dept. of Chemical Engineering, 2007. / Includes bibliographical references (p. 79-82).

by Wing-yu Tang. / Bibliography: leaves 129-138 / Thesis (M.Ph.)--Chinese University of Hong Kong, 1985

Liu, Pi-chu. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 155-173). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Chan Yiu Leung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 123-149). / Abstracts in English and Chinese. / Abstracts --- p.I / Acknowledgements --- p.VIII / List of Figures --- p.IX / Lists of Abbreviations --- p.X / Contents --- p.XII / Chapter Chapter One: --- Introduction and Literature Review --- p.1 / Chapter 1.1 --- Cancer in General --- p.1 / Chapter 1.2 --- Glioma --- p.3 / Chapter 1.2.1 --- Types of Glioma --- p.6 / Chapter 1.2.1.1 --- Astrocytomas --- p.6 / Chapter 1.2.1.2 --- Oligodendrogliomas --- p.8 / Chapter 1.2.1.3 --- Ependymomas --- p.9 / Chapter 1.2.2 --- Glioblastoma Multiforme (GBM) --- p.10 / Chapter 1.2.3 --- Molecular Biology of GBM --- p.11 / Chapter 1.2.4 --- Current Treatment for GBM --- p.15 / Chapter 1.3 --- HMG-Co A reductase inhibitors --- p.17 / Chapter 1.3.1 --- Pharmacology of HMG-Co A reductase inhibitor --- p.18 / Chapter 1.3.2 --- Epidemiological link between HMG-Co A Reductase Inhibitors and Cancer --- p.20 / Chapter 1.3.3 --- Current HMG-Co A reductase inhibitors research in cancer --- p.21 / Chapter 1.3.3.1 --- Inhibition of tumor cell growth --- p.21 / Chapter 1.3.3.2 --- Inhibition of Angiogenesis --- p.22 / Chapter 1.3.3.3 --- Anti-invasive effects of HMG-Co A reductase inhibitors.… --- p.23 / Chapter 1.3.3.4 --- Apoptosis induction by HMG-Co A reductase inhibitors --- p.24 / Chapter 1.3.4 --- In vivo efficacy and synergistic effects --- p.25 / Chapter 1.4 --- Tumor Necrosis Factor (TNF) related apoptosis-inducing Ligand (TRAIL) --- p.28 / Chapter 1.4.1 --- Molecular mechanisms of TRAIL-induced apoptosis --- p.29 / Chapter 1.4.2 --- Role for TRAIL in cancer therapy --- p.30 / Chapter 1.5 --- Objectives --- p.34 / Chapter Chapter 2 --- Methods and Materials --- p.35 / Chapter 2.1 --- Cell culture --- p.35 / Chapter 2.2 --- Cell proliferation detection (MTT) methods --- p.36 / Chapter 2.3 --- "Caspase 3,9 activities induced by lovastatin" --- p.37 / Chapter 2.4 --- Detection of apoptosis by Annexin V and PI staining --- p.39 / Chapter 2.5 --- Cell cycle analysis protocols --- p.41 / Chapter 2.6 --- DNA fragmentation ELISA detection kit protocols --- p.42 / Chapter 2.7 --- Reverse Transcription (RT) Polymerase Chain Reaction (PCR) --- p.44 / Chapter 2.8 --- Polymerase Chain Reaction (PCR) --- p.46 / Chapter 2.9 --- Bio-molecules extraction/purification protocols --- p.48 / Chapter 2.10 --- "Microarray analysis on lovastatin treated glioblastoma cells A172, M059J and M059K" --- p.51 / Chapter 2.10.1 --- Cells treatment and RNA extraction --- p.51 / Chapter 2.10.2 --- Synthesis of first strand cDNA --- p.53 / Chapter 2.10.3 --- Synthesis of second strand cDNA --- p.54 / Chapter 2.10.4 --- Purification of double stranded cDNA --- p.54 / Chapter 2.10.5 --- Synthesis of cRNA by in vitro transcription (IVT) --- p.55 / Chapter 2.10.6 --- Recovery of biotin-labelled cDNA --- p.56 / Chapter 2.10.7 --- Fragmentation of cRNA --- p.56 / Chapter 2.10.8 --- Preparation of hybridization reaction mixtures --- p.57 / Chapter 2.10.9 --- Loading of reaction mixtures into bioarray chambers --- p.58 / Chapter 2.10.10 --- Hybridization --- p.58 / Chapter 2.10.11 --- Post-hybridization wash --- p.59 / Chapter 2.10.12 --- 2.11.12Detection with streptavidin-dye conjugate --- p.59 / Chapter 2.10.13 --- Bioarray scanning and analysis --- p.61 / Chapter Chapter 3: --- Results --- p.62 / Chapter 3.1 --- Morphological effects of Lovastatin on human glioblastoma cells --- p.62 / Chapter 3.2 --- Anti-proliferation effects on glioblastoma cell lines --- p.64 / Chapter 3.3 --- Lovastatin-induced caspase3 and 9 activation in human glioblastoma cell lines --- p.69 / Chapter 3.4 --- Cell cycle determination by PI staining --- p.77 / Chapter 3.5 --- Quantification of apoptotic cell death by annexin V and propidium iodide staining --- p.79 / Chapter 3.6 --- Microarray analysis of lovastatin-modulated gene expression profiles --- p.82 / Chapter 3.7 --- Synergistic effects induced by lovastatin and Tumor Necrosis Factor related apoptosis-inducing Ligand (TRAIL) --- p.87 / Chapter 3.7.1 --- M059J and M059K glioblastoma cells was resistant to TRAIL attack --- p.87 / Chapter 3.7.2 --- Synergistic cell death was induced by lovastatin and TRAIL --- p.87 / Chapter 3.7.3 --- A combination of TRAIL and lovastatin induces synergistic apoptosis in glioblastoma cells --- p.93 / Chapter 3.7.4 --- DNA fragmentation on glioblastoma cells --- p.98 / Chapter 3.7.5 --- Four TRAIL receptors mRNA expression profiles on glioblastoma cells --- p.102 / Chapter Chapter 4 --- Discussion --- p.105 / Chapter 4.1 --- Lovastatin exhibited anti-proliferation effects in human glioblastoma cells --- p.107 / Chapter 4.2 --- Lovastatin activated caspase 3 and caspase 9 in human glioblastoma cells --- p.108 / Chapter 4.3 --- Gene expression profile modulated by Lovastatin in human glioblastoma cells --- p.110 / Chapter 4.4 --- Lovastatin-sensitized TRAIL-induced apoptosis in human glioblastoma cells --- p.117 / Chapter Chapter Five: --- Conclusion and Future perspective --- p.121 / References --- p.122 / Appendix --- p.150