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Is auditing useful in avoiding polypharmacy?Ng, Wing-yiu, George. January 2005 (has links)
Thesis (M. P. H.)--University of Hong Kong, 2005. / Also available in print.
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Is auditing useful in avoiding polypharmacy? /Ng, Wing-yiu, George. January 2005 (has links)
Thesis (M.P.H.)--University of Hong Kong, 2005.
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THE EFFECTS OF GLUTATHIONE DEPLETION BY L-BUTHIONINE-(S,R) SULFOXIMINE ON THE ANTITUMOR EFFICACY OF MODEL SULFHYDRYL-DEPENDENT ANTICANCER AGENTS (BSO)Soble, Michelle Joy, 1961- January 1986 (has links)
No description available.
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Is auditing useful in avoiding polypharmacy?Ng, Wing-yiu, George., 吳榮耀. January 2005 (has links)
published_or_final_version / Community Medicine / Master / Master of Public Health
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Mechanism-Based Computational Models to Study Pharmacological Actions of Anticancer DrugsYang, Jianning 16 September 2009 (has links)
No description available.
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The effects of combinations of a green tea extract and an active ingredient thereof, with standard antiretroviral drugs on SC-1 cells infected with the LP-BM5 virusDias, Andreia Sofia Pires January 2008 (has links)
Thesis (MSc.(Anatomy)--Faculty of Health Sciences)-University of Pretoria, 2008.] / Includes bibliographical references.
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Applications of evolutionary algorithms on biomedical systems.January 2007 (has links)
Tse, Sui Man. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 95-104). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgement --- p.v / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Motivation --- p.1 / Chapter 1.1.1 --- Basic Concepts and Definitions --- p.2 / Chapter 1.2 --- Evolutionary Algorithms --- p.5 / Chapter 1.2.1 --- Chromosome Encoding --- p.6 / Chapter 1.2.2 --- Selection --- p.7 / Chapter 1.2.3 --- Crossover --- p.9 / Chapter 1.2.4 --- Mutation --- p.10 / Chapter 1.2.5 --- Elitism --- p.11 / Chapter 1.2.6 --- Niching --- p.11 / Chapter 1.2.7 --- Population Manipulation --- p.13 / Chapter 1.2.8 --- Building Blocks --- p.13 / Chapter 1.2.9 --- Termination Conditions --- p.14 / Chapter 1.2.10 --- Co-evolution --- p.14 / Chapter 1.3 --- Local Search --- p.15 / Chapter 1.4 --- Memetic Algorithms --- p.16 / Chapter 1.5 --- Objective --- p.17 / Chapter 1.6 --- Summary --- p.17 / Chapter 2 --- Background --- p.18 / Chapter 2.1 --- Multiple Drugs Tumor Chemotherapy --- p.18 / Chapter 2.2 --- Bioinformatics --- p.22 / Chapter 2.2.1 --- Basics of Bioinformatics --- p.24 / Chapter 2.2.2 --- Applications on Biomedical Systems --- p.26 / Chapter 3 --- A New Drug Administration Dynamic Model --- p.29 / Chapter 3.1 --- Three Drugs Mathematical Model --- p.31 / Chapter 3.1.1 --- Rate of Change of Different Subpopulations --- p.32 / Chapter 3.1.2 --- Rate of Change of Different Drug Concen- trations --- p.35 / Chapter 3.1.3 --- Toxicity Effects --- p.35 / Chapter 3.1.4 --- Summary --- p.36 / Chapter 4 --- Memetic Algorithm - Iterative Dynamic Program- ming (MA-IDP) --- p.38 / Chapter 4.1 --- Problem Formulation: Optimal Control Problem (OCP) for Mutlidrug Optimization --- p.38 / Chapter 4.2 --- Proposed Memetic Optimization Algorithm --- p.40 / Chapter 4.2.1 --- Iterative Dynamic Programming (IDP) . . --- p.40 / Chapter 4.2.2 --- Adaptive Elitist-population-based Genetic Algorithm (AEGA) --- p.44 / Chapter 4.2.3 --- Memetic Algorithm 一 Iterative Dynamic Programming (MA-IDP) --- p.50 / Chapter 4.3 --- Summary --- p.56 / Chapter 5 --- MA-IDP: Experiments and Results --- p.57 / Chapter 5.1 --- Experiment Settings --- p.57 / Chapter 5.2 --- Optimization Results --- p.61 / Chapter 5.3 --- Extension to Other Mutlidrug Scheduling Model . --- p.62 / Chapter 5.4 --- Summary --- p.65 / Chapter 6 --- DNA Sequencing by Hybridization (SBH) --- p.66 / Chapter 6.1 --- Problem Formulation: Reconstructing a DNA Sequence from Hybridization Data --- p.70 / Chapter 6.2 --- Proposed Memetic Optimization Algorithm --- p.71 / Chapter 6.2.1 --- Chromosome Encoding --- p.71 / Chapter 6.2.2 --- Fitness Function --- p.73 / Chapter 6.2.3 --- Crossover --- p.74 / Chapter 6.2.4 --- Hill Climbing Local Search for Sequencing by Hybridization --- p.76 / Chapter 6.2.5 --- Elitism and Diversity --- p.79 / Chapter 6.2.6 --- Outline of Algorithm: MA-HC-SBH --- p.81 / Chapter 6.3 --- Summary --- p.82 / Chapter 7 --- DNA Sequencing by Hybridization (SBH): Experiments and Results --- p.83 / Chapter 7.1 --- Experiment Settings --- p.83 / Chapter 7.2 --- Experiment Results --- p.85 / Chapter 7.3 --- Summary --- p.89 / Chapter 8 --- Conclusion --- p.90 / Chapter 8.1 --- Multiple Drugs Cancer Chemotherapy Schedule Optimization --- p.90 / Chapter 8.2 --- Use of the MA-IDP --- p.91 / Chapter 8.3 --- DNA Sequencing by Hybridization (SBH) --- p.92 / Chapter 8.4 --- Use of the MA-HC-SBH --- p.92 / Chapter 8.5 --- Future Work --- p.93 / Chapter 8.6 --- Item Learned --- p.93 / Chapter 8.7 --- Papers Published --- p.94 / Bibliography --- p.95
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Gemcitabine and Docetaxel for Epithelioid Sarcoma: Results from a Retrospective, Multi-Institutional AnalysisPink, Daniel, Richter, Stephan, Gerdes, Sebastian, Andreou, Dimosthenis, Tunn, Per-Ulf, Busemann, Christoph, Ehninger, Gerhard, Reichardt, Peter, Schuler, Markus K. 20 May 2020 (has links)
Objective: Epithelioid sarcoma (ES) presents unique clinical features in comparison to other sarcoma subtypes. Data regarding the benefits of chemotherapy are very limited. Combination regimens using gemcitabine and docetaxel (Gem/Doce) have proven to be effective, especially in uterine and nonuterine leiomyosarcoma. Yet, there is no available data on the efficacy of Gem/Doce in ES. Methods: A retrospective analysis of the three participating institutions was performed. Twenty-eight patients with an ES diagnosis presented at one of the participating institutions between 1989 and 2012. Of this group, 17 patients received chemotherapy. Results: Patients’ median overall survival (OS) after the beginning of palliative chemotherapy was 21 months, and the 1-year OS was 87%. Twelve patients received Gem/Doce with a clinical benefit rate of 83%. The median progression-free survival (PFS) was 8 months for all patients receiving Gem/Doce. The best response was complete remission in 1 patient and partial remission in 6 patients. All 6 patients receiving Gem/Doce as a first-line treatment showed measurable responses with a median PFS of 9 months. Conclusions: In this retrospective study, Gem/Doce was an effective chemotherapeutic regimen for ES. Prospective studies are needed to better assess the effects of this combination drug therapy.
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In vitro evaluation of potential drug combination in cancer therapy: demethylcantharidin and platinum drug.January 2007 (has links)
Ng, Po Yan. / Thesis submitted in: November 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 109-120). / Abstracts in English and Chinese. / Acknowledgement --- p.i / Abstract --- p.ii / 摘要 --- p.iii / Table of Contents --- p.iv / List of Figures --- p.viii / List of Tables --- p.xi / List of Abbreviation --- p.xii / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- A General Introduction to the Development and Clinical Activities of Platinum Drugs --- p.1 / Chapter 1.1.1 --- Platinum Drugs used in a Clinical Setting --- p.4 / Chapter 1.1.2 --- Platinum Drugs under Clinical Trials --- p.5 / Chapter 1.1.3 --- Platinum Compounds with Dual Mechanisms --- p.7 / Chapter 1.2 --- Platinum Drug Antitumor Mechanism --- p.9 / Chapter 1.3 --- Limitations of Platinum Drugs --- p.12 / Chapter 1.3.1 --- Toxicity --- p.12 / Chapter 1.3.2 --- Drug Resistance or Cross Resistance --- p.15 / Chapter 1.3.2.1 --- Reduced Drug Accumulation or Increased Drug Efflux --- p.16 / Chapter 1.3.2.2 --- Drug Inactivation --- p.18 / Chapter 1.3.2.3 --- Enhanced DNA Repair --- p.19 / Chapter 1.4 --- Why Combinational Therapy? --- p.21 / Chapter 1.4.1 --- Antimetabolites --- p.20 / Chapter 1.4.2 --- Topoisomerase Inhibitors --- p.22 / Chapter 1.4.3 --- Tubulin-Active Antimitotic Agents --- p.24 / Chapter 1.4.4 --- Demethylcantharidin as a potential candidate for drug combination --- p.28 / Chapter 1.5 --- Study Objectives --- p.31 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Cell Lines --- p.33 / Chapter 2.2 --- Cancer Cell Preparation / Chapter 2.2.1 --- Chemicals and Reagents --- p.33 / Chapter 2.2.2 --- Cell Culture Practice --- p.34 / Chapter 2.2.2.1 --- Subcultures --- p.35 / Chapter 2.2.2.2 --- Cryopreservation --- p.37 / Chapter 2.2.2.3 --- Thawing Cryopreservated Cells --- p.38 / Chapter 2.2.3 --- Development of Drug-Resistant Cell Lines --- p.39 / Chapter 2.3 --- Growth Inhibition Assay / Chapter 2.3.1 --- Evaluation of Cytotoxicity in vitro --- p.40 / Chapter 2.3.2 --- Drug Pretreatment --- p.43 / Chapter 2.3.3 --- Drug Pre-sensitization with Concurrent Treatment --- p.44 / Chapter 2.4 --- Calculations for Drug Combinations --- p.46 / Chapter 2.5 --- Statistical Analysis --- p.49 / Chapter Chapter 3 --- Results and Discussions / Chapter 3.1 --- In vitro Cytotoxicity and Evaluation of Drug Resistance --- p.50 / Chapter 3.2 --- Role of Leaving Ligand in a Platinum Complex --- p.58 / Chapter 3.3 --- Priority in Selecting the Most Effective Drug Combination --- p.66 / Chapter 3.4 --- Drug Combination Studies / Chapter 3.4.1 --- Drug Combination Prescreening --- p.68 / Chapter 3.4.1.1 --- Comparison of the effectiveness of the three Drug Combinations --- p.72 / Chapter 3.4.1.2 --- Rationale for Drug Combination Studies presented in Section 3.4.2 & 3.4.3 --- p.73 / Chapter 3.4.2 --- Drug Pre-sensitization Studies in Colorectal Cancer Cell Lines --- p.74 / Chapter 3.4.2.1 --- Comparison of Drug Pre-sensitization Treatment in Sensitive Colorectal Cancer Cell Lines --- p.84 / Chapter 3.4.2.2 --- Comparison of Drug Pre-sensitization Treatment in Sensitive and Oxaliplatin Resistant HCT116 Colorectal Cancer Cell Lines --- p.87 / Chapter 3.4.3 --- Drug Pre-sensitization Studies in Liver Cancer Cell Lines --- p.89 / Chapter 3.4.3.1 --- Comparison of Drug Pre-sensitization Treatment in Sensitive Liver Cancer Cell Lines --- p.99 / Chapter 3.4.3.2 --- Comparison of Drug Pre-sensitization Treatment in Sensitive and Cisplatin Resistant SK-Hepl Liver Cancer Cell Line --- p.101 / Chapter 3.5 --- Possible Explanation to the Observed Drug Combination Effect --- p.103 / Chapter 3.6 --- General Protocols for Drug Combinations --- p.105 / Chapter Chapter 4 --- Conclusions / Reference --- p.109 / Appendices --- p.121 / Chapter I a. --- "Raw Data of Pre-screening for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.122 / Chapter I b. --- "Raw Data of Pre-screening for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.123 / Chapter II a. --- "Raw Data of Pre-screening for SK-Hepl (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.124 / Chapter II b. --- "Raw Data of Pre-screening for SK-Hepl ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.125 / Chapter III a. i) --- "Isobolograms for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.126 / Chapter III a. ii) --- "Raw Data for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.127 / Chapter III b. i) --- "Isobolograms for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.128 / Chapter III b. ii) --- "Raw Data for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.129 / Chapter IV a. i) --- "Isobolograms for HCT1160xaR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.130 / Chapter IV a. ii) --- "Raw Data for HCT1160xaR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.131 / Chapter IV b. i) --- "Isobolograms for HCT1160xaR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.132 / Chapter IV b. ii) --- "Raw Data for HCT1160xaR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.133 / Chapter V a. i) --- "Isobolograms for HT29 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.134 / Chapter V a. ii) --- "Raw Data for HT29 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.135 / Chapter V b. i) --- "Isobolograms for HT29 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.136 / Chapter V b. ii) --- "Raw Data for HT29 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.137 / Chapter VI a. i) --- Isobolograms for Hep G2 (Cisplatin and [Pt(DMC)(NH3)2]) --- p.138 / Chapter VI a. ii) --- Raw Data for Hep G2 (Cisplatin and [Pt(DMC)(NH3)2]) --- p.139 / Chapter VI b. i) --- "Isobolograms for Hep G2 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.140 / Chapter VI b. ii) --- "Raw Data for Hep G2 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.141 / Chapter VII a. i) --- "isobolograms for SK Hep 1 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.142 / Chapter VII a. ii) --- "Raw Data for SK Hep 1 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.143 / Chapter VII b.i) --- "Isobolograms for SK Hep 1 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.144 / Chapter VII b. ii) --- "Raw Data for SK Hep 1 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.145 / Chapter VIII a. i) --- "Isobolograms for SK Hep ICisR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.146 / Chapter VIII a. ii) --- "Raw Data for SK Hep ICisR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.147 / Chapter VIII b. i) --- "Isobolograms for SK Hep ICisR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.148 / Chapter VIII b. ii) --- "Raw Data for SK Hep ICisR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.149
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