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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

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.
2

Is auditing useful in avoiding polypharmacy? /

Ng, Wing-yiu, George. January 2005 (has links)
Thesis (M.P.H.)--University of Hong Kong, 2005.
3

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.
4

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
5

Mechanism-Based Computational Models to Study Pharmacological Actions of Anticancer Drugs

Yang, Jianning 16 September 2009 (has links)
No description available.
6

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 virus

Dias, Andreia Sofia Pires January 2008 (has links)
Thesis (MSc.(Anatomy)--Faculty of Health Sciences)-University of Pretoria, 2008.] / Includes bibliographical references.
7

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
8

Gemcitabine and Docetaxel for Epithelioid Sarcoma: Results from a Retrospective, Multi-Institutional Analysis

Pink, 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.
9

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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