Diss. (sammanfattning) Stockholm : Karolinska institutet, 2001. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst- / Härtill 8 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 5 uppsatser.

by Cheng Yuen Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves [106]-113). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.iv / Research out puts --- p.v / Abbreviations --- p.vii / List of Figures --- p.viii / List of Tables --- p.xiii / Table of contents --- p.xiv / Chapter Chapter 1 --- Introduction & Hypothesis / Chapter 1.1. --- General Introduction --- p.1 / Chapter 1.2. --- Hypothesis --- p.4 / Chapter 1.3. --- Objectives --- p.4 / Chapter Chapter 2 --- An Overview of Giant Cell Tumour of Bone / Chapter 2.1. --- Introduction --- p.5 / Chapter 2.2. --- Pathobiological features of GCT --- p.6 / Chapter 2.2.1. --- Radiological appearances and clinical classifications of GCT --- p.7 / Chapter 2.2.2. --- Histological characteristics --- p.10 / Chapter 2.2.3. --- Metastatic GCT --- p.13 / Chapter 2.3. --- Histogenesis of GCT --- p.14 / Chapter 2.4. --- Treatment --- p.19 / Chapter 2.5. --- Summary --- p.22 / Chapter Chapter 3 --- Pharmacological aspect of bisphosphonates / Chapter 3.1. --- Introduction --- p.23 / Chapter 3.2. --- Chemical structures of bisphosphonates --- p.28 / Chapter 3.3. --- Mechanisms and actions --- p.28 / Chapter 3.3.1. --- Bisphosphonates induce osteoclast apoptosis --- p.30 / Chapter 3.3.2. --- Bisphosphonates induce cell apoptosis --- p.32 / Chapter 3.3.3. --- Apoptosis --- p.33 / Chapter 3.3.3.1. --- Morphological characteristic of apoptosis --- p.35 / Chapter 3.4. --- Clinical applications of bisphosphonates --- p.36 / Chapter 3.5. --- Bisphosphonates used in this study --- p.38 / Chapter 3.6. --- Summary --- p.43 / Chapter Chapter 4 --- Materials and methods / Chapter 4.1. --- Introduction --- p.44 / Chapter 4.2. --- Primary GCT cell culture and maintenance --- p.46 / Chapter 4.3. --- Drug preparation --- p.46 / Chapter 4.4. --- MTT assay --- p.47 / Chapter 4.5. --- Annexin-V-flous staining assay --- p.48 / Chapter 4.6. --- Haematoxyline and Eosin staining --- p.51 / Chapter 4.7. --- TUNEL assay (Terminal deoxynucleotidyltrasferase - mediated dUTP-biotin nick end labelling) --- p.52 / Chapter 4.8. --- TEM (Transmission Electron Microscopy) --- p.54 / Chapter 4.9. --- Statistical analysis --- p.54 / Chapter Chapter 5 --- Bisphosphonates induce apoptosis in giant cell tumour of bone -in vitro study / Chapter 5.1. --- Introduction --- p.56 / Chapter 5.2. --- Experimental design --- p.57 / Chapter 5.3. --- Results / Chapter 5.3.1. --- Bisphosphonates reduce cell viability of GCT stromal tumour cell --- p.59 / Chapter 5.3.2. --- Bisphosphonates induce morphological changesin GCT primary culture --- p.59 / Chapter 5.3.3. --- Bisphosphonate significantly induce apoptosis in GCT stromal cells in a dose dependent manner --- p.62 / Chapter 5.4. --- Discussions and Summary --- p.68 / Chapter Chapter 6 --- Bisphosphonates induce apoptosis in giant cell tumour of bone -in vivo study / Chapter 6.1. --- Introduction --- p.73 / Chapter 6.2. --- Experiment design --- p.74 / Chapter 6.3. --- Results / Chapter 6.3.1. --- H & E observations / Chapter 6.3.2. --- Pamidronate significantly induce apoptosis in both osteoclast-like giant cells and stromal tumour cells by TUNEL labelling assay --- p.79 / Chapter 6.3.3. --- Pamidronate induced cellular ultrastructural changes of GCT by TEM examination --- p.83 / Chapter 6.3.4. --- Pamidronate reduce the recurrent characteristic of GCT --- p.95 / Chapter 6.4. --- Discussions and Summary --- p.97 / Chapter Chapter 7 --- Summary and Future Study / Chapter 7.1. --- Summary --- p.101 / Chapter 7.2. --- Future directions --- p.103 / Chapter Chapter 8 --- Reference --- p.105 / Chapter Chapter 9 --- Appendix - solution preparation

Leung Kam Tong. / Thesis submitted in: September 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 79-95). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese) --- p.iii / Acknowledgements --- p.v / Table of contents --- p.vi / List of figures --- p.ix / List of abbreviations --- p.xii / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1 --- Acute lymphoblastic leukemia --- p.1 / Chapter 1.2 --- T-cell acute lymphoblastic leukemia --- p.2 / Chapter 1.2.1 --- Chemotherapy --- p.2 / Chapter 1.2.1.1 --- Induction therapy --- p.2 / Chapter 1.2.1.2 --- Intensification therapy --- p.3 / Chapter 1.2.1.3 --- Maintenance therapy --- p.3 / Chapter 1.2.2 --- Chemoresistance in T-ALL --- p.3 / Chapter 1.3 --- Apoptosis and chemoresistance --- p.5 / Chapter 1.3.1 --- "Initiation, execution and regulation of apoptosis" --- p.5 / Chapter 1.3.1.1 --- Initiation of apoptosis --- p.5 / Chapter 1.3.1.2 --- Execution of apoptosis --- p.7 / Chapter 1.3.1.3 --- Regulation of apoptosis --- p.7 / Chapter 1.3.2 --- Mechanisms of resistance to apoptosis --- p.9 / Chapter 1.3.2.1 --- Overexpression of pro-survival proteins --- p.9 / Chapter 1.3.2.2 --- Downregulation and mutation of pro-apoptotic proteins --- p.11 / Chapter 1.3.2.3 --- Other mechanisms --- p.13 / Chapter 1.4 --- Bcl-2 interating mediator of cell death --- p.14 / Chapter 1.4.1 --- Role of Bim in apoptosis --- p.16 / Chapter 1.4.2 --- Regulation of Bim --- p.17 / Chapter 1.4.2.1 --- Transcriptional regulation of Bim --- p.18 / Chapter 1.4.2.2 --- Post-transcriptional regulation of Bim --- p.18 / Chapter 1.5 --- c-Jun N-terminal kinase --- p.20 / Chapter 1.5.1 --- Pro-apoptotic role of JNK --- p.21 / Chapter 1.5.2 --- Anti-apoptotic role of JNK --- p.21 / Chapter 1.6 --- Hypotheses --- p.22 / Chapter Chapter 2 --- Materials and Methods --- p.23 / Chapter 2.1 --- Cell culture --- p.23 / Chapter 2.2 --- Induction of quantification of apoptosis --- p.24 / Chapter 2.3 --- Determination of caspase activities --- p.24 / Chapter 2.4 --- Western blotting --- p.25 / Chapter 2.4.1 --- Protein extraction and determination of protein concentration --- p.25 / Chapter 2.4.2 --- SDS-PAGE and immunodetection --- p.26 / Chapter 2.5 --- Cell-free apoptosis reactions --- p.27 / Chapter 2.6 --- Analysis of mitochondrial membrane potential --- p.27 / Chapter 2.7 --- Transient transfection of Sup-Tl cells --- p.28 / Chapter 2.8 --- Reverse transcription-polymerase chain reaction (RT-PCR) --- p.28 / Chapter 2.8.1 --- RNA isolation --- p.28 / Chapter 2.8.2 --- Synthesis of first-strand cDNA --- p.29 / Chapter 2.8.3 --- Polymerase chain reaction --- p.29 / Chapter 2.9 --- Alkaline phosphatase digestion of Bim --- p.30 / Chapter Chapter 3 --- Results --- p.31 / Chapter 3.1 --- The T-ALL cell line Sup-Tl is resistant to etoposide-induced apoptosis --- p.31 / Chapter 3.2 --- Sup-Tl cells are resistant to etoposide-induced caspase activation --- p.40 / Chapter 3.3 --- Sup-Tl cells are insusceptible to etoposide-induced mitochondrial alterations --- p.46 / Chapter 3.4 --- BimEL is required for etoposide-induced apoptosis in Sup-Tl cells --- p.51 / Chapter 3.5 --- The reduced level of BimEL in Sup-Tl cells is owing to the presence of constitutively active JNK --- p.58 / Chapter Chapter 4 --- Discussion --- p.67 / References --- p.79

Previous studies have demonstrated that the interaction of CD40 on monocytes with CD40 ligand, present on activated CD4+ T cells, induces monocyte inflammatory cytokine synthesis and rescues monocytes from apoptosis. These findings suggest a role for CD40 signaling of monocyte activation in the maintenance and/or exacerbation of nonseptic (e.g., autoimmune) inflammatory responses. In the present study the effects of the modulatory cytokines IL-4 and IL-10 on CD40-mediated signaling of monocyte IL-1beta synthesis and rescue from apoptosis were examined. Both IL-4 and IL-10 decreased CD40-dependent IL-1beta synthesis in a dose-dependent manner individually and synergized in this effect when used concurrently, with minimal effect on CD40 surface expression. CD40 signaling of IL-1beta synthesis was shown to be dependent on the induction of protein tyrosine kinase (PTK) activity, and both IL-4 and IL-10 diminished CD40-mediated tyrosine phosphorylation of monocyte cellular proteins. However, IL-4, but not IL-10, blocked CD40-mediated rescue from apoptosis, an event that we have demonstrated previously to be dependent on PTK activity as well. Together these results suggest that in monocytes 1) both IL-4 and IL-10 target CD40-induced PTK activity in the down-regulation of IL-1beta synthesis; and 2) IL-4 and IL-10 have divergent effects on the CD40 signaling pathway, in that these cytokines are synergistic with respect to their abilities to inhibit CD40-mediated IL-1beta synthesis and differ in their abilities to block CD40-mediated rescue from apoptosis.

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.