by Pui-Kwong Chan. / Thesis -- The Chinese University of Hong Kong. / Bibliography: leaves 139-145.

Kwok-pui Fung. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1975. / Bibliography: leaves 122-131.

Thesis (M.Ph.)--Chinese University of Hong Kong. / Bibliography: leaves 87-96.

No description available.

O biglicam é um proteoglicano é altamente expresso em células trofoblásticas de patologias placentárias com invasividade exacerbada. No entanto, as funções do biglicam no trofoblasto ainda não foram elucidadas. Sendo assim, verificamos a expressão e as funções de biglicam e seus receptores Toll-like (TLR)-2 e TLR-4 nas células trofoblásticas durante a gestação. As células do citotrofoblasto extraviloso (CTEV) foram positivas para todas as moléculas, menos para o biglicam em placentas a termo. Adição exógena de biglicam promoveu migração e invasão das células trofoblásticas. O biglicam estimulou a fosforilação de AKT nos sítios Thr308 e Ser473 nas células trofoblásticas. A migração e a invasão biglicam-dependentes e as fosforilações de AKT foram inibidas após a adição de anticorpos bloqueadores anti-TLR-2 e anti-TLR-4. O silenciamento gênico de AKT1 em células SGHPL-5 aboliu os efeitos do biglicam na motilidade. Em conclusão, o biglicam aumenta a motilidade de células trofoblásticas após sinalização por AKT através da ativação de TLR-2 e TLR-4. / Biglycan is a highly expressed proteoglycan in trophoblast cells from invasiveness-changed placental pathologies. However, biglycan functions in the trophoblast were not yet identified. Therefore, it was verified the expression and functions of biglycan and its receptors Toll-like (TLR)-2 and TLR-4 in trophoblast cells throughout pregnancy. The extravillous cytotrophoblast cells (EVT) were positive to all the molecules, although biglycan was negative in term placentas. Exogenous biglycan promoted migration and invasion of trophoblast cells. Biglycan stimulated AKT phosphorilation at Thr308 and Ser473 sites in trophoblast cells. The biglycan-dependent migration, invasion and AKT phosphorilation were inhibited upon addiction of anti-TLR-2 and anti-TLR-4 blocking antibodies. AKT1 genic silencing in SGHPL-5 cells abolished the motility effects. In conclusion, biglycan increases the motility of trophoblast cells after AKT signaliing throughout TLR-2 and TLR-4 activation.

by Chung Hoi Sing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 92-106). / Abstract also in Chinese. / ABSTRACT --- p.i / 摘要 --- p.iii / ACKNOWLEDGMENT --- p.v / Chapter 1. --- Introduction / Chapter 1.1 --- Angiogenesis in general --- p.1 / Chapter 1.1.1 --- The concept of angiogenesis --- p.1 / Chapter 1.1.2 --- The process of angiogenesis --- p.1 / Chapter 1.2 --- Measurement of angiogenesis --- p.3 / Chapter 1.2.1 --- In vivo assays --- p.3 / Chapter 1.2.2 --- In vitro assays --- p.5 / Chapter 1.3 --- Angiogenic factors --- p.6 / Chapter 1.4 --- Angiogenesis in the female reproductive system --- p.7 / Chapter 1.5 --- Evidence of hormonally-regulated angiogenesis in endocrine tissues --- p.10 / Chapter 1.5.1 --- Ovary --- p.10 / Chapter 1.5.2 --- Thyroid --- p.11 / Chapter 1.6 --- Angiogenesis in the testis --- p.12 / Chapter 1.6.1 --- Structure of testicular vasculature --- p.12 / Chapter 1.6.2 --- Angiogenic factors in the testis --- p.13 / Chapter 1.6.3 --- Vascular effects of hCG/LH in the testis --- p.17 / Chapter 1.6.4 --- Postnatal development of testicular vasculature --- p.17 / Chapter 1.7 --- Aims of the present study --- p.19 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Animals --- p.20 / Chapter 2.2 --- Experimental design --- p.20 / Chapter 2.2.1 --- Testicular angiogenesis in adult rats - hormonal stimulation by hCG --- p.20 / Chapter 2.2.1.1 --- Changes with time after hCG treatment --- p.20 / Chapter 2.2.1.2 --- Effect of Leydig cell depletion --- p.22 / Chapter 2.2.1.3 --- Effect of Leydig cell suppression by subcutaneous testosterone-filled silastic implants --- p.22 / Chapter 2.2.1.4 --- Effect of testicular macrophage activation --- p.24 / Chapter 2.2.1.5 --- Effect of testicular macrophage depletion --- p.26 / Chapter 2.2.2 --- Developmental changes in testicular angiogenesis --- p.29 / Chapter 2.3 --- Perfusion of testes with fixative or Indian Ink --- p.29 / Chapter 2.4 --- Processing of the testes for histological sections --- p.30 / Chapter 2.5 --- Immunohistochemical staining for proliferating cell nuclear antigen (PCNA) --- p.31 / Chapter 2.6 --- Immunohistochemical staining for vascular endothelial growth factor --- p.32 / Chapter 2.7 --- Quantification of PCNA-positive endothelial cells --- p.33 / Chapter 2.8 --- Quantification of blood vessel density --- p.34 / Chapter 2.9 --- Estimation of intertubular area in testis section --- p.35 / Chapter 2.10 --- Preparation of liposome-entrapped dichloromethylene diphosphonate (Cl2MDP-lp) --- p.38 / Chapter 2.11 --- Radioimmunoassay of serum tsetosterone --- p.38 / Chapter 2.12 --- Statistical analyses --- p.40 / Chapter 3. --- Results / Chapter 3.1 --- hCG-induced increase in endothelial cell proliferation in adult rat testes --- p.41 / Chapter 3.1.1 --- Testicular histology --- p.41 / Chapter 3.1.2 --- Changes in the number of PCNA-positive endothelial cells --- p.41 / Chapter 3.1.3 --- Changes in blood vessel density --- p.44 / Chapter 3.1.4 --- Changes in testis weight and serum testosterone concentration --- p.44 / Chapter 3.2 --- Effect of Leydig cell depletion by ethane dimethane sulphonate (EDS) on hCG-induced endothelial cell proliferation in adult rat testes --- p.48 / Chapter 3.2.1 --- Testicular histology --- p.48 / Chapter 3.2.2 --- Changes in the number of PCNA-positive endothelial cells --- p.48 / Chapter 3.2.3 --- Changes in serum testosterone concentration and testis weight --- p.52 / Chapter 3.3 --- Effect ofLeydig cell suppression by testosterone-filled subcutaneous silastic implants on hCG-induced endothelial cell proliferation in adult rat testes --- p.54 / Chapter 3.3.1 --- "Changes in serum testosterone concentration, testis weight, and testicular intertubular area" --- p.54 / Chapter 3.3.2 --- Changes in the number of PCNA-positive endothelial cells --- p.58 / Chapter 3.3.3 --- Changes in the level of vascular endothelial growth factor (VEGF) immunoreactivity in the testis --- p.60 / Chapter 3.4 --- Effect of testicular macrophage activation by polystyrene latex beads on hCG-induced endothelial cell proliferation in adult rat testes --- p.60 / Chapter 3.4.1 --- Testicular histology --- p.60 / Chapter 3.4.2 --- Changes in the number of PCNA-positive endothelial cells --- p.63 / Chapter 3.4.3 --- Changes in testis weight and serum testosterone concentration --- p.65 / Chapter 3.5 --- Effect of testicular macrophage depletion by liposome-entrapped C12MDP treatment on hCG-induced endothelial cell proliferation in adult rat testes --- p.67 / Chapter 3.5.1 --- Testicular histology --- p.68 / Chapter 3.5.2 --- Changes in the number of PCNA-positive endothelial cells --- p.68 / Chapter 3.5.3 --- Changes in testis weight and serum testosterone --- p.72 / Chapter 3.6 --- Endothelial cell proliferation in rat testes during postnatal development --- p.74 / Chapter 3.6.1 --- Changes in the number of PCNA-positive endothelial cells --- p.74 / Chapter 3.6.2 --- Changes in blood vessel density --- p.74 / Chapter 3.6.3 --- Changes in testis weight and intertubular area of the testes --- p.77 / Chapter 4. --- Discussion / Chapter 4.1 --- hCG-induced endothelial cell proliferation and changes in blood vessel density --- p.79 / Chapter 4.2 --- Role of Leydig cells in hCG-induced endothelial cell proliferation in adult rat testes --- p.82 / Chapter 4.3 --- Role of testicular macrophages in hCG-induced endothelial cell proliferation in adult rat testes --- p.86 / Chapter 4.4 --- Testicular angiogenesis during postnatal development --- p.88 / Chapter 5. --- References --- p.92

Cheung Kwok Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 123-136). / ABSTRACT (English) --- p.i / ACKNOWLEDGMENTS --- p.1 / LIST OF FIGURES --- p.3 / LIST OF TABLES --- p.5 / LIST OF ABBREVIATIONS --- p.7 / Chapter I. --- INTRODUCTION AND OBJECTIVES --- p.8 / Chapter II. --- LITERATURE REVIEWS --- p.11 / Chapter II.A. --- Maternal Serum Alpha-fetoprotein Screeningin Singleton Pregnancies --- p.11 / Chapter II.A.1. --- Physiology of Alpha-fetoprotein --- p.12 / Chapter II.A.2. --- Historical Background of Screening by Alpha- fetoprotein --- p.12 / Chapter II.A.3. --- Factors that Influence Maternal Serum Alpha- fetoprotein Concentration --- p.13 / Chapter ILA.4. --- Elevated Maternal Serum Alpha-fetoprotein Concentration and Adverse Pregnancy Outcomes and Complications --- p.14 / Chapter II.A.4.a. --- Low Birth Weight --- p.16 / Chapter II.A.4.b. --- Fetal Loss --- p.17 / Chapter II.A.4.c. --- Pregnancy Induced Hypertension --- p.18 / Chapter II.B. --- Maternal Serum Human Chorionic Gonadotrophin Screening in Singleton Pregnancies --- p.18 / Chapter II.B.1. --- Physiology of Human Chorionic Gonadotrophin --- p.18 / Chapter II.B.2. --- Historical Background of Screening by Human Chorionic Gonadotrophin --- p.20 / Chapter II.B.3. --- Factors that Influence Maternal Serum Human Chorionic Gonadotrophin --- p.21 / Chapter II.B.4. --- Elevated Maternal Serum Human Chorionic Gonadotrophin Concentration and Pregnancy Complications --- p.21 / Chapter II.B.5. --- Maternal Serum AFP and hCG Concentrations and Adverse Outcomes or Complications in Twin Pregnancies --- p.23 / Chapter II.C. --- Mechanism for the Association between Adverse Outcomes and Elevated Maternal Serum Alpha- fetoprotein and Human Chorionic Gonadotrophin --- p.25 / Chapter III. --- METHODS --- p.28 / Chapter III.A. --- Study Population --- p.28 / Chapter III.B. --- Sample Collection and Analysis --- p.29 / Chapter III.C. --- Clinical Information --- p.30 / Chapter III.D. --- Microparticle Enzyme Immunoassay --- p.30 / Chapter III.D.1. --- Principles --- p.30 / Chapter III.D.1.a. --- Reaction Process --- p.31 / Chapter III.D.1.b. --- MEIA Assembly --- p.33 / Chapter III.D.1.c. --- Operation --- p.34 / Chapter III.D.2. --- AFP Assay --- p.34 / Chapter III.D.2.a. --- AFP Reagents --- p.34 / Chapter III.D.2.b. --- Sample Dilution --- p.36 / Chapter III.D.3. --- Total p-hCG Assay --- p.37 / Chapter III.D.3.a. --- Total p-hCG Reagents --- p.37 / Chapter III.D.3.b. --- Sample Dilution --- p.39 / Chapter III.D.4. --- Intra- and Inter-assay Variation --- p.39 / Chapter III.E. --- Data Handling --- p.42 / Chapter III.F. --- Statistical Analysis --- p.42 / Chapter III.F.1. --- Calculations of Median Values of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin Concentrations --- p.42 / Chapter III.F.2. --- Analysis for Adverse Outcomes or Complications --- p.43 / Chapter III.F.3. --- Adjustment of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Gestational Age and Maternal Weight --- p.46 / Chapter IV. --- RESULTS --- p.48 / Chapter IV.A. --- Median Values of Maternal Serum Alpha-fetoprotein Human Chorionic Gonadotrophin --- p.48 / Chapter IV.B. --- Prediction of Adverse Outcomes by Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin --- p.60 / Chapter IV.B. l. --- Preterm Delivery --- p.60 / Chapter IV.B.2. --- Spontaneous Preterm Delivery --- p.64 / Chapter IV.B.3. --- Premature Delivery --- p.68 / Chapter IV.B.4. --- Spontaneous Premature Delivery --- p.68 / Chapter IV.B.5. --- Other Outcomes or Complications --- p.72 / Chapter IV.B.6. --- Single Predictor for Most Adverse Outcomes --- p.74 / Chapter IV.C. --- Adjustment of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.75 / Chapter IV.C.1. --- Distribution of Alpha-fetoprotein and Human Chorionic Gonadotrophin during Mid-trimester --- p.76 / Chapter IV.C.2. --- Adjustment of Alpha-fetoprotein for Maternal Weight and Gestational Age --- p.79 / Chapter IV.C.3. --- Adjustment of Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.80 / Chapter IV.D. --- Predictiveness of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Adverse Outcomes after Adjusted for Maternal Weight and Gestational Age --- p.83 / Chapter IV.D.l. --- Preterm Delivery --- p.86 / Chapter IV.D.2. --- Spontaneous Preterm Delivery --- p.86 / Chapter IV.D.3. --- Premature Delivery --- p.92 / Chapter IV.D.4. --- Spontaneous Premature Delivery --- p.92 / Chapter IV.D.5. --- Other Adverse Outcomes or Complications --- p.98 / Chapter IV.D.6. --- Single Predictor for Most Adverse Outcomes --- p.98 / Chapter V. --- DISCUSSIONS --- p.100 / Chapter V.A. --- Median Values of Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadtrophin --- p.100 / Chapter V.B. --- Maternal Serum Alpha-fetoprotein and Human Chorionic Gonadotrophin Screening for Adverse Outcomes --- p.103 / Chapter V.C. --- Adjustment of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Maternal Weight and Gestational Age --- p.109 / Chapter V.D. --- Predictiveness of Alpha-fetoprotein and Human Chorionic Gonadotrophin for Adverse Outcomes after Maternal Weight and Gestational Age Adjustment --- p.112 / Chapter V.E. --- Conclusions --- p.113 / Chapter V.F. --- Future Directions --- p.116 / APPENDIX 1 DATA BASE OF CLINICAL INFORMATION --- p.117 / APPENDIX 2 SEVERITY AND CLASSIFICATION OF PREGNANCY INDUCED HYPERTENSION --- p.122 / REFERENCES --- p.123

名古屋大学博士学位論文 学位の種類 : 博士(医学)(論文) 学位授与年月日:平成9年2月28日 森脇崇之氏の博士論文として提出された

Thesis (M.S.) -- University of Texas Southwestern Medical Center at Dallas, 2005. / Embargoed. Vita. Bibliography: 33-36.

O biglicam é um proteoglicano é altamente expresso em células trofoblásticas de patologias placentárias com invasividade exacerbada. No entanto, as funções do biglicam no trofoblasto ainda não foram elucidadas. Sendo assim, verificamos a expressão e as funções de biglicam e seus receptores Toll-like (TLR)-2 e TLR-4 nas células trofoblásticas durante a gestação. As células do citotrofoblasto extraviloso (CTEV) foram positivas para todas as moléculas, menos para o biglicam em placentas a termo. Adição exógena de biglicam promoveu migração e invasão das células trofoblásticas. O biglicam estimulou a fosforilação de AKT nos sítios Thr308 e Ser473 nas células trofoblásticas. A migração e a invasão biglicam-dependentes e as fosforilações de AKT foram inibidas após a adição de anticorpos bloqueadores anti-TLR-2 e anti-TLR-4. O silenciamento gênico de AKT1 em células SGHPL-5 aboliu os efeitos do biglicam na motilidade. Em conclusão, o biglicam aumenta a motilidade de células trofoblásticas após sinalização por AKT através da ativação de TLR-2 e TLR-4. / Biglycan is a highly expressed proteoglycan in trophoblast cells from invasiveness-changed placental pathologies. However, biglycan functions in the trophoblast were not yet identified. Therefore, it was verified the expression and functions of biglycan and its receptors Toll-like (TLR)-2 and TLR-4 in trophoblast cells throughout pregnancy. The extravillous cytotrophoblast cells (EVT) were positive to all the molecules, although biglycan was negative in term placentas. Exogenous biglycan promoted migration and invasion of trophoblast cells. Biglycan stimulated AKT phosphorilation at Thr308 and Ser473 sites in trophoblast cells. The biglycan-dependent migration, invasion and AKT phosphorilation were inhibited upon addiction of anti-TLR-2 and anti-TLR-4 blocking antibodies. AKT1 genic silencing in SGHPL-5 cells abolished the motility effects. In conclusion, biglycan increases the motility of trophoblast cells after AKT signaliing throughout TLR-2 and TLR-4 activation.