Thesis advisor: Thomas O'Hare / The Behavior and Symptom Identification Scale 24 (BASIS-24) is a psychiatric outcome measure used for inpatient and outpatient populations. This 24-item measure comprises six subscales: depression/functioning; interpersonal relationships; self-harm; emotional lability; psychosis; and substance abuse. Earlier studies examined the reliability and validity of the BASIS-24, but none empirically examined its factor structure across gender. The purpose of this study was therefore to assess the construct validity of the BASIS-24 six-factor model and find evidence of configural, metric, strong and strict factorial invariance across gender. The sample consisted of 1398 psychiatric inpatients that completed BASIS-24 at admission and discharge at 11 facilities nation-wide. Confirmatory factor analyses were used to test measurement invariance of the BASIS-24 six-factor model across males and females. The single confirmatory factor analysis showed the original six-factor model of BASIS-24 provided an acceptable fit to the male sample at admission (RMSEA=0.058, SRMR=0.070, CFI=0.975, NNFI=0.971 and GFI=0.977) and at discharge (RMSEA=0.059, SRMR=0 .078, CFI=0.977, NNFI=0.972, and GFI=0.969). The goodness-of-fit indices for the female group at admission (RMSEA=0.055, SRMR=0.067, CFI=0.980, NNFI=0.976, and GFI=0.983), and at discharge (RMSEA=0.055, SRMR=0.079, CFI=0.98, NNFI=0.977, and GFI=0.971) also revealed that the six factor model fit reasonably well to the data. The goodness-of-fit indices between the unconstrained and constrained models showed that all four multi-group models were equivalent for both male and female samples at admission and discharge in terms of goodness-of-fit examined through the &#916;CFI and that all of them show an acceptable fit to the data. The decrease in CFI was <0.008 for admission sample and <0.003 for discharge sample and both fell below the 0.01 cut-off. This indicates that the configural, metric, as well as the strong and strict factorial invariance of BASIS-24 exist across males and females. The two important contributions of the present study are: 1) BASIS-24 can be used as a reliable and valid symptom measurement tool in assessing psychiatric inpatient populations which can compare quantitative differences in the magnitude of patient symptoms and functioning across genders; 2) the current study provides an example of useful statistical methodology for examining specific questions related to factorial invariance of the BASIS-24 instrument across gender. Implications of social work practice and research are discussed. / Thesis (PhD) — Boston College, 2008. / Submitted to: Boston College. Graduate School of Social Work. / Discipline: Social Work.

University of Macau / Institute of Chinese Medical Sciences

Doctor en Farmacología / Autorizada por el autor, pero con restricción para ser publicada a texto completo en el Portal de Tesis Electrónicas, hasta diciembre de 2018 / El cáncer es la 2° causa de muerte en Chile. El desarrollo del cáncer se ha propuesto que es consecuencia de la pérdida de función de los genes supresores de tumores beneficiando la acción de los oncogenes (genes que promueven el crecimiento de tumores). La activación del Factor inducible por hipoxia 1α (HIF1α) en un ambiente reducido en oxígeno (hipoxia) o por óxido nítrico (NO), permiten la proliferación y adaptación metabólica de las células tumorales. Por otro lado, Caveolina-1 es una proteína de andamiaje, que ha sido descrita como un supresor de tumores y promotor de metástasis. Resultados de nuestro laboratorio han demostrado que E-Cadherina y Caveolina-1 actúan cooperativamente en supresión de tumores in vivo. Sin embargo, Caveolina-1 suprime el crecimiento de tumores incluso en células carentes de E-Cadherina, de un modo menos eficiente. La isoforma endotelial de la sintasa de óxido nítrico (NOS3), es uno de los blancos inhibidos por Caveolina-1 más ampliamente descritos en la literatura, que recientemente ha sido implicado en mantenimiento tumoral. Cómo la inhibición de NOS mediada por Caveolina-1 afecta la activación de HIF1α contribuyendo a la función supresora de tumores de Caveolina-1 en ausencia de E-Cadherina, aún no ha sido evaluado. En este trabajo, evaluamos la posibilidad que la inhibición de NOS por Caveolina-1 pueda reducir la transcripción dependiente de HIF1α y contribuir así a la función supresora de tumores de Caveolina-1. Líneas celulares transfectadas con un plasmidio que codifica para Caveolina-1 [HT29(US), B16F10 y HEK293T] o células en que la expresión endógena de Caveolina-1 fue disminuida utilizando un shRNA [MDA-MB231], fueron tratadas en hipoxia (1% O2, 4-24 h). La actividad transcripcional de HIF, la expresión de genes blanco de HIF1α, la distribución subcelular de HIF1α, Caveolina-1 y NOS3, fueron evaluados mediante ensayos de gen reportero, RT-PCR/qPCR, Western Blot y microscopía confocal, respectivamente. Además, se realizaron ensayos de formación de tumores en ratones inmunosuprimidos SCID-Beige y en ratones inmunocompetentes C57BL/6. Los principales hallazgos de este trabajo fueron, que Caveolina-1 reduce la actividad transcripcional de HIF1α y la expresión de VEGF en hipoxia en las líneas celulares analizadas. Además, la reducción del crecimiento tumoral de células de melanoma murino B16F10(Cav-1) fue coincidente con la reducción de la expresión del mRNA de vegf in vivo. El tratamiento de las células con el dador de NO (DETA/NO) o el inhibidor de arginasa BEC, previnieron la inhibición de la actividad transcripcional de HIF1α mediada por Caveolina-1. Además, la inhibición de NOS con L-NAME o con el inhibidor selectivo de NOS3, L-NIO, reducen el incremento en la actividad transcripcional de HIF en hipoxia. In vivo, la sobreexpresión de HIF1α en células HT29(US)(Cav-1) revierte la supresión de tumores mediada por Caveolina-1 en ratones SCID-Beige. Finalmente, el tratamiento sistémico de ratones C57BL/6 con L-NAME, reduce el volumen tumoral a niveles comparables con los observados en los tumores formados por células B16F10(Cav-1). En resumen, nuestros resultados sugieren que la inhibición de NOS3 mediada por Caveolina-1 reduce la actividad transcripcional de HIF1α y la expresión de sus genes blanco, in vitro e in vivo, contribuyendo a la función supresora de tumores de Caveolina-1 en ausencia de E-Cadherina / Cancer, the 2nd most important cause of death in Chile, is thought to develop due to loss of tumor suppressor and gain of oncogene function. Activation of Hypoxia-inducible factor 1α (HIF1α) in the low oxygen environment (hypoxia) present in tumors or by nitric oxide (NO), favors cancer cell proliferation and metabolic adaptation. Caveolin-1 is a scaffolding protein that reportedly functions both as a tumor suppressor and promoter of metastasis. Results from this laboratory have shown that E-cadherin and Caveolin-1 cooperate in tumor suppression in vivo. However, Caveolin-1 expression suppresses tumor growth even in cancer cells lacking E-cadherin, albeit less efficiently. The endothelial isoform of nitric oxide synthase (NOS3), one of the best-established targets for inhibition by Caveolin-1, has recently been implicated in maintence of tumor growth. Whether, Caveolin-1-mediated NOS inhibition may impact on HIF1α activation and account for tumor suppression by Caveolin-1 in the absence of E-cadherin has not been yet assessed. Here, we evaluated the possibility that NOS inhibition by Caveolin-1 may reduce HIF1α - dependent transcription and thereby contribute to the tumor suppressor function of Caveolin-1. Cell lines transfected with a Caveolin-1-encoding plasmid [HT29(US), B16F10 and HEK293T] or cells where endogenous Caveolin-1 protein levels [MDA-MB231] were reduced using shRNA-technology, were exposed to hypoxia (1% O2, 4-24 h). In these cells, HIF transcriptional activity, HIF1α target-gene expression, HIF1α, Caveolin-1 and NOS3 protein levels and subcellular localization were evaluated by gene reporter assays, RT-PCR/qPCR, Western Blot and confocal microscopy, respectively. Tumor forming capacity was evaluated in immunodeficient SCID-Beige and immunocompetent C57BL/6 mouse strains. The main findings of this study are that Caveolin-1 reduced HIF1α transcriptional activity and VEGF expression in hypoxia in vitro in all cell lines. Also, reduced tumor growth of B16F10(Cav-1) melanoma cells in C57BL/6 mice correlated with reduced vegf gene expression in vivo. Treatment of cells with the NO donor (DETA/NO) o arginase inhibition with BEC, prevented Caveolin-1-mediated inhibition of HIF1α transcriptional activity. Furthermore, NOS inhibition with L-NAME or selective NOS3 inhibition with L-NIO, reduced hypoxia-enhanced HIF transcriptional activity. In vivo HIF1α overexpression in HT29(US)(Cav-1) cells reversed tumor suppression due to Caveolin-1 in SCID-Beige mice. Finally, systemic treatment of C57BL/6 mice with L-NAME, reduced tumor volumes to levels comparable to those observed for tumors formed by B16F10(Cav-1) cells. In summary, our observations suggest that Caveolin-1-mediated inhibition of NOS3 activity reduces HIF1α transcriptional activity and target gene expression, both in vitro and in vivo, and that this ability contributes to tumor suppression by Caveolin-1 in the absence of E-cadherin / CONICYT, FONDECYT, FONDAP, MECESUP

Regulation of gene expression in a spatiotemporal manner specifies cellular identity. Transcription factors (TFs) bind to DNA regulatory elements to remodel chromosome structure, to recruit transcription machinery to initiate gene transcription or to prevent the assembly of such machinery to repress gene transcription, thus they lie at the heart of gene regulation. Given important roles of TFs in gene regulation, numerous attentions have been attracted for engineered transcription factors (eTFs). The recent advance of generating customized DNA-sequence specific binding domains, including transcription activator-like effectors (TALEs) and RNA-guided clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (Cas) gene Cas9, has greatly accelerated the study and application of eTFs. The eTFs with these new binding domains offer a powerful and precise approach for modulating gene expression. / Oct4 is an important TF and it plays essential roles in the formation of inner cell mass during embryogenesis, and the maintenance of embryonic stem cells in culture as well as the reinstatement of cellular pluripotency from somatic cells. / In this study, we systematically investigated the potential of TALE-TFs and CRISPR/Cas9-TFs in activating Oct4. We designed a number of TALEs and small guide RNAs (sgRNAs) targeting various regions in the mouse and human Oct4 promoters. Using luciferase assays, we found that the most efficient TALE-VP64s bound on the region −120 to −80 bp upstream of transcription start site (TSS), while highly effective sgRNAs targeted −147 to −89 bp upstream of TSS to induce high activity of luciferase reporters. This positional effect can serve as a simple guideline for designing eTFs for activating transcription from a reporter system. Next, we examined the potential of TALE-VP64 and sgRNAs to activate endogenous Oct4 transcription. We found that the positional effect was less obvious as individual eTFs exhibited marginal activity to up-regulate endogenous gene expression. Interestingly, we found that when multiple eTFs were applied simultaneously, Oct4 could be induced significantly and synergistically. This phenomenon was well supported by activation of human SOX2, KLF4, cMYC, CDH1 and NANOG by TALE-VP64s. / Using optimized combinations of TALE-VP64s, we successfully enhanced endogenous Oct4 transcription up to 30-fold in mouse NIH3T3 cells and 20-fold in human HEK293T cells. More importantly, the enhancement of OCT4 transcription ultimately generated OCT4 proteins. Furthermore, examination of different epigenetic modifiers showed that histone acetyltransferase p300 could enhance both TALE-VP64- and sgRNA/dCas9-VP64-induced transcription of endogenous OCT4. Taken together, this study demonstrated that engineered TALE-TFs and dCas9-TFs are useful tools for modulating gene expression in mammalian cells. / 基因表達調控是決定細胞命運的關鍵。轉錄因子可以結合到DNA調控序列上，以重塑染色體的結構；而且可以募集轉錄機器，以起始轉錄, 或者幹擾轉錄機器的組裝，從而抑制基因轉錄；因此，在基因表達調控過程中轉錄因子處於核心地位。由于轉錄因子在基因調控方面的重要作用，研究者們越來越多的關注人工轉錄因子的研究。DNA 序列特異性結合域的發現與發展很大程度上促進了人工轉錄因子的研究與應用。最近從TALE和CRISPR/Cas9衍生而來的人工轉錄因子給我們提供了一個強大而且精確的調控基因表達的方法。Oct4是一個重要的轉錄因子，對胚胎發育過程中內細胞團的形成，和體外培養的胚胎幹細胞的維持，以及細胞多能性的重塑等多方面都至關重要。 / 在本研究中，我們系統性地探討了TALE和CRISPR/Cas9衍生而來的人工轉錄因子在激活Oct4基因方面的潛能。我們針對小鼠和人的Oct4的啓動子設計了一序列的TALEs和sgRNAs。通過熒光素酶實驗，我們發現結合到轉錄起始位點上遊120‐80bp位置的TALE‐VP64s，或者結合到147‐89bp位置的sgRNAs可以最有效地誘導熒光素酶報告基因的表達。在激活報告基因方面，這種位置效應可以作爲一條設計人工轉錄因子的簡單原則。然後，我們進一步檢測了這些人工轉錄因子在激活內源性Oct4轉錄方面的效果。結果顯示上述觀察到的位置效應並不明顯，因爲每一單個的人工轉錄因子都幾乎不能上調內源性基因的表達。但是，當同時導入多個人工轉錄因子時，我們可以顯著地激活Oct4的表達，而且可以觀察到明顯的疊加效應。利用人工轉錄因子激活SOX2, KLF4, cMYC, CDH1和NANOG,我們進一步證明了這種疊加效應。 / 通過篩查不同的人工轉錄因子組合，我們在小鼠NIH3T3細胞系把Oct4基因的表達提供到了原來水平的30多倍，而在人的HEK293T中，提高了20多倍。更重要的是，我們可以檢測到蛋白質表達水平的提高。通過檢測不同的表觀調控因子，我們發現組蛋白乙酰化轉移酶p300可以進一步提升這些人工轉錄因子誘導的Oct4基因表達。因此，本研究表明這些人工轉錄因子是調節哺乳動物細胞內基因表達的有效工具。 / Hu, Jiabiao. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2014.y066 / Includes bibliographical references (leaves 132-157). / Abstracts also in Chinese. / Title from PDF title page (viewed on 13, December, 2016). / Hu, Jiabiao. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only.

by Ngai Wing Keung Clement. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 172-206). / Chapter 1. --- Acknowledgment --- p.iv / Chapter 2. --- Abstract --- p.v / Chapter 3. --- Lists of Tables and Figures --- p.vii / Chapter 4. --- General Introduction --- p.1 / Chapter 5. --- Review of Literature --- p.5 / Chapter 5.1. --- Historical Background of Natriuretic Peptides --- p.5 / Chapter 5.2. --- Secretion of Natriuretic Peptides --- p.8 / Chapter 5.3. --- Structure and Function Relationships --- p.12 / Chapter 5.4. --- Physiological Actions --- p.17 / Chapter 5.5. --- Natriuretic Peptide Receptors and Second Messengers --- p.22 / Chapter 5.6. --- Clinical Implications --- p.28 / Chapter 5.7. --- Review on Astrocytes --- p.31 / Chapter 6. --- General Materials and Methods --- p.43 / Chapter 6.1. --- Sources of Chemicals --- p.43 / Chapter 6.2. --- Culture of Mouse Astrocytes --- p.43 / Chapter 6.3. --- Culture of human astrocytoma cells --- p.57 / Chapter 6.4. --- Protein Determination --- p.57 / Chapter 6.5. --- Gamma Counting --- p.58 / Chapter 6.6. --- Beta Counting --- p.58 / Chapter 7. --- Receptor Identification and Characterization --- p.59 / Chapter 7.2 --- Materials and Methods --- p.60 / Chapter 7.3 --- Results --- p.66 / Chapter 7.4 --- Discussion --- p.81 / Chapter 8. --- Second Messenger Systems --- p.83 / Chapter 8.1 --- Introduction --- p.83 / Chapter 8.2 --- Materials and Methods --- p.85 / Chapter 8.3 --- Results --- p.97 / Chapter 8.4 --- Discussion --- p.109 / Chapter 9. --- Biological Actions of Natriuretic Peptides --- p.113 / Chapter 9.1. --- Potassium Transport --- p.113 / Chapter 9.1.1. --- Introduction --- p.113 / Chapter 9.1.2. --- Materials and Methods --- p.116 / Chapter 9.1.3. --- Results --- p.121 / Chapter 9.1.4. --- Discussion --- p.131 / Chapter 9.2 --- Taurine Release --- p.135 / Chapter 9.2.1. --- Introduction --- p.135 / Chapter 9.2.2. --- Materials and Methods --- p.137 / Chapter 9.2.3. --- Results --- p.139 / Chapter 9.2.4. --- Discussion --- p.143 / Chapter 9.3 --- Thymidine Incorporation --- p.144 / Chapter 9.3.1. --- Introduction --- p.144 / Chapter 9.3.2. --- Materials and Methods --- p.146 / Chapter 9.3.3. --- Results --- p.148 / Chapter 9.3.4. --- Discussion --- p.156 / Chapter 10. --- Interaction with Other Hormonal Systems --- p.160 / Chapter 10.1 --- Introduction --- p.160 / Chapter 10.2 --- Materials and Methods --- p.162 / Chapter 10.3 --- Result --- p.163 / Chapter 10.4 --- Discussion --- p.167 / Chapter 11. --- Conclusion --- p.169 / Chapter 12. --- References --- p.172 / Chapter 13. --- Appendix --- p.208

by Chun-kwok Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1990. / Bibliography: leaves 181-196. / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.iii / ABBREVIATIONS --- p.iv / CHAPTER / Chapter 1. --- INTRODUCTION : An overview of Tumor Necrosis Factor ( TNF) / Chapter 1. --- The discovery of tumor necrosis factor (TNF) --- p.1 / Chapter 2. --- Production of tumor necrosis factor --- p.3 / Chapter 3. --- Physiochemical properties of TNF --- p.5 / Chapter 4. --- Biological activities of TNF on various cells in the mammal --- p.8 / Chapter 5. --- Mechanisms of anti-tumor action of TNF --- p.12 / Chapter 6. --- Clinical studies of Hr-TNF --- p.19 / Chapter 2. --- AIM OF INVESTIGATION --- p.23 / Chapter 3. --- MATERIALS AND METHODS / Chapter A. --- MATERIALS --- p.26 / Chapter B. --- METHODS / Chapter 1. --- Preparation of Reagents --- p.30 / Chapter 2. --- Cell Culture --- p.31 / Chapter 3. --- Lymphocytes proliferation --- p.32 / Chapter 4. --- In vitro production of tumor necrosis factor (TNF) by peritoneal macrophages of ICR mice --- p.33 / Chapter 5. --- Production of TNF in animals --- p.34 / Chapter 6. --- Determination of TNF titre --- p.35 / Chapter 7. --- Determination of TNF containing serum titre on EAT in vitro --- p.35 / Chapter 8. --- Mortality determination of mice --- p.36 / Chapter 9. --- "3H-Thymidine, 3H-uridine, 14C-leucine incorporation" --- p.36 / Chapter 10. --- Glucose uptake determination --- p.37 / Chapter 11. --- Whole body hyperthermic treatment of EAT bearing mice --- p.37 / Chapter 12. --- Lipolysis assay --- p.38 / Chapter 13. --- Statistical analysis --- p.39 / Chapter 4. --- IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR USING ZYMOSAN AND LIPOPOLYSACCHARIDE / INTRODUCTION --- p.40 / EXPERIMENTAL --- p.43 / RESULTS --- p.45 / DISCUSSION --- p.65 / Chapter 5. --- SIDE EFFECTS DURING IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR IN EHRLICH ASCITES TUMOR BEARING MICE / INTRODUCTION --- p.70 / EXPERIMENTAL --- p.72 / RESULTS --- p.74 / DISCUSSION --- p.93 / Chapter 6. --- MODIFIED PROCEDURE FOR THE IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR FOR THE TREATMENT OF EHRLICH ASCITES TUMOR BEARING MICE / INTRODUCTION --- p.98 / EXPERIMENTAL --- p.99 / RESULTS --- p.100 / DISCUSSION --- p.108 / Chapter 7. --- "COMBINED TREATMENTS OF IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR (TNF) WITH HYPERTHERMIA, METHOTREXATE (MTX), POLYRIBOINOSINIC-POLYRIBOCYTIDYLIC ACID (POLY I.C), N-(PHOSPHONACETYL)-L-ASPARTATE (PALA) ON EAT BEARING MICE" / INTRODUCTION --- p.111 / EXPERIMENTAL --- p.116 / RESULTS --- p.118 / DISCUSSION --- p.133 / Chapter 8. --- EFFECTS OF IN VIVO PRODUCTION OF TUMOR NECROSIS FACTOR ON EHRLICH ASCITES TUMOR CELLS CYTOTOXICITY / INTRODUCTION --- p.138 / EXPERIMENTAL --- p.140 / RESULTS --- p.142 / DISCUSSION --- p.151 / Chapter 9. --- SIDE EFFECTS OF TUMOR NECROSIS FACTOR AND LIPOPOLYSACCHARIDE ON RAT IN VITRO AND IN VIVO / INTRODUCTION --- p.154 / EXPERIMENTAL --- p.157 / RESULTS --- p.159 / DISCUSSION --- p.170 / Chapter 10. --- CONCLUSION AND OUTLOOK --- p.174 / BIBLIOGRAPHY --- p.181

by Chu, Pui-ya. / Thesis (M.Phil.)--Chinese University of Hong Kong. / Bibliography: leaves 115-126. / ACKNOWLEDGEMENT / LIST OF ABBREVIATIONS / ABSTRACT --- p.1 / Chapter CHAPTER 1 --- INTRODUCTION / Chapter 1.1 --- PLATELET-ACTIVATING FACTOR (PAF) --- p.4 / Chapter 1.1.1 --- Metabolism of PAF --- p.4 / Chapter 1.1.1.1 --- Biosynthesis of PAF --- p.4 / Chapter 1.1.1.2 --- Degradation of PAF --- p.9 / Chapter 1.1.2 --- Systemic effects of PAF --- p.12 / Chapter 1.1.3 --- Structure - activity relationship of PAF --- p.16 / Chapter 1.2 --- PAF RECEPTORS --- p.19 / Chapter 1.2.1 --- PAF receptor on platelets --- p.19 / Chapter 1.2.2 --- PAF receptor on leukocytes --- p.20 / Chapter 1.2.3 --- PAF receptor on macrophages --- p.20 / Chapter 1.2.4 --- Antagonists of PAF --- p.20 / Chapter 1.2.4.1 --- Nonspecific inhibitors of PAF --- p.21 / Chapter 1.2.4.2 --- Specific antagonists of PAF --- p.21 / Chapter 1.3 --- SECOND MESSENGER SYSTEMS OF PAF --- p.22 / Chapter 1.3.1 --- Adenylate cyclase - cyclic adenosine mono- phosphate system --- p.26 / Chapter 1.3.2 --- Phospholipase C - phosphatidylinositol system --- p.28 / Chapter 1.3.3 --- Intracellular calcium --- p.29 / Chapter 1.3.4 --- The role of prostaglandins and leukotrienes --- p.30 / Chapter 1.3.5 --- Protein kinase C --- p.30 / Chapter 1.3.5.1 --- Dual action of PKC --- p.31 / Chapter 1.3.5.2 --- Down regulation of PKC --- p.33 / Chapter 1.4 --- THE FUNCTION OF MACROPHAGES --- p.33 / Chapter 1.4.1 --- Phagocytosis --- p.34 / Chapter 1.4.2 --- Antigen presentation --- p.34 / Chapter 1.4.3 --- Release of cytokines --- p.34 / Chapter 1.4.4 --- Respiratory burst --- p.35 / Chapter CHAPTER 2 --- METHODS / Chapter 2.1 --- PREPARATION OF PERITONEAL MACROPHAGES --- p.37 / Chapter 2.1.1 --- Preparation of reagents --- p.37 / Chapter 2.1.2 --- Preparation of peritoneal macrophages --- p.37 / Chapter 2.2 --- RADIOLIGAND BINDING ASSAY --- p.38 / Chapter 2.2.1 --- Reagents --- p.38 / Chapter 2.2.2 --- [3H]-PAF binding to TG-PEC --- p.39 / Chapter 2.2.2.1 --- Preparation of thioglycollate-elicited peritoneal macrophages --- p.39 / Chapter 2.2.2.2 --- Preparation of working solutions --- p.39 / Chapter 2.2.2.3 --- Assay of [3H]-PAF binding --- p.40 / Chapter 2.2.3 --- [3H]-PAF binding to resident PEC --- p.40 / Chapter 2.2.3.1 --- Preparation of resident peritoneal mcrophages --- p.41 / Chapter 2.2.3.2 --- Preparation of working solutions --- p.41 / Chapter 2.2.3.3 --- Assay of [3H]-PAF binding --- p.41 / Chapter 2.2.4 --- Preparation of drugs --- p.41 / Chapter 2.2.5 --- Data analysis --- p.42 / Chapter 2.3 --- MEASUREMENT OF INOSITOL PHOSPHATES --- p.42 / Chapter 2.3.1 --- Preparation of reagents --- p.42 / Chapter 2.3.2 --- Dowex column preparation --- p.43 / Chapter 2.3.3 --- Cell plating in 24 - well plastic trays --- p.44 / Chapter 2.3.4 --- Determination of total inositol phosphates --- p.44 / Chapter 2.3.5 --- Column separation --- p.45 / Chapter 2.3.6 --- Determination of inositol trisphosphate (IP3) --- p.46 / Chapter 2.4 --- MEASUREMENT OF INOSITOL PHOSPHATES ACCUMULATION AFTER PROLONGED PMA PRETREATMENT --- p.46 / Chapter 2.4.1 --- Preparation of phorbol-12-myristate-13-acetate (PMA) solutions --- p.47 / Chapter 2.4.2 --- Preparation of cells with PMA --- p.47 / Chapter 2.5 --- DETERMINATION OF SUPEROXIDE ANION PRODUCTION --- p.47 / Chapter 2.5.1 --- Preparation of drugs --- p.47 / Chapter 2.5.2 --- Assay of superoxide anion production --- p.48 / Chapter 2.5.3 --- Data analysis --- p.48 / Chapter 2.6 --- STATISTICAL METHOD --- p.48 / Chapter CHAPTER 3 --- RESULTS / Chapter 3.1 --- [3H]-PAF BINDING TO TG-PEC --- p.50 / Chapter 3.1.1 --- General properties --- p.50 / Chapter 3.1.2 --- Stereospecific of PAF receptor --- p.57 / Chapter 3.1.3 --- Comparison of [3H]-PAF binding to TG-PEC and TG-PMΦ from Balb/c mice --- p.57 / Chapter 3.1.4 --- Inhibition of specific binding of [3H]-PAF to murine and guinea pig TG-PEC by PAF --- p.57 / Chapter 3.1.5 --- Effects of PAF antagonists on the binding of [3H]- PAF to TG-PEC from Balb/c mice and guinea pigs --- p.60 / Chapter 3.1.6 --- Scatchard analysis of [3H]-PAF binding to murine and guinea pig TG-PMΦ --- p.65 / Chapter 3.2 --- SUPEROXIDE ANION PRODUCTION IN PERITONEAL MACROPHAGES --- p.69 / Chapter 3.2.1 --- Superoxide anion production induced by PAFin murine and guinea pig TG-PMΦ --- p.69 / Chapter 3.2.2 --- Effect of PMA on superoxide anion production in murine and guinea pig TG-PMΦ --- p.69 / Chapter 3.2.3 --- Effect of calcium ionophore on superoxide anion production in murine and guinea pig TG-PMΦ --- p.75 / Chapter 3.2.4 --- Effect of PAF antagonists on PAF - induced superoxide anion production in guinea pig TG-PMΦ --- p.75 / Chapter 3.3 --- PHOSPHOLIPASE C - PHOSPHATIDYLINOSITOL SYSTEM IN PERITONEAL MACROPHAGES --- p.79 / Chapter 3.3.1 --- Effect of PAF on the accumulation of inositol phosphates in the absence of LiCl --- p.79 / Chapter 3.3.2 --- Effect of PAF on the accumulation of inositol phosphates in the presence of LiCl --- p.79 / Chapter 3.3.2.1 --- Time course of [3H]-inositol phosphates accumulation induced by PAF in TG-PMΦ --- p.86 / Chapter 3.3.2.2 --- Effect of PAF on the accumulation of [3H]-IPs in TG- PMΦ from Balb/c mice and guinea pigs --- p.86 / Chapter 3.3.2.3 --- Effect of PAF antagonists on PAF-induced [3H]-IPs accumulation in TG-PMΦ from Balb/c mice and guinea pigs --- p.86 / Chapter 3.3.2.4 --- Effect of PMA on PAF-induced [3H]-IPs formation in TG-PMΦ from Balb/c mice and guinea pigs --- p.90 / Chapter 3.3.2.5 --- Effect of prolonged PMA pretreatment on PAF and PMA-induced [3H]-IPs accumulation in murine and guinea pig TG-PMΦ --- p.90 / Chapter 3.4 --- STUDIES OF RESIDENT PEC FROM Balb/c MICE --- p.96 / Chapter 3.4.1 --- Binding of 2nM [3H]-PAF to Balb/c mice resident PEC --- p.96 / Chapter 3.4.2 --- PAF-induced [3H]-IPs accumulation in murine resident PMΦ --- p.100 / Chapter 3.4.3 --- Binding of 0.2 nM [3H]-PAF to Balb/c mice resident PEC --- p.100 / Chapter 3.4.4 --- Superoxide anion production induced by PAF and PMA in murine resident PMΦ --- p.104 / Chapter CHAPTER 4 --- DISCUSSIONS / Chapter 4.1 --- PAF RECEPTOR ON PERITONEAL MACROPHAGES --- p.125 / Chapter 4.1.1 --- [3H]-PAF binding to peritoneal macrophages --- p.105 / Chapter 4.1.2 --- Expression of PAF receptor on Balb/c mice peritoneal macrophages --- p.107 / Chapter 4.2 --- SUPEROXIDE ANION PRODUCTION IN PERITONEAL MACROPHAGES --- p.108 / Chapter 4.3 --- PAF RECEPTOR AND POLYPHOSPHATIDYLINOSITOL SYSTEM IN PERITONEAL MACROPHAGES --- p.109 / Chapter CHAPTER 5 --- CONCLUSIONS --- p.112 / REFERENCES --- p.115

by Chung-Pui Cheng. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 142-163.

by King-hong Leung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 110-111). / Chapter Chapter 1 --- Introduction --- p.1 / Chapter Chapter 2 --- Prediction Problem of Factor Scores --- p.5 / Chapter 2.1 --- The Basic Model --- p.5 / Chapter 2.2 --- Regression Formula in Predicting Factor Scores --- p.7 / Chapter 2.3 --- The Model with Polytomous Variables --- p.9 / Chapter Chapter 3 --- Prediction Methods of Factor Scores --- p.11 / Chapter 3.1 --- Model with Continuous and Polytomous Variables --- p.11 / Chapter 3.2 --- Model with Polytomous Variables --- p.16 / Chapter Chapter 4 --- Monte-Carlo Study --- p.20 / Chapter 4.1 --- Model with Continuous and Polytomous Variables --- p.20 / Chapter 4.1.1 --- Design of the Monte-Carlo Study --- p.20 / Chapter 4.1.2 --- Results of the Monte-Carlo Study --- p.24 / Chapter 4.2 --- Model with Polytomous Variables --- p.30 / Chapter 4.2.1 --- Design of the Monte-Carlo Study --- p.30 / Chapter 4.2.2 --- Results of the Monte-Carlo Study --- p.33 / Chapter Chapter 5 --- Summary and Conclusion --- p.38 / Tables --- p.41 / Figures --- p.56 / References --- p.110

by Chung Sai Ho. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 53-56). / SUMMARY / Chapter 1. --- Introduction --- p.1 / "Functional, Structural and Ultrastructural Relationships" --- p.2 / Identifiability --- p.4 / Non-normally Distributed Regressor --- p.5 / Chapter 2. --- Underlying Non-normality --- p.7 / Beta Regressor and Guassian Errors --- p.8 / Moments --- p.14 / Moment Generating Function & Characteristic Function --- p.17 / Modality --- p.18 / Distribution Portfolio --- p.21 / Chapter 3. --- Modified Maximum Likelihood Estimation --- p.24 / Consistency --- p.26 / Asymptotically Normality --- p.30 / Efficiency of the MMLE --- p.34 / Chapter 4. --- Monte Carlo Simulation Studies --- p.36 / The Use of MMLE --- p.36 / Third Order Moment Estimator with Asymptotically Minimal Variance --- p.42 / Robustness --- p.46 / Chapter 5. --- Discussions and Conclusions --- p.48 / Other Alternatives --- p.48 / Semiparametric and Nonparametric Maximum Likelihood Estimation --- p.51 / References --- p.53