Wong Lai Lok. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 162-173). / Abstracts in English and Chinese. / Abstract --- p.ii / Acknowledgements --- p.vi / Publications --- p.vii / Abbreviations --- p.viii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1. --- Historical Background --- p.2 / Chapter 1.2. --- Heterogeneity of mast cells --- p.3 / Chapter 1.3. --- Mast cell mediators --- p.5 / Chapter 1.3.1. --- Performed and granule associated mediators --- p.5 / Chapter 1.3.2. --- Newly synthesized mediators --- p.8 / Chapter 1.3.3. --- Cytokines --- p.10 / Chapter 1.4. --- Mast cell activation --- p.10 / Chapter 1.4.1. --- Aggregation of IgE Receptors (FcεRI) --- p.10 / Chapter 1.4.2. --- Activation of Phospholipase C --- p.11 / Chapter 1.4.3. --- Activation of Adenylate cyclase --- p.13 / Chapter 1.5. --- Adenosine --- p.14 / Chapter 1.5.1. --- Adenosine receptors --- p.14 / Chapter 1.5.2. --- Selective agonists and antagonists --- p.17 / Chapter 1.5.3. --- Physiological and pathological roles of adenosine --- p.20 / Chapter 1.6. --- Role of adenosine receptors in mast cell activation --- p.21 / Chapter 1.7. --- Aims of the study --- p.23 / Chapter Chapter 2 --- Materials and Methods --- p.30 / Chapter 2.1. --- Materials --- p.31 / Chapter 2.1.1. --- Mast cells secretagogues --- p.31 / Chapter 2.1.2. --- Anti-allergic compounds --- p.31 / Chapter 2.1.3. --- Adenosine receptor agonists and antagonists --- p.31 / Chapter 2.1.4. --- Materials for buffers --- p.32 / Chapter 2.1.5. --- Materials for rat sensitization --- p.32 / Chapter 2.1.6. --- Materials for histamine assay --- p.33 / Chapter 2.1.7. --- Miscellaneous --- p.33 / Chapter 2.2. --- Buffers and stock solutions --- p.34 / Chapter 2.2.1 --- Buffer ingredients --- p.34 / Chapter 2.2.2 --- Stock solutions --- p.34 / Chapter 2.3. --- Source of mast cells --- p.35 / Chapter 2.3.1. --- Animals --- p.35 / Chapter 2.3.2. --- Sensitization of animals --- p.35 / Chapter 2.3.3. --- Isolation of rat peritoneal mast cells --- p.35 / Chapter 2.3.4. --- Mast cells purification --- p.36 / Chapter 2.3.5. --- Cell counting --- p.36 / Chapter 2.4. --- General protocol for histamine release --- p.37 / Chapter 2.4.1. --- Histamine assay --- p.37 / Chapter 2.4.2. --- Antagonist studies --- p.38 / Chapter 2.4.3. --- Determination of histamine contents --- p.38 / Chapter 2.4.4. --- Calculation of histamine levels --- p.39 / Chapter 2.5. --- Statistical analysis --- p.40 / Chapter Chapter 3 --- "Effects of adenosine, adenosine deaminase and adenosine receptor agonists on mast cell activation" --- p.42 / Chapter 3.1. --- Introduction --- p.43 / Chapter 3.2. --- Materials and methods --- p.44 / Chapter 3.3. --- Results --- p.45 / Chapter 3.3.1. --- Effects of adenosine on anti-IgE induced histamine release in HEPES buffer --- p.45 / Chapter 3.3.2. --- Effects of NECA on anti-IgE induced histamine release in HEPES buffer --- p.46 / Chapter 3.3.3. --- Effects of CCPA on anti-IgE induced histamine release in HEPES buffer --- p.47 / Chapter 3.3.4. --- Effects of CPA on anti-IgE induced histamine release in HEPES buffer --- p.47 / Chapter 3.3.5. --- Effects of CGS21680 on anti-IgE induced histamine release in HEPES buffer --- p.48 / Chapter 3.3.6. --- Effects of Cl-MECA on anti-IgE induced histamine release in HEPES buffer --- p.49 / Chapter 3.3.7. --- Effects of adenosine deaminase on anti-IgE induced histamine release from rat peritoneal mast cells --- p.50 / Chapter 3.3.8. --- Effects of NECA on anti-IgE induced histamine release with and without adenosine deaminase --- p.50 / Chapter 3.3.9. --- Effects of Cl-MECA on anti-IgE induced histamine release with and without adenosine deaminase --- p.53 / Chapter 3.3.10. --- Effects of CV1808 on anti-IgE induced histamine release in HEPES buffer --- p.55 / Chapter 3.4. --- Discussion --- p.76 / Chapter 3.5. --- Conclusion --- p.83 / Chapter Chapter 4 --- Effects of adenosine receptor antagonists on mast cell activation --- p.88 / Chapter 4.1. --- Introduction --- p.89 / Chapter 4.2. --- Materials and methods --- p.90 / Chapter 4.3. --- Results --- p.91 / Chapter 4.3.1. --- Effects of A1 receptor antagonist DPCPX on modulations of anti-IgE induced histamine release by adenosine receptor agonists --- p.91 / Chapter 4.3.2. --- Effects of A2A receptor antagonist ZM241385 on modulations of anti-IgE induced histamine release by adenosine receptor agonists --- p.91 / Chapter 4.3.3. --- Effects of A2B receptor antagonist MRS 1706 on modulations of anti-IgE induced histamine release by adenosine receptor agonists --- p.92 / Chapter 4.3.4. --- Effects of A3 receptor antagonist VUF5574 on modulations of anti-IgE induced histamine release by adenosine receptor agonists --- p.93 / Chapter 4.3.5. --- Further characterization of adenosine mediated potentiation of anti-IgE histamine release using VUF5574 and ZM241385 --- p.93 / Chapter 4.3.6. --- Effects of theophylline on anti-IgE induced percentage potentiation in HEPES buffer --- p.95 / Chapter 4.4. --- Discussion --- p.130 / Chapter 4.5. --- Conclusion --- p.135 / Chapter Chapter 5 --- Further characterization of the effects of adenosine on mast cells --- p.138 / Chapter 5.1. --- Introduction --- p.139 / Chapter 5.2. --- Materials and methods --- p.141 / Chapter 5.3. --- Results --- p.142 / Chapter 5.3.1. --- Effects of anti-IgE induced histamine release in calcium free and HEPES buffers --- p.142 / Chapter 5.3.2. --- Effects of adenosine on anti-IgE induced histamine release in calcium free buffer --- p.143 / Chapter 5.3.3. --- Effects of adenosine deaminase on compound48/80 induced histamine release from rat peritoneal mast cells --- p.143 / Chapter 5.3.4. --- Effects of adenosine on compound 48/80 induced histamine release in HEPES buffer --- p.144 / Chapter 5.3.5. --- Effects of adenosine deaminase on A23187 induced histamine release from rat peritoneal mast cells --- p.144 / Chapter 5.3.6. --- Effects of adenosine on calcium ionophore A23187 induced histamine release in HEPES buffer --- p.145 / Chapter 5.3.7. --- Effects of adenosine receptor antagonists on inosine mediated enhancement of anti-IgE induced histamine release --- p.145 / Chapter 5.4. --- Discussion --- p.157 / Chapter 5.5. --- Conclusion --- p.160 / References --- p.162

The recognition accuracy of emotion in faces varies depending on the discrete emotion being expressed and the location of the stimulus. More specifically, emotion detection performance declines as facial stimuli are presented further out in the periphery. Interestingly, this is not always true for faces depicting happy emotional expressions, which can be associated with maintained levels of detection. The current study examined neurophysiological responses to emotional face discrimination in the periphery. Two event-related potentials (ERPs) that can be sensitive to the perception of emotion in faces, P1 and N170, were examined using EEG data recorded from electrodes at occipitotemporal sites on the scalp. Participants saw a face presented at a 0° angle of eccentricity, at a 10° angle of eccentricity, or at a 20° angle of eccentricity, and responded whether the face was a specific emotion or neutral. Results showed that emotion detection was higher when faces were presented at the center of the display than at 10° or 20° for both happy and angry expressions. Likewise, the voltage amplitude of the N170 component was greater when faces were presented at the center of the display than at 10° or 20°. Further exploration of the data revealed that high intensity expressions were more easily detected at each location and elicited a larger amplitude N170 than low intensity expressions for both emotions. For a peripheral emotion discrimination task like that which was employed in the current study, emotion cues seem to enhance face processing at peripheral locations.

Early-latency theories of emotional processing state that at least coarse monitoring of the emotional valence (a pleasure-displeasure continuum) of facial expressions should be both rapid and highly automated (LeDoux, 1995; Russell, 1980). Research has largely substantiated early-latency differential processing of emotional versus non-emotional facial expressions; however, the effect of valence on early-latency processing of emotional facial expression remains unclear. In an effort to delineate the effects of valence on early-latency emotional facial expression processing, the current investigation compared ERP responses to positive (happy and surprise), neutral, and negative (afraid and sad) basic facial expression photographs as well as to positive (happy-surprise), neutral (afraid-surprise, happy-afraid, happy-sad, sad-surprise), and negative (sad-afraid) morph facial expression photographs during a valence-rating task. Morphing manipulations have been shown to decrease the familiarity of facial patterns and thus preclude any overlearned responses to specific facial codes. Accordingly, it was proposed that morph stimuli would disrupt more detailed emotional identification to reveal a valence response independent of a specific identifiable emotion (Balconi & Lucchiari, 2005; Schweinberger, Burton & Kelly, 1999). ERP results revealed early-latency differentiation between positive, neutral, and negative morph facial expressions approximately 108 milliseconds post-stimulus (P1) within the right electrode cluster; negative morph facial expressions continued to elicit significantly smaller ERP amplitudes than other valence categories approximately 164 milliseconds post-stimulus (N170). Consistent with previous imaging research on emotional facial expression processing, source localization revealed substantial dipole activation within regions of the mesolimbic dopamine system. Thus, these findings confirm rapid valence processing of facial expressions and suggest that negative valence processing may continue to modulate subsequent structural facial processing.

Visual attention has long been described in terms of the spotlight metaphor, which assumes that two-dimensional regions of the visual field are selectively processed. However, evidence suggests that attention can be distributed to depth in addition to two-dimensional space (Andersen and Kramer, 1993; Gawryszewski, Riggio, Rizzolatti, and Umiltà, 1987). Research supporting this idea has induced depth through binocular disparity. Thus, the results of previous research may be specific to stereoscopic stimuli and not apply generally to the perception of depth. Three experiments were conducted in order to determine if visual attention could be distributed to a non-stereoscopic apparent depth. In these experiments, the perceptual experience of depth was induced in a visual scene using only pictorial depth cues. Subjects were required to attend either a near or far depth in this scene. Experiments 1 and 2 employed electrophysiological recordings and found a reliable modulation in the amplitude of the attention sensitive visual component, P1, when subjects directed attention to far depths. Behavioral measurements in Experiment 3 supported this result, finding speeded reaction time to attended far depth stimuli. No P1 modulation or reaction time facilitation was found when the pictorial depth cues of the visual scene were attenuated. These results suggest that visual attention may be distributed to pictorial depth and are further consistent with a viewer-centered asymmetry in attending to depth.

This dissertation investigates the possibility of producing zeolites from municipal solid waste ash, MSW ash, by using hydrothermal treatment alone and by introducing fusion at 550 °C prior to hydrothermal treatment. The study was performed at different treatment conditions where silica/aluminum ratio of 13.9 and 2.5, hydroxide concentrations of 1.5N, 2.5N and 3.5N, temperatures at 100°C and 60 °C and time at 6, 24 and 72 hours were the major variables used to study zeolites synthesis process. The possibility of forming zeolites A, P1 and X was of particular interest in the present study. Factors, mechanism and modeling of zeolite A were investigated thoroughly in the present study. Zeolite synthesis process was evaluated using X-Ray diffraction to study different formed zeolite types and their chemical composition as well as their percentages. Morphological and physical characteristics of the produced zeolitic materials were evaluated by scanning electron microscopy, and cation exchange capacity property, CEC.The findings indicate that hydrothermal process did not succeed in producing significant amounts of zeolites. Consequently, the CEC of the produced zeolitic materials were much below the available commercial zeolite materials.Fusing the ash prior to hydrothermal treatment successfully produced sodium aluminum silicates and sodium silicates precursors to zeolite A formation. Fusion followed by hydrothermal treatment yielded significant amounts of zeolite A, at maximum value of 38.8% with CEC up to 245.0 meq/100g, which is within the range of commercially available zeolites. Experimental design analysis performed on zeolite A synthesis showed that zeolite A formation was reproducible and equation of interaction between different used conditions was established. Mechanism of zeolite A formation was concluded to be solution transport mediated process that involved both gel and solution interaction rather than being pure solution reaction or pu re gel transformation process. Solution super saturation and optimum silica/aluminum ratio were the driving force for nucleation of zeolite A.

The ability to recognise an individual's affective state from their facial expression is crucial to human social interaction. However, understanding of facial expression recognition processes is limited because mounting evidence has revealed important differences between posed and genuine facial expressions of emotion. Most previous studies of facial expression recognition have used only posed or simulated facial expressions as stimuli, but posed expressions do not reflect underlying affective state unlike genuine expressions. The current study compared behavioural responses and Evoked Response Potentials (ERPs) to neutral expressions, posed smiles and genuine smiles, during three different tasks. In the first task, no behavioural judgment was required, whereas participants were required to judge whether the person was showing happiness in the second task or feeling happiness in the third task. Behavioural results indicated that participants exhibited a high degree of sensitivity in detecting the emotional state of expressions. Genuine smiles were usually labelled as both showing and feeling happiness, but posed smiles were far less likely to be labelled as feeling happiness than as showing happiness. Analysis of P1 and N170 components, and later orbitofrontal activity, revealed differential activity levels in response to neutral expressions as compared to posed and genuine smiles. This differential activity occurred as early as 135ms at occipital locations and from 450ms at orbitofrontal locations. There were significant interactions between participant behavioural sensitivity to emotional state and P1 and N170 amplitudes. However, no significant difference in ERP activity between posed smiles and genuine smiles was observed until 850ms at orbitofrontal locations. An additional finding was greater right temporal and left orbitofrontal activation suggesting hemispheric asymmetry of facial expression processing systems.

P1 is a low copy number plasmid that uses a dedicated partition system that actively ensures each daughter cell inherits a copy of the plasmid. P1 plasmid partition is a positioning reaction, ensuring that each plasmid copy is correctly localized to the one-quarter and three-quarter position or midcell in an E. coli cell prior to partition. The factors involved in this positioning process are not well understood. I utilized cell biology techniques and E. coli mukB mutants that produce cells with chromosomal condensation defects to study the role of the bacterial chromosome and P1 ParA as possible localization signals. P1 plasmid prefers to localize to the bacterial nucleoid even when the chromosome is perturbed. ParA is necessary for plasmid localization to the chromosome. In this study, live cell microscopy analysis of ParA indicates that an interaction between P1 ParA and the E. coli nucleoid may underlie the localization mechanism of the plasmid partition system.

P1 is a low copy number plasmid that uses a dedicated partition system that actively ensures each daughter cell inherits a copy of the plasmid. P1 plasmid partition is a positioning reaction, ensuring that each plasmid copy is correctly localized to the one-quarter and three-quarter position or midcell in an E. coli cell prior to partition. The factors involved in this positioning process are not well understood. I utilized cell biology techniques and E. coli mukB mutants that produce cells with chromosomal condensation defects to study the role of the bacterial chromosome and P1 ParA as possible localization signals. P1 plasmid prefers to localize to the bacterial nucleoid even when the chromosome is perturbed. ParA is necessary for plasmid localization to the chromosome. In this study, live cell microscopy analysis of ParA indicates that an interaction between P1 ParA and the E. coli nucleoid may underlie the localization mechanism of the plasmid partition system.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.