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A new version of the direct injection nebulizer (DIN) is used to interface liquid chromatographic (LC) separations with element - selective detection by inductively coupled plasma - mass spectrometry (ICP-MS). The advantages of using LC-DIN-ICP-MS include little dead volume, low sample and solvent consumption, excellent plasma stability when nebulizing samples containing concentrated organic solvent, excellent absolute detection limits, excellent precision, superior chromatographic resolution, and reduced memory effects from memory-prone elements (e.g., Hg);Various compounds containing arsenic (AsO[subscript]2[superscript]-, HAsO[subscript]4[superscript]2-, CH[subscript]3AsO[subscript]3[superscript]2- and (CH[subscript]3)[subscript]2AsO[subscript]2[superscript]-), tin (CH[subscript]3Sn[superscript]3+, (CH[subscript]3)[subscript]2Sn[superscript]2+, (C[subscript]2H[subscript]5)[subscript]2Sn[superscript]2+ and (CH[subscript]3)[subscript]3Sn[superscript]+), mercury (Hg[superscript]+2, CH[subscript]3Hg[superscript]+, C[subscript]2H[subscript]5Hg[superscript]+ and C[subscript]6H[subscript]5Hg[superscript]+) and lead (Pb[superscript]+2, (CH[subscript]3)[subscript]3Pb[superscript]+ and (C[subscript]2H[subscript]5)[subscript]3Pb[superscript]+) are separated by reversed-phase ion-pairing LC. Selenium species (SeO[subscript]3[superscript]2- and SeO[subscript]4[superscript]2-) are separated by ion chromatography (IC). Several metalloproteins containing Na, Fe, Cu, Zn, Cd, Ba, and Pb are separated by size-exclusion chromatography (SEC). Some of these compounds are separated and measured in biological and environmental samples such as human urine and human serum. Detection limits are ≈3, 0.7, 1, 0.5, 5, 0.5, 15, 7, and 0.2 pg for Fe, Cu, Zn, As, Se, Cd, Sn, Hg, and Pb, respectively. Microbore (1-2 mm i.d.) packed columns are employed because the liquid flow rates used (30-100 [mu]L min[superscript]-1) are compatible with the DIN;Aerosol droplet sizes and velocities from a DIN ar

Thesis (Sc. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, 1986., MICROFICHE COPY AVAILABLE IN ARCHIVES AND SCIENCE., Bibliography: leaves 284-290., by Chiu-Kin Steven Lai., Sc.D.

Chiu Kin., Thesis (M.Phil.)--Chinese University of Hong Kong, 1998., Includes bibliographical references (leaves 100-116)., also in Chinese., TABLE OF CONTENTS --- p.I, ACKNOWLEDGEMENTS --- p.V, LIST OF FIGURES --- p.VI, LIST OF ABBREVIATIONS --- p.VIII, p.1, Chapter 1. --- INTRODUCTION --- p.5, Chapter 2. --- LITERATURE REVIEW --- p.7, Chapter 2.1 --- RETINAL ISCHEMIA --- p.7, Chapter 2.1.1 --- INDUCTION OF RETINAL ISCHEMIA --- p.7, Chapter 2.1.2 --- MECHANISMS OF RETINAL ISCHEMIA/REPERFUSION DAMAGE --- p.8, Chapter 2.1.2.1. --- Free radical --- p.8, Chapter 2.1.2.2 --- Excitotoxicity --- p.9, Chapter 2.1.3 --- APOPTOSIS IN RETINAL ISCHEMIA/REPERFUSION INJURY --- p.10, Chapter 2.2 --- RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RAT --- p.15, Chapter 2.3 --- BCL-2 FAMILY MEMBERS --- p.16, Chapter 2.3.1 --- FAMILY MEMBERS AND THEIR INTERACTIONS --- p.16, Chapter 2.3.2 --- SUBCELLULAR LOCALIZATION --- p.18, Chapter 2.3.3 --- PHYSICAL STRUCTURE AND PORE FORMATION --- p.19, Chapter 2.3.4 --- BIOLOGICAL EFFECTS OF BCL-2 --- p.20, Chapter 3. --- OBJECTIVES --- p.24, Chapter 4. --- MATERIALS AND METHODS --- p.27, Chapter 4.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.27, Chapter 4.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED RETINAL ISCHEMIA/REPERFUSION INSULT --- p.27, Chapter 4.1.1.1. --- Induction of retinal ischemia/reperfusion insult with transient elevated intraocular pressure (IOP) --- p.27, Chapter 4.1.1.2. --- Animal experiments --- p.28, Chapter 4.1.1.3. --- Histopathology and measurement of inner retinal thickness (IRT) --- p.28, Chapter 4.1.1.4. --- Flat preparation of the retinas and retinal ganglion cell counts (RGCCs) --- p.29, Chapter 4.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTIONS AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.30, Chapter 4.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.30, Chapter 4.1.2.2. --- In-situ terminal deoxynucleotidyl transferase (TdT)-mediated biotin- dUTP nicked end labelling (TUNEL) --- p.31, Chapter 4.1.3. --- "IMMUNOHISTOCHEMISTRY OF BCL-2, BAX AND P53" --- p.32, Chapter 4.1.4. --- "DOUBLE LABELLING OF BCL-2, BAX AND TUNEL" --- p.33, Chapter 4.1.5. --- IN-SITU REVERSE TRANSCRIPTASE - POLYMERASE CHAIN REACTION OF BCL-2 AND BAX --- p.34, Chapter 4.1.5.1. --- Primers design and specificity test --- p.34, Chapter 4.1.5.2. --- In-situ RT-PCR --- p.36, Chapter 4.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEONS (RCS) RATS --- p.38, Chapter 4.2.1. --- HISTOPATHOLOGY --- p.38, Chapter 4.2.2 --- MORPHOMETRY OF CELLS IN THE RETINAL GANGLION CELL LAYER (RGCL) AND THE INNER NUCLEAR LAYER (INL) --- p.39, Chapter 4.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.39, Chapter 5. --- RESULTS --- p.40, Chapter 5.1. --- RETINAL ISCHEMIA AND REPERFUSION INDUCED LOSS OF INNER RETINAL ELEMENTS --- p.40, Chapter 5.1.1. --- TISSUE RESPONSES IN THE RAT RETINAS AFTER TRANSIENT ELEVATED INTRAOCULAR PRESSURE INDUCED ISCHEMIA/ REPERFUSION INSULT --- p.40, Chapter 5.1.1.1. --- Histopathology --- p.40, Chapter 5.1.1.2. --- Morphometry of inner retinal thickness --- p.40, Chapter 5.1.1.3. --- Retinal ganglion cell counts (RGCCs) --- p.41, Chapter 5.1.2. --- INTERNUCLEOSOMAL DNA FRAGMENTATION AND IN SITU NICKED DNA DETECTION AT DIFFERENT TIME AFTER REPERFUSION IN THE RAT RETINAS --- p.41, Chapter 5.1.2.1. --- Enzyme-linked immunosorbent assay (ELISA) of mono- and oligonucleosomes --- p.42, Chapter 5.1.2.2. --- In situ TUNEL --- p.42, Chapter 5.1.3. --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.42, Chapter 5.1.3.1. --- Immunohistochemistry of Bcl-2 --- p.42, Chapter 5.1.3.2. --- Double labelling of Bcl-2 and TUNEL --- p.43, Chapter 5.1.3.3. --- In situ RT-PCR for bcl-2 mRNA --- p.43, Chapter 5.1.4. --- BAX AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.44, Chapter 5.1.4.1. --- Immunohistochemistry of Bax --- p.44, Chapter 5.1.4.2. --- Double labelling of Bax and TUNEL --- p.45, Chapter 5.1.4.3. --- In situ RT-PCR for bax mRNA --- p.45, Chapter 5.1.5. --- P53 IMMUNOREACTIVITY AT VARIOUS TIME AFTER REPERFUSION --- p.46, Chapter 5.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RATS --- p.47, Chapter 5.2.1. --- HISTOPATHOLOGY --- p.47, Chapter 5.2.2. --- MORPHOMETRY OF CELLS IN THE RGCL AND INL --- p.47, Chapter 5.2.3. --- IMMUNOHISTOCHEMISTRY OF BCL-2 AND BAX --- p.47, Chapter 5.2.3.1. --- Bcl-2 --- p.47, Chapter 5.2.3.2. --- Bax --- p.48, Chapter 6. --- DISCUSSION --- p.49, Chapter 6.1. --- RETINA ISCHEMIA AND REPERFUSION INDUCED LOSS OF RETINAL ELEMENTS --- p.51, Chapter 6.1.1 --- REPERFUSION TIME DEPENDENT TISSUE RESPONSES IN RAT RETINAS --- p.51, Chapter 6.1.2 --- ISCHEMIA/REPERFUSION INDUCED APOPTOSIS IN RAT RETINAS --- p.52, Chapter 6.1.3 --- BCL-2 AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.53, Chapter 6.1.4 --- BAX AND RETINAL ISCHEMIA/REPERFUSION INSULT --- p.58, Chapter 6.1.5 --- P53 AND RETINAL ISCHEMIA/REPERFUSION INJURY --- p.60, Chapter 6.2. --- LOSS OF INNER RETINAL ELEMENTS IN THE RETINAL DYSTROPHIC ROYAL COLLEGE OF SURGEON (RCS) RAT --- p.61, Chapter 6.2.1. --- HISTOPATHOLOGY AND MORPHOMETRY --- p.62, Chapter 6.2.2. --- BCL-2 --- p.63, Chapter 6.2.3. --- BAX --- p.64, Chapter 7. --- CONCLUSION --- p.65, APPENDIX A FIGURES --- p.66, APPENDIX B REFERENCES --- p.100, http://library.cuhk.edu.hk/record=b5889774, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)