Lin, Wenhua. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 162-190). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Mo Flora. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references (leaves 168-184). / ACKNOWLEDGEMENT --- p.i / ABSTRACT --- p.ii / TABLE OF CONTENTS --- p.iv / Chapter CHAPTER ONE --- INTRODUCTION / Chapter 1.1 --- Stroke as a major disabling disease --- p.1 / Chapter 1.2 --- Classification of stroke --- p.4 / Chapter 1.3 --- Risk factors attributing to stroke --- p.15 / Chapter 1.4 --- Experimental methods to induce cerebral ischemia --- p.19 / Chapter 1.4.1 --- The establishment of animal models for stroke --- p.21 / Chapter 1.4.2 --- Gerbil as a putative model --- p.25 / Chapter 1.5 --- Mechanisms of focal ischemia damage --- p.30 / Chapter 1.6 --- Potential biochemical markers for cerebral ischemia --- p.38 / Chapter 1.7 --- Aim of investigation --- p.48 / Chapter CHAPTER TWO --- MATERIALS AND METHODS / Chapter 2.1 --- Common chemicals --- p.49 / Chapter 2.2 --- Common bench solutions --- p.52 / Chapter 2.3 --- Animals / Chapter 2.3.1 --- Gerbils --- p.52 / Chapter 2.3.2 --- Rabbit --- p.53 / Chapter 2.4 --- Establishment of an animal model / Chapter 2.4.1 --- Surgical methods for common carotid artery (CCA) ligation --- p.54 / Chapter 2.5 --- Methods to determine stroke conditions of gerbils / Chapter 2.5.1 --- Ocular fundus examination --- p.56 / Chapter 2.5.2 --- Stroke index --- p.56 / Chapter 2.5.3 --- Inclined plane method --- p.59 / Chapter 2.6 --- Preparation of gerbil brain for subsequent analysis / Chapter 2.6.1 --- Preparation of gerbil brain slices --- p.61 / Chapter 2.6.2 --- "2,3,5-triphenytetrazolium chloride (TTC) for quantitative staining of brain slices" --- p.61 / Chapter 2.6.3 --- Preparation of normal and stroke gerbil brain extract --- p.62 / Chapter 2.7 --- Polyacrylamide gel electrophoresis (PAGE) using a discontinuous buffer system / Chapter 2.7.1 --- Stock reagents --- p.63 / Chapter 2.7.2 --- Separation gel preparation --- p.65 / Chapter 2.7.3 --- Stacking gel preparation --- p.66 / Chapter 2.7.4 --- Electrophoresis conditions --- p.67 / Chapter 2.7.5 --- Staining and destaining --- p.67 / Chapter 2.8 --- Two dimensional slab gel electrophoresis / Chapter 2.8.1 --- Equipment --- p.70 / Chapter 2.8.2 --- Chemical --- p.70 / Chapter 2.8.3 --- Procedure --- p.74 / Chapter 2.9 --- Production of rabbit polyclonal antibodies against isolated stroke protein / Chapter 2.9.1 --- Isolation of stroke protein band from SDS-PAGE slab gel --- p.78 / Chapter 2.9.2 --- Production of anti-stroke protein serum in rabbits --- p.79 / Chapter 2.10 --- Western blotting method / Chapter 2.10.1 --- Reagents --- p.80 / Chapter 2.10.2 --- Procedures --- p.81 / Chapter 2.11 --- Extraction of total cellular RNA by lithium chloride method / Chapter 2.11.1 --- Reagents --- p.83 / Chapter 2.11.2 --- Procedures --- p.84 / Chapter 2.11.3 --- Checking the purity of the extracted RNA --- p.85 / Chapter 2.12 --- Purification of mRNA / Chapter 2.12.1 --- Reagents --- p.85 / Chapter 2.12.2 --- Procedure --- p.86 / Chapter 2.13 --- Verification of purity of mRNA / Chapter 2.13.1 --- Reagents --- p.87 / Chapter 2.13.2 --- Procedure --- p.88 / Chapter 2.14 --- Translation of gerbil brain mRNA in reticulocyte lysates and analysis of its product by SDS PAGE / Chapter 2.14.1 --- Reagents --- p.89 / Chapter 2.14.2 --- Procedures --- p.89 / Chapter CHAPTER THREE --- ESTABLISHMENT OF AN ANIMAL STROKE MODEL / Chapter 3.1 --- Foreword --- p.92 / Chapter 3.2 --- Preliminary studies / Chapter 3.2.1 --- Introduction --- p.92 / Chapter 3.2.2 --- Results --- p.93 / Chapter 3.2.3 --- Discussion --- p.96 / Chapter 3.3 --- Survival rate analysis / Chapter 3.3.1 --- Introduction --- p.97 / Chapter 3.3.2 --- Result --- p.98 / Chapter 3.3.3 --- Discussion --- p.102 / Chapter 3.4 --- Neurologic signs of ischemia / Chapter 3.4.1 --- Introduction --- p.103 / Chapter 3.4.2 --- Result --- p.105 / Chapter 3.4.3 --- Discussion --- p.111 / Chapter 3.5 --- Ocular fundus examination / Chapter 3.5.1 --- Introduction --- p.112 / Chapter 3.5.2 --- Result --- p.114 / Chapter 3.5.3 --- Discussion --- p.116 / Chapter 3.6 --- Inclined plane method / Chapter 3.6.1 --- Introduction --- p.117 / Chapter 3.6.2 --- Result --- p.118 / Chapter 3.6.3 --- Discussion --- p.121 / Chapter 3.7 --- Histologic examination using TTC as staining agent / Chapter 3.7.1 --- Introduction --- p.122 / Chapter 3.7.2 --- Result --- p.124 / Chapter 3.7.3 --- Discussion --- p.129 / Chapter CHAPTER FOUR --- IDENTIFICATION OF ALTERED PROTEIN PATTERN IN THE - BRAINS OF STROKE GERBILS BY ELECTROPHORETIC METHODS / Chapter 4.1 --- Separation of soluble brain extracts by SDS-PAGE analysis / Chapter 4.1.1 --- Introduction --- p.130 / Chapter 4.1.2 --- Result --- p.132 / Chapter 4.1.3 --- Discussion --- p.140 / Chapter 4.2 --- Two dimensional electrophoretic analysis of soluble brain extracts from stroke gerbils / Chapter 4.2.1 --- Introduction --- p.142 / Chapter 4.2.2 --- Result --- p.143 / Chapter 4.2.3 --- Discussion --- p.148 / Chapter CHAPTER FIVE --- ISOLATION OF STROKE-ASSOCIATED PROTEIN FROM BRAINS OF STROKE GERBILS BY IMMUNOCHEMICAL METHOD / Chapter 5.1 --- Introduction --- p.149 / Chapter 5.2 --- Result --- p.151 / Chapter 5.3 --- Discussion --- p.153 / Chapter CHAPTER SIX --- DETECTION OF NEW PROTEIN TRANSLATED FROM MESSENGER RIBONUCLEIC ACID FROM BRAINS OF STROKE GERBIL / Chapter 6.1 --- Introduction / Chapter 6.1.1 --- Extraction of stroke gerbil brain messenger ribonucleic acid --- p.154 / Chapter 6.1.2 --- Translation of mRNA --- p.154 / Chapter 6.2 --- Results / Chapter 6.2.1 --- Yield of total cellular RNA --- p.157 / Chapter 6.2.2 --- Verification of purity of mRNA --- p.157 / Chapter 6.2.3 --- Autoradiographic patterns of translated proteins --- p.159 / Chapter 6.3 --- Discussion --- p.163 / Chapter CHAPTER SEVEN --- GENERAL DISCUSSION --- p.165 / BIBLIOGRAPHY --- p.168

Magnetic resonance imaging (MRI) is a valuable research and clinical imaging modality for the non-invasive detection and characterization of cerebral ischemia. Specifically, diffusion-weighted imaging (DWI), which derives image contrast based on the diffusion of endogenous water molecules, is sensitive to cerebral ischemia within minutes of the onset of stroke. In combination with perfusion-weighted imaging (PWI) and T2-weighted imaging (T2WI), DWI can be used to characterize the temporal and spatial evolution of cerebral ischemia. The primary role of this dissertation is to outline several studies that investigate DWI, PWI, and T2WI changes in a rat stroke model of transient cerebral ischemia. Secondarily, this dissertation will introduce the method and results of an experiment designed to elucidate the relative roles of the intracellular (IC) or extracellular (EC) spaces to the water diffusion coefficient changes that occur as a result of cerebral ischemia. The use of MRI to detect cerebral ischemia is well established; however, the ability to distinguish between reversibly and irreversibly damaged tissues is limited. It has been shown in temporary focal ischemia models that the DWI abnormality (manifested as an image hyperintensity in the DWI) can be resolved if reperfusion is performed soon after the onset of the stroke. Initial studies suggested that the renormalization of water diffusion was associated with permanent restoration of cellular function (i.e., infarction was prevented). However, subsequent studies demonstrated that the disappearance of the acute ischemic lesion following reperfusion is not necessarily permanent and is related to the duration of the transient insult. Following short occlusions [e.g., 10 minutes in a rat middle cerebral artery occlusion (MCAO) model], there is complete tissue renormalization and restoration of normal neurological function. In contrast, following long periods of occlusion (e.g., 90 minutes), there are areas of the brain that do not recover and progress to infarction without delay. Intermediate durations of occlusion (e.g., 30 minutes) exhibit complete renormalization in all regions of ischemia; however, following several hours there is a gradual, secondary decline of the water diffusion coefficient values within the regions initially defined as abnormal. In this dissertation, the significant temporal and spatial heterogeneity in the secondary diffusion changes will be described and evaluated. Ultimately, MR techniques may provide valuable information regarding the response of tissue to transient ischemia as well as potential avenues for therapeutic intervention, which would have major clinical benefit. The significant changes in the apparent diffusion coefficient (ADC) of water that occur in ischemic brain are still not well understood. The leading hypothesis suggests that cellular swelling associated with the failure of the ionic gradient across the cell membrane results in an increase in EC tortuosity of the diffusion paths. Another theory suggests that the influx of fast-diffusing EC water, that occurs during cellular swelling, increases the proportion of water in the IC space, which is more restricted and viscous than the EC space. The final experiment presented herein demonstrates that significant cellular swelling remains in the regions of renormalized of ischemic ADC values that occur following reperfusion in transient ischemia. In short, the changes in the ADC values are not only the result of cellular swelling. Since conventional MR data contains the combined signals from the IC and EC spaces, it is difficult to determine the separate roles of these two compartments to the overall changes in water ADC. First, using a yeast-cell model, a method for separating the NMR signals is introduced. This method utilizes differences in the compartmental relaxation properties to isolate the MR signals from IC and EC spaces, and then secondarily the diffusion coefficients can be calculated. Using a modified version of this method, the experiment was performed in normal and ischemic rat brain. Intracerebroventricular (ICV) infusion of an MR contrast reagent (CR) was used to isolate IC T1, T2, and ADC values in vivo in normal and middle cerebral artery occluded (MCAO) rats using volume-localized, diffusion-weighted inversion-recovery spin-echo (DW-IRSE) spectroscopy and diffusion-weighted echo-planar imaging (DW-EPI). The presence of the EC contrast reagent (CR) selectively enhances the relaxation of water in the EC space and allows the IC and EC signal contributions to be separated based on T1-relaxation time differences between the two compartments. The results presented in this dissertation suggest that the IC ADC value is the major determinant of the overall ADC value measured in the normal rat brain. Further, the data suggests that the ADC decline experienced during acute ischemia is dictated largely by changes in the IC ADC, possibly due to failure of energy-dependent IC microcirculation (cytoplasmic streaming).

Acute myocardial infarction (AMI) rat model was adopted to test the effect of AngioT in vivo. AngioT was directly injected into the ischaemic region of the left ventricle immediately after the ligation of left anterior descending artery. The densities of vessels in AngioT treated hearts were on average 3-4 folds higher compared with non-treated hearts after two and seven days post infarction. Using TUNEL method, approximately 3-fold lower numbers of apoptotic cardiomyocytes were detected in AngioT treated AMI hearts compared with controls. The infarcted volume estimated by Masson's Trichrome staining was significantly decreased in AngioT treated hearts (27.44%+/-7.34% vs. 39.53%+/-5.97%, p<0.05) compared with control hearts 14 days post infarction. Echocardiography demonstrated that left ventricular ejection fraction and fraction shortening in AngioT treated hearts were significantly improved by 10.4% and 22.3% compared to those in the control hearts 2-day post infarction (p<0.05). These improvements were maintained for 2-week post infarction. / Based on the analysis of rat angiogenesis specific superarray, VEGFb, VEGFc and FGF7, were found to be highly expressed in AngioT treated AMI hearts compared to the controls. The expression levels of survival related genes Bcl2 and Akt1 were increased to 3.3 and 2.8 folds respectively in AngioT treated AMI hearts compared with the controls (both p<0.05). Based on the signal transduction pathway finder superarray, Jak-Stat pathway activators, Interleukin 4 receptor and Interferon regulatory factor 1 (IL4R and IRF1), were found to be highly expressed in the AngioT treated AMI heart. / In conclusion, bioactive angiogenic factors (AngioT) were isolated from Geum. japonicum Thunb. Var. Chinense F. Bolle (GJ). Intra-cardiomuscular injection of AngioT had beneficial effects on the acute myocardial infarction. The underlying mechanisms might be related to the activation of Jak-Stat Pathway and over expressions of angiogenic factors and survival associated genes. The therapeutic properties of AngioT appear entirely novel and may provide a new dimension for therapeutic angiogenesis for the treatment of acute ischaemic heart disease. / In the present study, an angiogenic tannins fraction (AngioT) was isolated from Geum. japonicum Thunb. Var. Chinense F. Bolle using bio-assay guided strategy. AngioT increased the proliferation of human umbilical vein endothelial cell (HUVEC) in culture within 24-hour, 48-hour and 72-hour treatment in a dose-dependent pattern. The EC50 of AngioT on HUVEC was less than 25mug/ml. Conditional media from AngioT treated HUVEC stimulated the proliferation of HUVEC significantly greater than conditional media from non-treated HUVEC. Using 2-dimensional electrophoresis and MALDI-TOF, VEGFa was identified in the AngioT treated conditional medium. / Ischaemic heart disease remains the leading cause of morbidity and mortality in most countries. Severe ischaemia of myocardium induces myocardial infarction and results in an irreversible loss of myocardium. Restoration of coronary blood flow by rapid angiogenesis may offer a direct and effective therapeutic way to intractable ischaemic heart diseases. / Key words. ischaemic heart disease; myocardial infarction; therapeutic angiogenesis; Geum japonicum; apoptosis; tannins; VEGF; Jak-Stat pathway / Gu, Xuemei. / "Sep 2007." / Adviser: Peter Tong Chun Yip. / Source: Dissertation Abstracts International, Volume: 69-08, Section: B, page: 4615. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (p. 159-177). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

Lam, Ming Yiu. / "September 2011." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 149-169). / Abstracts in English and Chinese. / Thesis / Assessment Committee --- p.ii / Abstract (English) --- p.iii / Abstract (Chinese) --- p.vi / Acknowledgements --- p.viii / Table of contents --- p.x / List of figures --- p.xvi / List of tables --- p.xix / Abbreviations --- p.xx / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Cerebral stroke --- p.1 / Chapter 1.2 --- Epidemiology --- p.2 / Chapter 1.3 --- Risk factors and symptoms --- p.5 / Chapter 1.3.1 --- Non-modifiable risks --- p.5 / Chapter 1.3.2 --- Modifiable risks --- p.6 / Chapter 1.3.3 --- Symptoms --- p.9 / Chapter 1.4 --- Mechanisms of cell injury --- p.10 / Chapter 1.4.1 --- Energy failure and loss of ionic homeostasis --- p.10 / Chapter 1.4.2 --- Excitotoxicity and calcium-modulated cell damage --- p.11 / Chapter 1.4.3 --- Oxidative stress --- p.13 / Chapter 1.4.4 --- Inflammation --- p.16 / Chapter 1.4.5 --- Apoptosis --- p.18 / Chapter 1.5 --- Current treatment of ischemia --- p.19 / Chapter 1.6 --- Chinese herbal medicine --- p.21 / Chapter 1.6.1 --- Traditional Chinese medicine theory on stroke --- p.21 / Chapter 1.6.2 --- Danshen --- p.22 / Chapter 1.6.3 --- Gegen --- p.25 / Chapter 1.6.4 --- Danshen-Gegen formula --- p.28 / Chapter 1.7 --- Aim of study --- p.30 / Chapter Chapter 2 --- General methodology --- p.31 / Chapter 2.1 --- Induction of transient focal cerebral ischemia by middle cerebral artery occlusion (MCAO) --- p.31 / Chapter 2.1.1 --- Intraluminal filament production --- p.32 / Chapter 2.1.2 --- Cerebral blood flow measurement by laser Doppler flowmetry --- p.33 / Chapter 2.1.3 --- Middle cerebral artery occlusion --- p.35 / Chapter 2.2 --- Neurological scoring --- p.38 / Chapter 2.3 --- Brain infarction measurement by triphenyltetrazolium chloride (TTC) staining --- p.40 / Chapter 2.4 --- Statistical analyses --- p.42 / Chapter Chapter 3 --- Preparation of herbal medicine --- p.43 / Chapter 3.1 --- Authentication of Chinese herbs --- p.43 / Chapter 3.1.1 --- Morphological authentication --- p.43 / Chapter 3.1.2 --- Chemical authentication using thin layer chromatography --- p.44 / Chapter 3.1.2.1 --- Danshen --- p.44 / Chapter 3.1.2.2 --- Gegen --- p.48 / Chapter 3.2 --- Danshen-Gegen (DG) extract preparation --- p.50 / Chapter 3.3 --- Chemical analysis of DG extract --- p.51 / Chapter 3.3.1 --- TLC --- p.51 / Chapter 3.3.2 --- HPLC --- p.54 / Chapter 3.4 --- Conclusion --- p.57 / Chapter Chapter 4 --- Protective effect of DG extract on cerebral ischemia --- p.58 / Chapter 4.1 --- Introduction --- p.58 / Chapter 4.1.1 --- Different models of ischemia --- p.58 / Chapter 4.1.2 --- Anti-oxidative enzymes in cerebral ischemia --- p.61 / Chapter 4.1.2.1 --- Superoxide dismutase (SOD) --- p.61 / Chapter 4.1.2.2 --- Catalase --- p.62 / Chapter 4.1.2.3 --- Glutathione peroxidase (GPX) --- p.62 / Chapter 4.2 --- Materials and methods --- p.64 / Chapter 4.2.1 --- "DG extract treatment, neurological deficit and brain infarction" --- p.64 / Chapter 4.2.2 --- Anti-oxidative enzymes activity determination --- p.65 / Chapter 4.2.2.1 --- Treatment with DG extract and induction of cerebral ischemia --- p.65 / Chapter 4.2.2.2 --- Extraction of enzymes from the brain --- p.66 / Chapter 4.2.2.3 --- Determination of protein concentration --- p.66 / Chapter 4.2.2.4 --- Assay kits --- p.67 / Chapter 4.3 --- Results --- p.70 / Chapter 4.4 --- Discussion --- p.80 / Chapter 4.4.1 --- Neurological score and percentage brain infarction --- p.80 / Chapter 4.4.2 --- Anti-oxidative enzyme induction --- p.82 / Chapter Chapter 5 --- Behavioral assessment using the shuttle box avoidance test on rats suffering from cerebral ischemia: effect of DG extract treatment --- p.86 / Chapter 5.1 --- Introduction --- p.86 / Chapter 5.1.1 --- Behavioral tests --- p.86 / Chapter 5.1.2 --- Theory of the test --- p.90 / Chapter 5.2 --- Materials and methods --- p.91 / Chapter 5.2.1 --- DG extract treatment --- p.91 / Chapter 5.2.2 --- Shuttle box training and MCAO --- p.92 / Chapter 5.2.3 --- Shuttle box testing --- p.96 / Chapter 5.2.4 --- Neurological score and brain infarction --- p.96 / Chapter 5.3 --- Results --- p.97 / Chapter 5.3.1 --- Shuttle box performance --- p.97 / Chapter 5.3.2 --- Neurological score --- p.105 / Chapter 5.3.3 --- Brain infarction --- p.109 / Chapter 5.4 --- Discussion --- p.112 / Chapter 5.4.1 --- The shuttle box protocol --- p.112 / Chapter 5.4.2 --- Shuttle box performance --- p.114 / Chapter 5.4.2.1 --- Pretreatment groups --- p.114 / Chapter 5.4.2.2 --- Pre + post treatment groups --- p.115 / Chapter 5.4.2.3 --- Comparison of pretreatment and pre + post treatment groups --- p.116 / Chapter 5.4.3 --- Neurological score --- p.117 / Chapter 5.4.4 --- Brain infarction --- p.118 / Chapter 5.4.5 --- Conclusion --- p.119 / Chapter Chapter 6 --- Anti-blood coagulation effect of DG extract --- p.121 / Chapter 6.1 --- Introduction --- p.121 / Chapter 6.2 --- Materials and methods --- p.125 / Chapter 6.2.1 --- Treatment with DG extract and warfarin --- p.125 / Chapter 6.2.2 --- Tail bleeding time and volume --- p.126 / Chapter 6.2.3 --- Prothrombin time --- p.127 / Chapter 6.2.4 --- Platelet aggregation --- p.127 / Chapter 6.3 --- Results --- p.128 / Chapter 6.4 --- Discussion --- p.138 / Chapter Chapter 7 --- General discussion --- p.141 / Chapter 7.1 --- General discussion and conclusion --- p.141 / Chapter 7.2 --- Clinical significance of the study --- p.145 / Chapter 7.3 --- Limitations of the study --- p.146 / Chapter 7.4 --- Future work --- p.147 / References --- p.149 / Publications --- p.170

Thesis (M.Sc.)--Memorial University of Newfoundland, 2005. / Bibliography: leaves 31-42.

Background:     The microdialysis (MD) technique is widely spread and used both experi­mentally and in clinical practice. The MD technique allows continuous collection of small molecules such as glucose, lactate, pyruvate and glycerol. Samples are often analysed using the CMA 600 analyser, an enzymatic and colorimetric analyser.  Data evaluating the performance of the CMA 600 analysis system and associated sample han­dling are sparse. The aim of this work was to identify sources of variability related to han­dling of microdialysis samples and sources of error associated with use of the CMA 600 analyser. Further, to develop and compare different application techniques of the micro­dialysis probes both within an organ and on the surface of an organ.  Material and Methods:  Papers I and II are mainly in vitro studies with the exception of the No Net Flux calibration method in paper I where a pig model (n=7) was used to exam­ine the true concen­tration of glucose and urea in subcutaneous tissue. Flow rate, sampling time, vial and caps material and performance of the analyser device (CMA 600) were examined. In papers III and IV normoventilated anaesthetised pigs (n=33) were used. In paper III, heart ischemia was used as intervention to compare microdialysis measurements in the myocardium with corresponding measurements on the heart surface. In paper IV, microdialysis measurements in the liver parenchyma were compared with measurements on the liver surface in associa­tion with induced liver ischemia. All animal studies were approved by the Animal Experi­mental Ethics Committee at Umeå University Sweden. Results:  In paper I we succeeded to measure true concentrations of glucose (4.4 mmol/L) and Urea (4.1 mmol/L) in subcutaneous tissue. Paper II showed that for a batch analyse of 24 samples it is preferred to store microdialysis samples in glass vials with crimp caps. For reliable results, samples should be centrifuged before analysis. Paper III showed a new application area for microdialysis sampling from the heart, i.e. surface sampling. The sur­face probe and myocardial probe (in the myocardium) showed a similar pattern for glucose, lactate and glycerol during baseline, short ischemic and long ischemic interventions. In paper IV, a similar pattern was observed as in paper III, i.e. data obtained from the probe on the liver surface showed no differences compared with data from the probe in liver paren­chyma for glucose, lactate and glycerol concentrations during baseline, ischemic and reperfusion interven­tions. Conclusion:  The MD technique is adequate for local metabolic monitoring, but requires methodological considerations before starting a new experimental serie. It is important to consider factors such as flow rate, sampling time and handling of samples in association with the analysis device chosen. The main finding in this thesis is that analyses of glucose, lactate and glycerol in samples from the heart surface and liver surface reflect concentra­tions sampled from the myocardium and liver parenchyma, respectively.

Thesis (Ph.D.)--Indiana University, 2009. / Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).

Dissertation (Ph.D.)--University of South Florida, 2008. / Includes vita. Includes bibliographical references. Also available online.

published_or_final_version / Paediatrics and Adolescent Medicine / Doctoral / Doctor of Philosophy