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This study was designed to follow up a chance observation in patients with an admission white blood cell (WBC) count showing an absolute lymphocytosis and relative neutropenia that changed to a lymphopenia and neutrophilia within 24 hours. As 15 of the 20 patients were admitted following trauma, we examined this association further by reviewing charts of 69 patients who had sustained stab wounds to the chest and abdomen. A prospective study involving 40 patients in the Intensive Care Unit was also undertaken because of the related hypothesis that the Adult Respiratory Distress Syndrome (ARDS) is associated with sequestration of complement activated polymorphonuclear leukocytes (PMN) by the lung. These studies show that trauma is frequently associated with a lymphocytosis and relative neutropenia. In cases where ARDS did develop, the onset of respiratory failure was associated with a profound fall in the circulating PMN count. To test the hypothesis that these leukocyte changes were due to catecholamine release and sequestration of PMN within the pulmonary micro-vasculature, we studied the effects of epinephrine infusion, lowered cardiac output and complement activation on WBC uptake and release from the dog lung. The data show that pulmonary blood flow has a marked effect on the uptake and release of WBC by the lung but has no effect on differential counts. Epinephrine infusion increases circulating WBC counts but also does not alter differential counts. In contrast, activation of the complement cascade alters differential values by causing preferential sequestration of PMN. We conclude that trauma is frequently associated with a lymphocytosis and relative neutropenia and speculate that this phenomenon is due to a combination of catecholamine release and sequestration of PMN within pulmonary and systemic microvasculatures. The findings that a profound fall in PMN counts occurs prior to the onset of ARDS and after activation of the complement pathway with cobra venom factor support the hypothesis that complement activated PMN play a role in the pathogenesis of ARDS. These data also suggest that prospective leukocyte counts may be a useful predictor with respect to determining which patients will develop this syndrome. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

Class of 2012 Abstract / Specific Aims: The objective of this study is to evaluate and compare clinical outcomes and economic impact involved with the use of beractant (B) compared to poractant (P) for the treatment of respiratory distress syndrome (RDS) in premature neonates admitted to a neonatal intensive care unit. Methods: Patients were included if they were less than 35 weeks gestational age at birth, survived at least 48 hours, and admitted to the neonatal intensive care unit and treated with P or B for RDS. The primary outcome of this study is the change in the fraction of inspired oxygen (FiO2) over the first 48 hours after surfactant administration. Secondary outcomes were the change in oxygen saturation, time spent on mechanical ventilation and continuous positive airway pressure (CPAP), complication occurrence and mortality of the neonates. Main Results: There were a total of 40 neonates whose charts were reviewed (n= 13 and n=27 in the P and B groups respectively). The mean gestational age of the neonates were 29.2+/-2.9 and 28.8+/-2.9 weeks in the P and B groups respectively. The FiO2 was found to not be lower between the P and B groups (35.5+/-22.2 and 42.4+/-24.2, respectively; p=0.379), as well as the O2 saturation (94.6+/-4.6 and 92.3+/-6.1; p=0.194). Significance was also not found for the other clinical or economic outcomes assessed in this study. Conclusions: There was not a significant difference between poractant and beractant in FiO2, O2 saturation, or in the other clinical outcomes evaluated in this study.

Gu Jia-Shi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 117-148). / Abstracts in English and Chinese. / Title --- p.i / Abstract (English) --- p.iii / Abstract (Chinese) --- p.iv / Acknowledgments --- p.v / Statement of Originality --- p.vi / List of Abbreviations --- p.viii / List of Figures --- p.xi / List of Tables --- p.xiii / Table of Contents --- p.xiv / Chapter Section One : --- Introduction & Literature Review / Introduction & Objective --- p.2 / Introduction / Objective of the present study / Chapter Chapter. 1 --- A Review of Chronic lung disease (CLD) --- p.6 / Chapter 1. --- BPD 226}0ؤ an example of CLD / Chapter 2. --- Pathological change & Clinical presentation / Chapter 3. --- Clinical sequel of CLD infants / Chapter 3.1 --- O2 consumption of CLD infants / Chapter 3.1-1 --- Oxygen consumption / Chapter 3.1-2 --- Oxygen transportation / Chapter 3.1-2a --- Dissolved O2 / Chapter 3.1-2b --- Haemoglobin / Chapter 3.2 --- Energy expenditure of CLD infants / Chapter 3.3 --- Growth rate of CLD infants / Chapter 4. --- Treatment & Management of CLD infants / Chapter 4.1 --- Diuretics / Chapter 4.2 --- Bronchodilators / Chapter 4.3 --- Corticosteroids / Chapter 5. --- "Interpretations of the observed phenomena, why does CLD impair growth?" / Chapter 5.1 --- The traditional view / Chapter 5.2 --- Disagreement with the traditional view / Chapter Chapter 2 --- Measurement of oxygen consumption --- p.20 / Chapter 1. --- Invasive measurement of VO2 / Chapter 1.1 --- Cardiac output / Chapter 1.2 --- Fick method / Chapter 1.3 --- Advantages and Disadvantages of Fick method in estimating VO2 / Chapter 1.4 --- Measurement of cardiac output by thermodilution / Chapter 1.4-1 --- Advantages and Disadvantages of Thermodilution Method / Chapter 2. --- Non-invasive measurement of VO2 / Chapter 2.1 --- Metabolic analyzer---DeltatraćёØII / Chapter 2.2 --- Paramagnetic sensor / Chapter 3. --- Measured and calculated oxygen consumption / Chapter 3.1 --- Difference between mVO2 and cVO2 / Chapter 4. --- Summary / Chapter Chapter 3 --- Hypothesis --- p.34 / Chapter 1. --- Possible explanations for the difference between mV02 & cV02 / Chapter 1.1 --- Measurement variability and Mathematical error / Chapter 1.2 --- Oxygen consumption of the lung / Chapter 1.3 --- VO2pul with lung damage / Chapter 1.4 --- "Neutrophils, Macrophages and oxygen consumption" / Chapter 2. --- Hypothesis / Chapter Section Two : --- Methods & Materials / Chapter Chapter 1 --- Animal Model --- p.41 / Chapter Chapter 2. --- Materials --- p.43 / Chapter 1. --- Animals / Chapter 2. --- Chemicals used for inducing lung damage / Chapter 2.1 --- Acute damage group / Chapter 2.1-1 --- N-nitroso-N-methylurethane (NNNMU) / Chapter 2.1-2 --- Administrations to rabbits / Chapter 2.2 --- Chronic damage group / Chapter 2.2-1 --- Bleomycin (BLM) / Chapter 2.2-2 --- Pulmonary toxicity of Bleomycin / Chapter 2.2-3 --- Administration to animals / Chapter Chapter 3 --- Instruments --- p.50 / Chapter 1. --- Measurement of VO2 and VCO2 226}0ؤDeltatracIÍёØ Metabolic analzyer / Measurement of cardiac outpu´tؤCardiomax II model85 / Chapter Chapter 4 --- Methods --- p.58 / Chapter 1. --- N-nitroso-N-methylurethane (NNNMU) Preparation / Chapter 2. --- Bleomycin Preparation / Chapter 3. --- 2.5% pentobarbitone Preparation / Chapter 4. --- Animal Preparation / Chapter 4.1 --- Control (Normal) group / Chapter 4.2 --- A cute lung damage group / Chapter 4.3 --- Chronic lung damage group / Chapter 5. --- Preparation of the animals for VO2 measurement / Chapter 6. --- Measurement of oxygen consumption / Chapter 6.1 --- VO2wb measurement / Chapter 6.2 --- VO2b measurement / Chapter 7. --- Histopathology / Chapter 8. --- Statistics / Chapter Section Three : --- Results --- p.69 / Chapter 1. --- Healthy (Control) group / Chapter 1.1 --- Pulmonary histology / Chapter 2. --- Acute lung damage group / Chapter 2.1 --- Pulmonary histology / Chapter 3. --- Chronic lung damage group / Chapter 3.1 --- Pulmonary histology / Chapter 4. --- Comparison of the pulmonary oxygen consumption among the three groups / Chapter Section Four : --- Discussion --- p.97 / Chapter Section Five : --- Conclusion --- p.111 / Chapter Section Six : --- Future Studies --- p.114 / Chapter Section Seven : --- Bibliography --- p.118

Given that pandemic swine flu outbreak led to substantial admission in intensive care unit, extracorporeal membrane oxygenation has been increasingly applied to those who suffered from H1N1 infection induced acute respiratory distress syndrome. This review is going to evaluate the effectiveness of using ECMO based on five related observational studies. The result, discussion and policy implication in Hong Kong are discussed. Since the ECMO system has been technological improved in recent years, there are less complications when applying ECMO. In view of evidence of reviewed studies, application of ECMO in Hong Kong can be considered as cost effective. And since only a few hospitals in Hong Kong can offer ECMO application, retrieval teams are needed to ensure safety transfer between hospitals. / published_or_final_version / Public Health / Master / Master of Public Health

Acute Respiratory Distress Syndrome (ARDS) is the most extreme form of acute lung injury and continues to have a significant morbidity and mortality. Unfortunately, the mechanisms involved in the recovery and repair of the lung following ARDS remain poorly understood. An understanding of these is pivotal to improving outcome from acute lung injury. Several observational studies have suggested a potential relationship between Vascular Endothelial Growth Factor (VEGF) in the lung and the development/outcome of ARDS. In this thesis, three potential mechanisms underlying these observations have been explored: 1. What is the anatomical distribution of VEGF receptor and isoform expression in normal and ARDS lung? How does this change at early and later time points following acute lung injury? 2. Are human type 2 alveolar epithelial (ATII) cells a source of and target for VEGF? How does exposure to a pro-inflammatory milieu modify their expression of VEGF isoforms and receptors? 3. Is there a relationship between a functional VEGF polymorphism and susceptibility to developing and severity of ARDS? I have demonstrated VEGF receptor expression on both sides of the alveolarcapillary membrane with upregulation in later ARDS. All three principal isoforms (VEGF121, VEGF165 and VEGF189) are expressed in normal human lung with uniform downregulation of all three in early ARDS, which normalises with increasing time following injury. I have not found any evidence of VEGF isoform switching. I have also demonstrated human ATII cells are both a significant cellular source of and a target for VEGF (via VEGF receptor expression) confirming autocrine VEGF activity in the lung. VEGF is an ATII cell survival factor. ATII cells differentially respond to pro-inflammatory stimuli by increasing VEGF isoform but not receptor expression, which may serve as a regulatory control mechanism. Finally, I have demonstrated the VEGF 936 T allele increases susceptibility to and the severity of lung injury. The T allele is associated with an increase in plasma VEGF level in ARDS patients but intra-alveolar levels are unaffected.

Neonatal respiratory distress syndrome (RDS) is a disease that affects premature infants born prior to 32 weeks gestation. The main cause is a deficiency in pulmonary surfactant due to immature type II pneumocyte cells found in the alveoli. These cells are not capable of producing the required surfactant which normally functions to reduce the surface tension at the air-liquid interface of the lungs, as well as reduce the work of breathing and prevent alveolar collapse. A current treatment method for RDS is exogenous surfactant replacement therapy involving application of an exogenous surfactant preparation directly into the lungs of premature infants. Current surfactant preparations are animal-derived and very costly. Synthetic preparations, on the other hand, are an attractive alternative. The goal of this research is to synthesize a diether phosphonolipid analogue of dipalmitoyl phosphatidylcholine (DPPC), designated DEPN-8. When incorporated into a synthetic exogenous surfactant mixture, DEPN-8 exhibits greater adsorption and surface activity compared to its natural counterpart, DPPC. The synthesis of several components related to the re-tailored synthesis of DEPN-8 will be presented and discussed below. / National Institute of Health, NSERC

Diss. (sammanfattning) Umeå : Univ., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 5 uppsatser.