Rocket plume flowfields have an importance due to their influence on the signature of the rocket and also on the distribution of the plume gases around the vehicle. Little information on the co-flowing situation exists other than a previous study at Oxford. This thesis thus represents a significant database for co-flowing rocket plumes of this form. The work presented deals with two new aspects of co- flowing rocket plumes in that detailed flowfield measurements have been made and plumes from twin nozzle have been investigated for the first time in this thesis. This study on twinjet rocket plumes was carried out using the University of Oxford Gun Tunnel. Twinjet rockets with nozzle exit Mach numbers of 3 and 5 were tested in quiescent and in co-flow at Mach 7 using nitrogen and hydrogen injections. A major feature of the twinjet case was the so-called impingement shock between the flows from the two nozzles. It was discovered that this shock was insensitive to the freestream and scaling parameters are suggested for its geometry. Comparisons with single equivalent thrust nozzles are made at downstream locations and similar Pitot pressure profiles were observed for nitrogen injection in a nitrogen freestream after approximately 3 nozzle diameters downstream. Shear layers were studied and fluctuations in this region were measured by fast-response Pitot pressure and heat transfer probes sampled at 1.1 MHz. The extent of the shear layer was deduced using a new Oxford Total Temperature Probe. With the freestream stagnation temperature at approximately 650 K and injected gas at 350 K, a linear variation for the deduced total temperature across the shear layer was obtained. This was consistent with the Pitot pressure variations across this region. Convective heat transfer coefficient fluctuations and flow total temperature fluctuations across rocket flowiields were obtained using three thin-film heat transfer probes and found to be closely correlated. Experimental results for the twinjet and the single jet were compared with CFD simulations and good overall agreements were achieved. Instrumentation for the hypersonic experiments was investigated and a fast-response (~ 20 kHz) Pitot probe suited for flows heavily contaminated with particulate was developed and tested.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 185-195).

Thesis (M.Sc.)--Aberdeen University, 2008. / Title from web page (viewed on June 1, 2009). Includes bibliographical references.

Thesis (M. S.)--Earth and Atmospheric Sciences, Georgia Institute of Technology, 2006. / Dickinson, Robert, Committee Chair ; Fu, Rong, Committee Co-Chair ; Yu, Hongbin, Committee Member.

Thesis (Ph.D.)--OGI School of Science & Engineering at OHSU, July 2006. / Includes bibliographical references (leaves 97-114).

abstract: Smoke entering a flight deck cabin has been an issue for commercial aircraft for many years. The issue for a flight crew is how to mitigate the smoke so that they can safely fly the aircraft. For this thesis, the feasibility of having a Negative Pressure System that utilizes the cabin altitude pressure and outside altitude pressure to remove smoke from a flight deck was studied. Existing procedures for flight crews call for a descent down to a safe level for depressurizing the aircraft before taking further action. This process takes crucial time that is critical to the flight crew's ability to keep aware of the situation. This process involves a flight crews coordination and fast thinking to manually take control of the aircraft; which has become increasing more difficult due to the advancements in aircraft automation. Unfortunately this is the only accepted procedure that is used by a flight crew. Other products merely displace the smoke. This displacement is after the time it takes for the flight crew to set up the smoke displacement unit with no guarantee that a flight crew will be able to see or use all of the aircraft's controls. The Negative Pressure System will work automatically and not only use similar components already found on the aircraft, but work in conjunction with the smoke detection system and pressurization system so smoke removal can begin without having to descend down to a lower altitude. In order for this system to work correctly many factors must be taken into consideration. The size of a flight deck varies from aircraft to aircraft, therefore the ability for the system to efficiently remove smoke from an aircraft is taken into consideration. For the system to be feasible on an aircraft the cost and weight must be taken into consideration as the added fuel consumption due to weight of the system may be the limiting factor for installing such a system on commercial aircraft. / Dissertation/Thesis / M.S.Tech Mechanical Engineering 2013

Cigarette smoke is the leading cause of preventable mortality worldwide. This excess death is attributable to an increased risk of acquiring a variety of conditions, including chronic respiratory/cardiovascular diseases and various types of cancer. Smokers are additionally predisposed to develop infectious diseases, notably including pneumonia caused by the influenza virus, one of the most prevalent and burdensome pathogens in existence today. Although cigarette smoke is well known to modulate many aspects of the immune system, the specific mechanisms by which this predisposition is mediated are incompletely understood. Also unclear is the effect of cigarette smoke on responses to intranasal immunization strategies aimed at eliciting immunity against pathogens such as influenza in the upper airways, where protection may substantially contribute to sterilizing immunity. This PhD thesis focused primarily on addressing these knowledge gaps. In the first study, we assessed the effect of cigarette smoke on antibody induction following intranasal immunization in the upper airways of mice, finding that smoke exposure attenuated antigen-specific IgA induction in the upper respiratory tract, reproductive tract, and systemic circulation. In addition, we found that these nasal IgA demonstrated a reduced antigen-binding avidity in the acute post-immunization period. Mechanistically, deficits in nasal IgA were associated with a reduced accumulation of antigen-specific IgA antibody-secreting cells (ASCs) in the nasal mucosa, induction of these cells in nasal-draining lymphoid tissues, and upregulation of molecules critical to ASC homing (vascular cell adhesion molecule-1; VCAM-1) and IgA transepithelial transport (polymeric immunoglobulin receptor; pIgR) in the nasal mucosa. Ultimately, in tandem with recent clinical work published by others, our study strongly suggests that cigarette smoke can attenuate IgA induction in the upper airways, which may have implications for aspects of intranasal vaccine efficacy. Thus, smoking status should be more consistently considered in the design of clinical trials for IgA-oriented intranasal vaccines. The second study did not assess smoking and host defense directly, but rather served to optimize protocols for assessing immunoglobulins in human mucoid respiratory samples as a precursor to future studies in smoking-related disease. In this regard we found that, relative to phosphate-buffered saline (PBS), dithiothreitol (DTT)-based processing of human sputum samples increased total IgA yields, decreased IgE yield, and improved the detection of a specific IgG autoantibody. These findings suggest that processing choices for human mucoid respiratory samples should be made with specific goals in mind as they pertain to antibody isotype(s) of interest. Finally, in the third study we investigated potential mechanisms by which cigarette smoke exposure promotes influenza, given that smokers are at increased risk of acquiring the pathogen, progressing to severe disease, and being admitted to hospital/ICU following infection. In doing so, we found that concurrent smoke exposure increased morbidity, hypoxemia, pulmonary edema, neutrophilia, and ultimately mortality in a mouse model of H1N1 infection. These changes were associated with an increased accumulation of viral (v)RNA in cells independent of any change in the shedding of replication-competent viral particles. Using a novel dysregulation score approach, we found that interleukin (IL)-6 and colony-stimulating factor (CSF)3 expression was highly exacerbated in the lungs and circulation of smoke-exposed, infected mice relative to controls. Supplementation of recombinant (r)CSF3 increased morbidity, hypothermia and edema, while blockade of the cognate receptor (CSF3R) improved alveolar-capillary barrier function. On the cellular level, single cell RNA-sequencing revealed a shift in the distribution of Csf3+ cells towards neutrophils. Finally, deep transcriptional analysis of neutrophils revealed a gene signature that was largely indicative of an exacerbated form of typical disease with select unique regulatory elements. Ultimately, this work identifies potential therapeutic targets (CSF3R signaling, excess vRNA accumulation) for the treatment of cigarette smoke-augmented influenza, and warns against clinical rCSF3 therapy to treat neutropenia during viral infectious disease. In conclusion, the work presented in this PhD dissertation expands our understanding of the relationship between cigarette smoke and antimicrobial host defense as it pertains to both IgA immunity in the upper airways, and the pathogenesis of cigarette smoke-augmented influenza. / Thesis / Doctor of Philosophy (PhD) / Cigarette smoke exposure is well known to have many harmful effects on human health, including through its ability to promote various infectious diseases such as influenza. However, the mechanisms by which it promotes infection are not fully known. This is an important knowledge gap given that over 1.1 billion individuals continue to smoke worldwide, and a large number of people are exposed to the harmful effects of second-hand smoke, both with fatal consequence. The central goal of this thesis was to gain a better understanding of this relationship between cigarette smoke and infectious disease, specifically by assessing how smoke exposure impacts immune responses in the upper and lower airways. In the first study, we found that smoke exposure interferes with the ability to activate immunoglobulin (Ig)A antibody responses in the nasal passages of mice, which may have important implications for human nasal vaccination strategies. The second study investigated different methods with which to best measure antibodies in human respiratory samples. Finally, in the third study we defined a role for a specific molecule, CSF3, in worsening health in a mouse model of concurrent cigarette smoke and influenza infection. Overall, this work provides new insights into the ways in which smoking can increase the risk of respiratory infection, thereby informing the future design and testing of vaccines and treatments for use in our highly smoke-exposed global population.

No description available.

This work is an experimental and theoretical analysis of factors and conditions affecting smoke and carbon monoxide (CO) production in corridor-like enclosure fires. Thirty eight experiments were performed in a three metre long corridor-like enclosure having a cross section 0.5 m x 0.5 m, door-like openings in the front panel and a propane gas burner located near the closed end. Measurements of smoke and carbon monoxide concentrations were performed at locations inside the enclosure and also in the exhaust duct of a hood collecting the combustion products. The main conclusion of this work is that smoke production depends not only on the fuel and Global Equivalence Ratio (GER) - as is reported in the literature - but also on the temperatures and residence time inside the enclosure, at least for the experimental conditions examined in this study. Additionally, it was found that the smoke concentration inside the enclosure was increasing during the ventilation controlled regime even after external burning started. Such increase was verified by temperature, smoke and velocity measurements inside the enclosure. The increase was due to reverse flow behind the flames travelling along the corridor. Namely, the gases reversed direction behind the flames with hot gases travelling in the upper layer backwards towards the closed end of the corridor in contrast to hot gas movements towards the opening in front of the flames. This recirculation was confirmed by velocity and oxygen concentration measurements in the upper and lower layers inside the enclosure. In addition, the present results show that the relationship reported in the literature between smoke and carbon monoxide production during overventilated conditions yco/ys ≈ constant, is no longer valid during an underventilated enclosure fire. The ratio yco/ys increases for the Global Equivalence Ratios of the enclosure greater than one. The obtained results are useful for CFD validation and specifically applicable for assessing smoke hazards in corridor fires in buildings where smoke concentrations can be much larger than anticipated owing to leakage to adjacent rooms behind travelling flames.

published_or_final_version / Mechanical Engineering / Doctoral / Doctor of Philosophy