In this investigation, two separate methods for determining oxygen transfer rates were applied to the oxidation ditches of an activated sludge plant. Steady state oxygen uptake rate testing and an oxygen mass balance technique were used to propose an in-process procedure for monitoring aeration efficiency using available resources. Although some overall averages offered promise, the testing results revealed that the mass balance analysis yielded results that do not accurately represent the oxygen transfer capabilities within the individual reactors due to shared variables that control the oxygen transfer rate. The steady state method provided more favorable results. Overall averages of daily oxygen transfer rates determined using the steady state method displayed a ratio of oxygen transfer rate between the reactors that corresponds to the expected ratio of 5/6 derived from the linear feet of aerator rotor present in each reactor.

The primary goal of this study was to evaluate a new device and system, designed to optimize the performance of standard low pressure air diffusers in two types of aerated systems (activated sludge and aerobic sludge digestion) and to decrease overall energy consumption. Aerated treatment systems are very important in the treatment of wastewaters and management of sludges. The activated sludge process is widely used to treat wastewater from both industrial and municipal sources. However, they are costly to operate because oxygen is marginally soluble in water and standard low pressure (8 psig) diffusers provide marginal mixing and minimum retention. The newly patented device is referred to as TotalMix and is a type of pneumatic mixing system. TotalMix introduces air under high pressure at regular fixed intervals. During the tests the frequency of air delivered, the pressure, and the period of pressured air delivery was varied manually or through feedback control to optimize oxygen transfer and the interaction with a regular aeration system. Various chemical parameters, most importantly dissolved oxygen, were measured and compared to the new approach, using the TotalMix in combination with standard diffuser systems. The new System was tested in different sized tanks (17,000 L and 380,000 L), different concentrations of total solids (TS), using different airflow rates and different diffusers (membrane fine bubble diffusers, ceramic fine bubble diffuser, and course bubble diffuser). The statistical evaluation of the experiments indicates an increase in oxygen transfer rate with a concomitant decrease in energy consumption at low airflow rates. / Master of Science

Atherosclerosis propagates when innate immune cells, myeloid-derived macrophages, undergo unregulated uptake of cholesterol-rich modified low-density lipoproteins (LDL). Excess storage and retention of this cholesterol leads to development of lipid-laden macrophage foam cells, that accumulate within the intima of arteries as developing plaque. Formation of atherosclerotic lesions reduces blood flow and can further lead to more serious complications such as myocardial infarction, stroke, and cardiovascular disease. AMP-activated protein kinase (AMPK), a master regulator of cellular energetics, has been shown to participate in many anti-atherogenic pathways within myeloid cells such as (but not limited to) the inhibition of cholesterol synthesis and stimulation of reverse cholesterol transport. However, a recent report described a pro-atherogenic role for myeloid AMPK, showing it is expression required for myeloid cell recruitment and longevity within the atherosclerotic microenvironment. Despite this, multiple reports all corroborate describing a protective role for systemic pharmacological AMPK activation. We sought to determine the consequence of modified LDL variants in myeloid AMPK signaling and to further clarify the role of myeloid AMPK signaling within atherosclerosis. In cultured macrophages primed with modified LDL variants underwent AMPK activation, which was also associated with increased markers of autophagy. In an in vivo model of intermediate atherosclerosis, we observed that neither myeloid AMPK expression nor systemic AMPK-activating therapy influenced lesion myeloid content, necrosis, or autophagic markers. Furthermore, despite a suggestive trend, both myeloid AMPK and AMPK-therapy did not significantly influence lesion size in male or female mice. Interestingly, we found that in animals lacking AMPK signaling to only one substrate, HMGCR (the rate limiting enzyme in cholesterol synthesis), knock-in mice developed accelerated atherosclerosis when compared to their wild-type littermate. Furthermore, we determined that AMPK signaling to HMGCR in the hematopoietic compartment alone is enough to protect against atherogenesis. Taken together, these studies show the benefit of interrogating specific AMPK-regulated pathways in the context of atherosclerosis, and sheds light on the benefit of utilization of single point mutation knock-in models opposed to global or cell type-specific knockout models for investigations into AMPK within atherosclerosis.

M.S.

No description available.

No description available.

No description available.

No description available.

No description available.

No description available.