This thesis project discusses the transitions of the physician profession and their struggle to maintain autonomy throughout American History until approximately the 1980's. Included in the historical account of the physician profession, is the development of the American Hospital System and its origins working under the physician profession. As history progresses from 1760 on, what comes to light is a cyclical struggle for physicians to remain independent from the corporations, while using them to gain social and economic prestige. This work focuses on how the establishment of private practice in the United States has lead to the current system in place today, illustrating a long fight for control of the medical field that still rages on today. As physicians gained power and autonomy in the medical field during the 20th century, constant attempts of government intervention can be seen within the convoluted history of this professional field. The rise of corporate healthcare, that works in tandem with private physicians, was a critical period in forgotten American History that subsequently allowed physicians to increase their stranglehold on the medical service industry. The goal of this research was to establish a better understanding of American Medicine's history to better tackle the new problems we face today. As America transitions to a period of public health outcry, it is important to establish a somewhat linear rendition of a mostly untold history that directly impacts the lives of every citizen in this country. This work attempts to mend the broken pieces of that history to give light to how healthcare evolved into what it is today.

The purpose of this thesis experiment was to design and create an Acoustically Active Cannula (AAC), which is furnished by a piezoelectric crystal placed at its tip that produces an acoustic navigation signal. I tested the functionality of the cannula in vitro and demonstrated its navigational abilities in vivo in anesthetized pigs. This experiment was based upon ultrasound science and technology, and thus some practical experience with conventional (B-mode) and Doppler ultrasound was achieved as well. The results of bench and experimental animal studies indicated proper functionality of the AAC for identification and spatial navigation of its tip with color Doppler ultrasound imaging.

Spatiotemporal processing in the mammalian olfactory bulb (OB), and its analog, the invertebrate antennal lobe (AL), is subject to plasticity driven by biogenic amines. I study plasticity using honey bees, which have been extensively studied with respect to nonassociative and associative based olfactory learning and memory. Octopamine (OA) release in the AL is the functional analog to epinephrine in the OB. Blockade of OA receptors in the AL blocks plasticity induced changes in behavior. I have now begun to test specific hypotheses related to how this biogenic amine might be involved in plasticity in neural circuits within the AL. OA acts via different receptor subtypes, AmOA1, which gates calcium release from intracellular stores, and AmOA-beta, which results in an increase of cAMP. Calcium also enters AL interneurons via nicotinic acetylcholine receptors, which are driven by acetylcholine release from sensory neuron terminals, as well as through voltage-gated calcium channels. I employ 2-photon excitation (2PE) microscopy using fluorescent calcium indicators to investigate potential sources of plasticity as revealed by calcium fluctuations in AL projection neuron (PN) dendrites in vivo. PNs are analogous to mitral cells in the OB and have dendritic processes that show calcium increases in response to odor stimulation. These calcium signals frequently change after association of odor with appetitive reinforcement. However, it is unclear whether the reported plasticity in calcium signals are due to changes intrinsic to the PNs or to changes in other neural components of the network. My studies were aimed toward understanding the role of OA for establishing associative plasticity in the AL network. Accordingly, I developed a treatment that isolates intact, functioning PNs in vivo. A second study revealed that cAMP is a likely component of plasticity in the AL, thus implicating the AmOA-beta; receptors. Finally, I developed a method for loading calcium indicators into neural components of the AL that have yet to be studied in detail. These manipulations are now revealing the molecular mechanisms contributing to associative plasticity in the AL. These studies will allow for a greater understanding of plasticity in several neural components of the honey bee AL and mammalian OB.