Browsing by Subject "Vascular"
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Item A Study of Microfluidic Reconfiguration Mechanisms Enabled by Functionalized Dispersions of Colloidal Material for Radio Frequency Applications(2010-07-14) Goldberger, Sean A.Communication and reconnaissance systems are requiring increasing flexibility concerning functionality and efficiency for multiband and broadband frequency applications. Circuit-based reconfiguration mechanisms continue to promote radio frequency (RF) application flexibility; however, increasing limitations have resulted in hindering performance. Therefore, the implementation of a "wireless" reconfiguration mechanism provides the required agility and amicability for microwave circuits and antennas without local overhead. The wireless reconfiguration mechanism in this thesis integrates dynamic, fluidic-based material systems to achieve electromagnetic agility and reduce the need for "wired" reconfiguration technologies. The dynamic material system component has become known as electromagnetically functionalized colloidal dispersions (EFCDs). In a microfluidic reconfiguration system, they provide electromagnetic agility by altering the colloidal volume fraction of EFCDs - their name highlights the special considerations we give to material systems in applied electromagnetics towards lowering loss and reducing system complexity. Utilizing EFCDs at the RF device-level produced the first circuit-type integration of this reconfiguration system; this is identified as the coaxial stub microfluidic impedance transformer (COSMIX). The COSMIX is a small hollowed segment of transmission line with results showing a full reactive loop (capacitive to inductive tuning) around the Smith chart over a 1.2 GHz bandwidth. A second microfluidic application demonstrates a novel antenna reconfiguration mechanism for a 3 GHz microstrip patch antenna. Results showed a 300 MHz downward frequency shift by dielectric colloidal dispersions. Magnetic material produced a 40 MHz frequency shift. The final application demonstrates the dynamically altering microfluidic system for a 3 GHz 1x2 array of linearly polarized microstrip patch antennas. The parallel microfluidic capillaries were imbedded in polydimethylsiloxane (PDMS). Both E- and H-plane designs showed a 250 MHz frequency shift by dielectric colloidal dispersions. Results showed a strong correlation between decreasing electrical length of the elements and an increase of the volume fraction, causing frequency to decrease and mutual coupling to increase. Measured, modeled, and analytical results for impedance, voltage standing wave ratio (VSWR), and radiation behavior (where applicable) are provided.Item Intracellular pH regulation in microvascular endothelial cells(Texas Tech University, 2000-05) Rojas, Jose DMany advances in vascular biology are a result of the use of cultured endothelial cells as a model. This model system has shown that endothelial cells synthesize and secrete various substances involved in regulating blood flow. There can be considerable heterogeneity in the properties and function of endothelial cells. These heterogeneities are a result of the tissue of origin and whether they are from macro- or microcirculation. Nitric oxide, a vasoactive substance synthesized by endothelial cells, has been shown to activate other second messenger systems in both a calcium-dependent and –independent fashion. There is a substantial body of work on intracellular calcium [Ca^2+] regulation in endothelial cells. Similarly, it is known that intracellular pH (pH'") is important in signal transduction following hormonal stimulation, and in regulating many physiological processes including cell growth, secretion, contraction, and invasion/migration. Significant work has been done on pH'" regulation in macrovascular endothelial cells; however, there remains a large gap in the knowledge of pH'" regulation in microvascular endothelial cells. Since there have been reported differences in [Ca^2+ ] regulation and nitric oxide production in microvascular and macrovascular endothelial cells, one specific aim of this dissertation was to perform an in-depth study of pH^in regulation in microvascular endothelial cells from different vascular beds. Microvascular endothelial cells are intimately involved in the invasive process of angiogenesis and there have been reports of plasma membrane vacuolar-type ATPase (pmV-ATPase) in several invasive cell types. These observations led to the formulation of the hypothesis that pmV-ATPase is required for invasion and was tested in this study. To our knowledge, this study is the first reported observation of pmV-ATPase as a pH^10 regulatory mechanism in microvascular endothelial cells along with evidence that the mechanism is involved in the process of invasion. Diabetes affects the cardiovascular system with complications that include acidosis, abnormalities in blood flow regulation, and altered microvascular proliferation and angiogenesis. Part of this study examined pH'" regulation in microvascular endothelial cells from a model of spontaneous diabetes. As a result of this work we determined that diabetic cells have decreased pmV-ATPase activity. Along with decreased pmV-ATPase activity diabetic cells also exhibit decreased invasive Potential and angiogenesis. Pharmacologic inhibition of pmV-ATPase activity in normal cells renders them as non-invasive as diabetic cells and unable to form capillary-like structures in an angiogenesis model. Finally, the study examines endothelial cells from lung micro vasculature. This vascular bed is known to undergo extensive vascular remodeling with prolonged hypoxia. Since prolonged hypoxia results in acidosis, it was predicted that these cells would have a dynamic pH'" regulatory that allows them to cope with this situation. Moreover, because vascular remodeling is an invasive process, it was predicted that these endothelial cells would also express pmV-ATPase. In support of the hypothesis; immunocytochemical, fluorescence spectroscopy, and pharmacologic studies reveal pmV-ATPase as a major pH'" regulatory mechanism in these cells. In summary this work demonstrates the presence of pmV-ATPase in several microvascular beds and provides functional evidence for its role in the invasive process of vascular remodeling.Item Regulation of calcium stores in normal and diabetic endothelial cells(Texas Tech University, 2000-12) Sanka, Shankar ChittaranjanCytosolic Ca^^ ([Ca^^]*'^^) mediates many cellular ftinctions, e.g.. cell growth, motility, secretion, etc. In many cell types, ion transport processes appear to be dependent on metabolism of glucose for maximal activity. In certain cell types, a strict coupling between glycolysis and the acfivity of Endoplasmic Reticulum Ca^"-ATPases (SERCA). involved in regulating Ca^^ homeostasis, has been suggested. In diabetes, glucose homeostasis is altered. We hypothesize that Ca^^ homeostasis in microvascular endothelial cells from diabetic animals is altered due to a dysfunction of glycolysis coupling the activity of SERCA. We further hypothesize that endosomal/lysosomal (E/L) compartments exhibiting SERCA are involved in this dysfunction. Our data indicated that agonist stimulation (ATP, vasopressin, angiotensin-II)elicited [Ca^"]^^* increases (independent of extracellular Ca^^) that were larger in endothelial cells from diabetic than from normal animals. Simultaneous measurements of [Ca^^]'^^' and Ca^^ in E/L compartments ([Ca^^]^) using fluorescence spectroscopy, indicated that E/L compartments released Ca^^ following agonist-stimulation. The magnitude of the Ca'* release was significantly larger in microvascular endothelial cells from diabetic rats. SERCA inhibitors elicited Ca^^ releases from E/L compartments in both normal and diabetic models. The magnitude of the [Ca^^]^ release was however similar among normal and diabetic cells. Immunocytochemical experiments demonstrated that 60% of E/L compartments exhibited SERCA. These data indicate that (a) E/L compartments are important for Ca^^ homeostasis in microvascular endothelial cells from both normal and diabetic models; (b) Ca^^ regulation in E/L compartments is different in cells from a diabefic model, (c) the compartment involved in altered Ca'* homeostasis in diabetes is unknown.Item Role of Vascular Oxidative Stress in Hypertension(2012-04-19) Bhatt, Siddhartha; Lokhandwala, Mustafa F.; Banday, Anees Ahmad; Marwaha, Aditi; Majid, Dewan; Lewis, Russell E.Hypertension affects 1 in 3 adult Americans and is a primary risk factor for cardiovascular diseases. Better understanding of hypertension pathogenesis is important for development of effective therapeutic agents. An important underlying factor present during hypertension is oxidative stress (OS). However, causal role of OS in hypertension is unclear. Increased vascular resistance resulting from enhanced vasoconstriction and impaired vasodilation is a hallmark of hypertension. Enhanced vasoconstriction is associated with increased reactivity to vasoconstrictors such as angiotensin (Ang) II. Ang II-induced vasoconstriction is exaggerated during hypertension and is associated with Ang II type 1 receptors (AT1R) upregulation, the cause of which is unknown. OS modulates redox sensitive transcription factors including nuclear factor kappa B (NFκB), which has been associated with AT1R upregulation. Thus, OS via NFκB can transcriptionally upregulate AT1R. The impaired vasodilation in hypertension is attributed to endothelial dysfunction resulting from attenuated nitric oxide (NO) availability. OS can also contribute to endothelial dysfunction by reducing NO production and increasing NO scavenging. Our objective was to study the role of OS in hypertension development. The first part of the study investigates whether OS is a cause or consequence of hypertension. Studies in 3-4 week old spontaneously hypertensive rats (SHR) revealed that OS precedes hypertension development and is associated with NFκB activation and AT1R upregulation. Treatment of young SHR with pyrrolidine dithiocarbamate, an antioxidant with NFκB inhibitory action, attenuated hypertension development and normalized NFκB and AT1R expression. Experiments in human aortic smooth muscle cells also exhibited OS-induced AT1R upregulation through mechanisms involving NFκB. The second part of the study investigates the role of early oxidative stress in endothelial dysfunction with focus on elucidating role of resveratrol, an antioxidant polyphenol. Our results demonstrate, early resveratrol treatment lowers oxidative stress and reduces NO scavenging and eNOS uncoupling thereby preventing endothelial dysfunction and attenuating hypertension development. In conclusion, early vascular OS in SHR could contribute to hypertension by modulating AT1 receptor upregulation, possibly via NFκB. Additionally, vascular OS could also contribute to endothelial dysfunction by increasing NO scavenging and eNOS uncoupling. Resveratrol treatment lowered oxidative stress, prevented endothelial dysfunction and attenuated hypertension development in SHR.