Production Well Performance Enhancement using Sonication Technology

The objective of this project was to develop a sonic well performance enhancement technology that focused on near wellbore formation damage. In order to successfully achieve this objective, a three-year project was defined. The entire project was broken into four tasks. The overall objective of all this was to foster a better understanding of the mechanisms involved in sonic energy interactions with fluid flow in porous media and adapt such knowledge for field applications. The fours tasks are: • Laboratory studies • Mathematical modeling • Sonic tool design and development • Field demonstration The project was designed to be completed in three years; however, due to budget cuts, support was only provided for the first year, and hence the full objective of the project could not be accomplished. This report summarizes what was accomplished with the support provided by the US Department of Energy. Experiments performed focused on determining the inception of cavitation, studying thermal dissipation under cavitation conditions, investigating sonic energy interactions with glass beads and oil, and studying the effects of sonication on crude oil properties. Our findings show that the voltage threshold for onset of cavitation is independent of transducer-hydrophone separation distance. In addition, thermal dissipation under cavitation conditions contributed to the mobilization of deposited paraffins and waxes. Our preliminary laboratory experiments suggest that waxes are mobilized when the fluid temperature approaches 40°C. Experiments were conducted that provided insights into the interactions between sonic wave and the fluid contained in the porous media. Most of these studies were carried out in a slim-tube apparatus. A numerical model was developed for simulating the effect of sonication in the nearwellbore region. The numerical model developed was validated using a number of standard testbed problems. However, actual application of the model for scale-up purposes was limited due to funding constraints. The overall plan for this task was to perlorm field trials with the sonication tooL These trials were to be performed in production and/or injection wells located in Pennsylvania, New York, and West Virginia. Four new wells were drilled in preparation for the field demonstration. Baseline production data were collected and reservoir simulator tuned to simulate these oil reservoirs. The sonication tools were designed for these wells. However, actual field testing could not be carried out because of premature termination of the project

Design of a differential protection scheme for a 345 kV transmission line using SEL 311L relays

Master of ScienceDepartment of Electrical and Computer EngineeringNoel SchulzTransmission networks are an important part of an electric power system. They help transfer power from the point of generation (power plants) to the substation. In order to minimize losses during power transfer, the lines are operated at high voltages. The high voltage lines not only have a high power transmission capacity, but they are also prone to faults of larger magnitudes. Thus the occurrence of such faults results in a need for the faults to be cleared quickly in order to limit damage caused to the system. Hence, relays are installed at the Buses to provide protection to the lines. Transmission lines in a power system are most commonly protected by distance relays that use directional comparison schemes. However, due to the simplicity of line differential schemes, there has been an increase in the use of differential relays for complex networks. Moreover, since the relays require only current as the operating parameter, their settings can be determined easily. This report discusses the design of a line current differential protection scheme for a transmission line using SEL 311L relays. The relay settings have been determined and then tested for seven fault scenarios, three internal fault points and four external fault points. To set and test the relays, AcSELerator Quickset, SEL 5030 and PowerWorld programs have been used. Real life power system is simulated with the help of SEL AMS (Adaptive Multichannel Source) that acts as the source to provide the required data to the relays. The relays trip and open the breaker contacts for an internal fault. During an external fault, the relays do not trip and the breaker contacts remain closed. The response of the relays in case of communication failures has been discussed

Connective Tissue Growth Factor in the Pathogenesis of Diabetic Nephropathy A Target for Therapeutic Intervention

Since its discovery in 1991, connective tissue growth factor (CCN2; formerly named CTGF), a member of the CCN family of genes, has been shown to have quite diverse biological functions. Our laboratory was among the first to provide evidence for a causal role for CCN2 in the pathogenesis of diabetic nephropathy (DN). We suggested its criticality as downstream profibrotic factor stimulated by both transforming growth factor (TGF)-βdependent and -independent mechanisms, and as such, a novel target for therapeutic intervention. Proof is now being provided for its role in the fibrosis and sclerosis that occurs in the glomerulus, and likely in the interstitium, in DN. This chapter will focus first on the evidence for a causal role, second on the recently discovered mechanisms and factors involved in regulation of CCN2, and third on the direction we envision the research heading, including possibilities for novel therapeutics and diagnostics targeting CCN

A current view of G protein-coupled receptor - mediated signaling in pulmonary hypertension: finding opportunities for therapeutic intervention

Pathological vascular remodeling is observed in various cardiovascular diseases including pulmonary hypertension (PH), a disease of unknown etiology that has been characterized by pulmonary artery vasoconstriction, right ventricular hypertrophy, vascular inflammation, and abnormal angiogenesis in pulmonary circulation. G protein-coupled receptors (GPCRs) are the largest family in the genome and widely expressed in cardiovascular system. They regulate all aspects of PH pathophysiology and represent therapeutic targets. We overview GPCRs function in vasoconstriction, vasodilation, vascular inflammation-driven remodeling and describe signaling cross talk between GPCR, inflammatory cytokines, and growth factors. Overall, the goal of this review is to emphasize the importance of GPCRs as critical signal transducers and targets for drug development in PH

Phosphorylation of the angiotensin II (AT(1A)) receptor carboxyl terminus: A role in receptor endocytosis

The molecular mechanism of angiotensin II type I receptor (AT(1)) endocytosis is obscure, although the identification of an important serine/threonine rich region (Thr(332)Lys(333)Met(334)Ser(335)Thr(336)Leu(337) Ser(338)) within the carboxyl terminus of the AT(1A) receptor subtype suggests that phosphorylation may be involved. In this study, we examined the phosphorylation and internalization of full-length AT(1A) receptors and compared this to receptors with truncations and mutations of the carboxyl terminus. Epitope-tagged full-length AT(1A) receptors, when transiently transfected in Chinese hamster ovary (CHO)-K1 cells, displayed a basal level of phosphorylation that was significantly enhanced by angiotensin II (Ang II) stimulation. Phosphorylation of AT(1A) receptors was progressively reduced by serial truncation of the carboxyl terminus, and truncation to Lys(325), which removed the last 34 amino acids, almost completely inhibited Ang II-stimulated P-32 incorporation into the AT(1A) receptor. To investigate the correlation between receptor phosphorylation and endocytosis, an epitope-tagged mutant receptor was produced, in which the carboxyl-terminal residues, Thr(332), Ser(335), Thr(336), and Ser(338), previously identified as important for receptor internalization, were substituted with alanine. Compared with the wild-type receptor, this mutant displayed a clear reduction in Ang II-stimulated phosphorylation. Such a correlation was further strengthened by the novel observation that the Ang II peptide antagonist, Sar(1)Ile(8)-Ang II, which paradoxically causes internalization of wild-type AT(1A) receptors, also promoted their phosphorylation. In an attempt to directly relate phosphorylation of the carboxyl terminus to endocytosis, the internalization kinetics of wild-type AT(1A) receptors and receptors mutated within the Thr(332)-Ser(338) region were compared. The four putative phosphorylation sites (Thr(332), Ser(335), Thr(336), and Ser(338)) were substituted with either neutral [alanine (A)] or acidic amino acids [glutamic acid (E) and aspartic acid (D)], the former to prevent phosphorylation and the latter to reproduce the acidic charge created by phosphorylation. Wildtype AT(1A) receptors, expressed in Chinese hamster ovary cells, rapidly internalized after Ang II stimulation [t(1/2) 2.3 min; maximal level of internalization (Y-max) 78.2%], as did mutant receptors carrying single acidic substitutions (T332E, t(1/2) 2.7 min, Y-max 76.3%; S335D, t(1/2) 2.4 min, Y-max 76.7%; T336E, t(1/2) 2.5 min, Y-max 78.2%; S338D, t(1/2) 2.6 min, Y-max 78.4%)