Thermal energy storage in a confined aquifer: Experimental results

This is the published version. Copyright 1979 American Geophysical UnionTo aid in testing the idea of storing thermal energy in aquifers, an experiment was performed by Auburn University in which 54,784 m3 of water was pumped from a shallow supply aquifer, heated to an average temperature of 55°C, and injected into a deeper confined aquifer where the ambient temperature was 20°C. After a storage period of 51 days, 55,345 m3 of water were produced from the confined aquifer. Throughout the experiment, which lasted approximately 6 months, groundwater temperatures were recorded at six depths in each of 10 observation wells, and hydraulic heads were recorded in five observation wells. In order to prevent errors due to thermal convection, most of the observation wells recording temperature had to be backfilled with sand. During the 41-day production period, the temperature of the produced water varied from 55° to 33°C, and 65% of the injected thermal energy was recovered. At no time was an appreciable amount of free thermal convection observed in the storage formation. The dominant heat dissipation mechanisms appeared to be hydrodynamic thermal dispersion and possible mixing of cold and hot water induced by clogging and unclogging of the injection-production well. On the basis of laboratory and field studies, it was concluded that clogging of the injection well, which constituted the major technical problem during the experiment, was caused by the freshwater-sensitive nature of the storage aquifer. Due to the relatively low concentration of cations in the supply water, clay particles would swell, disperse, and migrate until they became trapped in the relatively small pores connecting the larger pores. Surging the pump and back washing the injection well would dislodge the clogging particles and temporarily improve the storage formation permeability. The phenomenon seems largely independent of temperature because it was reproduced in the laboratory with unheated water. It may, however, depend on pore velocity. Future research should be directed toward procedures for selecting storage aquifers that will have minimal susceptibility to clogging and other geochemical problems. Procedures for overcoming such difficulties are needed also because clogging and related phenomena will be more the rule than the exception. Designing an aquifer thermal storage system for maximum energy recovery would involve selecting an appropriate aquifer, analyzing the effects of hydrodynamic thermal dispersion and thermal convection if it is predicted to occur, anticipating geochemical problems, designing the optimum supply-injection-production well configuration and injecting a sufficiently large volume of heated water to realize economies of scale related to increasing volume-surface area ratio

Expansion Thoracoplasty Affects Lung Growth and Morphology in a Rabbit Model: A Pilot Study

Background: Thoracic insufficiency syndrome represents a novel form of postnatal restrictive respiratory disease occurring in children with early-onset scoliosis and chest wall anomalies. Expansion thoracoplasty improves lung volumes in children with thoracic insufficiency syndrome; however, how it affects lung development is unknown. Questions/purposes: Using a rabbit model of thoracic insufficiency syndrome, we evaluated the effect of expansion thoracoplasty on the response of biologic mechanisms in the alveolar microstructure. Methods: Using archived material from a previous experiment, 10 4-week-old New Zealand rabbits were divided into three groups: normal (n = 3), disease (n = 3), and treated (n = 4). Left ribs four to eight were tethered in seven rabbits at age 5 weeks to induce hypoplasia of the left hemithorax (disease). At age 10 weeks, four of these rabbits were treated by expansion thoracoplasty (treated). At age 24 weeks, lungs were excised and processed. Alveolar density and parenchymal airspace were measured on histologic sections. Immunohistochemistry was performed for vascular endothelial growth factor receptor 2 (angiogenesis), KI-67 (cell proliferation), and RAM-11 (macrophages). Results: Alveolar walls were poorly perfused and airspace fraction was larger (emphysematous) in disease rabbits than normal or treated rabbits. Immunohistochemistry provided inconclusive evidence to support the concept that pulmonary hypoplasia is induced by thoracic insufficiency syndrome and controlled by expansion thoracoplasty. Conclusions: Treatment of thoracic insufficiency syndrome by expansion thoracoplasty may prevent emphysematous changes in the alveolar microstructure, thereby enhancing gas exchange

Near Threshold Pion Production via 2-H(p,pi-0)3-He

This research was sponsored by the National Science Foundation Grant NSF PHY-931478

Stratifying patients at the risk of heart failure hospitalization using existing device diagnostic thresholds

AbstractBackgroundHeart failure hospitalizations (HFHs) cost the US health care system ∼$20 billion annually. Identifying patients at risk of HFH to enable timely intervention and prevent expensive hospitalization remains a challenge. Implantable cardioverter defibrillators (ICDs) and cardiac resynchronization devices with defibrillation capability (CRT-Ds) collect a host of diagnostic parameters that change with HF status and collectively have the potential to signal an increasing risk of HFH. These device-collected diagnostic parameters include activity, day and night heart rate, atrial tachycardia/atrial fibrillation (AT/AF) burden, mean rate during AT/AF, percent CRT pacing, number of shocks, and intrathoracic impedance. There are thresholds for these parameters that when crossed trigger a notification, referred to as device observation, which gets noted on the device report. We investigated if these existing device observations can stratify patients at varying risk of HFH.MethodsWe analyzed data from 775 patients (age: 69 ± 11 year, 68% male) with CRT-D devices followed for 13 ± 5 months with adjudicated HFHs. HFH rate was computed for increasing number of device observations. Data were analyzed by both excluding and including intrathoracic impedance. HFH risk was assessed at the time of a device interrogation session, and all the data between previous and current follow-up sessions were used to determine the HFH risk for the next 30 days.Results2276 follow-up sessions in 775 patients were evaluated with 42 HFHs in 37 patients. Percentage of evaluations that were followed by an HFH within the next 30 days increased with increasing number of device observations. Patients with 3 or more device observations were at 42× HFH risk compared to patients with no device observation. Even after excluding intrathoracic impedance, the remaining device parameters effectively stratified patients at HFH risk.ConclusionAvailable device observations could provide an effective method to stratify patients at varying risk of heart failure hospitalization

High-bone-mass causing mutant LRP5 receptors are resistant to endogenous inhibitors in vivo

Certain missense mutations affecting LRP5 cause high bone mass (HBM) in humans. Based on in vitro evidence, HBM LRP5 receptors are thought to exert their effects by providing resistance to binding/inhibition of secreted LRP5 inhibitors such as sclerostin (SOST) and Dickkopf homolog-1 (DKK1). We previously reported the creation of two Lrp5 HBM knock-in mouse models, in which the human p.A214V or p.G171V missense mutations were knocked into the endogenous Lrp5 locus. To determine whether HBM knock-in mice are resistant to SOST- or DKK1-induced osteopenia, we bred Lrp5 HBM mice with transgenic mice that overexpress human SOST in osteocytes ((8kb) Dmp1-SOST) or mouse DKK1 in osteoblasts and osteocytes ((2.3kb) Col1a1-Dkk1). We observed that the (8kb) Dmp1-SOST transgene significantly lowered whole-body bone mineral density (BMD), bone mineral content (BMC), femoral and vertebral trabecular bone volume fraction (BV/TV), and periosteal bone-formation rate (BFR) in wild-type mice but not in mice with Lrp5 p.G171V and p.A214V alleles. The (2.3kb) Col1a1-Dkk1 transgene significantly lowered whole-body BMD, BMC, and vertebral BV/TV in wild-type mice and affected p.A214V mice more than p.G171V mice. These in vivo data support in vitro studies regarding the mechanism of HBM-causing mutations, and imply that HBM LRP5 receptors differ in their relative sensitivity to inhibition by SOST and DKK1