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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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11 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2019

Use of Cardiac Imaging to Evaluate Cardiac Function and Pulmonary Hemodynamics in Patients with Heart Failure

Purpose of Review: Noninvasive hemodynamic assessments in patients with heart failure (HF) are essential for appropriate diagnosis and establishment of the best treatment strategies. Recently, the impact of pulmonary circulation and right ventricular function on prognosis in HF patients has drawn increasing attention. In this article, we explore the usefulness of cardiac imaging for hemodynamic assessments, mainly focusing on echocardiographic evaluation. Recent Findings: The reliability of Doppler echocardiography as a noninvasive alternative to Swan-Ganz catheterization has been well investigated with higher than 80% accuracy for estimating pulmonary artery pressure. Strain measurement and three-dimensional echocardiography are useful for evaluating right ventricular function together with pulmonary circulation. The accuracy of analyzing left and right ventricular functions by cardiac computed tomography and cardiac magnetic resonate imaging has also been established. These modalities can provide myocardial tissue information and allow calculation of the extracellular volume fraction as well. Summary: According to the rapid improvement of technologies, cardiac imaging has become an essential tool for hemodynamic evaluation in HF management.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2016

A Novel Technique Using a Protection Filter During Fibrin Sheath Removal for Implanted Venous Access Device Dysfunction

With the increased use of implanted venous access devices (IVADs) for continuous long-term venous access, several techniques such as percutaneous endovascular fibrin sheath removal, have been described, to maintain catheter function. Most standard techniques do not capture the stripped fibrin sheath, which is subsequently released in the pulmonary circulation and may lead to symptomatic pulmonary embolism. The presented case describes an endovascular technique which includes stripping, capture, and removal of fibrin sheath using a novel filter device. A 64-year-old woman presented with IVAD dysfunction. Stripping was performed using a co-axial snare to the filter to capture the fibrin sheath. The captured fragment was subsequently removed for visual and pathological verification. No immediate complication was observed and the patient was discharged the day of the procedure.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2017

An efficient parallel simulation of unsteady blood flows in patient-specific pulmonary artery

Simulation of blood flows in the pulmonary artery provides some insight into certain diseases by examining the relationship between some continuum metrics, eg, the wall shear stress acting on the vascular endothelium, which responds to flow-induced mechanical forces by releasing vasodilators/constrictors. V. Kheyfets, in his previous work, studies numerically a patient-specific pulmonary circulation to show that decreasing wall shear stress is correlated with increasing pulmonary vascular impedance. We develop a scalable parallel algorithm based on domain decomposition methods to investigate an unsteady model with patient-specific pulsatile waveforms as the inlet boundary condition. The unsteady model offers tremendously more information about the dynamic behavior of the flow field, but computationally speaking, the simulation is a lot more expensive since a problem which is similar to the steady-state problem has to be solved many times, and therefore, the traditional sequential approach is not suitable anymore. We show computationally that simulations using the proposed parallel approach with up to 10 000 processor cores can be obtained with much reduced compute time. Finally, this makes the technology potentially usable for the routine study of the dynamic behavior of blood flows in the pulmonary artery, in particular, the changes of the blood flows and the wall shear stress in the spatial and temporal dimensions.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Cardiac Ischemia Reperfusion Injury Following Instillation of 20 nm Citrate-capped Nanosilver

Background: Silver nanoparticles (AgNP) have garnered much interest due to their antimicrobial properties, becoming one of the most utilized nano scale materials. However, any potential evocable cardiovascular injury associated with exposure has not been previously reported. We have previously demonstrated expansion of myocardial infarction after intratracheal (IT) instillation of other nanomaterials. We hypothesized that pulmonary exposure to Ag core AgNP induces persistent increase in circulating cytokines, expansion of cardiac ischemia-reperfusion (I/R) injury and associated with altered coronary vessel reactivity. Methods: Male Sprague-Dawley rats were exposed to 200 µg of 20 nm citrate capped Ag core AgNP, or a citrate vehicle intratracheally (IT). One and 7 days following IT instillation lungs were evaluated for inflammation and silver presence, serum was analyzed for concentrations of selected cytokines, and cardiac I/R injury and coronary artery reactivity was assessed. Results: AgNP instillation resulted in modest pulmonary injury with detection of silver in lung tissue and infiltrating cells, elevation of serum cytokines: G-CSF, MIP-1α, IL-1β, IL-2, IL-6, IL-13, IL-10, IL-18, IL-17, TNFα, and RANTES, expansion of I/R injury and depression of the coronary vessel reactivity at 1 day post IT compared to vehicle treated rats. Seven days post IT instillation was associated with persistent detection of silver in lungs, elevation in cytokines: IL-2, IL-13, and TNFα and expansion of I/R injury. Conclusions: Based on these data, IT instillation of AgNP increases circulating levels of several cytokines, which may contribute to persistent expansion of I/R injury possibly through an impaired vascular responsiveness.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Systemic metabolic derangement, pulmonary effects, and insulin insufficiency following subchronic ozone exposure in rats

Acute ozone exposure induces a classical stress response with elevated circulating stress hormones along with changes in glucose, protein and lipid metabolism in rats, with similar alterations in ozone-exposed humans. These stress-mediated changes over time have been linked to insulin resistance. We hypothesized that acute ozone-induced stress response and metabolic impairment would persist during subchronic episodic exposure and induce peripheral insulin resistance. Male Wistar Kyoto rats were exposed to air or 0.25 ppm or 1.00 ppm ozone, 5 h/day, 3 consecutive days/week (wk) for 13 wks. Pulmonary, metabolic, insulin signaling and stress endpoints were determined immediately after 13 wk or following a 1 wk recovery period (13 wk + 1 wk recovery). We show that episodic ozone exposure is associated with persistent pulmonary injury and inflammation, fasting hyperglycemia, glucose intolerance, as well as, elevated circulating adrenaline and cholesterol when measured at 13 wk, however, these responses were largely reversible following a 1 wk recovery. Moreover, the increases noted acutely after ozone exposure in non-esterified fatty acids and branched chain amino acid levels were not apparent following a subchronic exposure. Neither peripheral or tissue specific insulin resistance nor increased hepatic gluconeogenesis were present after subchronic ozone exposure. Instead, long-term ozone exposure lowered circulating insulin and severely impaired glucose-stimulated beta-cell insulin secretion. Thus, our findings in young-adult rats provide potential insights into epidemiological studies that show a positive association between ozone exposures and type 1 diabetes. Ozone-induced beta-cell dysfunction may secondarily contribute to other tissue-specific metabolic alterations following chronic exposure due to impaired regulation of glucose, lipid, and protein metabolism. - Highlights: • Subchronic episodic ozone exposure caused pulmonary and metabolic effects. • These effects were largely reversible upon one week recovery. • Ozone exposure did not cause liver or muscle insulin resistance. • Subchronic ozone exposure led to decrease in serum insulin. • Ozone severely impaired beta cell insulin secretion in response to glucose.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2019

The impact of combined cardiopulmonary exercise testing and SPECT myocardial perfusion imaging on downstream evaluation and management

Objective: The diagnostic yield of combined cardiopulmonary exercise testing (CPET) and myocardial perfusion imaging (MPI) in patients referred for stress testing has received limited study. Methods: We evaluated consecutive patients who underwent combined CPET-MPI at a single tertiary referral center between 2011 and 2015. An abnormal CPET was defined as any of the following: reduced oxygen consumption, cardiac output impairment, or pulmonary impairment. Normal MPI was defined as the absence of resting or stress perfusion defect. The primary study outcome was change in clinical decision-making after CPET-MPI including management of pulmonary disease, management of deconditioning, heart failure management, and referral for cardiac catheterization. Outcomes of patients with normal and abnormal MPI were presented based on the specific CPET abnormality. Results: 415 patients were included in the study. Of the 269 patients that had normal MPI, 206 (77%) had abnormal CPET. Patients with abnormal CPET and normal MPI, compared with patients that had normal CPET and normal MPI, were more frequently diagnosed with pulmonary disease (11.7% vs 3.2%, P = .04) and deconditioning (33.5% vs 17.4%, P = .01). Of the 146 patients that had abnormal MPI, 128 (88%) had abnormal CPET. Patients with abnormal CPET and abnormal MPI, compared with patients that had normal CPET and abnormal MPI, did not statistically differ with regard to the study outcome. Conclusion: An abnormal CPET, if the MPI was normal, prompted further evaluation and led to management of pulmonary disease and deconditioning.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2022

Quantile-Specific Heritability of Inflammatory and Oxidative Stress Biomarkers Linked to Cardiovascular Disease

Purpose: Heritability (h 2 , the proportion of the phenotypic variance attributable to additive genetic effects) is traditionally assumed to be constant throughout the distribution of the phenotype. However, the heritabilities of circulating C-reactive protein, interleukin-6, plasminogen activator inhibitor type-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) concentrations depend upon whether the phenotype is high or low relative to their distributions (quantile-dependent expressivity), which may account for apparent gene–environment interactions. Whether the heritabilities of other inflammatory biomarkers linked to cardiovascular disease are quantile-dependent remain to be determined. Patients and Methods: Quantile-specific offspring-parent (β OP ) and full-sib regression slopes (β FS ) were estimated by applying quantile regression to the age- and sex-adjusted phenotypes of families surveyed as part of the Framingham Heart Study. Quantile-specific heritabilities were calculated as: h 2 =2β OP /(1+r spouse ) and h 2 ={(1+8r spouse β FS ) 0.5 – 1}/(2r spouse ). Results: Heritability (h 2 ± SE) of lipoprotein-associated phospholipase A2 (Lp-PLA 2 ) mass concentrations increased from 0.11 ± 0.03 at the 10 th percentile, 0.08 ± 0.03 at the 25 th , 0.12 ± 0.03 at the 50 th , 0.20 ± 0.04 at the 75 th , and 0.26 ± 0.06 at the 90 th percentile, or 0.0023 ± 0.0006 per each one-percent increase in the phenotype distribution (P linear trend = 0.0004). Similarly, h 2 increased 0.0029 ± 0.0011 (P linear trend = 0.01) for sP-selectin, 0.0032 ± 0.0009 (P linear trend = 0.0001) for soluble intercellular adhesion molecule 1 (sICAM-1), and 0.0026 ± 0.0006 for tumor necrosis factor receptor 2 (TNFR2) (P linear trend = 5.0 × 10 -6 ) per each one-percent increase in their distributions when estimated from β OP . Osteoprotegerin and soluble ST2 heritability also increased significantly with increasing percentiles of their distributions when estimated from β FS . Lp-PLA 2 activity, CD40 ligand, TNFα, interleukin-18, and myeloperoxidase heritability showed no significant quantile-dependence. Conclusion: The heritabilities of circulating Lp-PLA 2 -mass, sP-selectin, sICAM-1, TNFR2, osteoprotegerin and soluble ST2 concentrations are quantile-dependent, which may contribute to purported genetic modulations of: 1) sP-selectin’s relationships to venous thrombosis, pulmonary hypertension, type 2 diabetes and atorvastatin treatment; 2) sICAM-I’s relationships to brain abscess and atorvastatin treatment; and 3) Lp-PLA 2 ’s relationships to myocardial infarction and preeclampsia.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Staphylococcal enterotoxin A regulates bone marrow granulocyte trafficking during pulmonary inflammatory disease in mice

Pulmonary neutrophil infiltration produced by Staphylococcal enterotoxin A (SEA) airway exposure is accompanied by marked granulocyte accumulation in bone marrow (BM). Therefore, the aim of this study was to investigate the mechanisms of BM cell accumulation, and trafficking to circulating blood and lung tissue after SEA airway exposure. Male BALB/C mice were intranasally exposed to SEA (1 μg), and at 4, 12 and 24 h thereafter, BM, circulating blood, bronchoalveolar lavage (BAL) fluid and lung tissue were collected. Adhesion of BM granulocytes and flow cytometry for MAC-1, LFA1-α and VLA-4 and cytokine and/or chemokine levels were assayed after SEA-airway exposure. Prior exposure to SEA promoted a marked PMN influx to BAL and lung tissue, which was accompanied by increased counts of immature and/or mature neutrophils and eosinophils in BM, along with blood neutrophilia. Airway exposure to SEA enhanced BM neutrophil MAC-1 expression, and adhesion to VCAM-1 and/or ICAM-1-coated plates. Elevated levels of GM-CSF, G-CSF, INF-γ, TNF-α, KC/CXCL-1 and SDF-1α were detected in BM after SEA exposure. SEA exposure increased production of eosinopoietic cytokines (eotaxin and IL-5) and BM eosinophil VLA-4 expression, but it failed to affect eosinophil adhesion to VCAM-1 and ICAM-1. In conclusion, BM neutrophil accumulation after SEA exposure takes place by integrated action of cytokines and/or chemokines, enhancing the adhesive responses of BM neutrophils and its trafficking to lung tissues, leading to acute lung injury. BM eosinophil accumulation in SEA-induced acute lung injury may occur via increased eosinopoietic cytokines and VLA-4 expression. - Highlights: • Airway exposure to SEA causes acute lung inflammation. • SEA induces accumulation of bone marrow (BM) in immature and mature neutrophils. • SEA increases BM granulocyte or BM PMN adhesion to ICAM-1 and VCAM-1, and MAC-1 expression. • SEA induces BM elevations of CXCL-1, INF-γ, TNF-α, GM-CSF, G-CSF and SDF-1α. • Our results contribute to elucidating BM events during SEA-induced lung inflammation.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2026

Naphthalene-DNA Adduct Formation in a Lung Airway Explant Model: The Role of Bioactivation and Naphthalene Metabolites

Humans are widely exposed to naphthalene. Once inhaled or ingested, naphthalene is metabolized by cytochrome P450 and other enzymes to form toxic metabolites known to harm lung epithelial cells. Naphthalene metabolites circulate in the blood. Chronic naphthalene inhalation promotes lesions in the epithelium of the mouse lung and rat nose. Oral naphthalene exposure leads to DNA adduct formation in mouse lung, but the contributions of different enzymatic pathways and the metabolites they generate are not fully understood. This study explores the influence of naphthalene metabolites on DNA adduct formation in the lungs of two species (mice and primates). To isolate the lung response, conducting airway explants containing Club cells, a target for pulmonary naphthalene toxicity, were microdissected from live lung tissue and incubated with 14 C-naphthalene or its metabolites: 14 C-1,2-naphthoquinone or 14 C-naphthalene-1,2-dihydrodiol. Explants were incubated for 1 h, then processed immediately (T1), or were transferred to clean media for the remainder of the 24 h (T24), to monitor 14 C in DNA over time. Accelerator mass spectrometry analysis revealed the formation of DNA adducts by all three radiolabeled compounds by T24. Our results support the notion that P450 enzymes of the Cyp2abfgs subfamily contribute to naphthalene-induced DNA adduct formation (approximately 4-fold reduction in male mice lacking the Cyp2abfgs genes, P < 0.01). The finding that naphthalene-1,2-dihydrodiol, a stable metabolite, formed DNA adducts (102–117 adducts/10 8 nucleotides) at 24 h following addition to the culture media validates the concern that circulating naphthalene metabolites can contribute to DNA adduct formation in the lung. DNA adducts persisted to 24 h after exposure in both mouse and primate airways and at comparable levels between species (77.8 vs 129 adducts/10 8 nucleotides, respectively). Together, these results support the importance of a potential genotoxic mechanism of naphthalene and its metabolites in vivo in both mice and nonhuman primates, and possibly also in humans.

Biological and medical sciences↗
DOE OSTI2018

Pitfalls in the Diagnosis of Acute Pulmonary Embolism on Computed Tomography: Common Pathologic and Imaging Mimics

Purpose of Review: Acute pulmonary embolism (PE) is the third most-common acute cardiovascular disease in the United States. Nearly 900,000 new diagnoses are made each year, with 250,000 associated hospitalizations and up to 100,000 deaths (Palacio et al. in Semin Roentgenol 50(3):217–225, 2015; Metter et al. in Am J Roentgenol 208(3):489–494, 2017; Jaff et al. in Circulation 123(16):1788–830, 2011). Timely and accurate diagnosis of acute PE is crucial for the prevention of most deaths associated with PE, even more so than optimal medical therapy (Palacio et al. in Semin Roentgenol 50(3):217–225, 2015; Jaff et al. in Circulation 123(16):1788–830, 2011; Raja et al. in Ann Intern Med 163(9):701, 2015). Recent Findings: Computed tomography (CT) has emerged as the primary imaging modality used in the diagnosis of acute PE. Thus, radiologists play a key role in the correct diagnosis of acute PE, and must differentiate this diagnosis from other conditions that mimic the imaging findings of acute PE, as well as from artifacts associated with imaging techniques (Palacio et al. in Semin Roentgenol 50(3):217–225, 2015; Jaff et al. in Circulation 123(16):1788–830, 2011; Raja et al. in Ann Intern Med 163(9):701, 2015). Understanding how these diagnoses present on CT is necessary for improved patient care. Summary: This article will discuss the diagnosis of acute PE with CT, the diagnosis of diseases that may be mistaken for acute PE, and how to identify imaging artifacts that may be mistaken for an acute PE.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2019

Exacerbation of ozone-induced pulmonary and systemic effects by β 2 -adrenergic and/or glucocorticoid receptor agonist/s

Agonists of β 2 adrenergic receptors (β 2 AR) and glucocorticoid receptors (GR) are prescribed to treat pulmonary diseases. Since ozone effects are mediated through the activation of AR and GR, we hypothesized that the treatment of rats with relevant therapeutic doses of long acting β 2 AR agonist (LABA; clenbuterol; CLEN) and/or GR agonist (dexamethasone; DEX) would exacerbate ozone-induced pulmonary and systemic changes. In the first study, male 12-week-old Wistar-Kyoto rats were injected intraperitoneally with vehicle (saline), CLEN (0.004 or 0.02 mg/kg), or DEX (0.02 or 0.1 mg/kg). Since dual therapy is commonly used, in the second study, rats received either saline or combined CLEN + DEX (each at 0.005 or 0.02 mg/kg) one day prior to and on both days of exposure (air or 0.8ppm ozone, 4 hr/day x 2-days). In air-exposed rats CLEN, DEX or CLEN + DEX did not induce lung injury or inflammation, however DEX and CLEN + DEX decreased circulating lymphocytes, spleen and thymus weights, increased free fatty acids (FFA) and produced hyperglycemia and glucose intolerance. Ozone exposure of vehicle-treated rats increased bronchoalveolar lavage fluid protein, albumin, neutrophils, IL-6 and TNF-α. Ozone decreased circulating lymphocytes, increased FFA, and induced hyperglycemia and glucose intolerance. Drug treatment did not reverse ozone-induced ventillatory changes, however, lung effects (protein and albumin leakage, inflammation, and IL-6 increase) were exacerbated by CLEN and CLEN + DEX pre-treatment in a dose-dependent manner (CLEN > CLEN + DEX). Systemic effects induced by DEX and CLEN + DEX but not CLEN in air-exposed rats were analogous to and more pronounced than those induced by ozone. These data suggest that adverse air pollution effects might be exacerbated in people receiving LABA or LABA plus glucocorticoids.

59 BASIC BIOLOGICAL SCIENCES↗