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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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At least 19 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS1975

Effect of shape and size of lung and chest wall on stresses in the lung

To understand better the effect of shape and size of lung and chest wall on the distribution of stresses, strains, and surface pressures, we analyzed a theoretical model using the technique of finite elements. First we investigated the effects of changing the chest wall shape during expansion, and second we studied lungs of a variety of inherent shapes and sizes. We found that, in general, the distributions of alveolar size, mechanical stresses, and surface pressures in the lungs were dominated by the weight of the lung and that changing the shape of the lung or chest wall had relatively little effect. Only at high states of expansion where the lung was very stiff did changing the shape of the chest wall cause substantial changes. Altering the inherent shape of the lung generally had little effect but the topographical differences in stresses and surface pressures were approximately proportional to lung height. The results are generally consistent with those found in the dog by Hoppin et al (1969).

Vawter, D. L.↗
DOE OSTI2023

Quasi‐dynamic breathing model of the lung incorporating viscoelasticity of the lung tissue

Abstract We advanced a novel model to calculate viscoelastic lung compliance and airflow resistance in presence of mucus, accounting for the quasi‐linear viscoelastic stress–strain response of the parenchyma (alveoli) tissue. We adapted a continuum‐based numerical modeling approach for the lung, integrating the fluid mechanics of the airflow within individual generations of the bronchi and alveoli. The model accounts for elasticity of the deformable bronchioles, resistance to airflow due to the presence of mucus within the bronchioles, and subsequent mucus flow. Simulated quasi‐dynamic inhalation and expiration cycles were used to characterize the net compliance and resistance of the lung, considering the rheology of the mucus and viscoelastic properties of the parenchyma tissue. The structure and material properties of the lung were identified to have an important contribution to the lung compliance and airflow resistance. The secondary objective of this work was to assess whether a higher frequency and smaller volume of harmonic air flow rate compared to a normal ventilator breathing cycle enhanced mucus outflow. Results predict, lower mucus viscosity and higher excitation frequency of breathing are favorable for the flow of mucus up the bronchi tree, towards the trachea.

60 APPLIED LIFE SCIENCES↗
NASA NTRS1992

High lung volume increases stress failure in pulmonary capillaries

We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.

Non-NASA Center↗
DOE OSTI2021

CLEC12B suppresses lung cancer progression by inducing SHP-1 expression and inactivating the PI3K/AKT signaling pathway

Lung cancer is the leading cause of cancer mortality worldwide. CLEC12B, a C-type lectin-like receptor, is low-expressed in lung cancer tissues. However, the function of CLEC12B in lung cancer and its underlying mechanism remain unclear. Here, an obvious down-regulation of CLEC12B was observed in lung cancer cells compared with the normal lung epithelial cells. CLEC12B over-expression suppressed cell viability and cell cycle entry in lung cancer, along with the reduction of PCNA and cyclin D1 expressions, while silencing CLEC12B possessed the opposite effects. Over-expression of CLEC12B promoted lung cancer cell apoptosis, accompanied by decreased Bcl-2 and increased Bax, cleaved caspase-3 and cleaved caspase-9. Moreover, CLEC12B decreased phosphorylation of PI3K-p85 and AKT proteins. By contrast, CLEC12B knockdown activated the PI3K/AKT pathway. In vivo, CLEC12B inhibited tumor growth in lung cancer, which can be reversed by CLEC12B inhibition. Co-IP and immunofluorescence assays confirmed the interaction between CLEC12B and SHP-1, and CLEC12B over-expression increased SHP-1 level. Furthermore, knocking down SHP-1 abrogated the above biological phenotypes caused by CLEC12B elevation. Taken together, our findings demonstrate that CLEC12B serves as a tumor-suppressing gene in lung cancer through positively regulating SHP-1 expression, which may be mediated by the PI3K/AKT signaling pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2022

Iraq/Afghanistan war lung injury reflects burn pits exposure

This descriptive case series retrospectively reviewed medical records from thirty-one previously healthy, war-fighting veterans who self-reported exposure to airborne hazards while serving in Iraq and Afghanistan between 2003 and the present. They all noted new-onset dyspnea, which began during deployment or as a military contractor. Twenty-one subjects underwent non-invasive pulmonary diagnostic testing, including maximum expiratory pressure (MEP) and impulse oscillometry (IOS). In addition, five soldiers received a lung biopsy; tissue results were compared to a previously published sample from a soldier in our Iraq Afghanistan War Lung Injury database and others in our database with similar exposures, including burn pits. We also reviewed civilian control samples (5) from the Stony Brook University database. Military personnel were referred to our International Center of Excellence in Deployment Health and Medical Geosciences, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell under the auspices of Northwell IRB: 17-0140-FIMR Feinstein Institution for Medical Research “Clinicopathologic characteristics of Iraq Afghanistan War Lung Injury.” We retrospectively examined medical records, including exposure data, radiologic imaging, and non-invasive pulmonary function testing (MGC Diagnostic Platinum Elite Plethysmograph) using the American Thoracic Society (ATS) standard interpretation based on Morgan et al., and for a limited cohort, biopsy data. Lung tissue, when available, was examined for carbonaceous particles, polycyclic aromatic hydrocarbons (Raman spectroscopy), metals, titanium connected to iron (Brookhaven National Laboratory, National Synchrotron Light Source II, Beamline 5-ID), oxidized metals, combustion temperature, inflammatory cell accumulation and fibrosis, neutrophil extracellular traps, Sirius red, Prussian Blue, as well as polarizable crystals/particulate matter/dust. Among twenty-one previously healthy, deployable soldiers with non-invasive pulmonary diagnostic tests, post-deployment, all had severely decreased MEP values, averaging 42% predicted. These same patients concurrently demonstrated abnormal airways reactance (X5Hz) and peripheral/distal airways resistance (D5–D20%) via IOS, averaging – 1369% and 23% predicted, respectively. These tests support the concept of airways hyperresponsiveness and distal airways narrowing, respectively. Among the five soldiers biopsied, all had constrictive bronchiolitis. We detected the presence of polycyclic aromatic hydrocarbons (PAH)—which are products of incomplete combustion—in the lung tissue of all five warfighters. All also had detectable titanium and iron in the lungs. Metals were all oxidized, supporting the concept of inhaling burned metals. Combustion temperature was consistent with that of burned petrol rather than higher temperatures noted with cigarettes. All were nonsmokers. Neutrophil extracellular traps were reported in two biopsies. Compared to our prior biopsies in our Middle East deployment database, these histopathologic results are similar, since all database biopsies have constrictive bronchiolitis, one has lung fibrosis with titanium bound to iron in fixed mathematical ratios of 1:7 and demonstrated polarizable crystals. These results, particularly constrictive bronchiolitis and polarizable crystals, support the prior data of King et al. (N. Engl. J. Med. 365:222–230, 2011) Soldiers in this cohort deployed to Iraq and Afghanistan since 2003, with exposure to airborne hazards, including sandstorms, burn pits, and improvised explosive devices, are at high risk for developing chronic clinical respiratory problems, including: (1) reduction in respiratory muscle strength; (2) airways hyperresponsiveness; and (3) distal airway narrowing, which may be associated with histopathologic evidence of lung damage, reflecting inhalation of burned particles from burn pits along with particulate matter/dust. Non-invasive pulmonary diagnostic tests are a predictor of burn pit-induced lung injury

36 MATERIALS SCIENCE↗
DOE OSTI2021

A novel lung-inspired 3D-printed desiccant-coated heat exchanger for high-performance humidity management in buildings

Offering an independent humidity management method for buildings, desiccant-coated heat exchangers (DCHXs) are deemed a promising approach to improve the overall energy efficiency of air conditioning (AC) systems. State-of-the-art DCHXs, however, are bound with conventional HX topologies either providing limited desiccant-air interfacial areas or introducing excessive pressure drop penalties. In this paper a novel 3D-printed DCHX concept inspired by the bronchi arrangement of a human lung is introduced to address the shortcomings inherent in existing DCHX designs. The proposed lung-inspired DCHX utilizes two intertwined bicontinuous flow networks enabling highly efficient heat and mass transfer characteristics for augmented adsorption and regeneration processes at low pressure drop penalties. While the first network evenly distributes an incoming air stream through the entire volume of the lung-inspired DCHX, the second network volumetrically splits a cooling water stream within and through the first network. Effects of various parameters including air flow rate, outdoor air humidity ratio, and regeneration temperature on dehumidification performance and energy efficiency of the proposed lung-inspired DCHX were investigated. Experimental results indicated the proposed lung-inspired 3D-printed DCHX outperforms existing DCHX systems by demonstrating an excellent balance between a high volumetric adsorption rate and a low pressure drop penalty. The volumetric adsorption rate of the proposed lung-inspired DCHX technology is 54.8 g/m 3 -s, a more than two-fold improvement compared with state-of-the-art DCHX systems. Additionally, the lung-inspired DCHX offers high thermal energy efficiency of 56% at a low regeneration temperature of 40 °C. Therefore, the proposed lung-inspired 3D-printed DCHX offers a new solid-desiccant-based air dehumidification pathway for next-generation high-performance AC systems.

32 ENERGY CONSERVATION, CONSUMPTION, AND UTILIZATI↗
DOE OSTI2023

Validation of a Proteomic Signature of Lung Cancer Risk from Bronchial Specimens of Risk-Stratified Individuals

A major challenge in lung cancer prevention and cure hinges on identifying the at-risk population that ultimately develops lung cancer. Previously, we reported proteomic alterations in the cytologically normal bronchial epithelial cells collected from the bronchial brushings of individuals at risk for lung cancer. The purpose of this study is to validate, in an independent cohort, a selected list of 55 candidate proteins associated with risk for lung cancer with sensitive targeted proteomics using selected reaction monitoring (SRM). Bronchial brushings collected from individuals at low and high risk for developing lung cancer as well as patients with lung cancer, from both a subset of the original cohort (batch 1: n = 10 per group) and an independent cohort of 149 individuals (batch 2: low risk (n = 32), high risk (n = 34), and lung cancer (n = 83)), were analyzed using multiplexed SRM assays. ALDH3A1 and AKR1B10 were found to be consistently overexpressed in the high-risk group in both batch 1 and batch 2 brushing specimens as well as in the biopsies of batch 1. Validation of highly discriminatory proteins and metabolic enzymes by SRM in a larger independent cohort supported their use to identify patients at high risk for developing lung cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2024

Evaluating county-level lung cancer incidence from environmental radiation exposure, PM 2.5 , and other exposures with regression and machine learning models

Characterizing the interplay between exposures shaping the human exposome is vital for uncovering the etiology of complex diseases. For example, cancer risk is modified by a range of multifactorial external environmental exposures. Environmental, socioeconomic, and lifestyle factors all shape lung cancer risk. However, epidemiological studies of radon aimed at identifying populations at high risk for lung cancer often fail to consider multiple exposures simultaneously. For example, moderating factors, such as PM 2.5 , may affect the transport of radon progeny to lung tissue. This ecological analysis leveraged a population-level dataset from the National Cancer Institute’s Surveillance, Epidemiology, and End-Results data (2013–17) to simultaneously investigate the effect of multiple sources of low-dose radiation (gross γ activity and indoor radon) and PM 2.5 on lung cancer incidence rates in the USA. County-level factors (environmental, sociodemographic, lifestyle) were controlled for, and Poisson regression and random forest models were used to assess the association between radon exposure and lung and bronchus cancer incidence rates. Tree-based machine learning (ML) method perform better than traditional regression: Poisson regression: 6.29/7.13 (mean absolute percentage error, MAPE), 12.70/12.77 (root mean square error, RMSE); Poisson random forest regression: 1.22/1.16 (MAPE), 8.01/8.15 (RMSE). The effect of PM 2.5 increased with the concentration of environmental radon, thereby confirming findings from previous studies that investigated the possible synergistic effect of radon and PM 2.5 on health outcomes. In summary, the results demonstrated (1) a need to consider multiple environmental exposures when assessing radon exposure’s association with lung cancer risk, thereby highlighting (1) the importance of an exposomics framework and (2) that employing ML models may capture the complex interplay between environmental exposures and health, as in the case of indoor radon exposure and lung cancer incidence.

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTAN↗
DOE OSTI2021

A census of the lung: CellCards from LungMAP

The human lung plays vital roles in respiration, host defense, and basic physiology. Recent technological advancements such as single-cell RNA sequencing and genetic lineage tracing have revealed novel cell types and enriched functional properties of existing cell types in lung. The time has come to take a new census. Initiated by members of the NHLBI-funded LungMAP Consortium and aided by experts in the lung biology community, we synthesized current data into a comprehensive and practical cellular census of the lung. Identities of cell types in the normal lung are captured in individual cell cards with delineation of function, markers, developmental lineages, heterogeneity, regenerative potential, disease links, and key experimental tools. This publication will serve as the starting point of a live, up-to-date guide for lung research at https://www.lungmap.net/cell-cards/. We hope that Lung CellCards will promote the community-wide effort to establish, maintain, and restore respiratory health.

COVID↗
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↗
NASA NTRS1972

Stresses, strains, and surface pressures in the lung caused by its weight.

In an effort to understand how the lung is deformed by its own weight, we have analyzed the distribution of regional expansion, stresses, and surface pressures in a theoretical elastic lung-shaped model using the technique of finite elements. In the upright position, the parenchyma was most expanded at the apex and least at the base. Stresses in both the vertical and lateral directions were maximal at the apex. As the lung was inflated from very low volumes to total lung capacity, parenchymal expansion and stress at the apex first decreased, then increased. This behavior can be explained by the increasing rigidity of the expanded lung which enabled it to resist distortion by its own weight. At functional residual capacity, the stress at the apex was near its minimum. The differences in intrapleural pressure down the lung were volume dependent, increasing at very low volumes. In the inverted lung, the regional differences in stress, strain, and surface pressures were less marked because of the shape of the chest.

West, J. B.↗
DOE OSTI2021

Dexmedetomidine preconditioning ameliorates lung injury induced by pulmonary ischemia/reperfusion by upregulating promoter histone H3K4me3 modification of KGF-2

Highlights: • DexP alleviates I/R-induced lung injury and endothelial barrier dysfunction in mice. • DexP reduces the inflammatory response and increases KGF-2 expression in I/R. • DexP regulates the H3K4me3 modification of KGF-2 promoter histone. • DexP promotes KGF-2 expression by downregulating the expression of JMJD3. • DexP has the potential to be used as a means of treating I/R-induced lung injury. Keratinocyte growth factor (KGF)-2 has been highlighted to play a significant role in maintaining the endothelial barrier integrity in lung injury induced by ischemia-reperfusion (I/R). However, the underlying mechanism remains largely unknown. The aims of this study were to determine whether dexmedetomidine preconditioning (DexP) modulates pulmonary I/R-induced lung injury through the alteration in KGF-2 expression. In our I/R-modeled mice, DexP significantly inhibited pathological injury, inflammatory response, and inflammatory cell infiltration, while promoted endothelial barrier integrity and KGF-2 promoter activity in lung tissues. Bioinformatics prediction and ChIP-seq revealed that I/R significantly diminished the level of H3K4me3 modification in the KGF-2 promoter, which was significantly reversed by DexP. Moreover, DexP inhibited the expression of histone demethylase JMJD3, which in turn promoted the expression of KGF-2. In addition, overexpression of JMJD3 weakened the protective effect of DexP on lung injury in mice with I/R. Collectively, the present results demonstrated that DexP ameliorates endothelial barrier dysfunction via the JMJD3/KGF-2 axis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2023

Reconstructed lung doses for the million person study cohort of 26,650 Tennessee Eastman corporation workers employed between 1942 and 1947

Abstract Tennessee Eastman Corporation workers were exposed to uranium dust resulting in high-linear energy transfer (LET) irradiation to lung tissue. In this work, radiation lung doses were reconstructed for 26 650 men and women working at the plant between 1942 and 1947. Site air monitoring data of uranium concentrations and payroll records were used to determine the daily inhaled activities and annualized lung doses. Variations in the activity median aerodynamic diameter of the uranium dust, the solubility of particulate matter in the lungs and the sex-specific breathing rate were investigated as part of a sensitivity analysis. Male and female mean lung doses of 18.9 and 32.7 mGy, respectively, from high-LET alpha irradiation, and there was general agreement with evaluations from previously published epidemiological studies. Annual lung dose estimates and sensitivity analysis for the 26 650 workers in the TEC cohort have been archived on the United States Department of Energy Comprehensive Epidemiologic Data Resource.

61 RADIATION PROTECTION AND DOSIMETRY↗
NASA NTRSDate not supplied

Plausible Biological Mechanisms Underlying Sex Differences in Radiation-Induced Lung Cancer Risk

Some epidemiological studies suggest that women are at greater risk for radiation-induced lung cancer than men, but this observation is not consistent across all studies. A scientific committee formed by the National Council on Radiation Protection and Measurement evaluated evidence for a sex difference in lung cancer risk from radiation exposuresby reviewing animal studies and assessing the biological plausibility that such a difference might exist. The committee identified four mechanisms that could potentially result in greater radiogenic lung cancer risks for women. The first of these is that radiation exposure increases the relative risk for a molecular subtype of spontaneous lung cancer that occurs predominantly in women. The second is that is that sex chromosome or gene expression differences between men and women places women at greater risk. The third is that hormonal differences between men and women, particularly for estrogen levels, puts women at greater risk. The fourth mechanism is that sex differences in immune system function underlie a sex difference in radiation associated lung cancer risk.None of these mechanisms hasyet been proven to play a role in radiogenic lung cancer risk.

radiation↗
DOE OSTI2021

Olivine Dissolution in Simulated Lung and Gastric Fluid as an Analog to the Behavior of Lunar Particulate Matter Inside the Human Respiratory and Gastrointestinal Systems

With the Artemis III mission scheduled to land humans on the Moon in 2025, work must be done to understand the hazards lunar dust inhalation would pose to humans. In this study, San Carlos olivine was used as an analog of lunar olivine, a common component of lunar dust. Olivine was dissolved in a flow-through apparatus in both simulated lung fluid and 0.1 M HCl (simulated gastric fluid) over a period of approximately 2 weeks at physiological temperature, 37°C. Effluent samples were collected periodically and analyzed for pH, iron, silicon, and magnesium ion concentrations. The dissolution rate data derived from our measurements allow us to estimate that an inhaled 1.0 μm diameter olivine particle would take approximately 24 years to dissolve in the human lungs and approximately 3 weeks to dissolve in gastric fluid. Results revealed that inhaled olivine particles may generate the toxic chemical, hydroxyl radical, for up to 5–6 days in lung fluid. Olivine dissolved in 0.1 M HCl for 2 weeks transformed to an amorphous silica-rich solid plus the ferric iron oxy-hydroxide ferrihydrite. Olivine dissolved in simulated lung fluid shows no detectable change in composition or crystallinity. Equilibrium thermodynamic models indicate that olivine in the human lungs can precipitate secondary minerals with fibrous crystal structures that have the potential to induce detrimental health effects similar to asbestos exposure. Our work indicates that inhaled lunar dust containing olivine can settle in the human lungs for years and could induce long-term potential health effects like that of silicosis.

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTAN↗