Experimental investigation of harmonic ion cyclotron wave propagation and attenuation.
Harmonic ion cyclotron wave propagation and attenuation investigated experimentally
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Harmonic ion cyclotron wave propagation and attenuation investigated experimentally
Temperature and frequency effects on amplitude- independent longitudinal ultrasonic attenuation in superconducting lead
Ultrasonic attenuation measurements at high magnetic fields in mixed state for clean and dirty limits
Longitudinal ultrasound attenuation in polycrystalline superconducting mercury at 9.3 GHz, studying temperature dependence
The purpose of this study is to investigate ways to combine estimates from the Surface Reference and Hitschfeld-Bordan methods into a hybrid path attenuation estimate and to study its performance using dual-frequency radar data provided by the Dual-Frequency Precipitation Radar (DPR) on board the Global Precipitation Mission (GPM) satellite.
Several algorithms to calculate a rain-rate profile from a single-frequency air- or space-borne radar backscatter profile and a given path-integrated attenuation have been proposed.
ABSTRACT CXCL12 is abundantly expressed in reticular cells associated with the perivascular niches of the bone marrow (BM) and is indispensable for B lymphopoiesis. Cxcl12 promotes osteoclastogenesis and has been implicated in pathologic bone resorption. We had shown earlier that estrogen receptor α deletion in osteoprogenitors and estrogen deficiency in mice increase Cxcl12 mRNA and protein levels in the BM plasma, respectively. We have now generated female and male mice with conditional deletion of a Cxcl12 allele in Prrx1 targeted cells (Cxcl12∆Prrx1) and show herein that they have a 90% decrease in B lymphocytes but increased erythrocytes and adipocytes in the marrow. Ovariectomy increased the expression of Cxcl12 and B-cell number in the Cxcl12f/f control mice, but these effects were abrogated in the Cxcl12∆Prrx1 mice. Cortical bone mass was not affected in Cxcl12∆Prrx1 mice. Albeit, the cortical bone loss caused by ovariectomy was greatly attenuated. Most unexpectedly, the rate of bone turnover in sex steroid–sufficient female or male Cxcl12∆Prrx1 mice was dramatically increased, as evidenced by a more than twofold increase in several osteoblast- and osteoclast-specific mRNAs, as well as increased mineral apposition and bone formation rate and increased osteoclast number in the endosteal surface. The magnitude of the Cxcl12∆Prrx1-induced changes were much greater than those caused by ovariectomy or orchidectomy in the Cxcl12f/f mice. These results strengthen the evidence that CXCL12 contributes to the loss of cortical bone mass caused by estrogen deficiency. Moreover, they reveal for the first time that in addition to its effects on hematopoiesis, CXCL12 restrains bone turnover—without changing the balance between resorption and formation—by suppressing osteoblastogenesis and the osteoclastogenesis support provided by cells of the osteoblast lineage. © 2020 American Society for Bone and Mineral Research.
Abstract Wogonoside (WG) is a flavonoid chemical component extracted from Scutellaria baicalensis, which exerts therapeutic effects on liver diseases. Ferroptosis, a novel form of programmed cell death, regulates diverse physiological/pathological processes. In this study, we attempted to investigate a novel mechanism by which WG mitigates liver fibrosis by inducing ferroptosis in hepatic stellate cells (HSCs). A CCl 4 ‐induced mouse liver fibrosis model and a rat HSC line were employed for in vivo and in vitro experiments, both treated with WG. Firstly, the levels of the fibrotic markers α‐smooth muscle actin (α‐SMA) and α1(I)collagen (COL1α1) were effectively decreased by WG in CCl 4 ‐induced mice and HSC‐T6 cells. Additionally, mitochondrial condensation and mitochondrial ridge breakage were observed in WG‐treated HSC‐T6 cells. Furthermore, ferroptotic events including depletion of SLC7A11, GPX4 and GSH, and accumulation of iron, ROS and MDA were discovered in WG‐treated HSC‐T6 cells. Intriguingly, these ferroptotic events did not appear in hepatocytes or macrophages. WG‐elicited HSC ferroptosis and ECM reduction were dramatically abrogated by ferrostatin‐1 (Fer‐1), a ferroptosis inhibitor. Importantly, our results confirm that SOCS1/P53/SLC7A11 is a signaling pathway which promotes WG attenuation of liver fibrosis. On the contrary, WG mitigated liver fibrosis and inducted HSC‐T6 cell ferroptosis were hindered by SOCS1 siRNA and pifithrin‐α (PFT‐α). These findings demonstrate that SOCS1/P53/SLC7A11‐mediated HSC ferroptosis is associated with WG alleviating liver fibrosis, which provides a new clue for the treatment of liver fibrosis.
Benzene homologues often used as organic raw materials or as detergents in chemical industry are prone to accidental release into the environment which can cause serious long-term soil pollutions. In a large former herbicide factory site, we investigated 43 locations for benzene homologues contaminations in soil, soil gas, and groundwater; and studied the hydrogeological conditions. An inverse distance weighted interpolation method was employed to determine the pollutants three-dimensional spatial distribution in the soils. Results showed that benzene homologues residues were mainly originated from the herbicide production workshop; and that the pollution had horizontally expanded at the deeper soil layer. Contaminants had already migrated 15m downward from ground surface. Contaminant phase distribution study showed that NAPL was the primary phase (>99%) for the pollutants accumulated in the unsaturated zone; while it had not migrated to groundwater. The primary mechanism for contaminant transport and attenuation included dissolution of “occluded” NAPL into pore water and pollutant volatilization into soil pore space. Risk assessment revealed that the pollutants brought unacceptable high carcinogenic and non-carcinogenic risks to public health. In order to convert this former chemical processing factory site into a residential area, a remediation to the polluted production workshop sites is urgently required.
Abstract While PSI-driven cyclic electron flow (CEF) and assembly of thylakoid supercomplexes have been described in model organisms like Chlamydomonas reinhardtii , open questions remain regarding their contributions to survival under long-term stress. The Antarctic halophyte, C. priscuii UWO241 (UWO241), possesses constitutive high CEF rates and a stable PSI-supercomplex as a consequence of adaptation to permanent low temperatures and high salinity. To understand whether CEF represents a broader acclimation strategy to short- and long-term stress, we compared high salt acclimation between the halotolerant UWO241, the salt-sensitive model, C. reinhardtii , and a moderately halotolerant Antarctic green alga, C. sp. ICE-MDV (ICE-MDV). CEF was activated under high salt and associated with increased non-photochemical quenching in all three Chlamydomonas species. Furthermore, high salt-acclimated cells of either strain formed a PSI-supercomplex, while state transition capacity was attenuated. How the CEF-associated PSI-supercomplex interferes with state transition response is not yet known. We present a model for interaction between PSI-supercomplex formation, state transitions, and the important role of CEF for survival during long-term exposure to high salt.
Uranium minerals are commonly found in soils and sediment across the United States at an average concentration of 2–4 mg/kg. Uranium occurs in the environment primarily in two forms, the oxidized, mostly soluble uranium(VI) form, or the reduced, sparingly soluble reduced uranium(IV) form. Here we describe subsurface geochemical conditions that result in low uranium concentrations in an alluvial aquifer with naturally occurring uranium in soils and sediments in the presence of complexing ligands under oxidizing conditions. Groundwater was saturated with respect to calcite and contained calcium (78–90 mg/L) with elevated levels of carbonate alkalinity (291–416 mg/L as HCO 3 -). X-ray adsorption near edge structure (XANES) spectroscopy identified that sediment-associated uranium was oxidized as a uranium(VI) form (85%). Calcite was the predominant mineral by mass in the ultrafine fraction in uranium-bearing sediments (>16 mg/kg). Furthermore, groundwater geochemical modeling indicated calcite and/or a calcium-uranyl-carbonate mineral such as liebigite in equilibrium with groundwater. The δ 13 C (0.57‰ ± 0.15‰) was indicative of abiotic carbonate deposition. Thus, solid-phase uranium(VI) associated with carbonate is likely maintaining uranium(VI) groundwater levels below the maximum contaminant level (MCL; 30 µg/L), presenting a deposition mechanism for uranium attenuation rather than solely a means of mobilization.
In this study, high-Cu weld material harvested from an ex service reactor pressure vessel (RPV) steel from Unit 1 of the decommissioned Zion Nuclear Generating Station has been characterized using atom probe tomography. Samples taken from 4 different positions through the thicknesses of the pressure vessel wall from the water-side to the air-side were characterized, along with an unirradiated baseline material. In the baseline material, no precipitates were found and the Cu was observed to be fully in solid solution; however, scanning transmission electron microscopy combined with energy dispersive spectroscopy (STEM-EDS) revealed the presence of ϵ -Cu that form during processing of the material and results in the concomitant decrease of matrix Cu. Following irradiation, a high number density of nano-scale Cu-rich precipitates (CRPs) were observed, uniformly distributed throughout the matrix. The Cu content within the CRPs was found to be ~30-35 at.% regardless of location in the wall. No statistically significant variation in the compositions, mean radius, number density, or volume fraction as a function of location within the wall was observed. The measured matrix Cu level excluding CRPs contribution was found to be ~90 appm higher than the solubility limit suggesting that further nucleation and growth of the CRPs under continued operations would have occurred. These results clearly demonstrate that the neutron energy attenuation has no significant effect on the precipitation kinetics of CRPs regardless of location in the wall in high-Cu RPV steels under irradiation.
Macrophage mediated inflammation and foam cell formation play crucial roles in the development of atherosclerosis. MiR-375 is a small noncoding RNA that significantly implicated in multiple tumor regulation and has been emerged as a novel biomarker for type 2 diabetes. However, the exact role of miR-375 on macrophage activation remains unknown. In the present study, we observed that miR-375 expression showed an up-regulated expression in atherosclerotic aortas, as well as in bone marrow derived macrophages (BMDMs) and mouse peritoneal macrophages (MPMs) isolated from ApoE deficiency mice and was gradually increased followed the Ox-LDL treated time. Functionally, miR-375 inhibition significantly decreased foam cell formation accompanied by up-regulated genes expression involved in cholesterol efflux but reduced genes expression implicated in cholesterol influx. Moreover, miR-375 silencing increased resolving M2 macrophage but reduced pro-inflammatory M1 macrophage markers expression. Such above effects can be reversed by miR-375 overexpression. Mechanistically, we noticed that miR-375 knockdown promoted KLF4 expression which was required for the ameliorated effect of miR-375 silencing on macrophage activation. Importantly, the consistent results in mRNA expression of M1 and M2 markers were observed in vivo, and miR-375{sup −/−}ApoE{sup −/−} mice significant decreased atherosclerotic lesions in the whole aorta and aortic sinus. Taken together, these evidences suggested that miR-375 knockdown attenuated macrophage activation partially through activation of KLF4-dependent mechanism.
Highlights: • Acute lung injury (ALI) is a leading cause of mortality and therapies for ALI are yet to be thoroughly investigated. • Recent evidence has shown that irisin attenuates lipopolysaccharide-induced acute lung injury. • Irisin can alleviate ALI by inhibiting miR-199a and upregulating Rad23b expression. Acute lung injury (ALI) is a leading cause of mortality as a result of inflammatory cytokine overexpression and increased rates of apoptosis. Therapies for ALI are yet to be thoroughly investigated. Recent evidence has shown that irisin exerts protective effects against many types of pathologies. The present study aimed to determine the function of irisin in an ALI mouse model induced by lipopolysaccharide (LPS) and the corresponding underlying mechanisms at the tissue, cellular, and molecular levels.
In situ mid-infrared spectroscopy is a powerful technique for understanding the mechanism of CO 2 reduction (CO 2 R) catalysts because it enables the direct detection of catalytic intermediates and products. Moreover, spectroelectrochemistry (SEC), the coupling of spectroscopy with electrochemistry, allows spectroscopic changes to be correlated with applied potentials to reveal potential-dependent intermediates that are often relevant to photoelectrochemical reactions. Hybrid photoelectrodes, comprised of a narrow bandgap semiconductor, like silicon (Si), with a covalently-linked molecular catalyst, are a promising platform for sunlight-driven catalysis, but characterization of the catalytic mechanism(s) is challenging under photoelectrochemical conditions, particularly when the catalyst is present in monolayer or less concentrations. Here, we have developed a new strategy to use multiple-reflection attenuated total reflectance IR spectroscopy (ATR-IR) coupled with electrochemistry to characterize catalysts directly integrated with a semiconductor surface under applied potential. We show that by surface-proximal n-type or p-type doping of the top ~100-200 nm of the crystal surface, Si ATR crystals can be used simultaneously as the internal reflection element and semiconductor working electrode for ATR-IR-SEC measurements. The surface-proximal doping strategy yields a quasi-equipotential surface with excellent infrared transparency that would have been compromised by free carrier absorption if the crystal was uniformly doped. This approach permits the catalytically-active functionalized surface to be directly probed without modification and overcomes signal-to-noise limitations of other strategies that use separately deposited working electrodes on Si ATR crystals. Proof-of-concept ATR-IR-SEC spectra were collected during the reduction and oxidation of monolayers of Re- and Ru-based transition metal carbonyl complexes, respectively, verifying the viability of the technique to probe redox processes associated with CO 2 R catalysts on Si electrode surfaces with high sensitivity.
Modulating gene expression in macrophages can be used to improve tissue regeneration and redirect tumor microenvironments (TMEs) toward positive therapeutic outcomes. We have developed Bacillus subtilis as an engineered endosymbiont (EES) capable of residing inside the eukaryotic host cell cytoplasm and controlling the fate of macrophages. Secretion of mammalian transcription factors (TFs) from B. subtilis that expresses listeriolysin O (LLO; allowing the EES to escape destruction by the macrophage) modulated expression of surface markers, cytokines, and chemokines, indicating functional changes in a macrophage/monocyte cell line. The engineered B. subtilis LLO TF strains were evaluated in murine bone marrow-derived macrophages (BMDMs) by flow cytometry, chemokine/cytokine profiling, metabolic assays, and RNA-Seq delivery of TFs by the EES shifted BMDM gene expression, production of cytokine and chemokines, and metabolic patterns, indicating that the TF strains could guide primary macrophage function. Thereafter, the ability of the TF strains to alter the TME was characterized in vivo in an orthotopic murine model of triple-negative breast cancer to assess therapeutic effects. The TF strains altered the TME by shifting immune cell composition and attenuating tumor growth. Additionally, multiple doses of the TF strains were well-tolerated by the mice. The use of B. subtilis LLO TF strains as EES showed promise as a unique cancer immunotherapy by directing the immune function intracellularly. The uses of EES could be expanded to modulate other mammalian cells over a range of biomedical applications.
Silica optical fiber sensors offer a fast, distributed measurement solution in various cryogenic and radiation environments, such as magnets for fusion power. Under these conditions, light-absorbing point defects limit lifetime via radiation-induced attenuation (RIA). To support RIA kinetics prediction, we present an in situ, broadband absorption spectroscopy setup combining gamma irradiation with liquid nitrogen cooling. The apparatus enables continuous monitoring of narrowband RIA levels and the use of secondary optical annealing light sources, alongside broadband spectrum measurements to characterize RIA defects through spectrum decomposition. Initial results confirm the inevitable photobleaching effect of the probe light source, which must be accounted for. In addition, we report RIA kinetics during cycles of gamma irradiation at 77 K and isochronal thermal annealing steps from liquid nitrogen to room temperature, showcasing the setup’s ability to replicate real fiber operation scenarios. These instruments form an ideal platform to further study the kinetics of RIA coupled with thermal and optical annealing.
The metazoan innate immune second messenger 2'3'-cGAMP is present both inside and outside cells. However, only extracellular cGAMP can be negatively regulated by the extracellular hydrolase ENPP1. Here, we determine whether ENPP1’s regulation of extracellular cGAMP is a ubiquitous mechanism of attenuating stimulator of interferon genes (STING) signaling. We identified ENPP1 H362A , a point mutation that cannot degrade the 2'-5' linkage in cGAMP while maintaining otherwise normal function. The selectivity of this histidine is conserved down to bacterial nucleotide pyrophosphatase/phosphodiesterase (NPP), allowing structural analysis and suggesting an unexplored ancient history of 2'-5' cyclic dinucleotides. Enpp1 H362A mice demonstrated that extracellular cGAMP is not responsible for the devastating phenotype in ENPP1-null humans and mice but is responsible for antiviral immunity and systemic inflammation. Our data define extracellular cGAMP as a pivotal STING activator, identify an evolutionarily critical role for ENPP1 in regulating inflammation, and suggest a therapeutic strategy for viral and inflammatory conditions by manipulating ENPP1 activity.