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Qiu, J.

Publications and source records attributed to Qiu, J..

8 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2022

A multimodal approach to revisiting oxidation defects in Cr 2 O 3

The oxidation of chromium in air at 700 °C was investigated with a focus on point defect behavior and transport during oxide layer growth. A comprehensive set of characterization techniques targeted characteristics of chromium oxide microstructure and chemical composition analysis. TEM showed that the oxide was thicker with longer oxidation times and that, for the thicker oxides, voids formed at the metal/oxide interface. PAS revealed that the longer the oxidation time, there was an overall reduction in vacancy-type defects, though chromium monovacancies were not found in either case. EIS found that the longer oxidized material was more electrochemically stable and that, while all oxides displayed p-type character, the thicker oxide had an overall lower charge carrier density. Together, the results suggest anion oxygen interstitials and chromium vacancy cluster complexes drive transport in an oxidizing environment at this temperature, providing invaluable insight into the mechanisms that regulate corrosion.

36 MATERIALS SCIENCE↗
DOE OSTI2022

Snowmass 2021 White Paper: Electron Ion Collider for High Energy Physics

Electron Ion Collider (EIC) is a particle accelerator facility planned for construction at Brookhaven National Laboratory on Long Island, New York by the United States Department of Energy. EIC will provide capabilities of colliding beams of polarized electrons with polarized beams of proton and light ions. EIC will be one of the largest and most sophisticated new accelerator facilities worldwide, and the only new large-scale accelerator facility planned for construction in the United States in the next few decades. The versatility, resolving power and intensity of EIC will present many new opportunities to address some of the crucial and fundamental open scientific questions in particle physics. This document provides an overview of the science case of EIC from the perspective of the high energy physics community.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
NASA NTRS2001

H-alpha Proxies for EIT Crinkles: Further Evidence for Pre-Flare "Breakout"-Type Activity in an Ejective Solar Eruption

We present Halpha observations from Big Bear Solar Observatory of an eruptive flare in NOAA AR 8210, occurring near 22:30 UT on 1998 May 1. Previously, using the EUV Imaging Telescope (EIT) on the SOHO spacecraft, we found that a pattern of transient, localized brightenings, which we call "EIT crinkles," appears in the neighborhood of the eruption near the time of flare onset. These EIT crinkles occur at a location in the active region well separated from the sheared core magnetic fields, which is where the most intense features of the eruption are concentrated. We also previously found that high-cadence images from the Soft X-ray Telescope (SXT) on Yohkoh indicate that soft X-ray intensity enhancements in the core begin after the start of the EIT crinkles. With the Halpha data, we find remote flare brightening counterparts to the EIT crinkles. Lightcurves as functions of time of various areas of the active region show that several of the remote flare brightenings undergo intensity increases prior to onset of principle brightenings in the core region, consistent with our earlier findings from EIT and SXT data. These timing relationships are consistent with the eruption onset mechanism known as the breakout model, introduced by Antiochos and colleagues, which proposes that eruptions begin with reconnection at a magnetic null high above the core region. Our observations are also consistent with other proposed mechanisms which do not involve early reconnection in the core region. As a corollary, our observations are not consistent with the so-called tether cutting models, which say that the eruption begins with reconnection in the core. The Halpha data further show that a filament in the core region becomes activated near the time of EIT crinkle onset, but little if any of the filament actually erupts, despite the presence of a halo Coronal Mass Ejection (CME) associated with this event.

Sterling, Alphonse C.↗
NASA NTRS2000

Ca(2+) regulates fluid shear-induced cytoskeletal reorganization and gene expression in osteoblasts

Osteoblasts subjected to fluid shear increase the expression of the early response gene, c-fos, and the inducible isoform of cyclooxygenase, COX-2, two proteins linked to the anabolic response of bone to mechanical stimulation, in vivo. These increases in gene expression are dependent on shear-induced actin stress fiber formation. Here, we demonstrate that MC3T3-E1 osteoblast-like cells respond to shear with a rapid increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) that we postulate is important to subsequent cellular responses to shear. To test this hypothesis, MC3T3-E1 cells were grown on glass slides coated with fibronectin and subjected to laminar fluid flow (12 dyn/cm(2)). Before application of shear, cells were treated with two Ca(2+) channel inhibitors or various blockers of intracellular Ca(2+) release for 0. 5-1 h. Although gadolinium, a mechanosensitive channel blocker, significantly reduced the [Ca(2+)](i) response, neither gadolinium nor nifedipine, an L-type channel Ca(2+) channel blocker, were able to block shear-induced stress fiber formation and increase in c-fos and COX-2 in MC3T3-E1 cells. However, 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, an intracellular Ca(2+) chelator, or thapsigargin, which empties intracellular Ca(2+) stores, completely inhibited stress fiber formation and c-fos/COX-2 production in sheared osteoblasts. Neomycin or U-73122 inhibition of phospholipase C, which mediates D-myo-inositol 1,4,5-trisphosphate (IP(3))-induced intracellular Ca(2+) release, also completely suppressed actin reorganization and c-fos/COX-2 production. Pretreatment of MC3T3-E1 cells with U-73343, the inactive isoform of U-73122, did not inhibit these shear-induced responses. These results suggest that IP(3)-mediated intracellular Ca(2+) release is required for modulating flow-induced responses in MC3T3-E1 cells.

Non-NASA Center↗
NASA NTRS1998

Fluid shear-induced mechanical signaling in MC3T3-E1 osteoblasts requires cytoskeleton-integrin interactions

Mechanical stimulation of bone induces new bone formation in vivo and increases the metabolic activity and gene expression of osteoblasts in culture. We investigated the role of the actin cytoskeleton and actin-membrane interactions in the transmission of mechanical signals leading to altered gene expression in cultured MC3T3-E1 osteoblasts. Application of fluid shear to osteoblasts caused reorganization of actin filaments into contractile stress fibers and involved recruitment of beta1-integrins and alpha-actinin to focal adhesions. Fluid shear also increased expression of two proteins linked to mechanotransduction in vivo, cyclooxygenase-2 (COX-2) and the early response gene product c-fos. Inhibition of actin stress fiber development by treatment of cells with cytochalasin D, by expression of a dominant negative form of the small GTPase Rho, or by microinjection into cells of a proteolytic fragment of alpha-actinin that inhibits alpha-actinin-mediated anchoring of actin filaments to integrins at the plasma membrane each blocked fluid-shear-induced gene expression in osteoblasts. We conclude that fluid shear-induced mechanical signaling in osteoblasts leads to increased expression of COX-2 and c-Fos through a mechanism that involves reorganization of the actin cytoskeleton. Thus Rho-mediated stress fiber formation and the alpha-actinin-dependent anchorage of stress fibers to integrins in focal adhesions may promote fluid shear-induced metabolic changes in bone cells.

Non-NASA Center↗
NASA NTRS1997

Mechanotransduction in bone: osteoblasts are more responsive to fluid forces than mechanical strain

Mechanical force applied to bone produces two localized mechanical signals on the cell: deformation of the extracellular matrix (substrate strain) and extracellular fluid flow. To study the effects of these stimuli on osteoblasts, MC3T3-E1 cells were grown on type I collagen-coated plastic plates and subjected to four-point bending. This technique produces uniform levels of physiological strain and fluid forces on the cells. Each of these parameters can be varied independently. Osteopontin (OPN) mRNA expression was used to assess the anabolic response of MC3T3-E1 cells. When fluid forces were low, neither strain magnitude nor strain rate was correlated with OPN expression. However, higher-magnitude fluid forces significantly increased OPN message levels independently of the strain magnitude or rate. These data indicate that fluid forces, and not mechanical stretch, influence OPN expression in osteoblasts and suggest that fluid forces induced by extracellular fluid flow within the bone matrix may play an important role in bone formation in response to mechanical loading.

Non-NASA Center↗