Engineering Papers⌕ Search

SEARCH · Engineering Papers

Results for “MIGRATION”

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.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

Transforming growth factor-beta1 promotes the migration and invasion of sphere-forming stem-like cell subpopulations in esophageal cancer

Esophageal cancer is one of the most lethal solid malignancies. Mounting evidence demonstrates that cancer stem cells (CSCs) are able to cause tumor initiation, metastasis and responsible for chemotherapy and radiotherapy failures. As CSCs are thought to be the main reason of therapeutic failure, these cells must be effectively targeted to elicit long-lasting therapeutic responses. We aimed to enrich and identify the esophageal cancer cell subpopulation with stem-like properties and help to develop new target therapy strategies for CSCs. Here, we found esophageal cancer cells KYSE70 and TE1 could form spheres in ultra low attachment surface culture and be serially passaged. Sphere-forming cells could redifferentiate and acquire morphology comparable to parental cells, when return to adherent culture. The sphere-forming cells possessed the key criteria that define CSCs: persistent self-renewal, overexpression of stemness genes (SOX2, ALDH1A1 and KLF4), reduced expression of differentiation marker CK4, chemoresistance, strong invasion and enhanced tumorigenic potential. SB525334, transforming growth factor-beta 1(TGF-β1) inhibitor, significantly inhibited migration and invasion of sphere-forming stem-like cells and had no effect on sphere-forming ability. In conclusion, esophageal cancer sphere-forming cells from KYSE70 and TE1 cultured in ultra low attachment surface possess cancer stem cell properties, providing a model for CSCs targeted therapy. TGF-β1 promotes the migration and invasion of sphere-forming stem-like cells, which may guide future studies on therapeutic strategies targeting these cells. - Highlights: • Esophageal cancer sphere-forming cells possess cancer stem cell properties. • Sphere-forming cells enhance TGF-β1 pathway activity. • TGF-β 1 inhibitor suppresses the migration and invasion of sphere-forming cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

IGF-I regulates HT1080 fibrosarcoma cell migration through a syndecan-2/Erk/ezrin signaling axis

Highlights: • IGF-I exhibits significant involvement in cancer progression. • Syndecan-2 (SDC-2), has a discrete role in mesenchymal tumors progression. • SDC2 facilitates IGF-I-dependent HT1080 fibrosarcoma cell chemotactic migration. • SDC2 / IGF-IR / ezrin co-localization is demonstrated. • Mediator co-localization enhances actin polymerization and membrane linking. Fibrosarcoma is a tumor of mesenchymal origin, originating from fibroblasts. IGF-I is an anabolic growth factor which exhibits significant involvement in cancer progression. In this study, we investigated the possible participation of syndecan-2 (SDC-2), a cell membrane heparan sulfate (HS) proteoglycan on IGF-I dependent fibrosarcoma cell motility. Our results demonstrate that SDC-2-deficient HT1080 cells exhibit attenuated IGF-I-dependent chemotactic migration (p IGF-I enhanced actin polymerization and ezrin/actin specific localization to cell membranes. Finally, treatment with IGF-I strongly increased SDC2 expression at both the mRNA and protein level (p contributes to actin polymerization and ezrin/actin specific localization to cell membranes, ultimately facilitating the progression of IGFI-dependent fibrosarcoma cell migration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

High YBX1 expression indicates poor prognosis and promotes cell migration and invasion in nasopharyngeal carcinoma

Highlights: • YBX1 overexpressed in cytoplasmic of nasopharyngeal carcinoma cells. • YBX1 expression associated with the EMT process in nasopharyngeal carcinoma. • TGF-β1 induced YBX1 expression in NPC cell lines. • TGF-β1/YBX1 signaling mediated the EMT process in NPC cell lines. Y-box binding protein-1 (YBX1) is a multifunctional protein and often acts as an indicator of poor prognosis in cancers. Increasing evidence has shown that the levels of YBX1 protein were closely associated with multidrug resistance, relapse, metastasis and poor prognosis in cancers. However, its role in nasopharyngeal carcinoma (NPC) metastasis remains unknown. In our study, we discovered that the expression of YBX1 was increased in nasopharyngeal carcinoma tissues. YBX1 protein levels positively correlated with T stage and metastasis of NPC patients. Moreover, expression of YBX1 was negatively correlated with membrane E-cadherin levels and positively correlated with Vimentin expression. In vitro, the expression of YBX1 was closely related to the invasive and migratory ability of nasopharyngeal carcinoma cells. Knockdown of YBX1 inhibited migration and invasion in 5–8 F cells, and over-expression of YBX1 promoted CNE1 cells migration and invasion. Transforming growth factor-β1 (TGF-β1) treatment led to epithelial-to-mesenchymal transition (EMT) in CNE1 cells accompanied by elevated YBX1 expression. On the contrary, knockdown of YBX1 partially inhibited the TGF-β1-induced CNE1 cell migration, together with changes of EMT-associated markers. Our study revealed that TGF-β1/YBX1 signaling might be one of novel mechanisms mediating EMT in NPC, providing a new target for the treatment of nasopharyngeal carcinoma.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Artemin regulates CXCR4 expression to induce migration and invasion in pancreatic cancer cells through activation of NF-κB signaling

Highlights: • Artemin regulates CXCR4 expression to induce migration and invasion in pancreatic cancer cells through activation of NF-κB signaling. • Artemin activates Akt and ERK, which cooperatively mediates activation of NF-κB and subsequent CXCR4 up-regulation. • Artemin induces an increase in migration and invasion potential in pancreatic cancer cell by regulating Akt and ERK1/2/NF-κB/CXCR4 signaling. Pancreatic ductal adenocarcinoma (PDAC) is the most lethal human malignant tumor because of the early onset of local invasion and distant metastasis. Perineural invasion is a prominent characteristic of pancreatic adenocarcinoma, which is a multifactorial process that involves various signaling molecules from different signaling pathways. The glial cell line-derived neurotrophic factor family of ligands was reported to be involved in perineural invasion in pancreatic cancer. Artemin is one member of the glial cell line-derived neurotrophic factor family of ligands. Although Artemin has previously been demonstrated to promote invasiveness of pancreatic cancer, the mechanisms remain poorly understood. In this study, we performed an analysis to determine the effects of Artemin on modulating tumor cell metastatic potential and invasion activity and explored its mechanisms in pancreatic cancer. We indicated that Artemin and CXCR4 were overexpressed in cancer tissues and widely expressed in pancreatic cancer cell lines. We observed that activation of ERK1/2 and Akt in Artemin-treated cells led to enhanced nuclear accumulation of NF-κB, which then induced CXCR4 expression. Through regulation of the expression of CXCR4, Artemin functionally promoted the migration and invasion in pancreatic cancer cells. The present study indicated that Artemin induced CXCR4 expression by activating Akt and ERK 1/2/NF-κB signaling, thereby modulating tumor cell metastatic potential and invasion activity in pancreatic cancer by regulating SDF-1α/CXCR4 axis. Artemin might be an effective and potent therapeutic target for pancreatic cancer metastasis, especially in perineural invasion.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Heregulin-induced cell migration is promoted by aryl hydrocarbon receptor in HER2-overexpressing breast cancer cells

Highlights: • Heregulin signaling up-regulates AhR expression at the transcriptional level in HER2-overexpressing breast cancer cells. • Heregulin signaling induces nuclear translocation of AhR. • Knockout of the AhR decreases cell migration by heregulin signaling in HER2-overexpressing breast cancer cells. HER2 overexpression accounts for approximately 15–20% of all breast cancers. We have shown that HER2 overexpression leads to elevated expression of the aryl hydrocarbon receptor (AhR) in breast cancer cells. In this study, firstly, we showed that AhR expression was up-regulated by treatment with the HER3 ligand heregulin (HRG) in HER2-overexpressing breast cancer cell lines. Induction of AhR was mediated by transcriptional activation of the region of AhR promoter corresponding to − 190 to − 100 bp. In addition, HRG treatment elicited nuclear translocation of AhR. To investigate the role of AhR in HRG-HER2/HER3 signaling in HER2-overexpressing cells, we established AhR knockout (KO) HER2-overexpressing cells to perform wound-healing assays. HRG-induced cell migration was markedly attenuated by AhR KO. HRG-induced cell migration was associated with increased expression of the inflammatory cytokines interleukin (IL)-6 and IL-8 in wild type cells, but not in AhR KO cells. These results elucidate that AhR is an important factor for the malignancy in HER2 overexpressing breast cancers.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

ER-localized protein-Herpud1 is a new mediator of IL-4-induced macrophage polarization and migration

Highlights: • Herpud1 is induced by IL-4 in M2 macrophages. • Herpud1 is involved in IL-4 promoted polarization and migration of M2 macrophage. • Herpud1-associated ER stress play an important role in polarization and migration of M2 macrophage. ER-localized proteins have been reported function in endoplasmic reticulum, unfolded protein degradation and destruction of misfolded proteins by the ER-associated protein degradation (ERAD) system, but their function in the chemotaxis of macrophage cells remained un-addressed. Here, we showed that ER protein with ubiquitin like domain 1(Herpud1) was upregulated in IL-4-treated M2 macrophage cells and its expression pattern was similar with macrophage polarization markers, such as Arg1, Mrc1 and Fizz1. Inhibition of Herpud1 by using specific target shRNA decreased these marker's expression at mRNA and protein level in IL-4-treated or -untreated M2 macrophage cells. IL-4 treatment promoted M2 macrophage cell migration and polarization, but this promotion was weakened by Herpud1 depletion and we got similar results by inhibition of ER stress response with chemical molecule 4-phenylbutyric acid (4-PBA) in IL-4-treated or untreated-M2 macrophage cells with Herpud1 overexpression. These results indicated that depending on ER-associated protein degradation (ERAD) to help unfolded protein degradation or destruction is not the only function of Herpud1 and acting as a mediator of IL-4 induced macrophage activation and polarization maybe another unrevealed function, elucidating the role of Herpud1-associated M2 macrophage cell polarization and activation are helpful for exploration the function of macrophage cells in immune response.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long non-coding RNA UCA1 upregulation promotes the migration of hypoxia-resistant gastric cancer cells through the miR-7-5p/EGFR axis

Highlights: • Two novel hypoxia-resistant gastric cancer (HRGC) cell lines were established. • UCA1 was upregulated in HRGC cells, which promoted their migration. • UCA1 directly interacted with miR-7-5p. • UCA1 suppressed the degradation of EGFR mRNA by sponging miR-7-5p. A variety of solid tumors are surrounded by a hypoxic microenvironment, which is known to be associated with high metastatic capability and resistance to various clinical therapies, contributing to a poor survival rate for cancer patients. Although the majority of previous studies on tumor-associated hypoxia have focused on acute hypoxia, chronic hypoxia more closely mimics the actual hypoxic microenvironment of a tumor. In this study, two novel hypoxia-resistant gastric cancer (HRGC) cell lines which could grow normally in 2% oxygen were established. The long non-coding RNA UCA1 was upregulated in HRGC cells, which promoted their migration. Bioinformatics analysis and a luciferase reporter assay showed that miR-7-5p could bind to specific sites of UCA1 to regulate the target EGFR through competitive endogenous RNA function. UCA1 directly interacted with miR-7-5p and decreased the binding of miR-7-5p to the EGFR 3′-untranslated region, which suppressed the degradation of EGFR mRNA by miR-7-5p. Therefore, long-term hypoxia induced UCA1 to promote cell migration by enhancing the expression of EGFR. This study thus reveals a new mechanism by which a hypoxic microenvironment promotes tumor metastasis, and highlights UCA1 as a potential biomarker for predicting the metastasis of gastric cancer to guide clinical treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Fibronectin amyloid-like aggregation alters its extracellular matrix incorporation and promotes a single and sparsed cell migration

Highlights: • Fibronectin can polymerize into amyloid-like aggregates. • Fibronectin amyloid-like aggregates promote a sparsed cell migration. • The supramolecular state of fibronectin could fine-tune cell phenotype. Fibronectin (Fn) is an extracellular matrix (ECM) multifunctional glycoprotein essential for regulating cells behaviors. Within ECM, Fn is found as polymerized fibrils. Apart from fibrils, Fn could also form other kind of supramolecular assemblies such as aggregates. To gain insight into the impact of Fn aggregates on cell behavior, we generated several Fn oligomeric assemblies. These assemblies displayed various amyloid-like properties but were not cytotoxic. In presence of the more amyloid-like structured assemblies of Fn, the cell-ECM networks were altered and the cell shapes shifted toward extended mesenchymal morphologies. Additionnaly, the Fn amyloid-like aggregates promoted a single-cell and sparsed migration of SKOV3 cancer cells, which was associated with a relocalization of αv integrins from plasma membrane to perinuclear vesicles. These data pointed out that the features of supramolecular Fn assemblies could represent a higher level of fine-tuning cell phenotype, and especially migration of cancer cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

MiR-940 promotes the proliferation and migration of gastric cancer cells through up-regulation of programmed death ligand-1 expression

Although anti-programmed death ligand-1 (PD-L1) therapy has shown light in treatment of gastric cancer, only a limited number of patients respond to the treatment. In addition to its immunosuppressive effect, PD-L1 is involved in other functions of tumor cells. Previously study showed that PD-L1 promoted EMT in lung cancer cells. However, the other effect and role of PD-L1 in gastric cancer remains unclear. In the present study, we first demonstrated that PD-L1 promoted the proliferation and migration in gastric cancer cell lines. We found that another STAT family member, STAT5a, is involved in regulating the expression of PD-L1 in gastric cancer. Additionally, Cbl-b interacted and ubiquitated STAT5a, down-regulated the expression of STAT5a and PD-L1. Moreover, bioinformatics predictions and experimental data showed that Cbl-b is a target gene of the microRNA miR-940. We further found that miR-940 promoted the proliferation and migration of gastric cancer in vivo and in vitro. Taken together, our findings suggest that miR-940/Cbl-b/STAT5a axis regulated the expression of PD-L1, which promotes the proliferation and migration of gastric cancer cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

PCGF3 promotes the proliferation and migration of non-small cell lung cancer cells via the PI3K/AKT signaling pathway

Highlights: • PCGF3 is highly expressed in non-small cell lung cancer (NSCLC) tissues. • PCGF3 overexpression positively correlates with lymph node metastasis and p-TNM staging. • PCGF3 promotes NSCLC cells proliferation by regulating CyclinB1, CyclinD1, and CDK4. • PCGF3 promotes NSCLC cells migration by regulating RhoA, RhoC, and CDC42. • PCGF3 promotes malignant behavior in NSCLC by positively regulating the PI3K/AKT signaling pathway. The Polycomb Group Ring Finger 3 (PCGF3) protein has been reported to be significantly upregulated in pancreatic islet tumors and related to signal transduction; however, its detailed mechanisms and biological roles in other tumors, including non-small cell lung cancer (NSCLC), remain unclear. This study investigated the function of PCGF3 in NSCLC and further elucidated its mechanism of action. The immunohistochemical analysis of 86 selected lung cancer tissues revealed that PCGF3 was highly expressed in NSCLC tissues and positively correlated with lymph node metastasis and p-TNM staging. Additionally, PCGF3 promoted cell proliferation in lung cancer by regulating CyclinB1, CyclinD1, and CDK4 expression, and also promoting their migration by regulating RhoA, RhoC, and CDC42. Furthermore, PCGF3 affected both the proliferation and migration of lung cancer cells by regulating the PI3K/AKT pathway, as verified by inhibiting this pathway using LY294002. The findings of this study suggested that PCGF3 is associated with poor prognosis in patients with NSCLC and could therefore be an important biomarker for treating and preventing NSCLC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Injectable platelet rich fibrin facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity

Hair follicle regeneration has been successful in mice but failed in human being for years. Dermal papilla cells, a specialized mesenchymal stem cell derived from dermal papilla within hair follicles, is considered the key cells for hair follicle regeneration function as both regeneration initiator and regulator. Injectable platelet rich fibrin (i-PRF), a novel biomaterial rich in a variety of growth factors and three-dimensional scaffolds, has shown promising effects on tissue regeneration. In this study, we aimed to evaluate the application of i-PRF in human hair follicle regeneration by examining the biological effects of i-PRF on human dermal papilla cells (hDPCs). Biomaterial compatibility, cell viability, proliferation, migration, alkaline phosphatase activity and trichogenic inductivity were assessed after exposing hDPCs to different concentrations of i-PRF extracts. In addition, we investigated the ultrastructure of i-PRF with all cell components filtered. The results revealed that i-PRF possessing excellent biocompatibility and could significantly promote hDPCs proliferation, migration, and trichogenic inductivity. Furthermore, the concentration of i-PRF is able to remarkably influence hDPCs behavior in a dose-dependent pattern. Different concentrations exhibited differential effects on hDPCs behavior. In general, lower concentration promotes cell proliferation better than higher concentration, while higher concentration promotes cell function better reversely. Best concentration for hDPCs in vitro expending is 1% concentration. 20% concentration is optimal for hair follicle regeneration. In summary, our findings concluded that i-PRF facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2019

Strain Relaxation-Induced Twin Interface Migration and Morphology Evolution of Silver Nanoparticles

The twinned structure of nanoscale metal particles is considered to be an important factor in the formation of novel morphologies. Nevertheless, most studies are focused on the growth of nanoparticles with stable twinned structures, and little is known about the intrinsic relationship between the morphological evolution and the strain relaxation induced by twin boundary migration. In this study, we elucidated the mechanisms of symmetry breaking induced by strain relaxation in Ag nanoparticles by employing transmission electron microscopy, electron tomography, and strain analysis. The experimental results reveal that decahedral nanoparticles larger than ~ 50 nm evolve into asym-metrical rhomboid pyramids to relax the lattice strain energy in the fivefold twin through twin pole migration. This migration is achieved by coordinating slipping and dissociating of partial and perfect dislocations. In addition, we found that the rhomboid pyramid further evolves into a rhomboid bar during growth in a specific way to avoid in-creasing the strain energy in the crystal.

Song, Miao↗
DOE OSTI2019

Probing Mg Migration in Spinel Oxides

Mg batteries utilizing oxide cathodes can theoretically surpass the energy density of current Li-ion technologies. The absence of functional devices so far has been ascribed to impeded Mg 2+ migration within oxides, which severely handicaps intercalation reactions at the cathode. Broadly, knowledge of divalent cation migration in solid frameworks is surprisingly deficient. In this paper, we present a combined experimental and theoretical study of Mg migration within three spinel oxides, which reveal critical features that influence it. Experimental activation energies for a Mg 2+ hop to an adjacent vacancy, as low as ~0.6 eV, are reported. These barriers are low enough to support functional electrodes based on the intercalation of M g2+ . Subsequent electrochemical experiments demonstrate that significant demagnesiation is indeed possible, but the challenges instead lie with the chemical stability of the oxidized states. Our findings enhance the understanding of cation transport in solid structures and renew the prospects of finding materials capable of high density of energy storage.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2022

Sand Migration Simulation during Gas Production from Gas Hydrate Reservoir at Kuparuk 7–11–12 site in the Prodhoe Bay Unit, Alaska

Uncontrolled sand production impedes continuous gas production from a hydrate reservoir as observed in the past field-scale gas production tests. Sand mobilization is strongly linked with sediment deformation and high pressure gradient. Sand production occurs when the mobilized sands reach the well. Throughout gas production from a hydrate reservoir, because of hydrate dissociation, deformation and pressure gradient change both in time and space. Therefore, it is necessary to consider the entire process to identify where sand is likely mobilized and how much mobilized sand could reach the well. Here, this study utilizes a coupled thermal, hydrological, chemical, and mechanical (thermo-hydro-chemo-mechanical) sand migration model to simulate a year long gas production from the hydrate reservoir at the Kuparuk 7–11–12 site in the Prodhoe Bay Unit, Alaska. It is found that sand would mainly come from the lower portion of the production zone where faster hydrate dissociation occurs. The relatively faster hydrate dissociation coupled with the fact that hydrate-bearing sediments and hydrate-free sediments have similar stiffness but different strengths causes complex stress transfer, which results in excessive shear deformation when the upper portion of the production zone starts to dissociate. This is evident not only near the well but also away from the well, leading to a large amount of sand mobilization. Another focus of the modeling study is evaluation of the effect of sand migration on gas production. The comparison of two extreme cases–with sandscreen and without sandscreen–suggests that migrated and settled solids around a sand control device can prevent pressure drop across the near-wellbore zone and lead to reduction of the gas production rate.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2018

Comparison of Sintering by Particle Migration and Ripening through First-Principles-Based Simulations

Here, we introduce a kinetic Monte Carlo (kMC) based model that can simulate migration of different size Pt nanoparticles on supports with point defects. Diffusion constants are obtained from 3D-lattice kMC simulations based on activation energies calculated from DFT. We study the effects of temperature, particle size, and particle concentration as well as defect concentration and defect binding on sintering. Additionally, we perform simulations that combine particle migration with ripening, where the latter is simulated through a mean-field model. This allows us to assess the relative importance of particle migration and ripening as well as their interaction.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2023

Kinetic Suppression of Photoinduced Halide Migration in Wide Bandgap Perovskites via Surface Passivation

In this work, we study the kinetics of photoinduced halide migration in FA 0.8 Cs 0.2 Pb(I 0.8 Br 0.2 ) 3 wide (~1.69 eV) bandgap perovskites and show that halide migration slows down following surface passivation with (3-aminopropyl) trimethoxysilane (APTMS). We use scanning Kelvin probe microscopy (SKPM) to probe the contact potential difference (CPD) shift under illumination and the kinetics of surface potential relaxation in the dark. Our results show that APTMS-passivated perovskites exhibit a smaller CPD shift under illumination and a slower surface potential relaxation in the dark. We compare the evolution of the photoluminescence spectra of APTMS-passivated and unpassivated perovskites under illumination. We find that APTMS-passivated perovskites exhibit more than 5 times slower photoluminescence red-shift, consistent with the slower surface potential relaxation as observed by SKPM. In conclusion, these observations provide evidence for kinetic suppression of photoinduced halide migration in APTMS-passivated samples, likely due to reduced halide vacancy densities, opening avenues to more efficient and stable devices.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2017

Atomic Resolution Structural and Chemical Imaging Revealing the Sequential Migration of Ni, Co, and Mn upon the Battery Cycling of Layered Cathode

Layered lithium transition metal oxides (LTMO) are promising candidate cathode materials for next generation high energy density lithium ion battery. The challenge for using this category of cathode is the capacity and voltage fading, which is believed to be associated with the layered structure disordering, a process that is initiated from the surface or solid-electrolyte interface and facilitated by transition metal (TM) reduction and oxygen vacancy formation. However, the atomic level dynamic mechanism of such a layered structure disordering is still not fully clear. In this work, utilizing atomic resolution electron energy loss spectroscopy (EELS), we map, for the first time at atomic scale, the spatial evolution of Ni, Co and Mn in a cycled LiNi1/3M1/3Co1/3O2 layered cathode. In combination with atomic level structural imaging, we discovered the direct correlation of TM ions migration behavior with lattice disordering, featuring the residing of TM ions in the tetrahedral site and a sequential migration of Ni, Co, and Mn upon the increased lattice disordering of the layered structure. This work highlights that Ni ions, though acting as the dominant redox species in many LTMO, are labile to migrate to cause lattice disordering upon battery cycling; while the Mn ions are more stable as compared with Ni and Co and can act as pillar to stabilize layered structure. Direct visualization of the behavior of TM ions during the battery cycling provides insight for designing of cathode with structural stability and correspondingly a superior performance.

annular bright field image↗
DOE OSTI2021

Sea Level-Driven Marsh Migration Results in Rapid Net Loss of Carbon

Sea level rise alters coastal carbon cycling by driving the rapid migration of coastal ecosystems, salinization of freshwater systems, and replacement of terrestrial forests with tidal wetlands. Wetland soils accumulate carbon (C) at faster rates than terrestrial soils, implying that sea level rise may lead to enhanced carbon accumulation. Here, we show that carbon stored in tree biomass greatly exceeds carbon stored in adjacent marsh soils so that marsh migration reduces total carbon stocks by ~50% in less than 100 years. Continued marsh soil carbon accumulation may eventually offset forest carbon loss, but we estimate that the time for replacement is similar to estimates of marsh survival (i.e., centuries), which suggests that forest C may never be replaced. These findings reveal a critical C source not included in coastal C budgets driven by migrating ecosystems and rapidly shifting allocations between carbon stored in soils and biomass.

58 GEOSCIENCES↗