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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 1,045 records · Page 58
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver

Highlights: • GOLGA2/GM130 loss induces autophagy with Golgi disruption in liver cells and transgenic mice. • GOLGA2/GM130 loss leads to degradation of lipid structures (LBs and LDs) by autophagy. • GOLGA2/GM130 loss causes liver and lung fibrosis. Autophagy is a biological recycling process via the self-digestion of organelles, proteins, and lipids for energy-consuming differentiation and homeostasis. The Golgi serves as a donor of the double-membraned phagophore for autophagosome assembly. In addition, recent studies have demonstrated that pulmonary and hepatic fibrosis is accompanied by autophagy. However, the relationships among Golgi function, autophagy, and fibrosis are unclear. Here, we show that the deletion of GOLGA2, encoding a cis-Golgi protein, induces autophagy with Golgi disruption. The induction of autophagy leads to fibrosis along with the reduction of subcellular lipid storage (lipid droplets and lamellar bodies) by autophagy in the lung and liver. GOLGA2 knockout mice clearly demonstrated fibrosis features such as autophagy-activated cells, densely packed hepatocytes, increase of alveolar macrophages, and decrease of alveolar surfactant lipids (dipalmitoylphosphatidylcholine). Therefore, we confirmed the associations among Golgi function, fibrosis, and autophagy. Moreover, GOLGA2 knockout mice may be a potentially valuable animal model for studying autophagy-induced fibrosis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

GhoT of the GhoT/GhoS toxin/antitoxin system damages lipid membranes by forming transient pores

Highlights: • Determined that toxin GhoT disrupts membranes by forming transient pores. • Determined that membrane charge affects the activity of GhoT. • Determined through molecular dynamic simulations why GhoT F38R is inactive. GhoT is a bacterial toxin of the type V toxin/antitoxin system that allows Escherichia coli to reduce its metabolism in response to oxidative and bile stress. GhoT functions by increasing membrane permeability and reducing both ATP levels and the proton motive force. However, how GhoT damages the inner membrane has not been elucidated. Here we investigated how GhoT damages membranes by studying its interaction with lipid bilayers and determined that GhoT does not cause macroscopic disruption of the lipid bilayer to increase membrane permeability to the dye carboxyfluorescein. Using circular dichroism, we found that GhoT forms an alpha helical structure in lipid bilayers that agrees with the structure predicted by the I-TASSER protein structure prediction program. The structure generated using I-TASSER was used to conduct coarse-grained molecular dynamics simulations, which indicate that GhoT damages the cell membrane, as a multimer, by forming transient transmembrane pores.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

A novel 1-acyl-sn-glycerol-3-phosphate O-acyltransferase homolog for the synthesis of membrane phospholipids with a branched-chain fatty acyl group in Shewanella livingstonensis Ac10

Highlights: • A new 1-acyl-sn-glycerol-3-phosphate O-acyltransferase (PlsC) was discovered. • The enzyme introduces a branched-chain fatty acyl group into membrane phospholipids. • The substrate specificity of the enzyme is unprecedented in the PlsC family enzymes. • Multiple PlsC homologs contribute to generation of membrane phospholipid diversity. 1-Acyl-sn-glycerol-3-phosphate O-acyltransferase (PlsC) plays an essential role in the formation of phosphatidic acid, a precursor of various membrane phospholipids (PLs), in bacteria by catalyzing the introduction of an acyl group into the sn-2 position of lysophosphatidic acid. Various bacteria produce more than one PlsC. However, the physiological significance of the occurrence of multiple PlsCs is poorly understood. A psychrotrophic bacterium, Shewanella livingstonensis Ac10, which produces eicosapentaenoic acid at low temperatures, has five putative PlsCs (PlsC1-5). We previously showed that PlsC1 is responsible for the production of PLs containing an eicosapentaenoyl group. Here, we characterized another putative PlsC of this bacterium named PlsC4. We generated a plsC4-disrupted mutant and found that PLs containing 13:0 found in the parental strain were almost completely absent in the mutant. The loss of these PLs was suppressed by introduction of a plsC4-expression plasmid. PLs containing 15:0 were also drastically decreased by plsC4 disruption. Gas chromatography-mass spectrometry analysis of fatty acyl methyl esters derived from PLs of the parental strain showed that the 13:0 and 15:0 groups were an 11-methyllauroyl group and a 13-methylmyristoyl group, respectively. Phospholipase A2 treatment revealed that these fatty acyl groups were linked to the sn-2 position of PLs. Thus, PlsC4 is a new type of PlsC homolog that is responsible for the synthesis of PLs containing a branched-chain fatty acyl group at the sn-2 position and plays a clearly different role from that of PlsC1 in vivo.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Lysophosphatidic acid receptor, LPA6, regulates endothelial blood-brain barrier function: Implication for hepatic encephalopathy

Highlights: • Serum autotaxin activity is elevated in the mouse with brain edema. • LPA{sub 6} is predominantly expressed in rat brain capillary endothelial cells. • LPA–LPA{sub 6}–G{sub 12/13}–Rho pathway regulates blood brain barrier permeability. Cerebral edema is a life-threatening neurological condition characterized by brain swelling due to the accumulation of excess fluid both intracellularly and extracellularly. Fulminant hepatic failure (FHF) develops cerebral edema by disrupting blood-brain barrier (BBB). However, the mechanisms by which mediator induces brain edema in FHF remain to be elucidated. Here, we assessed a linkage between brain edema and lysophosphatidic acid (LPA) signaling by utilizing an animal model of FHF and in vitro BBB model. Azoxymethane-treated mice developed FHF and hepatic encephalopathy, associated with higher autotaxin (ATX) activities in serum than controls. Using in vitro BBB model, LPA disrupted the structural integrity of tight junction proteins including claudin-5, occludin, and ZO-1. Furthermore, LPA decreased transendothelial electrical resistances in in vitro BBB model, and induced cell contraction in brain endothelial monolayer cultures, both being inhibited by a Rho-associated protein kinase inhibitor, Y-27632. The brain capillary endothelial cells predominantly expressed LPA{sub 6} mRNA, whose knockdown blocked the LPA-induced endothelial cell contraction. Taken together, the up-regulation of serum ATX in hepatic encephalopathy may activate the LPA–LPA{sub 6}–G{sub 12/13}–Rho pathway in brain capillary endothelial cells, leading to enhancement of BBB permeability and brain edema.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Dual-specificity phosphatase 18 modulates the SUMOylation and aggregation of Ataxin-1

Highlights: • MAPK phosphatase DUSP18 binds to ataxin-1 and suppresses JNK activation. • DUSP18 inhibits the SUMOylation of ataxin-1 without affecting phosphorylation. • DUSP18 blocks ataxin-1 aggregation and disrupt its association with Sp100. We previously reported that SUMOylation promotes the aggregation of ataxin-1 and JNK is involved in the process. Here we show that dual-specificity phosphatase 18 (DUSP18), a member of protein tyrosine phosphatases, exerts the opposite effects on ataxin-1. DUSP18 associated with ataxin-1 and suppressed JNK activated by ataxin-1. Interestingly DUSP18, but not the other DUSPs interacting with ataxin-1, caused the mobility shift of ataxin-1. De-phosphorylation by DUSP18 was initially suspected as a cause for such an effect; however, the phosphorylation of ataxin-1 was unchanged. Instead DUSP18 inhibited SUMOylation and reduced ataxin-1 aggregation. The catalytic mutant of DUSP18 failed to reduce the SUMOylation and aggregation of ataxin-1 indicating that the phosphatase activity is indispensable for the effects. Moreover, DUSP18 disrupted the co-localization of ataxin-1 with the PML component Sp100. These results together implicate that JNK and DUSP18 reciprocally modulate the SUMOylation, which plays a regulatory role in the aggregation of ataxin-1.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

TMEM16F/ANO6, a Ca2+-activated anion channel, is negatively regulated by the actin cytoskeleton and intracellular MgATP

Highlights: • ANO6 current shows sluggish activation even with high [Ca{sup 2+}]{sub i}, and inactivation. • Actin cytoskeleton disruption accelerate both activation and inactivation of ANO6. • Intracellular MgATP further delays ANO6 activation, and prevent inactivation. • The effects of MgATP on ANO6 were overcome by actin inhibitor, cytochalasin-D. • State actin cytoskeleton is crucial for determining ANO6 activity in intact cells. Anoctamin 6 (ANO6/TMEM16F) is a recently identified membrane protein that has both phospholipid scramblase activity and anion channel function activated by relatively high [Ca{sup 2+}]{sub i}. In addition to the low sensitivity to Ca{sup 2+}, the activation of ANO6 Cl{sup −} conductance is very slow (>3–5 min to reach peak level at 10 μM [Ca{sup 2+}]{sub i}), with subsequent inactivation. In a whole-cell patch clamp recording of ANO6 current (I{sub ANO6,w-c}), disruption of the actin cytoskeleton with cytochalasin-D (cytoD) significantly accelerated the activation kinetics, while actin filament-stabilizing agents (phalloidin and jasplakinolide) commonly inhibited I{sub ANO6,w-c}. Inside-out patch clamp recording of ANO6 (I{sub ANO6,i-o}) showed immediate activation by raising [Ca{sup 2+}]{sub i}. We also found that intracellular ATP (3 mM MgATP in pipette solution) decelerated the activation of I{sub ANO6,w-c}, and also prevented the inactivation of I{sub ANO6,w-c}. However, the addition of cytoD still accelerated both activation and inactivation of I{sub ANO6,w-c}. We conclude that the actin cytoskeleton and intracellular ATP play major roles in the Ca{sup 2+}-dependent activation and inactivation of I{sub ANO6,w-c}, respectively.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Stabilization of HDAC1 via TCL1-pAKT-CHFR axis is a key element for NANOG-mediated multi-resistance and stem-like phenotype in immune-edited tumor cells

Highlights: • NANOG contributes to stabilization of HDAC1 protein through AKT signaling pathway. • NANOG-AKT axis leads to phosphor-dependent inactivation of CHFR, which is an E3 ligase for HDAC1 protein. • HDAC1 confers immune-resistance, drug-resistance and stem-like phenotype through its catalytic activity. • AKT inhibition disrupts HDAC1-mediated multi-resistance and stem-like phenotype. Cancer immunoediting enriches NANOG expression in tumor cells, resulting in multi-drug resistance and stem-like phenotypes. We previously demonstrated that these NANOG-associated phenotypes are promoted through HDAC1 transcriptional upregulation. In this study, we identified that NANOG also contributes to the stabilization of HDAC1 protein through the AKT signaling pathway. NANOG-AKT axis leads to phosphor-dependent inactivation of CHFR, an E3 ligase for HDAC1 protein, and thereby inhibiting the ubiquitin-mediated degradation of HDAC1. Furthermore, AKT inhibition disrupts HDAC1 WT-mediated phenotypes but had no effect on the phenotypes mediated by HDAC1 FM, a mutant that is unable to interact with CHFR. Critically, we applied a catalytic dead mutant, HDAC1-H141A, to uncover that HDAC1 confers immune-resistance, drug-resistance and stem-like phenotype in tumor cells through its catalytic activity. Collectively, our results establish a firm molecular link in immune-edited tumor cells among NANOG, AKT, CHFR, and HDAC1, identifying HDAC1 as a molecular target in controlling NANOGHIGH immune-refractory cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

In vitro analysis of drugs that improve hyperglycemia-induced blood-brain barrier dysfunction

Highlights: • Blood-brain barrier (BBB) disruptions are a key feature of hyperglycemia (HG)-induced cerebral damage. • Pitavastatin and candesartan may act as BBB-protective drugs in diabetic cerebral vessel disease. • Our HG-induced BBB dysfunction model will contribute to the search for BBB protective drugs. Blood-brain barrier (BBB) disruptions are a key feature of hyperglycemia (HG)-induced cerebral damage. Patients with diabetes mellitus often have other cerebrovascular disease risk factors including hypertension, dyslipidemia, arrhythmia, and atherosclerosis obliterans. However, whether the drugs for these comorbidities are effective for improving HG-induced BBB damage is unclear.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Unexpected role of a conserved domain in the first extracellular loop in G protein-coupled receptor trafficking

Highlights: • Most Class A GPCRs contain a conserved WxFG motif. • Substitution of the W with a non-aromatic amino acid disrupts GPCR functioning. • Disrupted GPCR functioning is the due to aberrant plasma membrane localization. G protein-coupled receptors are the largest superfamily of cell surface receptors in the Metazoa and play critical roles in transducing extracellular signals into intracellular responses. This action is mediated through conformational changes in the receptor following ligand binding. A number of conserved motifs have critical roles in GPCR function, and here we focus on a highly conserved motif (WxFG) in extracellular loop one (EL1). A phylogenetic analysis documents the presence of the WxFG motif in ∼90% of Class A GPCRs and the motif is represented in 17 of the 19 Class A GPCR subfamilies. Using site-directed mutagenesis, we mutagenized the conserved tryptophan residue in eight receptors which are members of disparate class A GPCR subfamilies from different taxa. The modification of the Drosophila leucokinin receptor shows that substitution of any non-aromatic amino acid for the tryptophan leads to a loss of receptor function. Additionally, leucine substitutions at this position caused similar signaling defects in the follicle-stimulating hormone receptor (FSHR), Galanin receptor (GALR1), AKH receptor (AKHR), corazonin receptor (CRZR), and muscarinic acetylcholine receptor (mACHR1). Visualization of modified receptors through the incorporation of a fluorescent tag revealed a severe reduction in plasma membrane expression, indicating aberrant trafficking of these modified receptors. Taken together, these results suggest a novel role for the WxFG motif in GPCR trafficking and receptor function.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

PAS-histidine kinases PHK1 and PHK2 exert oxygen-dependent dual and opposite effects on gametophore formation in the moss Physcomitrella patens

Highlights: • Two unique histidine kinases repress a developmental process in a moss plant. • These kinases promote the same process when submerged under water. • Similarly, they promote the process in artificial hypoxic condition. • Thus, these kinases have dual and opposite functions depending on oxygen condition. • This study adds insight into flexibility and evolution of two-component systems. Two-component systems, versatile signaling mechanisms based on phosphate transfer between component proteins, must have played important roles in adaptation and diversification processes in land plant evolution. We previously demonstrated that two Per-Arnt-Sim (PAS)-histidine kinases, PHK1 and PHK2, repress gametophore formation in the moss Physcomitrella patens under aerobic conditions, and that, in eukaryotes, the presence of their homologs is restricted to early-diverging streptophyte linages. We assessed here whether or not PHKs play a role in oxygen signaling. When submerged under water, the double disruption line for PHK1 and PHK2 formed fewer gametophores than the wild-type line (WT) both under light-dark cycles or continuous light, indicating that PHKs promote gametophore formation under an aquatic environment, in contrast to aerobic conditions. Similarly, in an artificial low-oxygen condition, the double disruption line formed fewer gametophores than WT. These results indicate that PHKs exert dual and opposite effects on gametophore formation depending on oxygen status. This study adds important insight into functional versatility and evolutionary significance of two-component systems in land plants.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Crystal structure of the human glial fibrillary acidic protein 1B domain

Highlights: • The first crystal structure of the human GFAP 1B domain was determined. • Two parallel coiled-coils pack together lengthwise in an antiparallel configuration. • H-bonds, salt bridges, and hydrophobic interactions stabilize the homotetramer. • Alexander disease mutations disrupt the interactions and the GFAP filament network. Glial fibrillary acidic protein (GFAP) is a homopolymeric type III intermediate filament (IF) that plays essential roles in cell migration, mitosis, development, and signaling in astrocytes and a specific type of glial cells. Its overexpression and genetic mutations lead to abnormal IF networks and accumulation of Rosenthal fibers, which results in the fatal neurodegenerative disorder Alexander disease. Herein, we present the first crystal structure of human GFAP spanning the central coiled-coil 1B domain at 2.5 Å resolution. The domain forms a tetramer comprising two equivalent parallel coiled-coil dimers that pack together in an antiparallel manner. Its assembly is stabilized by extensive networks of intermolecular hydrogen bonds, salt bridges, and hydrophobic interactions. Furthermore, mapping of the GFAP mutations associated with Alexander disease reveals that most involve residues buried in the core of the interface, and are likely to disrupt the intermolecular interactions and/or introduce steric clashes, thereby decreasing GFAP solubility and promoting aggregation. Based on our structural analysis and previous biochemical studies, we propose that GFAP assembles in the A11 mode in which coiled-coil 1B dimers lie in close axial proximity in an antiparallel fashion to provide a stable tetrameric platform for the organization of the GFAP filament.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

A novel role for Bcl2l13 in promoting beige adipocyte biogenesis

Highlights: • Bcl2l13 expression is induced in Browning of white adipose tissues in Mice. • Knockdown of Bcl2l13 in beige adipocytes represses adipogenesis and thermogenic programing. • Bcl2l13 induces thermogenic programing by regulating mitochondrial dynamic and biogenesis. Bcl2l13 is a member of the Bcl-2 family that has been found to play a central role in regulating apoptosis. Recently Bcl2l13 has been reported to induce mitophagy as a functional mammalian homolog of Atg32. However, the role of Bcl2l13 in adipose tissue has not been investigated yet. In the present study, we found that Bcl2l13 expression was increased in white adipose tissue browning process stimulated by cold exposure or β3-adrenergic agonist CL-316,243 in vivo as well as during brown adipocytes differentiation in vitro. Moreover, Bcl2l13 disruption dramatically inhibited the browning program of preadipocytes, evidenced by reduced Prdm16, Ucp1, Dio2 and Adrb3 expression. Our findings revealed that the inhibition effect of Bcl2l13 disruption on browning program may be independent of altering autophagy activity, but through regulating mitochondrial dynamic and biogenesis, supported by decreased mitochondrial fission/fussion genes, PGC-1α and mitochondrial respiratory chain complexes expression. Taken together, our study uncovered a novel function of Bcl2l13 in adipocytes differentiation and promoting browning program.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Green leaf volatile-burst in Arabidopsis is governed by galactolipid oxygenation by a lipoxygenase that is under control of calcium ion

Plants form green leaf volatiles (GLVs) almost instantly after tissue disruption caused by damages, such as herbivore damage. This rapid formation of GLVs, namely GLV-burst, is an essential factor for the plants’ GLV-dependent direct and indirect defenses. However, mechanism of GLV-burst remains unknown. We observed that the formation of monogalactosyldiacylglycerol hydroperoxides (MGDG-OOHs) by Arabidopsis lipoxygenase 2 (AtLOX2) governs GLV-burst in Arabidopsis. Addition of a Ca{sup 2+} selective chelating reagent, BAPTA, during tissue disruption effectively suppressed the formation of MGDG-OOHs as well as GLV-burst. This suppression was relieved by the addition of Ca{sup 2+}. Therefore, we propose that Ca{sup 2+}-dependent activation of AtLOX2 facilitates GLV-burst formation as observed in leukotriene formation, which is regulated by Ca{sup 2+}-dependent activation of LOXs in animal cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

IFN-γ, IL-17A, or zonulin rapidly increase the permeability of the blood-brain and small intestinal epithelial barriers: Relevance for neuro-inflammatory diseases

Highlights: • Zonulin rapidly (within 60 min) increases the permeability of the IEB and BBB in vitro. • Both IL-17A and IFN-γ enhance the permeability of the BBB and IEB within 1 h. • All three pro-inflammatory mediators rapidly modify IEB TJs, by causing mislocalization of ZO-1, claudin-5, and occludin. • Rapid TJ disassembly by all mediators was accompanied by dramatic depolymerization of the peri-junctional actin cytoskeleton. Breakdown of the blood-brain barrier (BBB) precedes lesion formation in the brains of multiple sclerosis (MS) patients. Since recent data implicate disruption of the small intestinal epithelial barrier (IEB) in the pathogenesis of MS, we hypothesized that the increased permeability of the BBB and IEB are mechanistically linked. Zonulin, a protein produced by small intestine epithelium, can rapidly increase small intestinal permeability. Zonulin blood levels are elevated in MS, but it is unknown whether zonulin can also disrupt the BBB. Increased production of IL-17A and IFN-γ has been implicated in the pathogenesis of MS, epilepsy, and stroke, and these cytokines impact BBB integrity after 24 h. We here report that primary human brain microvascular endothelial cells expressed the EGFR and PAR2 receptors necessary to respond to zonulin, and that zonulin increased BBB permeability to a 40 kDa dextran tracer within 1 h. Moreover, both IL-17A and IFN-γ also rapidly increased BBB and IEB permeability. By using confocal microscopy, we found that exposure of the IEB to zonulin, IFN-γ, or IL-17A in vitro rapidly modified the localization of the TJ proteins, ZO-1, claudin-5, and occludin. TJ disassembly was accompanied by marked depolymerization of the peri-junctional F-actin cytoskeleton. Our data indicate that IFN-γ, IL-17A, or zonulin can increase the permeability of the IEB and BBB rapidly in vitro, by modifying TJs and the underlying actin cytoskeleton. These observations may help clarify how the gut-brain axis mediates the pathogenesis of neuro-inflammatory diseases.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

ESSENCE- A rapid, shear-enhanced, flow-through, capacitive electrochemical platform for rapid detection of biomolecules

The rapid, sensitive, and selective detection of target analytes using electrochemical sensors are challenging. ESSENCE, a new Electrochemical Sensor that uses a Shear-Enhanced, flowthrough Nanoporous Capacitive Electrode, overcomes current electrochemical sensors' response limitations, selectivity, and sensitivity limitations. ESSENCE is a microfluidic channel packed with transducer material sandwiched by a top and bottom microelectrode. The room-temperature instrument less integration process allows the switch of the transducer materials to make up the porous electrode without modifying the electrode architecture or device protocol. ESSENCE can be used to detect both biomolecules and small molecules by simply changing the packed transducer material. Electron microscopy results confirm the high porosity. In conjunction with the non-planar interdigitated electrode, the packed transducer material results in a flow-through porous electrode. Electron microscopy results confirm the high porosity. The enhanced shear forces and increased convective fluxes disrupt the electric double layer's (EDL) diffusive process in ESSENCE. This disruption migrates the EDL to high MHz frequency allowing the capture signal to be measured at around 100 kHz, significantly improving device timing (rapid detection) with a low signal-to-noise ratio. The device’s unique architecture allows us multiple configuration modes for measuring the impedance signal. This allows us to use highly conductive materials like carbon nanotubes. We show that by combining single-walled carbon nanotubes as transducer material with appropriate capture probes, NP-µIDE has high selectivity and sensitivity for DNA (fM sensitivity, selective against non-target DNA), breast cancer biomarker proteins (p53, pg/L sensitivity, selective against non-target HER2).

Cheng, Yu-Hsuan↗
DOE OSTI2019

SAR optimization studies on modified salicylamides as a potential treatment for acute myeloid leukemia through inhibition of the CREB pathway

Disruption of cyclic adenosine monophosphate response element binding protein (CREB) provides a potential new strategy to address acute leukemia, a disease associated with poor prognosis, and for which conventional treatment options often carry a significant risk of morbidity and mortality. In this paper, we describe the structure-activity relationships (SAR) for a series of XX-650-23 derived from naphthol AS-E phosphate that disrupts binding and activation of CREB by the CREB-binding protein (CBP). Through the development of this series, we identified several salicylamides that are potent inhibitors of acute leukemia cell viability through inhibition of CREB-CBP interaction. Among them, a biphenyl salicylamide, compound 71, was identified as a potent inhibitor of CREB-CBP interaction with improved physicochemical properties relative to previously described derivatives of naphthol AS-E phosphate.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2021

Ineffectiveness of ultrasound at low frequency for treating per- and polyfluoroalkyl substances in sewage sludge

Concerns have been raised about per- and polyfluoroalkyl substances (PFAS) in sewage sludge given the urgent need of finding suitable disposal methods for sludge. Here in this study, we evaluated the effect of ultrasonication on PFAS changes in sewage sludge. It was revealed that although ultrasonication at 20 kHz increased the soluble chemical oxygen demand (SCOD) of treated sewage sludge, this technique was ineffective for degrading perfluoroalkyl acids (PFAAs) and their precursors. Ultrasonic treatment for longer time (>15 min) led to concentration increase of perfluorooctanoic acid (PFOA), perfluoroheptanoic acid (PFHpA), and perfluorohexanoic acid (PFHxA) in the liquid phase, possibly due to their release from disrupted sludge flocs during cavitation. Adding permanganate (10 mM) to the ultrasonic system could also enhance the disruption of sludge particles, resulting in higher concentrations of PFOA and PFHxA in the solid phase and PFOA, PFHpA, PFHxA, and perfluorobutanesulfonic acid (PFBS) in the liquid phase. Overall, ultrasonic pretreatment at 20 kHz and 0.7 W/mL is unlikely to remove PFAS from sewage sludge. Instead, it could increase the risk of PFAS pollution upon final sludge disposal. Effective treatment technologies are thus demanded if PFAS in sludge are regulated.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2023

On a fully-implicit VMS-stabilized FE formulation for low Mach number compressible resistive MHD with application to MCF

This study presents the development and evaluation of a fully-implicit variational multiscale (VMS) stabilized unstructured finite element (FE) formulation for compressible magnetohydrodynamics (MHD) model, at low Mach number regime. The model describes the dynamics of a compressible conducting fluid in the low Mach number limit in the presence of electromagnetic fields and can be used to study aspects of astrophysical phenomena, important science and technology applications, and basic plasma physics phenomena. The specific applications that motivate this study are macroscopic simulations of the longer time-scale stability and disruptions of magnetic confinement fusion (MCF) devices, specifically the ITER tokamak. The discussion considers the development of the VMS FE representation, the structure of the stabilizing terms that deal with significant convective flows, the stabilization of the nearly incompressible response of the fluid flow, and the stabilization of the constraint that enforces the solenoidal involution on the magnetic field. The nonlinear discretized system is solved with scalable preconditioned Newton–Krylov iterative methods, which employs a multiphysics block preconditioning method based on approximate block factorizations and Schur complements. The study presents an evaluation of the VMS method on a 2D cartesian tearing mode instability, and illustrates the scalability of the solvers on MCF relevant problems. A set of results are also presented for longer time-scale stability and disruptions for the ITER tokamak. These include a vertical displacement event (VDE), and a (1,1) internal kink mode. Here, the formulation is demonstrated to be scalable and also reasonably robust with respect to the Lundquist number scaling.

42 ENGINEERING↗