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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 289 records · Page 16
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Emergence and selection of isoniazid and rifampin resistance in tuberculosis granulomas

Drug resistant tuberculosis is increasing world-wide. Resistance against isoniazid (INH), rifampicin (RIF), or both (multi-drug resistant TB, MDR-TB) is of particular concern, since INH and RIF form part of the standard regimen for TB disease. While it is known that suboptimal treatment can lead to resistance, it remains unclear how host immune responses and antibiotic dynamics within granulomas (sites of infection) affect emergence and selection of drug-resistant bacteria. We take a systems pharmacology approach to explore resistance dynamics within granulomas. We integrate spatio-temporal host immunity, INH and RIF dynamics, and bacterial dynamics (including fitness costs and compensatory mutations) in a computational framework. We simulate resistance emergence in the absence of treatment, as well as resistance selection during INH and/or RIF treatment. There are four main findings. First, in the absence of treatment, the percentage of granulomas containing resistant bacteria mirrors the non-monotonic bacterial dynamics within granulomas. Second, drug-resistant bacteria are less frequently found in non-replicating states in caseum, compared to drug-sensitive bacteria. Third, due to a steeper dose response curve and faster plasma clearance of INH compared to RIF, INH-resistant bacteria have a stronger influence on treatment outcomes than RIF-resistant bacteria. Finally, under combination therapy with INH and RIF, few MDR bacteria are able to significantly affect treatment outcomes. Overall, our approach allows drug-specific prediction of drug resistance emergence and selection in the complex granuloma context. Since our predictions are based on pre-clinical data, our approach can be implemented relatively early in the treatment development process, thereby enabling pro-active rather than reactive responses to emerging drug resistance for new drugs. Furthermore, this quantitative and drug-specific approach can help identify drug-specific properties that influence resistance and use this information to design treatment regimens that minimize resistance selection and expand the useful life-span of new antibiotics.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

Experimental and numerical study of the effective thermal conductivity of silica nanocomposites with thermal boundary resistance

The thermal interface resistance at the macro scale is mainly described by the physical gap between two interfaces and constriction resistance due to this gap. The small gaps between the two material faces makes up the majority of thermal interface resistance at the macro scale. So, most of the studies have been focused on characterizing effect of surface geometry and material properties to thermal interface resistance. This resistance is more widely known as thermal contact resistance, represented with Rc. There are various models to predict thermal contact resistance at macro scale. These models predict thermal resistance Rc for given two materials by utilizing their bulk thermomechanical properties. Although, Rc represents thermal resistance accurately for macro size contacts between two metals, it is not suitable to describe interface resistance of particles in modern TIMs, aka particulate composites. The particles inside recently available TIMs are micron size and with effort to further increase surface area this particle size is approaching nano scale. At this small scale, Rc does not accurately predict thermal interface, as it is very difficult to characterize the surface topography. The thermal discontinuity at perfectly bonded interface of two dissimilar materials is termed as thermal boundary resistance (Rb) or Kapitza resistance. The macroscopic assumptions that thermal discontinuity only exists due to gaps and surface geometry leads to substantial error in determining interface thermal properties at micron and nano scale. The phenomenon of thermal boundary resistance is an inherent material property and arises due to fundamental mechanism of thermal transport. For metal-matrix particulate composites, Rb plays more important role than Rc. The free flowing nature of the polymer would eliminate most of the gaps between the two materials at their interface. This means almost all of the thermal resistance at particle/matrix interface would occur due to Rb. The current study presents experimental study of thermal boundary resistance for silica nano particles embedded inside epoxy resin. The bulk conductivity of the sample is measured and Rc is back calculated using Hasselman-Johnson s (H-J) equation. The numerical validation of the equation is also presented, including extrapolation study to predict effective conductivity of the nanocomposite TIM.

silica nanocomposites↗
DOE OSTI2018

Three-dimensional electronic resistivity mapping of solid electrolyte interphase on Si anode materials

Silicon is a promising candidate for the lithium ion battery (LIB) anode because of the order-of-magnitude improvement in capacity over current state-of-the-art graphite anodes. In systems featuring both C and Si anodes, electronic resistivity of the solid-electrolyte interphase (SEI) layer is a critical factor for preventing continuous electrolyte-decomposition reactions at the electrode/electrolyte interface. However, the in-situ measurement of SEI electronic resistance has been complicated by ion transport and electronic contributions from other parts of the battery circuit. Ex-situ measurements of SEI resistivity at microscopic scales are also lacking. We report on a nanometer-resolution three-dimensional technique that enables ex-situ mapping of electronic resistivity of SEI formed on a model single-crystalline wafer Si anode. Our novel experimental approach uses scanning spreading-resistance microscopy resistance imaging and mechanical depth profiling. In addition to resistance mapping, this method also provides an alternative technique for locating buried interfaces, where mechanical or electronic properties differ sufficiently between layers. Further validation of this method was obtained by resistance mapping of a reference sample with a designed a-Si:H layer stack of different doping concentrations. The results show relatively uniform lateral resistivity distribution of the SEIs but steep decreases in resistivity in the vertical direction. Resistivity vs. depth profiles are highly dependent on cycling conditions, but they generally show a resistivity decrease from the most superficial levels of SEI and a thickness increase with continued cycling prior to SEI stabilization. The most prominent resistivity increase was observed on SEI formed in Gen2 electrolyte (EC:EMC [3:7 by wt.] + 1.2 M LiPF6) with 10 wt% fluoroethylene carbonate additive; this result may partially explain the significant improvements of sustained electrochemical cycling and coulombic efficiency observed with this electrolyte additive. Our approach provides a novel and unparalleled three-dimensional approach in characterizing electronic resistivity, which contributes significantly to understanding SEI formation and the intrinsic properties critical to battery performance.

25 ENERGY STORAGE↗
DOE OSTI2018

Exosomal transfer of miR-214 mediates gefitinib resistance in non-small cell lung cancer

Highlights: • Gefitinib-resistant PC-9GR cells derived exosomes can be taken up and internalized by sensitive PC-9 cells and confer gefitinib resistance in NSCLC. • miR-214 level was upregulated in gefitinib-resistant PC-9GR cells and their derived exosomes. • miR-214 antagomir reversed gefitinib resistance conferred by geiftinib resistant PC-9GR cells-derived exosomes in vitro and in vivo. Recent studies have demonstrated that exosomal miRNAs mediate as intercellular bio-messengers of drug resistance in lung cancer. Our objective was to investigate whether exosomes derived from gefitinib resistant non-small cell lung cancer cells could confer resistance to its recipient cells. Exosomes were successfully isolated by ultracentrifugation and exosomes morphologies and sizes were determined by transmission electron microscopy and dynamic light scattering analysis. Fluorescent PKH-67 labeled exosomes derived from PC-9GR cells could be taken up and internalized by PC-9 cells. CCK8 measurement showed that PC-9GR-derived exosomes could confer gefitinib resistance in PC-9 cells. MiRNA-214 was upregulated in gefitinib resistant PC-9GR cells and its derived exosomes by qPCR analysis. Inhibition of exosomal miR-214 with antagomir reversed gefitinib resistance conferred by PC-9GR-derived exosomes in vitro, which was confirmed by flow cytometry analysis and westernblot of apoptotic protein (caspase-3, caspase-3 cleaved, bax) and anti-apoptotic protein (bcl-2). Finally, exosomes enriched with miR-214 antagomir was further confirmed to reverse gefitinib resistance in vivo. Our results are the first to show that exosomes derived from gefitinib-resistant PC-9GR cells could transfer resistance to its recipient sensitive PC-9 cells, which might be mediated by exosomal transfer of miR-214.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2014

Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ{sub m}) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H{sub 2}O{sub 2}), they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ{sub m} depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H{sub 2}O{sub 2}-induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ{sub m} depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin-resistance. • Inhibition of DRP or ROS failed to improve palmitate-induced insulin-resistance. • Mitochondrial dysfunction by lipid metabolites would induce insulin-resistance.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2015

Targeting glucosylceramide synthase induction of cell surface globotriaosylceramide (Gb3) in acquired cisplatin-resistance of lung cancer and malignant pleural mesothelioma cells

Background: Acquired resistance to cisplatin treatment is a caveat when treating patients with non-small cell lung cancer (NSCLC) and malignant pleural mesothelioma (MPM). Ceramide increases in response to chemotherapy, leading to proliferation arrest and apoptosis. However, a tumour stress activation of glucosylceramide synthase (GCS) follows to eliminate ceramide by formation of glycosphingolipids (GSLs) such as globotriaosylceramide (Gb3), the functional receptor of verotoxin-1. Ceramide elimination enhances cell proliferation and apoptosis blockade, thus stimulating tumor progression. GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux. We investigated the expression of Gb3, MDR1 and MRP1 in NSCLC and MPM cells with acquired cisplatin resistance, and if GCS activity or MDR1 pump inhibitors would reduce their expression and reverse cisplatin-resistance. Methods: Cell surface expression of Gb3, MDR1 and MRP1 and intracellular expression of MDR1 and MRP1 was analyzed by flow cytometry and confocal microscopy on P31 MPM and H1299 NSCLC cells and subline cells with acquired cisplatin resistance. The effect of GCS inhibitor PPMP and MDR1 pump inhibitor cyclosporin A for 72 h on expression and cisplatin cytotoxicity was tested. Results: The cisplatin-resistant cells expressed increased cell surface Gb3. Cell surface Gb3 expression of resistant cells was annihilated by PPMP whereas cyclosporin A decreased Gb3 and MDR1 expression in H1299 cells. No decrease of MDR1 by PPMP was noted in using flow cytometry, whereas a decrease of MDR1 in H1299 and H1299res was indicated with confocal microscopy. No certain co-localization of Gb3 and MDR1 was noted. PPMP, but not cyclosporin A, potentiated cisplatin cytotoxicity in all cells. Conclusions: Cell surface Gb3 expression is a likely tumour biomarker for acquired cisplatin resistance of NSCLC and MPM cells. Tumour cell resistance to MDR1 inhibitors of cell surface MDR1 and Gb3 could explain the aggressiveness of NSCLC and MPM. Therapy with GCS activity inhibitors or toxin targeting of the Gb3 receptor may substantially reduce acquired cisplatin drug resistance of NSCLC and MPM cells. - Highlights: • The cisplatin-resistant cells had increased cell surface Gb3 and MDR1. • PPMP decreased extracellular Gb3 in the resistant cell lines. • Cyclosporin A decreased extracellular Gb3 and MDR1 in H1299 cells. • PPMP, but not cyclosporin A, potentiated cisplatin cytotoxicity in all cells. • Resistance to inhibitors of MDR1 and Gb3 could explain aggressiveness of NSCLC and MPM.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2025

Integrative path modeling and QTL mapping identify maturity, stem strength, and cell wall composition driving lettuce resistance to Sclerotinia minor

Lettuce ( Lactuca sativa ) is highly vulnerable to Sclerotinia minor , the pathogen causing lettuce drop. Breeding for resistance is the most effective control strategy; however, full resistance has not been achieved, and current partial resistance sources are often linked with undesirable traits, such as early bolting. This study aimed to unravel the genetic basis of partial resistance to S. minor and its relationship with plant maturity (bolting), stem mechanical strength (SMS), and cell wall composition (CWC) using a recombinant inbred line (RIL) population derived from a cross between the susceptible iceberg cv. ‘Salinas’ and the resistant oil-seed accession PI 251246. Field evaluations indicated that resistance was linked to earlier bolting, stronger stems, and higher pentose content. Path analysis demonstrated that earlier-maturing plants exhibited increased resistance through enhanced SMS and modified CWC, particularly with higher xylose and lower arabinose levels. Further analysis indicated a significant relationship between syringyl lignin content and resistance, especially in plants with varying bolting responses. Three key quantitative trait loci (QTLs) on linkage groups (LG) 2, 6, and 7 were consistently associated with resistance, bolting, and SMS. Importantly, residual QTL analysis revealed that the resistance locus on LG7 acted independently of maturity, suggesting a distinct resistance mechanism. Callose synthase emerged as a key candidate gene within the LG7 resistance QTL, located near - but distinct from - genes associated with plant maturity and flowering. These findings provide valuable insights into decoupling resistance from early bolting, suggesting a pathway for breeding lettuce cultivars with improved disease resistance and delayed bolting.

Lactuca↗
DOE OSTI2018

Genome-wide association study of Gossypium arboreum resistance to reniform nematode

Background: Reniform nematode ( Rotylenchulus reniformis ) has emerged as one of the most destructive root pathogens of upland cotton ( Gossypium hirsutum ) in the United States. Management of R. reniformis has been hindered by the lack of resistant G. hirsutum cultivars; however, resistance has been frequently identified in germplasm accessions from the G. arboreum collection. To determine the genetic basis of reniform nematode resistance, a genome-wide association study (GWAS) was performed using 246 G. arboreum germplasm accessions that were genotyped with 7220 single nucleotide polymorphic (SNP) sequence markers generated from genotyping-by-sequencing. Results: Fifteen SNPs representing 12 genomic loci distributed over eight chromosomes showed association with reniform nematode resistance. For 14 SNPs, major alleles were shown to be associated with resistance. From the 15 significantly associated SNPs, 146 genes containing or physically close to these loci were identified as putative reniform nematode resistance candidate genes. These genes are involved in a broad range of biological pathways, including plant innate immunity, transcriptional regulation, and redox reaction that may have a role in the expression of resistance. Eighteen of these genes corresponded to differentially expressed genes identified from G. hirsutum in response to reniform nematode infection. Conclusions: The identification of multiple genomic loci associated with reniform nematode resistance would indicate that the G. arboreum collection is a significant resource of novel resistance genes. The significantly associated markers identified from this GWAS can be used for the development of molecular tools for breeding improved reniform nematode resistant upland cotton with resistance introgressed from G. arboreum . Additionally, a greater understanding of the molecular mechanisms of reniform nematode resistance can be determined through genetic structure and functional analyses of candidate genes, which will aid in the pyramiding of multiple resistance genes.

Cotton↗
DOE OSTI2021

Natural Horizontal Gene Transfer of Antimicrobial Resistance Genes in Campylobacter spp. From Turkeys and Swine

Antibiotic-resistant Campylobacter constitutes a serious threat to public health. The clonal expansion of resistant strains and/or the horizontal spread of resistance genes to other strains and species can hinder the clinical effectiveness of antibiotics to treat severe campylobacteriosis. Still, gaps exist in our understanding of the risks of acquisition and spread of antibiotic resistance in Campylobacter. While the in vitro transfer of antimicrobial resistance genes between Campylobacter species via natural transformation has been extensively demonstrated, experimental studies have favored the use of naked DNA to obtain transformants. In this study, we used experimental designs closer to real-world conditions to evaluate the possible transfer of antimicrobial resistance genes between Campylobacter strains of the same or different species (Campylobacter coli or Campylobacter jejuni) and originating from different animal hosts (swine or turkeys). This was evaluated in vitro through co-culture experiments and in vivo with dual-strain inoculation of turkeys, followed by whole genome sequencing of parental and newly emerged strains. In vitro, we observed four independent horizontal gene transfer events leading to the acquisition of resistance to beta-lactams (blaOXA), aminoglycosides [aph(2")-If and rpsL] and tetracycline [tet(O)]. Observed events involved the displacement of resistance-associated genes by a mutated version, or the acquisition of genomic islands harboring a resistance determinant by homologous recombination; we did not detect the transfer of resistance-carrying plasmids even though they were present in some strains. In vivo, we recovered a newly emerged strain with dual-resistance pattern and identified the replacement of an existing non-functional tet(O) by a functional tet(O) in the recipient strain. Whole genome comparisons allowed characterization of the events involved in the horizontal spread of resistance genes between Campylobacter following in vitro co-culture and in vivo dual inoculation. Our study also highlights the potential for antimicrobial resistance transfer across Campylobacter species originating from turkeys and swine, which may have implications for farms hosting both species in close proximity.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2022

Genetic mapping of sugarcane aphid resistance in sorghum line SC112-14

Sugarcane aphid [Melanaphis sacchari (Zehntner)] is a destructive pest that has had an economic effect on sorghum in North America since 2013. The identification, development, and use of resistant sorghum germplasm is the most feasible strategy to control the pest. Nevertheless, the genetic control of sugarcane aphid (SCA) resistance is unknown for most sorghum resistant lines. To identify the genetic regions that confer SCA resistance in sorghum line SC112-14, 103 recombinant inbred lines (RILs) derived by its cross with the susceptible line PI 609251 were evaluated for their SCA resistance response in Georgia during two consecutive years. The resistance response was determined based on two ratings (2 wk apart) for aphid population size (APS) and aphid-induced plant damage (APD) each year. Segregation for SCA resistance was observed for the first APS and both APD ratings, and the broad-sense heritability estimate ranged from .71 to .76, respectively. A quantitative trait locus analysis using a high-density linkage map of 3,852 single nucleotide polymorphisms (SNPs) detected an 81-kb genomic region on chromosome 6 that explained 50–55% of the phenotypic variation. Comparative mapping analysis found that the resistance locus in SC112-14 is located 8- and 10-cM upstream of the Henong 16 (RMES1) and Tx2783 resistance loci, respectively, and encloses the SNP Sbv3.1_06_2316351 associated in Haitian resistant lines. Therefore, the line SC112-14 is an additional SCA resistance source that can be combined or strategically used with other resistance sources to assure a more robust host plant resistance to the SCA.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Mechanism of c-Met and EGFR tyrosine kinase inhibitor resistance through epithelial mesenchymal transition in non-small cell lung cancer

According to currently available estimates from Cancer Research UK, 14.1 million new lung cancer cases were diagnosed and a staggering 8.2 million people worldwide died from lung cancer in 2012. EGFR and c-Met are two tyrosine kinase receptors most commonly overexpressed or mutated in Non-small Cell Lung Cancer (NSCLC) resulting in increased proliferation and survival of lung cancer cells. Tyrosine kinase inhibitors (TKIs), such as erlotinib, approved by the FDA as first/second line therapy for NSCLC patients have limited clinical efficacy due to acquired resistance. In this manuscript, we investigate and discuss the role of epithelial mesenchymal transition (EMT) in the development of resistance against EGFR and c-Met TKIs in NSCLC. Our findings show that Zeb-1, a transcriptional repressor of E-Cadherin, is upregulated in TKI-resistant cells causing EMT. We observed that TKI-resistant cells have increased gene and protein expression of EMT related proteins such as Vimentin, N-Cadherin, β-Catenin and Zeb-1, while expression of E-Cadherin, an important cell adhesion molecule, was suppressed. We also confirmed that TKI-resistant cells display mesenchymal cell type morphology, and have upregulation of β-Catenin which may regulate expression of Zeb-1, a transcriptional repressor of E-Cadherin in TKI-resistant NSCLC cells. Finally, we show that down-regulating Zeb-1 by inducing miR-200a or β-Catenin siRNA can increase drug sensitivity of TKI-resistant cells. - Highlights: • Resistance to TKIs in NSCLC cells is mediated via modulation in EMT related proteins. • EMT may induce c-Met mediated TKI resistance, similar to EGFR TKI resistance. • Role of β-catenin and cadherins in TKI resistance was validated by FACS and qPCR. • Knockdown of β-catenin or Zeb-1 can increase TKI sensitivity in TKI-resistant cells. • Targeting key EMT related proteins may overcome TKI resistance in NSCLC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

H19 mediates methotrexate resistance in colorectal cancer through activating Wnt/β-catenin pathway

Colorectal cancer (CRC) is a common malignancy, most of which remain unresponsive to chemotherapy. As one of the earliest cytotoxic drugs, methotrexate (MTX) serves as an anti-metabolite and anti-folate chemotherapy for various cancers. Unfortunately, MTX resistance prevents its clinical application in cancer therapy. Thereby, overcoming the drug resistance is an alternative strategy to maximize the therapeutic efficacy of MTX in clinics. Long noncoding RNAs (lncRNAs) have gained widespread attention in recent years. More and more emerging evidences have demonstrated that they play important regulatory roles in various biological activities and disease progression including drug resistance. In the present study, a MTX-resistant colorectal cell line HT-29 (HT-29-R) was developed, which displayed the active proliferation and shortened cell cycle. LncRNA H19 was found to be significantly upregulated in this resistant cell line. Further investigation showed that H19 knockdown sensitized the MTX resistance in HT-29-R cells while its overexpression improved the MTX resistance in the parental cells, suggesting that H19 mediate MTX resistance. The Wnt/β-catenin signaling was activated in HT-29-R cells, and H19 knockdown suppressed this signaling in the parental cells. In conclusion, H19 mediated MTX resistance via activating Wnt/β-catenin signaling, which help to develop H19 as a promising therapeutic target for MTX resistant CRC. - Highlights: • A methotrexate (MTX) -resistant colorectal cancer cell line HT-29 (HT-29-R) has been developed. • H19 was upregulated in HT-29-R cells. • H19 mediated MTX resistance in colorectal cancer (CRC). • Wnt/β-catenin pathway was involved in the H19-mediated MTX resistance in CRC cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2019

Advancing next generation nanolithography with infiltration synthesis of hybrid nanocomposite resists

Organic–inorganic hybrid resists are emerging as an effective way of addressing stringent process requirements for aggressive down-scaling of semiconducting devices. Yet, hybrid resists generally require complex chemical synthesis while being predominantly negative-tone with high dose requirements. For positive-tone processes and high-aspect-ratio pattern transfers, resist choices are limited to costly, non-hybrid alternatives, whose etch resistance is still inferior compared with hybrid resists. In this work, we demonstrate a novel hybrid positive-tone resist platform utilizing simple ex situ vapor-phase inorganic infiltration into standard resist materials. A model system based on poly(methyl methacrylate) (PMMA) thin film hybridized with aluminum oxide has been demonstrated for electron-beam lithography patterning, featuring a fully controllable critical exposure dose, contrast, and etch resistance. The hybrid resist not only achieves contrast as high as ~30, six-fold enhancement over standard PMMA, but also enables Si nanostructures with resolution down to ~30 nm and an aspect ratio as high as ~17, owing to enhancement of the Si etch selectivity to ~70, with an estimated achievable maximum of ~300, far exceeding known commercial positive-tone resist systems. The easy implementabilility, combined with versatile ex situ control of resist characteristics, makes this hybrid resist synthesis method uniquely suited for addressing the resist performance and high throughput required for advanced nanolithography techniques, such as extreme ultraviolet lithography, possibly.

29 ENERGY PLANNING, POLICY, AND ECONOMY↗
DOE OSTI2019

Experimental Evolution of Extreme Resistance to Ionizing Radiation in Escherichia coli after 50 Cycles of Selection

In prior work (D. R. Harris et al., J Bacteriol 191:5240–5252, 2009, https://doi.org/10.1128/JB.00502-09; B. T. Byrne et al., Elife 3:e01322, 2014, https://doi.org/10.7554/eLife.01322), we demonstrated that Escherichia coli could acquire substantial levels of resistance to ionizing radiation (IR) via directed evolution. Major phenotypic contributions involved adaptation of organic systems for DNA repair. We have currently undertaken an extended effort to generate E. coli populations that are as resistant to IR as Deinococcus radiodurans . After an initial 50 cycles of selection using high-energy electron beam IR, four replicate populations exhibit major increases in IR resistance but have not yet reached IR resistance equivalent to D. radiodurans . Regular deep sequencing reveals complex evolutionary patterns with abundant clonal interference. Prominent IR resistance mechanisms involve novel adaptations to DNA repair systems and alterations in RNA polymerase. Adaptation is highly specialized to resist IR exposure, since isolates from the evolved populations exhibit highly variable patterns of resistance to other forms of DNA damage. Sequenced isolates from the populations possess between 184 and 280 mutations. IR resistance in one isolate, IR9-50-1, is derived largely from four novel mutations affecting DNA and RNA metabolism: RecD A90E, RecN K429Q, and RpoB S72N/RpoC K1172I. Additional mechanisms of IR resistance are evident. IMPORTANCE Some bacterial species exhibit astonishing resistance to ionizing radiation, with Deinococcus radiodurans being the archetype. As natural IR sources rarely exceed mGy levels, the capacity of Deinococcus to survive 5,000 Gy has been attributed to desiccation resistance. To understand the molecular basis of true extreme IR resistance, we are using experimental evolution to generate strains of Escherichia coli with IR resistance levels comparable to Deinococcus . Experimental evolution has previously generated moderate radioresistance for multiple bacterial species. Yet, these efforts could not take advantage of modern genomic sequencing technologies. In this report, we examine four replicate bacterial populations after 50 selection cycles. Genomic sequencing allows us to follow the genesis of mutations in populations throughout selection. Novel mutations affecting genes encoding DNA repair proteins and RNA polymerase enhance radioresistance. However, more contributors are apparent.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2023

Genetic diversity, population structure and anthracnose resistance response in a novel sweet sorghum diversity panel

Sweet sorghum is an attractive feedstock for the production of renewable chemicals and fuels due to the readily available fermentable sugars that can be extracted from the juice, and the additional stream of fermentable sugars that can be obtained from the cell wall polysaccharides in the bagasse. An important selection criterion for new sweet sorghum germplasm is resistance to anthracnose, a disease caused by the fungal pathogen Colletotrichum sublineolum. The identification of novel anthracnose-resistance sources present in sweet sorghum germplasm offers a fast track towards the development of new resistant sweet sorghum germplasm. We established a sweet sorghum diversity panel (SWDP) of 272 accessions from the USDA-ARS National Plant Germplasm (NPGS) collection that includes landraces from 22 countries and advanced breeding material, and that represents ~15% of the NPGS sweet sorghum collection. Genomic characterization of the SWDP identified 171,954 single nucleotide polymorphisms (SNPs) with an average of one SNP per 4,071 kb. Population structure analysis revealed that the SWDP could be stratified into four populations and one admixed group, and that this population structure could be aligned to sorghum’s racial classification. Results from a two-year replicated trial of the SWDP for anthracnose resistance response in Texas, Georgia, Florida, and Puerto Rico showed 27 accessions to be resistant across locations, while 145 accessions showed variable resistance response against local pathotypes. A genome-wide association study identified 16 novel genomic regions associated with anthracnose resistance. Four resistance loci on chromosomes 3, 6, 8 and 9 were identified against pathotypes from Puerto Rico, and two resistance loci on chromosomes 3 and 8 against pathotypes from Texas. In Georgia and Florida, three resistance loci were detected on chromosomes 4, 5, 6 and four on chromosomes 4, 5 (two loci) and 7, respectively. One resistance locus on chromosome 2 was effective against pathotypes from Texas and Puerto Rico and a genomic region of 41.6 kb at the tip of chromosome 8 was associated with resistance response observed in Georgia, Texas, and Puerto Rico. This publicly available SWDP and the extensive evaluation of anthracnose resistance represent a valuable genomic resource for the improvement of sorghum.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2019

Mesoscopic modeling of transport resistances in a polymer-electrolyte fuel-cell catalyst layer: Analysis of hydrogen limiting currents

Understanding transport resistances in a polymer-electrolyte fuel cell (PEFC) catalyst layer (CL) is essential to mitigate the unexpected voltage loss when using low loadings of precious metals. In this paper, we explore through mesoscopic modeling the quantification analyses of the transport resistances in CL as derived using hydrogen-pump limiting current. Numerical treatments on the conjugated interfacial conditions at interfaces of ionomer/pore and Pt/ionomer are proposed to describe the mesoscopic transport processes of hydrogen and proton. Characterizations of the reconstructed microstructure of CL are performed. Parameter analyses on the influences of the critical transport properties such as the permeation coefficient and the dissolution and adsorption reaction rates at the surfaces of ionomer/pore and Pt/ionomer on the local transport resistance are presented. It is found that the local transport resistance is mainly originated from the diffusion resistance of the ionomer thin-film, which is more resistive than its bulk analogue with its permeation coefficient fitted to be 5.9% of the bulk one. The interfacial transport resistances and the diffusion resistance are coupled. The local transport resistance increases with I/C ratio due to thicker ionomer coated on the particles. Higher Pt/C ratio and bare carbon fraction lead to higher local transport resistance since the ionomer loading relative to Pt roughness factor decreases. The local transport resistance decreases with the porosity. Furthermore, the contribution of pores to the CL resistance, which decreases with the porosity, is comparatively small at low loadings.

25 ENERGY STORAGE↗
DOE OSTI2015

Impurity-limited resistance and phase interference of localized impurities under quasi-one dimensional nano-structures

The impurity-limited resistance and the effect of the phase interference among localized multiple impurities in the quasi-one dimensional (quasi-1D) nanowire structures are systematically investigated under the framework of the scattering theory. We derive theoretical expressions of the impurity-limited resistance in the nanowire under the linear response regime from the Landauer formula and from the Boltzmann transport equation (BTE) with the relaxation time approximation. We show that the formula from the BTE exactly coincides with that from the Landauer approach with the weak-scattering limit when the energy spectrum of the in-coming electrons from the reservoirs is narrow and, thus, point out a possibility that the distinction of the impurity-limited resistances derived from the Landauer formula and that of the BTE could be made clear. The derived formulas are applied to the quasi-1D nanowires doped with multiple localized impurities with short-range scattering potential and the validity of various approximations on the resistance are discussed. It is shown that impurity scattering becomes so strong under the nanowire structures that the weak-scattering limit breaks down in most cases. Thus, both phase interference and phase randomization simultaneously play a crucial role in determining the impurity-limited resistance even under the fully coherent framework. When the impurity separation along the wire axis direction is small, the constructive phase interference dominates and the resistance is much greater than the average resistance. As the separation becomes larger, however, it approaches the series resistance of the single-impurity resistance due to the phase randomization. Furthermore, under the uniform configuration of impurities, the space-average resistance of multiple impurities at room temperature is very close to the series resistance of the single-impurity resistance, and thus, each impurity could be regarded as an independent scattering center. The physical origin of this “self-averaging” under the fully coherent environments is attributed to the broadness of the energy spectrum of the in-coming electrons from the reservoirs.

71 CLASSICAL AND QUANTUM MECHANICS, GENERAL PHYSIC↗
DOE OSTI2024

Flow resistance of phloem sieve plates revisited using an experimental model

Sieve plate resistance has been identified as the key to understanding the efficiency of phloem transport of carbohydrates in trees. These plates with small holes connecting sieve tubes are responsible for the largest resistance to flow in the phloem. Their structure determines how fast sugars can be transported through the phloem with certain pressure differences and what the limits for phloem transport in different plants are. Because experiments with the phloem are very challenging, our understanding of sieve plate resistance is mostly based on anatomical studies and hydrodynamic modeling of flow through sieve plates. These models calculate the resistance of the entire sieve tube–sieve plate system using the Hagen–Poiseuille flow resistance for the sieve cell lumen and a combination of the Hagen–Poiseuille resistance and Sampson flow resistance through the sieve pores. The resistance of the entire sieve plate is calculated by summing the Hagen–Poiseuille and Sampson flow resistances of each pore. To test the validity of this model formulation, an experimental model with aspect parameters similar to phloem sieve tubes was built using polyvinyl chloride (PVC) piping and plastic straws of different diameters and lengths. This system was used to measure flow rates and calculate flow resistance at Reynolds numbers 0.5–300. The results suggest that the current models may significantly overestimate the flow resistance caused by sieve plates and that the resistance might be better described by formulations used for perforated plates.

54 ENVIRONMENTAL SCIENCES↗