SEARCH · Engineering Papers
Results for “LAI”
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.
Insight into lithium distribution in lithium-stuffed garnet oxides through neutron diffraction and atomistic simulation: Li7-xLa3Zr2-xTaxO12 (x = 0-2) series
Explore the source record for details and available documents.
Low-index surface energies, cleavage energies, and surface relaxations for crystalline NiAl from first-principles calculations
NiAl surfaces frequently serve as a platform for studying a broad range of physical and chemical phenomena including chemisorption, catalysis, oxidation, alloy growth, and surface nanostructure formation. Knowledge of precise values for low-index surface energies of NiAl, the most fundamental quantities characterizing surface thermodynamics, is often invaluable for understanding of these phenomena. In all previous analyses for NiAl(100) and NiAl(111), Ni- and Al-terminations are not distinguished, and half of the cleavage energy (or equivalently, the average of the surface energies of two differently terminated surfaces) is always identified as the “surface energy”. No values are available for individual surface energies of Ni- or Al-terminated NiAl(100) or NiAl(111) surfaces, whereas knowledge of only cleavage energy is often insufficient for analyzing surface-associated behavior. As such, in this work we perform extensive first-principles density-functional-theory (DFT) calculations for surface energies and cleavage energies of NiAl(110), NiAl(100) and NiAl(111) by considering the chemical-potential-based formulations to clarify the ambiguity in their surface energies and cleavage energies. We obtain a surface-energy phase diagram for these three low-index surfaces versus the relevant chemical potential, as well as the chemical-potential-dependent Wulff plots for NiAl crystal equilibrium shapes. We also provide the surface-relaxation information from our DFT calculations for comparison with previous experimental data.
Formation and coarsening of epitaxially-supported metal nanoclusters
This mini-review describes developments over the last ~30 years in characterizing the nucleation & growth of epitaxially-supported metal nanoclusters (NCs) or islands during vapor deposition, as well as their post-deposition coarsening. A beyond-mean-field treatment for homogeneous nucleation & growth corrects the deficiencies of traditional treatments in describing, e.g., the island size distribution, but also necessitates consideration of the spatial distribution of islands and their capture zones. We discuss advances in modeling capabilities, including those based upon on an ab-initio level treatment of periphery diffusion kinetics, for description of the non-equilibrium growth shapes of these NCs, focusing on 2D NCs. For post-deposition coarsening of arrays of NCs, there is generally a competition between Ostwald Ripening (OR) and Smoluchowski Ripening (SR). SR is also known as Particle Migration & Coalescence. For 2D NCs in homoepitaxial systems, conventional OR is observed on pristine fcc(111) surfaces, dramatically enhanced OR in the presence of even trace amounts of chalcogens for Cu(111) and Ag(111), and anomalous OR on anisotropic fcc(110) surfaces. The unexpected discovery of SR for fcc(100) homoepitaxial systems prompted extensive analysis of the underlying diffusivities of 2D NCs as a function of size, as well as of NC coalescence dynamics. A comprehensive understanding of these processes is now available. Self-assembly of 3D NCs during deposition, issues related to heterogeneous nucleation, directed assembly, NC growth structure selection, and coarsening are addressed. Finally, for SR of 3D epitaxial NCs, recent insights into the size-dependence of diffusivity are described.
Nitrogen fixation in Pampinifervens , a new species-rich genus of Aquificaceae that inhabits a wide pH range in terrestrial hot springs
Members of the Aquificota play important roles in hydrogen, sulfur, and carbon cycles in geothermal systems as ubiquitous and abundant chemolithoautotrophs; however, their roles in the nitrogen cycle are poorly defined. Here, we show that Aquificaceae isolate T-2 T from Tengchong, China, fixes nitrogen based on growth with dinitrogen as the sole nitrogen source and incorporation of 15 N atoms when grown with 15 N 2 . We further show evidence that suggests its nitrogen fixation (nif) genes are transcribed in situ in a nearby spring. We propose the name Pampinifervens diazotrophicum gen. et sp. nov., with strain T-2 T (= JCM 35475 T = DSM 116324 T ) as the nomenclatural type. Its close relative designated Pampinifervens florentissimum sp. nov. T-8 T (= CGMC 1.5214 T = JCM 33569 T ) does not fix nitrogen but respires nitrate. Analysis of 104 metagenome-assembled genomes from 84 metagenomes allowed us to circumscribe the genus Pampinifervens and identify at least 16 sympatric Pampinifervens species that dominate the Aquificaceae populations in diverse hot springs in southwest China, with distinct species globally. Analysis of these Pampinifervens genomes revealed variable presence of nif and denitrification genes and frequent gene loss and horizontal transfer. Genes for pH homeostasis were also present in Pampinifervens genomes, with a proliferation in species from Tengchong, consistent with the wide pH growth range of both Pampinifervens isolates and the prevalence of Pampinifervens in both alkaline and acidic springs. The dynamic evolution of nif and denitrification genes, along with pH homeostasis genes, may facilitate the diversification of Pampinifervens into diverse springs with different nitrogen availability.
Polymorphism of inflammatory genes and arsenic methylation capacity are associated with urothelial carcinoma
Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8). TNF-α, IL-6 and IL-8 have been shown to be involved in the development and progression of various cancers, including bladder cancer. This study aimed to investigate the joint effect of the polymorphism of TNF-α − 308 G/A, IL-6 − 174 G/C, IL-8 − 251 T/A and urinary arsenic profiles on urothelial carcinoma (UC) risk. This study evaluated 300 pathologically-confirmed cases of UC and 594 cancer-free controls. Urinary arsenic species were detected using high-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry. The polymorphism of TNF-α − 308 G/A, IL-6 − 174 G/C and IL-8 − 251 T/A was determined using polymerase chain reaction-restriction fragment length polymorphism. The joint effects on UC risk were estimated by odds ratios and 95% confidence intervals using unconditional logistic regression. We found that the TNF-α − 308 A/A and IL-8 − 251 T/T polymorphisms were significantly associated with UC. Moreover, significant dose–response joint effect of TNF-α − 308 A/A or IL-8 − 251 T/T genotypes and arsenic methylation indices were seen to affect UC risk. The present results also showed a significant increase in UC risk in subjects with the IL-8 − 251 T/T genotype for each SD increase in urinary total arsenic and MMA%. In contrast, a significant decrease in UC risk was found in subjects who carried the IL-8 − 251 T/T genotype for each SD increase in DMA%. - Highlights: • Joint effect of the TNF-α -308 A/A genotype and urinary total arsenic affected UC. • Joint effect of the IL-8 -251 T/T genotype and urinary total arsenic affected UC. • Urinary total arsenic level, TNF-α -308 A/A and IL-8 -251 T/T genotype affected UC.
Biphasic influence of dexamethasone exposure on embryonic vertebrate skeleton development
Dexamethasone (Dex) has anti-inflammatory and immunomodulatory properties against many conditions. There is a potential teratogenic risk, however, for pregnant women receiving Dex treatment. It has been claimed that Dex exposure during pregnancy could affect osteogenesis in the developing embryo, which still remains highly controversial. In this study, we employed chick embryos to investigate the effects of Dex exposure on skeletal development using combined in vivo and in vitro approach. First, we demonstrated that Dex (10{sup −8}–10{sup −6} μmol/egg) exposure resulted in a shortening of the developing long bones of chick embryos, and it accelerated the deposition of calcium salts. Secondly, histological analysis of chick embryo phalanxes exhibited Dex exposure inhibited the proliferation of chondrocytes, increased apoptosis of chondrocytes and osteocytes, and led to atypical arranged hypertrophic chondrocytes. The expression of genes related to skeletogenesis was also analyzed by semi-quantitative RT-PCR. The expression of ALP, Col1a2 and Col2a1 was decreased in the Dex treated phalanxes. A detectable increase was observed in Runx-2 and Mmp-13 expression. We next examined how Dex affected the different stages of skeletogenesis in vitro. Utilizing limb bud mesenchyme micromass cultures, we determined that Dex exposure exerted no effect on apoptosis but impaired chondrogenic cell proliferation. Interestingly, low dose of Dex moderately prompted nodule formation as revealed by alcian blue staining, but higher doses of Dex significantly inhibited similar chondrogenic differentiation. Dex exposure did not induce apoptosis when the chondrogenic precursors were still at the mesenchymal stage, however, cell viability was suppressed when the mesenchyme differentiated into chondrocytes. Alizarin red staining revealed that the capacity to form mineralized bone nodules was correspondingly enhanced as Dex concentrations increased. The mRNA level of Sox-9 was slightly increased in mesenchymal cell mass treated by low concentration of Dex. Mmp-13 expression was obviously up-regulated by Dex in both mesenchymal cells and primary chondrocyte cultures. And Col10a1 expression was also increased by Dex exposure in chondrocyte. In summary, we have revealed that different concentrations of Dex exposure during early gestation could exert a biphasic effect on vertebrate skeletal development. - Highlights: • Chick embryos occurred shortening of the long bone following Dex exposure. • Dex suppressed chondrocytes proliferation and promoted apoptosis. • Dex exposure decreased ALP production and up-regulated Runx-2 and Mmp-13. • Dex exhibited biphasic effects on chondrogenic proliferation and nodule formation. • The hypertrophy and ossification were accelerated by Dex both in vivo and in vitro.
Ginsenoside-Rg{sub 1} induces angiogenesis by the inverse regulation of MET tyrosine kinase receptor expression through miR-23a
Therapeutic angiogenesis has been implicated in ischemic diseases and wound healing. Ginsenoside-Rg{sub 1} (Rg{sub 1}), one of the most abundant active components of ginseng, has been demonstrated as an angiogenesis-stimulating compound in different models. There is increasing evidence implicating microRNAs (miRNAs), a group of non-coding RNAs, as important regulators of angiogenesis, but the role of microRNAs in Rg{sub 1}-induced angiogenesis has not been fully explored. In this report, we found that stimulating endothelial cells with Rg{sub 1} could reduce miR-23a expression. In silico experiments predicted hepatocyte growth factor receptor (MET), a well-established mediator of angiogenesis, as the target of miR-23a. Transfection of the miR-23a precursor or inhibitor oligonucleotides validated the inverse relationship of miR-23a and MET expression. Luciferase reporter assays further confirmed the interaction between miR-23a and the MET mRNA 3′-UTR. Intriguingly, ginsenoside-Rg{sub 1} was found to increase MET protein expression in a time-dependent manner. We further demonstrated that ginsenoside-Rg{sub 1}-induced angiogenic activities were indeed mediated through the down-regulation of miR-23a and subsequent up-regulation of MET protein expression, as confirmed by gain- and loss-of-function angiogenic experiments. In summary, our results demonstrated that ginsenoside-Rg{sub 1} could induce angiogenesis by the inverse regulation of MET tyrosine kinase receptor expression through miR-23a. This study has broadened our understanding of the non-genomic effects of ginsenoside-Rg{sub 1,} and provided molecular evidence that warrant further development of natural compound as novel angiogenesis-promoting therapy. - Highlights: • Therapeutic angiogenesis has been implicated in ischemic diseases and wound healing. • Ginsenoside-Rg{sub 1} (Rg{sub 1}) has been demonstrated as an angiogenesis-stimulating compound. • We found that Rg{sub 1} induces angiogenesis by decreasing miR-23a expression. • Hepatocyte growth factor receptor (MET) is a direct regulatory target of miR-23a. • Rg{sub 1} could induce angiogenesis by the inverse regulation of MET through miR-23a.
The influence of N-acetyl-L-cysteine on damage of porcine oocyte exposed to zearalenone in vitro
Zearalenone (ZEA), one of the mycotoxins produced by Fusarium fungi, impacts porcine reproduction by interfering with the estrogen signaling pathway. Previous studies have shown that ZEA inhibits porcine oocyte maturation through the formation of aberrant spindle. To explore the effect of ZEA on porcine oocyte meiotic maturation, the extent of both nuclear and cytoplasmic maturation was examined in this study. Compared with control group, presence of ZEA (3 μM) during oocyte maturation, significantly inhibited the polar body extrusions from 71% to 51%, and significantly increased intracellular reactive oxygen species (ROS) level (12.01 vs. 5.89). Intracellular glutathione (GSH) content in ZEA treatment group was lower than in the control group (1.08 pmol/oocyte vs. 0.18 pmol/oocyte), and cortical granules of cortical area distributed oocytes were reduced (88% vs. 62%). ZEA decreases cumulus expansion in both morphology and mRNA level (HAS2, PTX3, TNFAIP6 and CX43). Addition of N-acetyl-L-cysteine (NAC) to the oocyte maturation media reversed the ZEA-induced inhibition of polar body extrusion (from 69% to 81%), up-regulated ROS (from 7.9 to 6.5), down-regulated GSH content (from 0.16 to 0.82 pmol/oocyte) and recovered cumulus cells expansion in morphology and mRNA level. It is concluded that ZEA affects both oocyte nucleus and cytoplasmic maturation during in vitro maturation, and NAC can reverse these damages to some extent. - Highlights: • ZEA significantly inhibited the polar body extrusions during oocyte maturation. • ZEA significantly increased intracellular ROS level and reduced GSH content. • ZEA disturbed cortical granules of cortical area distributed oocytes. • NAC reversed the ZEA-induced inhibition of oocyte maturation.
Inhibition by ketamine and amphetamine analogs of the neurogenic nitrergic vasodilations in porcine basilar arteries
The abuse of ketamine and amphetamine analogs is associated with incidence of hypertension and strokes involving activation of sympathetic activities. Large cerebral arteries at the base of the brain from several species receive dense sympathetic innervation which upon activation causes parasympathetic-nitrergic vasodilation with increased regional blood flow via axo-axonal interaction mechanism, serving as a protective mechanism to meet O{sub 2} demand in an acutely stressful situation. The present study was designed to examine effects of ketamine and amphetamine analogs on axo-axonal interaction-mediated neurogenic nitrergic vasodilation in porcine basilar arteries using techniques of blood-vessel myography, patch clamp and two-electrode voltage clamp, and calcium imaging. In U46619-contracted basilar arterial rings, nicotine (100 μM) and electrical depolarization of nitrergic nerves by transmural nerve stimulation (TNS, 8 Hz) elicited neurogenic nitrergic vasodilations. Ketamine and amphetamine analogs concentration-dependently inhibited nicotine-induced parasympathetic-nitrergic vasodilation without affecting that induced by TNS, nitroprusside or isoproterenol. Ketamine and amphetamine analogs also concentration-dependently blocked nicotine-induced inward currents in Xenopus oocytes expressing α3β2-nicotinic acetylcholine receptors (nAChRs), and nicotine-induced inward currents as well as calcium influxes in rat superior cervical ganglion neurons. The potency in inhibiting both inward-currents and calcium influxes is ketamine > methamphetamine > hydroxyamphetamine. These results indicate that ketamine and amphetamine analogs, by blocking nAChRs located on cerebral perivascular sympathetic nerves, reduce nicotine-induced, axo-axonal interaction mechanism-mediated neurogenic dilation of the basilar arteries. Chronic abuse of these drugs, therefore, may interfere with normal sympathetic-parasympathetic interaction mechanism resulting in diminished neurogenic vasodilation and, possibly, normal blood flow in the brainstem. - Highlights: • Ketamine/amphetamines inhibit nicotine-induced cerebral neurogenic vasdilation. • Ketamine/amphetamines block cerebral perivascular sympathetic nAChR-mediated current. • The inhibitory potency is ketamine > D-amphetamine > methamphetamine > OH-amphetamine.
Coarse-grained resource allocation modeling for decoding and rewiring microbial metabolism
Microbial metabolism is a complex, emergent system driven by the coordinated interplay of intricate and dynamic molecular processes. To elucidate cellular behavior and enable biotechnological applications, quantitative models that address the inherent complexity of metabolism have been developed from a resource allocation perspective. Here, we synthesize recent advances in coarse-grained resource allocation frameworks and their applications in understanding microbial physiology and guiding gene circuit design. Here, these frameworks reveal global regulatory constraints and predict cellular adaptation to nutrient and environmental changes. In addition, they enable the quantification of metabolic costs, the dissection of circuit–host interactions, and the development of strategies for burden mitigation. Collectively, these modeling frameworks provide a powerful platform for uncovering quantitative principles of microbial growth and engineering robust synthetic biological systems.
Changes in atmospheric circulation amplify extreme snowfall fueled by Arctic sea ice loss over high-latitude land
Arctic sea-ice retreat has been linked to increased winter precipitation and heavy snowfall over land, likely due to a combination of enhanced evaporation from ice-free Arctic marginal seas (AMS) and changes in atmospheric circulation. However, their relative roles and contributions remain uncertain. Here, we show that a greater proportion of AMS evaporative moisture reached high-latitude land during the cold seasons from 1980–1989 to 2012–2021. Atmospheric circulation changes added an additional 13 % increase in the AMS moisture contribution, accounting for 11 % of the total increase in AMS-sourced land precipitation. Notably, 46 % of the increase in AMS-sourced extreme snowfall is attributed to circulation-driven landward moisture transport, representing an 84 % increase beyond the effect of enhanced AMS evaporation alone. Further analysis indicates that both the rise in Arctic moisture and the atmospheric circulation shifts are primarily driven by anthropogenic forcing. These findings highlight how atmospheric circulation changes amplify extreme snowfall fueled by AMS evaporation, underscoring the synergistic effects of Arctic sea ice loss and circulation change on high-latitude winter precipitation.
Addressing solar photochemistry durability with an amorphous nickel antimonate photoanode
Not Available
Therapeutic efficacy of improved α-fetoprotein promoter-mediated tBid delivered by folate-PEI600-cyclodextrin nanopolymer vector in hepatocellular carcinoma
SNPs in human AFP promoter are associated with serum AFP levels in hepatocellular carcinoma (HCC), suggesting that AFP promoter variants may generate better transcriptional activities while retaining high specificity to AFP-producing cells. We sequenced human AFP promoters, cloned 15 different genotype promoters and tested their reporter activities in AFP-producing and non-producing cells. Among various AFP variant fragments tested, EA4D exhibited the highest reporter activity and thus was selected for the further study. EA4D was fused with tBid and coupled with nano-particle vector (H1) to form pGL3-EA4D-tBid/H1. pGL3-EA4D-tBid/H1 could express a high level of tBid while retain the specificity to AFP-producing cells. In a HCC tumor model, application of pGL3-EA4D-tBid/H1 significantly inhibited the growth of AFP-producing-implanted tumors with minimal side-effects, but had no effect on non-AFP-producing tumors. Furthermore, pGL3-EA4D-tBid/H1 could significantly sensitize HCC cells to sorafenib, an approved anti-HCC agent. Collectively, pGL3-EA4D-tBid/H1, a construct with the AFP promoter EA4D and the novel H1 delivery system, can specifically target and effectively suppress the AFP-producing HCC. This new therapeutic tool shows little toxicity in vitro and in vivo and it should thus be safe for further clinical tests. - Highlights: • The nano-particle vector H1 has advantages in mediating gene therapy construct pGL3-EA4D-tBid for HCC treatment. • pGL3-EA4D-tBid/H1, a construct with the AFP promoter EA4D, can specifically target the AFP-producing HCC. • pGL3-EA4D-tBid/H1effectively suppresses the proliferation and growth of AFP-producing HCC. • This novel pGL3-EA4D-tBid/H1 therapeutic tool shows little toxicity in vitro and in vivo.
SWAP-70 contributes to spontaneous transformation of mouse embryo fibroblasts
Mouse embryo fibroblasts (MEFs) grow slowly after cultivation from animals, however, after an extended period of cultivation, their growth accelerates. We found that SWAP-70 deficient MEFs failed to increase growth rates. They maintain normal growth rates and proliferation cycles for at least 5 years. Complementing SWAP-70 deficiency in one of these MEF clones, MEF1F2, by expressing human SWAP-70 resulted in fast growth of the cells after further cultivation for a long period. The resulting cells show a transformation phenotype, since they grow on top of each other and do not show contact inhibition. This phenotype was reverted when sanguinarine, a putative SWAP-70 inhibitor, was added. Two SWAP-70 expressing clones were examined in detail. Even after cell density became very high their cdc2 and NFκB were still activated suggesting that they do not stop growing. One of the clones formed colonies in soft agar and formed tumors in nude mice. Lately, one more clone became transformed being able to make colonies in soft agar. We maintain 4 human SWAP-70 expressing MEF1F2 cell lines. Three out of 4 clones exhibited transforming phenotypes. The mouse SWAP-70 gene also promoted transformation of MEFs. Taken together our data suggest that SWAP-70 is not a typical oncogene, but is required for spontaneous transformation of MEFs. - Highlights: • Mouse embryo fibroblasts (MEFs) lacking SWAP-70 do not cause spontaneous transform. • Adding back of SWAP-70 to SWAP-70-deficient MEFs induces spontaneous transformation. • SWAP-70 is required for spontaneous transformation of MEFs.
Effects of oxidative stress on hyperglycaemia-induced brain malformations in a diabetes mouse model
Pregestational diabetes mellitus (PGDM) enhances the risk of fetal neurodevelopmental defects. However, the mechanism of hyperglycaemia-induced neurodevelopmental defects is not fully understood. In this study, several typical neurodevelopmental defects were identified in the streptozotocin-induced diabetes mouse model. The neuron-specific class III beta-tubulin/forkhead box P1-labelled neuronal differentiation was suppressed and glial fibrillary acidic protein-labelled glial cell lineage differentiation was slightly promoted in pregestational diabetes mellitus (PGDM) mice. Various concentrations of glucose did not change the U87 cell viability, but glial cell line-derived neurotrophic factor expression was altered with varying glucose concentrations. Mouse maternal hyperglycaemia significantly increased Tunel{sup +} apoptosis but did not dramatically affect PCNA{sup +} cell proliferation in the process. To determine the cause of increased apoptosis, we determined the SOD activity, the expression of Nrf2 as well as its downstream anti-oxidative factors NQO1 and HO1, and found that all of them significantly increased in PGDM fetal brains compared with controls. However, Nrf2 expression in U87 cells was not significantly changed by different glucose concentrations. In mouse telencephalon, we observed the co-localization of Tuj-1 and Nrf2 expression in neurons, and down-regulating of Nrf2 in SH-SY5Y cells altered the viability of SH-SY5Y cells exposed to high glucose concentrations. Taken together, the data suggest that Nrf2-modulated antioxidant stress plays a crucial role in maternal hyperglycaemia-induced neurodevelopmental defects. - Highlights: • Typical neurodevelopmental defects could be observed in STZ-treated mouse fetuses. • Nrf2 played a crucial role in hyperglycaemia-induced brain malformations. • The effects of hyperglycaemia on neurons and glia cells were not same.