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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 487 records · Page 27
All sourcesNASA NTRSDOE OSTI
DOE OSTI2023

Comparison of inclusive and photon-tagged jet suppression in 5.02 TeV Pb+Pb collisions with ATLAS

Parton energy loss in the quark–gluon plasma (QGP) is studied with a measurement of photon-tagged jet production in 1.7 nb –1 of Pb+Pb data and 260 pb –1 of pp data, both at $\sqrt{^S{\text{NN}}}$ = 5.02 TeV, with the ATLAS detector. The process $pp$ → γ +jet+X and its analogue in Pb+Pb collisions is measured in events containing an isolated photon with transverse momentum ($p_{\text{T}}$) above 50 GeV and reported as a function of jet $p_{\text{T}}$. This selection results in a sample of jets with a steeply falling $p_{\text{T}}$ distribution that are mostly initiated by the showering of quarks. The $pp$ and Pb+Pb measurements are used to report the nuclear modification factor, $R_{\text{AA}}$, and the fractional energy loss, $S_{\text{loss}}$, for photon-tagged jets. In addition, the results are compared with the analogous ones for inclusive jets, which have a significantly smaller quark-initiated fraction. The $R_{\text{AA}}$ and $S_{\text{loss}}$ values are found to be significantly different between those for photon-tagged jets and inclusive jets, demonstrating that energy loss in the QGP is sensitive to the colour-charge of the initiating parton. Finally, the results are also compared with a variety of theoretical models of colour-charge-dependent energy loss.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2024

Suppressed electric quadrupole collectivity in 49 Ti

Single-step Coulomb excitation of 46,48,49,50 Ti is presented. A complete set of E2 matrix elements for the quintuplet of states in 49 Ti, centred on the core excitation, was measured for the first time. A total of nine E2 matrix elements are reported, four of which were previously unknown. $^{49}_{22}$Ti 27 shows a 20% quenching in electric quadrupole transition strength as compared to its semi-magic $^{50}_{22}$Ti 28 neighbour. This 20% quenching, while empirically unprecedented, can be explained with a remarkably simple two-state mixing model, which is also consistent with other ground-state properties such as the magnetic dipole moment and electric quadrupole moment. A connection to nucleon transfer data and the quenching of single-particle strength is also demonstrated. The simplicity of the 49 Ti- 50 Ti pair (i.e., approximate single-j 0 7/2 valence space and isolation of yrast states from non-yrast states) provides a unique opportunity to disentangle otherwise competing effects in the ground-state properties of atomic nuclei, the emergence of collectivity, and the role of proton-neutron interactions.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗
DOE OSTI2020

Staphylococcus pseudintermedius 5'-nucleotidase suppresses canine phagocytic activity

Staphylococcus pseudintermedius is a major opportunistic bacterial pathogen and the leading cause of pyoderma in dogs. In canines it is also often associated with infections of the urinary system and wounds and occasionally infects people. Widespread antimicrobial resistance has made the development of alternative treatments a high priority. The development of a staphylococcal vaccine, however, has proven challenging. Identification of virulence factors that inhibit phagocytosis and avoid innate immunity may play a significant role in preventing or treating infection with S. pseudintermedius. In this study, we identified a putative 5'-nucleotidase provisionally named SpAdsA, a S. pseudintermedius cell- wall protein encoded by SpAdsA. SpAdsA shares approximately 52% identity with the orthologous protein of Staphylococcus aureus and 14.8% identity with that of Streptococcus suis type2. It catalyzes the dephosphorylation of adenosine triphosphate and attenuation of this enzyme with critical amino acid substitutions nearly eliminated its hydrolytic activity. Furthermore, exogenous adenosine inhibited phagocytosis of S. pseudintermedius by canine neutrophils and monocytes. Conversely, the addition of SpAdsA inhibitor or A2A adenosine receptor antagonist impaired the capacity of S. pseudintermedius to escape from killing by phagocytic cells. The neutralizing ability of canine antibody produced against SpAdsA-M was determined. Taken together, these results suggest that SpAdsA likely plays an important role in S. pseudintermedius virulence and that attenuated SpAdsA may be a good candidate for inclusion in a vaccine against S. pseudintermedius.

5'-nucleotidase↗
DOE OSTI2021

Long non-coding RNA GClnc1 knockdown suppresses progression of epithelial ovarian cancer by recruiting FOXC2 to disrupt the NOTCH1/NF-κB/Snail pathway

Highlights: • GClnc1 is highly expressed in EOC patients and is associated with poor prognosis. • shGClnc1 inhibits the growth and metastasis of EOC cells and promotes apoptosis. • GClnc1 transcriptionally activates NOTCH1 by recruiting FOXC2 in the nucleus. • NOTCH1 promotes the activation of the NF-κB/Snail signaling. • GClnc1 may be one of the possible targets for the treatment of EOC. Epithelial ovarian cancer (EOC) is a highly fatal gynecological cancer. A long noncoding RNA (lncRNA) gastric cancer-associated lncRNA1 (GClnc1) has been revealed to play critical roles in metastasis. Therefore, the present study aims to explore the correlation between GClnc1 and the metastasis and progression of EOC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Adipose-specific knockout of Protein Kinase D1 suppresses de novo lipogenesis in mice via SREBP1c-dependent signaling

Highlights: • Protein Kinase D1 is a functional regulator in adipocyte and white adipose tissue. • PKD1 drives de novo lipogenesis in adipocyte. • SREBP1c signaling regulates lipogenesis in adipocyte. • PKD1-mediated de novo lipogenesis relies on SREBP1c. Having healthy adipose tissue is essential for metabolic health, as excessive adipose tissue in the body can cause its dysregulation and driving chronic metabolic diseases. Protein kinase D1 (PKD1) is considered to be a key kinase in signal transduction, which regulates multiple cellular functions, but its physiological functions in adipose are still not fully understood. This study aimed at elucidating the function of adipocyte PKD1 on lipogenesis. From RNA-Sequencing data, we found that the fatty acid biosynthesis pathway in white adipose tissue lacking PKD1 was significantly affected. Critical rate-limiting enzymes for de novo lipogenesis in adipocytes, such as FASN, ACCα, and SCD1, were significantly repressed after deleting PKD1 in vivo and in vitro. Further studies revealed that blockade of PKD1 significantly increased phosphorylation of SREBP1c at serine 372 site. Co-immunoprecipitation analysis showed that PKD1 interacts with SREBP1c in vitro and in vivo. Importantly, overexpression of SREBP1c reversed the inhibition of FASN and ACCα expression caused by PKD1 silencing. Together, adipocyte PKD1 promotes de novo lipogenesis via SREBP1c-dependent manner in visceral white adipose tissue and might provide a new target for the development of anti-obesity therapies.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Exosomes derived from hypoxic bone marrow mesenchymal stem cells rescue OGD-induced injury in neural cells by suppressing NLRP3 inflammasome-mediated pyroptosis

Exosomes have been shown to have therapeutic potential for cerebral ischemic diseases. In this study, we investigated the neuroprotective effects of normoxic and hypoxic bone marrow mesenchymal stromal cells-derived exosomes (N-BM-MSCs-Exo and H-BM-MSCs-Exo, respectively) on oxygen-glucose deprivation (OGD) injury in mouse neuroblastoma N2a cells and rat primary cortical neurons. The proportions of dead cells in N2a and primary cortical neurons after OGD injury were significantly increased, and N-BM-MSCs-Exo (40 μg/ml) could reduce the ratios, noteworthily, the protective effects of H-BM-MSCs-Exo (40 μg/ml) were more potent. Western blotting analysis indicated that N-BM-MSCs-Exo decreased the expression of NLRP3, ASC, Caspase-1, GSDMD-N, cleaved IL-1β and IL-18 in N2a cells. However, H-BM-MSCs-Exo (40 μg/ml) was more powerful in inhibiting the expression of these proteins in comparison with N-BM-MSCs-Exo. Similar results were obtained in primary cortical neurons. Immunofluorescence assays showed that after N-BM-MSCs-Exo and H-BM-MSCs-Exo treatment, the co-localization of NLRP3, ASC, Caspase-1 and the GSDMD translocation from the nucleus to the cytoplasm and membrane after OGD injury were reduced in N2a cells and primary cortical neurons, and H-BM-MSCs-Exo had a more obvious effect. In addition, N-BM-MSCs-Exo and H-BM-MSCs-Exo significantly reduced lactate dehydrogenase (LDH) release and the IL-18 levels in cell culture medium in N2a cells and primary cortical neurons. Once again H-BM-MSCs-Exo induced these effects more potently than N-BM-MSCs-Exo. All of these results demonstrated that N-BM-MSCs-Exo and H-BM-MSCs-Exo have significant neuroprotective effects against NLRP3 inflammasome-mediated pyroptosis. H-BM-MSCs-Exo has a more pronounced protective effect than N-BM-MSCs-Exo and may be used to ameliorate the progression of cerebral ischemia and hypoxia injury in patients.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

SMYD2 suppresses p53 activity to promote glucose metabolism in cervical cancer

Reprogrammed energy metabolism, especially the Warburg effect, is emerged as a hallmark of cancer. The protein lysine methyltransferase SMYD2 functions as an oncogene and is implicated in various malignant phenotypes of human cancers. However, the role of SMYD2 in tumor metabolism is still largely unknown. Here, we report that SMYD2 is highly expressed in human cervical cancer and its aberrant expression is linked to a poor prognosis. Bioinformatic analysis revealed a novel link between SMYD2 expression and aerobic glycolysis. Through loss-of-function experiments, we demonstrated that SMYD2 knockdown or inhibition induced a metabolic shift from aerobic glycolysis to oxidative phosphorylation, as evidenced by glucose uptake, lactate production, extracellular acidification, and the oxygen consumption rate. In contrast, SMYD2 overexpression promoted glycolytic metabolism in cervical cancer cells. Moreover, SMYD2 was required for tumor growth in cervical cancer and this oncogenic activity was largely glycolysis-dependent. Mechanistically, SMYD2 altered the methylation status of p53 and inhibited its transcriptional activity. Genetic silencing of p53 largely abrogated the effects of SMYD2 in promoting aerobic glycolysis. Taken together, our findings reveal a novel function of SMYD2 in regulating the Warburg effect in cervical cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Suppression of latent transforming growth factor-β (TGF-β)-binding protein 1 (LTBP1) inhibits natural killer/ T cell lymphoma progression by inactivating the TGF-β/Smad and p38MAPK pathways

Natural killer/T cell lymphoma (NKTCL) is a distinct subtype of Non-Hodgkin's lymphoma with highly aggressive clinical behavior. We aim to investigate the function of Latent transforming growth factor β binding protein 1 (LTBP1) and transforming growth factor beta1 (TGF-β1) and complex molecular pathogenesis of this disease.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

ESR1 mediated circ{sub 0}004018 suppresses angiogenesis in hepatocellular carcinoma via recruiting FUS and stabilizing TIMP2 expression

Angiogenesis has been certified to account for tumor pathobiology. Circular RNAs (circRNAs) have been demonstrated to be involved in angiogenesis-related diseases, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory roles of most circRNAs remain obscure. This study aims to uncover the function of hsa{sub c}irc{sub 0}004018 on angiogenesis in HCC. Firstly, quantitative real-time RT-PCR (RT-qPCR) analyzed that circ{sub 0}004018 was definitely down-regulated in HCC. Western blot analysis was conducted to detect the protein level of fused protein in sarcoma (FUS) and TIMP metallopeptidase inhibitor 2 (TIMP2). Functional assays were carried out to assess the impacts of circ{sub 0}004018 on HCC. From the experimental results, we found that overexpression of circ{sub 0}004018 significantly inhibited angiogenesis in HCC. The regulatory mechanism of circ{sub 0}004018 in HCC was determined by chromatin immunoprecipitation (ChIP), luciferase reporter assays and RNA immunoprecipitation (RIP) assay. Therefore, we proved that estrogen receptor 1 (ESR1) mediated circ{sub 0}004018 regulated TIMP2 by recruiting FUS. A series of rescue assays verified that circ{sub 0}004018 participated in angiogenesis in HCC via modulating TIMP2. In summary, this paper disclosed that ESR1 activated circ{sub 0}004018 inhibited angiogenesis in HCC via binding to FUS and stabilizing TIMP2 expression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

SIRT3 mediates mitofusin 2 ubiquitination and degradation to suppress ischemia reperfusion-induced acute kidney injury

Ischemia reperfusion-induced acute kidney injury (IR-induced AKI) is a life-threatening disease with many complications. Mitofusin 2 (Mfn2) ubiquitination is related to AKI. But the underlying molecular mechanisms remain unknown. This study aimed to probe the mechanism of Mfn2 ubiquitination in IR-induced AKI development. In IR-induced AKI mouse models, orbital blood and urine were collected for assessing kidney function. The kidney injury, ultrastructure of mitochondria, and histopathology in mice were evaluated after injection of G5, an ubiquitination inhibitor. Oxygen glucose deprivation/reoxygenation (OGD/R) models were established in HK-2 cells, and the mitochondria were extracted. Cell viability, apoptosis, oxidative stress, inflammatory reaction, mitochondrial membrane potential, and ATP production were measured. Mfn2 ubiquitination in mouse and cell models was evaluated. si-SIRT3 and pcDNA3.1-SIRT3 were transfected into cell models. Consequently, kidney function in mice was impaired by IR-induced AKI. Mfn2 ubiquitination and degradation promoted IR-induced AKI. OGD/R induced renal tubular epithelial cell injury and disrupted mitochondrial dynamics and functions through promoting Mfn2 ubiquitination. SIRT3 knockdown led to Mfn2 ubiquitination by binding to UBC; while its overexpression alleviated tubular epithelial cell injury. Briefly, SIRT3 mediates Mfn2 ubiquitination to relieve IR-induced AKI. This investigation may offer new insights for the treatment of IR-induced AKI injury.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2025

Suppression of the collisionless tearing mode by flow shear: implications for reconnection onset in the Alfvénic solar wind

We analyse the collisionless tearing mode instability of a current sheet with a strong shear flow across the layer. The growth rate decreases with increasing shear flow, and is completely stabilised as the shear flow becomes Alfvénic. We also show that, in the presence of strong flow shear, the tearing mode growth rate decreases with increasing background ion-to-electron temperature ratio, the opposite behaviour to the tearing mode without flow shear. We find that even a relatively small flow shear is enough to dramatically alter the scaling behaviour of the mode, because the growth rate is small compared with the shear flow across the ion scales (but large compared with shear flow across the electron scales). Our results may explain the relative absence of reconnection events in the near-Sun Alfvénic solar wind observed recently by NASA’s Parker Solar Probe.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗