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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 1,135 records · Page 63
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

HIF-2alpha-dependent PAI-1 induction contributes to angiogenesis in hepatocellular carcinoma

Hypoxia promotes progression of hepatocellular carcinoma (HCC), not only affecting tumor cell proliferation and invasion, but also angiogenesis and thus, increasing the risk of metastasis. Hypoxia inducible factors (HIF)-1α and -2α cause adaptation of tumors to hypoxia, still with uncertainties towards the angiogenic switch. We created a stable knockdown of HIF-1α and HIF-2α in HepG2 cells and generated cocultures of HepG2 spheroids with embryonic bodies as an in vitro tumor model mimicking the cancer microenvironment. The naturally occuring oxygen and nutrient gradients within the cocultures allow us to question the role of distinct HIF isoforms in regulating HCC angiogenesis. In cocultures with a HIF-2α knockdown, angiogenesis was attenuated, while the knockdown of HIF-1α was without effect. Microarray analysis identified plasminogen activator inhibitor 1 (PAI-1) as a HIF-2α target gene in HepG2 cells. The knockdown of PAI-1 in HepG2 cells also lowered angiogenesis. Blocking plasmin, the downstream target of PAI-1, with aprotinin in HIF-2α knockdown (k/d) cells proved a cause–effect relation and restored angiogenesis, with no effect on control cocultures. Suggestively, HIF-2α increases PAI-1 to lower concentrations of active plasmin, thereby supporting angiogenesis. We conclude that the HIF-2α target gene PAI-1 favors the angiogenic switch in HCC. - Highlights: • HepG2 were cocultured with stem cells to mimic a cancer microenvironment in vitro. • A knockdown of HIF-2α reduces angiogenesis. • PAI-1 was identified as a HIF-2α target gene in HCC by microarray analysis. • HIF-2α induces the angiogenic switch via inhibition of plasmin.

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 OSTI2016

Induction of oxidative and nitrosative stresses in human retinal pigment epithelial cells by all-trans-retinal

Delayed clearance of free form all-trans-retinal (atRAL) is estimated be the key cause of retinal pigment epithelium (RPE) cells injury during the pathogenesis of retinopathies such as age-related macular degeneration (AMD), however, the underlying molecular mechanisms are far from clear. In this study, we investigated the cytotoxicity effect and underlying molecular mechanism of atRAL on human retinal pigment epithelium ARPE-19 cells. The results indicated that atRAL could cause cell dysfunction by inducing oxidative and nitrosative stresses in ARPE-19 cells. The oxidative stress induced by atRAL was mediated through up-regulation of reactive oxygen species (ROS) generation, activating mitochondrial-dependent and MAPKs signaling pathways, and finally resulting in apoptosis of ARPE-19 cells. The NADPH oxidase inhibitor apocynin could partly attenuated ROS generation, indicating that NADPH oxidase activity was involved in atRAL-induced oxidative stress in ARPE-19 cells. The nitrosative stress induced by atRAL was mainly reflected in increasing nitric oxide (NO) production, enhancing iNOS, ICAM-1 and VCAM-1 expressions, and promoting monocyte adhesion. Furthermore, above effects could be dramatically blocked by using a nuclear factor kappa B (NF-κB) inhibitor SN50, indicated that atRAL-induced oxidative and nitrosative stresses were mediated by NF-κB. The results provide better understanding of atRAL-induced toxicity in human RPE cells. - Highlights: • atRAL induces oxidative stress-mediated apoptosis in ARPE-19 cells. • atRAL induces oxidative stress-mediated inflammation in ARPE-19 cells. • NF-κB is involved in atRAL-induced oxidative and nitrosative stresses.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2012

Selective killing of ovarian cancer cells through induction of apoptosis by nonequilibrium atmospheric pressure plasma

Two independent ovarian cancer cell lines and fibroblast controls were treated with nonequilibrium atmospheric pressure plasma (NEAPP). Most ovarian cancer cells were detached from the culture dish by continuous plasma treatment to a single spot on the dish. Next, the plasma source was applied over the whole dish using a robot arm. In vitro cell proliferation assays showed that plasma treatments significantly decreased proliferation rates of ovarian cancer cells compared to fibroblast cells. Flow cytometry and western blot analysis showed that plasma treatment of ovarian cancer cells induced apoptosis. NEAPP could be a promising tool for therapy for ovarian cancers.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2013

Induction of electron injection and betatron oscillation in a plasma-waveguide-based laser wakefield accelerator by modification of waveguide structure

By adding a transverse heater pulse into the axicon ignitor-heater scheme for producing a plasma waveguide, a variable three-dimensionally structured plasma waveguide can be fabricated. With this technique, electron injection in a plasma-waveguide-based laser wakefield accelerator was achieved and resulted in production of a quasi-monoenergetic electron beam. The injection was correlated with a section of expanding cross-section in the plasma waveguide. Moreover, the intensity of the X-ray beam produced by the electron bunch in betatron oscillation was greatly enhanced with a transversely shifted section in the plasma waveguide. The technique opens a route to a compact hard-X-ray pulse source.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗
DOE OSTI2021

Observation of second harmonic electron cyclotron resonance heating and current-drive transition during non-inductive plasma start-up experiment in QUEST

Here, noninductive plasma current start-up using 2nd harmonic electron cyclotron resonance heating (ECRH) with oblique radio frequency (RF) injection is demonstrated in a Q-shu University experiment with steady-state spherical tokamak. A strong transition was observed in the heating and plasma current ramp-up. The initial bulk electron heating regime exhibits T ebulk ~ 140 eV and no hard x-ray (HXR) emission with a low I p of ~15 kA; it abruptly transitions to a regime that exhibits a low T ebulk of ~10 eV and a strong HXR emission with a high I p of ~50 kA. This behavior is distinctly different from that observed in previous fundamental ECRH experiments. The mechanism of the heating and current drive transition are investigated considering wave power absorption and plasma power balance. The results indicate that the transition is caused by the favorable heating of tail electrons where the RF power absorption at the 2nd harmonic increases nearly linearly with T etail , while the power transfer from the tail electrons to the bulk electrons decreases with 1/T etail 0.5 . This causes a rapid transition to a state with high T etail while reducing T ebulk towards colder ion temperature. The understanding of the transition mechanism helps to consider plasma current start-up using 2nd harmonic ECRH for tokamak reactors such as JT-60 SA and ITER.

QUEST↗
DOE OSTI2013

Spin-flip induction of Fano resonance upon electron tunneling through atomic-scale spin structures

The inclusion of inelastic spin-dependent electron scatterings by the potential profiles of a single magnetic impurity and a spin dimer is shown to induce resonance features due to the Fano effect in the transport characteristics of such atomic-scale spin structures. The spin-flip processes leading to a configuration interaction of the system's states play a fundamental role for the realization of Fano resonance and antiresonance. It has been established that applying an external magnetic field and a gate electric field allows the conductive properties of spin structures to be changed radically through the Fano resonance mechanism.

75 CONDENSED MATTER PHYSICS, SUPERCONDUCTIVITY AND↗