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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 685 records · Page 38
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Effects of amiloride on physiological activity of stem cells of human lung cancer and possible mechanism

Lung cancer is a common malignant tumor, the cancer stem cells (CSCs) were regarded responsible for the development of cancer tissue. The effects of amiloride on lung cancer stem cells and the possible mechanism were not much investigated. In this study, human NCI-H1975 lung CSCs were selected by flow cytometry, and the effects of amiloride at different concentrations (0, 12.5, 25, 50, and 100 μmol/L) were evaluated on proliferation, migration, invasion and apoptosis of CSCs using cell counting kit-8 and Transwell migration assays as well as flow cytometry. Wstern blot analysis was performed to investigate the effect of amiloride on the level of proteins in uPA system, NF-kB pathway, and PI3K-AKT-mTOR pathway in CSCs. As a result, we found that amiloride inhibited proliferation, migration and invasion of lung CSCs, and promoted apoptosis. Further, we found that amiloride decreased levels of target proteins in the uPA system, as well as the NF-kB and PI3K-AKT-mTOR pathways. These results indicated that amiloride could inhibit proliferation, migration and invasion of lung CSCs, and promotes apoptosis, these effects may be related to decreased levels of proteins in the uPA system, the NF-kB pathway, and the PI3K-AKT-mTOR pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

A negative feedback loop between nuclear factor 90 (NF90) and an anti-oncogenic microRNA, miR-7

Highlights: • miR-7, an anti-oncogenic miRNA, represses NF90 at the mRNA level. • The coding region of the NF90 mRNA is directly targeted by miR-7. • A rise in NF90 is attributed to negative feedback between NF90 and miR-7 in tumors. Alterations in microRNAs (miRNAs) levels deeply correlate with tumorigenesis. However, the molecular mechanism for the regulation of the miRNA production in tumors is not fully understood. We previously reported that downregulation of miR-7, which is an anti-oncogenic miRNA, was caused by overexpression of the nuclear factor 90 (NF90)-nuclear factor 45 (NF45) complex through the binding of double-stranded (ds) RNA-binding proteins to primary miR-7, resulting in promotion of tumorigenesis (Higuchi et al 2016). During this study, we found that the level of NF90 protein was dramatically decreased by overexpression of miR-7. Interestingly, the miR-7-mediated reduction in NF90 family proteins was only observed in NF90 protein, but not in NF110 protein, which is a longer form of the NF90 gene. Luciferase reporter analysis indicated that the overexpression of miR-7 significantly repressed the luciferase activity in the coding region of NF90 mRNA harboring a predicted target sequence of miR-7. The luciferase activity of the reporter vector, which has a mutated miR-7 target site in the coding region, was the same in the control and miR-7 overexpressed cells. Furthermore, the translation of TARGET-tagged NF90 mRNA without the 3′UTR of the NF90 mRNA was inhibited by the overexpression of miR-7. These results imply that miR-7 suppresses NF90 at the protein level through the binding of miR-7 to the complementary site of the seed sequence in the coding region of the NF90 mRNA. We further confirmed increased endogenous NF90 protein levels in SK-N-SH cells transfected with antisense oligonucleotides targeting miR-7, indicating that miR-7-mediated translational repression of NF90 is a physiological event. Taken together with our previous findings (Higuchi et al 2016), it suggests that the level of NF90 is increased by a negative feedback loop between NF90 and miR-7 in tumor tissues under physiological conditions.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Administration of ubiquitin-activating enzyme UBA1 inhibitor PYR-41 attenuates angiotensin II-induced cardiac remodeling in mice

Highlights: • Ang II induces UBA1 expression. • PYR-41 inhibits cardiac remodeling. • PYR-41 stabilizes PTEN. Pathological cardiac hypertrophy is the main risk factor for heart diseases. The ubiquitin-proteasome system (UPS) is the major intracellular protein degradation system involved in the development of cardiac hypertrophic remodeling. Ubiquitin-activating enzyme E1, a key component of the UPS, catalyzes the first step in ubiquitin conjugation to mark cellular proteins for degradation via proteasome. However, the functional role of E1 (UBA1) in regulation of hypertrophic remodeling in angiotensin II (Ang II)-infused mice remains unknown. In this study, male wild-type mice were treated with UBA1 inhibitor PYR-41 at two doses of 5 and 10 mg and infused with Ang II (1000 ng/kg/min) for 14 days. Systolic blood pressure was detected by using tail-cuff system. Cardiac function was assessed by echocardiography. Hypertrophic remodeling was analyzed examined by histological examinations. The expressions of genes and proteins were detected by quantitative real-time PCR and immunoblotting analysis. After 14 days, Ang II infusion significantly increased UBA1 expression at both mRNA and protein levels in the hearts. Furthermore, Ang II-infused mice showed a significant increase in systolic blood pressure compensatory cardiac function, hypertrophy, interstitial fibrosis, inflammation and oxidative stress compared with saline-treated controls, whereas these effects were dose-dependently attenuated in PYR-41-treated mice. These beneficial actions were associated mainly with inhibition of PTEN degradation and multiple downstream mediators (AKT, ERK1/2, STAT3, TGF-β/Smad2/3 and NF-kB(p65)). In conclusion, these results indicate that inhibition of UBA1 suppresses Ang II-induced hypertrophic remodeling, and suggest that administration of low dose PYR-41 may be a new potential therapeutic approach for treating hypertensive heart diseases.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Evaluation of collagen mixture on promoting skin wound healing in zebrafish caused by acetic acid administration

The aim of this study is to use zebrafish embryos as a quick platform for wound healing studies. At beginning, we optimized a protocol to induce skin lesion by acetic acid injection. The acetic acid injection induced regional inflammation wound hyperpigmentation by recruiting pigment cells to the wound area. Later, we applied established platform to evaluate the effect of tilapia's collagen peptide mixtures, including demonstration on promoting skin wound healing and eliminating inflammatory response. Results showed that after treating TY001, one of the above fish collagen peptide mixtures, not only repair and proliferation were induced, but also death and apoptosis cells were cleared within cutaneous lesion. Moreover, inflammatory response was suppressed along with collagen mixture treatment. Finally, the TY001-associated signaling was validated by real time-PCR, and numbers of gene associated with tissue repair and vessel proliferation were induced. To sum up, our findings provided a permissive model that may apply to generate a platform for further screening on repair and restoration technology. In addition, the tilapia fish collagen peptide mixture we applied on our model has great potential on developing clinical application on wound healing.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Co-production of bio-ethanol, xylonic acid and slow-release nitrogen fertilizer from low-cost straw pulping solid residue

In this paper, a novel bio-refinery sequence yielding varieties of co-products was developed using straw pulping solid residue. This process utilizes neutral sulfite pretreatment which under optimal conditions (160 °C and 3% (w/v) sulfite charge) provides 64.3% delignification while retaining 90% of cellulose and 67.3% of xylan. The pretreated solids exhibited excellent enzymatic digestibility, with saccharification yields of 86.9% and 81.1% for cellulose and xylan, respectively. After pretreatment, the process of semi-simultaneous saccharification and fermentation (S-SSF) and bio-catalysis was investigated. The results revealed that decreased ethanol yields were achieved when solid loading increased from 5% to 30%. An acceptable ethanol yield of 76.8% was obtained at 20% solid loading. After fermentation, bio-catalysis of xylose remaining in fermentation broth resulted in near 100% xylonic acid (XA) yield at varied solid loadings. Finally, to complete the co-product portfolio, oxidation ammoniation of the dissolved lignin successfully transformed it into biodegradable slow-release nitrogen fertilizer with excellent agricultural properties.

09 BIOMASS FUELS↗
DOE OSTI2022

Revealing the mechanism of surfactant-promoted enzymatic hydrolysis of dilute acid pretreated bamboo

Here, to improve the enzymatic digestibility of dilute acid pretreated bamboo residue (DABR), surfactants including PEG 4000 and Tween 80 were added to prevent the non-productive adsorption between residual lignin and enzyme. At the optimal loadings (e.g., 0.2 and 0.3 g surfactant/g lignin), the enzymatic digestibility of DABR improved from 29.4% to 64.6% and 61.6% for PEG 4000 and Tween 80, respectively. Furthermore, the promoting mechanism of these surfactants on enzymatic hydrolysis was investigated by real-time surface plasmon resonance (SPR) and fluorescence spectroscopy. Results from SPR analysis showed that Tween 80 outperformed PEG 4000 in terms of dissociating the irreversible cellulase adsorption onto lignin. Fluorescence quenching mechanism revealed that PEG 4000 and Tween 80 intervened the interaction between lignin and cellulase by hydrogen bonds/Van der Waals and hydrophobic action, respectively. This work provided an in-depth understanding of the mechanisms of PEG 4000 and Tween 80 on enhancing the enzymatic hydrolysis efficiency.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2021

Unlocking the secret of lignin-enzyme interactions: Recent advances in developing state-of-the-art analytical techniques

Bioconversion of renewable lignocellulosics to produce liquid fuels and chemicals is one of the most effective ways to solve the problem of fossil resource shortage, energy security, and environmental challenges. Among the many biorefinery pathways, hydrolysis of lignocellulosics to fermentable monosaccharides by cellulase is arguably the most critical step of lignocellulose bioconversion. In the process of enzymatic hydrolysis, the direct physical contact between enzymes and cellulose is an essential prerequisite for the hydrolysis to occur. However, lignin is considered one of the most recalcitrant factors hindering the accessibility of cellulose by binding to cellulase unproductively, which reduces the saccharification rate and yield of sugars. This results in high costs for the saccharification of carbohydrates. The various interactions between enzymes and lignin have been explored from different perspectives in literature, and a basic lignin inhibition mechanism has been proposed. However, the exact interaction between lignin and enzyme as well as the recently reported promotion of some types of lignin on enzymatic hydrolysis is still unclear at the molecular level. Multiple analytical techniques have been developed, and fully unlocking the secret of lignin-enzyme interactions would require a continuous improvement of the currently available analytical techniques. This review summarizes the current commonly used advanced research analytical techniques for investigating the interaction between lignin and enzyme, including quartz crystal microbalance with dissipation (QCM-D), surface plasmon resonance (SPR), attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy, atomic force microscopy (AFM), nuclear magnetic resonance (NMR) spectroscopy, fluorescence spectroscopy (FLS), and molecular dynamics (MD) simulations. Interdisciplinary integration of these analytical methods is pursued to provide new insight into the interactions between lignin and enzymes. Finally, this review will serve as a resource for future research seeking to develop new methodologies for a better understanding of the basic mechanism of lignin-enzyme binding during the critical hydrolysis process.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2022

Structure-based optimization of hydroxylactam as potent, cell-active inhibitors of lactate dehydrogenase

Structure-based design was utilized to optimize 6,6-diaryl substituted dihydropyrone and hydroxylactam to obtain inhibitors of lactate dehydrogenase (LDH) with low nanomolar biochemical and single-digit micromolar cellular potencies. Surprisingly the replacement of a phenyl with a pyridyl moiety in the chemical structure revealed a new binding mode for the inhibitors with subtle conformational change of the LDHA active site. Finally, this led to the identification of a potent, cell-active hydroxylactam inhibitor exhibiting an in vivo pharmacokinetic profile suitable for mouse tumor xenograft study.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗