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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 379 records · Page 21

Inhibition of Rev-erbα ameliorates muscular dystrophy

Highlights: • Rev-erbα ablation in mdx mice protects against muscle damage and wasting. • Loss of Rev-erbα promoted regenerative myogenesis in mdx mice. • Rev-erbα deficiency in dystrophic muscle reduced inflammatory response. • Loss of Rev-erbα in mdx primary myoblasts promoted proliferation and differentiation. Duchene muscular dystrophy leads to progressive muscle structural and functional decline due to chronic degenerative-regenerative cycles. Enhancing the regenerative capacity of dystrophic muscle provides potential therapeutic options. We previously demonstrated that the circadian clock repressor Rev-erbα inhibited myogenesis and Rev-erbα ablation enhanced muscle regeneration. Here we show that Rev-erbα deficiency in the dystrophin-deficient mdx mice promotes regenerative myogenic response to ameliorate muscle damage. Loss of Rev-erbα in mdx mice improved dystrophic pathology and muscle wasting. Rev-erbα-deficient dystrophic muscle exhibit augmented myogenic response, enhanced neo-myofiber formation and attenuated inflammatory response. In mdx myoblasts devoid of Rev-erbα, myogenic differentiation was augmented together with up-regulation of Wnt signaling and proliferative pathways, suggesting that loss of Rev-erbα inhibition of these processes contributed to the improvement in regenerative myogenesis. Collectively, our findings revealed that the loss of Rev-erbα function protects dystrophic muscle from injury by promoting myogenic repair, and inhibition of its activity may have therapeutic utilities for muscular dystrophy.

60 APPLIED LIFE SCIENCES↗

Heterogeneous response of cancer-associated fibroblasts to the glucose deprivation through mitochondrial calcium uniporter

Highlights: • CAFs from a tumor mass are heterogeneous under the glucose deficient condition. • CAFs survive under glucose deficient condition by activation of TGF-β and calcium. • Calcium influx to mitochondria is critical for survival of glucose-deficient CAFs. • MCU in CAFs could be a feasible target for the development of anticancer drugs. Cancer-associated fibroblasts (CAFs) are an abundant component of the tumor microenvironment and have distinct features from normal fibroblasts (NFs). However, the discriminative nature of heterogeneous CAFs under glucose starvation remains unknown. In this study, we investigated the changes in the mitochondrial calcium concentration and relevant intracellular machinery in CAFs under glucose-deficient conditions. Xenografted tumor masses were dissected into multiple pieces and subjected to the CAF isolation using magnetically activated cell sorting (MACS). NFs were separated from the normal lung and skin. Under glucose starvation, CAFs from the tumor mass exhibited heterogeneity in cell proliferation, ATP production and calcium concentration. Compared to NFs, mitochondrial calcium concentration was significantly higher in glucose-starved CAFs with upregulation of mitochondrial calcium uniporter (MCU) that led to enhancement of ATP production and cell growth. Intriguingly, treatment of glucose-starved CAFs with oligomycin increased apoptosis by disrupted calcium homeostasis following overactivation of the mPTP. Moreover, oligomycin-induced apoptosis was mitigated by calcium chelation. This study demonstrated that the discriminative calcium influx to mitochondria through MCU coordinated cell growth and apoptosis in glucose-starved CAFs but not in NFs.

60 APPLIED LIFE SCIENCES↗

EPS8 supports pancreatic cancer growth by inhibiting BMI1 mediated proteasomal degradation of ALDH7A1

Aldehyde dehydrogenase 7 family member A1 (ALDH7A1) is an enzyme catalyzing lipid peroxidation of fatty aldehydes. It plays a critical role in sustaining high oxygen consumption rate (OCR) and ATP production in pancreatic ductal adenocarcinoma (PADC). However, why PADC cells maintain a relatively high level of ALDH7A1 concentration is still not well understood. In the current study, we explored the interplay between epidermal growth factor receptor kinase substrate 8 (EPS8) and ALDH7A1 in PADC cells. PADC cell lines MIA PaCa-2 and AsPANC-1 were used for in vitro and in vivo studies. The co-IP assay showed mutual interactions between Flag-EPS8 and Myc-ALDH7A1 in both MIA PaCa-2 and AsPANC-1 cells. EPS8 knockdown resulted in decreased ALDH7A1 protein levels and increased poly-ubiquitination. An interaction was observed between ALDH7A1 and BMI1 but not between BMI1 and EPS8. BMI1 knockdown reduced ALDH7A1 poly-ubiquitination and degradation caused by EPS8 knockdown. Dual EPS8 and ALDH7A1 knockdown had a synergistic effect on suppressing PADC cell proliferation in vitro and in vivo. In conclusion, this study revealed that EPS8 supports PADC growth by interacting with ALDH7A1 and inhibiting BMI1 mediated proteasomal degradation of ALDH7A1.

60 APPLIED LIFE SCIENCES↗

MIG/CXCL9 exacerbates the progression of metabolic-associated fatty liver disease by disrupting Treg/Th17 balance

CD4{sup +}CD25{sup +} regulatory T (Treg) cells and Th17 cells play important roles in the progression of metabolic-associated fatty liver disease (MAFLD). However, the contribution of monokine induced by interferon-gamma (MIG)/CXCL9 to the Treg/Th17 imbalance in MAFLD is only partially understood. In the present study, we detected increased levels of MIG/CXCL9 and a Treg/Th17 imbalance in the setting of metabolic-associated steatohepatitis (MASH). Recombinant adeno-associated virus-mediated gene transfer and silencing of MIG/CXCL9 expression in mice alleviated MASH and increased the Treg/Th17 ratio. Furthermore, the percentage of Th17 cells, but not Treg cells, differentiated from splenic CD4{sup +} T cells was significantly increased by administration of MIG/CXCL9. MIG/CXCL9 also promoted Th17 cell proliferation, and its effects were dose dependent. Levels of phosphorylated c-Jun N-terminal kinase (JNK) decreased dramatically when MIG/CXCL9 was inhibited in a murine MASH model. In cultured Treg cells, phosphorylated JNK levels decreased dose-dependently in response to MIG/CXCL9 inhibition, but increased in cultured Th17 cells. This effect was blocked in the presence of a JNK inhibitor. These findings underline the fundamental importance of MIG/CXCL9 in maintaining the Treg/Th17 balance in MAFLD and provide the foundations for a novel approach to preventing and treating MAFLD.

60 APPLIED LIFE SCIENCES↗

Antitumor CD8 T cell responses in glioma patients are effectively suppressed by T follicular regulatory cells

Regulatory T (Treg) cells are thought to contribute to tumor pathogenesis by suppressing tumor immunosurveillance and antitumor immunity. T follicular regulatory (Tfr) cells are a recently characterized Treg subset that expresses both the Treg transcription factor (TF) Foxp3 and the T follicular helper (Tfh) TF Bcl-6. The role of Tfr cells in glioma patients remains unclear. In this study, we found that the level of Tfr cells, identified as Foxp3{sup +}Bcl-6{sup +} CD4 T cells, was significantly elevated in tumor-infiltrating CD4 T cells from resected glioma tumors. Both Tfr cells and Treg cells significantly suppressed the proliferation and the cytotoxic capacity of CD8 T cells toward glioma tumor cells, and the suppression was positively associated with the proportion of Tfr cells and Treg cells, respectively. Tfr and Treg cells from glioma tumor samples demonstrated higher suppression potency than those from healthy blood samples and glioma blood samples. Interestingly, canonical CXCR5{sup -} Treg cells could suppress both CXCR5{sup +} and CXCR5{sup -} CD8 T cells, albeit with stronger potency toward CXCR5{sup -} CD8 T cells. However, Tfr cells presented much higher suppression potency toward CXCR5{sup +} CD8 T cells, whereas CXCR5{sup +} CD8 T cells are a potent CD8 T cell subset previously described to have antiviral and antitumor roles. Overall, these data indicate that Tfr cells are enriched in glioma tumors and have suppressive capacity toward CD8 T cell-mediated effector functions.

60 APPLIED LIFE SCIENCES↗

Human α-defensin 5 suppressed colon cancer growth by targeting PI3K pathway

Defensins are highly conserved antimicrobial peptides, which ubiquitously expressed in different species. In addition to the functions in host defense, their aberrant expression have also been documented in cancerous tissue including breast cancer, lung caner and renal carcinoma etc. Whereas, roles of Defensin Alpha 5 (DEFA5) in colon cancer has not been explored. Bioinformatic analysis was used to study the expression of DEFA5 and its correlation with clinical outcomes; Western blot, qPCR, Co-immunoprecipitation, xenograft models were used to the study the molecular mechanism. Decreased expression of DEFA5 at protein level was observed in colon tissues. Colon cancer cell lines proliferation and colony formation capacity were significantly suppressed by DEFA5 overexpression. Moreover, in vivo tumor growth in nude mice was also suppressed by DEFA5 overexpression, suggesting a tumor suppressor role of DEFA5 in colon cancer. Mechanistically, DEFA5 directly binds to the subunits of PI3K complex, thus attenuates the downstream signaling transduction, leads to delayed cell growth and metastasis. Collectively, we concluded that DEFA5 showed an inhibitory effect in colon cancer cell growth and may serve as a potential tumor suppressor in colon cancer.

60 APPLIED LIFE SCIENCES↗

MiR-10b-5p inhibits tumorigenesis in gastric cancer xenograft mice model through down-regulating Tiam1

Highlights: • MiR-10b-5p acted as a tumor suppressor in gastric cancer by targeting and down-regulating Tiam1. • Overexpression of miR-10b-5p induced apoptosis of gastric cancer cells. • As a specifically chemically modified miRNA mimics, agomir-10b-5p can accumulate in target cells after overcoming membrane and tissue barriers in vivo. • Agomir-10b-5p could be a potential therapeutic agent for the treatment of gastric cancer. The miR-10b-5p plays an important role in gastric cancer development but its exact effect on gastric cancer development in vivo has not been fully studied. We showed that miR-10b-5p inhibited the proliferation and migration of gastric cancer cells by down-regulating Tiam1 which was up-regulated in both gastric cancer cells and tissues. Gastric cancer xenograft experiment showed that lenti-miR-10b-5p treatment and agomir-10b-5p injection could significantly retard tumor growth and reduce tumor size and induced apoptosis. Therefore, our results elucidate the tumor suppressor role of miR-10b-5p in gastric cancer in which it acts as a negative regulator of Tiam1 and also provide a molecular mechanism for agomir-10b-5p to treat gastric cancer.

60 APPLIED LIFE SCIENCES↗

Kindlin-2 promoted the progression of keloids through the Smad pathway and Fas/FasL pathway

Keloids are benign skin tumors characterized by aggressive growth. To date, there is no exact treatment because little is known about its pathological mechanism. Therefore, it is important to investigate the mechanism of its occurrence and development to identify therapeutic targets. In this study, the expression of Kindlin-2 was higher in keloid fibroblasts (KFs) than in normal skin fibroblasts (NFs). In vitro experiments showed that knocking down Kindlin-2 in KFs could promote cell apoptosis and inhibit cell proliferation, cell migration and invasion, and contractile capability. Western blot results showed that the phosphorylation of Smad3 in KFs was inhibited after knocking down Kindlin-2, inhibiting the activation of the Smad pathway. Moreover, knocking down Kindlin-2 increased the expression of Fas and FasL in KFs, which demonstrated that knocking down Kindlin-2 promoted the activation of the exogenous apoptotic pathway of KFs and then facilitated apoptosis. The above results revealed that knocking down Kindlin-2 in KFs can inhibit the activation of the Smad pathway and promote the activation of the Fas/FasL exogenous apoptosis pathway, thereby altering the cytological function of KFs. Therefore, Kindlin-2 might play an important role in the occurrence and development of keloids and could become a new target to treat keloids.

60 APPLIED LIFE SCIENCES↗

MicroRNA-7 overexpression positively regulates the CD8+ SP cell development via targeting PIK3R1

Highlights: • MicroRNA-7 overexpression promotes CD8{sup +} SP cell development. • We identified PIK3R1 as a target of miR-7. • The miR-7/PIK3R1 axis regulates CD8{sup +} SP cell development via modulating the balance of AKT/ERK pathways. microRNA-7 (miR-7), a distinct miRNA family member, has been reported to be involved in the biological functions of immune cells. However, the potential role of miR-7 in the CD8{sup +} T cell development remains to be elucidated. In this study, we estimated the potential effects of miR-7 overexpression in the thymic CD8{sup +} SP cell development using miR-7 overexpression mice. Our results showed that compared with those in control wild type (WT) mice, the volume, weight and total cell numbers of thymus in miR-7 overexpression (OE) mice increased significantly. The absolute cell number of CD8{sup +} SP cells in miR-7 OE mice increased and its ability of activation and proliferation enhanced. Futhermore, we clarified that miR-7 overexpression had an intrinsic promote role in CD8{sup +} SP cell development by adoptive cell transfer assay. Mechanistically, the expression level of PIK3R1, a target of miR-7, decreased significantly in CD8{sup +} SP cells of miR-7 OE mice. Moreover, the expression level of phosphorylated (p)-AKT and p-ERK changed inversely and indicating that miR-7 overexpression impaired the balance of AKE and ERK pathways. In summary, our work reveals an essential role of miR-7 in promoting CD8{sup +} SP cell development through the regulation of PIK3R1 and balance of AKT and ERK pathways.

60 APPLIED LIFE SCIENCES↗

WISP3 suppresses ESCC progression by inhibiting the IGF-2-IGF1R-AKT signaling cascade

Esophageal squamous cell carcinoma (ESCC) is a major health problem worldwide, especially in the Chinese population. However, the intrinsic molecular mechanisms of ESCC progression are largely unclear, thus there is an unmet need to identify essential genes governing this disease. Here, we discovered WISP3, an important member of the CCN family, is markedly downregulated in ESCC tissues compared to the normal esophageal epithelium. Downregulation of WISP3 in cancer tissue correlates with worse overall survival of ESCC patients. Using ESCC cell lines as models, we found that forced expression of WISP3 not only suppressed proliferation and migration of cancer cells in vitro, but also inhibited ESCC tumor growth and metastasis in vivo. On the contrary, WISP3 depletion strongly promoted the tumorigenicity of ESCC cells. Mechanistically, we found that WISP3 negates the activity of AKT via inhibiting the IGF-2-IGF1R signaling cascade, which mediates the tumor-suppressive function of WISP3 in esophageal cancers. Together, we identified a novel factor driving the development of ESCC, and revealed a potential therapeutic target for ESCC treatment.

60 APPLIED LIFE SCIENCES↗

LOXG473A induces the formation of osteoclasts in RAW264.7 cells via IL-6/JAK2/STAT3 signaling

Formation of osteoclasts is known to be closely associated with osteoporosis progression. LOX is a key enzyme that catalyzes the synthesis of collagen, which is the new mediator in osteoclast formation. However, the effect of LOXG473A on of osteoclast formation needs to be explored. Thereby, we sought to explore the effect of LOX{sub G473A} on formation of osteoclasts and its underlying mechanism. To investigate the function of LOX{sub G473A} in osteoclast formation, Raw264.7 cells were stably transfected with LOX-WT or LOX-MUT (LOX{sub G473A}). Real-time PCR and western blotting were used to detect the relative levels of osteoclast formation related genes and proteins. TRAP staining and immunofluorescence staining were used to test the ability of Raw264.7 cells to form osteoclasts and the ability of cells to form rings, respectively. Bone erosion assay was used to test bone resorptive activity. The data indicated that LOX{sub G473A} significantly enhanced the ability of osteoclasts forming, ring-forming and bone resorpting in Raw264.7 cells. Mechanically, LOX{sub G473A} upregulated the expressions of NFATC1, ACP5, CTSK, IL-6, and the proportion of p-JAK2/JAK2 and p-STAT3/STAT3, thereby promoting the formation of osteoclasts. In conclusion, we have verified that LOX{sub G473A} induces the proliferation of osteoclasts in Raw264.7 cells via IL-6/JAK2/STAT3 signaling, suggesting a novel strategy for studying osteoporosis.

60 APPLIED LIFE SCIENCES↗

The protein 4.1R downregulates VEGFA in M2 macrophages to inhibit colon cancer metastasis

Highlights: • Protein 4.1R knockout reduced the phagocytosis of M2 macrophages. • Co-culture with 4.1R knockout M2 macrophages enhances the malignancy of colon cancer. • Protein 4.1R knockout upregulates vascular endothelial growth factor A secreted by M2 macrophages. • Protein 4.1R knockout activates the PI3K/AKT signaling pathway and promotes the progression of colon cancer. M2 macrophages are crucial components of the tumour microenvironment and have been shown to be closely related to tumour progression. Co-culture with 4.1R{sup −/−} M2 macrophages enhances the malignancy of colon cancer (CC), but the mechanism remains unclear. Here, we report that protein 4.1R knockout reduced the phagocytosis of M2 macrophages (M-CSF/IL-4-treated bone marrow cells) and promoted MC38 colon cancer cell proliferation, migration, invasion, tumour formation and epithelial-mesenchymal transition (EMT), which are regulated by M2 macrophages. Further mechanistic dissection revealed that the 4.1R knockout upregulated vascular endothelial growth factor A (VEGFA) secreted by M2 macrophages and promoted colon cancer progression by activating the PI3K/AKT signalling pathway. In summary, our present study identified that 4.1R downregulates VEGFA secretion in M2 macrophages and delays the malignant potential of colon cancer by inhibiting the PI3K/AKT signalling pathway.

60 APPLIED LIFE SCIENCES↗

Incomplete radiofrequency ablation induced chemoresistance by up-regulating heat shock protein 70 in hepatocellular carcinoma

Highlights: • iRFA treatment inhibited cisplatin-induced pyroptosis of HCC cells. • Heat shock protein 70 was involved in the suppression of NLRP3 activation. • iRFA treatment decreased the cisplatin sensitivity of HCC through regulating HSP70. Radiofrequency ablation (RFA) is a common minimally invasive treatment for hepatocellular carcinoma (HCC). Incomplete RFA (iRFA) due to the sub-lethal heat shock challenge of some cell populations leads to the generation of transformed survivor cells with enhanced chemoresistance. However, the underlying mechanism of iRFA on HCCs chemoresistance remains unknown. In the present study, we investigated the effect of iRFA on HCCs sensitivity to cisplatin. Cells treated with the sub-lethal heat shock challenge were used to mimic iRFA treatment in vitro. An orthotopic implantation HCC model was established and also performed iRFA treatment. Flow cytometry, transwell assay, and cell counting kit-8 assay were used to determine the effect of iRFA treatment on cisplatin-induced HCC cell apoptosis, invasion, and cell viability. ELISA and Western blot were used to detect the effect of iRFA treatment on cisplatin-induced HCC cell pyroptosis. We found that iRFA treatment increased the HCC cell proliferation and invasion ability, and inhibited cisplatin-induced pyroptosis. Further experiments showed that iRFA treatment induced upregulation of HSP70, which inhibited the cisplatin-induced NLRP3 inflammasome activation, leading to inhibition of pyroptosis. HSP70 knockdown or NLRP3 overexpression could reverse the effect of iRFA treatment in vitro. In vivo, HSP70 knockdown reversed the chemosensitivity of HCC to cisplatin, which was decreased by iRFA. In conclusion, we demonstrated that iRFA induced drug resistance by HSP70-mediated inhibition of cell pyroptosis in HCC.

60 APPLIED LIFE SCIENCES↗

LncRNA HOTTIP from synovial fibroblast-derived exosomes: A novel molecular target for rheumatoid arthritis through the miR-1908–5p/STAT3 axis

Rheumatoid arthritis (RA) is a chronic inflammation mediated by autoimmune responses. HOTTIP, a long noncoding RNA (lncRNA), participates in cell proliferation and invasion. However, the correlation between HOTTIP and RA remains unclear. Therefore, this study aimed to clarify how HOTTIP works in RA and to investigate its role in the development of RA. Flow cytometry was used to analyze cell cycle progression. Binding between HOTTIP, signal transducer and activator of transcription 3 (STAT3) and miR-1908–5p was demonstrated by dual-luciferase assays. Quantitative real-time polymerase chain reaction (qRT–PCR) was used to measure the expression of T cell differentiation-related proteins. We found that HOTTIP was upregulated in rheumatoid arthritis synovial fibroblasts (RASFs). HOTTIP directly bound to miR-1908–5p and negatively modulated miR-1908–5p expression while positively regulating STAT3. The effects of HOTTIP overexpression on regulating the balance of the Th17/Treg cell ratio were partly reversed by miR-1908–5p overexpression. In addition, in vivo experiments demonstrated that overexpression of HOTTIP aggravated inflammation in RA mice, which was demonstrated by hematoxylin and eosin (HE) staining and the increased expression levels of CD4{sup +} interleukin (IL)-17{sup +}, forkhead Box P3 (FOXP3) and retinoid-related orphan receptor gamma-t (RORγt). In summary, our study suggests that HOTTIP plays a damaging role in RA by promoting inflammation, which may be related to the regulation of miR-1908–5p expression and the STAT3 signaling pathway. These results suggest that the regulation of HOTTIP may be a promising therapeutic strategy for RA.

60 APPLIED LIFE SCIENCES↗

4th Big Data for Nuclear Power Plants Workshop 2023

The Ohio State University and Idaho National Laboratory organized the 4 th Big Data for Nuclear Power Plants Workshop in November, 2023 in Columbus, Ohio. Workshop topics were chosen to understand the challenges and gaps that need to be addressed to maximize the impact of data on the nuclear industry, as well as the associated applications and risks. Discussions were focused around six specific application areas: Operation and Maintenance; Machine Learning in Nuclear Materials and Advanced Manufacturing; Cybersecurity; High-Performance Computing and Massive Computation; Big Data and Digital Twins; and Nuclear Non-Proliferation. The opportunities, challenges, and risks identified in the six focus areas explored in this workshop are diverse, but some common themes emerge, such as the importance of data integrity, quality, coverage, privacy, and traceability. Big data and AI/ML tools can be leveraged to reduce costs, optimize human tasking, and reduce human error across various application areas. In order for the nuclear industry to benefit from big data and advanced analytic capabilities, it is essential to address challenges and risks, such as data privacy, model reliability, and computational resource availability. Learning from other industries that have successfully implemented big data and AI/ML technologies, like the aerospace industry, can help the nuclear industry successfully integrate these technologies.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗

Utility Experience with Inverter Based Resource Impacts on Transmission Protection

High penetration of inverter-based resources (IBR) can adversely affect the transmission protection schemes in the area. With the proliferation of IBRs, utilities are finding out that conventional protection schemes are not adequately equipped to protect the electric systems because the existing system has been designed based on the fault current response of conventional rotating-machine-based generators. In several cases, the available literature does not provide any clear solution for the issues when the protection scheme does not operate properly near IBRs. This report identifies various protection challenges due to IBRs that industry is facing, from the utility perspective. It includes a broad review of all challenges that system protection has experienced so far with high penetration of IBRs. Key issues have been identified based on a survey of different utility protection engineers. Finally, fault event recordings are shown to demonstrate some actual cases of mis-operations of relays near IBRs.

24 POWER TRANSMISSION AND DISTRIBUTION↗

The Future of Arms Control in a Multilateral and Multi-Domain Environment

The crisis of arms control is obvious and broadly discussed among states, within the world’s expert community and to a lesser extent the media. This crisis has at least three building blocks: Russia continues to violate or undermine key arms control treaties and commitments; China rejects to join the existing arms control architecture; and both countries heavily invest in the modernization of their armed forces, including development of the nuclear arsenals. In the current highly competitive environment, arms control is more difficult to achieve and is likely to accomplish less than what was optimistically anticipated a generation ago. The growing pressure to “save arms control at all cost”, often expressed by the Western expert community, further complicates the situation. The excessively aspirational and ideological approach to arms control – in which arms control, disarmament, and non-proliferation (ADN) become a silver bullet solution – is as dangerous as security and defence policies which entirely exclude ADN. As James Cameron rightly points out, “history should teach policy-makers to look beyond formulae for strategic stability to other ways in which arms control can help to contain disruptive challenges to the balance of power and minimize the chances of war”.

98 NUCLEAR DISARMAMENT, SAFEGUARDS, AND PHYSICAL P↗