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Background: The progression of non-small cell lung cancer (NSCLC) is significantly influenced by circular RNAs (circRNAs), especially in tumor hypoxia microenvironment. However, the precise functions and underlying mechanisms of dysregulated circRNAs in NSCLC remain largely unexplored. Methods: Differentially expressed circRNAs in NSCLC tissues were identified through high-throughput RNA sequencing. The characteristics of circ_0007386 were rigorously confirmed via Sanger sequencing, RNase R treatment and actinomycin D treatment. The effects of circ_0007386 on proliferation and apoptosis were investigated using CCK8, cloning formation assays, TUNEL staining, and flow cytometry assays in vitro. In vivo, xenograft tumor models were used to evaluate its impact on proliferation. Mechanistically, the regulatory relationships of circ_0007386, miR-383-5p and CIRBP were examined through dual luciferase reporter assays and rescue experiments. Additionally, we detected the binding of EIF4A3 to CRIM1 pre-mRNA by RNA immunoprecipitation and the interaction between YAP1 and EIF4A3 under hypoxic conditions by co-immunoprecipitation. Results: Our investigation revealed a novel circRNA, designated as circ_0007386, that was upregulated in NSCLC tissues and cell lines. Circ_0007386 modulated proliferation and apoptosis in NSCLC both in vitro and in vivo. Functionally, circ_0007386 acted as a sponge for miR-383-5p, targeting CIRBP, which influenced NSCLC cell proliferation and apoptosis via the PI3K/AKT signaling pathway. Furthermore, under hypoxic conditions, the interaction between YAP1 and EIF4A3 was enhanced, leading to the displacement of EIF4A4 from binding to CRIM1 pre-mRNA. This facilitated the back-splicing of CRIM1 pre-mRNA, increasing the formation of circ_0007386. The circ_0007386/miR-383-5p/CIRBP axis was significantly associated with the clinical features and prognosis of NSCLC patients. Conclusions: Circ_0007386, regulated by YAP1-EIF4A3 interaction under hypoxia conditions, plays an oncogenic role in NSCLC progression via the miR-383-5p/CIRBP axis. [ABSTRACT FROM AUTHOR]

When large-scale electric vehicles are connected to the grid for unordered charging, it will seriously affect the stability and security of the power system. To solve this problem, this paper proposes a regional power network optimization scheduling method considering vehicle network interaction. Initially, based on the user behavior characteristics and charging and discharging characteristics of electric vehicles, a charging and discharging behavior model of electric vehicles was established. Based on the Monte Carlo sampling algorithm, the scheduling upper and lower limits of each scheduling cycle of electric vehicles were described, and the scheduling potential of each scheduling cycle of electric vehicles was obtained. Then, the electricity price is then used as an incentive parameter to guide EV users to charge during periods of low electricity prices and participate in discharge during periods of peak electricity prices. Aiming at the highest economic efficiency, the best consumption effect of new energy and the smoothest demand-side power curve of regional power grid, a three-objective optimal dispatching model was established. In the later stage, uncertainty factors are taken into consideration by introducing the concept of interval numbers, and an interval multi-objective optimization dispatching model is established. The two dispatching models are solved by NSGA-II algorithm and improved NSGA-II algorithm, and the Pareto solution set is obtained. Finally, based on the analytic Hierarchy Process (AHP), the optimal scheduling scheme is determined. The Monte Carlo sampling method is used to simulate the user side charging demand, and the effectiveness of this method is verified. In addition, the results of the interval multi-objective optimization model and the deterministic multi-objective optimization model are compared, and it is proved that the solution results of the interval multi-objective model are more adaptive, practical and robust to the uncertain factors. [ABSTRACT FROM AUTHOR]

The objective of this study was to optimize the extraction process of total sterols from wild Pyracantha fortuneana leaves (WPFL), and explore their antioxidant and whitening activities. The yield of total sterols (WPFLTPS) was used as indicator, and the single factor experiment was used to investigate the effects of extraction solvent, solid-liquid ratio, ultrasonic temperature and ultrasonic time on the yield of WPFLTPS. Based on this, the orthogonal experimental design was used to optimize the extraction conditions. The DPPH (2,2-diphenyl-1-picrylhydrazyl), ABTS [2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)] and nitrite methods were used to evaluate the antioxidant activity of WPFLTPS in vitro. The whitening activity was evaluated by the inhibitory effect on tyrosinase. The results showed that for optimal extraction process of WPFLTPS, the extraction solvent was absolute ethanol, ultrasonic temperature was 50 °C, solid-liquid ratio was 1:16 g/mL, and ultrasonic time was 25 minutes. Under these conditions, the yield of WPFLTPS was (11.00± 0.03) mg/g. In the range of 0.5~5 mg/mL, WPFLTPS had strong scavenging effects on DPPH radicals, ABTS+ radicals and nitrite ions, as well as a strong inhibitory effect on tyrosinase, demonstrating a good dose-response relationship. This extraction process was stable and reliable for extracting WPFLTPS. The WPFLTPS can be used as a new, natural antioxidant and tyrosinase inhibitor in functional foods. [ABSTRACT FROM AUTHOR]

In this work, a novel NiCo/ZIF-67/rGO catalyst was prepared via a facile impregnation-reduction method, followed by comprehensive characterization using XRD, SEM, TEM, XPS, and ICP-OES techniques. This catalyst featured a hierarchical porous support consisting of Zeolitic Imidazolate Framework-67 (ZIF-67) with a high specific surface area and reduced graphene oxide (rGO) with considerable electronic conductivity, along with strong synergistic interactions between Ni and Co species as well as between the deposited metals and the carbon in rGO. The NiCo/ZIF-67/rGO catalyst exhibited excellent activity in catalyzing the hydrolysis of NaBH4, resulting in a low activation energy (Ea) of 21.08 kJ mol−1 and a high turnover frequency (TOF) value of 5420 m L H 2 g M - 1 min - 1 . The hydrogen generation rate was increased by nearly double after five cyclic experiments, demonstrating the exceptional catalytic durability of NiCo/ZIF-67/rGO. The as-prepared NiCo/ZIF-67/rGO catalyst exhibits the advantages of cost-effectiveness, durability, and superior performance for NaBH4 hydrolysis, rendering it a promising candidate for industrial applications. [ABSTRACT FROM AUTHOR]

Background: Autism spectrum disorder (ASD) encompasses a diverse range of neurodevelopmental disorders, but the precise underlying pathogenesis remains elusive. This study aim to explore the potential mechanism of TREM2 in regulating microglia function in ASD. Materials and methods: The offspring rat model of ASD was established through prenatal exposure to valproic acid (VPA), and the behavioral symptoms of the ASD model were observed. On postnatal day (PND) 7 and PND 28, the effects of prenatally exposure to VPA on synaptic development and microglia phenotype of offspring rats were observed. Primary microglia were cultured in vitro. Lentivirus and adenovirus were utilized to interfere with TREM2 and overexpress TREM2. Results: Prenatally VPA exposure induced offspring rats to show typical ASD core symptoms, which led to abnormal expression of synapse-related proteins in the prefrontal cortex of offspring rats, changed the phenotype of microglia in offspring rats, promoted the polarization of microglia to pro-inflammatory type, and increased inflammatory response. The experimental results in vitro showed that overexpression of TREM2 could increase the expression of Gephyrin, decrease the content of CD86 protein and increase the content of CD206 protein. In addition, after the expression of TREM2 was interfered, the content of p-P38 MAPK protein increased and the content of p-ELK-1 protein decreased. Conclusion: The protective influence of TREM2 on the VPA-induced ASD model is attributed to its inhibition of the P38 MAPK pathway, this protective effect may be achieved by promoting the polarization of microglia to anti-inflammatory phenotype and improving the neuronal synaptic development. [ABSTRACT FROM AUTHOR]

The sluggish redox reaction kinetics and "shuttle effect" of lithium polysulfides (LPSs) impede the advancement of high-performance lithium-sulfur batteries (LSBs). Transition metal phosphides exhibit distinctive polarity, metallic properties, and tunable electron configuration, thereby demonstrating enhanced adsorption and electrocatalytic capabilities towards LPSs. Consequently, they are regarded as exceptional sulfur hosts for LSBs. Moreover, the introduction of a heterogeneous structure can enhance reaction kinetics and expedite the transport of electrons/ions. In this study, a composite of hollow CoP-FeP cubes with heterostructure modified carbon nanotube (CoFeP-CNTs) was fabricated and utilized as sulfur host in advanced LSBs. The presence of carbon nanotubes (CNTs) facilitates enhanced electron and Li + transport. Meanwhile, the active sites within the heterogeneous interface of CoP-FeP suppress the "shuttle effect" and enhance the conversion kinetics of LPSs. Therefore, the CoFeP-CNTs/S electrode exhibited exceptional cycling stability and demonstrated a capacity attenuation of merely 0.051 % per cycle over 600 cycles at 1C. This study presents a highly effective tactic for synthesizing dual-acting transition metal phosphides with heterostructure, which will play a pivotal role in advancing the development of efficient LSBs., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

This study aimed to investigate the mechanism of the effect of TREM2 on cognitive function in autistic mice. TREM2 overexpression and knockdown viruses were given to autism spectrum disorder (ASD) mice and BV2 microglia cell line. To assess cognitive performance, all groups of mice took part in the open field, new object recognition, Morris water maze, and three-box social experiments. Double immunofluorescence labeling demonstrated co-localization of LC3II and NeuN. Proteins from the PI3K/Akt/mTOR pathway were identified. In vivo, behavior studies revealed that TREM2 could successfully improve ASD mice's social interaction and cognitive performance. Besides, we discovered that TREM2 could increase autophagy in ASD mice. In vitro, overexpressing TREM2 reduced the expression of PI3K/AKT/mTOR pathway proteins, whereas knocking down TREM2 increased the expression of PI3K/AKT/mTOR pathway proteins. In conclusion, TREM2 could inhibit PI3K/Akt/mTOR signaling pathway, enhance autophagy, and improve the social communication ability and cognitive function of ASD mice.

Background: Non-small cell lung cancer (NSCLC) is a type of lung cancer that occurs in the cells of the respiratory tract, and its development is influenced by the regulation of circular RNAs (circRNAs). However, the role of circRNA carboxypeptidase A4 (circCPA4) in the progression of NSCLC and the underlying mechanism remain relatively clear., Methods: The study utilized both real-time quantitative polymerase chain reaction (RT-qPCR) and western blot techniques to evaluate the levels of circCPA4, microRNA-145-5p (miR-145-5p), alanine, serine, or cysteine-preferring transporter 2 (ASCT2). To assess cell proliferation, cell counting kit-8 (CCK8) and 5-ethynyl-2'-deoxyuridine (EdU) assays were performed. Apoptosis was determined using flow cytometry, while cell migration and invasive capacity were evaluated through transwell and wound-healing assays. Intracellular levels of glutamine, glutamate, and α-KG were measured using specific kits. The relationship between miR-145-5p and circCPA4 or ASCT2 was confirmed using dual-luciferase reporter assay and RNA immunoprecipitation assay., Results: CircCPA4 and ASCT2 RNA levels were elevated, while miR-145-5p was downregulated in both NSCLC tissues and cells. Depletion of circCPA4 significantly inhibited NSCLC cell proliferation, migration, invasion, and intracellular levels of glutamine, glutamate, and α-KG, and promoted apoptosis. Moreover, circCPA4 knockdown delayed tumor growth in vivo. Furthermore, circCPA4 was found to bind to miR-145-5p, thereby regulating the progression of NSCLC in vitro. ASCT2 was also identified as a downstream target of miR-145-5p, and its upregulation rescued the effects of miR-145-5p overexpression on NSCLC cell processes., Conclusion: CircCPA4 knockdown inhibited tumor property of NSCLC cells by modulating the miR-145-5p/ASCT2 axis., (© 2024 The Authors. Thoracic Cancer published by John Wiley & Sons Australia, Ltd.)