Publications by authors named "Lili Chai"

3 Publications

  • Page 1 of 1

A current collect-free LiNiCoMnOflexible film for high-performance lithium-ion batteries.

Nanotechnology 2021 Nov 3;33(4). Epub 2021 Nov 3.

Department of Physics, Nanchang University, Nanchang 330031, People's Republic of China.

Due to the high demand for more convenient flexible devices, there are more requirements for higher performance of flexible batteries. The layered lithium-rich manganese-based LiNiCoMnOcathode material has the advantages of higher energy density, higher discharge capacity and environmentally friendly, so it can be used for high-performance flexible electrode cathode material. Its theoretical capacity can reach more than 250 mAh g, which is higher than most cathode materials currently used in commercialization. Here we synthesize LiNiCoMnO(LNCM) cathode, and then use a simple method to make a current collect-free LNCM flexible film. This film has excellent flexibility and electrochemical performance. At 25 mA g, its initial discharge capacity reaches 314.0 mAh g. After 200 cycles of 500 mA g, its capacity retention rate is 82.1%, the attenuation is about 0.08% per cycle. Moreover, by bending at any position of the flexible film, it can still remain intact, and the soft-packaged battery made by the flexible film can still be used under the bending condition and keep the brightness of the LED lamp unchanged. This shows that using LiNiCoMnOto make high-performance flexible electrodes is a simple and effective method, which is expected to be practically applied to flexible electronic devices.
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http://dx.doi.org/10.1088/1361-6528/ac302aDOI Listing
November 2021

Chemoprotective effect of atorvastatin against benzo(a)pyrene-induced lung cancer via the inhibition of oxidative stress and inflammatory parameters.

Ann Transl Med 2021 Feb;9(4):355

Department of Respiratory, Affiliated Xi'an Central Hospital, The Medical School of Xi'an Jiaotong University, Xi'an, China.

Background: Lung cancer affects approximately 9% of women and 17% of men worldwide, and has a mortality rate of 17%. Previously published studies have suggested that oxidative stress expansion can lead to lung cancer. The aim of the current study was to analyze the possible inhibitory pathway of atorvastatin against lung cancer cells in an model.

Methods: The cytotoxic effects of atorvastatin on lung cancer cell lines H460 and A549 were analyzed, as well as cell cycle arrest and cell morphology. Benzo(a)pyrene (BaP) was used for the induction of lung cancer in experimental rats, and atorvastatin (5, 10, and 20 mg/kg body weight) was used for treatment in a dose-dependent manner. Body weight and lung tumors were calculated at regular intervals. Antioxidants, pro-inflammatory cytokines, phase I and II antioxidant enzymes, polyamine enzymes, and apoptosis markers were determined at end of the experimental study.

Results: Cell cycle arrest occurred at the G2/M phase after atorvastatin treatment. Atorvastatin increased cytochrome C expression and caspase activity in a dose-dependent manner, and increased the activity of antioxidative enzymes, such as GPx, SOD, GST, reduced glutathione, and catalase, and reduced the level of nitrate and LPO. It also altered the xanthine oxidase (XO), Lactic Acid Dehydrogenase (LDH), quinone reductase (QR), UDP-glucuronosyltransferase (UDP-GT), adenosine deaminase (ADA), Aryl hydrocarbon hydroxylase (AHH), 5'-nucleotidase, cytochrome P450, cytochrome B5 and NADPH cytochrome C reductase levels. Atorvastatin was found to modulate polyamine enzyme levels, such as histamine, spermine, spermidine, and putrescine, and significantly (P<0.001) reduced the pro-inflammatory cytokine levels, such as tumor necrosis factor-α. Interleukin (IL)-6 and interleukin-1β (IL-1β) increased caspase-3 and caspase-9 levels in a dose-dependent manner.

Conclusions: Our findings indicate that atorvastatin can inhibit lung cancer through apoptosis.
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http://dx.doi.org/10.21037/atm-20-7770DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7944302PMC
February 2021

Fetal Calf Serum Exerts an Inhibitory Effect on Replication of Duck Hepatitis A Virus Genotype 1 in Duck Embryo Fibroblast Cells.

Viruses 2020 01 9;12(1). Epub 2020 Jan 9.

Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.

Among the causative agents of duck viral hepatitis, duck hepatitis A virus genotype 1 (DHAV-1) is the most common virus reported in most outbreaks worldwide. How to propagate DHAV-1 in cell cultures efficiently remains a problem to be explored. Here, we aimed to test the effect of serum type on DHAV-1 replication in duck embryo fibroblast (DEF) cells. Comparative studies involved virus culture and passage, observation of cytopathic effect (CPE), virus quantification, and plaque formation assay. From the results of these investigations, we conclude that use of chicken serum (CS) in maintenance medium allows DHAV-1 to establish productive, cytocidal infection in DEF cells, whereas FCS exerts inhibitory effects on DHAV-1 replication, CPE development, and plaque formation. By using a neutralization test, we found that the direct action of FCS on virions is likely to play a key role in inhibiting DHAV-1 replication in DEF cells. Mechanism analyses revealed that FCS inhibits DHAV-1 replication at virus adsorption and reduces extracellular virus yields. The present work may shed light on a new perspective for antiviral agent development, and have provided a virus-host cell system for further studies on molecular mechanism involved DHAV-1 replication and pathogenesis.
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http://dx.doi.org/10.3390/v12010080DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7019637PMC
January 2020
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