Automating literature screening and curation with applications to computational neuroscience.

OBJECTIVE: ModelDB (https://modeldb.science) is a discovery platform for computational neuroscience, containing over 1850 published model codes with standardized metadata. These codes were mainly supplied from unsolicited model author submissions, but this approach is inherently limited. For example, we estimate we have captured only around one-third of NEURON models, the most common type of models in ModelDB. To more completely characterize the state of computational neuroscience modeling work, we aim to identify works containing results derived from computational neuroscience approaches and their standardized associated metadata (eg, cell types, research topics). MATERIALS AND METHODS: Known computational neuroscience work from ModelDB and identified neuroscience work queried from PubMed were included in our study. After pre-screening with SPECTER2 (a free document embedding method), GPT-3.5, and GPT-4 were used to identify likely computational neuroscience work and relevant metadata. RESULTS: SPECTER2, GPT-4, and GPT-3.5 demonstrated varied but high abilities in identification of computational neuroscience work. GPT-4 achieved 96.9% accuracy and GPT-3.5 improved from 54.2% to 85.5% through instruction-tuning and Chain of Thought. GPT-4 also showed high potential in identifying relevant metadata annotations. DISCUSSION: Accuracy in identification and extraction might further be improved by dealing with ambiguity of what are computational elements, including more information from papers (eg, Methods section), improving prompts, etc. CONCLUSION: Natural language processing and large language model techniques can be added to ModelDB to facilitate further model discovery, and will contribute to a more standardized and comprehensive framework for establishing domain-specific resources.

Development and validation of a scale for the assessment of the knowledge-attitude-practice of parents towards children snoring.

BACKGROUND: Children Snoring is a common childhood disorder that affects the growth and development of children and is detrimental to their health. Increasing awareness of Children Snoring among parents is important. AIM: To develop the Knowledge-Attitude-Practice of Parents towards Children Snoring Scale and test the reliability and validity of the scale. METHODS: The development of the tool was divided into two phases involving 1257 parents from China. In the first phase, an initial project bank was created through a literature review. This was followed by a Delphi expert consultation, group discussion and pre-survey. The second stage screened the items and conducted an exploratory factor analysis, then conducted a confirmatory factor analysis and tested for reliability and validity. RESULTS: Support was found for the 25-item Knowledge-Attitude-Practice toward Children Snoring scale. Exploratory and confirmatory factor analyses provide support for four subscales: (parental basic cognition toward Children Snoring; parents' perception of complications of Children Snoring; parents' attitude towards Children Snoring; parents' concern and prevention of Children Snoring). Internal consistency for the total scale was high (Cronbach's α = 0.93). The intraclass correlation coefficient of test-retest reliability was 0.92 (95%CI: 0.85 to 0.95), which provided support for the stability of the scale. CONCLUSION: The Knowledge-Attitude-Practice of Parents towards Children Snoring scale shows promise as a measure that may be used by medical workers and community children's health managers.

Eriodictyol regulated ferroptosis, mitochondrial dysfunction, and cell viability via Nrf2/HO-1/NQO1 signaling pathway in ovarian cancer cells.

This study aimed to investigate the antitumor effect and the underlying molecular mechanism of eriodictyol on ovarian cancer cells. CaoV3 and A2780 were exposed to eriodictyol at different concentrations of 0-800 µM. Cell apoptosis and viability were determined by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay and Cell Counting Kit-8 (CCK-8) assay, respectively. Mitochondrial membrane potential was evaluated by flow cytometers with a JC-1 detection kit. Fe2+ content was evaluated using an iron assay kit. The section of tumor tissues was observed using hematoxylin-eosin (H&E) staining and nuclear factor erythroid 2-related factor 2 (Nrf2) expression was detected by immunohistochemistry (IHC) staining. Eriodictyol suppressed cell viability and induced cell apoptosis of CaoV3 and A2780 cells. Half maximal inhibitory concentration (IC50 ) value of CaoV3 at 24 and 48 h was (229.74 ± 5.13) µM and (38.44 ± 4.68) µM, and IC50 value of A2780 at 24 and 48 h was (248.32 ± 2.54) µM and (64.28 ± 3.19) µM. Fe2+ content and reactive oxygen species production were increased and protein levels of SLC7A11 and GPX4 were decreased by eriodictyol. Besides, eriodictyol reduced the ratio of JC-1 fluorescence ratio, glutathione and malondialdehyde contents but elevated Cytochrome C level. Nrf2 phosphorylation were obviously downregulated by eriodictyol. Finally, eriodictyol suppressed tumor growth, aggravated mitochondrial dysfunction and downregulated Nrf2 expression in tumor tissue in mice. Eriodictyol regulated ferroptosis, mitochondrial dysfunction and cell viability via Nrf2/HO-1/NQO1 signaling pathway in ovarian cancer.

[Retracted] MicroRNA­379 acts as a tumor suppressor in non­small cell lung cancer by targeting the IGF­1R­mediated AKT and ERK pathways.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell migration and invasion assay data shown in Figs. 2F, 5D and 6D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 38: 1857­1866, 2017; DOI: 10.3892/or.2017.5835].

Encapsulation of curcumin in soluble soybean polysaccharide-coated gliadin nanoparticles: interaction, stability, antioxidant capacity, and bioaccessibility.

BACKGROUND: Gliadin nanoparticles are used as a delivery system for active substances because of their amphiphilicity and bioavailability. However, they are susceptible to destabilization by external agents. In this study, gliadin nanoparticles stabilized by soluble soybean polysaccharide (SSPS) were prepared by antisolvent precipitation. Formed stable complex nanoparticles were applied to protect and deliver curcumin (Cur). RESULTS: Gliadin/SSPS nanoparticles with the smallest particle size (196.66 nm, polydispersity index < 0.2) were fabricated when the mass ratio of gliadin to SSPS was 1:1 at pH 5.0. SSPS-stabilized gliadin nanoparticles had excellent stability at pH 3.0-8.0, 0.02-0.1 mol L-1 NaCl and at 90 °C heat. Gliadin/SSPS nanoparticles were used to encapsulate the Cur. The encapsulation efficiency of the Cur-loaded gliadin/SSPS nanoparticles was 84.59%. Fourier transform infrared spectroscopy and fluorescence spectrophotometry showed that the main forces were hydrogen bonds, electrostatic interactions and hydrophobic interactions between gliadin and SSPS. The X-ray diffraction patterns exhibited that the crystalline form of Cur converted to an amorphous substance. The retention rates of Cur-loaded gliadin/SSPS nanoparticles reached 79.03%, 73.43% and 87.92% after ultraviolet irradiation for 4 h, heating at 90 °C and storage at 25 °C for 15 days, respectively. Additionally, simulated digestion demonstrated that the bioavailability of gliadin/SSPS-Cur nanoparticles was four times higher than that of free Cur. CONCLUSION: This study showed that SSPS improved the stability of gliadin nanoparticles. Gliadin/SSPS nanoparticles have the function of loading and delivering Cur. © 2022 Society of Chemical Industry.

Encapsulation of Ultrafine Metal-Organic Framework Nanoparticles within Multichamber Carbon Spheres by a Two-Step Double-Solvent Strategy for High-Performance Catalysts.

Carbon-encapsulated metal-organic framework (MOF) composite is one kind of emerging new catalyst with high efficiency and has gained much attention. However, for this kind of composite catalyst, the key to improving its catalytic activity and durability is to realize the effective dispersion of MOF nanoparticles (NPs) and enhance the interaction between MOF NPs and the carbon matrix, which remain a significant challenge. Herein, ultrafine MOF NPs within multichamber carbon spheres (MOF@MCCS), for the first time, have been rationally synthesized by a two-step double-solvent strategy for high-performance catalysts. The precise loading of guest MOFs can be achieved by adjusting the multichamber structure and calcination extent of the multichamber polymer (MCP), and the particle size of MOFs can be as low as 13.2 nm. Due to the formation of abundant carbon defects in the pyrolysis process of MCPs, the special structure and synergistic effect make the material exhibit higher catalytic activity and durability. More importantly, this method is universal and can be extended to different MOF systems. The two-step double-solvent strategy not only prepares a unique structure of MOF@MCCS-type host-guest-encapsulated catalysts but also provides a new idea for the design of high-efficiency catalysts with better performance and higher durability.

Gel properties of transglutaminase-induced soy protein isolate-polyphenol complex: influence of epigallocatechin-3-gallate.

BACKGROUND: Traditional soy protein isolate (SPI)-based gel products, such as tofu, are generally produced by heating and by addition of metal salt ions to adjust the hydrophobicity and electrostatic force of soybean protein to facilitate the formation of a uniform network structure. However, the gelation rate of the soy protein gel network structure is difficult to control. Theoretically, epigallocatechin-3-gallate (EGCG) could be used to alter the surface hydrophobicity of thermally induced SPI to improve its gelation rate and form a more uniform network structure, thus improving SPI-based gel properties (hardness, water holding capacity and rheological properties). RESULTS: An SPI-EGCG complex (SPIE) was prepared, and properties of the resulting gel, following induction of transglutaminase (TG), were evaluated. Results showed that EGCG is bound to thermally induced SPI primarily via hydrophobic and hydrogen bonding, thus altering the secondary structure composition and reducing surface hydrophobicity of proteins in thermally induced SPI. Furthermore, the optimum amount of EGCG required to improve the gel strength, water holding capacity and rheological properties was ≤0.04:1 (SPI 1 g L-1 ; EGCG:SPI, w/w). Thermal stability analysis further indicated that EGCG in SPIE was more stable than free EGCG after heating. CONCLUSION: This study demonstrated that EGCG can improve the gel properties of TG-crosslinked SPIE, while EGCG in SPIE exhibits enhanced thermal stability. Additionally, the results of this study provide a novel strategy for the development of SPI-based gel foods with improved gel properties and that are enriched with bioactive compounds. © 2020 Society of Chemical Industry.

Inhibition of hepatocellular carcinoma cell proliferation, migration, and invasion by a disintegrin and metalloproteinase-17 inhibitor TNF484.

BACKGROUND: The aim of this study was to test the effect of TNF484 on cell proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells. MATERIALS AND METHODS: Various doses (0, 1, 10, 50, and 100 nM) of TNF484 were applied to the HepG2 and Bel7402 cells, and cell proliferation was measured by using 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay after 72 h. Cell migration rate was measured using the xCELLigence system, and the cell invasion ability was examined by the three-dimensional spheroid BME cell invasion assay. The expression level of ADAM17 was also measured with RT-PCR. RESULTS: With the treatment of TNF484, the cell proliferation of HepG2 and Bel7402 cells was inhibited in a dose-dependent manner. Moreover, under TNF484 treatment, the cell migration rate as well as cell invasion ability of the HepG2 and Bel7402 cells were suppressed. CONCLUSION: TNF484 could inhibit the cell proliferation, migration, and invasion of some HCC cell lines, making it a potential therapeutic option for liver cancer treatment.

[Rapid untargeted screening and determination of unknown contaminants in aquatic products by high performance liquid chromatography-quadrupole/electrostatic field orbitrap high resolution mass spectrometry].

A method has been developed for rapid untargeted screening and determination of unknown contaminants in aquatic products by high performance liquid chromatography-quadrupole/electrostatic field orbitrap high resolution mass spectrometry. The samples were extracted by acetonitrile, dried under nitrogen, dissolved in methanol-water (3:7, v/v), and analyzed via the full MS scan/data dependent MS2 mode during the screening process. The Trace Finder software was used to match the precise mass, the isotope abundance ratio, the fragment ion to search for unknown contaminants in aquatic samples. The optimized QuEChERS method is used to purify the samples when quantifying. The quantitative analyses of triazole, caffeine, and ethoxyquinoline were performed via the target-MS2 mode. The correlation coefficients of the three compounds in fish and shrimp samples were higher than 0.99 in the linear range of 5-1000 µg/L. The limit of detection was 1 µg/kg, and the limit of quantitation was 5 µg/kg. The average recoveries were between 70.5% and 90.9% with the relative standard deviations ranging from 5.4% to 12.8%. The screening method has the advantages of fast, accurate, and high throughput; when combined with the quantitative method, it can be used to screen and determine unknown contaminants in the actual aquatic products.

[Determination of characteristic compound in manuka honey by automatic on-line solid phase extraction-liquid chromatography-high resolution mass spectrometry].

A method for the determination of characteristic compound 3,5-dimethoxybenzoate-4-diglucoside (leptosperin) in manuka honey was developed by automatic on-line solid phase extraction-liquid chromatography-high resolution mass spectrometry (SPE-LC-HRMS). The samples were separated on a Dikma Diamonsil Plus C18 column (150 mm×4.6 mm, 5 µm) using the mobile phases of 0.1% (v/v) formic acid aqueous solution and acetonitrile with gradient elution. The compound was detected with negative electrospray ionization (ESI-) in Target-MS2 mode. The results showed that the linear range was 0.5-100.0 mg/L, the correlation coefficient was 0.9993. The limit of detection (LOD, S/N ≥ 3) and limit of quantification (LOQ, S/N ≥ 10) of the method was 3 mg/kg and 10 mg/kg, respectively. The recoveries at the spiked levels of 50.0, 100.0, 200.0 mg/kg (10.0, 20.0, 50.0 mg/kg in black locust samples) were in the range of 82.0%-95.2% with the relative standard deviations ranging from 2.7% to 9.7% (n=6). The proposed method was applied to 95 mature honey samples from hives in New Zealand including 12 different kinds and 50 commercial honey samples from four different countries. The method is fast, sensitive and accurate to provide technical support to solve the judgment of the manuka honey imported from New Zealand.

MicroRNA-379 acts as a tumor suppressor in non-small cell lung cancer by targeting the IGF­1R-mediated AKT and ERK pathways.

Lung cancer is one of the most common types of malignancy in humans and is a leading cause of cancer-related deaths among men and women worldwide. Aberrantly expressed microRNAs in non-small cell lung cancer (NSCLC) contribute to tumor occurrence and development as either tumor suppressors or promoters. MicroRNA-379 (miR­379) is dysregulated in several types of human cancer. However, its expression pattern, role and underlying mechanism in NSCLC progression and metastasis are poorly understood. In this study, assay of reverse transcription-quantitative polymerase chain reaction showed that miR­379 was downregulated in both NSCLC tissue and cell lines. Low miR­379 expression in NSCLC tissues was significantly correlated with TNM stage and lymph node metastasis. In addition, functional experiments revealed that restoring the expression of miR­379 inhibited cell proliferation, migration and invasion of NSCLC. The insulin-like growth factor receptor-1 (IGF­1R) was identified as a direct target of miR­379 in NSCLC. IGF­1R was highly expressed in NSCLC tissues and inversely correlated with miR­379 expression. Downregulation of IGF­1R had tumor suppressive roles similar to that of miR­379 overexpression on NSCLC cell proliferation, migration and invasion. Moreover, the upregulation of IGF­1R effectively rescued the tumor suppressive roles induced by miR­379 overexpression in NSCLC. The resumption of the expression of miR­379 inhibited the activation of AKT and ERK signaling pathways in NSCLC. These findings suggested that miR­379 acts as a tumor suppressor in NSCLC by directly targeting IGF­1R and indirectly regulating AKT and ERK signaling pathways. miR­379 provides novel therapeutic targets for the treatment of patients with this disease.

PARP-1 promotes autophagy via the AMPK/mTOR pathway in CNE-2 human nasopharyngeal carcinoma cells following ionizing radiation, while inhibition of autophagy contributes to the radiation sensitization of CNE-2 cells.

It was previously reported that poly-(adenosine diphosphate-ribose) polymerase-1 (PARP-1) regulated ionizing radiation (IR)-induced autophagy in CNE-2 human nasopharyngeal carcinoma cells. The present study aimed to investigate whether PARP-1-mediated IR-induced autophagy occurred via activation of the liver kinase B1 (LKB1)/adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway in CNE-2 cells. In addition, the effect of PARP-1 and AMPK inhibition on the radiation sensitization of CNE-2 cells was investigated. CNE-2 cells were treated with 10 Gy IR in the presence or absence of the AMPK activator 5-amino-1-ß-D-ribofuranosyl-1H-imid-azole-4-carboxamide (AICAR). In addition, IR-treated CNE-2 cells were transfected with lentivirus-delivered small-hairpin RNA or treated with the AMPK inhibitor Compound C. Western blot analysis was used to assess the protein expression of PARP-1, phosphorylated (p)-AMPK, microtubule-associated protein 1 light chain 3 (LC3)-II and p-P70S6K. Cell viability and clone formation assays were performed to determine the effect of PARP-1 silencing and AMPK inhibition on the radiation sensitization of CNE-2 cells. The results showed that IR promoted PARP-1, p-AMPK and LC3-II protein expression as well as decreased p-P70S6K expression compared with that of the untreated cells. In addition, AICAR increased the expression of p-AMPK and LC3-II as well as decreased p-P70S6K expression compared with that of the IR-only group; however, AICAR did not increase PARP-1 expression. Furthermore, PARP-1 gene silencing decreased the expression of PARP-1, p-AMPK and LC3-II as well as increased p-P70S6K expression. Compound C decreased p-AMPK and LC3-Ⅱ expression as well as increased p-P70S6K expression; however, Compound C did not increase PARP-1 expression. Western blot analysis detected limited expression of p-LKB1 in all treatment groups. Cell viability and clone formation assays revealed that PARP-1 or AMPK inhibition reduced the proliferation of CNE-2 cells following IR. In conclusion, the present study demonstrated that PARP-1 promoted autophagy via the AMPK/mTOR pathway; in addition, PARP-1 or AMPK inhibition contributed to the radiation sensitization of CNE-2 cells following IR. However, it remains to be elucidated whether PARP-1 is an upstream mediator of the LKB1 pathway in CNE­2 cells following IR.

RNAi-mediated knockdown of the c-jun gene sensitizes radioresistant human nasopharyngeal carcinoma cell line CNE-2R to radiation.

This study aimed to investigate the effect of RNA interference (RNAi)-mediated downregulation of the expression of the c-jun gene (a proto-oncogene) on the radiosensitivity of a radioresistant human nasopharyngeal carcinoma cell line (CNE-2R) and to validate its potential as an anticancer target. A lentiviral vector with c-jun small hairpin RNA (shRNA) was constructed and transfected into CNE-2R cells. The gene silencing efficiency of these recombinants was confirmed by RT-PCR and western blotting. Radiosensitivity, cell proliferation, cell cycle profile and apoptosis were assessed using colony formation assay, CCK-8 assay and flow cytometry, respectively. The lentiviral shRNA efficiently knocked down the expression of c-jun at both the mRNA and protein levels (P<0.05). c-jun-downregulated CNE-2R cells exhibited significantly decreased cell proliferation and enhanced radiosensitivity compared to the control group (P<0.05), and the effects were likely due to G2/M phase arrest and enhanced cell apoptosis. These data provide evidence that c-jun may be involved in the radioresistance of nasopharyngeal carcinoma (NPC) and knockdown of the c-jun gene may be a potential strategy to enhance the radiation sensitivity of NPC.