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Background Growing evidences indicate that circular RNAs (circRNAs) play an important role in the regulation of biological behavior of tumor. We aim to explore the role of circRNA in glioma and elucidate how circRNA acts. Methods Real-time PCR was used to examine the expression of circPTN in glioma tissues and normal brain tissues (NBT). Assays of dual- luciferase reporter system, biotin label RNA pull-down and FISH were used to determine that circPTN could sponge miR-145-5p and miR-330-5p. Tumor sphere formation assay was performed to determine self- renewal of glioma stem cell (GSCs). Cell counting Kit-8 (CCK8), EdU assay and flow cytometry were used to investigate proliferation and cell cycle. Intracranial xenograft was established to determine how circPTN impacts in vivo. Tumor sphere formation assay was performed to determine self- renewal of glioma stem cell (GSCs). Results We demonstrated circPTN was significantly higher expression in glioma tissues and glioma cell lines, compared with NBT and HEB (human astrocyte). In gain- and loss-of-function experiments, circPTN significantly promoted glioma growth in vitro and in vivo. Furthermore, we performed dual-luciferase reporter assays and RNA pull-down assays to verify that circPTN acts through sponging miR-145-5p and miR-330-5p. Increasing expression of circPTN rescued the inhibition of proliferation and downregulation of SOX9/ITGA5 in glioma cells by miR-145-5p/miR-330-5p. In addition, we found that circPTN promoted self-renewal and increased the expression of stemness markers (Nestin, CD133, SOX9, and SOX2) via sponging miR-145-5p. Moreover, this regulation was disappeared when circPTN binding sites in miR-145-5p were mutated. Conclusions Our results suggest that circPTN is an oncogenic factor that acts by sponging miR-145-5p/miR-330-5p in glioma.

Background Preserving the integrity of the blood-brain barrier (BBB) is beneficial to avoid further brain damage after acute ischemic stroke (AIS). Astrocytes, an important component of the BBB, promote BBB breakdown in subjects with AIS by secreting inflammatory factors. The glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 (Ex-4) protects the BBB and reduces brain inflammation from cerebral ischemia, and GLP-1R is expressed on astrocytes. However, the effect of Ex-4 on astrocytes in subjects with AIS remains unclear. Methods In the present study, we investigated the effect of Ex-4 on astrocytes cultured under oxygen-glucose deprivation (OGD) plus reoxygenation conditions and determined whether the effect influences bEnd.3 cells. We used various methods, including permeability assays, western blotting, immunofluorescence staining, and gelatin zymography, in vitro and in vivo. Results Ex-4 reduced OGD-induced astrocyte-derived vascular endothelial growth factor (VEGF-A), matrix metalloproteinase-9 (MMP-9), chemokine monocyte chemoattractant protein-1 (MCP-1), and chemokine C-X-C motif ligand 1 (CXCL-1). The reduction in astrocyte-derived VEGF-A and MMP-9 was related to the increased expression of tight junction proteins (TJPs) in bEnd.3 cells. Ex-4 improved neurologic deficit scores, reduced the infarct area, and ameliorated BBB breakdown as well as decreased astrocyte-derived VEGF-A, MMP-9, CXCL-1, and MCP-1 levels in ischemic brain tissues from rats subjected to middle cerebral artery occlusion. Ex-4 reduced the activation of the JAK2/STAT3 signaling pathway in astrocytes following OGD. Conclusion Based on these findings, ischemia-induced inflammation and BBB breakdown can be improved by Ex-4 through an astrocyte-dependent manner.

Under unfavorable environmental conditions, eukaryotic cells may form stress granules (SGs) in the cytosol to protect against injury and promote cell survival. The initiation, mRNA and protein composition, distribution and degradation of SGs are subject to multiple intracellular post-translational modifications and signaling pathways to cope with stress damage. Despite accumulated comprehensive knowledge of their composition and dynamics, the function of SGs remains poorly understood. When the stress persists, aberrant and/or persistent intracellular SGs and aggregation of SGs-related proteins may lead to various diseases. In the present article, the research progress regarding the generation, modification and function of SGs was reviewed. The regulatory effects and influencing factors of SGs in the development of tumors, cardiovascular diseases, viral infections and neurodegenerative diseases were also summarized, which may provide novel insight for preventing and treating SG-related diseases.

Glioblastoma stem cells (GSCs) play a key role in glioblastoma (GBM) resistance to temozolomide (TMZ) chemotherapy. With the increase in research on the tumour microenvironment, exosomes secreted by GSCs have become a new focus in GBM research. However, the molecular mechanism by which GSCs affect drug resistance in GBM cells via exosomes remains unclear. Using bioinformatics analysis, we identified the specific expression of ABCB4 in GSCs. Subsequently, we established GSC cell lines and used ultracentrifugation to extract secreted exosomes. We conducted in vitro and in vivo investigations to validate the promoting effect of ABCB4 and ABCB4-containing exosomes on TMZ resistance. Finally, to identify the transcription factors regulating the transcription of ABCB4, we performed luciferase assays and chromatin immunoprecipitation-quantitative PCR. Our results indicated that ABCB4 is highly expressed in GSCs. Moreover, high expression of ABCB4 promoted the resistance of GSCs to TMZ. Our study found that GSCs can also transmit their highly expressed ABCB4 to differentiated glioma cells (DGCs) through exosomes, leading to high expression of ABCB4 in these cells and promoting their resistance to TMZ. Mechanistic studies have shown that the overexpression of ABCB4 in GSCs is mediated by the transcription factor ATF3. In conclusion, our results indicate that GSCs can confer resistance to TMZ in GBM by transmitting ABCB4, which is transcribed by ATF3, through exosomes. This mechanism may lead to drug resistance and recurrence of GBM. These findings contribute to a deeper understanding of the mechanisms underlying drug resistance in GBM and provide novel insights into its treatment.

Astaxanthin is an important antioxidant with many biological activities such as anti-tumor, anti-obesity, cardioprotective, and immuno-modulatory activities. Most of these biological activities are derived from (3S,3′S)-astaxanthin, while the activities of (3R,3′R)-astaxanthin are rarely reported. The purpose of this study was to investigate the effect of (3R,3′R)-astaxanthin on lipid metabolism and gut microbiota in mice fed with a high-fat diet. In this work, 40 male C57BL/6 mice were divided into 8 groups fed a high-fat diet supplemented or not with (3R,3′R)-astaxanthin or Xanthophyllomyces dendrorhous for 8 weeks. The weight gain, energy intake, fat index, plasma triacylglycerol and cholesterol, liver triacylglycerol and cholesterol, and gut microbiota were determined. The results showed that the addition of (3R,3′R)-astaxanthin/X. dendrorhous to the high-fat diet as a supplement prevented weight gain, reduced plasma and liver triacylglycerol, and decreased plasma and liver total cholesterol. The addition of (3R,3′R)-astaxanthin/X. dendrorhous also regulated the gut microbiota of the mice, which optimized the ratio of Bacteroides to Firmicutes and increased the content of Verrucomicrobia, especially Akkermansia. The changes in the gut microflora achieved a healthier structure, thus reducing the incidence of obesity. Thus (3R,3′R)-Astaxanthin has the function of regulating lipid metabolism and gut microbiota to prevent obesity caused by a high-fat diet. The production strain of (3R,3′R)-astaxanthin, X. dendrorhous, has the same function as astaxanthin in preventing obesity caused by a high-fat diet, which reflects its potential ability as a probiotic drug.

Glioma is a devastating cancer with a dismal prognosis and there is an urgent need to discover novel glioma-specific antigens for glioma therapy. Previous studies have identified CD163-positive tumour cells in certain solid tumours, but CD163 expression in glioma remains unknown. In this study, via an analysis of public datasets, we demonstrated that CD163 overexpression in glioma specimens correlated with an unfavourable patient prognosis. CD163 expression was increased in glioma cells, especially primary glioma cells. The loss of CD163 expression inhibited both cell cycle progression and the proliferation of glioblastoma multiforme (GBM) cell lines and primary glioma cells. CD163 interacted directly with casein kinase 2 (CK2) and CD163 silencing reduced AKT/GSK3β/β-catenin/cyclin D1 pathway activity via CK2. Moreover, CD163 was upregulated in CD133-positive glioma stem cells (GSCs), and CD163 downregulation decreased the expression of GSC markers, including CD133, ALDH1A1, NANOG and OCT4. The knockdown of CD163 impaired GSC stemness by inhibiting the CK2/AKT/GSK3β/β-catenin pathway. Finally, a CD163 antibody successfully induced complement-dependent cytotoxicity against glioma cells. Our findings indicate that CD163 contributes to gliomagenesis via CK2 and provides preclinical evidence that CD163 and the CD163 pathway might serve as a therapeutic target for glioma.

Chlorella pyrenoidosa is an excellent source of protein, and in this research, we assessed the antioxidant and emulsifying effects of Chlorella protein hydrolysate (CPH) using neutral proteases and alkaline proteases, as well as the properties of CPH-derived krill oil-in-water (O/W) emulsions. The CPHs exhibited the ability to scavenge several kinds of free radicals, including 1,1-diphenyl-2-picrylhydrazyl (DPPH), O2−, hydroxyl, and ABTS. Additionally, the CPHs (5 mg/mL) scavenged approximately 100% of the DPPH and ABTS. The CPHs showed similar emulsifying activities to Tween 20 and excellent foaming activities (max FS 74%), which helped to stabilize the krill oil-in-water emulsion. Less than 10 mg/mL CPHs was able to form fresh krill oil-in-water emulsions; moreover, the CPHs (5 mg/mL) in a krill O/W emulsion were homogenous, opaque, and stable for at least 30 days. Based on their inhibitory effects on the peroxide value (POV) and thiobarbituric acid reactive substances (TRABS), the CPHs were found to be able to inhibit lipid oxidation in both emulsifying systems and krill O/W emulsions. Thus, the CPHs could improve superoxide dismutase (SOD) activities by 5- or 10-fold and decrease the high reactive oxygen species (ROS) level caused by the addition of H2O2 in vitro. In conclusion, health-promoting CPHs could be applied in krill oil-in-water emulsions as both emulsifiers and antioxidants, which could help to improve the oxidative and physical stability of emulsions.

The purpose of this study was to reveal the changes in total phenolic content and antioxidant capacity of broccoli, and an untargeted metabolomics approach was developed to investigate the effect of lactic acid bacteria fermentation on the metabolome of broccoli florets. The results showed that the total phenolic content and antioxidant capacity significantly increased after fermentation. The untargeted metabolite profile showed that the main chemical components of fermented and unfermented broccoli are lipids and lipid-like molecules, organic acids and derivatives and organoheterocyclic compounds. Univariate and multivariate statistical analyses of the identified metabolites showed some metabolites such as sorbitol are upregulated after fermentation, and that other metabolites such as l-malic acid are downregulated after fermentation. Moreover, metabolite pathway analyses were used to study the identification of subtle but significant changes among groups of related metabolites that cannot be observed with conventional approaches. KEGG pathway analysis showed that metabolites are mainly enriched in the glucagon signaling pathway, pyruvate metabolism, glycolysis/gluconeogenesis and fructose and mannose metabolism after fermentation, compared with raw broccoli. The results of this study can help to further our understanding of the impact of LAB fermentation on bioactivity changes in and the metabolites profile of fermented broccoli, and the application of fermented broccoli in health foods and special dietary foods.

Deep network fault diagnosis requires a lot of labeled data and assumes identical data distributions for training and testing. In industry, varying equipment conditions lead to different data distributions, making it challenging to maintain consistent fault diagnosis performance across conditions. To this end, this paper designs a transfer learning model named the multi-adversarial joint distribution adaptation network (MAJDAN) to achieve effective fault diagnosis across operating conditions. MAJDAN uses a one-dimensional lightweight convolutional neural network (1DLCNN) to directly extract features from the original bearing vibration signal. Combining the distance-based domain-adaptive method, maximum mean difference (MMD), with the multi-adversarial network will simultaneously reduce the conditional and marginal distribution differences between the domains. As a result, MAJDAN can efficiently acquire domain-invariant feature information, addressing the challenge of cross-domain bearing fault diagnosis. The effectiveness of the model was verified based on two sets of different bearing vibration signals, and one-to-one and one-to-many working condition migration task experiments were carried out. Simultaneously, various levels of noise were introduced to the signal to enable analysis and comparison. The findings demonstrate that the suggested approach achieves exceptional diagnostic accuracy and exhibits robustness.

In some countries, yeasts are still not allowed in the production of commercially fermented sausages. Therefore, further research is needed on producing fermented meat products using different strains of yeasts. In this study, two strains of Debaryomyces hansenii (D. hansenii Y61 and Y67) were inoculated in fermented sausages to study their effects as starter cultures. The inoculation of D. hansenii strains affected ripening by decreasing the pH and aw. The sausages inoculated with Y61 and Y67 exhibited decreases in lipid oxidation of 40.70% and 36.04%, respectively, and Enterobacteriaceae counts of 50% and 100%, respectively. The inoculating yeasts Y61 and Y67 increased the lightness (L*) and redness (a*) of fermented sausages. The D. hansenii-inoculated sausages had higher levels of free amino acids and fatty acids, which improved the digestibility, sensory value, and safety of these sausages. Moreover, the total amount of ester compounds increased by 87.14% and 83.31% in the Y61- and Y67-inoculated groups, respectively, which contributed to the aroma. Better sensory attributes were also found in the sausages inoculated with Y61 and Y67 D. hansenii. Native D. hansenii Y61 and Y67 are, therefore, good starter cultures for fermented sausage production. Together, the results provide data supporting future research and the use of yeast-fermented sausages.