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Abstract This study aimed to evaluate the regulatory effect and molecular mechanism of long noncoding RNA small nucleolus RNA host gene 8 (LncRNA SNHG8) in the migration and angiogenesis of primary human umbilical vein endothelial cells (pHUVECs) under high-glucose (HG) conditions. The HG-induced endothelial injury model was established in vitro.The cell model of silencing SNHG8, overexpressing SNHG8, and silencing TRPM7 was established by transfecting SNHG8-siRNA, SNHG8 plasmid and TRPM7-siRNA into cells with liposomes.The SNHG8 level was determined through reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of transient receptor potential melastatin 7 (TRPM7), endothelial nitric oxide synthase (eNOS), p-eNOS, extracellular signal-regulated kinase 1/2(ERK1/2), and p-ERK1/2 were assessed through western blot. Nitric oxide (NO) levels were measured with DAF-FM. pHUVEC migration was examined through wound healing and Transwell assay, and pHUVEC angiogenesis was observed through a tube formation assay. Results showed that HG promoted the expression of lncRNA SNHG8 and TRPM7 and decreased the ratio of p-eNOS/eNOS and p-ERK1/2/ERK1/2 in pHUVECs . NO production, migration , and angiogenesis were inhibited in pHUVECs under HG conditions. Silencing lncRNA SNHG8 and TRPM7 could significantly reverse the HG-induced decrease in eNOS activation, NO production , migration, and angiogenesis . SNHG8 and U0126 (ERK pathway inhibitor) overexpression enhanced the HG effects, whereas using U0126 did not affect the TRPM7 expression. In conclusion, lncRNA SNHG8 participates in HG-induced endothelial cell injury and likely regulates NO production, migration, and angiogenesis of pHUVECs via the TRPM7/ERK1/2 signaling axis.

Abstract Public metabolites such as vitamins play critical roles in maintaining the ecological functions of microbial community. However, the biochemical and physiological bases for fine-tuning of public metabolites in the microbiome remain poorly understood. Here, we examine the interactions between myxobacteria and Phytophthora sojae, an oomycete pathogen of soybean. We find that host plant and soil microbes complement P. sojae’s auxotrophy for thiamine. Whereas, myxobacteria inhibits Phytophthora growth by a thiaminase I CcThi1 secreted into extracellular environment via outer membrane vesicles (OMVs). CcThi1 scavenges the required thiamine and thus arrests the thiamine sharing behavior of P. sojae from the supplier, which interferes with amino acid metabolism and expression of pathogenic effectors, probably leading to impairment of P. sojae growth and pathogenicity. Moreover, myxobacteria and CcThi1 are highly effective in regulating the thiamine levels in soil, which is correlated with the incidence of soybean Phytophthora root rot. Our findings unravel a novel ecological tactic employed by myxobacteria to maintain the interspecific equilibrium in soil microbial community.

Abstract Background Pulmonary arterial hypertension (PAH) is a pathophysiological syndrome, characterized by pulmonary vascular remodeling. Immunity and inflammation are progressively recognized properties of PAH, which are crucial for the initiation and maintenance of pulmonary vascular remodeling. This study explored immune cell infiltration characteristics and potential biomarkers of PAH using comprehensive bioinformatics analysis. Methods Microarray data of GSE117261, GSE113439 and GSE53408 datasets were downloaded from Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified in GSE117261 dataset. The proportions of infiltrated immune cells were evaluated by CIBERSORT algorithm. Feature genes of PAH were selected by least absolute shrinkage and selection operator (LASSO) regression analysis and validated by fivefold cross-validation, random forest and logistic regression. The GSE113439 and GSE53408 datasets were used as validation sets and logistic regression and receiver operating characteristic (ROC) curve analysis were performed to evaluate the prediction value of PAH. The PAH-associated module was identified by weighted gene association network analysis (WGCNA). The intersection of genes in the modules screened and DEGs was used to construct protein–protein interaction (PPI) network and the core genes were selected. After the intersection of feature genes and core genes, the hub genes were identified. The correlation between hub genes and immune cell infiltration was analyzed by Pearson correlation analysis. The expression level of LTBP1 in the lungs of monocrotaline-induced PAH rats was determined by Western blotting. The localization of LTBP1 and CD4 in lungs of PAH was assayed by immunofluorescence. Results A total of 419 DEGs were identified, including 223 upregulated genes and 196 downregulated genes. Functional enrichment analysis revealed that a significant enrichment in inflammation, immune response, and transforming growth factor β (TGFβ) signaling pathway. CIBERSORT analysis showed that ten significantly different types of immune cells were identified between PAH and control. Resting memory CD4+ T cells, CD8+ T cells, γδ T cells, M1 macrophages, and resting mast cells in the lungs of PAH patients were significantly higher than control. Seventeen feature genes were identified by LASSO regression for PAH prediction. WGCNA identified 15 co-expression modules. PPI network was constructed and 100 core genes were obtained. Complement C3b/C4b receptor 1 (CR1), thioredoxin reductase 1 (TXNRD1), latent TGFβ binding protein 1 (LTBP1), and toll-like receptor 1 (TLR1) were identified as hub genes and LTBP1 has the highest diagnostic efficacy for PAH (AUC = 0.968). Pearson correlation analysis showed that LTBP1 was positively correlated with resting memory CD4+ T cells, but negatively correlated with monocytes and neutrophils. Western blotting showed that the protein level of LTBP1 was increased in the lungs of monocrotaline-induced PAH rats. Immunofluorescence of lung tissues from rats with PAH showed increased expression of LTBP1 in pulmonary arteries as compared to control and LTBP1 was partly colocalized with CD4+ cells in the lungs. Conclusion LTBP1 was correlated with immune cell infiltration and identified as the critical diagnostic maker for PAH.

Abstract MnSe and Co0.85Se embedded in nitrogen‐doped carbon nanofibers (MnSe/Co0.85Se/N‐CNFs) were synthesized by electrospinning and high‐temperature calcination, and evaluated for the first time as sodium/potassium‐ion battery anode material via constant current charge/discharge, cyclic voltammetry, electrochemical impedance spectroscopy.Ex‐situ XRD revealed the potassium storage mechanism of MnSe/Co0.85Se/N‐CNFs, indicating that its capacity was mainly provided by the conversion reaction. Compared with MnSe/N‐CNFs and Co0.85Se/N‐CNFs, the reversible capacity and cycling performance of MnSe/Co0.85Se/N‐CNFs were significantly improved due to the synergistic effect of bimetals. The MnSe/Co0.85Se/N‐CNFs electrode showed a charging capacity of 262.3 mAh g−1 after 700 cycles at 1 A g−1 in Na‐ion batteries and a discharge capacity of 183.4 mAh g−1 after 400 cycles at 0.1 A g−1 in K‐ion batteries, The results showed that binder‐free binary metal MnSe/Co0.85Se/N‐CNFs have a certain development prospect as anode for sodium/potassium‐ion batteries.

Background: The aim of this study was to explore the correlation between high-risk human papillomavirus (HR-HPV) infection and changes in vaginal microecology, as well as the severity of cervical intraepithelial lesions (CIN). Methods: A retrospective analysis was conducted on 221 inpatients (aged 23–80 years) who underwent simultaneous testing of vaginal secretions for microecological parameters, HR-HPV genotyping, and cervical tissue biopsy at the Department of Gynecology, Second Affiliated Hospital of Xinjiang Medical University, Urumqi, from October 2021 to January 2023. The study subjects were analyzed to determine the association between HR-HPV infection and alterations in vaginal microecology, as well as CIN. Results: Among the 221 cases, 69 were positive for HR-HPV, resulting in a positivity rate of 31.22% (69/221). Out of the 139 cases with normal vaginal microecology, 26 were positive for HR-HPV, yielding a positivity rate of 18.71% (26/139). Among the 82 cases with abnormal vaginal microecology, 43 were positive for HR-HPV, resulting in a positivity rate of 52.44% (43/82). Out of the 162 cases with normal cervix, 26 were positive for HR-HPV, resulting in a positivity rate of 16.00% (26/162). Among the 59 cases with abnormal cervix, 43 were positive for HR-HPV, resulting in a positivity rate of 72.88% (43/59). In the cases of abnormal cervix, 10 presented cervical inflammation, with a HR-HPV positivity rate of 70.00% (7/10); 20 cases had cervical intraepithelial lesions (CIN) I, with a HR-HPV positivity rate of 70.00% (14/20); 20 cases had CIN II, with a HR-HPV positivity rate of 75.00% (15/20); and 9 cases had CIN III, with a HR-HPV positivity rate of 77.80% (7/9). Moreover, among the 162 cases with normal cervix, 36 had abnormal vaginal microecology, resulting in an abnormality rate of 22.22% (36/162). Among the 59 cases with abnormal cervix, 46 had abnormal vaginal microecology, resulting in an abnormality rate of 77.97% (46/59). In the cases of abnormal cervix, 10 had cervical inflammation, with an abnormal vaginal microecology rate of 70.00% (7/10); 20 cases had CIN I, with an abnormal vaginal microecology rate of 70.00% (14/20); 20 cases had CIN II, with an abnormal vaginal microecology rate of 80.00% (16/20); and 9 cases had CIN III, with an abnormal vaginal microecology rate of 100.00% (9/9). The differences in HR-HPV positivity rates between the group with normal vaginal microecology and the group with abnormal vaginal microecology were statistically significant (p < 0.05). Similarly, the differences in HR-HPV positivity rates for different degrees of CIN were statistically significant (p < 0.05), as well as the differences in abnormal vaginal microecology rates for different degrees of CIN (p < 0.05). Conclusions: HR-HPV infection was found to be significantly associated with alterations in vaginal microecology and CIN.

Background: This study aimed to assess the efficacy and safety of laparoscopic and transvaginal cervical cerclage treatments in patients with cervical insufficiency before and during pregnancy. Methods: A total of 70 patients diagnosed with cervical insufficiency and undergoing cervical cerclage at the Second Affiliated Hospital of Xinjiang Medical University between January 2020 and December 2022 were included. The patients were divided into three groups based on different surgical methods: transvaginal loop during pregnancy (Group 1, n = 30), transabdominal loop before pregnancy (Group 2, n = 20), and transabdominal loop during pregnancy (Group 3, n = 20). The groups were compared in terms of general clinical data, operation time, intraoperative bleeding, hospital stay, delivery gestational weeks, preterm delivery rate, prolonged gestational weeks, and neonatal births. Results: (1) There were no statistically significant differences in age, pregnancy, delivery, number of miscarriages, cervical length, and history of midterm pregnancy loss among the three groups (p > 0.05). (2) Prolonged gestational week, delivery gestational week, term delivery, and neonatal birth weight were higher in Groups 2 and 3 compared to Group 1, with statistically significant differences (p < 0.05). There was no statistically significant difference (p > 0.05) when comparing Group 2 and Group 3. Premature rupture of membranes and preterm delivery were higher in Group 1 compared to Groups 2 and 3, with statistically significant differences (p < 0.05). There was no statistically significant difference when comparing Group 2 and Group 3 (p > 0.05). (3) The amount of surgical bleeding and surgical time showed statistically significant differences (p < 0.05) among the three groups. Group 1 had more surgical bleeding than Groups 2 and 3, with statistically significant differences (p < 0.05). When comparing Group 2 and Group 3, Group 3 had more surgical bleeding than Group 2, with a statistically significant difference (p < 0.05). Group 2 had a shorter surgical time than Group 1 and Group 3, with statistically significant differences (p < 0.05). When comparing Group 1 and Group 3, Group 3 had a longer surgical time than Group 1, with a statistically significant difference (p < 0.05). There was no statistically significant difference in hospital stay when comparing three groups (p > 0.05). Conclusions: Laparoscopic cervical cerclage is a safe and effective treatment option, yielding better pregnancy outcomes than transvaginal cervical cerclage, particularly for patients with previous failed transvaginal cerclage. Preconception laparoscopic cervical cerclage carries lower surgical risks and should be considered for clinical application.

Abstract Diabetes is a potential risk factor for gastric cancer (GC). Pin1, a peptidyl–prolyl cis/trans isomerase, promotes GC cell proliferation and migration. The role and underlying mechanism of the Pin1/BRD4 axis in hyperglycemia-induced proliferation and migration of GC cells were analyzed in vivo and in vitro. Proliferation and migration of GC cells were measured; Pin1 and BRD4 expression of the cell cycle were determined. Pin1 and BRD4 were downregulated by transfecting Pin1 shRNA lentivirus into GC cells and JQ1-intervention GC cells. Tumor formation and lung metastasis were assessed in vivo. Inhibition of Pin1 and BRD4 significantly suppressed high-glucose (HG)-induced GC cell proliferation and migration. HG enhanced G1/S cell-cycle transition, associated with increased Pin1 and BRD4 expression. Silencing Pin1 significantly downregulated the expression of BRD4 and NAP1L1 and upregulated that of P21 in GC cells. In vivo studies indicated that hyperglycemia promotes tumor growth and lung metastasis by inducing Pin1 and BRD4 expression. Thus, Pin1/BRD4 plays an important role in hyperglycemia-promoted tumor growth. The significance of these findings toward improved prognosis of diabetic patients with GC cannot be underestimated.

Background: Corneal fluorescein sodium staining is a valuable diagnostic method for various ocular surface diseases. However, the examination results are highly dependent on the subjective experience of ophthalmologists. Objectives: To develop an artificial intelligence system based on deep learning to provide an accurate quantitative assessment of sodium fluorescein staining score and the size of cornea epithelial patchy defect. Design: A prospective study. Methods: We proposed an artificial intelligence system for automatically evaluating corneal staining scores and accurately measuring patchy corneal epithelial defects based on corneal fluorescein sodium staining images. The design incorporates two segmentation models and a classification model to forecast and assess the stained images. Meanwhile, we compare the evaluation findings from the system with ophthalmologists with varying expertise. Results: For the segmentation task of cornea boundary and cornea epithelial patchy defect area, our proposed method can achieve the performance of dice similarity coefficient (DSC) is 0.98/0.97 and Hausdorff distance (HD) is 3.60/8.39, respectively, when compared with the manually labeled gold standard. This method significantly outperforms the four leading algorithms (Unet, Unet++, Swin-Unet, and TransUnet). For the classification task, our algorithm achieves the best performance in accuracy, recall, and F1-score, which are 91.2%, 78.6%, and 79.2%, respectively. The performance of our developed system exceeds seven different approaches (Inception, ShuffleNet, Xception, EfficientNet_B7, DenseNet, ResNet, and VIT) in classification tasks. In addition, three ophthalmologists were selected to rate corneal staining images. The results showed that the performance of our artificial intelligence system significantly outperformed the junior doctors. Conclusion: The system offers a promising automated assessment method for corneal fluorescein staining, decreasing incorrect evaluations caused by ophthalmologists’ subjective variance and limited knowledge.

Abstract The development of social networking services (SNSs) revealed a surge in image sharing. The sharing mode of multi-page photo collage (MPC), which posts several image collages at a time, can often be observed on many social network platforms, which enables uploading images and arrangement in a logical order. This study focuses on the construction of MPC for an image collection and its formulation as an issue of joint optimization, which involves not only the arrangement in a single collage but also the arrangement among different collages. Novel balance-aware measurements, which merge graphic features and psychological achievements, are introduced. Non-dominated sorting genetic algorithm is adopted to optimize the MPC guided by the measurements. Experiments demonstrate that the proposed method can lead to diverse, visually pleasant, and logically clear MPC results, which are comparable to manually designed MPC results.

Abstract Transformers, the dominant architecture for natural language processing, have also recently attracted much attention from computational visual media researchers due to their capacity for long-range representation and high performance. Transformers are sequence-to-sequence models, which use a self-attention mechanism rather than the RNN sequential structure. Thus, such models can be trained in parallel and can represent global information. This study comprehensively surveys recent visual transformer works. We categorize them according to task scenario: backbone design, high-level vision, low-level vision and generation, and multimodal learning. Their key ideas are also analyzed. Differing from previous surveys, we mainly focus on visual transformer methods in low-level vision and generation. The latest works on backbone design are also reviewed in detail. For ease of understanding, we precisely describe the main contributions of the latest works in the form of tables. As well as giving quantitative comparisons, we also present image results for low-level vision and generation tasks. Computational costs and source code links for various important works are also given in this survey to assist further development.

Complement C3 plays a prominent role in inflammatory processes, and its increase exacerbates ischemia reperfusion injury (IRI)-induced acute kidney injury (AKI). Infiltrated neutrophils can be stimulated to form neutrophil extracellular traps (NETs), leading to renal injury. However, the relationship between the increase of C3 and the release of NETs in AKI was not clear. Here we found that IRI in the mouse kidney leads to increased neutrophils infiltration and NET formation. Furthermore, neutrophils depletion by anti-Ly6G IgG (1A8) did not reduce C3 activation but reduced kidney injury and inflammation, indicating a link between neutrophils infiltration and renal tissue damage. Pretreatment with 1A8 suppressed ischemia-induced NET formation, proving that extracellular traps (ETs) in renal tissue were mainly derived from neutrophils. Renal ischemia injury also leads to increased expression of C3. Moreover, C3 KO mice (C3 KO) with IRI exhibited attenuated kidney damage and decreased neutrophils and NETs. In vitro, C3a primed neutrophils to form NETs, reflected by amorphous extracellular DNA structures that colocalized with CitH3 and MPO. These data reveal that C3 deficiency can ameliorate AKI by reducing the infiltration of neutrophils and the formation of NETs. Targeting C3 activation may be a new therapeutic strategy for alleviating the necroinflammation of NETs in AKI.

Background. Myocardial ischemia/reperfusion (MI/R) injury is a common pathology in ischemia heart disease. Long noncoding RNAs (lncRNAs) are significant regulators related to many ischemia/reperfusion conditions. This study is aimed at exploring the molecule mechanism of lncRNA-mediated competing endogenous RNA (ceRNA) network in MI/R. Methods. The dataset profiles of MI/R and normal tissues (GSE130217 and GSE124176) were obtained from the GEO database. Integrated bioinformatics were performed to screen out differentially expressed genes (DEGs). Thereafter, an lncRNA-mediated ceRNA network was constructed by the starBase database. The GO annotations and KEGG pathway analysis were conducted to study action mechanism and related pathways of DEGs in MI/R. A model of hypoxia/reoxygenation- (H/R-) treated HL-1 cell was performed to verify the expression of lncRNAs through qRT-PCR. Results. 2406 differentially expressed- (DE-) mRNAs, 70 DE-lncRNAs, and 156 DE-miRNAs were acquired. These DEGs were conducted to construct an lncRNA-mediated ceRNA network, and a subnetwork including lncRNA Xist/miRNA-133c/mRNA (Slc30a9) was screen out. The functional enrichment analyses revealed that the lncRNAs involved in the ceRNA network might functions in oxidative stress and calcium signaling pathway. The lncRNA Xist expression is reduced under H/R conditions, followed by the increased level of miRNA-133c, thus downregulating the expression of Slc30a9. Conclusion. In sum, the identified ceRNA network which included the lncRNA Xist/miR-133c/Slc30a9 axis might contribute a better understanding to the pathogenesis and development of MI/R injury and offer a novel targeted therapy way.

Metal responsive transcription factor 1 (MTF-1) is a zinc-dependent transcription factor involved in the development of pulmonary arterial hypertension (PAH), which is a life-threatening disease characterized by elevated pulmonary artery pressure and pulmonary vascular remodeling. However, little is known about the role and regulatory signaling of MTF-1 in PAH. This study aimed to investigate the effect and mechanism of MTF-1 on the proliferation of pulmonary arterial smooth muscle cells (PASMCs). Several techniques including intracellular-free zinc detected by fluorescent indicator-fluozinc-3-AM, western blot, luciferase reporter, and cell proliferation assay were conducted to perform a comprehensive analysis of MTF-1 in proliferation of PASMCs in PAH. Increased cytosolic zinc was shown in monocrotaline (MCT)-PASMCs and ZnSO4-treated PASMCs, which led to overexpression and overactivation of MTF-1, followed by the up-regulation of placental growth factor (PlGF). Elevated MTF-1 and PlGF were observed in western blot, and high transcriptional activity of MTF-1 was confirmed by luciferase reporter in ZnSO4-treated cells. Further investigation of cell proliferation revealed a favorable impact of zinc ions on PASMCs proliferation, with the deletion of Mtf-1/Plgf attenuating ZnSO4-induced proliferation. Flow cytometry analysis showed that blockade of PKC signaling inhibited the cell cycle of MCT-PASMCs and ZnSO4-treated PASMCs. The Zinc/PKC/MTF-1/PlGF pathway is involved in the up-regulatory effect on the PASMCs proliferation in the process of PAH. This study provided novel insight into zinc homeostasis in the pathogenesis of PAHs, and the regulation of MTF-1 might be a potential target for therapeutic intervention in PAH. [ABSTRACT FROM AUTHOR]

The β-1,6-glucan is the key linker between mannoproteins in the outermost part of the cell wall and β-1,3-glucan/chitin polysaccharide to maintain the rigid structure of the cell wall. The β-1,6-glucanase GluM, which was purified from the fermentation supernatant of Corallococcus sp. EGB, was able to inhibit the germination of Fusarium oxysporum f. sp. cucumerinum conidia at a minimum concentration of 2.0 U/mL (0.08 μg/mL). The survival rates of GluM-treated conidia and monohyphae were 10.4% and 30.7%, respectively, which were significantly lower than that of β-1,3-glucanase treatment (Zymolyase, 20.0 U/mL; equate to 1.0 mg/mL) (72.9% and 73.9%). In contrast to β-1,3-glucanase treatment, the high-osmolarity glycerol (HOG) pathway of F. oxysporum f. sp. cucumerinum cells was activated after GluM treatment, and the intracellular glycerol content was increased by 2.6-fold. Moreover, the accumulation of reactive oxygen species (ROS) in F. oxysporum f. sp. cucumerinum cells after GluM treatment induced apoptosis, but it was not associated with the increased intracellular glycerol content. Together, the results indicate that β-1,6-glucan is a promising target for the development of novel broad-spectrum antifungal agents. [ABSTRACT FROM AUTHOR]

Generalizing the electroencephalogram (EEG) decoding methods to unseen subjects is an important research direction for realizing practical application of brain-computer interfaces (BCIs). Since distribution shifts across subjects, the performance of most current deep neural networks for decoding EEG signals degrades when dealing with unseen subjects. Domain generalization (DG) aims to tackle this issue by learning invariant representations across subjects. To this end, we propose a novel domain-generalized EEG classification framework, named FDCL, to generalize EEG decoding through category-relevant and -irrelevant Feature Decorrelation and Cross-view invariant feature Learning. Specifically, we first devise data augmented regularization through mixing the segments of same-category features from multiple subjects, which increases the diversity of EEG data by spanning the space of subjects. Furthermore, we introduce feature decorrelation regularization to learn the weights of the augmented EEG trials to remove the dependencies between their features, so that the true mapping relationship between relevant features and corresponding labels can be better established. To further distill subject-invariant EEG feature representations, cross-view consistency learning regularization is introduced to encourage consistent predictions of category-relevant features induced from different augmented EEG views. We seamlessly integrate three complementary regularizations into a unified DG framework to jointly improve the generalizability and robustness of the model on unseen subjects. Experimental results on motor imagery (MI) based EEG datasets validate that the proposed FDCL outperforms the available state-of-the-art methods.