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The tear strength of textiles is a crucial characteristic of product quality. However, during the laboratory testing of this indicator, factors such as equipment operation, human intervention, and test environment can significantly influence the results. Currently, there is a lack of traceable records for the influencing factors during the testing process, and effective classification of testing activities is not achieved. Therefore, this study proposes a state-awareness and classification approach for fabric tear performance testing based on multi-source data. A systematic design is employed for fabric tear performance testing activities, which can real-time monitor electrical parameters, operational environment, and operator behavior. The data are collected, preprocessed, and a Decision Tree Support Vector Machine (DTSVM) is utilized for classifying various working states, and introducing ten-fold cross-validation to enhance the performance of the classifier, forming a comprehensive awareness of the testing activities. Experimental results demonstrate that the system effectively perceives fabric tear performance testing processes, exhibiting high accuracy in the classification of different fabric testing states, surpassing 98.73%. The widespread application of this system contributes to continuous improvement in the workflow and traceability of fabric tear performance testing processes.

Previous studies have shown that both age and hemoglobin are closely associated with the prognosis of septic shock. A recent study found that hemoglobin may change with age. Hemoglobin-to-Age Ratio (HAR) takes both age and hemoglobin into consideration as essential factors. So far, the effect of HAR on the prognosis of septic shock is still unclear. This research aimed to investigate the association between the HAR and the prognosis of patients with septic shock. Cox proportional hazards regression analysis, restricted cubic spline, Kaplan-Meier survivor analysis and stratified interaction analysis were used to elucidate the relationship between the HAR and prognosis of patients with septic shock. There is a nonlinear association between the HAR and mortality within 28 days after intensive care unit admission. When the HAR was lower than 0.13, mortality within 28 days after ICU admission decreased significantly as the HAR increased. When the HAR was higher than 0.13, the HAR was not a protective factor for mortality within 28 days after ICU admission. In patients with septic shock, the HAR was more effective in reducing the risk of death in patients with atrial fibrillation than in patients without atrial fibrillation. There is a nonlinear association between the HAR and mortality within 28 days after intensive care unit admission. When the HAR was at a low level, mortality within 28 days after ICU admission decreased significantly as the HAR increased. When the HAR was at high levels, the HAR might not be a protective factor for mortality within 28 days after ICU admission. In patients with septic shock, the HAR was more effective in reducing the risk of death in patients with atrial fibrillation than in patients without atrial fibrillation.

Background Hypoxia can impair cell and organ function, and cause apoptosis and various diseases. At present, there are many studies on pulmonary hypoxia but few studies on bronchial injury. The study aimed to research the impact of hypoxia on the barrier function of human bronchial epithelial cells and the expression level of tight junction proteins. Methods Primary human bronchial epithelial cells were allocated into four groups: (1) control group, (2) intermittent hypoxia group, (3) sustained hypoxia group, and (4) cigarette smoke exposure group. Apoptosis in each group was assessed by flow cytometric analysis. The expression levels of ZO-1, occludin, and claudin-1 were evaluated via Western blotting. Furthermore, trans-epithelial electrical resistance (TEER) was measured using an epithelial voltohmmeter to assess barrier function. Results (1) Compared with the control group, the intermittent hypoxia group exhibited no significant differences in apoptosis rate, TEER, or the expression of tight junction proteins ZO-1, occludin, and claudin-1 (P > 0.05). In contrast, both the sustained hypoxia and cigarette smoke groups demonstrated significantly elevated apoptosis rates (P < 0.05). Claudin-1 expression was significantly reduced in the sustained hypoxia group (P < 0.05), while the increase in ZO-1 expression was not statistically significant (P > 0.05). In the cigarette smoke group, expression levels of ZO-1, occludin, and claudin-1 were all markedly decreased (P < 0.05). (2) Compared with the control group, TEER values were significantly reduced in both the sustained hypoxia and cigarette smoke groups (P < 0.05). (3) A significant difference in ZO-1 expression was observed between the sustained hypoxia and cigarette smoke groups (P < 0.05). Conclusions Hypoxia modulates the expression of tight junction proteins in human bronchial epithelial cells, disrupts intercellular junctional integrity, increases epithelial permeability, and ultimately impairs barrier function.

Background Isatis tinctoria Linnaeus and Isatis indigotica Fortune are very inconsistent in their morphological characteristics, but the Flora of China treats them as the same species. In this work, a new technology that differs from conventional barcodes is developed to prove that they are different species and to clarify their classification. Results and methods I. indigotica was indistinguishable from I. tinctoria when using ITS2. CPGAVAS2 was used to construct the chloroplast genomes. MAFFT and DnaSP were used to calculate nucleotide polymorphism, the chloroplast genomes of the two have high diversity in the rpl 32 ~  trn L-UAG short region. When using this region as a mini barcode, it was found that there are obvious differences in the base numbers of I. tinctoria and different ploidy I. indigotica were found, but diploid and tetraploid I. indigotica had the same number of bases. Moreover, the reconstruction of the maximum likelihood (ML) tree, utilizing the mini-barcode, demonstrated that I. tinctoria and both diploid and tetraploid I. indigotica are located on distinct branches. The genome size of tetraploid I. indigotica was approximately 643.773 MB, the heterozygosity rate was approximately 0.98%, and the repeat sequence content was approximately 90.43%. This species has a highly heterozygous, extremely repetitive genome. Conclusion A new method was established to differentiate between I. indigotica and I. tinctoria . Furthermore, this approach provides a reference and basis for the directional breeding of Isatis .

Background/Aims: Stroke is a major cerebrovascular disease threatening human health and life with high morbidity, disability and mortality. It is aimed to find effective biomarkers for the early diagnosis on stroke. Methods: The expressions of 17 previously reported stroke-associated miRNAs were measured using quantitative RT-PCR and the expressions of plasma high-sensitivity C reactive protein (hs-CRP) and serum interleukin 6 (IL-6), the pro-inflammation markers in brain injury, were examined using enzyme-linked immunosorbent assay in 128 acute ischemic stroke (AIS) patients and control group. Results: Serum miR-146b expression was significantly increased within 24 hours after stroke onset in patients compared with control group. In addition, the upregulation of serum miR-146b was strong positively correlated with plasma hs-CRP, infarct volume and National Institutes of Health Stroke Scale (NIHSS) score, and moderate positively correlated with serum IL-6 of patients. Importantly, the combination of plasma hs-CRP and serum miR-146b gained a better sensitivity/specificity for prediction of AIS (AUC from 0.782 to 0.863). Conclusion: Our preliminary findings suggested that upregulated serum miR-146b in acute ischemic stroke might be a potential biomarker for AIS evaluation.

The treatment of diabetic periodontitis poses a significant challenge due to the presence of local inflammation characterized by excessive glucose concentration, bacterial infection, and high oxidative stress. Herein, mesoporous silica nanoparticles (MSN) are embellished with gold nanoparticles (Au NPs) and loaded with manganese carbonyl to prepare a carbon monoxide (CO) enhanced multienzyme cooperative hybrid nanoplatform (MSN‐Au@CO). The Glucose‐like oxidase activity of Au NPs catalyzes the oxidation of glucose to hydrogen peroxide (H2O2) and gluconic acid，and then converts H2O2 to hydroxyl radicals (•OH) by peroxidase‐like activity to destroy bacteria. Moreover, CO production in response to H2O2, together with Au NPs exhibited a synergistic anti‐inflammatory effect in macrophages challenged by lipopolysaccharides. The underlying mechanism can be the induction of nuclear factor erythroid 2‐related factor 2 to reduce reactive oxygen species, and inhibition of nuclear factor kappa‐B signaling to diminish inflammatory response. Importantly, the antibacterial and anti‐inflammation effects of MSN‐Au@CO are validated in diabetic rats with ligature‐induced periodontitis by showing decreased periodontal bone loss with good biocompatibility. To summarize, MSN‐Au@CO is fabricate to utilize glucose‐activated cascade reaction to eliminate bacteria, and synergize with gas therapy to regulate the immune microenvironment, offering a potential direction for the treatment of diabetic periodontitis. MSN‐Au@CO nanozymes are designed with enzyme‐like cascade reactions and resultant carbon monoxide (CO) gas release ability. The MSN‐Au@CO nanozymes consume glucose to generate hydroxyl radicals (•OH) that kill bacteria, and the resultant CO can synergistically enhance MSN‐Au to inhibit inflammation through Nrf2 and NF‐κB signaling. The anti‐bacterial and anti‐inflammation effects of MSN‐Au@CO show excellent efficacy in the treatment of periodontitis in diabetic rats.

Purpose To evaluate and identify the effects and explore the mechanisms of pyruvate kinase M2 (PKM2) on stroke‐induced post stroke depression (PSD). Methods Rats were separated into six different groups, including sham + saline, Stroke + saline, PSD + saline, PSD + recombinant pyruvate kinase M2 (rPKM2) (112 ng/kg), PSD + rPKM2 (224 ng/kg), and PSD + rPKM2 (224 ng/kg) + bevacizumab. Then, the body weight, sucrose preference rate, immobility time, horizontal movement, and vertical movement were determined to evaluate the effect of PKM2 on improving the depressive behavior of PSD rats. Subsequently, the proliferation of oligodendrocytes in subventricular zone (SVZ) of rats in each group was examined by western blot and immunofluorescent staining. Furthermore, the mRNA and protein expression levels of TNF‐α, IL‐6, and IL‐1β were also detected by qPCR and ELISA to verify the anti‐inflammatory effects of PKM2 on PSD rats. In addition, the protein expression levels of MDA, LDH, and NO were tested to reveal that PKM2 can reduce oxidative stress in PSD rats. The western blot and IHC assays were employed to examine the protein expression levels of VEGF, PKM2, and ERK in PSD rats. Results In this study, the results showed that PKM2 can improve the depressive behavior and proliferation of oligodendrocytes in PSD rats. In addition, PKM2 has anti‐inflammatory and anti‐oxidative stress effects on PSD rats. Meanwhile, PKM2 activated the expression level of VEGF/MAPK/ERK pathway. Conclusion PKM2 improves symptoms of post‐ischemic stroke depression by activating VEGF‐mediated MAPK/ERK pathway.

Background The relationship between cancer development and alterations in IgG N-glycosylation has been well-established. However, comprehensive profiling of the N-glycome and N-glycoproteome in gastric cancer (GC) remains limited. Furthermore, the prognostic potential of IgG N-glycan patterns in identifying precursors to GC has yet to be fully elucidated. Methods The IgG N-glycome in GC was characterized using a custom high-throughput orthogonal mass spectrometry approach. Multivariate analysis was employed to identify and assess glycomic alterations. A comprehensive bioinformatics analysis was also conducted to investigate the differential expression of N-glycosylation-related genes and their potential roles in GC pathogenesis. Additionally, interleukin-11 (IL-11) levels were quantified using a standardized enzyme-linked immunosorbent assay (ELISA). Results Galactosylation and sialylation of IgG decreased mainly in the IgG1 and IgG2 subclasses in GC, with subclass-specific changes in IgG3 and IgG4 galactosylation. These glycan modifications were represented by unique glycopeptides (IgG1_H5N5, IgG2_H4N3F1, IgG2_H4N4, IgG2_H4N4F1S1, IgG3/4_H4N4F1, IgG3/4_H4N4F1S1), which outperformed CA72-4 for GC diagnosis. Analysis of key glycogenes revealed differential expression patterns, implicating a functional role for IgG N-glycosylation in GC. Notably, the abundance of specific IgG glycosylation exhibited a significant correlation with serum level of IL-11. Conclusions Alterations in subclass-specific IgG N-glycosylation represent promising biomarkers for the detection and monitoring of GC progression, potentially influenced by cytokine-driven inflammation. Understanding these changes could improve our knowledge of molecular mechanisms, aiding in diagnostic improvements and therapeutic development.

ObjectiveThe aim of this study was to explore the safety and efficacy of multiple peptide-pulsed autologous dendritic cells (DCs) combined with cytotoxic T lymphocytes (CTLs) in patients with cancer.MethodsFive patients diagnosed with cancer between November 2020 and June 2021 were enrolled and received DC-CTLs therapy. Peripheral blood was collected and antigenic peptides were analyzed. The phenotype and function of DC-CTLs and the immune status of patients were detected using flow cytometry or IFN-γ ELISPOT analysis.ResultsDCs acquired a mature phenotype and expressed high levels of CD80, CD86, CD83, and HLA-DR after co-culture with peptides, and the DC-CTLs also exhibited high levels of IFN-γ. Peripheral blood mononuclear cells from post-treatment patients showed a stronger immune response to peptides than those prior to treatment. Importantly, four of five patients maintained a favorable immune status, of which one patient’s disease-free survival lasted up to 28.2 months. No severe treatment-related adverse events were observed.ConclusionOur results show that multiple peptide-pulsed DCs combined with CTLs therapy has manageable safety and promising efficacy for cancer patients, which might provide a precise immunotherapeutic strategy for cancer.