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To resolve the issue of predicting the leak rate in proton exchange membrane fuel cells (PEMFCs) under long-term random vibration conditions. Considering the mechanism of bolt vibration loosening and rubber vibration relaxation, a leakage mechanism model of the PEMFC sealing structure under vibration conditions is proposed, and the validity of the model is verified by experimental comparison. The model clearly reveals the quantitative effects of structural parameters and material parameters on the leakage rate of PEMFC under vibration conditions. The research results show that under long-term random vibration conditions, the change of PEMFC leakage rate with time is mainly divided into three stages: response stage, stable stage, and leakage stage. Compared to bolt vibration loosening, the rubber vibration relaxation has a more significant impact on PEMFC leakage, the leakage rate of the fuel cell stack is 433ppm after 10,000 hrs of vibration. In addition, increasing the bolt preload, changing the bolt distribution, reducing surface roughness, and reducing gasket thickness can effectively suppress PEMFC leakage under random vibration conditions, the minimum leakage rate of the fuel cell stack can be reduced to around 170ppm per 10,000 hours. The proposed mechanism model provides an effective method for predicting the leakage rate of PEMFC sealing structures. [ABSTRACT FROM AUTHOR]

Metastasis is a crucial stage in tumour progression, and cancer‐associated fibroblasts (CAFs) support metastasis through their participation in extracellular matrix (ECM) stiffness. CD248 is a possible biomarker for non‐small cell lung cancer (NSCLC)‐derived CAFs, but its role in mediating ECM stiffness to promote NSCLC metastasis is unknown. We investigated the significance of CD248+ CAFs in activating the Hippo axis and promoting connective tissue growth factor (CTGF) expression, which affects the stromal collagen I environment and improves ECM stiffness, thereby facilitating NSCLC metastasis. In this study, we found that higher levels of CD248 in CAFs induced the formation of collagen I, which in turn increased extracellular matrix stiffness, thereby enabling NSCLC cell infiltration and migration. Hippo axis activation by CD248+ CAFs induces CTGF expression, which facilitates the formation of the collagen I milieu in the stromal matrix. In a tumour lung metastasis model utilizing fibroblast‐specific CD248 gene knockout mice, CD248 gene knockout mice showed a significantly reduced ability to develop tumour lung metastasis compared to that of WT mice. Our findings demonstrate that CD248+ CAFs activate the Hippo pathway, thereby inducing CTGF expression, which in turn facilitates the collagen I milieu of the stromal matrix, which promotes NSCLC metastasis. [ABSTRACT FROM AUTHOR]

This study used the two-dimensional fluid volume method to investigate the effect of vibration on the detachment and removal of droplets in the two-dimensional/three-dimensional flow channel of proton exchange membrane fuel cell (PEMFC). The vibration frequency was used as the main variable to study the dynamic process of droplets in the channel, and typical droplet flow modes and separation methods were determined. The water removal ability of the two-dimensional/three-dimensional flow channel under vibration conditions was evaluated using droplet breakage time and coverage rate as evaluation indicators. Finally, the orthogonal table method was used to analyze the effects of vibration frequency, vibration amplitude, wind speed, and droplet size on the water removal ability of the three-dimensional flow field. The results indicate that under vibration conditions, the main motion modes of droplets are rolling mode and crushing mode and that the drainage capacity of the three-dimensional flow field is much higher than that of the two-dimensional flow field in both modes. The impact of vibration on the removal of droplets in the flow channel in the crushing mode is more significant compared to the rolling mode, and the vibration frequency has a greater impact on the drainage efficiency of the three-dimensional flow channel compared to the vibration amplitude. This study is of great significance for understanding the dynamics of droplets in PEMFC gas channels under vibration conditions as well as for optimizing the design and operating conditions of these channels. [ABSTRACT FROM AUTHOR]

African horse sickness (AHS) is an acute and subacute infectious disease of equine species caused by the African horse sickness virus (AHSV). The VP7 of AHSV is a group-specific protein conserved in all serotypes and is an excellent candidate for the serological diagnosis and an AHS vaccine component. However, to date, B-cell epitopes on the AHSV VP7 recognized by humoral immune responses remain unclear. This study expressed the recombinant AHSV VP7 soluble in Escherichia coli and purified it for mouse immunization. Four monoclonal antibodies (mAbs) were screened and identified by hybridoma cell fusion, clonal purification, and immunological assays. The B-cell epitopes, recognized by monoclonal antibodies 4B5, 3G10, 3D7, and 4D6, were identified by a series of truncated overlapping peptides expressed as glutathione S-transferase (GST)-fusion proteins. The results revealed that 4B5 recognized the 124VQTGRYAGA132 motif, 3G10 recognized the 140RYYVPQGRT148 motif, while 3D7 and 4D6 recognized the 292QPINPPIFP300 motif. Amino acid sequence alignment indicated that three novel B-cell epitopes were conserved among various AHSV serotypes but unconserved in other orbiviruses, such as the bluetongue and epidemic hemorrhagic disease viruses. This study informs on the antigenic epitopes of AHSV VP7, facilitating future investigations into the serological diagnosis method and epitope-based vaccines against AHSV. • Altering key amino acids at the C-terminus achieved soluble expression of AHSV. • VP7 protein in E. coli for the first time. • Hybridoma technology prepared four monoclonal antibodies specific to the AHSV VP7 protein. • Three new linear B cell epitopes of AHSV VP7 protein were originally mapped using monoclonal antibodies. • This study will facilitate future investigations into diagnosis and epitope-based vaccination against AHSV. [ABSTRACT FROM AUTHOR]

Objective: To investigate the inhibitory effect of chrysanthemum extract on myocardial fibrosis in rats with renovascular hypertension, and explore the possible mechanism underlying this effect., Methods: Sixty Wistar rats were randomly divided into six groups: sham operation, model, positive control, and low-, medium-, and high-dose Huai chrysanthemum extract groups (ten rats per group). With the exception of the sham operation group, a renal hypertensive model was established in rats using the ""two-kidney, one clip"" method. After 6 weeks, low-, medium-, and high-dose groups were intragastrically administered chrysanthemum extract at 1, 2, or 4 g/kg, respectively, once daily for 4 weeks. The positive control group was administered Kato Pury at 50 mg/kg once daily for 4 weeks, while sham operation and model groups received an equal volume of distilled water once daily for 4 weeks. Blood pressure changes were examined before modeling, 6 weeks after modeling, and after 4 weeks of treatment administration. Ventricular remodeling indexes were measured by high frequency echocardiography after 4 weeks of treatment administration. Pathological changes were observed by hematoxylin and eosin, and Masson's trichrome staining methods. Collagen typeⅠ (Col Ⅰ) and type Ⅲ (Col Ⅲ) expression were examined by enzyme-linked immunosorbent assays. Transforming growth factor-β1 (TGF-β1), sma mad 3 (Smad3), Smad7, Ras homolog gene family, member A (RhoA), and Rho-associated protein kinase 1 (ROCK1) protein expression were detected by Western blot., Results: Compared with the model group, chrysanthemum-administered groups and the positive control group showed significant improvement of arterial blood pressure, echocardiography indicators, and degree of myocardial fibrosis (P < 0.05). In addition, these groups exhibited decreased expression of Col Ⅰ, Col Ⅲ, RhoA, ROCK1, TGF-β1, and Smad3, and increased Smad7 expression. Such improvements were most obvious in the high-dose chrysanthemum extract group (P < 0.05)., Conclusion: Chrysanthemum extract could effectively reduce myocardial fibrosis in rats with renovascular hypertension by a mechanism that potentially involves inhibition of RhoA/ROCK1 and TGF-β1/Smad signaling pathways.