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Anesthesia‐related drugs cause various side effects and health‐related illnesses after surgery. In particular, neurogenerative disorder is a common problem of anesthesia‐related drugs. A patient gets anesthesia as a requirement of the preoperative evaluation to diagnose the medical illness, which is caused by anesthetic drug treatment. Different blood‐based biomarkers help in identifying the changes appearing in patients after anesthesia treatment. Among them, tau protein is a sensitive biomarker of neurodegenerative diseases, and the fluctuations in tau proteins are highly associated with various diseases. Furthermore, researchers have found unstable levels of tau protein after the anesthesia process. The current research has focused on quantifying tau protein via impedance spectroscopy to identify the problems caused by anesthesia‐related drugs. An impedance spectroscopy electrode was modified into a multiwalled carbon nanotube, and an amine‐ended aptamer was then attached. This electrode surface was used to quantify the tau protein level and reached the detection limit of 1 fM. The determination coefficient was found to be y = 369.93x + 1144.9, with R2 = 0.9846 in the linear range of 1 fM–1 nM. Furthermore, tau protein spiked human serum was clearly identified on the immobilized aptamer surface, indicating the specific detection. [ABSTRACT FROM AUTHOR]

Objectives: Mesenchymal stem cells (MSCs) have shown great potential in treating autoimmune diseases (ADs). Unlike the traditional immunosuppressants, which inadvertently impair patients' antimicrobial immunity, MSCs reduce the incidence and duration of respiratory infection. However, the underlying mechanisms are unknown. Methods: To investigate how MSCs regulate the lung immunity and improve the defence against respiratory infection, we infected MSC‐treated wild‐type and lupus‐prone mice with Haemophilus influenzae intranasally and determined the clearance of bacteria. Tissue damage and inflammatory cytokines were measured by H&E staining and ELISA separately. Immune cell subsets in the tissues were analysed by flow cytometry. Results: MSC pretreatment prevented overwhelming inflammation and accelerated bacterial clearance in both wild‐type and lupus‐prone mice. Tregs increased dramatically in the lung after MSC treatment. Adoptive transfer of Tregs isolated from MSC‐treated mice offered similar protection, while deletion of Tregs abrogated the protective effects of MSCs. The majority of the intravenously injected MSCs were engulfed by lung phagocytes, which in turn produced CXCL9 and CXCL10 and recruited tremendous CXCR3+ Tregs into the lung. Compared with their CXCR3− counterparts, CXCR3+ Tregs displayed enhanced proliferation and stronger inhibitory functions. Neutralisation of CXCL9 and CXCL10 significantly downregulated the migration of CXCR3+ Tregs and eliminated the benefits of MSC pretreatment. Conclusion: Here, we showed that by recruiting CXCR3+ Tregs, MSC treatment restricted the overactivation of inflammatory responses and prevented severe symptoms caused by infection. By discovering this novel property of MSCs, our study sheds light on optimising long‐term immunosuppressive regimen for autoimmune diseases and other immune disorders. [ABSTRACT FROM AUTHOR]

A porous 3D graphene lubricant is designed using a polyurethane (PU) foam vehicle and a self‐lubricating composite is thereafter prepared by pouring monomer casting polyamide 6 (MCPA6) into the 3D graphene lubricant. The microstructure of the composite is studied using infrared (IR), thermogravimetric analysis (TGA), X‐ray diffractometer (XRD), and scanning electron microscopy (SEM). The results of tribological properties and mechanical properties show that the composite exhibits enhanced tribological behaviors while inheriting excellent mechanical properties of neat MCPA6; the wear resistance of the composite is over 160 times higher than that of neat MCPA6 (1.3 m s−1, 140 N). The friction and wear mechanism of the composite is determined. The designed porous 3D graphene composite shows the merits of the increased friction reduction and antiwear performances with decreased loading content of graphene. This research opens a new insight for designing 3D graphene composite in severe tribological conditions. [ABSTRACT FROM AUTHOR]

Background. Immunosuppressants such as cyclophosphamide (CTX) have been employed to treat a wide array of autoimmune diseases. The most unfavourable side effects of these drugs are their suppression on the antimicrobial immunity and increasing the risk of infection. As a promising substitution/adjunct, mesenchymal stem cells (MSCs) are currently being tested in several clinical trials. However, their influence on the recipients' antimicrobial immunity remains unclear. Methods. In this study, C57BL/6 mice were treated with either CTX or MSCs, and then both the innate and adaptive immunity of the lung were determined. To investigate the influence of CTX and MSCs on the immune defence against infection, the treated mice were intranasally infected with opportunistic pathogen Haemophilus influenzae (Hi). Bacterial clearance and antibacterial immune responses were analysed. Results. Our data showed that CTX strongly inhibited the proliferation of lung immune cells, including alveolar macrophages (AMs) and T cells, whereas MSCs increased the numbers of these cells. CTX suppressed the phagocytic activity of AMs; on the contrary, MSCs enhanced it. Notably, infusion of MSCs led to a remarkable increase of regulatory T cells and Th1 cells in the lung. When infected by Hi, CTX did not significantly impair the elimination of invaded bacteria. However, MSC-treated mice exhibited accelerated bacterial clearance and moderate inflammation and tissue damage. Conclusion. Our study reported that unlike traditional immunosuppressants, modulation of MSCs on the recipient's immune response is more elegant. It could preserve and even enhance the antimicrobial defence, suggesting that MSCs are better choice for patients with high risk of infection or those who need long-term immunosuppressive regimen. [ABSTRACT FROM AUTHOR]

Infection is a common cause of hospitalization and mortality in patients with systemic lupus erythematosus (SLE). How the underlying immune dysfunctions affect the antimicrobial immunity remains largely unknown. In the present study, employing the pulmonary infection model, we determined the antimicrobial defence of lupus-prone mice. After infecting with opportunistic bacterium Haemophilus influenzae (Hi), lupus-prone mice (B6/lpr) exhibited inefficient bacterial elimination and recovered slowly. They generated severer inflammation at the early stage of infection, as excessive accumulation of neutrophils and enhanced production of proinflammatory cytokines were observed in the lung. In addition, a large number of apoptotic cells were detected in the lungs of B6/lpr mice. For adaptive immune responses, B6/lpr mice were capable to generate enough protective Hi-specific Th17 cells. They evoked stronger Hi-specific γδ T17 response in both lungs and spleens. Unexpectedly, both CD4 and γδ T cells from lupus-prone mice showed deficiency in IFN-γ production. For humoral immune responses, compared with those of WT mice, the concentrations of Hi-specific IgA, IgM, and IgG, especially IgG, were significantly higher in the B6/lpr mice. Our findings suggest that lupus mice are capable to generate antibacterial immune responses; however, the overwhelming inflammation and overactivated immune responses increase the severity of infection. [ABSTRACT FROM AUTHOR]

Aim: Cardiovascular complications related to atherosclerosis are major causes of morbidity and mortality in patients with systemic lupus erythematosus (SLE). However, the underlying mechanisms are not fully understood. Endothelial dysfunction has been identified as having involvement in pathogenesis of cardiovascular diseases and SLE. This study aims to evaluate endothelial cell injury in mice with the combination of lupus and atherosclerosis. Methods: The mouse model of accelerated atherosclerosis in lupus (gld.apoE−/− mouse) was generated from apolipoprotein E‐deficient (apoE−/−) and Faslgld C57BL/6 mice. The lupus‐like autoimmunity and atherosclerotic lesions were evaluated. The endothelial cell injury was determined. Results: The results showed that the double‐mutant gld.apoE−/− mice were generated. Spleens from 5‐month‐old gld.apoE−/− mice were significantly enlarged compared with wild‐type mice (WT mice). The gld.apoE−/− mice produced high levels of total immunoglobulin G (IgG) and IgM and showed marked increase of IgG and C3 deposits in the glomeruli. The gld.apoE−/− mice displayed a pattern of glomerulonephritis typically found in SLE. The gld.apoE−/− mice have high levels of serum creatinine. The total cholesterol, low‐density lipoprotein cholesterol and triglycerides were significantly increased, while high‐density lipoprotein cholesterol decreased in the double‐mutant mice. The circulating endothelial progenitor cells were significantly decreased. The serum levels of thrombomodulin and vascular cell adhesion molecule‐1 were significantly elevated in gld.apoE−/− mice. The gld.apoE−/− mice simultaneously exhibited SLE and atherosclerosis characteristics. Conclusion: Our findings indicated that endothelial cell injury might be a biomarker for evaluating risks of cardiovascular disease in SLE and targeting endothelial cell dysfunction might prevent and treat atherosclerosis in SLE. [ABSTRACT FROM AUTHOR]