Anti-icing is a technology urgently needed for human society to take production activities in high latitude and cold regions. Superhydrophobic coating is widely used to prevent important facilities ...from icing, such as power lines, building roof and aircraft skin. In this work, PTFE (PTFE, polytetrafluoroethylene) super hydrophobic coating was prepared on titanium alloy surface, a falling droplet impacted the PTFE super hydrophobic coating and froze on it. Then continuous freezing and thawing were carried out on the PTFE super hydrophobic coating. The result shows that the adhesion between PTFE super hydrophobic coating and droplet is extremely small. Droplet can bounce and roll along the surface, even at low temperatures. Freezing of droplet on PTFE super hydrophobic coating lasts 760 s, much longer than that of unmodified titanium alloy surface. Furthermore, the PTFE super hydrophobic coating has high wear resistance and can resist freezing and thawing permanently.
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•A PTFE super hydrophobic coating with simple structure and low cost was prepared on titanium alloy surface.•It prevent droplets from adhering to its surface under ambient temperature and cold weather, even if the slope of titanium alloy surface is extremely gently.•It also has high wear resistance and can resist freezing and thawing permanently.
Advanced oxidation processes (AOPs) are a class of highly efficient pollution remediation technologies that produce oxidising radicals under specific conditions to degrade organic pollutants. The ...Fenton reaction is a commonly applied AOP. To combine the advantages of AOPs and biodegradation in the remediation of organic pollutants, some studies have developed coupled systems between Fenton AOPs and white rot fungi (WRF) for environmental organic pollutant remediation and have achieved some success. Moreover, a promising system, termed as advanced bio-oxidation processes (ABOPs), mediated by the quinone redox cycling of WRF, has attracted increasing attention in the field. In this ABOP system, the radicals and H2O2 produced through the quinone redox cycling of WRF can strengthen Fenton reaction. Meanwhile, in this process, the reduction of Fe3+ to Fe2+ ensures the maintenance of Fenton reaction, leading to a promising application potential for the remediation of environmental organic pollutants. ABOPs combine the advantages of bioremediation and advanced oxidation remediation. Further understanding the coupling of Fenton reaction and WRF in the degradation of organic pollutants will be of great significance for the remediation of organic pollutants. Therefore, in this study, we reviewed recent remediation techniques for organic pollutants involving the coupled application of WRF and the Fenton reaction, focusing on the application of new ABOPs mediated by WRF, and discussed the reaction mechanism and conditions of ABOPs. Finally, we discussed the application prospects and future research directions of the joint application of WRF and advanced oxidation technologies for the remediation of environmental organic pollutants.
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•Reviewed organic pollution remediation technologies that coupled WRF with the Fenton reaction.•The advanced bio-oxidation processes mediated by quinone redox cycling of WRF were discussed.•Provided an insight into the mechanisms and reaction conditions of ABOPs in bioremediation.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. Although previous studies have demonstrated that SLE is related to the imbalance of cells in the immune system, including B cells, ...T cells, and dendritic cells, etc., the mechanisms underlying SLE pathogenesis remain unclear. Therefore, effective and low side-effect therapies for SLE are lacking. Recently, mesenchymal stem cell (MSC) therapy for autoimmune diseases, particularly SLE, has gained increasing attention. This therapy can improve the signs and symptoms of refractory SLE by promoting the proliferation of Th2 and Treg cells and inhibiting the activity of Th1, Th17, and B cells, etc. However, MSC therapy is also reported ineffective in some patients with SLE, which may be related to MSC- or patient-derived factors. Therefore, the therapeutic effects of MSCs should be further confirmed. This review summarizes the status of MSC therapy in refractory SLE treatment and potential reasons for the ineffectiveness of MSC therapy from three perspectives. We propose various MSC modification methods that may be beneficial in enhancing the immunosuppression of MSCs in SLE. However, their safety and protective effects in patients with SLE still need to be confirmed by further experimental and clinical evidence.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that was traditionally thought to be closely related to genetic and environmental risk factors. Although treatment options for SLE ...with hormones, immunosuppressants, and biologic drugs are now available, the rates of clinical response and functional remission of these drugs are still not satisfactory. Currently, emerging evidence suggests that gut microbiota dysbiosis may play crucial roles in the occurrence and development of SLE, and manipulation of targeting the gut microbiota holds great promises for the successful treatment of SLE. The possible mechanisms of gut microbiota dysbiosis in SLE have not yet been well identified to date, although they may include molecular mimicry, impaired intestinal barrier function and leaky gut, bacterial biofilms, intestinal specific pathogen infection, gender bias, intestinal epithelial cells autophagy, and extracellular vesicles and microRNAs. Potential therapies for modulating gut microbiota in SLE include oral antibiotic therapy, fecal microbiota transplantation, glucocorticoid therapy, regulation of intestinal epithelial cells autophagy, extracellular vesicle-derived miRNA therapy, mesenchymal stem cell therapy, and vaccination. This review summarizes novel insights into the mechanisms of microbiota dysbiosis in SLE and promising therapeutic strategies, which may help improve our understanding of the pathogenesis of SLE and provide novel therapies for SLE.
Hepatocellular carcinoma (HCC) is a malignancy with one of the worst prognoses. Long noncoding RNA (lncRNA) are emerging as an important regulator of gene expression and function, leading to the ...development of cancer. The aim of this study was to determine the relationship between lncRNA and HCC and to further guide clinical therapy. lncRNA in HCC and adjacent tissues were screened, and the correlation between lncRNA‐PDPK2P expression in liver tissues and the pathological characteristics and severity of HCC was assessed. The effects of PDPK2P on HCC proliferation, apoptosis, metastasis, and invasion were also systematically investigated via CCK‐8 assay, flow cytometry, scratch wound healing, and transwell assay, respectively. The relationship between PDPK2P and PDK1 was verified by RNA pull‐down, rescue experiments and western blot. lncRNA‐PDPK2P was highly expressed in HCC tissues with a distinct positive correlation between PDPK2P and PDK1, and the upregulation was clinically associated with a larger tumor embolus, low differentiation, and poor survival. Mechanistically, lncRNA‐PDPK2P interacted with PDK1 and promoted HCC progression through the PDK1/AKT/caspase 3 signaling pathway. lncRNA‐PDPK2P can promote HCC progression, suggesting it may be a clinically valuable biomarker and serve as a molecular target for the diagnosis, prognosis, and therapy of hepatocellular carcinoma.
lnc‐PDPK2P that binds to microRNA increases with increased lnc‐PDPK2P expression, resulting in a decrease in the amount of microRNA bound to mRNA‐PDK1 and thereby increasing the amount of PDK1 involved in the AKT pathway. Finally, lncRNA‐PDPK2P promotes HCC progression through the PDK1 /AKT/caspase 3 signaling pathway.
A critical challenge for chemotherapy is the development of chemoresistance in breast cancer. However, the underlying mechanisms and validated predictors remain unclear. Extracellular vesicles (EVs) ...have gained attention as potential means for cancer cells to share intracellular contents. In adriamycin-resistant human breast cancer cells (MCF-7/ADM), we analyzed the role of transient receptor potential channel 5 (TrpC5) in EV formation and transfer as well as the diagnostic implications. Up-regulated TrpC5, accumulated in EVs, is responsible for EV formation and trapping of adriamycin (ADM) in EVs. EV-mediated intercellular transfer of TrpC5 allowed recipient cells to acquire TrpC5, consequently stimulating multidrug efflux transporter P-glycoprotein production through a Ca ²⁺- and activated T-cells isoform c3-mediated mechanism and thus, conferring chemoresistance on nonresistant cells. TrpC5-containing circulating EVs were detected in nude mice bearing MCF-7/ADM tumor xenografts, and the level was lower after TrpC5–siRNA treatment. In breast cancer patients who underwent chemotherapy, TrpC5 expression in the tumor was significantly higher in patients with progressive or stable disease than in patients with a partial or complete response. TrpC5-containing circulating EVs were found in peripheral blood from patients who underwent chemotherapy but not patients without chemotherapy. Taken together, we found that TrpC5-containing circulating EVs may transfer chemoresistance property to nonchemoresistant recipient cells. It may be worthwhile to further explore the potential of using TrpC5-containing EVs as a diagnostic biomarker for chemoresistant breast cancer.
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•Vitexin could alleviate liver injury caused by ulcerative colitis.•Vitexin could inhibit the activation of TLR4/NF-κB signaling pathway.•Vitexin could be a promising drug for liver ...injury induced by acute ulcerative colitis.
As one of commonly used herbs with dual-purpose of drug and food, it has been reported that vitexin has hepatoprotective effects. However, the protective effects of vitexin on colitis-induced liver injury as well as the underlying molecular mechanisms remain unclear. The purpose of the current study was to investigate the effects and mechanisms of vitexin on liver injury induced by acute ulcerative colitis in mice. In this study, the mice model of acute ulcerative colitis was induced by 4 % dextran sodium sulphate (DSS). And then, the degree of liver injury in colitis mice was evaluated, the hepatic ALT, AST, TC and TG levels were measured by specific determination kits, the levels of TNF-α, IL-6 and IL-1β were examined by ELISA, the expressions of TLR4/NF-κB pathway related protein were detected by western blot analysis. The results indicated that hepatic histopathological changes induced by DSS were normalized by vitexin treatment, administration of vitexin decreased the liver levels of ALT and TC in mice with liver injury and reduced the release amounts of DSS-induced pro-inflammatory cytokines TNF-α, IL-6 and IL-1β. Furthermore, we found that vitexin inhibited the activation of TLR4/NF-κB signaling pathway induced by DSS. In conclusion, vitexin possess hepatoprotective activities against colitis-induced liver injury, it has potential application prospects in the treatment of liver injury induced by ulcerative colitis.
The incidence of hepatocellular carcinoma (HCC) is extremely high, and China accounts for approximately 50% of global liver cancer cases. Previous studies reported that CDC20 is involved in the ...occurrence and progression of a variety of malignant tumors. So, whether CDC20 will affect the development of HCC, we have conducted in-depth research on this.
We selected Hep3B and HepG2 for cell culture, and performed siRNA transfection, lentiviral infection, western blot, MTS determination, cell cycle determination, apoptosis test, immunodeficiency test, clone survival test and subcutaneous parthenogenesis in nude mice.
Knockdown of CDC20 greatly enhanced the radiation efficacy on the growth retardation in HepG2, and protein level of CDC20 was decreased for the activation of P53 by radiation. Downregulation of CDC20 combined with radiation can inhibit proliferation, aggravate DNA damage, increase G2/M arrest, and promote apoptosis of HCC cells to a greater extent, and the relative survival fraction of HCC cells was gradually reduced with radiation dose increased in P53 mutated Hep3B cells. After knocking down CDC20 in HCC, Bcl-2 was down-regulated and Bax expression increased. Down-regulation of CDC20 can inhibit further invasion by promoting the radiosensitivity of HCC.
In this study, we found that that CDC20 was highly expressed in HCC and participated in radio resistance of HCC cells with P53 mutation Bcl-2/Bax via signaling pathway. This study is the first to present evidence that CDC20 may play a role in improving the efficacy of radiotherapy in HCC.
Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are two common multisystem autoimmune diseases that share, among others, many clinical manifestations and serological features. The ...role of long non-coding RNAs (lncRNAs) has been of particular interest in the pathogenesis of autoimmune diseases. Here, we aimed to summarize the roles of lncRNAs as emerging novel biomarkers and therapeutic targets in SLE and RA. We conducted a narrative review summarizing original articles on lncRNAs associated with SLE and RA, published until November 1, 2021. Based on the studies on lncRNA expression profiles in samples (including PBMCs, serum, and exosomes), it was noted that most of the current research is focused on investigating the regulatory mechanisms of these lncRNAs in SLE and/or RA. Several lncRNAs have been hypothesized to play key roles in these diseases. In SLE, lncRNAs such as GAS5, NEAT1, TUG1, linc0949, and linc0597 are dysregulated and may serve as emerging novel biomarkers and therapeutic targets. In RA, many validated lncRNAs, such as HOTAIR, GAS5, and HIX003209, have been identified as promising novel biomarkers for both diagnosis and treatment. The shared lncRNAs, for example, GAS5, may participate in SLE pathogenesis through the mitogen-activated protein kinase pathway and trigger the AMP-activated protein kinase pathway in RA. Here, we summarize the data on key lncRNAs that may drive the pathogenesis of SLE and RA and could potentially serve as emerging novel biomarkers and therapeutic targets in the coming future.
Commensal bacteria generate immensely diverse active metabolites to maintain gut homeostasis, however their fundamental role in establishing an immunotolerogenic microenvironment in the intestinal ...tract remains obscure. Here, we demonstrate that an understudied murine commensal bacterium, Dubosiella newyorkensis, and its human homologue Clostridium innocuum, have a probiotic immunomodulatory effect on dextran sulfate sodium-induced colitis using conventional, antibiotic-treated and germ-free mouse models. We identify an important role for the D. newyorkensis in rebalancing Treg/Th17 responses and ameliorating mucosal barrier injury by producing short-chain fatty acids, especially propionate and L-Lysine (Lys). We further show that Lys induces the immune tolerance ability of dendritic cells (DCs) by enhancing Trp catabolism towards the kynurenine (Kyn) pathway through activation of the metabolic enzyme indoleamine-2,3-dioxygenase 1 (IDO1) in an aryl hydrocarbon receptor (AhR)-dependent manner. This study identifies a previously unrecognized metabolic communication by which Lys-producing commensal bacteria exert their immunoregulatory capacity to establish a Treg-mediated immunosuppressive microenvironment by activating AhR-IDO1-Kyn metabolic circuitry in DCs. This metabolic circuit represents a potential therapeutic target for the treatment of inflammatory bowel diseases.
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