When testing the electrochemical performance of metal oxide anode for lithium-ion batteries (LIBs), binder played important role on the electrochemical performance. Which binder was more suitable for preparing transition metal oxides anodes of LIBs has not been systematically researched. Herein, five different binders such as polyvinylidene fluoride (PVDF) HSV900, PVDF 301F, PVDF Solvay5130, the mixture of styrene butadiene rubber and sodium carboxymethyl cellulose (SBR+CMC), and polyacrylonitrile (LA133) were studied to make anode electrodes (compared to the full battery). The electrochemical tests show that using SBR+CMC and LA133 binder which use water as solution were significantly better than PVDF. The SBR+CMC binder remarkably improve the bonding capacity, cycle stability, and rate performance of battery anode, and the capacity retention was about 87% after 50th cycle relative to the second cycle. SBR+CMC binder was more suitable for making transition metal oxides anodes of LIBs.

These findings suggest that coronary artery calcification is associated with increased IL-18 levels. IL-18 enhances VSMCs osteogenic differentiation and subsequent VC induced by β-glycerophosphate via TRPM7 channel activation. Accordingly, IL-18 may contribute to VC in proinflammatory conditions.

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Vascular calcification (VC) is a significant risk factor for cardiovascular morbidity and mortality. We recently reported that apocynin had benefits for preventing cardiovascular diseases. However, whether apocynin could attenuate VC is unknown. Here, we investigated the role of apocynin in VC and its underlying mechanisms. 163 participants with high or normal ankle–brachial index (ABI) were enrolled in this study for analyzing the demographic and biochemical data. In vitro, vascular smooth muscle cells (VSMCs) were exposed to calcification medium containing b-glycerophosphate and angiotensin II (Ang II) for 24 hours. The results showed that serum level of Ang II was significantly increased in patients with high ABI (P<0.05). In cultured VSMCs, Ang II significantly exacerbated osteogenic switching. The expression of osteogenic phenotype markers, including bone morphogenetic protein 2 (BMP2), runt-related transcription factor 2 (Runx2) and osteopontin (OPN), were significantly upregulated, whereas contractile markers expression, including alpha smooth muscle actin (a-SMA) and smooth muscle 22 alpha (SM22a) were simultaneously downregulated. However, these effects were greatly attenuated by apocynin. Apocynin enhanced expression of a-SMA by 5.3%, and reduced expression of BMP2, Runx2, OPN by 3.37%, 0.61% and 3.07%, respectively. Furthermore, extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation was upregulated by Ang II, and this effect was also reversed by apocynin. Intriguingly, pretreatment with U0126, an inhibitor of ERK1/2, had similar effects with apocynin. Apocynin may act as a novel molecular candidate to protect against VSMCs osteogenic switching through suppressing ERK1/2 pathway.

Advanced oxidation protein products (AOPPs) are independent risk factor for various cardiovascular diseases. Cardiomyocyte apoptosis has been implicated as an important mechanism in cardiac remodeling in chronic kidney disease (CKD). However, whether AOPPs affect cardiomyocyte apoptosis and subsequent cardiac remodeling in CKD is still not very clear. Here, we assessed the role of AOPPs in cardiomyocyte apoptosis in CKD. H9C2 rat cardiomyoblast cells were exposed to AOPPs. Apoptotic cells were determined by TUNEL assay. The expression of apoptotic markers (cleaved caspase-3 and Bax), JNK signaling, and endoplasmic reticulum stress were explored. Serum AOPPs were measured in male Sprague-Dawley rats that underwent sham surgery and 5/6 nephrectomy, respectively. In vitro, our findings showed that AOPPs activated JNK signaling and endoplasmic reticulum stress and significantly aggravated H9C2 rat cardiomyoblast cells apoptosis. These effects were partially ameliorated by apocynin with inhibition of oxidative stress. In vivo, serum levels of AOPPs were progressively elevated with the increasing time course in CKD rats compared with sham-operated rats ( P < 0.05). Serum AOPP levels were positively associated with cardiomyocyte apoptosis ( R = 0.76, P < 0.01). In conclusion, AOPPs aggravate cardiomyocyte apoptosis in vitro, and these effects are partially prevented by apocynin via suppressing JNK signaling and endoplasmic reticulum stress with oxidative stress inhibition. In vivo, AOPPs are increased in the CKD model and may contribute to the cardiac pathogenesis, but at this point it is unclear if that is true. These results suggest that pharmacological approaches to attenuate AOPP-aggravated cardiomyocyte apoptosis may be beneficial to improve cardiac remodeling in CKD. NEW & NOTEWORTHY Here, we present new evidence to show that advanced oxidation protein products aggravate cardiomyocyte apoptosis and subsequent cardiac remodeling via upregulations of JNK signaling and endoplasmic reticulum stress in chronic kidney disease. Such processes are mainly prevented by apocynin via oxidative stress inhibition.

Background: Canonical Wnt/β-catenin signaling is frequently dysregulated in acute myeloid leukemia (AML) and has been implicated in leukemogenesis. γ-catenin was previously demonstrated to be associated with the nuclear localization of β-catenin, the central mediator, and to exert oncogenic effects in AML; however, the underlying mechanisms remain unclear. Our study aimed to investigate the expression characteristics of γ-catenin in AML patients, explore the mechanisms by which γ-catenin regulates β-catenin, and discuss the feasibility of targeting γ-catenin for AML treatment. Methods: The mRNA expression levels of γ-catenin in AML patients were measured by qRT-PCR. Cell proliferation was examined via Cell Counting Kit-8 (CCK-8) assays. The expression levels of related proteins were measured via Western blotting. Specific siRNA was used to modulate the expression level of the γ-catenin gene. Apoptosis and cell cycle distribution were quantified by flow cytometry. The subcellular localization of γ-catenin and β-catenin was examined via immunofluorescence with a confocal laser scanning microscope. Results: Overexpression of γ-catenin was frequently observed in AML and correlated with poor prognosis. Consistent with this finding, suppression of γ-catenin in the AML cell line THP-1 induced growth inhibition, promoted apoptosis and blocked β-catenin nuclear translocation. Interestingly, γ-catenin knockdown sensitized THP-1 cells to cytotoxic chemotherapeutic agents such as cytarabine and homoharringtonine and further inhibited β-catenin nuclear localization. Moreover, our data implied the relationship between γ-catenin and GSK3β (whose effect on β-catenin is mediated by its own phosphorylation), which may be the principal mechanism underlying the anti-AML effect of γ-catenin inhibition. Conclusion: Taken together, our results revealed a potential role of γ-catenin in AML pathogenesis-mainly through the inhibition of GSK3β-mediated nuclear localization of β-catenin-and indicate that targeting γ-catenin might offer new AML treatments.

The electron channeling contrast imaging technique was used to investigate the microstructure of copper coatings fabricated by cold gas dynamic spray. The high velocity impact characteristics for cold spray led to the formation of many substructures, such as high density dislocation walls, dislocation cells, deformation twins, and ultrafine equiaxed subgrains/grains. A schematic model is proposed to explain structure refinement of Cu during cold spray, where an emphasis is placed on the role of dislocation configurations and twinning.