Hard carbon (HC) represents an attractive anode material for sodium‐ion batteries. However, most HC materials deliver limited capacity and the sodium storage mechanisms in the slope and plateau regions are controversial. Herein, a series of hard carbon nanofibers (HCNFs) with tunable interlayer spacings are designed to understand the sodium storage manners in HC. The optimized HCNFs featuring short‐range graphitic layers with sufficient interlayer spacings (0.37–0.40 nm) for Na+ intercalation deliver a high reversible capacity (388 mAh g–1 at 30 mA g–1) and good rate capability. In‐situ X‐ray diffraction and Raman characterizations reveal a revised adsorption/insertion–filling sodium storage mechanism. Combined with the density functional theory (DFT) calculation, the detailed relationship between pore‐filling plateau capacity and interlayer spacing is disclosed. It is found that sufficient interlayer spacings (>0.37 nm) provide diffusion channels for Na+ to reach the pores for further filling. Additionally, the reason for plateau‐region capacity degradation of the HCNFs is completely demonstrated. This contribution provides insights into the sodium storage mechanism and rational construction of high‐performance HC anode materials.

Abstract. Emodin is an active ingredient derived from root and rhizome of Rheum palmatum L and many studies have reported that it exhibits anticancer effects in a number of human tumors. However, there is little information demonstrating the possible effects of emodin on the proliferation and apoptosis of hepatocellular carcinoma (HCC). In the present study, we show that emodin may inhibit the proliferation of SMMC-7721 cells in a dose-and time-dependent manner and induced apoptosis of cells in a concentration-dependent manner after treatment for 24 h. Moreover, we further discovered that the possible molecular mechanisms involved may relate to the mitogenactivated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT signaling pathways. Emodin may induce the phosphorylation of extracellular-signal-regulated kinase (ERK) and p38 while mildly suppressed the expression of p-c-Jun-N-terminal kinase (p-JNK). However, emodin did not affect the expression of the total (t)-ERK, t-p38 or t-JNK. Furthermore, emodin also suppressed the activation of p-AKT, but not the t-AKT. In vivo, we found that emodin suppressed tumor growth in experimental mice without an obvious change in body weight, which may work through the antiproliferation and apoptosis inducing effects. Moreover, emodin improves the liver and kidney function in mice, revealing that emodin may improve the life quality of the mice with implanted tumors. In conclusion, the above findings indicate that emodin may be a potentially effective and safe drug to induce apoptosis of HCC.

Increasing evidence suggests that microRNAs, which control gene expression at the post-transcriptional level, are aberrantly expressed in cancers and play significant roles in carcinogenesis and cancer progression. In this study, we show differential miR-133b down-expression in human esophageal squamous cell carcinoma (ESCC) cells and tissues. In addition, squalene epoxidase (SQLE), a key enzyme of cholesterol synthesis, is identified as the direct downstream target gene of miR-133b by luciferase gene reporter assay. Furthermore, ectogenic miR-133b expression and SQLE knockdown can inhibit proliferation, invasion, and metastasis, and diminish epithelial-to-mesenchymal transition (EMT) traits of ESCC in vitro, implying that miR-133b-dependent SQLE can induce tumorigenicity and that SQLE is an EMT inducer. Xenograft experiment results also proved the biological function of SQLE in vivo. Therefore, we conclude that miR-133b-dependent SQLE plays a critical role in the potential metastasis mechanisms in ESCC.

Source reduction of hazardous Cr6+ containing wastes has significance in the cleaner production of chromate and environmental protection.

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each series it is expected that two to three stages whose boundaries correspond to horizons that can be correlated with a high degree of confidence through all paleocontinents will be recognized. As emphasized by Geyer and Shergold (2000), communication of timestratigraphic information will be maximized if the internal subdivisions of the system correspond to horizons recognizable on all paleocontinents. Traditional, regional stratigraphic schemes, based principally on unit stratotypes, do not meet this goal, and it is for this reason that the ISCS is now engaged in further developing our understanding of key horizons for correlation within the Cambrian, and newly defined series and stages that are readily traceable among Cambrian regions. The newly defined chronostratigraphic units are based on the principle of boundary stratotypes, in which the base of one unit (marked by a Global boundary Stratotype Section and Point, or GSSP) automatically delimits the top of the underlying unit. So defined, these intervals differ in substance from unit stratotypes, which have been variously defined in Cambrian regions (Geyer and Shergold, 2000; Peng et al., 2004a, 2006; Babcock et al., 2005). Apart from the Guzhangian Stage (discussed here), the boundary positions relevant to the Cambrian (Figure 1) that have been ratified are: 1, the conterminant base of the Paleozoic Erathem, Cambrian System,

The Toll-like receptor 3 (TLR3) agonists as polyriboinosinic–polyribocytidylic acid (poly (I:C)) have been implicated as potential immunotherapy adjuvant for cancer whereas the exact roles of TLR3 agonists in hepatocellular carcinoma (HCC) treatment have not been clearly evaluated. In consistent with previous reports, we found that poly (I:C) triggering of TLR3 inhibited cell proliferation and induced apoptosis in HCC cells. However, poly (I:C), when used at lower concentration that cannot remarkably inhibit proliferation and induce apoptosis in HCC cells, enhanced the migration and invasion in vitro and the metastasis in vivo. More importantly, we found that bufalin, a prominent component of toad venom, could suppress poly (I:C)-inspired migration, invasion and metastasis of HCC cells despite that bufalin could not potentiate poly (I:C)-induced inhibition of proliferation and induction of apoptosis. In MHCC97 H cells, bufalin impaired poly (I:C)-induced activation of Tank-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3) pathway and NF-κB pathway. Inhibitor for TBK1 but not NF-κB suppressed poly (I:C)-inspired migration and invasion, which was further supported by using TBK1 deficient (Tbk1–/–) cells. In another model using poly (I:C) transfection, bufalin could also suppress the migration and invasion of HCC cells, which was not observed in Tbk1–/– MHCC97 H cells. Our data suggest that bufalin can suppress the metastasis of HCC cells in poly (I:C) therapy by impairing TBK1 activation, indicating that bufalin may be used in combination with poly (I:C) therapy in HCC treatment for the sake of reversing poly (I:C)-triggered metastasis of HCC cells.

AIM:To investigate the safety of combined cranioplasty (CP) and ventriculoperitoneal shunt (VPS) placement. Furthermore, we investigated whether the sequence of these procedures affects the postoperative complication rates associated with staged CP and VPS placement. MATERIAL and METHODS:We retrospectively investigated patients who developed communicating hydrocephalus after decompressive craniectomy and subsequently underwent VPS placement and CP at the hospital at which this study was performed between January 2009 and December 2019. Patients were categorized into group 1 (simultaneous CP and VPS placement) and group 2 (CP and VPS placement performed separately). Group 2 was subcategorized into subgroup 2a (CP performed before VPS placement) and subgroup 2b (VPS placement performed before CP). The Student's t and Chi square tests were used to analyze intergroup differences. RESULTS:This study included 86 patients; 22 in group 1 and 64 in group 2 (24 patients in subgroup 2a and 40 patients in subgroup 2b). No statistically significant difference was observed in the overall complication rates between groups 1 and 2 (36.4% vs. 28.1%, P=0.591). However, the incidence of infections was significantly higher in group 1 than in group 2 (22.7% vs. 4.7%, P=0.024). Subgroup analysis showed that the overall complication rate was significantly lower in subgroup 2a than in subgroup 2b (12.5% vs. 37.5%, P=0.031). CONCLUSION:Simultaneous CP and VPS placement is associated with a high incidence of infections. Moreover, compared with initial CP, initial VPS placement is associated with a significantly higher risk of overall complications in patients who undergo a staged procedure.