Multifunctional Heterostructured Fe3O4-FeTe@MCM Electrocatalyst Enabling High-Performance Practical Lithium-Sulfur Batteries Via Built-in Electric Field.

The development of capable of simultaneously modulating the sluggish electrochemical kinetics, shuttle effect, and lithium dendrite growth is a promising strategy for the commercialization of lithium-sulfur batteries. Consequently, an elaborate preparation method is employed to create a host material consisting of multi-channel carbon microspheres (MCM) containing highly dispersed heterostructure Fe3O4-FeTe nanoparticles. The Fe3O4-FeTe@MCM exhibits a spontaneous built-in electric field (BIEF) and possesses both lithophilic and sulfophilic sites, rendering it an appropriate host material for both positive and negative electrodes. Experimental and theoretical results reveal that the existence of spontaneous BIEF leads to interfacial charge redistribution, resulting in moderate polysulfide adsorption which facilitates the transfer of polysulfides and diffusion of electrons at heterogeneous interfaces. Furthermore, the reduced conversion energy barriers enhanced the catalytic activity of Fe3O4-FeTe@MCM for expediting the bidirectional sulfur conversion. Moreover, regulated Li deposition behavior is realized because of its high conductivity and remarkable lithiophilicity. Consequently, the battery exhibited long-term stability for 500 cycles with 0.06% capacity decay per cycle at 5 C, and a large areal capacity of 7.3 mAh cm-2 (sulfur loading: 9.73 mg cm-2) at 0.1 C. This study provides a novel strategy for the rational fabrication of heterostructure hosts for practical Li-S batteries.

Radioactive Stent for Malignant Esophageal Obstruction: A Meta-Analysis of Randomized Controlled Trials.

Purpose: To compare the relative clinical efficacies of radioactive and normal stent insertion methods as a means of treating patients suffering from malignant esophageal obstruction (MEO). Materials and Methods: The Pubmed, Embase, and Cochrane Library databases were searched for relevant randomized controlled trials (RCTs) from the date of inception through to July 2020. RevMan v5.3 was used for all data analyses. Results: This meta-analysis included six RCTs that included a total of 194 patients who had undergone radioactive stent insertion and 209 who had normal stent insertion. There were no significant differences in pooled improvement of dysphagia scores (P = .40), rates of stent restenosis (24.7% versus 28.7%, P = .35), stent migration (3.3% versus 4.4%, P = .61), severe chest pain (22.8% versus 20.3%, P = .61), hemorrhage (11.0% versus 9.8%, P = .80), or fistula formation (6.1% versus 4.2%, P = .55) between two groups. The pooled time to restenosis (P < .00001) and survival (P < .00001) were significant longer in the radioactive stent group. Significant heterogeneity was detected in the endpoint of improvement of dysphagia score (I2 = 89%; P = .0002). Funnel plot analyses did not detect any evidence of publication bias pertaining to the selected study endpoints. Conclusions: Our meta-analysis demonstrated that radioactive stent insertion can prolong stent patency and survival for patients with MEO compared with normal stent insertion.

Low expression of BEX1 predicts poor prognosis in patients with esophageal squamous cell cancer.

The brain expressed x­linked gene 1 (BEX1) is a member of the BEX family and is aberrantly expressed in many cancers. However, the clinical significance of BEX1 expression level and its role in the pathology of esophageal squamous cell cancer (ESCC) remain unknown. In the present study, we determined BEX1 expression in the tumor and adjacent normal tissues from 118 ESCC patients by immunohistochemistry and determined the proliferation and growth of ESCC cells following ectopic overexpression of BEX1 in cultured cells and in mouse­ESCC xenografts. We observed that BEX1 was downregulated in ESCC tissues compared to adjacent normal tissues, and low BEX1 expression was significantly associated with larger ESCC tumor volume (P<0.001), advanced T stage (P=0.011) and advanced clinical stage (P=0.039). Additionally, survival analysis revealed that low expression of BEX1 significantly predicted poor prognosis in patients with ESCC (P<0.001). Multivariate analysis revealed that low BEX1 expression was an independent prognostic factor of poor survival (P=0.039). In vitro analysis revealed that overexpression of BEX1 inhibited ESCC cell proliferation and colony formation. Furthermore, in vivo tumorigenesis assays revealed that ectopic overexpression of BEX1 suppressed ESCC tumor growth in mice. Further immunoblotting analysis demonstrated that BEX1 upregulation led to reduced expression and phosphorylation of NF­κB p65, indicating inhibition of the NF­κB signaling pathway by BEX1. Our findings indicated that low BEX1 expression may be an independent prognostic marker for poor survival and may serve as a potential target for ESCC therapy.

Overexpression of Hepatocyte Cell Adhesion Molecule (hepaCAM) Inhibits the Proliferation, Migration, and Invasion in Colorectal Cancer Cells.

Hepatocyte cell adhesion molecule (hepaCAM), a new type of CAM, belongs to the immunoglobulin superfamily. Recently, hepaCAM was reported to be implicated in cancer development, and many researchers investigated its biological function in the tumorigenesis of various cancers. However, what kind of role hepaCAM plays in colorectal cancer (CRC) remains unknown. In this study, we found that hepaCAM was downregulated in CRC tissues and cell lines. Overexpression of hepaCAM inhibited CRC cell proliferation, migration, and invasion in vitro. Furthermore, the tumorigenesis assay showed that increased expression of hepaCAM suppressed CRC tumor growth and metastasis in vivo. We also demonstrated that overexpression of hepaCAM reduced the protein expression levels of ß-catenin, cyclin D1, and c-Myc, indicating its inhibitory effect on the Wnt/ß-catenin signaling pathway. In conclusion, our study results suggest hepaCAM as a promising therapeutic target for CRC and provide a better understanding for the molecular basis of CRC progression.