rGO@TiO2-x Schottky heterojunction for enhanced bidirectional catalysis in polysulfide conversion.

The shuttling and sluggish conversion kinetics of lithium polysulfides (LiPSs) lead to poor cycling performance and low energy efficiency in lithium-sulfur batteries (LSBs). In this work, a hierarchically structured nanocomposite, synthesized through a surfactant-directed hydrothermal growth following dopamine-protected pyrolysis, serves as a bidirectional catalyst for LSBs. This nanocomposite comprises N-doped reduced graphene oxide (rGO) nanosheets anchored with uniformly distributed TiO2-x nanoparticles via interfacial N-Ti and C-Ti bonding, resulting in the formation of abundant 2D/0D Schottky heterojunctions (rGO/TiO2-x). Density functional theory (DFT) calculations and in situ Raman characterizations demonstrate that rGO/TiO2-x effectively inhibits the shuttling of LiPSs with enhanced redox kinetics, achieving high utilization of the sulfur cathode and improving the overall reversibility. A high areal capacity is attained at a high sulfur loading and a low electrolyte/sulfur ratio. The initial specific capacity reaches 1010 mA h g-1 at a current density of 0.2C (1C = 1675 mA g-1), and a retention of 86.4 % is attained over 100 cycles. A light-emitting diode (LED) screen using two LSBs with rGO/TiO2-x demonstrates their high potential for practical applications.

Nitrogen-doped hollow carbon@tin disulfide as a bipolar dynamic host for lithium-sulfur batteries with enhanced kinetics and cyclability.

Lithium-sulfur batteries (LSBs) are promising next-generation electrochemical energy storage systems owing to high theoretical specific capacity (1675 mAh/g) and low cost. However, the shuttling effect of soluble polysulfides with slow conversion kinetics has deferred their commercial applications. The feasible design and synthesis of composite cathode hosts offer a promise solution to improving their electrochemical performances. In this work, tin disulfide (SnS2) nanosheets were anchored on nitrogen-doped hollow carbon with mesoporous shells, forming a bipolar dynamic host ("SnS2@NHCS"). It can efficiently confine the polysulfides and promote their conversion during (dis)charge. The as-assembled LSBs delivered a high capacity, superior rate and cyclability. This work presents a new view on the exploration of novel composite electrode materials for various rechargeable batteries with emerging applications.

15-hydroxy-6α,12-epoxy-7ß,10αH,11ßH-spiroax-4-ene-12-one sensitizes rectal tumor cells to anti-PD1 treatment through agonism of CD11b.

PURPOSE: Although immunotherapies have resulted in durable clinical responses, not all tumor types have seen substantial benefit. Extensive recruitment and accumulation of immunosuppressive myeloid cells into the tumor tissues has been postulated as a major mechanism of resistance to immunotherapies. Strategies targeting on single immunosuppressive cell type, in combination with checkpoint inhibitors, have resulted in promising outcomes in animal studies. However, compensatory actions by untargeted cells may limit the therapeutic efficacy. CD11b is highly expressed on the myeloid cell surface with an important role in their trafficking and cellular functions.In this study, we demonstrated that activation of CD11b with 15-hydroxy-6α,12-epoxy-7ß,10αH,11ßH-spiroax-4-ene-12-one (HESEO) enhanced the therapeutic efficacy of anti-PD1 treatment in the tumor model. MATERIALS AND METHODS: A syngeneic rectal tumor model was established. Different types of cells from the peripheral blood and tumor tissues were analyzed by flow cytometry. Real-time PCR was used to detect the gene expression. Therapeutic effects of HESEO combining with anti-PD1 antibody were assessed by the tumor model. RESULTS: Our data demonstrated that HESEO repolarized tumor-associated macrophages and reduced the number of tumor-infiltrating immunosuppressive myeloid cells. We further demonstrated that HESEO and immunotherapy combination promoted tumor growth control in a syngeneic tumor model. CONCLUSIONS: Our results showed that HESEO improved anti-tumor T cell immunity and rendered anti-PD1 treatment effective in unresponsive tumor models, providing proof of concept for a new combination strategy involving molecular agonism of CD11b to bypass the limitations of current clinical strategies to overcome resistance to immunotherapies.

Reversible posterior leukoencephalopathy syndrome induced by apatinib: a case report and literature review.

Reversible posterior leukoencephalopathy syndrome (RPLS) is a rare clinical-radiologic syndrome. There are reports that RPLS may be associated with cancer therapy including some chemotherapy drugs and antiangiogenic drugs. This paper reported a case of RPLS induced by apatinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor. A 47-year-old cervical cancer patient was administered apatinib, and 3 months later, headache, dizziness, blurred vision, and hypertension appeared. She was diagnosed with RPLS by nuclear magnetic resonance imaging (MRI). After apatinib discontinuation and normotensive treatment, her symptoms completely reversed. Antiangiogenic drugs potentially damage the balance of the blood-brain barrier by directly injuring vascular endothelial cells, resulting in the occurrence of RPLS. This case is the first report of RPLS induced by apatinib.

ING5 inhibits epithelial-mesenchymal transition in breast cancer by suppressing PI3K/Akt pathway.

Epithelial-mesenchymal transition (EMT) is a crucial step in tumor progression and has an important role during cancer invasion and metastasis. The proteins of the inhibitor of growth (ING) candidate tumor suppressor family are involved in multiple cellular functions such as cell cycle regulation and apoptosis. ING5 is a member of the family. However, the role of ING5 in breast cancer is still unclear. Thus, the aim of this study is to explore the role of ING5 in breast cancer. In the present study, we showed that ING5 is involved in the pathogenesis of breast cancer. ING5 is down-regulated in breast cancer tissues and cell lines. Overexpression of ING5 significantly inhibited breast cancer cell migration, invasion, and EMT phenotype, moreover, overexpression of ING5 significantly the phosphorylation of PI3K and Aktin in breast cancer cells. In conclusion, our findings show that ING5 can efficiently inhibit the EMT progression in breast cancer cells by suppressing PI3K/Akt signaling pathway. Therefore, ING5 may be a good molecular target for the prevention and treatment of breast cancer.

Systematic analysis of gene expression and molecular interactions in cardiac and non-cardiac gastric carcinomas.

BACKGROUND/AIMS: : This study aims to comparing the gene expression profiles and molecular interactions among gastric cardiac adenocarcinomas (GCA), gastric noncardiac adenocarcinomas (GNCA) and their adjacent normal tissues. METHODOLOGY: Gene expression profile of GSE29272 was downloaded from Gene expression omnibus. Differentially expressed genes (DEGs) were identified at the cut-off of p-value ≤ 0.01. Gene ontology (GO) enrichment analysis was further performed for the DEGs, and then the binding sites of the transcriptional factors and the specific protein-protein interactions were analyzed. RESULTS: Total 1024 DEGs were screened, including 741 up-regulated genes and 283 down-regulated genes. VSNL1 (visinin-like protein-1) is expressed relatively higher in the GNCA and could be its molecular biomarker, as KRT14 (cytokeratin 14) in the GCA. GO analysis showed that the analogous cancer-relevant factors network appears in these two cancer subgroups. The DEGs in the GCA tend to be bound by SPIB and ZNF354C. FN1 lies in the center of the protein-protein interaction networks of the two cancer subgroups. CONCLUSIONS: We found out the RNA expression level of the two gastric cancers varied greatly from the normal tissues while gene expression profile of them were very similar, however, the different biomarker and transcriptional factors indicate the differences of two mechanisms.