Multimodality imaging for the diagnosis of left ventricular apical hypoplasia: A case presentation and review of the literatures.

Left ventricular apical hypoplasia is a rare malformation recently described congenital abnormality characterized by: (1) truncation of the left ventricle, with the septum projecting toward the right ventricle; (2) abnormal papillary muscle originating from the flattened left ventricular apex; (3) a narrow right ventricle encompassing the periapical area of the left ventricle; (4) fatty infiltration of the apex of the left ventricle. We reported a case of LVAH and reviewed the patient's clinical presentation. And its morphologic characteristics were revealed by multimodality imaging, including echocardiography and cardiac magnetic resonance imaging. Additionally, we reviewed 41 cases from 32 reports to summarize the pathogenesis and analyzed the imaging manifestations of LVAH in this study, aiming to provide new ideas for the diagnosis and clinical management of LVAH patients.

Intestinal aberrant sphingolipid metabolism shaped-gut microbiome and bile acids metabolome in the development of hepatic steatosis.

Conjugated bile acids (CBAs) play major roles in hepatic gene regulation via nuclear S1P-inhibited histone deacetylase (HDACs). Gut microbiota modifies bile acid pool to generate CBAs and then CBAs returned to liver to regulate hepatic genes, fatty liver, and non-alcoholic fatty liver disease (NAFLD). However, it is not yet known how the gut microbiota was modified under the environment of inflammatory bowel disease (IBD). Here, we revealed that aberrant intestinal sphingosine kinases (SphKs), a major risk factor of IBD, modified gut microbiota by increasing the proportions of Firmicutes and Verrucomicrobia, which were associated with the increase in CBAs. When exposed to a high-fat diet (HFD), sphingosine kinases 2 knockout (SphK2KO) mice developed more severity of intestinal inflammation and hepatic steatosis than their wild-type (WT) littermates. Due to knockdown of nuclear SphK2, Sphk2KO mice exhibited an increase in sphingosine kinases 1 (SphK1) and sphingosine-1-phosphate (S1P) in intestinal epithelial cells. Therefore, the microbiota was modified in the environment of the SphK1/S1P-induced IBD. 16S rDNA amplicon sequencing of cecal contents indicated an increase of Firmicutes and Verrucomicrobia. Ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS) measured an increase in CBAs, including taurocholic acid (TCA), taurodeoxycholic acid (TDCA), and glycocholic acid (GCA), in cecal contents and liver tissues of Sphk2KO mice. These CBAs accumulated in the liver promoted hepatic steatosis through downregulating the acetylation of H3K9, H3K14, H3K18 and H3K27 due to the CBAs-S1PR2-nuclear SphK2-S1P signaling pathway was blocked in HFD-SphK2KO mice. In summary, intestinal aberrant sphingolipid metabolism developed hepatic steatosis through the increase in CBAs associated with an increase in Firmicutes and Verrucomicrobia.

Atypical chemokine receptor 3 induces colorectal tumorigenesis in mice by promoting ß-arrestin-NOLC1-fibrillarin-dependent rRNA biogenesis.

Atypical chemokine receptor 3 (ACKR3) has emerged as a key player in various biological processes. Its atypical "intercepting receptor" properties have established ACKR3 as the major regulator in the pathophysiological processes in many diseases. In this study, we investigated the role of ACKR3 activation in promoting colorectal tumorigenesis. We showed that ACKR3 expression levels were significantly increased in human colon cancer tissues, and high levels of ACKR3 predicted the increased severity of cancer. In Villin-ACKR3 transgenic mice with a high expression level of CKR3 in their intestinal epithelial cells, administration of AOM/DSS induced more severe colorectal tumorigenesis than their WT littermates. Cancer cells of Villin-ACKR3 transgenic mice were characterised by the nuclear ß-arrestin-1 (ß-arr1)-activated perturbation of rRNA biogenesis. In HCT116 cells, cotreatment with CXCL12 and AMD3100 selectively activated ACKR3 and induced nuclear translocation of ß-arr1, leading to an interaction of ß-arr1 with nucleolar and coiled-body phosphoprotein 1 (NOLC1). NOLC1, as the phosphorylated protein, further interacted with fibrillarin, a conserved nucleolar methyltransferase responsible for ribosomal RNA methylation in the nucleolus, thereby increasing the methylation in histone H2A and promoting rRNA transcription in ribosome biogenesis. In conclusion, ACKR3 promotes colorectal tumorigenesis through the perturbation of rRNA biogenesis by the ß-arr1-induced interaction of NOLC1 with fibrillarin.

Targeting NQO1/GPX4-mediated ferroptosis by plumbagin suppresses in vitro and in vivo glioma growth.

BACKGROUND: Ferroptosis has attracted increasing interest in cancer therapy. Emerging evidences suggest that naturally occurring naphthoquinones exhibit potent anti-glioma effects via various mechanisms. METHODS: The anti-glioma effects of plumbagin were evaluated by in vitro and in vivo experiments. Anti-glioma mechanism of plumbagin was studied by proteomics, flow cytometry, MDA assay, western blot, and RT-PCR. Gene knockdown/overexpression, molecular docking, PharmMappper database, and coimmunoprecipitation were used to study the targets of plumbagin. RESULTS: Plumbagin showed higher blood-brain barrier penetration ability than that of lapachol and shikonin and elicited significant growth inhibitory effects in vitro and in vivo. Ferroptosis was the main mechanism of plumbagin-induced cell death. Mechanistically, plumbagin significantly downregulated the protein and mRNA levels of xCT and decreased GPX4 protein levels. NAD(P)H quinone dehydrogenase 1 (NQO1) was revealed as a plumbagin predictive target using PharmMappper database and molecular docking. Plumbagin enhanced NQO1 activity and decreased xCT expression, resulting in NQO1-dependent cell death. It also induced GPX4 degradation via the lysosome pathway and caused GPX4-dependent cell death. CONCLUSIONS: Plumbagin inhibited in vitro and in vivo glioma growth via targeting NQO1/GPX4-mediated ferroptosis, which might be developed as a novel ferroptosis inducer or anti-glioma candidate.

Green synthesis of MIL-100(Fe) derivatives and revealing their structure-activity relationship for 2,4-dichlorophenol photodegradation.

MIL-100(Fe), a kind of iron-based metal-organic framework materials (MOFs), can be synthesized at room temperature or hydrothermal conditions, which are promising precursor materials for preparing photocatalysts to degrade some recalcitrant chlorophenols in industrial wastewater. However, the relationship between the structural characterization of MIL-100(Fe) derivatives and their photodegradation behavior of chlorophenol pollutants is still unclear. Thus, in this work, a porous Z-scheme α-Fe2O3/MIL-100(Fe) composite was successfully fabricated via partial-pyrolysis of MIL-100(Fe) precursor synthesized through green synthesis route, which was further used for degrading high-concentration of 2,4-dichlorophenol under visible-light illumination (λ > 420 nm). The effects of synthesis route and pyrolysis temperature of MIL-100(Fe) on the degradation efficiencies of as-derived materials for 2,4-dichlorophenol were investigated. The structure-activity relationship was illuminated in detail. Otherwise, the influence of several process factors, i.e., initial concentration and pH of the 2,4-dichlorophenol solution, catalyst dosage on the degradation efficiency of 2,4-dichlorophenol has also been performed. The removal efficiency of 2,4-dichlorophenol with the initial concentration of 100 mg L-1 reached up to 87.65% under optimized conditions. Lastly, the possible mechanism was explored based on trapping experiments and some other characterization results. The study in this paper not only exhibited new insight into the modified α-Fe2O3 material with high photocatalytic activity but also provided a promising method for treating wastewater containing 2,4-dichlorophenol or other similar organic pollutants.

Resource utilization of agricultural residues: one-step preparation of biochar derived from Pennisetum giganteum for efficiently removing chromium from water in a wide pH range.

Biochars derived from agricultural residues, Pennisetum giganteum, were prepared by a one-step activation method after impregnated with H3PO4. The effects of activation temperature and the H3PO4 impregnation method on the structure and performance of biochar were investigated. The characterization results of XPS, FTIR, and N2 adsorption-desorption showed that the P-containing biochar prepared by the one-step method had a large specific surface area, large pores, and abundant surface functional groups. And, the groups including C-P, O-P, and C-O participated in the adsorption of Cr(VI). Moreover, the target adsorbent has a good removal effect on Cr (VI) in a wide range of pH. The Cr(VI) removal efficiency was more than 55.92% at pH≤9. Interestingly, the adsorption results also showed that the adsorbent could offer acid groups for regulating the pH of the bulk solution and thus keep the adsorption surroundings in a narrow pH range. In addition, the target adsorbent has been proved to have good selective removal of Cr(VI). Even after repeated use for 5 times, the removal capacity of Cr(VI) is still 77.4%. This work provides a simple scheme for the high-value utilization of Pennisetum agricultural solid waste, and also confirms that the biochar activated by phosphoric acid can effectively remove Cr(VI) in the solution with wide pH range.

Effects of Tamoxifen vs. Toremifene on fatty liver development and lipid profiles in breast Cancer.

BACKGROUND: Tamoxifen (TAM) and Toremifene (TOR), two kinds of selective estrogen receptor modulators (SERMs), have equal efficacy in breast cancer patients. However, TAM has been proved to affect serum lipid profiles and cause fatty liver disease. The study aimed to compare the effects of TAM and TOR on fatty liver development and lipid profiles. METHODS: This study performed a retrospective analysis of 308 SERMs-treated early breast cancer patients who were matched 1:1 based on propensity scores. The follow-up period was 3 years. The primary outcomes were fatty liver detected by ultrasonography or computed tomography (CT), variation in fibrosis indexes, and serum lipid profiles change. RESULTS: The cumulative incidence rate of new-onset fatty liver was higher in the TAM group than in the TOR group (113.2 vs. 67.2 per 1000 person-years, p < 0.001), and more severe fatty livers occurred in the TAM group (25.5 vs. 7.5 per 1000 person-years, p = 0.003). According to the Kaplan-Meier curves, TAM significantly increased the risk of new-onset fatty liver (25.97% vs. 17.53%, p = 0.0243) and the severe fatty liver (5.84% vs. 1.95%, p = 0.0429). TOR decreased the risk of new-onset fatty liver by 45% (hazard ratio = 0.55, p = 0.020) and showed lower fibrotic burden, independent of obesity, lipid, and liver enzyme levels. TOR increased triglycerides less than TAM, and TOR increased high-density lipoprotein cholesterol, while TAM did the opposite. No significant differences in total cholesterol and low-density lipoprotein cholesterol are observed between the two groups. CONCLUSIONS: TAM treatment is significantly associated with more severe fatty liver disease and liver fibrosis, while TOR is associated with an overall improvement in lipid profiles, which supports continuous monitoring of liver imaging and serum lipid levels during SERM treatment.

Myricetin and M10, a myricetin-3-O-ß-d-lactose sodium salt, modify composition of gut microbiota in mice with ulcerative colitis.

Our previous studies found that M10, a myricetin-3-O-ß-d-lactose sodium salt, possessed higher effects of ameliorating ulcerative colitis (UC) than Myricetin in mice. Here, we aim to investigate whether the inhibition of UC is the consequence of the effects of M10 that leads to the changed microbiota. Mice model of UC was induced by dextran sulfate sodium (DSS) treatment. M10 and Myricetin were orally administrated for 12 weeks. We performed 16S rDNA sequencing assay to analyze the composition of gut microbiota isolated from ileocecum. Both M10 and Myricetin normalized the composition of Firmicutes and Actinobacteria as healthy mice had. At genus level, the effects of M10 and Myricetin on colitis were associated to the increase of probiotics, such as Akkermansia, and the inhibition of pathogenic microorganisms, such as Ruminococcus and Parabacteroides. M10 had stronger activity than Myricetin in the improvement of biosynthesis and degradation activities, resulting to increasing metabolism of sulfur, pyruvate, steroid biosynthesis and unsaturated fatty acid biosynthesis in gut. Furthermore, M10 normalized the proportion of Firmicutes and Actinobacteria in gut microbiota. It suggests that the improvements in UC are the consequence of the effect of M10 that leads to the changed intestinal microbiota. Conclusion: M10 contributed the pharmacological effects on UC by modification of the intestinal microbiota.

From wastes to functions: A paper mill sludge-based calcium-containing porous biochar adsorbent for phosphorus removal.

With the increased awareness of reusing solid wastes for higher sustainability and the concern of water pollution associated with phosphorus over-emission, there are strong interests in developing solid waste based adsorbents for purifying phosphorus-containing wastewater. As a rich calcium resource, paper mill sludge (i.e., a major solid waste from pulping industry) can be used as phosphorus removal adsorbent after calcination. Thus, in this work, a simple and clean thermally treating route has been proposed for preparing calcium-containing biochar from paper mill sludge. The effect of the physicochemical properties of paper mill sludge and its carbonization condition on phosphorus adsorption has been analyzed. Moreover, the influence of some key adsorption parameters, e.g., biochar dosage, initial pH of solution, co-existing anions, initial phosphorus concentration and contact time has also been investigated. The results showed that the phosphorus adsorption data could be fitted well with pseudo-second-order kinetic and Langmuir isothermal models. The calculated maximum adsorption capacity of the as-prepared optimal calcium-containing biochar could reach to 68.49 mg·g-1 at 25 °C. Combined with the characterization results, it can be reasonably inferred that the adsorption process was chemisorption-dominated. Lastly, the application of this spent adsorbent in agriculture field has also been discussed. In brief, this work provided a feasible strategy for converting paper mill solid waste to an environmental functional material (i.e., calcium-rich biochar) for remediation of eutrophic water.

Synthesis of NiMo/La-Al2O3 powders for efficient catalytic transesterification of triglyceride with the high yield of 95.2.

Enhancement of the transesterification efficiency of triglyceride has come under heated study in biodiesel-making industry. In this research, the NiMo/La-Al2O3 nanopowders have been prepared for producing biodiesel efficiently. The screening test showed that the NiMo/La-Al2O3 catalyst has the best catalytic activity for triglyceride transesterification. Besides, the process parameters including reaction temperature, time, oil-to-alcohol ratio and catalyst loading etc., also have been investigated for optimization of the transesterification process. The results showed that with 5 wt% of catalyst loading, and oil to methanol molar ratio of 1:9, the conversion yield of triglyceride could be up to 95.2% within 120 min at 160°C. The NiMo/La-Al2O3 catalyst has the outstanding recycle property, which proved that the prepared NiMo/La-Al2O3 powders can be suitable for biodiesels' production.

Long Non-Coding RNA NLIPMT as a Tumor Suppressor and Inhibitor of Cell Proliferation and Metastasis in Papillary Thyroid Carcinoma.

INTRODUCTION: Gene expression association studies of tumor samples have uncovered several long non-coding RNAs (lncRNAs) closely related to various types of cancer. Several lncRNAs have been reported to play essential roles in the progression of papillary thyroid carcinoma (PTC). Novel lncRNA inhibiting proliferation and metastasis (lnc-NLIPMT) is a known regulator of mammary cell proliferation and motility, but its involvement in PTC is unclear. MATERIALS AND METHODS: We investigated the role of lnc-NLIPMT in PTC by quantitative real-time polymerase chain reaction (qRT-PCR) on various PTC tissue samples and cell lines. We assessed the effects of overexpression or knockdown of lnc-NLIPMT on the proliferation, migration, and invasion of PTC cells using CCK-8, cell clone formation, and transwell assays. Changes in the expression of N-cadherin and vimentin were detected by immunoblotting. RESULTS: Our results revealed a downregulation of the expression of lnc-NLIPMT in PTC and a negative correlation between lnc-NLIPMT expression and tumor size (P=0.006). Overexpression of lnc-NLIPMT in TPC-1 and B-CPAP cells significantly suppressed cell proliferation, migration, and invasion, while lnc-NLIPMT knockdown had the opposite effect. In addition, lnc-NLIPMT played an important role in the regulation of the expression of N-cadherin and vimentin. CONCLUSION: lnc-NLIPMT inhibits cell proliferation and metastasis of PTC cells and is a potential diagnostic and prognostic biomarker in PTC.

M10, a Myricetin-3-O-b-D-Lactose Sodium Salt, Prevents Ulcerative Colitis Through Inhibiting Necroptosis in Mice.

BACKGROUND: M10 is a derivative of Myricetin by adding a hydrophilic glycosylation group. Our previous study revealed that M10 by oral administration prevented colitis-associated colonic cancer (CAC) through attenuating endoplasmic reticulum stress in mice. In current study, we evaluated the inhibitory effects of M10 on ulcerative colitis in mice model, the mechanism of M10 in preventing colitis was further investigated. METHODS: Mice model of ulcerative colitis was induced by continuous oral dextran sodium sulfate (DSS). M10 was given gavage once a day for 12 consecutive weeks. Disease activity index (DAI) was recorded by analyzing the symptoms of colitis. Intestinal barrier was analyzed by the Immunofluorescence staining assay. The structure of microvilli of intestinal epithelial cells was analyzed under Transmission electron microscopy (TEM). TEM assay was also performed to determine the formation of necroptosis in the colonic epithelium with ulcerative colitis. We performed Western blotting assay to analyze the IL-6 and NF-κB pathways, as well as the cytokine cascades related to TNF-α signaling pathway during necroptosis. RESULTS: M10 by oral administration demonstrated a prevention of ulcerative colitis, showing a significant decrease of DAI as compared to the model mice. Pathological analysis indicated that M10 attenuated the degree of colonic inflammation in colonic tissues. M10 restored the structures of intestinal barrier damaged by DSS. M10 prevented the activation of the IL-6 and NF-κB signaling pathways in the inflamed colonic epithelium. Further, M10 prevented necroptosis in the inflamed colonic mucosal cells through down-regulating the TNF-α pathway. Importantly, M10 demonstrated higher activities in preventing ulcerative colitis than Myricetin and control drug Mesalazine. CONCLUSIONS: Myricetin derivative M10 prevents chronic ulcerative colitis through inhibiting necroptosis. M10 could be developed as a promising drug for the treatment of chronic ulcerative colitis.

Value-added utilization of paper sludge: Preparing activated carbon for efficient adsorption of Cr(VI) and further hydrogenation of furfural.

After normal alkali treatment process, the industrial Cr(VI) containing wastewater still contains a ppm level of Cr(VI) ions which should be further purified before discharging. In this study, the Cr(VI)-containing wastewater has been efficiently treated by the porous paper sludge-based activated carbon (psAC) with an excellent specific surface area and rich oxygen functional groups. The batch experimental results showed that under acidic conditions, pH has little effect on the Cr(VI) removal. The kinetic and isotherms studies showed that the Elovich and Freundlich model could describe the adsorption process well and the maximum adsorption capacity of psAC was 54.04 mg/g. The thermodynamic studies indicated that the reaction process was endothermic and spontaneous. Adsorption enthalpy was 17.37 kJ/mol, showing that the chemisorption process was a hydrogen bonding-controlled that has been also verified by some analytical techniques. Lastly, this study also provided an idea for reutilization of waster Cr(VI)-contained psAC in furfural hydrogenation.

SphK2 confers 5-fluorouracil resistance to colorectal cancer via upregulating H3K56ac-mediated DPD expression.

Aberrant sphingolipid metabolism has been implicated in chemoresistance, but the underlying mechanisms are still poorly understood. Herein we revealed a previously unrecognized mechanism of 5-fluorouracil (5-FU) resistance contributed by high SphK2-upregulated dihydropyrimidine dehydrogenase (DPD) in colorectal cancer (CRC), which is evidenced from human CRC specimens, animal models, and cancer cell lines. TMA samples from randomly selected 60 CRC specimens firstly identified the clinical correlation between high SphK2 and increased DPD (p < 0.001). Then the regulatory mechanism was explored in CRC models of villin-SphK2 Tg mice, SphK2-/-mice, and human CRC cells xenografted nude mice. Assays of ChIP-Seq and luciferase reporter gene demonstrated that high SphK2 upregulated DPD through promoting the HDAC1-mediated H3K56ac, leading to the degradation of intracellular 5-FU into inactive α-fluoro-ß-alanine (FBAL). Lastly, inhibition of SphK2 by SLR080811 exhibited excellent inhibition on DPD expression and potently reversed 5-FU resistance in colorectal tumors of villin-SphK2 Tg mice. Overall, this study manifests that SphK2high conferred 5-FU resistance through upregulating tumoral DPD, which highlights the strategies of blocking SphK2 to overcome 5-FU resistance in CRC.

CXCL12/CXCR4 promotes inflammation-driven colorectal cancer progression through activation of RhoA signaling by sponging miR-133a-3p.

BACKGROUND: Activation of CXCL12/CXCR4 axis has been found to be associated with invasion and metastasis in many cancers. However, the underlying mechanism remains elusive. Increasing data highlight that non-coding RNAs are linked to CRC progression. METHODS: The effects of CXCR4 were investigated using villin-CXCR4 transgenic mice model by flow cytometry assay, immunohistochemistry, and Western blot. The mechanism was explored through bioinformatics, luciferase reporter assay and RNA immunoprecipitation assay. RESULTS: We found that high CXCR4 expression exacerbated colitis-associated cancer in villin-CXCR4 transgenic mice. CXCR4+/-Apcmin/+ compound mutant mice demonstrated higher colorectal tumorigenesis than Apcmin/+ mice. Furthermore, overexpression of CXCR4 was found to promote the epithelial-mesenchymal transition (EMT) and infiltration of myeloid-derived suppressor cells (MDSCs) and macrophages in colonic tissue, accelerating colitis-associated and Apc mutation-driven colorectal tumorigenesis and progression. Notably, miR-133a-3p was found to be significantly decreased in HCT116 cells overexpressing CXCR4 by miRNA sequencing. miR-133a-3p was proved to target RhoA, which is involved in cytoskeletal reorganization that drive cell motility. Importantly, CXCL12/CXCR4-induced upregulation of lncRNA XIST functioned as a ceRNA to sponge miR-133a-3p, thereby liberating the repression of RhoA by miR-133a-3p. The negative correlation of miR-133a-3p with RhoA was also confirmed in human CRC tissues and CXCR4+/- mice. CONCLUSIONS: Our findings revealed the critical role of CXCR4 in promoting progression of inflammatory colorectal cancer through recruiting immunocytes and enhancing cytoskeletal remodeling by lncRNA XIST/ miR-133a-3p/ RhoA signaling. These results provide novel potential therapeutic targets for hindering CXCL12/CXCR4-induced CRC progression.

Overexpression of novel lncRNA NLIPMT inhibits metastasis by reducing phosphorylated glycogen synthase kinase 3ß in breast cancer.

Long noncoding RNAs (lncRNAs) are considered as regulators of gene expression in cancers. However, cancer profiling has little focused on noncoding genes. Here, we reported that RP11-115N4.1 (here renamed novel lncRNA inhibiting proliferation and metastasis [NLIPMT]) was downregulated in breast cancer tissues. Ectopic expression of NLIPMT inhibited mammary cell proliferation, motility in vitro. Moreover, lnc-NLIPMT reduced the growth of implanted MDA-MB-231 cells in vivo. Mechanistically, glycogen synthase kinase 3ß (GSK3ß) was identified as an effector protein regulated by lnc-NLIPMT. Inhibition of GSK3ß activity restored NLIPMT-induced inhibition of proliferation and motility in breast cancer cells. These data reveal that lnc-NLIPMT functions as a driver of breast cancer progression and might serve as a potential target for antimetastatic therapies.

Enhanced removal of Cr(VI) from aqueous solution by supported ZnO nanoparticles on biochar derived from waste water hyacinth.

Biochar derived from waste water hyacinth was prepared and modified by ZnO nanoparticles for Cr(VI) removal from aqueous solution with the aim of Cr(VI) removal and management of waste biomass. The effect of carbonization temperature (500-800 °C), ZnO content (10-50 wt%) loaded on biochar and contact time (0.17-14 h) on the Cr(VI) removal were investigated. It was found that higher than 95% removal efficiency of Cr(VI) can be achieved with the biochar loaded 30 wt% ZnO. The adsorption kinetics of the sorbent is consistent with the pseudo-second-order kinetic model and adsorption isotherm follows the Langmuir model with maximum adsorption capacity of 43.48 mg g-1 for Cr(VI). Multiple techniques such as XRD, XPS, SEM, EDX and FT-IR were performed to investigate the possible mechanisms involved in the Cr (VI) adsorption. The results show that there is precipitation between chromium ions and Zn oxide. Furthermore, the ZnO nanoparticles acts as photo-catalyst to generate photo-generated electrons to enhance the reduction of Cr(VI) to Cr(III). The as-prepared ZnO/BC possess good recyclability and the removal ratio remained at about 70% in the fifth cycle, which suggests that both contaminants removal and effective management of water hyacinth can be achieved by the approach.

Enhanced Performance of a Lithium-Sulfur Battery Using a Carbonate-Based Electrolyte.

The lithium-sulfur battery is regarded as one of the most promising candidates for lithium-metal batteries with high energy density. However, dendrite Li formation and low cycle efficiency of the Li anode as well as unstable sulfur based cathode still hinder its practical application. Herein a novel electrolyte (1 m LiODFB/EC-DMC-FEC) is designed not only to address the above problems of Li anode but also to match sulfur cathode perfectly, leading to extraordinary electrochemical performances. Using this electrolyte, lithium|lithium cells can cycle stably for above 2000 hours and the average Coulumbic efficiency reaches 98.8 %. Moreover, the Li-S battery delivers a reversible capacity of about 1400 mAh g(-1) sulfur with retention of 89 % for 1100 cycles at 1 C, and a capacity above 1100 mAh g(-1) sulfur at 10 C. The more advantages of this cell system are its outstanding cycle stability at 60 °C and no self-discharge phenomena.

A new ether-based electrolyte for dendrite-free lithium-metal based rechargeable batteries.

A new ether-based electrolyte to match lithium metal electrode is prepared by introducing 1, 4-dioxane as co-solvent into lithium bis(fluorosulfonyl)imide/1,2-dimethoxyethane solution. Under the synergetic effect of solvents and salt, this simple liquid electrolyte presents stable Li cycling with dendrite-free Li deposition even at relatively high current rate, high coulombic efficiency of ca. 98%, and good anodic stability up to ~4.87 V vs Li RE. Its excellent performance will open up a new possibility for high energy-density rechargeable Li metal battery system.