Fast-charging aluminium-chalcogen batteries resistant to dendritic shorting.

Although batteries fitted with a metal negative electrode are attractive for their higher energy density and lower complexity, the latter making them more easily recyclable, the threat of cell shorting by dendrites has stalled deployment of the technology1,2. Here we disclose a bidirectional, rapidly charging aluminium-chalcogen battery operating with a molten-salt electrolyte composed of NaCl-KCl-AlCl3. Formulated with high levels of AlCl3, these chloroaluminate melts contain catenated AlnCl3n+1- species, for example, Al2Cl7-, Al3Cl10- and Al4Cl13-, which with their Al-Cl-Al linkages confer facile Al3+ desolvation kinetics resulting in high faradaic exchange currents, to form the foundation for high-rate charging of the battery. This chemistry is distinguished from other aluminium batteries in the choice of a positive elemental-chalcogen electrode as opposed to various low-capacity compound formulations3-6, and in the choice of a molten-salt electrolyte as opposed to room-temperature ionic liquids that induce high polarization7-12. We show that the multi-step conversion pathway between aluminium and chalcogen allows rapid charging at up to 200C, and the battery endures hundreds of cycles at very high charging rates without aluminium dendrite formation. Importantly for scalability, the cell-level cost of the aluminium-sulfur battery is projected to be less than one-sixth that of current lithium-ion technologies. Composed of earth-abundant elements that can be ethically sourced and operated at moderately elevated temperatures just above the boiling point of water, this chemistry has all the requisites of a low-cost, rechargeable, fire-resistant, recyclable battery.

Large dynamic range dual-mode pH sensors via dye-doped ionic liquid fiber optofluidic lasers.

We report a fiber optofluidic laser (FOFL) using an RhB-doped ionic liquid (BmimPF6) as the gain medium and explore its application for large dynamic range highly sensitive pH sensing. Due to the high Q-factor of the FOFL and the unique merits of BmimPF6, lasing emission presents a threshold of only 0.61 µJ mm-1. Particularly, lasing emission behaviors are strongly dependent on the pH value of the gain medium, i.e., in the pH range 4.28-6.37, the lasing central wavelength blue-shifts monotonically with a sensitivity as high as 5.02 nm per pH unit, which we attribute to the conversion of the cationic form of RhB to the zwitterionic form caused by the deprotonation of the COOH group. Under alkaline conditions (pH 7.20-11.17), the lasing emission intensity exhibits a significant decrease and the corresponding lasing central wavelength is also blue-shifted due to the solvent effect. The sensitivity based on the wavelength shift is 3.03 nm per pH unit, which is 4-fold higher than that of fluorescence-based sensing, while the sensitivity based on the variation of the lasing emission intensity is almost three orders of magnitude higher than that of fluorescence-based sensing. Our work presents a novel dual sensing paradigm in response to different pH conditions, which can greatly improve the reliability and discrimination of pH sensing.

Comprehensive role of prostate-specific antigen identified with proteomic analysis in prostate cancer.

Current treatments including androgen deprivation fail to prevent prostate cancer (PrCa) from progressing to castration-resistant PrCa (CRPC). Accumulating evidence highlights the relevance of prostate-specific antigen (PSA) in the development and progression of PrCa. The underlying mechanism whereby PSA functions in PrCa, however, has yet been elucidated. We demonstrated that PSA knockdown attenuated tumorigenesis and metastasis of PrCa C4-2 cells in vitro and in vivo, whereas promoted the apoptosis in vitro. To illuminate the comprehensive role of PSA in PrCa, we performed an isobaric tag for relative and absolute quantitation (iTRAQ)-based proteomic analysis to explore the proteomic change induced by PSA knockdown. Among 121 differentially expressed proteins, 67 proteins were up-regulated, while 54 proteins down-regulated. Bioinformatics analysis was used to explore the mechanism through which PSA exerts influence on PrCa. Protein-protein interaction analysis showed that PSA may mediate POTEF, EPHA3, RAD51C, HPGD and MCM4 to promote the initiation and progression of PrCa. We confirmed that PSA knockdown induced the up-regulation of MCM4 and RAD51C, while it down-regulated POTEF and EPHA3; meanwhile, MCM4 was higher in PrCa para-cancerous tissue than in cancerous tissue, suggesting that PSA may facilitate the tumorigenesis by mediating MCM4. Our findings suggest that PSA plays a comprehensive role in the development and progression of PrCa.

Overexpression of immunoglobulin G prompts cell proliferation and inhibits cell apoptosis in human urothelial carcinoma.

Only B lymphocytes can express immunoglobulins according to the traditional immunological theories, and the expression of immunoglobulin G (IgG) messenger RNA (mRNA) and protein was found in certain human cancer cells recently. However, the expression pattern of IgG and its possible role in human urothelial carcinoma are still elusive. In this study, we investigated the expression of IgG in two human urothelial carcinoma cell lines, T24 and BIU-87, and in 56 cases of clinical urothelial carcinoma tissues. The mRNA of IgG was positively detected by in situ hybridization and reverse transcription PCR; furthermore, IgG protein was also positively detected by immunohistochemistry and Western blot. Moreover, blockade of tumor-derived IgG by either antihuman IgG antibody or antisense oligonucleotides increased cell apoptosis and inhibited cell growth in bladder cancer cell lines in vitro, and antihuman IgG antibody could suppress the growth of xenotransplant tumor in vivo. In addition, either antihuman IgG antibody or antisense oligonucleotides enhanced the sensitivity to mitomycin C in bladder cancer cell line T24. Furthermore, blockade of IgG in bladder cancer cell T24 resulted in upregulation of cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase. Our results indicated that bladder cancer cells were capable of expressing IgG, and blockade of IgG expression induced cell apoptosis through activation of caspase-dependent pathway. A novel potential targeted therapy for bladder cancer will be possibly developed based on these data.

Activation-Induced Cytidine Deaminase Expression Facilitates the Malignant Phenotype and Epithelial-to-Mesenchymal Transition in Clear Cell Renal Cell Carcinoma.

Although advances have been made in the development of antiangiogenesis targeted therapy and surgery, metastatic clear cell renal cell carcinoma (ccRCC) is still incurable. Activation-induced cytidine deaminase (AID) is mainly expressed in a variety of germ and somatic cells, and induces somatic hypermutation and class-switch recombination, playing a vital role in antibody diversification. We confirmed that AID was expressed at a higher level in ccRCC tissues than in the corresponding nontumor renal tissues. We explored the impact of AID on ccRCC proliferation, invasion, and migration. In 769-p and 786-0 cells, expression of an AID-specific short hairpin RNA significantly reduced AID expression, which markedly inhibited tumor cell invasion, proliferation, and migration. Previous studies showed that AID is associated with Wnt ligand secretion mediator (WLS/GPR177), cyclin-dependent kinase 4 (CDK4), and stromal cell-derived factor-1 (SDF-1/CXCL12) regulation, which was further confirmed in human ccRCC tissues. Therefore, we studied the relationship between AID and these three molecules, and the impact of AID on epithelial-to-mesenchymal transition in ccRCC. WLS/GPR177, SDF-1/CXCL12, and CDK4 were sensitive to 5-azacytidine (a DNA demethylation agent), which reverted the inhibition of carcinogenesis caused by AID repression. In summary, AID is an oncogene that might induce tumorigenesis through DNA demethylation. Targeting AID may represent a novel therapeutic approach to treat metastatic ccRCC.

AID modulates carcinogenesis network via DNA demethylation in bladder urothelial cell carcinoma.

Bladder cancer is one of the most common malignant diseases in the urinary system, with poor survival after metastasis. Activation-induced cytidine deaminase (AID), a versatile enzyme involved in antibody diversification, is an oncogenic gene that induces somatic hypermutation and class-switch recombination (CSR). However, the contribution of AID-mediated DNA demethylation to bladder urothelial cell carcinoma (BUCC) remains unclear. Herein, we evaluated the impact on BUCC caused by AID and explored the gene network downstream of AID by using a proteomic approach. Lentiviral vector containing AID-specific shRNA significantly reduced AID expression in T24 and 5637 cells. Silencing AID expression remarkably inhibited tumour malignancies, including cell proliferation, invasion and migration. We used Isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomics analysis technology to study the underpinning mechanism in monoclonal T24 cells, with or without AID knockdown. Among the 6452 proteins identified, 99 and 142 proteins in shAICDA-T24 cells were significantly up- or downregulated, respectively (1.2-fold change) compared with the NC-T24 control. After a pipeline of bioinformatics analyses, we identified three tumour-associated factors, namely, matrix metallopeptidase 14 (MMP14), C-X-C motif chemokine ligand 12 and wntless Wnt ligand secretion mediator, which were further confirmed in human BUCC tissues. Nonetheless, only MMP14 was sensitive to the DNA demethylation molecule 5-aza-2'-deoxycytidine (5-azadC; 5 µM), which reversed the inhibition of carcinogenesis by AID silence in T24 and 5637 cells. Overall, AID is an oncogene that mediates tumourigenesis via DNA demethylation. Our findings provide novel insights into the clinical treatment for BUCC.

Efficient Compact-Layer-Free, Hole-Conductor-Free, Fully Printable Mesoscopic Perovskite Solar Cell.

A compact-layer-free, hole-conductor-free, fully printable mesoscopic perovskite solar cell presents a power conversion efficiency of over 13%, which is comparable to that of the device with a TiO2 compact layer. The different wettability of the perovskite precursor solution on the surface of FTO and TiO2 possesses a significant effect on realizing efficient mesoscopic perovskite solar cell. This result shows a promising future in printable solar cells by further simplifying the fabrication process and lowering the preparation costs.