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Conventional Al‐air batteries are not suitable as portable power devices due to their complicated water management and bulky system. To resolve this issue, the fiber paper‐ and cotton cloth‐based Al‐air batteries were proposed, which exploited the capillary force from the paper (FP) and cotton cloth (CC) to deliver the solutions and eliminated the external pump. The physical features of the FP and CC were gained including the surface morphologies, surface elementary analysis, liquid absorption and flow rates. CC owned larger liquid absorption and faster flow rate due to its hierarchically woven‐spun fiber structure, compared to the randomly oriented fibers of the FP, although the surface of the CC demonstrated lower O/C ratio than that of the FP. So, the performance of the CC‐based Al‐air battery was largely higher than that of the FP‐based battery. The performance of the CC‐based Al‐air battery was optimal at 1.0 M NaOH electrolyte and the anode‐to‐cathode surface area ratio of 1 : 4, with the peak power density of 14.95±0.28 mW cm−2, and the maximum current density of 36.61±0.54 mA cm−2. To apply the CC‐based Al‐air battery, the two‐battery pack connected in series was assembled to drive a timer and light 9 LEDs. [ABSTRACT FROM AUTHOR]

Despite evidence that MRTF-A/B, co-activators of serum response factor (SRF), promotes tumor cell invasion and metastasis in cancer, there are no studies describing MRTF-A/B in pancreatic cancer. To clarify involvement of MRTF-A/B expression in pancreatic cancer, we used quantitative reverse transcription-polymerase chain reaction and western blot analysis to detect MRTF-A/B in pancreatic cancer, intraductal papillary mucinous neoplasm (IPMN) and non-neoplastic pancreata. MRTF-A/B expression differs significantly between cancer and non-neoplastic tissues as well as between non-neoplastic tissues and IPMN bulk tissues. Next, we studied the roles of MRTF-A/B in vitro. Overexpression of MRTF-A/B promoted epithelial-mesenchymal transition (EMT) and generated stem cell-like cells in normal pancreatic cells. We performed quantitative reverse transcription-polymerase chain reaction to detect the level of MRTF-A/B in 19 pancreatic cancer cell lines. We found that their expression was associated with gemcitabine resistance. Like in normal pancreatic cells, MRTF-A/B also promoted EMT and promoted formation of stem cell-like cells in pancreatic cancer and they could regulate microRNA expression associated with EMT and CICs. Finally, to further demonstrate the roles of MRTF-A/B in vivo, we performed nude mouse model of s.c. xenograft and found that overexpression of MRTF-A and MRTF-B promoted pancreatic cancer growth. Elucidating the roles of MRTF-A/B will help us to further understand molecular basis of the disease and offer new gene targets for effective therapies.