Guan Wang

Cellular reprogramming can manipulate the identity of cells to generate the desired cell types1– 3. The use of cell intrinsic components, including oocyte cytoplasm and transcription factors, can enforce somatic cell reprogramming to pluripotent stem cells4– 7. By contrast, chemical stimulation by exposure to small molecules offers an alternative approach that can manipulate cell fate in a simple and highly controllable manner8– 10. However, human somatic cells are refractory to chemical stimulation owing to their stable epigenome2,11,12 and reduced plasticity13,14; it is therefore challenging to induce human pluripotent stem cells by chemical reprogramming. Here we demonstrate, by creating an intermediate plastic state, the chemical reprogramming of human somatic cells to human chemically induced pluripotent stem cells that exhibit key features of embryonic stem cells. The whole chemical reprogramming trajectory analysis delineated the induction of the intermediate plastic state at the early stage, during which chemical-induced dedifferentiation occurred, and this process was similar to the dedifferentiation process that occurs in axolotl limb regeneration. Moreover, we identified the JNK pathway as a major barrier to chemical reprogramming, the inhibition of which was indispensable for inducing cell plasticity and a regeneration-like program by suppressing pro-inflammatory pathways. Our chemical approach provides a platform for the generation and application of human pluripotent stem cells in biomedicine. This study lays foundations for developing regenerative therapeutic strategies that use well-defined chemicals to change cell fates in humans.

Internet-enabled technologies have provided a way for people to communicate and collaborate with each other. The collaboration and communication made crowdsourcing an efficient and effective activity. Crowdsourcing is a modern paradigm that employs cheap labors for accomplishing different types of tasks. The task is usually posted online as an open call, and members of the crowd self-select a task to be carried out. Crowdsourcing involves initiators or crowdsourcers, the crowd, crowdsourcing task, the process, and the crowdsourcing platform where requesters offer various tasks and crowd workers complete these tasks. As the crowdsourcing is carried out in the online environment, it gives rise to certain challenges. The major problem is the selection of crowd that is becoming a challenging issue with the growth in crowdsourcing popularity. Crowd selection has been significantly investigated in crowdsourcing processes. Nonetheless, it has observed that the selection is based only on a single feature of the crowd worker which was not sufficient for appropriate crowd selection. For addressing the problem of crowd selection, a novel “ant colony optimization-based crowd selection method” is presented in this paper that selects a crowd worker based on multicriteria features. By utilizing the proposed model, the efficiency and effectiveness of crowdsourcing activity will be increased.

The cyclooxygenase 2 pathway has been implicated in the molecular pathogenesis of many malignancies, including lung cancer. Apricoxib, a selective COX-2 inhibitor, has been described to inhibit epithelial-mesenchymal transition in human malignancies. The mechanism by which apricoxib may alter the tumor microenvironment by affecting EMT through other important signaling pathways is poorly defined. IL-27 has been shown to have anti-tumor activity and our recent study showed that IL-27 inhibited EMT through a STAT1 dominant pathway.The purpose of this study is to investigate the role of apricoxib combined with IL-27 in inhibiting lung carcinogenesis by modulation of EMT through STAT signaling.Western blot analysis revealed that IL-27 stimulation of human non-small cell lung cancer cell lines results in STAT1 and STAT3 activation, decreased Snail protein and mesenchymal markers and a concomitant increase in expression of epithelial markers, and inhibition of cell migration. The combination of apricoxib and IL-27 resulted in augmentation of STAT1 activation. However, IL-27 mediated STAT3 activation was decreased by the addition of apricoxib. STAT1 siRNA was used to determine the involvement of STAT1 pathway in the enhanced inhibition of EMT and cell migration by the combined IL-27 and apricoxib treatment. Pretreatment of cells with STAT1 siRNA inhibited the effect of combined IL-27 and apricoxib in the activation of STAT1 and STAT3. In addition, the augmented expression of epithelial markers, decreased expression mesenchymal markers, and inhibited cell migration by the combination treatment were also inhibited by STAT1 siRNA, suggesting that the STAT1 pathway is important in the enhanced effect from the combination treatment.Combined apricoxib and IL-27 has an enhanced effect in inhibition of epithelial-mesenchymal transition and cell migration in human lung cancer cells through a STAT1 dominant pathway.

Lithium-oxygen cells are a promising power source, and carbons are an attractive non-metal catalyst for air electrodes. To improve the electrochemical performance, various carbons are heated in an inert atmosphere. It is found that heat treatment at 900 C can differently improve the electrochemical performance of multiwalled carbon nanotubes, acetylene carbon black and activated carbon, but the improvement of CNTs is the most obvious. After heat treatment, the peak current density of the oxygen reduction reaction and the 1st discharge capacity of CNTs increase ∼30% and ∼125%, respectively, while the charge transfer reaction resistance and the Warburg diffusion resistance decrease ∼7.0% and ∼11.1%, respectively. AC has the highest charge capacities and capacity retention ratio in spite of little influence by heat treatment. The possible mechanism and reasons are analyzed using different techniques. Microstructure is superior to conductivity for enhancing the rechargeability and the cyclability, and heat treatment is effective for some carbon materials in improving the electrochemical performance of Li-O2 cells. © 2014 Elsevier Ltd.