In this paper we report the growth and superconductivity of N axT aS2 crystals. The structural data deduced from X-ray diffraction pattern shows that the sample has the same structure as 2H − T aS2. A series of crystals with different superconducting transition temperatures (Tc) ranging from 2.5 K to 4.4 K were obtained. It is found that the Tc rises with the increase of N a content determined by Energy-Dispersive x-ray microanalysis(EDX) of Scanning Electron Microscope (SEM) on these crystals. Compared with the resistivity curve of un-intercalated sample 2H − T aS2 (Tc = 0.8 K, TCDW ≈ 70 K), no signal of charge density wave (CDW) was observed in samples N a0.1T aS2 and N a0.05T aS2. However, in some samples with lower Tc, the CDW appears again at about 65 K. Comparison between the anisotropic resistivity indicates that the anisotropy becomes smaller in samples with more N a intercalation (albeit a weak semiconducting behavior along c-axis) and thus higher Tc. It is thus concluded that there is a competition between the superconductivity and the CDW. With the increase of sodium content, the rise of Tc in N axT aS2 is caused mainly by the suppression to the CDW in 2H − T aS2, and the conventional rigid band model for layered dichalcogenide may be inadequate to explain the changes induced by the slight intercalation of sodium in 2H − T aS2.

The role of M2 macrophages in the resolution and fibroproliferation of acute lung injury (ALI) is poorly understood. In this study, we investigated the effects of two M2 macrophage subtypes, M2a induced by interleukin (IL)-4/IL-13 and M2c induced by IL-10/transforming growth factor -β, on the pathogenesis of ALI. M2a and M2c were adoptively transferred into lipopolysaccharide-induced ALI mice model. Data showed that Vybrant-labeled macrophages appeared in the lungs of ALI mice. Subsequently, we observed that both subsets significantly reduced lung inflammation and injury including a reduction of neutrophil influx into the lung and an augmentation of apoptosis. Interestingly, M2c macrophages more effectively suppressed indices of lung injury than M2a macrophages. M2c macrophages were also more effective than M2a in reduction of lung fibrosis. In addition, we found that M2c but not M2a macrophages increased IL-10 level in lung tissues of the recipient ALI mice partially mediated by activating the JAK1/STAT3/suppressor of cytokine signaling 3 signaling pathway. After blocking IL-10, these superior effects of M2c over M2a were abolished. These data imply that M2c are more potent than M2a macrophages in protecting against lung injury and subsequent fibrosis due to their ability to produce IL-10. Therefore, reprogramming macrophages to M2c subset may be a novel treatment modality with transitional potential.

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