Understanding the origins and roles of cardiac progenitor cells is important for elucidating the pathogenesis of congenital and acquired heart diseases. Moreover, manipulation of cardiac myocyte progenitors has potential for cell-based repair strategies for various myocardial disorders. Here we report the identification in mouse of a previously unknown cardiac myocyte lineage that derives from the proepicardial organ. These progenitor cells, which express the T-box transcription factor Tbx18, migrate onto the outer cardiac surface to form the epicardium, and then make a substantial contribution to myocytes in the ventricular septum and the atrial and ventricular walls. Tbx18-expressing cardiac progenitors also give rise to cardiac fibroblasts and coronary smooth muscle cells. The pluripotency of Tbx18 proepicardial cells provides a theoretical framework for applying these progenitors to effect cardiac repair and regeneration.

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As an important research area, the development of antibacterial materials has attracted extensive interest from researchers. Typical antibacterial materials involve the use of biocides and antibacterial metallic ions, such as Ag + , as well as killing by highly reactive species, such as hydroxyl radical, hydrogen peroxide and superoxide produced by the photocatalysis of TiO 2 . However, the intensive usage of biocides has a growing concern in the increase of bacterial resistance and cross-resistance to antibiotics and antibacterial Ag + depending on its dissolution property may have potential implications on human health and environment. Currently TiO 2 is mainly activated with UVA light and research on visible light photocatalysis is still under development. Recently, a new scheme using superhydrophobicity has raised more attention and interests especially for its ability in reducing bacterial adhesion. This paper provides a detailed review on the basics, recent developments, existing challenges and future perspectives of superhydrophobic surfaces especially in reducing bacterial adhesion.

Vitamin A signals play critical roles during embryonic development. In particular, heart morphogenesis depends on vitamin A signals mediated by the retinoid X receptor ␣ (RXR␣), as the systemic mutation of this receptor results in thinning of the myocardium and embryonic lethality. However, the molecular and cellular mechanisms controlled by RXR␣ signaling in this process are unclear, because a myocardium-restricted RXR␣ mutation does not perturb heart morphogenesis. Here, we analyze a series of tissuerestricted mutations of the RXR␣ gene in the cardiac neural crest, endothelial, and epicardial lineages, and we show that RXR␣ signaling in the epicardium is required for proper cardiac morphogenesis. Moreover, we detect an additional phenotype of defective coronary arteriogenesis associated with RXR␣ deficiency and identify a retinoid-dependent Wnt signaling pathway that cooperates in epicardial epithelial-to-mesenchymal transformation.coronary vessels ͉ epicardium ͉ retinoids ͉ wnt ͉ FGF