Age-related bone loss and osteoporosis are associated with bone remodeling changes that are featured with decreased trabecular and periosteal bone formation relative to bone resorption. Current anticatabolic therapies focusing on the inhibition of bone resorption may not be sufficient in the prevention or reversal of age-related bone deterioration and there is a big need in promoting osteoblastogenesis and bone formation. Enhanced understanding of the network formed by key signaling pathways and molecules regulating bone forming cells in health and diseases has therefore become highly significant. The successful development of agonist/antagonist of the PTH and Wnt signaling pathways are profits of the understanding of these key pathways. As the core component of an approved antiosteoporosis agent, strontium takes its effect on osteoblasts at multilevel through multiple pathways, representing a good example in revealing and exploring anabolic mechanisms. The recognition of strontium effects on bone has led to its expected application in a variety of biomaterial scaffolds used in tissue engineering strategies aiming at bone repairing and regeneration. While summarizing the recent progress in these respects, this review also proposes the new approaches such as systems biology in order to reveal new insights in the pathology of osteoporosis as well as possible discovery of new therapies.

We show that in the recent artificial light-harvesting experiment [Angewandte Chemie Intl. Ed. 55, 2759(2016] on organic nanocrystals self-assembled from difluoroboron chromophores, the spontaneous emission of an excited pigment should undergo a two-step process. It would first decay to an excitonic polariton confined by cavity resonance via strong photon-exciton coupling.The captive intermediate could then funnel the energy directly to doped acceptors, leading to the observed over 90% transfer efficiency at less than 1/1000 acceptor-donor ratio. Theoretical, parameter-free analyses are in quantitative agreement with the experiment. Abstract This supplementary information covers additional algebra needed for the main article published in [1]. It consists of the following parts: A. The standing-wave solutions of Maxwell equations in a rectangle cavity of homogeneous dielectric medium. B. Diagonalization of the photon-exciton coupling Hamiltonian in the rectangle cavity. C. Escape rate of the intermediate polariton out of confinement. D. Transition rate from a trapped exciton-polariton to doped acceptors.

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Background: The roles of lncRNA PLAC2 in bladder cancer (BC) were explored. Methods: The expression of PLAC2 in two types of tissue of BC patients was detected by RT-qPCR and the expression data were compared by paired t test. The 56 patients were staged according to the AJCC criteria, and 12, 15, 15 and 14 cases were classified into stage I-IV, respectively. The expression of TGF-β1 and miR-663 in BC tissues were also detected by RT-qPCR experiments. Results: Our data showed that the expression levels of PLAC2 were significantly lower in BC tissues than that in non-cancer tissues. The expression of PLAC2 was not affect by clinical stages and low expression levels of PLAC2 predicted lower survival rate. The expression of PLAC2 was positively correlated with miR-663 and inversely correlated with TGF-β1 in BC tissues. In BC cells, downregulated TGF-β1 and upregulated miR-663 were observed after the overexpression of PLAC2. Overexpression of PLAC2 also resulted in suppressed invasion and migration of BC cells. Overexpression of miR-663 resulted in downregulated TGF-β1 but did not affect the expression of PLAC2. Overexpression of TGF-β1 reduced the inhibitory effects of overexpression of PLAC2 and miR-663 on cell migration and invasion. Conclusion: PLAC2 can upregulate miR-663 to downregulate TGF-β1 and suppress BC cell migration and invasion.