Enhancing extraction of light from metal composite structures for plasmonic emitters using light-coupling effect.

This work demonstrates the efficiency and directionality of a method of extracting light from thin-film emissive devices by near-field evanescent waves in plasmonic emitters used in metal composite grating structures. A near-field evanescent wave can induce a surface plasmon wave on the surface of a metal under resonant conditions. Enhancing the near-field evanescent wave generates strong far-field nonlinear optical effects. This effect is highly efficient in some plasmonic emitter structures. Theoretical and experimental results demonstrate that such a metal composite grating structure exhibits good performance, a high coupling ratio, a small coupling angle, enhanced light extraction and a small FWHM. It also improves luminous efficiency, emitter angle, and directivity.

The migration speed of cancer cells influenced by macrophages and myofibroblasts co-cultured in a microfluidic chip.

We employ a microfluidic chip with three culture chambers to investigate the interactions among lung cancer cells, macrophages and myofibroblasts. By mixing the conditioned media of macrophages and myofibroblasts in this chip, we confirm that these two stromal cells have synergistic effects in accelerating the migration of cancer cells. However, as the myofibroblasts are pretreated with the conditioned medium of macrophages, the myofibroblasts' ability to enhance the migration of cancer cells is lowered. The tumour necrosis factor-α produced by macrophages reduces the expression of α-smooth muscle actin and the secretion of transforming growth factor-ß1 in myofibroblasts. Once the tumour necrosis factor-α in the macrophage conditioned medium is neutralized, the macrophage medium-pretreated myofibroblasts can still accelerate the migration of cancer cells.

Analysis of the paracrine loop between cancer cells and fibroblasts using a microfluidic chip.

We use a microfluidic cell culture chip equipped with pneumatic microvalves to analyze the paracrine loop between lung cancer cells and fibroblasts. In order to assess the cellular responses in the paracrine loop, we measure the migration speeds of cancer cells and the aspect ratios of fibroblasts which reflect the phenotype of myofibroblasts. With well-controlled interaction sequences between these two types of cells, we verify that the cytokines from cancer cells effectively stimulate the fibroblasts into myofibroblasts. The cytokines from myofibroblasts, rather than fibroblasts, increase the migration speeds of cancer cells. We confirm that the transforming growth factor-ß1 (TGF-ß1) is involved in the interaction between cancer cells and fibroblasts, and we also interrupt this paracrine loop in the cell culture chip by inhibiting the TGF-ß1 receptors on fibroblasts.