Robust digital watermarking for color images in combined DFT and DT-CWT domains.

Image watermarking focuses on hiding secret data into the cover image imperceptibly to protect the copyright of the original image. In this paper, we propose a new framework of robust digital watermarking for color images using combined embedding techniques of Discrete Fourier Transform (DFT) and Dual Tree Complex Wavelet Transform (DTCWT). The cover image is first divided into Y, U and V channels. The Y channel is then transformed by DFT and partitioned into the ring shapes. With an embedding key, we generate pseudo-random patterns to represent the watermark. These patterns are also transformed and partitioned. The watermark represented by the selection of patterns is then embedded into the rings of the DFT coefficients. We further embed a rectification watermark into the U channel, in which DTCWT is applied to achieve a capability of geometric distortion resilience. On the recipient's side, the detection and extraction of watermark can be successfully done. Compared with previous schemes, the proposed method is better on preserving the image quality. Meanwhile, the robustness against typical attacks is also stronger.

Autophagy inhibition promotes gambogic acid-induced suppression of growth and apoptosis in glioblastoma cells.

OBJECTIVE: To investigate the effects of gambogic acid (GA) on the growth of human malignant glioma cells. METHODS: U251MG and U87MG human glioma cell lines were treated with GA and growth and proliferation were investigated by MTT and colony formation assays. Cell apoptosis was analyzed by annexin V FITC/PI flow cytometry, mitochondrial membrane potential assays and DAPI nuclear staining. Monodansylcadaverine (MDC) staining and GFP-LC3 localisation were used to detect autophagy. Western blotting was used to investigate the molecular changes that occurred in the course of GA treatment. RESULTS: GA treatment significantly suppressed cell proliferation and colony formation, induced apoptosis in U251 and U87MG glioblastoma cells in a time- and dose-dependent manner. GA treatment also lead to the accumulation of monodansylcadaverine (MDC) in autophagic vacuoles, upregulated expressions of Atg5, Beclin 1 and LC3-II, and the increase of punctate fluorescent signals in glioblastoma cells pre-transfected with GFP-tagged LC3 plasmid. After the combination treatment of autophagy inhitors and GA, GA mediated growth inhibition and apoptotic cell death was further potentiated. CONCLUSION: Our results suggested that autophagic responses play roles as a self-protective mechanism in GA-treated glioblastoma cells, and autophagy inhibition could be a novel adjunctive strategy for enhancing chemotherapeutic effect of GA as an anti-malignant glioma agent.