Recovering Sign Bits of DCT Coefficients in Digital Images as an Optimization Problem

Recovering unknown, missing, damaged, distorted or lost information in DCT coefficients is a common task in multiple applications of digital image processing, including image compression, selective image encryption, and image communications. This paper investigates recovery of a special type of information in DCT coefficients of digital images: sign bits. This problem can be modelled as a mixed integer linear programming (MILP) problem, which is NP-hard in general. To efficiently solve the problem, we propose two approximation methods: 1) a relaxation-based method that convert the MILP problem to a linear programming (LP) problem; 2) a divide-and-conquer method which splits the target image into sufficiently small regions, each of which can be more efficiently solved as an MILP problem, and then conducts a global optimization phase as a smaller MILP problem or an LP problem to maximize smoothness across different regions. To the best of our knowledge, we are the first who considered how to use global optimization to recover sign bits of DCT coefficients. We considered how the proposed methods can be applied to JPEG-encoded images and conducted extensive experiments to validate the performances of our proposed methods. The experimental results showed that the proposed methods worked well, especially when the number of unknown sign bits per DCT block is not too large. Compared with other existing methods, which are all based on simple error-concealment strategies, our proposed methods outperformed them with a substantial margin, both according to objective quality metrics (PSNR and SSIM) and also our subjective evaluation. Our work has a number of profound implications, e.g., more sign bits can be discarded to develop more efficient image compression methods, and image encryption methods based on sign bit encryption can be less secure than we previously understood.Comment: 13 pages, 8 figure

Acquisition or greenfield entry into Africa? Responding to institutional dynamics in an emerging continent

Research Summary The dynamic development of a host country's institutional and factor market conditions is a critical consideration for multinational enterprises when entering emerging countries. By studying 2,245 foreign direct investments into Africa during the period 2008–2013, we find that MNEs are more likely to enter African countries that have formal institutions that are rapidly improving via greenfield investments. This is especially true for those MNEs with prior investment experience in Africa or with local government connections. We also find that acquisition modes are more likely to be adopted in African countries with rapidly improving factor market conditions, especially by MNEs with local government connections. We promote a dynamic perspective for MNEs for assessing business opportunities and entry modes in Africa. Managerial summary Foreign direct investment establishment mode literature has focused on the impact of unidimensional measures of institutional status, despite that institutional environments in emerging economies undergo substantial and continuous changes in multiple dimensions. This study integrates the dynamic institution-based view with the theoretical construct of institutional competitive advantages to examine the heterogeneous strategic responses of investing firms to host country institutional dynamics. Empirical results from 2,245 FDIs into Africa during the period 2008–2013 show that multinational enterprises MNEs are more likely to adopt: (1) a greenfield mode in countries with rapid development of formal institutions; and (2) an acquisition mode in countries with rapid development of factor markets. Moreover, the regional experience of MNEs strengthens the first effect, while the institutional ties strengthen both effects.This project was funded by research grants from CIBER University of South Carolina and the National Natural Science Foundation of China (71472038

Brassinosteroids regulate root meristem development by mediating BIN2-UPB1 module in Arabidopsis.

Plant steroid hormones brassinosteroids (BRs) regulate plant growth and development at many levels. While negative regulatory factors that inhibit development and are counteracted by BRs exist in the root meristem, these factors have not been characterized. The functions of UPB1 transcription factor in BR-regulated root growth have not been established, although its role in regulating root are well documented. Here, we found that BIN2 interacts with and phosphorylates the UPB1 transcription factor consequently promoting UPB1 stability and transcriptional activity. Genetic analysis revealed that UPB1 deficiency could partially recover the short-root phenotype of BR-deficient mutants. Expression of a mutated UPB1S37AS41A protein lacking a conserved BIN2 phosphorylation sites can rescue shorter root phenotype of bin2-1 mutant. In addition, UPB1 was repressed by BES1 at the transcriptional level. The paclobutrazol-resistant protein family (PRE2/3) interacts with UPB1 and inhibits its transcriptional activity to promote root meristem development, and BIN2-mediated phosphorylation of UPB1 suppresses its interaction with PRE2/3, and subsequently impairing root meristem development. Taken together, our data elucidate a molecular mechanism by which BR promotes root growth via inhibiting BIN2-UPB1 module

Electric Eel-Skin-Inspired Mechanically Durable and Super-Stretchable Nanogenerator for Deformable Power Source and Fully Autonomous Conformable Electronic-Skin Applications

Electric eel-skin-inspired mechanically durable and super-stretchable nanogenerator is demonstrated for the first time by using triboelectric effect. This newly designed nanogenerator can produce electricity by touch or tapping despite under various extreme mechanical deformations or even after experiencing damage. This device can be used not only as deformable and wearable power source but also as fully autonomous and self-sufficient adaptive electronic skin system

Light-Triggered Pyroelectric Nanogenerator Based on a pn-Junction for Self-Powered Near-Infrared Photosensing

A nanogenerator, as a self-powered system, can operate without an external power supply for energy harvesting, signal processing, and active sensing. Here, near-infrared (NIR) photothermal triggered pyroelectric nanogenerators based on pn-junctions are demonstrated in a p-Si/n-ZnO nanowire (NW) heterostructure for self-powered NIR photosensing. The pyroelectric-polarization potential (pyro-potential) induced within wurtzite ZnO NWs couples with the built-in electric field of the pn-junction. At the moment of turning on or off the NIR illumination, external current flow is induced by the time-varying internal electric field of the pn-heterostructure, which enables a bias-free operation of the photodetectors (PDs). The NIR PD exhibits a high on/off photocurrent ratio up to 10⁷ and a fast photoresponse component with a rise time of 15 μs and a fall time of 21 μs. This work provides an unconventional strategy to achieve active NIR sensing, which may find promising applications in biological imaging, optoelectronic communications, and optothermal detections

Triptolide attenuates pulmonary fibrosis by inhibiting fibrotic extracellular matrix remodeling mediated by MMPs/LOX/integrin

Background: Fibrotic extracellular matrix (ECM) remodeling characterized different types of pulmonary fibrosis, and its regulation could be a potential shared treatment strategy for pulmonary fibrosis. Purpose: We aimed to investigate the effect of triptolide on pulmonary fibrosis through the inhibition of several important aspects of fibrotic ECM remodeling. Methods: Bleomycin-induced pulmonary fibrosis mice and TGF-β1-induced primary lung fibroblasts were used. The effect of triptolide on pulmonary fibrosis was detected using histopathology, immunostaining, RT-qPCR, western blotting, ELISA, and protein activity assay. Results: Triptolide significantly alleviated bleomycin-induced pulmonary fibrosis in mice. It inhibited the expression of fibrotic genes α-SMA, collagen I, fibronectin, and vimentin and blocked the TGF-β-SMAD signaling pathway both in vivo and in vitro. In addition, triptolide regulated the expression and activity of MMPs during fibrosis. Interestingly, it suppressed the expression of lysyl oxidase, which was responsible for matrix cross-linking and elevated ECM stiffness. Furthermore, triptolide blocked the biomechanical stress transduction pathway integrin-β1-FAK-YAP signaling and attenuated the pro-fibrotic feedback of fibrotic ECM on fibroblasts via integrin inhibition. Conclusion: These findings show that triptolide prevents the key linkages of fibrotic ECM remodeling, including deposition, degradation, cross-linking, and pro-fibrotic feedback and, therefore, has potential therapeutic value for pulmonary fibrosis