Contrast Enhancement of Brightness-Distorted Images by Improved Adaptive Gamma Correction

As an efficient image contrast enhancement (CE) tool, adaptive gamma correction (AGC) was previously proposed by relating gamma parameter with cumulative distribution function (CDF) of the pixel gray levels within an image. ACG deals well with most dimmed images, but fails for globally bright images and the dimmed images with local bright regions. Such two categories of brightness-distorted images are universal in real scenarios, such as improper exposure and white object regions. In order to attenuate such deficiencies, here we propose an improved AGC algorithm. The novel strategy of negative images is used to realize CE of the bright images, and the gamma correction modulated by truncated CDF is employed to enhance the dimmed ones. As such, local over-enhancement and structure distortion can be alleviated. Both qualitative and quantitative experimental results show that our proposed method yields consistently good CE results

Acceleration of Histogram-Based Contrast Enhancement via Selective Downsampling

In this paper, we propose a general framework to accelerate the universal histogram-based image contrast enhancement (CE) algorithms. Both spatial and gray-level selective down- sampling of digital images are adopted to decrease computational cost, while the visual quality of enhanced images is still preserved and without apparent degradation. Mapping function calibration is novelly proposed to reconstruct the pixel mapping on the gray levels missed by downsampling. As two case studies, accelerations of histogram equalization (HE) and the state-of-the-art global CE algorithm, i.e., spatial mutual information and PageRank (SMIRANK), are presented detailedly. Both quantitative and qualitative assessment results have verified the effectiveness of our proposed CE acceleration framework. In typical tests, computational efficiencies of HE and SMIRANK have been speeded up by about 3.9 and 13.5 times, respectively.Comment: accepted by IET Image Processin

Progressive Feedback-Enhanced Transformer for Image Forgery Localization

Blind detection of the forged regions in digital images is an effective authentication means to counter the malicious use of local image editing techniques. Existing encoder-decoder forensic networks overlook the fact that detecting complex and subtle tampered regions typically requires more feedback information. In this paper, we propose a Progressive FeedbACk-enhanced Transformer (ProFact) network to achieve coarse-to-fine image forgery localization. Specifically, the coarse localization map generated by an initial branch network is adaptively fed back to the early transformer encoder layers for enhancing the representation of positive features while suppressing interference factors. The cascaded transformer network, combined with a contextual spatial pyramid module, is designed to refine discriminative forensic features for improving the forgery localization accuracy and reliability. Furthermore, we present an effective strategy to automatically generate large-scale forged image samples close to real-world forensic scenarios, especially in realistic and coherent processing. Leveraging on such samples, a progressive and cost-effective two-stage training protocol is applied to the ProFact network. The extensive experimental results on nine public forensic datasets show that our proposed localizer greatly outperforms the state-of-the-art on the generalization ability and robustness of image forgery localization. Code will be publicly available at https://github.com/multimediaFor/ProFact

In situ measurements and thermo-mechanical simulation of Ti–6Al–4V laser solid forming processes

Residual stresses and distortions are two technical obstacles for popularizing the additive manufacturing (AM) technology. The evolution of the stresses in AM components during the thermal cycles of the metal depositing process is not yet clear, and more accurate in situ measurements are necessary to calibrate and validate the numerical tools developed for its simulation. In this work a fully coupled thermo-mechanical analysis to simulate the laser solid forming (LSF) process is carried out. At the same time, an exhaustive experimental campaign is launched to measure the temperature evolution at different locations, as well as the distortions and both the stress and strain fields. The thermal and mechanical responses of single-wall coupons under different process parameters are recorded and compared with the numerical models. Good agreement between the numerical results and the experimental measurements is obtained. Sensitivity analysis demonstrates that the AM process is significantly affected by the laser power and the feeding rate, while poorly influenced by the scanning speed.Peer ReviewedPostprint (author's final draft

PI-3K and Akt are mediators of AP-1 induction by 5-MCDE in mouse epidermal Cl41 cells

5-Methylchrysene has been found to be a complete carcinogen in laboratory animals. However, the tumor promotion effects of (±)-anti-5-methylchrysene-1,2-diol-3,4-epoxide (5-MCDE) remain unclear. In the present work, we found that 5-MCDE induced marked activator protein-1 (AP-1) activation in Cl41 cells. 5-MCDE also induced a marked activation of phosphatidylinositol 3-kinase (PI-3K). Inhibition of PI-3K impaired 5-MCDE–induced AP-1 transactivation, suggesting that PI-3K is an upstream kinase involved in AP-1 activation by 5-MCDE. Furthermore, we found that Akt is a PI-3K downstream mediator for 5-MCDE–induced AP-1 transactivation, whereas another PI-3K downstream kinase, p70S6K, was not involved in AP-1 activation by 5-MCDE. Moreover, inhibition of Akt activation blocked 5-MCDE–induced activation of extracellular signal–regulated protein kinases (ERKs) and c-Jun NH2-terminal kinases (JNKs), whereas it did not affect p38K activation. Consistently, overexpression of a dominant-negative mutant of ERK2 or JNK1 blocked the AP-1 activation by 5-MCDE. These results demonstrate that 5-MCDE is able to induce AP-1 activation, and the AP-1 induction is specifically through a PI-3K/Akt–dependent and p70S6K-independent pathway

In situ measurements and thermo-mechanical simulation of Ti–6Al–4V laser solid forming processes

Residual stresses and distortions are two technical obstacles for popularizing the additive manufacturing (AM) technology. The evolution of the stresses in AM components during the thermal cycles of the metal depositing process is not yet clear, and more accurate in situ measurements are necessary to calibrate and validate the numerical tools developed for its simulation. In this work a fully coupled thermo-mechanical analysis to simulate the laser solid forming (LSF) process is carried out. At the same time, an exhaustive experimental campaign is launched to measure the temperature evolution at different locations, as well as the distortions and both the stress and strain fields. The thermal and mechanical responses of single-wall coupons under different process parameters are recorded and compared with the numerical models. Good agreement between the numerical results and the experimental measurements is obtained. Sensitivity analysis demonstrates that the AM process is significantly affected by the laser power and the feeding rate, while poorly influenced by the scanning speed

ErbB2 and p38γ MAPK Mediate Alcohol-Induced Increase in Breast Cancer Stem Cells and Metastasis

Background: Both epidemiological and experimental studies suggest that excessive alcohol exposure increases the risk for breast cancer and enhances metastasis/recurrence. We have previously demonstrated that alcohol enhanced the migration/invasion of breast cancer cells and cancer cells overexpressing ErbB2/HER2 were more sensitive to alcohol exposure. However, the underlying mechanisms remain unclear. This study was designed to investigate the mechanisms underlying alcohol-enhanced aggressiveness of breast cancer. Cancer stem cells (CSCs) play a critical role in cancer metastasis and recurrence. Methods: We evaluated the effect of chronic alcohol exposure on mammary tumor development/metastasis in MMTV-neu transgenic mice and investigated the cell signaling in response to alcohol exposure in breast cancer cells overexpressing ErbB2/HER2. Results and discussion: Chronic alcohol exposure increased breast cancer stem cell-like CSC population and enhanced the lung and colon metastasis in MMTV-neu transgenic mice. Alcohol exposure caused a drastic increase in CSC population and mammosphere formation in breast cancer cells overexpressing ErbB2/HER2. Alcohol exposure stimulated the phosphorylation of p38γ MAPK (p-p38γ) which was co-localized with phosphorylated ErbB2 and CSCs in the mammary tumor tissues. In vitro results confirmed that alcohol activated ErbB2/HER2 and selectively increased p-p38γ MAPK as well as the interaction between p38γ MAPK and its substrate, SAP97. However, alcohol did not affect the expression/phosphorylation of p38α/β MAPKs. In breast cancer cell lines, high expression of ErbB2 and p-p38γ MAPK was generally correlated with more CSC population. Blocking ErbB2 signaling abolished heregulin β1- and alcohol-stimulated p-p38γ MAPK and its association with SAP97. More importantly, p38γ MAPK siRNA significantly inhibited an alcohol-induced increase in CSC population, mammosphere formation and migration/invasion of breast cancer cells overexpressing ErbB2. Conclusions: p38γ MAPK is downstream of ErbB2 and plays an important role in alcohol-enhanced aggressiveness of breast cancer. Therefore, in addition to ErbB2/HER2, p38γ MAPK may be a potential target for the treatment of alcohol-enhanced cancer aggressiveness