Image Quality Evaluation in Professional HDR/WCG Production Questions the Need for HDR Metrics.

In the quality evaluation of high dynamic range and wide color gamut (HDR/WCG) images, a number of works have concluded that native HDR metrics, such as HDR visual difference predictor (HDR-VDP), HDR video quality metric (HDR-VQM), or convolutional neural network (CNN)-based visibility metrics for HDR content, provide the best results. These metrics consider only the luminance component, but several color difference metrics have been specifically developed for, and validated with, HDR/WCG images. In this paper, we perform subjective evaluation experiments in a professional HDR/WCG production setting, under a real use case scenario. The results are quite relevant in that they show, firstly, that the performance of HDR metrics is worse than that of a classic, simple standard dynamic range (SDR) metric applied directly to the HDR content; and secondly, that the chrominance metrics specifically developed for HDR/WCG imaging have poor correlation with observer scores and are also outperformed by an SDR metric. Based on these findings, we show how a very simple framework for creating color HDR metrics, that uses only luminance SDR metrics, transfer functions, and classic color spaces, is able to consistently outperform, by a considerable margin, state-of-the-art HDR metrics on a varied set of HDR content, for both perceptual quantization (PQ) and Hybrid Log-Gamma (HLG) encoding, luminance and chroma distortions, and on different color spaces of common use.

Coupling of Grb2 to Gab1 mediates hepatocyte growth factor-induced high intensity ERK signal required for inhibition of HepG2 hepatoma cell proliferation.

Activation of the extracellular signal-regulated kinase (ERK) pathway is a key factor in the regulation of cell proliferation by growth factors. Hepatocyte growth factor (HGF)-induced cell cycle arrest in the human hepatocellular carcinoma cell line HepG2 requires strong activation of the ERK pathway. In this study, we investigated the molecular mechanism of the activation. We constructed a chimeric receptor composed of the extracellular domain of the NGF receptor and the cytoplasmic domain of the HGF receptor (c-Met) and introduced a point mutation (N1358H) into the chimeric receptor, which specifically abrogates the direct binding of Grb2 to c-Met. The mutant chimeric receptor failed to mediate the strong activation of ERK, up-regulation of the expression of a Cdk inhibitor p16(INK4a) and inhibition of HepG2 cell proliferation by ligand stimulation. Moreover, the mutant receptor did not induce tyrosine phosphorylation of the docking protein Gab1. Knockdown of Gab1 using siRNA suppressed the HGF-induced strong activation of ERK and inhibition of HepG2 cell proliferation. These results suggest that coupling of Grb2 to Gab1 mediates the HGF-induced strong activation of the ERK pathway, which is required for the inhibition of HepG2 cell proliferation.