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Video Watermarking Algorithm for H.264 Scalable Video Coding
( Jianfeng Lu ),( Li Li ),( Zhenhua Yang ) 한국인터넷정보학회 2013 KSII Transactions on Internet and Information Syst Vol.7 No.1
Because H.264/SVC can meet the needs of different networks and user terminals, it has become more and more popular. In this paper, we focus on the spatial resolution scalability of H.264/SVC and propose a blind video watermarking algorithm for the copyright protection of H.264/SVC coded video. The watermark embedding occurs before the H.264/SVC encoding, and only the original enhancement layer sequence is watermarked. However, because the watermark is embedded into the average matrix of each macro block, it can be detected in both the enhancement layer and base layer after downsampling, video encoding, and video decoding. The proposed algorithm is examined using JSVM, and experiment results show that is robust to H.264/SVC coding and has little influence on video quality.
Huang Guangwei,Bao Hailong,Zhan Peng,Lu Xiyang,Duan Zonggang,Xiong Xinlin,Lin Muzhi,Wang Bing,An Hongxin,Xiahou Luanda,Zhou Haiyan,Luo Zhenhua,Li Wei 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Objectives This study aimed at investigating the role of the proprotein convertase subtilisin/Kexin type 9 (PCSK9)-mediated autophagy on myocardial ischemia/reperfusion injury (MIRI). To determine the relationship between autophagy, apoptosis, fibrosis, and inflammation in the myocardium, to provide experience in preventing and treating the myocardial ischemia/reperfusion (I/R) injury. Methods An AC16 hypoxia-reoxygenation model and a rat myocardial ischemia–reperfusion model were established. The concentrations of cardiac troponin T (cTnT) and creatine kinase-MB (CKMB) in plasma were measured by ELISA. To determine the size of the myocardial infarction, TTC/EB staining was performed. In addition to identifying pathological changes in myocardial tissue, Masson’s trichrome stains and H&E stains were used to identify pathological changes. Echocardiography was employed to detect cardiac function. Western blot analysis was then performed to detect the protein expression of Parkin, Pink1, and markers associated with autophagy (Beclin-1, p62, LC3). Results A significant increase in PCSK9 was observed in the myocardium during H/R. In the cardiac-specific PCSK9 knockdown model, cardiac autophagy was significantly inhibited, whereas cardiac-specific PCSK9 overexpression promoted cardiac autophagy. In vivo studies have demonstrated a significant decrease in cardiac autophagy when the PCSK9 inhibitor was administered. Apoptosis induced by I/R was greatly decreased, and myocardial infarction size and function were both improved by PCSK9 inhibitors. Mechanistically, the PCSK9 inhibitor improved the degree of myocardial fibrosis and inhibited the development of inflammation. Conclusions Our results demonstrated that increased PCSK9 via the parkin/pink1 signaling pathway contributes to I/R and H/R by exaggerating excessive autophagy during reperfusion/reoxygenation. In addition, the PCSK9 inhibitor blocked the development of inflammation and improved Infarct size, myocardial function, and myocardial fibrosis.