Robust Object-Based Watermarking Using SURF Feature Matching and DFT Domain

In this paper we propose a robust object-based watermarking method, in which the watermark is embedded into the middle frequencies band of the Discrete Fourier Transform (DFT) magnitude of the selected object region, altogether with the Speeded Up Robust Feature (SURF) algorithm to allow the correct watermark detection, even if the watermarked image has been distorted. To recognize the selected object region after geometric distortions, during the embedding process the SURF features are estimated and stored in advance to be used during the detection process. In the detection stage, the SURF features of the distorted image are estimated and match them with the stored ones. From the matching result, SURF features are used to compute the Affine-transformation parameters and the object region is recovered. The quality of the watermarked image is measured using the Peak Signal to Noise Ratio (PSNR), Structural Similarity Index (SSIM) and the Visual Information Fidelity (VIF). The experimental results show the proposed method provides robustness against several geometric distortions, signal processing operations and combined distortions. The receiver operating characteristics (ROC) curves also show the desirable detection performance of the proposed method. The comparison with a previously reported methods based on different techniques is also provided

Temporal and spatial variations in hydrothermal fluid abundances of degassing metals across an eruptive cycle at 9 degrees 50 minutes N East Pacific Rise

The influence of eruptive activity on hydrothermal fluid trace metal abundances, especially those inferred to degas from shallow mid ocean ridge (MOR) magma bodies, remains poorly understood. These data and their variations in time and space are critical to improving our understanding of the quantitative links between mantle, crust, and MOR biological communities. Frequent sampling of hydrothermal vents at the 9°50\u27N East Pacific Rise provides an ideal suite for evaluating the evolution of vent fluid chemistry during eruption cycles. Fluid metal abundances are presented for metals with high degassing potential (210Pb, Pb and Cd) for a subset of these time-series samples. These results are then considered with chloride, silica, magmatic volatile and more refractory metal contents. Taken together, vapor-phase vents with the highest degassing signal as indicated by volatile contents contain elevated 210Pb/Pb. Additionally, high levels of CO2 are associated with increasing concentrations of Cd as well as 210Pb

Ten Dimensional Black Hole and the D0-brane Threshold Bound State

We discuss the ten dimensional black holes made of D0-branes in the regime where the effective coupling is large, and yet the 11D geometry is unimportant. We suggest that these black holes can be interpreted as excitations over the threshold bound state. Thus, the entropy formula for the former is used to predict a scaling region of the wave function of the latter. The horizon radius and the mass gap predicted in this picture agree with the formulas derived from the classical geometry.Comment: 11 pages, harvmac; v2: typos corrected, argument for the convergence of two integrals improved, v3: one ref. adde

El precondicionamiento isquémico produce cambios en las proteínas de las fosforilación oxidativa y atenúa el daño oxidativo durante la isquemia-reperfusión por mecanismos independientes de la señalización citosólica

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Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning

Risc cardiovascular; Isquèmia/reperfusióCardiovascular risk; Ischemia/reperfusionRiesgo cardiovascular; Isquemia/reperfusiónPreconditioning, postconditioning, and remote conditioning of the myocardium enhance the ability of the heart to withstand a prolonged ischemia/reperfusion insult and the potential to provide novel therapeutic paradigms for cardioprotection. While many signaling pathways leading to endogenous cardioprotection have been elucidated in experimental studies over the past 30 years, no cardioprotective drug is on the market yet for that indication. One likely major reason for this failure to translate cardioprotection into patient benefit is the lack of rigorous and systematic preclinical evaluation of promising cardioprotective therapies prior to their clinical evaluation, since ischemic heart disease in humans is a complex disorder caused by or associated with cardiovascular risk factors and comorbidities. These risk factors and comorbidities induce fundamental alterations in cellular signaling cascades that affect the development of ischemia/reperfusion injury and responses to cardioprotective interventions. Moreover, some of the medications used to treat these comorbidities may impact on cardioprotection by again modifying cellular signaling pathways. The aim of this article is to review the recent evidence that cardiovascular risk factors as well as comorbidities and their medications may modify the response to cardioprotective interventions. We emphasize the critical need for taking into account the presence of cardiovascular risk factors as well as comorbidities and their concomitant medications when designing preclinical studies for the identification and validation of cardioprotective drug targets and clinical studies. This will hopefully maximize the success rate of developing rational approaches to effective cardioprotective therapies for the majority of patients with multiple comorbidities. Significance Statement Ischemic heart disease is a major cause of mortality; however, there are still no cardioprotective drugs on the market. Most studies on cardioprotection have been undertaken in animal models of ischemia/reperfusion in the absence of comorbidities; however, ischemic heart disease develops with other systemic disorders (e.g., hypertension, hyperlipidemia, diabetes, atherosclerosis). Here we focus on the preclinical and clinical evidence showing how these comorbidities and their routine medications affect ischemia/reperfusion injury and interfere with cardioprotective strategies.P.F. was supported by the National Research, Development and Innovation Office of Hungary (Research Excellence Program–TKP, National Heart Program NVKP 16-1-2016-0017) and by the Higher Education Institutional Excellence Program of the Ministry of Human Capacities in Hungary, within the framework of the Therapeutic Development thematic program of Semmelweis University. D.D. is supported by grants from National Institutes of Health National Heart, Lung, and Blood Institute [R01-HL136389, R01-HL131517, R01-HL089598, and R01-HL163277], the German Research Foundation [DFG, Do 769/4-1], the European Union (large-scale integrative project MAESTRIA, no. 965286). G.H. is supported by the German Research Foundation [SFB 1116 B8]. D.H. is supported by the Duke–NUS Signature Research Programme funded by the Ministry of Health, Singapore Ministry of Health’s National Medical Research Council under its Clinician Scientist–Senior Investigator scheme [NMRC/CSA-SI/0011/2017], Centre Grant [CGAug16M006], and Collaborative Centre Grant scheme [NMRC/CGAug16C006]. I.A. is supported from Boehringer-Ingelheim for the investigation of the effects of empagliflozin on the myocardium and from the European Union (ERDF) and Greek national funds through the Operational Program “Competitiveness, Entrepreneurship and Innovation,” under the call “RESEARCH – CREATE – INNOVATE” (project code: 5048539). S.M.D. acknowledges the support of the British Heart Foundation [PG/19/51/34493 and PG/16/85/32471]. S.L. is supported by the South African National Research Foundation and received COST Seed funding from the Department of Science and Innovation in South Africa. M.R-M. is supported by the Instituto de Salud Carlos III of the Spanish Ministry of Health [FIS-PI19-01196] and a grant from the Spanish Society of Cardiology [SEC/FEC-INV-BAS 217003]. C.J.Z. is supported by a grant from European Foundation for the Study of Diabetes (EFSD), a research grant from Boehringer-Ingelheim and an institutional grant from Amsterdam UMC Cardiovascular Research. R.S. is supported by Deutsche Forschungsgemeinschaft (DFG; German Research Foundation) [Project number 268555672—SFB 1213, Project B05]

Ischemic preconditioning and ischaemia-reperfusion: key role of connexin43 and mitochondrial complexes

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