A Novel Image Encryption Scheme Using the Composite Discrete Chaotic System

The composite discrete chaotic system (CDCS) is a complex chaotic system that combines two or more discrete chaotic systems. This system holds the chaotic characteristics of different chaotic systems in a random way and has more complex chaotic behaviors. In this paper, we aim to provide a novel image encryption algorithm based on a new two-dimensional (2D) CDCS. The proposed scheme consists of two parts: firstly, we propose a new 2D CDCS and analysis the chaotic behaviors, then, we introduce the bit-level permutation and pixel-level diffusion encryption architecture with the new CDCS to form the full proposed algorithm. Random values and the total information of the plain image are added into the diffusion procedure to enhance the security of the proposed algorithm. Both the theoretical analysis and simulations confirm the security of the proposed algorithm

Thermal Functionalization of Alkanes with Carbon Electrophiles

Alkane functionalization with carbon-electrophiles remains virtually unexplored under thermo-driven hydrogen atom transfer (HAT) conditions due to a challenge of integrating oxidation and reduction in a single operation. We report here a Ni-catalyzed arylation and alkylation of alkane C‒H bonds with organohalides to forge C(sp3)‒C bonds by merging easily accessible Zn and tBuOOtBu (DTBP) as the external reductant and oxidant. The mild and easy-to-operate protocol enables facile carbofunctionalization of N-/O-α- and cyclohexane CH bonds, and preparation of a number of bioactive compounds and drug derivatives. Preliminary mechanistic studies implied a Ni(I)-mediated DTBP reduction followed by alkane HAT to tBuO radical. The marked compatibility of Zn and DTBP with nickel-catalysis may invoke the development of external oxidant and reductant co-trigged thermoredox bond forming approaches based upon challenging substrates

A-kinase Anchoring Protein 5 Anchors Protein Kinase A to Mediate PLN/SERCA to Reduce Cardiomyocyte Apoptosis Induced by Hypoxia and Reoxygenation

A-kinase anchoring protein (AKAP) 5 has a variety of biological activities. This study explored whether AKAP5 is involved in cardiomyocyte apoptosis induced by H/R and its possible mechanism. H9C2 cells were used to construct an H/R model in vitro, followed by overexpression of AKAP5 in the cells. Flow cytometry was used to detect the rate of cardiomyocyte apoptosis. The expression of phospholamban (PLN) phosphorylation, SERCA2a and apoptosis-related proteins were determined by western blot. Immunofluorescence staining and immunoprecipitation were used to detect the distribution of and interaction between AKAP5, PKA, and PLN. After H/R induction, H9C2 cells had significantly reduced expression of AKAP5 protein. Upregulation of AKAP5 promoted cell survival and significantly reduced LDH level and apoptosis rate of H9C2 cells. In addition, the overexpression of AKAP5 was accompanied by the activation of the PLN/SERCA2a signaling pathway and a reduction in apoptosis. Immunofluorescence staining and immunoprecipitation revealed that AKAP5 colocalized and interacted with PLN and PKA.Interestingly,St-Ht31 inhibited the effect of AKAP5 overexpression on H/R-induced apoptosis in H9C2 cardiomyocytes. AKAP5 overexpression alleviated H/R-induced cardiomyocyte apoptosis, possibly through anchoring to PKA to mediate the PLN/SERCA pathway, suggesting that AKAP5 is a potential therapeutic target for the prevention and treatment of ischemia-reperfusion injury.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Changes of I_Kr in heart failure (HF).

<p>(A) Recording of I_kr tail current in a representative left ventricle (LV) myocyte before (left) and 10 min after exposure to dofetilide (1 µM) (right). (B) Representative tail traces of I_Kr in LV myocytes isolated from control (CTL, left) and HF guinea pigs (right). (C) The average current-voltage relationship of I_Kr plotted for control (n = 24 cells, 8 hearts) and HF (n = 33 cells, 10 hearts) myocytes (***p<0.001, HF vs. CTL). Test pulses were applied at various voltages from −40 to +40 mV (step width 20 mV, step duration 200 ms) before returning to −40 mV for tail current recording.</p

β₂-AR mediates the inhibition of I_kr by fenoterol (Feno) in heart failure (HF) myocytes.

<p>(A and B) Superimposed tail current traces of I_kr recorded before and 10 min after application of 10 µM fenoterol in the presence of the selective β₂-AR antagonist ICI118551 (ICI, 10 µM) and β₁-AR antagonist CGP20712A (CGP, 10 µM) in a HF myocyte, respectively. (C) Summarized data for percent decrease in the amplitude of I_Kr tail current evoked by ICI plus fenoterol, CGP plus fenoterol, and fenoterol alone (n = 5 and 6 cells, 3 hearts, *P<0.05, Feno+ICI versus Feno). Current amplitudes were measured at the voltage of +40 mV.</p

Effects of cAMP inhibition and PKA inhibition on I_kr response to β₂-AR stimulation.

<p>(A) Superimposed tail current traces of I_kr recorded before and 10 min after application of 10 µM fenoterol (Feno) in the presence of RpCAMPS (100 µM) in pipette solution in a heart failure (HF) myocyte. (B) Superimposed tail current traces of I_kr recorded before and 10 min after application of 10 µM Feno in the presence of PKA inhibitor, KT5720 (2.5 µM) in a HF myocyte. (C) Summarized data for percent decrease in the amplitude of I_Kr tail current evoked by Feno alone, RpCAMPS plus fenoterol, and KT5720 plus Feno in HF myocytes (n = 6, 6, and 5 cells, 3 hearts, *p<0.05, RpCAMPS+ Feno vs. Feno). Current amplitudes were measured at the voltage of +40 mV.</p