In Malik et al.'s method, each pixel can be embedded with log 2 3 bits by being modified at most 1. Thus, their method achieves significant hiding capacity while maintaining good visual quality. However, in their method, the first lower and the first upper quantization levels must be excluded from data embedding in order to ensure reversibility. To this end, we propose a two-layer reversible data hiding (RDH) scheme in combination with (7,4) Hamming code. In the 1st-layer embedding, each block can be embedded with 16 bits. In the 2nd-layer embedding, each already-modified block can carry 6 bits or 12 bits by taking advantage of (7,4) Hamming code that hides three bits by modifying only one bit. At most 2-bit additional information is needed to help decoders to correctly extract the original lower and upper quantization levels. By means of two-layer embedding, our method achieves higher embedding capacity while maintaining almost the same visual quality, compared with Malik et al.'s method. Experimental results also demonstrate our effectivity. INDEX TERMS Reversible data hiding, AMBTC (absolute moment block truncation coding), (7, 4) hamming code, two-layer.
Bleeding is one of the most serious side effects of antiplatelet drugs. Efforts have been made to find new antiplatelet agents without bleeding complications. Shear-induced platelet aggregation (SIPA) occurs only under pathological conditions and is a promising target for overcoming bleeding problems. This work demonstrates that the ginsenoside Re selectively inhibits platelet aggregation induced by high shear stress. Human platelets were exposed to high shear stress using microfluidic chip technology, and aggregation, activation, and phosphatidylserine (PS) exposure were measured. The Von Willebrand Ristocetin Cofactor (vWF:RCo) assay and western blot were used to evaluate the effect of the vWF-GPⅠb/PI3K/Akt signal pathway. The coagulation and bleeding risk were evaluated by measuring the coagulation parameters PT, APTT, TT, and thromboelastography. The 3-dimensional morphology of platelet aggregates was observed by a microscopic 3-dimensional imaging. Re was a potent inhibitor of SIPA, with an IC50 of 0.071 mg/mL. It effectively blocked shear stress–induced platelet activation without any significant toxicity. It was highly selective against SIPA, effectively inhibiting vWF–GPIb and the downstream PI3K/Akt signaling pathway. Most importantly, Re did not affect normal blood coagulation and did not increase the risk of bleeding. In conclusion, Re inhibits platelet activation through the inhibition of the vWF-GPIb/PI3K/Akt pathway. Thus, it might be considered as a new antiplatelet drug in the prevention of thrombosis without increasing the risk of bleeding.
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