RESUMEN
An effective post-processing algorithm is essential for achieving high rates of secret key generation in quantum key distribution. This work introduces an approach to quantum key distribution post-processing by integrating the three main steps into a unified procedure: syndrome-based error estimation, rate-adaptive reconciliation, and subblock confirmation. The proposed scheme employs low-density parity-check codes to estimate the quantum bit error rate using the syndrome information, and to optimize the channel coding rates based on the Slepian-Wolf coding scheme for the rate-adaptive method. Additionally, this scheme incorporates polynomial-based hash verification in the subblock confirmation process. The numerical results show that the syndrome-based estimation significantly enhances the accuracy and consistency of the estimated quantum bit error rate, enabling effective code rate optimization for rate-adaptive reconciliation. The unified approach, which integrates rate-adaptive reconciliation with syndrome-based estimation and subblock confirmation, exhibits superior efficiency, minimizes practical information leakage, reduces communication rounds, and guarantees convergence to the identical key. Furthermore, the simulations indicate that the secret key throughput of this approach achieves the theoretical limit in the context of a BB84 quantum key distribution system.
RESUMEN
As one of the important paths for China to achieve the "dual carbon" strategyï¼ developing hydrogen fuel cell vehicles is currently being promoted in various regions across the countryï¼ including passenger carsï¼ coachesï¼ and heavy-duty trucks. Quantifying the carbon reduction potential of hydrogen fuel cell vehicles for different vehicle types and regions has become a hot research topic. Using a life cycle assessment method that considers future vehicle fuel economyï¼ power generation carbon emission factorsï¼ hydrogen production carbon emission factorsï¼ and regional differences in the scale and hydrogen production methodsï¼ this study quantitatively evaluated the life cycle carbon emissions of different types of vehiclesï¼ including fuel cell vehicles ï¼FCVï¼ï¼ traditional fuel vehicles ï¼ICEVï¼ï¼ and battery electric vehicles ï¼BEVï¼. We compared and analyzed the carbon reduction potential of hydrogen fuel cell vehicles at different times and in different regions and conducted an uncertainty analysis on hydrogen consumption per hundred kilometers. The results showed that by 2025ï¼ the life cycle carbon emissions of hydrogen fuel cell coaches would decrease by 36.0% compared to that of traditional fuel coachesï¼ but the reduction in carbon emissions for hydrogen fuel cell heavy-duty trucks was not significant. By 2035ï¼ as the hydrogen energy source structure in China continues to improveï¼ the life cycle carbon emissions of hydrogen fuel cell heavy-duty trucks were predicted to decrease by 36.5% compared to that of traditional fuel heavy-duty trucks. The decarbonization potential was most significant for heavy-duty trucks compared to that of passenger cars and coaches. Taking the Beijing-Tianjin-Hebei demonstration group as an example in 2035ï¼ as the hydrogen consumption per hundred kilometers decreases by 20%ï¼ the carbon reduction potential of FCV passenger carsï¼ coachesï¼ and heavy-duty trucks would increase by 7.29%ï¼ 9.93%ï¼ and 19.57%ï¼ respectively. Thereforeï¼ it is recommended to prioritize the promotion of hydrogen fuel cell coaches in the short termï¼ heavy-duty trucks in the long termï¼ and passenger cars as a supplement. Promoting hydrogen fuel cell vehicles in different regions and stages will help advance the low-carbon development of the automotive industry in China.
RESUMEN
Cardiac remodeling is the primary pathological feature of chronic heart failure (HF). Exploring the characteristics of cardiac remodeling in the very early stages of HF and identifying targets for intervention are essential for discovering novel mechanisms and therapeutic strategies. Silent mating type information regulation 2 homolog 3 (SIRT3), as a major mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, is required for mitochondrial metabolism. However, whether SIRT3 plays a role in cardiac remodeling by regulating the biosynthesis of mitochondrial cardiolipin (CL) is unknown. In this study, we induced pressure overload in wild-type (WT) and SIRT3 knockout (SIRT3-/-) mice via transverse aortic constriction (TAC). Compared with WT mouse hearts, the hearts of SIRT3-/- mice exhibited more-pronounced cardiac remodeling and fibrosis, greater reactive oxygen species (ROS) production, decreased mitochondrial-membrane potential (ΔΨm), and abnormal mitochondrial morphology after TAC. Furthermore, SIRT3 deletion aggravated TAC-induced decrease in total CL content, which might be associated with the downregulation of the CL synthesis related enzymes cardiolipin synthase 1 (CRLS1) and phospholipid-lysophospholipid transacylase (TAFAZZIN). In our in vitro experiments, SIRT3 overexpression prevented angiotensin II (AngII)- induced aberrant mitochondrial function, CL biosynthesis disorder, and peroxisome proliferator-activated receptor gamma (PPARγ) downregulation in cardiomyocytes; meanwhile, SIRT3 knockdown exacerbated these effects. Moreover, the addition of GW9662, a PPARγ antagonist, partially counteracted the beneficial effects of SIRT3 overexpression. In conclusion, SIRT3 regulated PPARγ-mediated CL biosynthesis, maintained the structure and function of mitochondria, and thereby protected the myocardium against cardiac remodeling.