Sending-or-Not-Sending Twin-Field Quantum Key Distribution with a Passive Decoy-State Method.

Twin-field quantum key distribution (TF-QKD) has attracted considerable attention because it can exceed the basic rate-distance limit without quantum repeaters. Its variant protocol, sending or not-sending quantum key distribution (SNS-QKD), not only fixes the security vulnerability of TF-QKD, but also can tolerate large misalignment errors. However, the current SNS-QKD protocol is based on the active decoy-state method, which may lead to side channel information leakage when multiple light intensities are modulated in practice. In this work, we propose a passive decoy-state SNS-QKD protocol to further enhance the security of SNS-QKD. Numerical simulation results show that the protocol not only improves the security in source, but also retains the advantages of tolerating large misalignment errors. Therefore, it may provide further guidance for the practical application of SNS-QKD.

Prefixed-Threshold Real-Time Selection for Free-Space Sending-or-Not Twin-Field Quantum Key Distribution.

As a variant of the twin-field quantum key distribution (TF-QKD), the sending-or-not twin-field quantum key distribution (SNS TF-QKD) is famous for its higher tolerance of misalignment error, in addition to the capacity of surpassing the rate-distance limit. Importantly, the free-space SNS TF-QKD will guarantee the security of the communications between mobile parties. In the paper, we first discuss the influence of atmospheric turbulence (AT) on the channel transmittance characterized by the probability distribution of the transmission coefficient (PDTC). Then, we present a method called prefixed-threshold real-time selection (P-RTS) to mitigate the interference of AT on the free-space SNS TF-QKD. The simulations of the free-space SNS TF-QKD with and without P-RTS are both given for comparison. The results showed that it is possible to share the secure key by using the free-space SNS TF-QKD. Simultaneously, the P-RTS method can make the free-space SNS TF-QKD achieve better and more stable performance at a short distance.

Decoy-state phase-matching quantum key distribution with source errors.

The phase-matching quantum key distribution (PM-QKD), one of the variants of Twin-Field (TF) QKD protocol, was recently proposed to overcome the rate-distance limits of point to point protocol without quantum repeaters. In this paper, we propose a more practical PM-QKD protocol version with four-intensity decoy states and source errors, since neither the infinite decoy states nor the precise control of the light source is available in practice. We present the formulation of the secure key rate of the proposed protocol and analyze the performances of the protocol with and without source errors by numerical simulations.

Exploring the Mechanism of Salvianolic Acid B against Myocardial Ischemia-Reperfusion Injury Based on Network Pharmacology.

This study aimed to explore the mechanisms through which salvianolic acid B (Sal-B) exerts its effects during myocardial ischemia-reperfusion injury (MI/RI), aiming to demonstrate the potential pharmacological characteristics of Sal-B in the management of coronary heart disease. First, Sal-B-related targets and MI/RI-related genes were compiled from public databases. Subsequent functional enrichment analyses using the protein-protein interaction (PPI) network, gene ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG) predicted the core targets and approaches by which Sal-B counters MI/RI. Second, a Sal-B-treated MI/RI mouse model and oxygen-glucose deprivation/reoxygenation (OGD/R) H9C2 cell model were selected to verify the main targets of the network pharmacological prediction. An intersectional analysis between Sal-B and MI/RI targets identified 69 common targets, with a PPI network analysis highlighting caspase-3, c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38) as central targets. GO and KEGG enrichment analyses indicated remarkable enrichment of the apoptosis pathway among these targets, suggesting their utility in experimental studies in vivo. Experimental results demonstrated that Sal-B treatment not only mitigated myocardial infarction size following MI/RI injury in mice but also modulated the expression of key apoptotic regulators, including Bcl-2-Associated X (Bax), caspase-3, JNK, and p38, alongside enhancing the B-cell lymphoma-2 (Bcl-2) expression, thereby inhibiting myocardial tissue apoptosis. This study leveraged an integrative network pharmacology approach to predict Sal-B's potential targets in MI/RI treatment and verified the involvement of key target proteins within the predicted signaling pathways through both in vivo and in vitro experiments, offering a comprehensive insight into Sal-B's pharmacological mechanism in MI/RI management.

Salvianolic acid B inhibits atherosclerosis and TNF-α-induced inflammation by regulating NF-κB/NLRP3 signaling pathway.

BACKGROUND: Inflammation is critical in the pathophysiology of atherosclerosis (AS). The aim of this study was to investigate the protective effect of salvianolic acid B (Sal B) on AS and to explore the molecular mechanism of tumor necrosis factor-α (TNF-α)-induced damage in human umbilical vein endothelial cells (HUVECs). METHODS: In vivo studies, LDLR-/- mice were fed a high-fat diet (HFD) for 14 weeks to establish an AS model to evaluate the protective effect of Sal B on the development of AS. Total cholesterol (TC), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) levels were determined in the blood serum. En face and cross section lipid deposits were measured and quantified with Oil Red O staining. Hematoxylin and eosin (H&E) and Masson's trichrome staining were used to quantify atherosclerotic plaque size and collagen fiber content in aortic root sections. Reactive oxygen species (ROS) were detected in aortic root using dihydroethylenediamine (DHE) staining. Apoptosis rate was determined by TdT-mediated dUTP nick end labeling (TUNEL) staining. Immunofluorescence (IF) staining was used to detect the expression of the nuclear factor kappa-B (NF-κB) p65 and NOD-like receptor family pyrin domain containing 3 (NLRP3). To further investigate the protective effect of Sal B, we used TNF-α induced HUVECs inflammation model. We examined cell viability, lactate dehydrogenase (LDH) content, and ROS production. The transcription of NF-κB was evaluated by immunofluorescence. The mRNA levels of NLRP3, caspase-1, and IL-1ß were detected by RT-PCR. Pyroptosis related proteins were detected by Western blot. RESULTS: The change in the weight of the mice over time was an indication that Sal B had an effect on weight gain. IN VIVO STUDIES: we were able to show that the serum lipids TC, TG and LDL-C were increased in the model group and that the treatment with Sal B reduced the levels of serum lipids. Histological staining showed that the LDLR-/- mice had a large amount of foam cell deposition accompanied by inflammatory cell infiltration and the formation of atherosclerotic plaques in theMOD group. The pathological abnormalities were significantly improved by Sal B treatment. ROS release and apoptosis were significantly increased after HFD in aortic root, which was attenuated by Sal B. IF results showed that the expression of NF-κB p65 and NLRP3 was significantly increased in the MOD group and significantly decreased in the Sal B group, suggesting that Sal B may act through the NF-κB/NLRP3 pathway. And in vitro studies: inflammatory damage of HUEVCs was induced by TNF-α, and Sal B treatmented significantly increased cell viability and reduced LDH release. It was also found that Sal B inhibited ROS level increase after TNF-α-induced HUEVCs. Activation of NF-κB p65 by TNF-α stimulation, NF-κB p65 is transferred to the nucleus. Sal B treatment could reverse this effect. RT-PCR and Western blot showed that Sal B affected NF-κB transcription and NLRP3 inflammasome activation and could significantly inhibit TNF-α-induced NLRP3 inflammasome activation. These results suggest that Sal B may participate in antiatherosclerotic and inflammatory responses through the NF-κB/NLRP3 pathway. CONCLUSIONS: This study shows that Sal B ameliorates the development of AS lesions in HFD-induced LDLR-/- mice. Furthermore, under TNF-α conditions, Sal B reduced ROS release and reversed nuclear translocation of NF-κB, and inhibited atherosclerosis and inflammation by modulating the NF-κB/NLRP3 pathway.

Plug-and-play round-robin differential phase-shift quantum key distribution.

The round-robin differential-phase-shift quantum key distribution (RRDPS-QKD) protocol could provide an effective way to estimate the leakage information without monitoring the signal disturbance. Moreover, the self-compensating property of plug-and-play (P&P) setup can eliminate the variations of phase or polarization in QKD procedure. In the paper, we introduce the P&P concept into RRDPS-QKD, and propose a QKD protocol, named P&P RRDPS-QKD protocol, to make the RRDPS-QKD scheme more practical. We analyze the security, and discuss the key generation rate with infinite-intensity decoy state method. The results show that the proposed protocol is a good solution to RRDPS-QKD protocol with untrusted sources. It has a high security and its key generation rate could be as good as the protocol with trusted sources when the average input photon number N is greater than 106. In addition, the proposed protocol has a high noise tolerance in comparison with P&P BB84-QKD protocol.