Sja-let-7 suppresses the development of liver fibrosis via Schistosoma japonicum extracellular vesicles.

Schistosomiasis is a fatal zoonotic parasitic disease that also threatens human health. The main pathological features of schistosomiasis are granulomatous inflammation and subsequent liver fibrosis, which is a complex, chronic, and progressive disease. Extracellular vesicles (EVs) derived from schistosome eggs are broadly involved in host-parasite communication and act as important contributors to schistosome-induced liver fibrosis. However, it remains unclear whether substances secreted by the EVs of Schistosoma japonicum, a long-term parasitic "partner" in the hepatic portal vein of the host, also participate in liver fibrosis. Here, we report that EVs derived from S. japonicum worms attenuated liver fibrosis by delivering sja-let-7 into hepatic stellate cells (HSCs). Mechanistically, activation of HSCs was reduced by targeting collagen type I alpha 2 chain (Col1α2) and downregulation of the TGF-ß/Smad signaling pathway both in vivo and in vitro. Overall, these results contribute to further understanding of the molecular mechanisms underlying host-parasite interactions and identified the sja-let-7/Col1α2/TGF-ß/Smad axis as a potential target for treatment of schistosomiasis-related liver fibrosis.

Ultrafast Imaging of Jahn-Teller Distortion and the Correlated Proton Migration in Photoionized Cyclopropane.

The Jahn-Teller (JT) distortion is one of the fundamental processes in molecules and condensed phase matters. For photoionized organic molecules with high symmetry, the JT effect leads to geometric instability in certain electron configurations and thus has a significant effect on the subsequent isomerization and proton migration processes. Utilizing the femtosecond pump-probe Coulomb explosion method, we probe the isomerization dynamics process of a monovalent cyclopropane cation (C3H6+) caused by proton migration and reveal the relationship between proton migration and JT distortion. We found that the C3H6+ cation evolves from the D3h symmetric equilateral triangle geometry either to the acute triangle via two elongated C-C bonds (JT1) or to the obtuse triangle via a single elongated C-C bond (JT2). The JT1 pathway does not involve proton migration, while the JT2 pathway drives proton migration and can be mapped into the indirect dissociation channel of Coulomb explosion. The time-resolved experiment indicates that the delay time between those two JT pathways can be as large as ∼600 fs. After the JT distortion, the cyclopropane cation undergoes a subsequent structural evolution, which brings a greater variety of dissociation channels.

New Insights into Decabromodiphenyl Ether-Induced Splenic Injury in Chickens: Involvement of ROS-Mediated Endoplasmic Reticulum Stress Pathway Triggering Autophagy and Apoptosis.

Decabromodiphenyl ether (BDE-209) is a widely used brominated flame retardant that can easily detach from materials and enter into feed and foodstuffs, posing a serious risk to human and animal health and food safety of animal origin. However, the immunotoxic effects of BDE-209 on the avian spleen and the exact mechanism of the toxicity remain unknown. Therefore, we established an experimental model of BDE-209-exposed chickens and a positive control model of cyclophosphamide-induced immunosuppression in vivo and treated MDCC-MSB-1 cells and chicken splenic primary lymphocytes with BDE-209 in vitro. The results showed that BDE-209 treatment caused morphological and structural abnormalities in the chicken spleens. Mechanistically, indicators related to oxidative stress, endoplasmic reticulum stress (ERS), autophagy, and apoptosis were significantly altered by BDE-209 exposure in both the spleen and lymphocytes, but the use of the N-acetylcysteine or the 4-phenylbutyric acid significantly reversed these changes. In addition, BDE-209 exposure decreased the spleen antimicrobial peptide and immunoglobulin gene expression. In conclusion, the present research revealed that BDE-209 exposure enhanced lymphocyte autophagy and apoptosis in chicken spleen via the ROS-mediated ERS pathway. This signaling cascade regulatory relationship not only opens up a new avenue for studying BDE-209 immunotoxicity but also provides important insights into preventing BDE-209 hazards to animal health.

The scaffold of neutrophil extracellular traps promotes CCA progression and modulates angiogenesis via ITGAV/NFκB.

Neutrophil extracellular traps (NETs) have garnered attention for their dual role in host defense and tumor promotion. With their involvement documented across a spectrum of tumors, their influence on the progression of cholangiocarcinoma (CCA) is of paramount interest. We employed immunohistochemistry and immunofluorescence to detect NET deposition in CCA tissues. Through in vitro and in vivo investigation, including CCA organoid and transposon-based models in PAD4 KO mice, we explored the effects of NETs on cell proliferation and metastasis. Molecular insights were gained through RNA sequencing, enzyme linked immunosorbent assay, and chromatin immunoprecipitation. Elevated intratumoral NET deposition within CCA tissues was associated with poor survival. The influence of NETs on CCA proliferation, migration and invasion was primarily mediated by NET-DNA. RNA sequencing unveiled the activation of the NFκB signaling pathway due to NET-DNA stimulation. NET-DNA pull-down assay coupled with mass spectrometry revealed the interaction between NET-DNA and αV integrin (ITGAV), culmination in the activation of the NFκB pathway. Furthermore, NET-DNA directly upregulated the expression of VEGF-A in cancer cells. The study unequivocally establishes NETs as facilitators of CCA progression, orchestrating proliferation, metastasis, and angiogenesis through ITGAV/NFκB pathway activation. This novel insight positions NETs as prospective therapeutic targets for managing CCA patients. By implementing a variety of methodologies and drawing intricate connections between NETs, DNA interactions, and signaling pathways, this research expands our comprehension of the complex interplay between the immune system and cancer progression, offering promising avenues for intervention.

Nano­selenium alleviates the pyroptosis of cardiovascular endothelial cells in chicken induced by decabromodiphenyl ether through ERS-TXNIP-NLRP3 pathway.

Decabromodiphenyl ether (BDE-209) is one of the most widely used flame retardants that can infect domestic and wildlife through contaminated feed. Nano­selenium (Nano-Se) has the advantage of enhancing the anti-oxidation of cells. Nonetheless, it remains uncertain whether Nano-Se can alleviate vascular Endothelial cells damage caused by BDE-209 exposure in chickens. Therefore, we established a model with 60 1-day-old chickens, and administered BDE-209 intragastric at a ratio of 400 mg/kg bw/d, and mixed Nano-Se intervention at a ratio of 1 mg/kg in the feed. The results showed that BDE-209 could induce histopathological and ultrastructural changes. Additionally, exposure to BDE-209 led to cardiovascular endoplasmic reticulum stress (ERS), oxidative stress and thioredoxin-interacting protein (TXNIP)-pyrin domain-containing protein 3 (NLRP3) pathway activation, ultimately resulting in pyroptosis. Using the ERS inhibitor 4-PBA in Chicken arterial endothelial cells (PAECs) can significantly reverse these changes. The addition of Nano-Se can enhance the body's antioxidant capacity, inhibit the activation of NLRP3 inflammasome, and reduce cellular pyroptosis. These results suggest that Nano-Se can alleviate the pyroptosis of cardiovascular endothelial cells induced by BDE-209 through ERS-TXNIP-NLRP3 pathway. This study provides new insights into the toxicity of BDE-209 in the cardiovascular system and the therapeutic effects of Nano-Se.

CO2 emission prediction based on carbon verification data of 17 thermal power enterprises in Gansu Province.

The energy and power industry is an important field for CO2 emission reduction. The CO2 emitted by thermal power enterprises is a major cause of global climate change, and also a key challenge for China to achieve the goals of "carbon peaking and carbon neutrality." Therefore, it is essential to scientifically and accurately predict the CO2 emissions of key thermal power enterprises in the region. This will guide carbon reduction strategies and policy recommendations for leaders, and also provide a valuable reference for similar regions globally. This study utilizes the factor analysis method to extract the common factors influencing CO2 emissions based on the carbon verification data of 17 thermal power enterprises in Gansu Province. Additionally, the DISO (distance between indices of simulation and observation) index is employed to comprehensively evaluate three prediction models, namely multiple linear regression, support vector regression, and GA-BP neural network. Ultimately, this study provides a reasonable prediction of CO2 emissions for the aforementioned enterprises in Gansu Province. The results show that the three common factors obtained by factor analysis, namely energy consumption and output factor, energy quality factor, and energy efficiency factor, can effectively predict the CO2 emissions from thermal power enterprises. In the three prediction models, GA-BP neural network has the best overall performance with DISO value of 0.95, RMSE value of 11848.236, and MAE value of 7880.543. Over the period 2022-2030, CO2 emissions from 17 thermal power enterprises in Gansu Province are predicted to increase. Under the low-carbon, scenario baseline, and high-carbon scenarios, the CO2 emissions will reach 71.58 Mt, 79.25 Mt, and 87.97 Mt, respectively, by 2030.

Selenomethionine alleviates decabromodiphenyl ether-induced oxidative stress and ferroptosis via the NRF2/GPX4 pathway in the chicken brain.

Decabromodiphenyl ether (BDE209) is a toxic environmental pollutant that can cause neurotoxicity, behavioral abnormalities, and cognitive impairment in animals. However, the specific mechanisms of BDE209-induced neurological injury and effective preventative and therapeutic interventions are lacking. Even though selenomethionine (Se-Met) has a significant detoxification effect and protects the nervous system, it remains unclear whether Se-Met can counteract the toxic effects of BDE209. For the in vivo test, we randomly divided 60 1-week-old hy-line white variety chicks into the Con, BDE209, Se-Met, and BDE209 +Se-Met groups. In vitro experiments were performed, exposing chick embryo brain neurons to BDE209, Se-Met, N-Acetylcysteine (NAC, a ROS inhibitor), and RSL3 (a GPX4 inhibitor). We demonstrated that BDE209 induced oxidative stress and ferroptosis in the chicken brain, which mainly manifested as mitochondrial atrophy, cristae breakage, increased Fe2+ and MDA content, decreased antioxidant enzyme activity, and the inhibition of the NRF2/GPX4 signaling pathway in the brain neurons. However, Se-Met supplementation reversed these changes by activating the NRF2/GPX4 pathway, reducing mitochondrial damage, enhancing antioxidant enzyme activity, and alleviating ferroptosis. This study provides insight into the mechanism of BDE209-related neurotoxicity and suggests Se-Met as an effective preventative and control measure against BDE209 poisoning.

Molecular and functional characterization of Schistosoma japonicum annexin A13.

Schistosomiasis is a neglected tropical disease that affects humans and animals in tropical and subtropical regions worldwide. Schistosome eggs are responsible for the pathogenesis and transmission of schistosomiasis, thus reducing egg production is vital for prevention and control of schistosomiasis. However, the mechanisms underlying schistosome reproduction remain unclear. Annexin proteins (ANXs) are involved in the physiological and pathological functions of schistosomes, but the specific regulatory mechanisms and roles of ANX A13 in the development of Schistosoma japonicum and host-parasite interactions remain poorly understood. Therefore, in this study, the expression profiles of SjANX A13 at different life cycle stages of S. japonicum were assessed using quantitative PCR. In addition, the expression profiles of the homolog in S. mansoni were analyzed in reference to public datasets. The results of RNA interference showed that knockdown of SjANX A13 significantly affected the development and egg production of female worms in vivo. The results of an immune protection assay showed that recombinant SjANX A13 increased production of immunoglobulin G-specific antibodies. Finally, co-culture of S. japonicum exosomes with LX-2 cells using a transwell system demonstrated that SjANX A13 is involved in host-parasite interactions via exosomes. Collectively, these results will help to clarify the roles of SjANX A13 in the development of S. japonicum and host-parasite interactions as a potential vaccine candidate.

Sja-Let-7 Attenuates Carbon Tetrachloride-Induced Liver Fibrosis in a Mouse Model via Col1α2.

Liver fibrosis (LF) is a chronic progressive disease with no definitive treatment. The aim of this study was to assess helminth-derived molecules as potential therapeutic targets to prevent or reverse LF. A mouse model of carbon tetrachloride (CCL4)-induced LF was established and sja-let-7 was overexpressed by treatment with a miRNA agomir once per week. After four weeks, serum biochemistry, hepatic hydroxyproline content measurements, liver histology, mRNA expression profiling of fibrotic markers, the dual-luciferase reporter assay, and fluorescence in situ hybridization (FISH) were performed. Administration of the sja-let-7 agomir markedly ameliorated hepatosplenomegaly and reduced the liver hydroxyproline content. Liver histological analysis showed significant reductions in collagen deposition in the sja-let-7 agomir-treated mice. Additionally, the mRNA levels of both pro-fibrotic markers and pro-inflammatory cytokines were diminished after treatment. Furthermore, the dual-luciferase reporter assay and FISH identified the α2 chain of collagen type 1 (Col1α2) as the direct target of sja-let-7. Accordingly, the progression of LF was attenuated by targeting Col1α2 and the TGF-ß/Smad signaling pathway.

Corrigendum: Alterations via inter-regional connective relationships in Alzheimer's disease.

[This corrects the article DOI: 10.3389/fnhum.2023.1276994.].

Alterations via inter-regional connective relationships in Alzheimer's disease.

Disruptions in the inter-regional connective correlation within the brain are believed to contribute to memory impairment. To detect these corresponding correlation networks in Alzheimer's disease (AD), we conducted three types of inter-regional correlation analysis, including structural covariance, functional connectivity and group-level independent component analysis (group-ICA). The analyzed data were obtained from the Alzheimer's Disease Neuroimaging Initiative, comprising 52 cognitively normal (CN) participants without subjective memory concerns, 52 individuals with late mild cognitive impairment (LMCI) and 52 patients with AD. We firstly performed vertex-wise cortical thickness analysis to identify brain regions with cortical thinning in AD and LMCI patients using structural MRI data. These regions served as seeds to construct both structural covariance networks and functional connectivity networks for each subject. Additionally, group-ICA was performed on the functional data to identify intrinsic brain networks at the cohort level. Through a comparison of the structural covariance and functional connectivity networks with ICA networks, we identified several inter-regional correlation networks that consistently exhibited abnormal connectivity patterns among AD and LMCI patients. Our findings suggest that reduced inter-regional connectivity is predominantly observed within a subnetwork of the default mode network, which includes the posterior cingulate and precuneus regions, in both AD and LMCI patients. This disruption of connectivity between key nodes within the default mode network provides evidence supporting the hypothesis that impairments in brain networks may contribute to memory deficits in AD and LMCI.

NK Receptors Replace CD28 As the Dominant Source of Signal 2 for Cognate Recognition of Cancer Cells by TAA-specific Effector CD8+ T Cells.

CD28-driven "signal 2" is critical for naïve CD8+ T cell responses to dendritic cell (DC)-presented weak antigens, including non-mutated tumor-associated antigens (TAAs). However, it is unclear how DC-primed cytotoxic T lymphocytes (CTLs) respond to the same TAAs presented by cancer cells which lack CD28 ligands. Here, we show that NK receptors (NKRs) DNAM-1 and NKG2D replace CD28 during CTL re-activation by cancer cells presenting low levels of MHC I/TAA complexes, leading to enhanced proximal TCR signaling, immune synapse formation, CTL polyfunctionality, release of cytolytic granules and antigen-specific cancer cell killing. Double-transduction of T cells with recombinant TCR and NKR constructs or upregulation of NKR-ligand expression on cancer cells by chemotherapy enabled effective recognition and killing of poorly immunogenic tumor cells by CTLs. Operational synergy between TCR and NKRs in CTL recognition explains the ability of cancer-expressed self-antigens to serve as tumor rejection antigens, helping to develop more effective therapies.

High-Accuracy Maize Disease Detection Based on Attention Generative Adversarial Network and Few-Shot Learning.

This study addresses the problem of maize disease detection in agricultural production, proposing a high-accuracy detection method based on Attention Generative Adversarial Network (Attention-GAN) and few-shot learning. The method introduces an attention mechanism, enabling the model to focus more on the significant parts of the image, thereby enhancing model performance. Concurrently, data augmentation is performed through Generative Adversarial Network (GAN) to generate more training samples, overcoming the difficulties of few-shot learning. Experimental results demonstrate that this method surpasses other baseline models in accuracy, recall, and mean average precision (mAP), achieving 0.97, 0.92, and 0.95, respectively. These results validate the high accuracy and stability of the method in handling maize disease detection tasks. This research provides a new approach to solving the problem of few samples in practical applications and offers valuable references for subsequent research, contributing to the advancement of agricultural informatization and intelligence.

SeNPs alleviates BDE-209-induced intestinal damage by affecting necroptosis, inflammation, intestinal barrier and intestinal flora in layer chickens.

As environmental pollutants, polybrominated diphenyl ethers (PBDEs) can have toxic effects on living organisms and has a bioaccumulative effect. Low doses of selenium nanoparticles (SeNPs) can exert antioxidant, anti-inflammatory and anti-toxin functions on the organism. This experiment evaluated SeNPs' ability to prevent chicken's intestinal damage from decabromodiphenyl ether (BDE-209) exposure. Sixty layer chickens were separated into four groups at randomly and equally: Control group, SeNPs group (1 mg/kg SeNPs), BDE-209 group (400 mg/kg BDE-209), and BDE-209 +SeNPs group (400 mg/kg BDE-209 and 1 mg/kg SeNPs), for 42 days. The results showed that BDE-209 increased MDA content, decreased the activities of T-SOD, T-AOC, GSH and iNOS, up-regulated the expression of TNF-α, RIPK1, RIPK3 and MLKL, promoted the production of inflammatory factors, reduced the levels of tight junction proteins (Claudin-1, Occludin, ZO-1). SeNPs attenuated intestinal oxidative stress, necroptosis, inflammation and intestinal barrier damage caused by BDE-209. This protective effect is associated with the MAPK/NF-κB signaling pathway. Moreover, SeNPs restores flora alpha and beta diversity, improves intestinal flora composition and its abundance. It shifts the dysbiosis of intestinal flora caused by BDE-209 to normal. Overall, SeNPs can alleviate BDE-209-induced intestinal barrier damage and intestinal flora disorders, which are associated with intestinal oxidative stress, necroptosis and inflammation.

Toward a stable and low-resource PLM-based medical diagnostic system via prompt tuning and MoE structure.

Machine learning (ML) has been extensively involved in assistant disease diagnosis and prediction systems to emancipate the serious dependence on medical resources and improve healthcare quality. Moreover, with the booming of pre-training language models (PLMs), the application prospect and promotion potential of machine learning methods in the relevant field have been further inspired. PLMs have recently achieved tremendous success in diverse text processing tasks, whereas limited by the significant semantic gap between the pre-training corpus and the structured electronic health records (EHRs), PLMs cannot converge to anticipated disease diagnosis and prediction results. Unfortunately, establishing connections between PLMs and EHRs typically requires the extraction of curated predictor variables from structured EHR resources, which is tedious and labor-intensive, and even discards vast implicit information.In this work, we propose an Input Prompting and Discriminative language model with the Mixture-of-experts framework (IPDM) by promoting the model's capabilities to learn knowledge from heterogeneous information and facilitating the feature-aware ability of the model. Furthermore, leveraging the prompt-tuning mechanism, IPDM can inherit the impacts of the pre-training in downstream tasks exclusively through minor modifications. IPDM remarkably outperforms existing models, proved by experiments on one disease diagnosis task and two disease prediction tasks. Finally, experiments with few-feature and few-sample demonstrate that IPDM achieves significant stability and impressive performance in predicting chronic diseases with unclear early-onset characteristics or sudden diseases with insufficient data, which verifies the superiority of IPDM over existing mainstream methods, and reveals the IPDM can powerfully address the aforementioned challenges via establishing a stable and low-resource medical diagnostic system for various clinical scenarios.

Downregulated Acetyl-CoA Acyltransferase 2 Promoted the Progression of Hepatocellular Carcinoma and Participated in the Formation of Immunosuppressive Microenvironment.

Background: The aim of this study is to explore the role of acetyl-CoA acyltransferase 2 (ACAA2) in the progression of hepatocellular carcinoma (HCC). Methods: Bulk RNA data and single-cell RNA data were acquired from The Cancer Genome Atlas and Gene Expression Omnibus. Both in vitro and in vivo studies were used to determine the effect of ACAA2 on the progression of HCC, and RNA sequencing analysis was performed to explore the mechanism. Results: We found downregulation of ACAA2 was involved in the malignant progression of HCC. The patient with low ACAA2 level had an immunosuppressive microenvironment in the HCC and predicted to have a poor prognosis. Decreased ACAA2 facilitated HCC proliferation and metastasis by activating the nuclear factor-κB (NFκB) signaling pathway. And increased CXCL1 induced by NFκB signaling pathway might be responsible for low level of ACAA2 related immunosuppressive microenvironment. Furthermore, the expression of ACAA2 was also detected in immune cells. The expression of ACAA2 in CD4+TCF7+T, CD4+FOXP3+T, CD8+GZMK+T, and CD8+KLRD1+T cells was inversely correlated with the composition of CD8+PDCD1+T cells in HCC. This effect might be due to the CCL5-CCRs and HLA-E-KLRCs ligand-receptor networks. Conclusion: In a conclusion, downregulated ACAA2 promoted the progression of hepatocellular carcinoma and might be participated in the formation of immunosuppressive microenvironment. ACAA2 could be served as a favorable indicator for the prognosis of HCC and an ideal biomarker for immunotherapy.

Metabolic Dysregulation Explains the Diverse Impacts of Obesity in Males and Females with Gastrointestinal Cancers.

The prevalence of obesity, defined as the body mass index (BMI) ≥ 30 kg/m2, has reached epidemic levels. Obesity is associated with an increased risk of various cancers, including gastrointestinal ones. Recent evidence has suggested that obesity disproportionately impacts males and females with cancer, resulting in varied transcriptional and metabolic dysregulation. This study aimed to elucidate the differences in the metabolic milieu of adenocarcinomas of the gastrointestinal (GI) tract both related and unrelated to sex in obesity. To demonstrate these obesity and sex-related effects, we utilized three primary data sources: serum metabolomics from obese and non-obese patients assessed via the Biocrates MxP Quant 500 mass spectrometry-based kit, the ORIEN tumor RNA-sequencing data for all adenocarcinoma cases to assess the impacts of obesity, and publicly available TCGA transcriptional analysis to assess GI cancers and sex-related differences in GI cancers specifically. We applied and integrated our unique transcriptional metabolic pipeline in combination with our metabolomics data to reveal how obesity and sex can dictate differential metabolism in patients. Differentially expressed genes (DEG) analysis of ORIEN obese adenocarcinoma as compared to normal-weight adenocarcinoma patients resulted in large-scale transcriptional reprogramming (4029 DEGs, adj. p < 0.05 and |logFC| > 0.58). Gene Set Enrichment and metabolic pipeline analysis showed genes enriched for pathways relating to immunity (inflammation, and CD40 signaling, among others) and metabolism. Specifically, we found alterations to steroid metabolism and tryptophan/kynurenine metabolism in obese patients, both of which are highly associated with disease severity and immune cell dysfunction. These findings were further confirmed using the TCGA colorectal adenocarcinoma (CRC) and esophageal adenocarcinoma (ESCA) data, which showed similar patterns of increased tryptophan catabolism for kynurenine production in obese patients. These patients further showed disparate alterations between males and females when comparing obese to non-obese patient populations. Alterations to immune and metabolic pathways were validated in six patients (two obese and four normal weight) via CD8+/CD4+ peripheral blood mononuclear cell RNA-sequencing and paired serum metabolomics, which showed differential kynurenine and lipid metabolism, which corresponded with altered T-cell transcriptome in obese populations. Overall, obesity is associated with differential transcriptional and metabolic programs in various disease sites. Further, these alterations, such as kynurenine and tryptophan metabolism, which impact both metabolism and immune phenotype, vary with sex and obesity together. This study warrants further in-depth investigation into obesity and sex-related alterations in cancers that may better define biomarkers of response to immunotherapy.

Multi-omics analysis of expression profile and prognostic values of connexin family in LUAD.

PURPOSE: Our study first explored the expression differences and prognostic significance of Cx genes in pan-cancer and then focused on LUAD. Our objectives were to conducted a comprehensive analysis of the expression profile, prognostic significance, genetic alterations, potential biological functions and drug sensitivity of the Connexin gene family in LUAD. METHODS: We developed a comprehensive prognostic model for LUAD by combining risk scores with clinical features and created a nomogram to predict 1-, 3-, and 5-year overall survival. Using single-cell sequencing, we examined the expression and biological functions of the identified prognostic markers. RESULTS: Our risk model revealed that GJB2-5 play a critical role in the prognosis of LUAD patients, associated with many biological processes such as cell cycle, DNA damage, EMT, hypoxia, invasion, and metastasis. Furthermore, the connexin gene family is linked to transcriptional mechanisms such as the extracellular matrix (ECM), migration, mobility, angiogenesis, and the epithelial-mesenchymal transition (EMT) genetic program. CONCLUSION: The risk model can be used as a potential prognostic factor for LUAD patients and may provide new insights into cancer treatment from perspective of the expression of Cx genes.

Cost-Optimization-Based Quantum Key Distribution over Quantum Key Pool Optical Networks.

The Measurement-Device-Independent-Quantum Key Distribution (MDI-QKD) has the advantage of extending the secure transmission distances. The MDI-QKD combined with the Hybrid-Trusted and Untrusted Relay (HTUR) is used to deploy large-scale QKD networks, which effectively saves deployment cost. We propose an improved scheme for the QKD network architecture and cost analysis, which simplifies the number of QKD transmitters and incorporates the quantum key pool (QKP) in the QKD network. We developed a novel Hybrid-QKD-Network-Cost (HQNC) heuristic algorithm to solve the cost optimization problem. Simulations verified that the scheme in this paper could save the cost by over 50 percent and 90 percent, respectively.

A Resource-Adaptive Routing Scheme with Wavelength Conflicts in Quantum Key Distribution Optical Networks.

Quantum key distribution (QKD) has great potential in ensuring data security. Deploying QKD-related devices in existing optical fiber networks is a cost-effective way to practically implement QKD. However, QKD optical networks (QKDON) have a low quantum key generation rate and limited wavelength channels for data transmission. The simultaneous arrival of multiple QKD services may also lead to wavelength conflicts in QKDON. Therefore, we propose a resource-adaptive routing scheme (RAWC) with wavelength conflicts to achieve load balancing and efficient utilization of network resources. Focusing on the impact of link load and resource competition, this scheme dynamically adjusts the link weights and introduces the wavelength conflict degree. Simulation results indicate that the RAWC algorithm is an effective approach to solving the wavelength conflict problem. Compared with the benchmark algorithms, the RAWC algorithm can improve service request success rate (SR) by up to 30%.