Inhibition of ferroptosis reverses heart failure with preserved ejection fraction in mice.

BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of heart failure cases. The molecular mechanisms by which HFpEF leads to impaired diastolic function of the heart have not been clarified, nor have the drugs that target the clinical symptoms of HFpEF patients. METHODS: HFpEF chip data (GSE180065) was downloaded from the National Center for Biotechnology Information (NCBI) database. Differentially expressed genes (DEGs) were filtered by the limma package in R and processed for GO and KEGG pathway analyses. Then, ferroptosis-related genes in HFpEF were identified by taking the intersection between DEGs and ferroptosis-related genes. CytoHubba and MCODE were used to screen ferroptosis-related hub DEGs in the protein-protein interaction (PPI) network. Establishment of a mouse HFpEF model to validate the transcript levels of ferroptosis-related hub DEGs and ferroptosis-related phenotypes. Transcript levels of ferroptosis-related hub DEGs and HFpEF phenotypic changes in the hearts of HFpEF mice were further examined after the use of ferroptosis inhibitors. RESULTS: GO and KEGG enrichment analyses suggested that the DEGs in HFpEF were significantly enriched in ferroptosis-related pathways. A total of 24 ferroptosis-related DEGs were identified between the ferroptosis gene dataset and the DEGs. The established PPI network was further analyzed by CytoHubba and MCODE modules, and 11 ferroptosis-related hub DEGs in HFpEF were obtained. In animal experiments, HFpEF mice showed significant abnormal activation of ferroptosis. The expression trends of the 11 hub DEGs associated with ferroptosis, except for Cdh1, were consistent with the results of the bioinformatics analysis. Inhibition of ferroptosis alters the transcript levels of 11 ferroptosis-related hub DEGs and ameliorates HFpEF phenotypes. CONCLUSIONS: The present study contributes to a deeper understanding of the specific mechanisms by which ferroptosis is involved in the development of HFpEF and suggests that inhibition of ferroptosis may mitigate the progression of HFpEF. In addition, eleven hub genes were recognized as potential drug binding targets.

Students' 2018 PISA reading self-concept: Identifying predictors and examining model generalizability for emergent bilinguals.

Decades of research have indicated that reading self-concept is an important predictor of reading achievement. During this period, the population of emergent bilinguals has continued to increase within United States' schools. However, the existing literature has tended to examine native English speakers' and emergent bilinguals' reading self-concept in the aggregate, thereby potentially obfuscating the unique pathways through which reading self-concept predicts reading achievement. Furthermore, due to the overreliance of native English speakers in samples relating to theory development, researchers attempting to examine predictors of reading achievement may a priori select variables that are more aligned with native English speakers' experiences. To address this issue, we adopted Elastic Net, which is a theoretically agnostic methodology and machine learning approach to variable selection to identify the proximal and distal predictors of reading self-concept for the entire population; in our study, participants from the United States who participated in PISA 2018 served as the baseline group to determine significant predictors of reading self-concept with the intent of identifying potential new directions for future researchers. Based on Elastic Net analysis, 20 variables at the student level, three variables at the teacher level, and 12 variables at the school level were identified as the most salient predictors of reading self-concept. We then utilized a multilevel modeling approach to test model generalizability of the identified predictors of reading self-concept for emergent bilinguals and native English speakers. We disaggregated and compared findings for both emergent bilinguals and native English speakers. Our results indicate that although some predictors were important for both groups (e.g., perceived information and communications technologies competence), other predictors were not (e.g., competitiveness). Suggestions for future directions and implications of the present study are examined.

lhCLIP reveals the in vivo RNA-RNA interactions recognized by hnRNPK.

RNA-RNA interactions play a crucial role in regulating gene expression and various biological processes, but identifying these interactions on a transcriptomic scale remains a challenge. To address this, we have developed a new biochemical technique called pCp-biotin labelled RNA hybrid and ultraviolet crosslinking and immunoprecipitation (lhCLIP) that enables the transcriptome-wide identification of intra- and intermolecular RNA-RNA interactions mediated by a specific RNA-binding protein (RBP). Using lhCLIP, we have uncovered a diverse landscape of intermolecular RNA interactions recognized by hnRNPK in human cells, involving all major classes of noncoding RNAs (ncRNAs) and mRNA. Notably, hnRNPK selectively binds with snRNA U4, U11, and U12, and shapes the secondary structure of these snRNAs, which may impact RNA splicing. Our study demonstrates the potential of lhCLIP as a user-friendly and widely applicable method for discovering RNA-RNA interactions mediated by a particular protein of interest and provides a valuable tool for further investigating the role of RBPs in gene expression and biological processes.

Hepatocellular carcinoma cell differentiation trajectory predicts immunotherapy, potential therapeutic drugs, and prognosis of patients.

The aim of this study is to explore a novel classification and investigate the clinical significance of hepatocellular carcinoma (HCC) cells. We analyzed integrated single-cell RNA sequencing and bulk RNA-seq data obtained from HCC samples. Cell trajectory analysis divided HCC cells into three subgroups with different differentiation states: state 1 was closely related to phosphoric ester hydrolase activity, state 2 was involved in eukaryotic initiation factor 4E binding, translation regulator activity and ribosome, and state 3 was associated with oxidoreductase activity and metabolism. Three molecular classes based on HCC differentiation-related genes (HDRGs) from HCC samples were identified, which revealed immune checkpoint gene expression and overall survival (OS) of HCC patients. Moreover, a prognostic risk scoring (RS) model was generated based on eight HDRGs, and the results showed that the OS of the high-risk group was worse than that of the low-risk group. Further, potential therapeutic drugs were screened out based on eight prognostic RS-HDRGs. This study highlights the importance of HCC cell differentiation in immunotherapy, clinical prognosis, and potential molecular-targeted drugs for HCC patients, and proposes a direction for the development of individualized treatments for HCC.

Umbilical cord blood exosomes from very preterm infants with bronchopulmonary dysplasia aggravate lung injury in mice.

Bronchopulmonary dysplasia (BPD) is characterized by abnormal development of the blood vessels and alveoli in lungs, which largely occurs in premature infants. Exosomes (EXO) from very preterm infants (VPI) with BPD (BPD-EXO) impair angiogenic activities of human umbilical vein endothelial cells (HUVECs) via EXO-miRNAs cargo. This study aimed to determine whether and how BPD-EXO affect the development of BPD in a mouse model. We showed that treating BPD mice with BPD-EXO chronically and irreversibly aggravated lung injury. BPD-EXO up-regulated 139 and down-regulated 735 genes in the mouse lung tissue. These differentially expressed genes were enriched to the MAPK pathway (e.g., Fgf9 and Cacna2d3), which is critical to angiogenesis and vascular remodeling. BPD-EXO suppressed expression of Fgf9 and Cacna2d3 in HUVECs and inhibited migration, tube formation, and increased cell apoptosis in HUVECs. These data demonstrate that BPD-EXO aggravate lung injury in BPD mice and impair lung angiogenesis, plausibly leading to adverse outcomes of VPI with BPD. These data also suggest that BPD-EXO could serve as promising targets for predicting and treating BPD.

Umbilical cord blood-derived exosomes from healthy term pregnancies protect against hyperoxia-induced lung injury in mice.

Bronchopulmonary dysplasia (BPD) is a chronic, devastating disease primarily occurring in premature infants. To date, intervention strategies to prevent or treat BPD are limited. We aimed to determine the effects of umbilical cord blood-derived exosomes (UCB-EXOs) from healthy term pregnancies on hyperoxia-induced lung injury and to identify potential targets for BPD intervention. A mouse model of hyperoxia-induced lung injury was created by exposing neonatal mice to hyperoxia after birth until the 14th day post birth. Age-matched neonatal mice were exposed to normoxia as the control. Hyperoxia-induced lung injury mice were intraperitoneally injected with UCB-EXO or vehicle daily for 3 days, starting on day 4 post birth. Human umbilical vein endothelial cells (HUVECs) were insulted with hyperoxia to establish an in vitro model of BPD to investigate angiogenesis dysfunction. Our results showed that UCB-EXO alleviated lung injuries in hyperoxia-insulted mice by reducing histopathological grade and collagen contents in the lung tissues. UCB-EXO also promoted vascular growth and increased miR-185-5p levels in the lungs of hyperoxia-insulted mice. Additionally, we found that UCB-EXO elevated miR-185-5p levels in HUVECs. MiR-185-5p overexpression inhibited cell apoptosis, whereas promoted cell migration in HUVECs exposed to hyperoxia. The luciferase reporter assay results revealed that miR-185-5p directly targeted cyclin-dependent kinase 6 (CDK6), which was downregulated in the lungs of hyperoxia-insulted mice. Together, these data suggest that UCB-EXO from healthy term pregnancies protect against hyperoxia-induced lung injuries via promoting neonatal pulmonary angiogenesis partially by elevating miR-185-5p.

Experimental Mode-Pairing Measurement-Device-Independent Quantum Key Distribution without Global Phase Locking.

In the past two decades, quantum key distribution networks based on telecom fibers have been implemented on metropolitan and intercity scales. One of the bottlenecks lies in the exponential decay of the key rate with respect to the transmission distance. Recently proposed schemes mainly focus on achieving longer distances by creating a long-arm single-photon interferometer over two communication parties. Despite their advantageous performance over long communication distances, the requirement of phase locking between two remote lasers is technically challenging. By adopting the recently proposed mode-pairing idea, we realize high-performance quantum key distribution without global phase locking. Using two independent off-the-shelf lasers, we show a quadratic key-rate improvement over the conventional measurement-device-independent schemes in the regime of metropolitan and intercity distances. For longer distances, we also boost the key rate performance by 3 orders of magnitude via 304 km commercial fiber and 407 km ultralow-loss fiber. We expect this ready-to-implement high-performance scheme to be widely used in future intercity quantum communication networks.

Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.

Background: The molecular mechanisms underlying obstructive sleep apnea (OSA) and its comorbidities may involve mitochondrial dysfunction. However, very little is known about the relationships between mitochondrial dysfunction-related genes and OSA. Methods: Mitochondrial dysfunction-related differentially expressed genes (DEGs) between OSA and control adipose tissue samples were identified using data from the Gene Expression Omnibus database and information on mitochondrial dysfunction-related genes from the GeneCards database. A mitochondrial dysfunction-related signature of diagnostic model was established using least absolute shrinkage and selection operator Cox regression and then verified. Additionally, consensus clustering algorithms were used to conduct an unsupervised cluster analysis. A protein-protein interaction network of the DEGs between the mitochondrial dysfunction-related clusters was constructed using STRING database and the hub genes were identified. Functional analyses, including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene set enrichment analysis (GSEA), and gene set variation analysis (GSVA), were conducted to explore the mechanisms involved in mitochondrial dysfunction in OSA. Immune cell infiltration analyses were conducted using CIBERSORT and single-sample GSEA (ssGSEA). Results: we established mitochondrial dysfunction related four-gene signature of diagnostic model consisted of NPR3, PDIA3, SLPI, ERAP2, and which could easily distinguish between OSA patients and controls. In addition, based on mitochondrial dysfunction-related gene expression, we identified two clusters among all the samples and three clusters among the OSA samples. A total of 10 hub genes were selected from the PPI network of DEGs between the two mitochondrial dysfunction-related clusters. There were correlations between the 10 hub genes and the 4 diagnostic genes. Enrichment analyses suggested that autophagy, inflammation pathways, and immune pathways are crucial in mitochondrial dysfunction in OSA. Plasma cells and M0 and M1 macrophages were significantly different between the OSA and control samples, while several immune cell types, especially T cells (γ/δ T cells, natural killer T cells, regulatory T cells, and type 17 T helper cells), were significantly different among mitochondrial dysfunction-related clusters of OSA samples. Conclusion: A novel mitochondrial dysfunction-related four-gen signature of diagnostic model was built. The genes are potential biomarkers for OSA and may play important roles in the development of OSA complications.

TMUB1 Correlated with Immune Infiltration Is a Prognostic Marker for Colorectal Cancer.

Background: Transmembrane and ubiquitin-like domain-containing protein 1 (TMUB1) is overexpressed in a large number of liver and esophageal tumors. However, only a few reports on the clinical significance of TMUB1 in colorectal cancer (CRC) exist. Methods: Here, we evaluated the clinical significance and potential biological role of TMUB1 using bioinformatics analysis. Univariate and multivariate analyses were performed to evaluate the relationship of TMUB1 with clinicopathological features. Gene set enrichment analysis (GSEA) was performed to identify the biological function of TMUB1, while any associations between the expression of TMUB1 and the infiltration of 24 immune cells were analyzed using simple-sample GSEA. Results: TMUB1 was significantly overexpressed in CRC tissues compared with normal controls. The high expression of TMUB1 in CRC was associated with T stage, neotype, and residual tumor. Moreover, TMUB1 was identified as an independent factor of poor disease-free survival (DFS) and short overall survival (OS). GSEA demonstrated that TMUB1 was related to hypoxia, angiogenesis, adipogenesis, inflammatory response, IL6-JAK-STAT3 signaling, apoptosis, mitotic spindle, and IL2-STAT5 signaling. The expression of TMUB1 negatively correlated with the abundance of T helper cells, Tcm cells, macrophages, and Th2 cells, whereas it positively correlated with the abundance of several immune cell types, including CD56bright and CD56dim NK cells. Conclusions: The high expression of TMUB1 is closely related to a poor prognosis in patients with CRC. TMUB1 may be a potential prognostic biomarker and be used for therapeutic approaches in CRC.

Effects and mechanism of ultrasound treatment on Chironomus kiiensis eggs.

Chironomids are abundant insects in freshwater ecosystems and lay in still or slow-moving water. The walls of sedimentation tanks in drinking water treatment plants (DWTP) provide such laying habitat, which can lead to larval outbreaks in plant effluent. While chironomid larvae are often associated with poor hygiene, effective methods to control outbreaks are needed. Here, we assessed the effect of ultrasound treatment on Chironomus kiiensis' eggs. The mortality rate of eggs was examined after ultrasound treatment, and the protein content (heat shock protein 70 and hemoglobin) and enzymatic activities of acetylcholinesterase, cytochrome P450, and glutathione S-transferases involved in the ultrasound-induced stress response were analyzed before and after treatment. COMSOL software was also used to examine the characteristics of the ultrasonic field, including frequency, power, exposure distance, and time. Higher egg mortality was observed at lower frequencies. At 28 kHz, 450 W, 15-mm exposure distance, and 75-s exposure time, 72.4% of eggs showed apoptosis after exposure. At higher frequencies (68 kHz), mortality decreased to 50.9%. Exposure time and distance also significantly affected egg mortality. From the geometric models, it could be seen that C. kiiensis' eggs sustained much greater acoustic pressure (2379 Pa) with 28-kHz exposure than that with 68-kHz exposure (422 Pa); however, the propagation distance was greater at the higher frequency. The hydraulic shear force effect of the ultrasonic radiation appeared to be the primary factor in egg mortality. We expected that array of ultrasonic transducers embedded in the walls of water treatment plants could be effective in killing Chironomus' eggs and highlight the potential for ultrasound as an effective treatment for the prevention of Chironomus outbreaks in treatment plant effluents.

Revisited Cyclophosphamide in the Treatment of Lupus Nephritis.

Lupus nephritis (LN) is the most common serious complication of systemic lupus erythematosus (SLE). The pathogenesis of LN is complex, and the majority causes of LN are the renal deposition of circulating or/and in situ-formed immune complexes. These immune complexes trigger glomerular and tubulointerstitial inflammation, which finally leads to proteinuria and loss of renal function. Despite the emergence of new biological agents, cyclophosphamide (CY), an alkylating agent, is still the first-line drug widely used to treat patients with severe LN. In this review, we outline the application history, molecular structure, and pharmacokinetics of CY in the treatment of LN. We also detail its latest known immunopharmacological mechanisms, with a focus on supplemental regulation and inhibition of CD4 and CD8 positive T cells, differences in the use of various guidelines, and the combination with other drugs. The side effects of CY are also mentioned in this review.

Microbial composition and nitrogen removal pathways in a novel sequencing batch reactor integrated with semi-fixed biofilm carrier: evidence from a pilot study for low- and high-strength sewage treatment.

The sequencing batch reactor (SBR) activated sludge process is a well-established technology for sewage treatment. One of the drawbacks of SBRs, however, total nitrogen (TN) removals is insufficient. By means of introducing four improvements, including semi-fixed biofilm carrier, sludge elevation mixing and change for the mode of influent and effluent, compliant standard for TN discharge was obtained in this novel SBR configuration during low- and high-strength sewage load. To illustrate the microbial compositions and functions of the attached biofilm on semi-fixed carrier and the suspended aggregates, as well as the nitrogen removal pathway, high throughput 16S rRNA gene amplicon sequencing, PICRUSt2 algorithm, and KEGG database were applied. The results revealed that (i) the microbial communities from suspended aggregates and biofilm samples were significantly different from each other; (ii) during low-strength sewage loads, TN removal was mainly by nitrification-denitrification. The suspended aggregates was responsible for denitrification, while the biofilm was focused on ammonium oxidation; (iii) during high-strength sewage loads, function of nitrate reductase from suspended aggregates was faded, and anammox and N assimilation by biofilm became dominant. Meanwhile, TN removal referring to the formation of L-glutamine via assimilation was the main pathway.

Modulating Oxidative Stress in B Cells Promotes Immunotherapy in Food Allergy.

Allergen-specific immunotherapy (SIT) is the mainstay in the treatment of allergic diseases; its therapeutic efficacy is to be improved. Bacterial flagellin (FGN) has immune regulatory functions. This study investigates the role of FGN in promoting immunotherapy efficacy through modulating oxidative stress in regulatory B cells (Bregs). Blood samples were collected from patients with food allergy (FA) and healthy control (HC) subjects. CD19+ CD5+ Bregs were purified from blood samples by flow cytometry cell sorting. A murine FA model was developed with ovalbumin as the specific antigen. The results showed that peripheral Bregs from FA patients showed lower TLR5-related signals and higher apoptotic activities. The peripheral Breg frequency was negatively correlated with serum FGN levels in FA patients. Exposure to a specific antigen in culture induced antigen-specific Breg apoptosis that was counteracted by the presence of FGN. FGN diminished specific antigen-induced oxidative stress in Bregs. The STAT3/MAPKp38/NF-κB signal pathway was involved in the FGN/TLR5 signal-promoted superoxide dismutase expression in Bregs. Administration of FGN promotes the SIT efficacy in suppressing experimental FA. In summary, administration of FGN promotes SIT efficacy on FA, suggesting that the combination of FGN and SIT can be a novel therapy that has the translational potential to be employed in the treatment of allergic diseases.

DNA N6-methyladenine involvement and regulation of hepatocellular carcinoma development.

DNA N6-methyladenine (6 mA) is a new type of DNA methylation identified in various eukaryotic cells. However, its alteration and genomic distribution features in hepatocellular carcinoma (HCC) remain elusive. In this study, we found that N6AMT1 overexpression increased HCC cell viability, suppressed apoptosis, and enhanced migration and invasion, whereas ALKBH1 overexpression induced the opposite effects. Further, 23,779 gain-of-6 mA regions and 11,240 loss-of-6 mA regions were differentially identified in HCC tissues. The differential gain and loss of 6 mA regions were considerably enriched in intergenic regions. Moreover, 7% of the differential 6 mA modifications were associated with tumors, with 60 associated with oncogenes and 57 with tumor suppressor genes (TSGs), and 17 were common to oncogenes and TSGs. The candidate genes affected by 6 mA were filtered by gene ontology (GO) and RNA-seq. Using quantitative polymerase chain reaction (qPCR), BCL2 and PARTICL were found to be correlated with DNA 6 mA in certain HCC processes.

Efficacy and safety of early oral feeding in postoperative patients with upper gastrointestinal tumor: A systematic review and meta-analysis.

BACKGROUND: Early oral feeding (EOF) is an important measure for early recovery of patients with gastrointestinal tumors after surgery, which has emerged as a safe and effective postoperative strategy for improving clinical outcomes. AIM: To determine the safety and efficacy of early oral feeding in postoperative patients with upper gastrointestinal tumor. METHODS: This meta-analysis was analyzed using Review Manager version 5.3 and Stata version 14. All clinical studies that analyzed efficacy and safety of EOF for postoperative patients with upper gastrointestinal tumor were included. RESULTS: Fifteen studies comprising 2100 adult patients met all the inclusion criteria. A significantly lower risk of pneumonia was presented in the EOF compared with TOF group [relative risk (RR) = 0.63, 95% confidence interval (CI): 0.44-0.89, P = 0.01]. Length of hospital stay was significantly shorter in the EOF group than in the TOF group [weighted mean difference (WMD) = -1.91, 95%CI: -2.42 to -1.40; P < 0.01]. Cost of hospitalization was significantly lower (WMD = -4.16, 95%CI: -5.72 to -2.61; P < 0.01), and CD4 cell count and CD4/CD8 cell ratio on postoperative day 7 were significantly higher in the EOF group than in the TOF group: CD4 count (WMD = 7.17, 95%CI: 6.48-7.85; P < 0.01), CD4/CD8 ratio (WMD = 0.29, 95%CI: 0.23-0.35; P < 0.01). There was no significant difference in risk of anastomotic leak and total postoperative complications. CONCLUSION: EOF as compared with TOF was associated with lower risk of pneumonia, shorter hospital length of stay, lower cost of hospitalization, and significantly improved postoperative immune function of patients.

HDAC inhibitor Trichostatin A suppresses adipogenesis in 3T3-L1 preadipocytes.

BACKGROUND AND PURPOSE: Obesity is becoming a major global health issue and is mainly induced by the accumulation of adipose tissues mediated by adipogenesis, which is reported to be regulated by peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα). Trichostatin A (TSA) is a novel histone deacetylase inhibitor (HDACI) that was recently reported to exert multiple pharmacological functions. The present study will investigate the inhibitory effect of TSA on adipogenesis, as well as the underlying mechanism. METHODS: The adipogenesis of 3T3-L1 cells was induced by stimulation with a differentiation cocktail (DMI) medium for 8 days. MTT assay was used to measure the cell viability and Oil Red O staining was used to evaluate the adipogenesis of 3T3-L1 cells. The total level of triglyceride and released glycerol were detected to evaluate the lipolysis during 3T3-L1 adipogenesis. The expression levels of Leptin, fatty acid-binding protein 4 (FABP4), and sterol regulatory element-binding protein (SREBP1C) were determined by qRT-PCR. qRT-PCR assay was utilized to detect the expression levels of PPARγ and C/EBPα in 3T3-L1 cells. A high-fat diet (HFD) was used to construct an obese mice model, followed by the treatment with TSA. HE staining was conducted to evaluate the pathological state of adipose tissues. Body weights and the weights of adipose tissues were recorded to evaluate the anti-obesity property of TSA. RESULTS: Firstly, the promoted lipid accumulation induced by DMI incubation was significantly reversed by the treatment with TSA in a dose-dependent manner. The elevated expression levels of Leptin, FABP4, SREBP1C, PPARγ, and C/EBPα induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK). Secondly, the inhibitory effect of TSA against the expression level of PPARγ and lipid accumulation was greatly abolished by an AMPK inhibitor. Lastly, the increased body weights and visceral adipocyte tissue weight, as well as the enlarged size of adipocytes induced by HFD were pronouncedly reversed by the administration of TSA. CONCLUSION: TSA inhibited adipogenesis in 3T3-L1 preadipocytes by activating the AMPK pathway.

Field Test of Twin-Field Quantum Key Distribution through Sending-or-Not-Sending over 428 km.

Quantum key distribution endows people with information-theoretical security in communications. Twin-field quantum key distribution (TF-QKD) has attracted considerable attention because of its outstanding key rates over long distances. Recently, several demonstrations of TF-QKD have been realized. Nevertheless, those experiments are implemented in the laboratory, and therefore a critical question remains about whether the TF-QKD is feasible in real-world circumstances. Here, by adopting the sending-or-not-sending twin-field QKD (SNS-TF-QKD) with the method of actively odd parity pairing (AOPP), we demonstrate a field-test QKD over 428 km of deployed commercial fiber and two users are physically separated by about 300 km in a straight line. To this end, we explicitly measure the relevant properties of the deployed fiber and develop a carefully designed system with high stability. The secure key rate we achieved breaks the absolute key rate limit of repeaterless QKD. The result provides a new distance record for the field test of both TF-QKD and all types of fiber-based QKD systems. Our work bridges the gap of QKD between laboratory demonstrations and practical applications and paves the way for an intercity QKD network with measurement-device-independent security.

Spatial patterns of leaf δ13C and δ15N of aquatic macrophytes in the arid zone of northwestern China.

Analysis of stable isotope composition is an important tool in research on plant physiological ecology. However, large-scale patterns of leaf-stable isotopes for aquatic macrophytes have received considerably less attention. In this study, we examined the spatial pattern of stable isotopes of carbon (δ13C) and nitrogen (δ15N) of macrophytes leaves collected across the arid zone of northwestern China (approximately 2.4 × 106 km2) and attempted to illustrate its relationship with environmental factors (i.e., temperature, precipitation, potential evapotranspiration, sediment total carbon and nitrogen). Our results showed that the mean values of the leaf δ13C and δ15N in the macrophytes sampled from the arid zone were -24.49‰ and 6.82‰, respectively, which were far less depleted than those measured of terrestrial plants. The order of averaged leaf δ13C from different life forms was as follows: submerged > floating-leaved > emergent. Additionally, our studies indicated that the values of foliar δ13C values of all the aquatic macrophytes were only negatively associated with precipitation, but the foliar δ15N values were mainly associated with temperature, precipitation, and potential evapotranspiration. Therefore, we speculated that water-relation factors are the leaf δ13C determinant of macrophytes in the arid zone of northwestern China, and the main factors affecting leaf δ15N values are the complex combination of water and energy factors.

Effects of ultrasound on invasive golden mussel Limnoperna fortunei mortality and tissue lesions.

Biofouling by the invasive golden mussel Limnoperna fortunei deleteriously affects artificial water systems, but few effective, environmentally friendly antifouling strategies exist. We propose ultrasound for control of this invasive mussel and report minimum exposure times to kill juveniles and adults at ultrasonic powers ranging 300-600 W from a fixed distance of 8.5 cm. Analysis using a PMA + RT-qPCR assay revealed the formation of tissue lesions in response to ultrasound, with gill tissue more prone to injury than adductor muscle tissue. Shell microstructure determined using scanning electron microscopy (SEM) + energy dispersive X-ray spectroscopy (EDS) is plywood-like, with a thicker shell and increased numbers of prism and nacre layers in adult mussels that provide greater resistance to ultrasound, reducing mortality and tissue lesions. Our results suggest L. fortunei biomass could be effectively reduced by ultrasound, especially for early life-history stages without, or with only immature shells.