Effects of different stocking densities on the CO2 fluxes at water-air interface and the respiration metabolism in sea cucumber Apostichopus japonicus (Selenka)

Recently, abundant research has been devoted to investigating the variations of CO2 concentration in the atmosphere. However, the information of CO2 fluxes at the water-air interface remains limited, especially those from the respiratory metabolism of aquatic organisms. In the present study, a comprehensive analysis was carried out to evaluate the effects of different stocking densities of sea cucumber (Apostichopus japonicus) on the CO2 fluxes at water-air interface, and to explore the relationships between CO2 fluxes and respiratory metabolism. A total of 60 sea cucumbers were randomly classified into 4 groups with different stocking densities, including 2, 5 and 8 ind./tank (namely D2, D5 and D8 groups). After 34-day feeding trial, individuals in D5 had superior growth performance rather than D2 and D8. The analysis of modified floating static chambers clearly showed that the mean CO2 flux at the water-air interface in D5 was significantly higher than D2 and D8. Meanwhile, energy budget analysis revealed that D5 had higher carbon and nitrogen utilization, excretion energy and metabolizable energy, suggesting relatively active respiration metabolism in moderate stocking density. The activities of pyruvate dehydrogenase (PDH) and α-ketoglutarate dehydrogenase (OGDH) in respiratory tree and body wall tissues provided additional evidence for the higher respiration metabolism rate of individuals at D5, which may be responsible for the higher CO2 fluxes at the water-air interface. Transcriptome analysis was performed to uncover the molecular mechanism of respiratory metabolism affected by different stocking densities. The differentially expressed genes in respiration trees and body walls were significantly enriched in peroxisome, fatty acid degradation, and oxidative phosphorylation pathways. It may explain the differences of respiration metabolism rates at different stocking densities. The present study preliminarily revealed the CO2 fluxes variation at the water-air interface from aquatic invertebrates, and provided the scientific basis for the efficient and low-carbon agricultural technologies of sea cucumber

Neglected environmental health impacts of China's supply-side structural reform

“Supply-side structural reform” (SSSR) has been the most important ongoing economic reform in China since 2015, but its important environmental health effects have not been properly assessed. The present study addresses that gap by focusing on reduction of overcapacity in the coal, steel, and iron sectors, combined with reduction of emissions of sulfur dioxide (SO2), nitrogen oxide (NOx), and fine particulate matter (PM2.5), and projecting resultant effects on air quality and public health across cities and regions in China. Modeling results indicate that effects on air quality and public health are visible and distributed unevenly across the country. This assessment provides quantitative evidence supporting projections of the transregional distribution of such effects. Such uneven transregional distribution complicates management of air quality and health risks in China. The results challenge approaches that rely solely on cities to improve air quality. The article concludes with suggestions on how to integrate SSSR measures with cities’ air quality improvement attainment planning and management performance evaluation

Novel NIR-II organic fluorophores for bioimaging beyond 1550 nm

This work was partially supported by grants from NSFC (81773674, 81573383, and 21473041), NSFHP (2017CFA024, 2017CFB711, and 2016ACA126), the Applied Basic Research Program of WMBST (2019020701011429), Tibet Autonomous Region Science and Technology Plan Project Key Project (XZ201901-GB-11), Project First-Class Disciplines Development Supported by Chengdu University of Traditional Chinese Medicine (CZYJC1903), and Health Commission of Hubei Province Scientific Research Project (WJ2019M177 and WJ2019M178).Peer reviewedPublisher PD

Association of plasma galectin-3 and fetuin-A levels with diabetic retinopathy in type 2 diabetes mellitus patients

Introduction: Galectin-3 (Gal-3) and fetuin-A (Fet-A) are cytokines that participate in inflammation and insulin resistance. Previous studies have found that altered Gal-3 and Fet-A levels in circulation correlate with diabetic complications. However, whether they are all associated with diabetic retinopathy (DR) has been little investigated. The aim of this study was to assess plasma Gal-3 and Fet-A concentrations, and to investigate their associations with the presence of DR in type 2 diabetes mellitus (T2DM) patients. Material and methods: A total of 100 T2DM patients were enrolled, among which there were 50 patients without DR (non diabetic retinopathy, NDR group) and 50 patients with DR (DR group). Clinical parameters were collected, and plasma Gal-3 and Fet-A levels were measured by enzyme-linked immunosorbent assay (ELISA). Results: Both Gal-3 and Fet-A were found to be increased in DR patients with respect to NDR controls, and Gal-3 correlated positively with Fet-A. Bivariate correlation analysis revealed that Gal-3 levels were positively correlated with haemoglobin A1c (HbA1c), while Fet-A correlated negatively with fasting C peptide (FC-P) and positively with homocysteine (Hcy). Binary logistic regression suggested that elevated Gal-3 and Fet-A levels were related to increased risk of DR. ROC curve displayed that the combination of Fet-A and Gal-3 exhibited better diagnostic value for DR. Conclusions: Both Gal-3 and Fet-A were elevated in the circulation of DR patients, and they were positively associated with the occurrence of DR. The combination of 2 indicators showed better diagnostic value for DR.

Organic NIR-II dyes with ultralong circulation persistence for image-guided delivery and therapy

Acknowledgments This work was partially supported by grants from the National Key R&D Program of China (2020YFA0908800), NSFC (82111530209, 81773674, 91959103, 81573383, 21763002), Shenzhen Science and Technology Research Grant (JCYJ20190808152019182), the Applied Basic Research Program of Wuhan Municipal Bureau of Science and Technology (2019020701011429), Hubei Province Scientific and Technical Innovation Key Project (2020BAB058), the Local Development Funds of Science and Technology Department of Tibet (XZ202102YD0033C, XZ202001YD0028C), and the Fundamental Research Funds for the Central Universities.Peer reviewedPublisher PD

H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response

The inflammatory response and apoptosis have been proved to have a crucial role in the pathogenesis of the influenza A virus (IAV). Previous studies indicated that while IAV commonly causes pancreatitis and pancreatic damage in naturally and experimentally infected animals, the molecular mechanisms of the pathogenesis of IAV infection are less reported. In the present study, we showed for the first time that both avian-like (α-2,3-linked) and human-like (α-2,6-linked) sialic acid (SA) receptors were expressed by the mouse pancreatic cancer cell line PAN02 and the human pancreatic cancer cell line PANC-1. Using growth kinetics experiments, we also showed that PAN02 and PANC-1 cells supported the productive replication of the H5N1 highly pathogenic avian influenza while exhibited the limited replication of IAV subtypes H1N1 and H7N2 in vitro. The in vivo infection of H5N1 in pancreatic cells was confirmed by the histopathological and immunohistochemical staining of pancreas tissue from mice. Other than H1N1 and H7N2, severe damage and extensive positive signals were observed in pancreas of H5N1 infected mice. All three virus subtypes induced apoptosis but also triggered the infected PAN02 and PANC-1 cells to release pro-inflammatory cytokines and chemokines including interferon (IFN)-α, IFN-β, IFN-γ, chemokine (C-C motif) ligand 2 (CCL2), tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Notably, the subtypes of H5N1 could significantly upregulate these cytokines and chemokines in both two cells when compared with H1N1 and H7N2. The present data provide further understanding of the pathogenesis of H5N1 IAV in pancreatic cells derived from humans and mammals and may also benefit the development of new treatment against H5N1 influenza virus infection