Photo-corrosion inhibition of Ag₃PO₄ by polyaniline coating

<p>In this paper, polyaniline-coated silver phosphate has been successfully prepared via a facile chemisorption method in order to improve the stability of Ag₃PO₄ under light irradiation. The crystalline phase, band gap energy, and microstructure of the obtained PANI/Ag₃PO₄ composites were characterized by X-ray diffraction, UV–vis diffuse reflection spectroscopy, scanning electron microscopy, and transmission electron microscopy, respectively. The photocatalytic degradation of methlylene blue was performed to test the activities of PANI/Ag₃PO₄ composites with different coating amounts and the results indicate that the stabilities of PANI/Ag₃PO₄ composites were successfully enhanced. The correlation between photocatalytic performance and the properties of PANI/Ag₃PO₄ composites is discussed in detail.</p

Table_1_Can supplementary private health insurance further supplement health.DOCX

BackgroundChina advocates a health insurance system with social health insurance (SHI) as the main body and private health insurance (PHI) as the supplement. The study of PHI's complementary role in health is conducive to providing evidence for PHI's policy expansion and encouraging the public to participate in PHI, which is insufficient in China.MethodsWe used the three-wave balanced panel data of the China Health and Retirement Longitudinal Survey (CHARLS). Taking the ownership of supplementary PHI as the independent variable and EQ-5D index scores as the dependent variable, the panel instrumental variable (IV) method was used to analyze the impact of participation in PHI on health. We also assessed the heterogeneity of the health effects of PHI between chronic and non-chronic disease groups and between low- and high-income groups.ResultsThe coverage rate of PHI at baseline was 10.53%. The regression results showed that participating in PHI on the basis of SHI could result in an additional 8.21% health gain (p ConclusionParticipating in supplementary PHI can effectively enhance the health status of the insured, and has a more significant effect on patients with chronic diseases. The development of PHI should be further supported, while the health inequality in different income groups should be paid attention to.</p

DataSheet4_Efficacy and Safety of Various First-Line Therapeutic Strategies for Fetal Tachycardias: A Network Meta-Analysis and Systematic Review.PDF

Background: Fetal arrhythmias are common cardiac abnormalities associated with high mortality due to ventricular dysfunction and heart failure, particularly when accompanied by hydrops. Although several types of common fetal tachycardias have been relatively identified medications, such as digoxin, flecainide, and sotalol, there is no first-line drug treatment protocol established for the treatment of various types of fetal tachycardias.Methods: We conducted a network meta-analysis using a Bayesian hierarchical framework to obtain a model for integrating both direct and indirect evidence. All tachycardia types (Total group), supraventricular tachycardia (SVT subgroup), atrial flutter (AF subgroup), hydrops subgroup, and non-hydrops subgroup fetuses were analyzed, and five first-line regimens were ranked according to treatment outcomes: digoxin monotherapy (D), flecainide monotherapy (F), sotalol monotherapy (S), digoxin plus flecainide combination therapy (DF), and digoxin plus sotalol combination therapy (DS). Effectiveness and safety were determined according to the cardioversion rate and intrauterine death rate.Results: The pooled data indicated that DF combination therapy was always superior to D monotherapy, regardless of the tachycardia type or the presence of hydrops: Total, 2.44 (95% CrI: 1.59, 3.52); SVT, 2.77 (95% CrI: 1.59, 4.07); AF, 67.85 (95% CrI: 14.25, 168.68); hydrops, 6.03 (95% CrI: 2.54, 10.68); and non-hydrops, 5.06 (95% CrI: 1.87, 9.88). DF and F had a similar effect on control of fetal tachycardias. No significant differences were observed when comparing S, DS with D therapies across the subgroup analyses for the SVT, hydrops, and non-hydrops groups. No significant differences in mortality risks were among the various treatment regimens for the total group. And no significant differences were found in rates of intrauterine death rates at the same cardioversion amount.Conclusion The flecainide monotherapy and combination of digoxin and flecainide should be considered the most superior therapeutic strategies for fetal tachycardia.Systematic Review Registration: (https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=288997), identifier (288997).</p

DataSheet2_Efficacy and Safety of Various First-Line Therapeutic Strategies for Fetal Tachycardias: A Network Meta-Analysis and Systematic Review.PDF

Background: Fetal arrhythmias are common cardiac abnormalities associated with high mortality due to ventricular dysfunction and heart failure, particularly when accompanied by hydrops. Although several types of common fetal tachycardias have been relatively identified medications, such as digoxin, flecainide, and sotalol, there is no first-line drug treatment protocol established for the treatment of various types of fetal tachycardias.Methods: We conducted a network meta-analysis using a Bayesian hierarchical framework to obtain a model for integrating both direct and indirect evidence. All tachycardia types (Total group), supraventricular tachycardia (SVT subgroup), atrial flutter (AF subgroup), hydrops subgroup, and non-hydrops subgroup fetuses were analyzed, and five first-line regimens were ranked according to treatment outcomes: digoxin monotherapy (D), flecainide monotherapy (F), sotalol monotherapy (S), digoxin plus flecainide combination therapy (DF), and digoxin plus sotalol combination therapy (DS). Effectiveness and safety were determined according to the cardioversion rate and intrauterine death rate.Results: The pooled data indicated that DF combination therapy was always superior to D monotherapy, regardless of the tachycardia type or the presence of hydrops: Total, 2.44 (95% CrI: 1.59, 3.52); SVT, 2.77 (95% CrI: 1.59, 4.07); AF, 67.85 (95% CrI: 14.25, 168.68); hydrops, 6.03 (95% CrI: 2.54, 10.68); and non-hydrops, 5.06 (95% CrI: 1.87, 9.88). DF and F had a similar effect on control of fetal tachycardias. No significant differences were observed when comparing S, DS with D therapies across the subgroup analyses for the SVT, hydrops, and non-hydrops groups. No significant differences in mortality risks were among the various treatment regimens for the total group. And no significant differences were found in rates of intrauterine death rates at the same cardioversion amount.Conclusion The flecainide monotherapy and combination of digoxin and flecainide should be considered the most superior therapeutic strategies for fetal tachycardia.Systematic Review Registration: (https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=288997), identifier (288997).</p

Monodispersed Nanodiamonds for Enhanced Anticorrosion of Waterborne Epoxy Coatings

Nanodiamonds (NDs) prepared by the explosion method possess very large surface energies, resulting in serious agglomerates, limiting their further application. Herein, we employed the strong shearing action of hydroxyl ion (OH–) to induce the hydrolysis of esters between the ND primary particles, generating the carboxyl and hydroxyl groups, breaking hard agglomeration of NDs, and successfully constructed electrical double layers on the surface of NDs via deprotonation of surface oxygen-containing groups induced by the strong shearing action of hydroxyl ion (OH–), leading to a significant increase of zeta potential absolute value (−54.2 mV), achieving the long-term stable (200 days) monodispersion of NDs (m-NDs). The as-obtained m-NDs, as efficient nanofillers, were added into the waterborne epoxy (WEP) to produce a composite coating of m-NDs/WEP, displaying a considerable improvement in anticorrosion performance. The results of electrochemical impedance spectroscopy show that the |Z|f = 0.01 Hz of m-NDs/WEP is nearly 3 orders of magnitude higher than that of pure WEP after 168 h of immersion. The excellent anticorrosion performance of m-NDs/WEP can be ascribed to the excellent compatibility, electrical insulation property, and physical barrier behavior of m-NDs, inhibiting the infiltration of corrosive medium. The molecular dynamics simulation reveals that m-NDs have good barrier properties against a corrosive medium

DataSheet3_Efficacy and Safety of Various First-Line Therapeutic Strategies for Fetal Tachycardias: A Network Meta-Analysis and Systematic Review.PDF

Background: Fetal arrhythmias are common cardiac abnormalities associated with high mortality due to ventricular dysfunction and heart failure, particularly when accompanied by hydrops. Although several types of common fetal tachycardias have been relatively identified medications, such as digoxin, flecainide, and sotalol, there is no first-line drug treatment protocol established for the treatment of various types of fetal tachycardias.Methods: We conducted a network meta-analysis using a Bayesian hierarchical framework to obtain a model for integrating both direct and indirect evidence. All tachycardia types (Total group), supraventricular tachycardia (SVT subgroup), atrial flutter (AF subgroup), hydrops subgroup, and non-hydrops subgroup fetuses were analyzed, and five first-line regimens were ranked according to treatment outcomes: digoxin monotherapy (D), flecainide monotherapy (F), sotalol monotherapy (S), digoxin plus flecainide combination therapy (DF), and digoxin plus sotalol combination therapy (DS). Effectiveness and safety were determined according to the cardioversion rate and intrauterine death rate.Results: The pooled data indicated that DF combination therapy was always superior to D monotherapy, regardless of the tachycardia type or the presence of hydrops: Total, 2.44 (95% CrI: 1.59, 3.52); SVT, 2.77 (95% CrI: 1.59, 4.07); AF, 67.85 (95% CrI: 14.25, 168.68); hydrops, 6.03 (95% CrI: 2.54, 10.68); and non-hydrops, 5.06 (95% CrI: 1.87, 9.88). DF and F had a similar effect on control of fetal tachycardias. No significant differences were observed when comparing S, DS with D therapies across the subgroup analyses for the SVT, hydrops, and non-hydrops groups. No significant differences in mortality risks were among the various treatment regimens for the total group. And no significant differences were found in rates of intrauterine death rates at the same cardioversion amount.Conclusion The flecainide monotherapy and combination of digoxin and flecainide should be considered the most superior therapeutic strategies for fetal tachycardia.Systematic Review Registration: (https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=288997), identifier (288997).</p

DataSheet1_Efficacy and Safety of Various First-Line Therapeutic Strategies for Fetal Tachycardias: A Network Meta-Analysis and Systematic Review.PDF

Background: Fetal arrhythmias are common cardiac abnormalities associated with high mortality due to ventricular dysfunction and heart failure, particularly when accompanied by hydrops. Although several types of common fetal tachycardias have been relatively identified medications, such as digoxin, flecainide, and sotalol, there is no first-line drug treatment protocol established for the treatment of various types of fetal tachycardias.Methods: We conducted a network meta-analysis using a Bayesian hierarchical framework to obtain a model for integrating both direct and indirect evidence. All tachycardia types (Total group), supraventricular tachycardia (SVT subgroup), atrial flutter (AF subgroup), hydrops subgroup, and non-hydrops subgroup fetuses were analyzed, and five first-line regimens were ranked according to treatment outcomes: digoxin monotherapy (D), flecainide monotherapy (F), sotalol monotherapy (S), digoxin plus flecainide combination therapy (DF), and digoxin plus sotalol combination therapy (DS). Effectiveness and safety were determined according to the cardioversion rate and intrauterine death rate.Results: The pooled data indicated that DF combination therapy was always superior to D monotherapy, regardless of the tachycardia type or the presence of hydrops: Total, 2.44 (95% CrI: 1.59, 3.52); SVT, 2.77 (95% CrI: 1.59, 4.07); AF, 67.85 (95% CrI: 14.25, 168.68); hydrops, 6.03 (95% CrI: 2.54, 10.68); and non-hydrops, 5.06 (95% CrI: 1.87, 9.88). DF and F had a similar effect on control of fetal tachycardias. No significant differences were observed when comparing S, DS with D therapies across the subgroup analyses for the SVT, hydrops, and non-hydrops groups. No significant differences in mortality risks were among the various treatment regimens for the total group. And no significant differences were found in rates of intrauterine death rates at the same cardioversion amount.Conclusion The flecainide monotherapy and combination of digoxin and flecainide should be considered the most superior therapeutic strategies for fetal tachycardia.Systematic Review Registration: (https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=288997), identifier (288997).</p

BAG6 induces viral PB2 degradation through K48-linked ubiquitination pathway.

(A) HEK293T cells transfected with PB2-Flag expression plasmid, in combination with empty vector or BAG6-HA plasmid were treated with 50 μg/mL CHX for the indicated time periods. The protein levels of PB2 were determined by western blotting (left panel) and quantified using grayscale analysis (right panel). (B) HEK293T cells transfected with PB2-Flag expression plasmid, in combination with empty vector or BAG6-HA plasmid were treated with DMSO, MG132 or CQ for 8 h. The protein levels of PB2-Flag were determined by western blotting. (C) A549 cells were transfected with empty vector or BAG6-HA plasmid, respectively, and then infected with PR8 virus (MOI = 1) for 16 h post-infection, and then treated with DMSO, MG132 or CQ for 8 h, respectively. The protein levels of PB2 were determined by western blotting. (D) HEK293T cells transfected with HA-BAG6, Flag-PB2 and HA-Ub plasmids were immunoprecipitated with M2/Flag antibody, followed by western blot analysis using anti-HA monoclonal antibody. All cells were treated with 20 μM MG132 for 4 h before being harvested. (E) HEK293T cells transfected with HA-BAG6, Flag-PB2 and HA-K48-Ub (left panel) or HA-K63-Ub (right panel) plasmids were immunoprecipitated with M2/Flag antibody, followed by western blot analysis using anti-HA monoclonal antibody. All cells were treated with 20 μM MG132 for 4 h before being harvested. (F) HEK293T cells transfected with HA-BAG6, HA-K48-Ub and Flag-PB2 or its mutants were immunoprecipitated with M2/Flag antibody, followed by western blot analysis using anti-HA monoclonal antibody. All cells were treated with 20 μM MG132 for 4 h before being harvested. (G) HEK293T cells transfected with Flag-PB2 or Flag-PB2-K189R plasmid, in combination with increasing amounts of BAG6-HA. The protein levels of Flag-PB2 and HA-BAG6 were determined by western blotting (left panel) and the relative protein levels of PB2 were quantified by densitometry and normalized to the levels of β-actin (right panel).</p

BAG6 knockout enhances IAV replication.

(A and B) BAG6-KO and BAG6-WT A549 cells were infected with IAV H1N1 (MOI = 1.0), and viral NP expression were measured by western blotting at different time points post-infection, as indicated (A, left panels), and densitometry analysis and quantification were performed (A, right panels). Viral titers in the supernatants were determined by TCID50 assay at 12, 24 and 36 h post-infection (B). (C and D) BAG6-KO and BAG6-WT A549 cells were infected with IAV H7N9 or H9N2 or H5N1 (MOI = 1.0), and the NP expression were measured by western blotting at different time points post-infection (C, left panels), and densitometry analysis and quantification were performed (C, right panels). Viral titers in the supernatants were determined by TCID50 assay at 12 and 24 h post-infection (D). (E and F) BAG6-KO A549 cells were transfected BAG6-HA expression plasmid or HA-vector. At 24 h post-transfection, the cells were infected with IAV H1N1 (MOI = 1.0). The NP expression were measured by western blotting at different time points post-infection, as indicated (E, upper panels), and densitometry analysis and quantification were performed (E, lower panels). Viral titers in the supernatants were determined by TCID50 assay at 6, 12, 24 and 36 h post-infection (F). BAG6-WT A549 cells were infected with IAV H1N1 (MOI = 1.0) as a control. Data presented as means ± SD and are representative of three independent experiments. *p p p < 0.001, Unpaired Student’s t test.</p

List of primer pairs used in this study.

The interaction between influenza A virus (IAV) and host proteins is an important process that greatly influences viral replication and pathogenicity. PB2 protein is a subunit of viral ribonucleoprotein (vRNP) complex playing distinct roles in viral transcription and replication. BAG6 (BCL2-associated athanogene 6) as a multifunctional host protein participates in physiological and pathological processes. Here, we identify BAG6 as a new restriction factor for IAV replication through targeting PB2. For both avian and human influenza viruses, overexpression of BAG6 reduced viral protein expression and virus titers, whereas deletion of BAG6 significantly enhanced virus replication. Moreover, BAG6-knockdown mice developed more severe clinical symptoms and higher viral loads upon IAV infection. Mechanistically, BAG6 restricted IAV transcription and replication by inhibiting the activity of viral RNA-dependent RNA polymerase (RdRp). The co-immunoprecipitation assays showed BAG6 specifically interacted with the N-terminus of PB2 and competed with PB1 for RdRp complex assembly. The ubiquitination assay indicated that BAG6 promoted PB2 ubiquitination at K189 residue and targeted PB2 for K48-linked ubiquitination degradation. The antiviral effect of BAG6 necessitated its N-terminal region containing a ubiquitin-like (UBL) domain (17-92aa) and a PB2-binding domain (124-186aa), which are synergistically responsible for viral polymerase subunit PB2 degradation and perturbing RdRp complex assembly. These findings unravel a novel antiviral mechanism via the interaction of viral PB2 and host protein BAG6 during avian or human influenza virus infection and highlight a potential application of BAG6 for antiviral drug development.</div