Colorimetric and ECL dual-mode aptasensor for smartphone-based onsite sensitive detection of aflatoxin B1 in combination with ZnO@MWCNTs/g-C3N4 nanosheets and CuO@CuPt nanocomposites.

The development of dual-mode strategies with superior sensitivity and accuracy have garnered increasing attention for researchers in Aflatoxin B1 (AFB1) analysis. Herein, a colorimetric-electrochemiluminescence (ECL) dual-mode biosensor was constructed for onsite and ultrasensitive determination of AFB1. The multi-wall carbon nanotubes (MWCNTs) were integrated with the ZnO metal organic frameworks (MOFs) to accelerate the electron transfer and boost the ECL intensity of g-C3N4 nanoemitters. Through the aptamer-based DNA sandwich assay, the CuO@CuPt nanocomposites were introduced onto the electrode and acted as the dual functional signal nanoprobes. Due to the good spectrum overlap between the CuO@CuPt nanoprobes and g-C3N4 nanosheets, ECL signal could be efficiently quenched. Additionally, the CuO@CuPt nanoprobes show superior catalytic properties towards the TMB and H2O2 colorimetric reactions, and an obvious color alteration from colorless to blue can be observed using the smartphone. Under optimized conditions, a sensitive and accurate dual-mode analysis of the AFB1 was accomplished with the colorimetric detection limit of 3.26 fg/mL and ECL detection limit of 0.971 fg/mL (S/N = 3). This study combines innovative nanomaterial properties of ZnO@MWCNTs, g-C3N4 and CuO@CuPt for ultrasensitive dual-mode detection, which offers new opportunities for the innovative engineering of the dual-mode sensors and demonstrates significant potential in food safety analysis.

Suppressed humoral immunity is associated with dengue nonstructural protein NS1-elicited anti-death receptor antibody fractions in mice.

Dengue virus (DENV) infections may cause life-threatening dengue hemorrhagic fever (DHF). Suppressed protective immunity was shown in these patients. Although several hypotheses have been formulated, the mechanism of DENV-induced immunosuppression remains unclear. Previously, we found that cross-reactive antibodies against tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 1 (death receptor 4 [DR4]) were elicited in DHF patients, and that anti-DR4 autoantibody fractions were elicited by nonstructural protein 1 (NS1) immunizations in experimental mice. In this study, we found that anti-DR4 antibodies could suppress B lymphocyte function in vitro and in vivo. Treatment with the anti-DR4 immunoglobulin (Ig) induced caspase-dependent cell death in immortalized B lymphocyte Raji cells in vitro. Anti-DR4 Igs elicited by NS1 and DR4 immunizations markedly suppressed mouse spleen transitional T2 B (IgM+IgD+), bone marrow pre-pro-B (B220+CD43+), pre-B (B220+CD43-), and mature B cell (B220+IgD+) subsets in mice. Furthermore, functional analysis revealed that the pre-elicitation of anti-NS1 and anti-DR4 Ig titers suppressed subsequently neutralizing antibody production by immunization with DENV envelop protein. Our data suggest that the elicitation of anti-DR4 titers through DENV NS1 immunization plays a suppressive role in humoral immunity in mice.

Improving the efficiency of Fenton reactions and their application in the degradation of benzimidazole in wastewater.

Reducing the quantity of sludge produced in Fenton reactions can be partly achieved by improving their efficiency. This paper firstly studies the effect of uniform deceleration feeding (ferrous iron and hydrogen peroxide) on the efficiency of a Fenton reaction by measuring the yield of hydroxyl radicals (˙OH) and chemical oxygen demand (COD) removal rate. The dynamic behavior of ˙OH was also investigated. The results indicated that uniform deceleration feeding was the best feeding method compared with one-time feeding and uniform feeding methods when the same amount of Fenton reagents and the same reaction times were used. Besides, it was found the COD removal rate reached 79.3% when this method was applied to degrade 2-(a-hydroxyethyl)benzimidazole (HEBZ); this COD removal rate is larger than those when the other two modes were used (they reached 60.7% and 72.1%, respectively). The degradation pathway of HEBZ was determined using PL, UV-vis, FTIR, HPLC and GC-MS. Ultimately, HEBZ was decomposed into three small molecules (2-hydroxypropylamine, oxalic acid, and 2-hydroxypropamide). This research is of great significance for the application of Fenton reactions in wastewater treatment.

Process design of high-concentration benzimidazole wastewater treatment based on the molecular structure of contaminants.

Benzimidazole is an important intermediate in industry and it is usually difficult to be degraded by many treatment technologies. Looking for a highly effective, environment-friendly degradation process for benzimidazole wastewater is of great significance to reduce pollution. Based on the structure of contaminants, the micro-electrolysis (ME) coupled with the Fenton technique was chosen to degrade the industrial benzimidazole wastewater. Special feeding was applied to maintain the suitable hydrogen peroxide (H2O2) concentration to produce the hydroxyl radicals (•OH) as much as possible and protect •OH from being quenched by excess H2O2 according to the reaction mechanism. The results showed that this combined technique was highly efficient to decompose benzimidazole compounds. More chemical oxygen demand (COD) could be reduced when flow control was used, compared to the flow not being controlled. The COD removal rate could reach 85.2% at optimal parameters. Then the effluent of this process was combined with the existing biochemical system for further degradation. The studies of Ultraviolet Spectrophotometry, Fourier Transform Infrared Spectroscopy and Liquid Chromatography Mass Spectrometry showed that both 2-(a-Hydroxyethyl) benzimidazole and 2-Acetylbenzimidazole were decomposed to the isopropanolamine and aniline after the ME treatment; then the intermediates were oxidized into oxalic acid after the Fenton reaction.

Endothelial Cell Sensitization by Death Receptor Fractions of an Anti-Dengue Nonstructural Protein 1 Antibody Induced Plasma Leakage, Coagulopathy, and Mortality in Mice.

The mechanisms leading to the life-threatening dengue hemorrhagic fever (DHF) remain elusive. DHF preferentially occurs during secondary dengue infections, suggesting that aberrant immune responses are involved in its development. We previously demonstrated that the autoantibodies elicited by dengue virus (DENV) nonstructural protein 1 (NS1; anti-NS1 Igs) induce plasma leakage and mortality in mice with warfarinized anticoagulant suppression. However, the involved pathogenic Ig fractions of anti-NS1 Igs remain unclear. In this study, the autoreactive Igs in patients with DHF and in NS1-immunized rabbits crossreacted with TNF-related apoptosis-inducing ligand receptor 1 (death receptor [DR]4). Challenges with the DENV in a subcytotoxic dose sensitized endothelial cells to apoptosis. Treatments with the autoantibodies induced proapoptotic activities and suppressed the surface expression of endothelial anticoagulant thrombomodulin. Combined treatments comprising the DENV and DR4 affinity-purified fractions of anti-NS1 IgGs (anti-NS1-DR4 Ig), but not preimmune control IgGs, in subcytotoxic doses led to apoptosis in endothelial cells. Treatments with the anti-NS1-DR4 Ig led to plasma leakage, coagulopathy, and morality in mice with warfarinized anticoagulant suppression. These results suggest that DR4-induced endothelial cell sensitization through NS1-elicited autoantibodies exacerbates anticoagulant suppression, vascular injury, and plasma leakage. Detecting and blocking anti-DR Igs in patients may be novel strategies for managing severe DENV infection.

Acquired coagulant factor VIII deficiency induced by Bacillus anthracis lethal toxin in mice.

Mice treated with anthrax lethal toxin (LT) exhibit hemorrhage caused by unknown mechanisms. Moreover, LT treatment in mice induced liver damage. In this study, we hypothesized that a suppressed coagulation function may be associated with liver damage, because the liver is the major producing source of coagulation factors. The hepatic expression of coagulant factors and the survival rates were analyzed after cultured cells or mice were exposed to LT. In agreement with our hypothesis, LT induces cytotoxicity against hepatic cells in vitro. In addition, suppressed expression of coagulation factor VIII (FVIII) in the liver is associated with a prolonged plasma clotting time in LT-treated mice, suggesting a suppressive role of LT in coagulation. Accordingly, we further hypothesized that a loss-of-function approach involving treatments of an anticoagulant should exacerbate LT-induced abnormalities, whereas a gain-of-function approach involving injections of recombinant FVIII to complement the coagulation deficiency should ameliorate the pathogenesis. As expected, a sublethal dose of LT caused mortality in the mice that were non-lethally pretreated with an anticoagulant (warfarin). By contrast, treatments of recombinant FVIII reduced the mortality from a lethal dose of LT in mice. Our results indicated that LT-induced deficiency of FVIII is involved in LT-mediated pathogenesis. Using recombinant FVIII to correct the coagulant defect may enable developing a new strategy to treat anthrax.