A review of microplastic pollution in aquaculture: Sources, effects, removal strategies and prospects.

As microplastic pollution has become an emerging environmental issue of global concern, microplastics in aquaculture have become a research hotspot. For environmental safety, economic efficiency and food safety considerations, a comprehensive understanding of microplastic pollution in aquaculture is necessary. This review outlines an overview of sources and effects of microplastics in aquaculture. External environmental inputs and aquaculture processes are sources of microplastics in aquaculture. Microplastics may release harmful additives and adsorb pollutants in aquaculture environment, cause deterioration of aquaculture environment, as well as cause toxicological effects, affect the behavior, growth and reproduction of aquaculture products, ultimately reducing the economic benefits of aquaculture. Microplastics entering the human body through aquaculture products also pose potential health risks at multiple levels. Microplastic pollution removal strategies used in aquaculture in various countries are also reviewed. Ecological interception and purification are considered to be effective methods. In addition, strengthening aquaculture management and improving fishing gear and packaging are also currently feasible solutions. As proactive measures, new portable microplastic monitoring system and remote sensing technology are considered to have broad application prospects. And it was encouraged to comprehensively strengthen the supervision of microplastic pollution in aquaculture through talent exchange and strengthening the construction of laws and regulations.

Progress on the Effects of Microplastics on Aquatic Crustaceans: A Review.

It is impossible to overlook the effects of microplastics on aquatic life as they continuously accumulate in aquatic environments. Aquatic crustaceans, as both predator and prey, play an important role in the food web and energy transmission. It is of great practical significance to pay attention to the toxic effects of microplastics on aquatic crustaceans. This review finds that most studies have shown that microplastics negatively affect the life history, behaviors and physiological functions of aquatic crustaceans under experimental conditions. The effects of microplastics of different sizes, shapes or types on aquatic crustaceans are different. Generally, smaller microplastics have more negative effects on aquatic crustaceans. Irregular microplastics have more negative effects on aquatic crustaceans than regular microplastics. When microplastics co-exist with other contaminants, they have a greater negative impact on aquatic crustaceans than single contaminants. This review contributes to rapidly understanding the effects of microplastics on aquatic crustaceans, providing a basic framework for the ecological threat of microplastics to aquatic crustaceans.

Foot-and-Mouth Disease Virus Structural Protein VP1 Destroys the Stability of TPL2 Trimer by Degradation TPL2 to Evade Host Antiviral Immunity.

Tumor progression locus 2 (TPL2) is a serine/threonine kinase that belongs to the mitogen-activated protein 3 kinase (MAP3K) family, and it plays an important role in pathogen infection. The trimer complex of TPL2, p105, and ABIN2 is essential for maintenance of TPL2 steady-state levels and host cell response to pathogens. Foot-and-mouth disease virus (FMDV) is a positive-strand RNA virus of the family Picornaviridae that encodes proteins capable of antagonizing host immune responses to achieve infection. The VP1 protein of FMDV is a multifunctional protein that can bind host cells and induce an immune response as well as cell apoptosis. However, the role and mechanisms of TPL2 in FMDV infection remain unknown. Here, we determined that FMDV infection could inhibit TPL2, p105, and ABIN2 at the transcription and protein levels, while VP1 could only inhibit TPL2, p105 and ABIN2 at protein level. TPL2 inhibited the replication of FMDV in vivo and in vitro, the 268 to 283 amino-acid region in the TPL2 kinase domain was essential for interaction with VP1. Moreover, VP1 promoted K48-linked polyubiquitination of TPL2 and degraded TPL2 by the proteasome pathway. However, VP1-induced degradation of p105 and ABIN2 was independent of proteasome, autophagy, lysosome, and caspase-dependent pathways. Further studies showed that VP1 destroyed the stability of the TPL2-p105-ABIN2 complex. Taken together, these results revealed that VP1 antagonized TPL2-meditated antivirus activity by degrading TPL2 and destroying its complex. These findings may contribute to understand FMDV-host interactions and improve development of a novel vaccine to prevent FMDV infection.Importance Virus-host interactions are critical for virus infection. This study was the first to demonstrate the antiviral effect of host TPL2 during FMDV replication by increasing production of interferons and antiviral cytokines. Both FMDV and VP1 protein can reduce host TPL2, ABIN2 and p105 to destroy TPL2-p105-ABIN2 trimer complex. VP1 interacted with TPL2 and degrade TPL2 via proteasome pathway to repress TPL2-mediated antivirus activity. This study provided new insights into FMDV immune evasion mechanisms, elucidating new informations regarding FMDV counteraction of host antivirus activity.

PEG modification enhances the in vivo stability of bioactive proteins immobilized on magnetic nanoparticles.

OBJECTIVE: To increase the in vivo stability of bioactive proteins via optimized loading methods. RESULTS: ß-Glucosidase (ß-Glu), as a model protein, was immobilized on magnetic nanoparticles(denoted as MNP-ß-Glu) by chemical coupling methods and was further modified by poly(ethylene glycol) (PEG) molecules (denoted as MNP-ß-Glu-PEG) to increase its stability. The physicochemical properties of the as-prepared nanohybrids, including the particle size, zeta potential, and enzyme activity, were well characterized. The proper MNP/ß-Glu feed ratio was important for optimizing the particle size. Analysis of enzyme activity showed that the stability of immobilized ß-Glu compared with free ß-Glu was lower in deionized water and higher in blood serum at 37 °C. MNP-ß-Glu-PEG retained 77.9% of the initial activity within 30 days at 4 °C, whereas the free enzyme retained only 58.2%. Pharmacokinetic studies of Sprague-Dawley (SD) rats showed that the MNP-ß-Glu-PEG group retained a higher enzyme activity in vivo (41.46% after 50 min) than the MNP-ß-Glu group (0.03% after 50 min) and the ß-Glu group (0.37% after 50 min). Moreover, in contrast to the MNP-ß-Glu group, the enzyme activity was not fully synchronous with the decrease in the Fe concentration in the MNP-ß-Glu-PEG group. CONCLUSIONS: All findings indicated that the method of immobilization on magnetic nanoparticles and PEG modification is promising for the application of bioactive proteins in vivo.

Environmental biodegradation of haloarchaea-produced poly(3-hydroxybutyrate-co-3-hydroxyvalerate) in activated sludge.

Novel poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBHV) copolymers produced by haloarchaea are excellent candidate biomaterials. However, there is no report hitherto focusing on the biodegradation of PHBHV synthesized by haloarchaea. In this study, an environmental biodegradation of haloarchaea-produced PHBHV films, with 10~60 mol% 3-hydroxyvalerate (3HV) composition and different microchemical structures, was studied in nutrition-depleted activated sludge. The changes in mass, molar mass, chemical composition, thermal properties, and surface morphology were monitored. The mass and molar mass of each film decreased significantly, while the PHA monomer composition remained unchanged with time. Interestingly, the sample of random copolymer PHBHV-2 (R-PHBHV-2) (3HV, 30 mol%) had the lowest crystallinity and was degraded faster than R-PHBHV-3 containing the highest 3HV content or the higher-order copolymer PHBHV-1 (O-PHBHV-1) possessing the highest surface roughness. The order of biodegradation rate was in the opposite trend to the degree of crystallizability of the films. Meanwhile, thermal degradation temperature of most films decreased after biodegradation. Additionally, the surface erosion of films was confirmed by scanning electron microscopy. The dominant bacteria probably responsible for the degradation process were identified in the activated sludge. It was inferred that the degradation rate of haloarchaea-produced PHBHV films mainly depended on sample crystallinity, which was determined by monomer composition and microchemical structure and in turn strongly influenced surface morphology.

Propionyl coenzyme A (propionyl-CoA) carboxylase in Haloferax mediterranei: Indispensability for propionyl-CoA assimilation and impacts on global metabolism.

Propionyl coenzyme A (propionyl-CoA) is an important intermediate during the biosynthesis and catabolism of intracellular carbon storage of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) in haloarchaea. However, the haloarchaeal propionyl-CoA carboxylase (PCC) and its physiological significance remain unclear. In this study, we identified a PCC that catalyzed propionyl-CoA carboxylation with an acetyl-CoA carboxylation side activity in Haloferax mediterranei. Gene knockout/complementation demonstrated that the PCC enzyme consisted of a fusion protein of a biotin carboxylase and a biotin-carboxyl carrier protein (PccA [HFX_2490]), a carboxyltransferase component (PccB [HFX_2478]), and an essential small subunit (PccX [HFX_2479]). Knockout of pccBX led to an inability to utilize propionate and a higher intracellular propionyl-CoA level, indicating that the PCC enzyme is indispensable for propionyl-CoA utilization. Interestingly, H. mediterranei DBX (pccBX-deleted strain) displayed multiple phenotypic changes, including retarded cell growth, decreased glucose consumption, impaired PHBV biosynthesis, and wrinkled cells. A propionyl-CoA concentration equivalent to the concentration that accumulated in DBX cells was demonstrated to inhibit succinyl-CoA synthetase of the tricarboxylic acid cycle in vitro. Genome-wide microarray analysis showed that many genes for glycolysis, pyruvate oxidation, PHBV accumulation, electron transport, and stress responses were affected in DBX. This study not only identified the haloarchaeal PCC for the metabolism of propionyl-CoA, an important intermediate in haloarchaea, but also demonstrated that impaired propionyl-CoA metabolism affected global metabolism in H. mediterranei.

Characterization of genes for chitin catabolism in Haloferax mediterranei.

Chitin is the second most abundant natural polysaccharide after cellulose. But degradation of chitin has never been reported in haloarchaea. In this study, we revealed that Haloferax mediterranei, a metabolically versatile haloarchaeon, could utilize colloidal or powdered chitin for growth and poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) accumulation, and the gene cluster (HFX_5025-5039) for the chitin catabolism pathway was experimentally identified. First, reverse transcription polymerase chain reaction results showed that the expression of the genes encoding the four putative chitinases (ChiAHme, ChiBHme, ChiCHme, and ChiDHme, HFX_5036-5039), the LmbE-like deacetylase (DacHme, HFX_5027), and the glycosidase (GlyAHme, HFX_5029) was induced by colloidal or powdered chitin, and chiA Hme, chiB Hme, and chiC Hme were cotranscribed. Knockout of chiABC Hme or chiD Hme had a significant effect on cell growth and PHBV production when chitin was used as the sole carbon source, and the chiABCD Hme knockout mutant lost the capability to utilize chitin. Knockout of dac Hme or glyA Hme also decreased PHBV accumulation on chitin. These results suggested that ChiABCDHme, DacHme, and GlyAHme were indeed involved in chitin degradation in H. mediterranei. Additionally, the chitinase assay showed that each chitinase possessed hydrolytic activity toward colloidal or powdered chitin, and the major product of colloidal chitin hydrolysis by ChiABCDHme was diacetylchitobiose, which was likely further degraded to monosaccharides by DacHme, GlyAHme, and other related enzymes for both cell growth and PHBV biosynthesis. Taken together, this study revealed the genes and enzymes involved in chitin catabolism in haloarchaea for the first time and indicated the potential of H. mediterranei as a whole-cell biocatalyst in chitin bioconversion.

Haloarchaeal-type ß-ketothiolases involved in Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) synthesis in Haloferax mediterranei.

The key enzymes for poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) biosynthesis in haloarchaea have been identified except the ß-ketothiolase(s), which condense two acetyl coenzyme A (acetyl-CoA) molecules to acetoacetyl-CoA, or one acetyl-CoA and one propionyl-CoA to 3-ketovaleryl-CoA. Whole-genome analysis has revealed eight potential ß-ketothiolase genes in the haloarchaeon Haloferax mediterranei, among which the PHBV-specific BktB and PhaA were identified by gene knockout and complementation analysis. Unlike all known bacterial counterparts encoded by a single gene, the haloarchaeal PhaA that was involved in acetoacetyl-CoA generation, was composed of two different types of subunits (PhaAα and PhaAß) and encoded by the cotranscribed HFX_1023 (phaAα) and HFX_1022 (phaAß) genes. Similarly, the BktB that was involved in generation of acetoacetyl-CoA and 3-ketovaleryl-CoA, was also composed of two different types of subunits (BktBα and BktBß) and encoded by cotranscribed HFX_6004 (bktBα) and HFX_6003 (bktBß). BktBα and PhaAα were the catalytic subunits and determined substrate specificities of BktB and PhaA, respectively. Their catalytic triad "Ser-His-His" was distinct from the bacterial "Cys-His-Cys." BktBß and PhaAß both contained an oligosaccharide-binding fold domain, which was essential for the ß-ketothiolase activity. Interestingly, BktBß and PhaAß were functionally interchangeable, although PhaAß preferred functioning with PhaAα. In addition, BktB showed biotechnological potential for the production of PHBV with the desired 3-hydroxyvalerate fraction in haloarchaea. This is the first report of the haloarchaeal type of PHBV-specific ß-ketothiolases, which are distinct from their bacterial counterparts in both subunit composition and catalytic residues.

Multiple propionyl coenzyme A-supplying pathways for production of the bioplastic poly(3-hydroxybutyrate-co-3-hydroxyvalerate) in Haloferax mediterranei.

Haloferax mediterranei is able to accumulate the bioplastic poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) with more than 10 mol% 3-hydroxyvalerate (3HV) from unrelated carbon sources. However, the pathways that produce propionyl coenzyme A (propionyl-CoA), an important precursor of 3HV monomer, have not yet been determined. Bioinformatic analysis of H. mediterranei genome indicated that this strain uses multiple pathways for propionyl-CoA biosynthesis, including the citramalate/2-oxobutyrate pathway, the aspartate/2-oxobutyrate pathway, the methylmalonyl-CoA pathway, and a novel 3-hydroxypropionate pathway. Cofeeding of pathway intermediates and inactivating pathway-specific genes supported that these four pathways were indeed involved in the biosynthesis of 3HV monomer. The novel 3-hydroxypropionate pathway that couples CO2 assimilation with PHBV biosynthesis was further confirmed by analysis of (13)C positional enrichment in 3HV. Notably, (13)C metabolic flux analysis showed that the citramalate/2-oxobutyrate pathway (53.0% flux) and the 3-hydroxypropionate pathway (30.6% flux) were the two main generators of propionyl-CoA from glucose. In addition, genetic perturbation on the transcriptome of the ΔphaEC mutant (deficient in PHBV accumulation) revealed that a considerable number of genes in the four propionyl-CoA synthetic pathways were significantly downregulated. We determined for the first time four propionyl-CoA-supplying pathways for PHBV production in haloarchaea, particularly including a new 3-hydroxypropionate pathway. These results would provide novel strategies for the production of PHBV with controllable 3HV molar fraction.

Microplastics in cultivated soil environment: Construction of toxicity grading evaluation system, development of priority control checklist, and toxicity mechanism analysis.

The present study aimed to comprehensively evaluate the toxicological effects of microplastics (MPs) on cultivated soil quality. Based on improved G1 evaluation method, we first constructed a grading evaluation system comprising of the indicators of toxicological effects of cultivated soil quality under MPs exposure, while focusing on types of MPs that had significant/non-significant toxicity effects. Furthermore, we verified reliability of screening results of significance-links at each level, using several data processing methods. Then, using natural breakpoint classification method, a priority control checklist of toxicological effects of 18 types of MPs on cultivated soil was developed to determine the types of MPs having significant toxicity risks and cultivated soil quality links significantly affected by the toxicity of MPs exposure. Finally, quantum-mechanics/molecular-mechanics (QM/MM) methods were used to carry out the differential toxicity mechanism analysis. The results showed that MPs with higher non-polar surface area may lead to stronger toxicity effect to the cultivated soil quality. Notably, the MPs that have abundant binding sites enhance the binding affinity, and less polar MPs bind more strongly to the non-polar amino acids of target receptors. Our study provides a new theoretical perspective for multi-dimensional analysis toxicological effects of different MPs exposure on cultivated soil quality.

Complete genome sequence of the metabolically versatile halophilic archaeon Haloferax mediterranei, a poly(3-hydroxybutyrate-co-3-hydroxyvalerate) producer.

Haloferax mediterranei, an extremely halophilic archaeon, has shown promise for production of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) from unrelated cheap carbon sources. Here we report the complete genome (3,904,707 bp) of H. mediterranei CGMCC 1.2087, consisting of one chromosome and three megaplasmids.

Evaluation of two polymeric blends (EVA/PLA and EVA/PEG) as coating film materials for paclitaxel-eluting stent application.

The ethylene vinyl acetate copolymer (EVA)/Poly (lactic acid) (PLA) blend and EVA/Poly (ethylene glycol) (PEG) blend were applied as the drug carrier materials for a bi-layer drug-loaded stent coating film, which consisted of a paclitaxel (PTX)-loaded layer and a drug-free EVA layer. The changes of weight and appearance of the drug-free polymeric blend films with increasing time were examined by X-ray diffraction analysis (XRD), gel permeation chromatography (GPC) tests and scanning electronic microscopy (SEM), and the results showed the degradation of PLA and the leaching of PEG from the films. The effects of PLA, PEG and drug contents on in vitro drug release were investigated, and the results demonstrated that the addition of PLA promoted the drug release while the addition of PEG almost did not. Franz cells diffusion test results indicated that the bi-layer structure successfully endowed the stent coating with the release of drug in a unidirectional fashion. The release profiles of films incorporated PTX and the mechanical performance of the film could be customized by readily adjusting the contents of the blend components. Therefore, the polymeric blends could be useful drug carrier materials for drug-loaded stent coating capable of releasing drug in a highly tunable manner.

Corrigendum: Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-ß Signaling Pathway to Facilitate the Virus Replication.

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Wide distribution among halophilic archaea of a novel polyhydroxyalkanoate synthase subtype with homology to bacterial type III synthases.

Polyhydroxyalkanoates (PHAs) are accumulated as intracellular carbon and energy storage polymers by various bacteria and a few haloarchaea. In this study, 28 strains belonging to 15 genera in the family Halobacteriaceae were investigated with respect to their ability to synthesize PHAs and the types of their PHA synthases. Fermentation results showed that 18 strains from 12 genera could synthesize polyhydroxybutyrate (PHB) or poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV). For most of these haloarchaea, selected regions of the phaE and phaC genes encoding PHA synthases (type III) were cloned via PCR with consensus-degenerate hybrid oligonucleotide primers (CODEHOPs) and were sequenced. The PHA synthases were also examined by Western blotting using haloarchaeal Haloarcula marismortui PhaC (PhaC(Hm)) antisera. Phylogenetic analysis showed that the type III PHA synthases from species of the Halobacteriaceae and the Bacteria domain clustered separately. Comparison of their amino acid sequences revealed that haloarchaeal PHA synthases differed greatly in both molecular weight and certain conserved motifs. The longer C terminus of haloarchaeal PhaC was found to be indispensable for its enzymatic activity, and two additional amino acid residues (C143 and C190) of PhaC(Hm) were proved to be important for its in vivo function. Thus, we conclude that a novel subtype (IIIA) of type III PHA synthase with unique features that distinguish it from the bacterial subtype (IIIB) is widely distributed in haloarchaea and appears to be involved in PHA biosynthesis.

Magnetically Directed Enzyme/Prodrug Prostate Cancer Therapy Based on ß-Glucosidase/Amygdalin.

BACKGROUND: ß-Glucosidase (ß-Glu) can activate amygdalin to kill prostate cancer cells, but the poor specificity of this killing effect may cause severe general toxicity in vivo, limiting the practical clinical application of this approach. MATERIALS AND METHODS: In this study, starch-coated magnetic nanoparticles (MNPs) were successively conjugated with ß-Glu and polyethylene glycol (PEG) by chemical coupling methods. Cell experiments were used to confirm the effects of immobilized ß-Glu on amygdalin-mediated prostate cancer cell death in vitro. Subcutaneous xenograft models were used to carry out the targeting experiment and magnetically directed enzyme/prodrug therapy (MDEPT) experiment in vivo. RESULTS: Immobilized ß-Glu activated amygdalin-mediated prostate cancer cell death. Tumor-targeting studies showed that PEG modification increased the accumulation of ß-Glu-loaded nanoparticles in targeted tumor tissue subjected to an external magnetic field and decreased the accumulation of the nanoparticles in the liver and spleen. Based on an enzyme activity of up to 134.89 ± 14.18mU/g tissue in the targeted tumor tissue, PEG-ß-Glu-MNP/amygdalin combination therapy achieved targeted activation of amygdalin and tumor growth inhibition in C57BL/6 mice bearing RM1 xenografts. Safety evaluations showed that this strategy had some impact on liver and heart function but did not cause obvious organ damage. CONCLUSION: All findings indicate that this magnetically directed enzyme/prodrug therapy strategy has the potential to become a promising new approach for targeted therapy of prostate cancer.

Foot-and-mouth disease virus degrades Rab27a to suppress the exosome-mediated antiviral immune response.

Foot-and-mouth disease (FMD) is a highly contagious infection caused by foot-and-mouth disease virus (FMDV). Exosomes are extracellular vesicles that mediate antiviral immune responses in host cells and could be used by pathogens to evade host cell immune responses. Whether FMDV affects exosome secretion or whether exosomes derived from FMDV-infected cells mediate host cell antiviral immune responses is not yet clarified. In this study, the exosomes were identified and extracted from FMDV-infected PK-15 cells, and it was found that FMDV inhibits exosome secretion. Further investigation revealed that FMDV suppresses exosomes by degrading Rab27a via the autophagy-lysosome pathway. Also, microRNA (miRNA) differential analysis was performed in exosomes, which revealed that miRNA-136 was highly differentially expressed in exosomes and may be the key miRNA that inhibits the proliferation of FMDV. In summary, these results showed that host cells take advantage of exosomes to mediate their antiviral immune response, while FMDV evades exosome-mediated immune responses by degrading the exosome molecular switch, Rab27a.

Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-ß Signaling Pathway to Facilitate the Virus Replication.

Foot-and-mouth disease (FMD) is a severe, highly contagious viral disease of cloven-hoofed animals. In order to establish an infection, the FMD virus (FMDV) needs to counteract host antiviral responses. Tumor progression locus 2 (TPL2), a mitogen-activated protein kinase, can regulate innate and adaptive immunity; however, its exact mechanisms underlying TPL2-mediated regulation of the pathogenesis of FMDV infection remain unknown. In this study, we confirmed that TPL2 could inhibit FMDV replication in vitro and in vivo. The virus replication increased in Tpl2-deficient suckling mice in association with reduced expression of interferon-stimulated genes interferon-α (IFN-α) and myxovirus resistance (MX2) and significantly reduced expression of C-X-C motif chemokine ligand 10 (CXCL10), interferon regulatory factor 3 (IRF3), and IRF7, while the phosphorylation of IRF3 was not detected. Moreover, the interactions between TPL2 and VP1 were also confirmed. The overexpression of TPL2 promoted IRF3-mediated dose-dependent activation of the IFN-ß signaling pathway in association with interactions between IRF3 and TPL2. VP1 also inhibited phosphorylation of TPL2 at Thr290, while Thr290 resulted as the key functional site associated with the TPL2-mediated antiviral response. Taken together, this study indicated that FMDV capsid protein VP1 antagonizes TPL2-mediated activation of the IRF3/IFN-ß signaling pathway for immune escape and facilitated virus replication.

Molecular Mechanisms of Immune Escape for Foot-and-Mouth Disease Virus.

Foot-and-mouth disease virus (FMDV) causes a highly contagious vesicular disease in cloven-hoofed livestock that results in severe consequences for international trade, posing a great economic threat to agriculture. The FMDV infection antagonizes the host immune responses via different signaling pathways to achieve immune escape. Strategies to escape the cell immune system are key to effective infection and pathogenesis. This review is focused on summarizing the recent advances to understand how the proteins encoded by FMDV antagonize the host innate and adaptive immune responses.

Toxicity responses of different organs of zebrafish (Danio rerio) to silver nanoparticles with different particle sizes and surface coatings.

Silver nanoparticles (AgNPs) in aquatic ecosystems are toxic to aquatic organisms. In this study, we aimed to investigate the toxicities and molecular mechanisms of AgNPs with different surface coatings (sodium citrate and polyvinylpyrrolidone) and particle sizes (20 nm and 100 nm) in the gills, intestines, and muscles of zebrafish after 96 h of exposure. Our results indicated that the contribution of particle size to AgNP toxicity was greater than that of the surface coating. Citrate-coated AgNPs were more toxic than polyvinylpyrrolidone-coated AgNPs, and 20-nm AgNPs were more toxic than 100-nm AgNPs. The toxic effects of AgNPs to the tissues were in the order intestines > gills > muscles. Differential expression of genes with the different AgNPs confirmed that they had toxic effects in the zebrafish tissues at the molecular level. Our comprehensive comparison of the toxicities of different AgNPs to aquatic ecosystems will be helpful for further risk assessments of AgNPs.

The characteristics of optics polished with a polyurethane pad.

The effect of polishing an optical workpiece with a polyurethane pad was studied in this paper, including material removal rate, surface roughness and subsurface damage. Usually, optical polishing pitch is applied to polish optical workpieces, but the material removal rate (MRR) of pitch is quite low, and polyurethane foam is thus substituted for polishing pitch. With the polyurethane pad a much higher MRR was obtained. Surface roughness and subsurface damage of workpieces were also examined. We were gratified to find that there was almost no subsurface damage in the workpieces manufactured with pad polishing and surface roughness was comparable to the result of pitch polishing. Finally, a hypothesis was proposed in an attempt to explain the result that workpieces were defect-free.