Polystyrene nano-plastics impede skeletal muscle development and induce lipid accumulation via the PPARγ/LXRß pathway in vivo and in vitro in mice.

Nano-plastics (NPs) have emerged as a significant environmental pollutant, widely existing in water environment, and pose a serious threat to health and safety with the intake of animals. Skeletal muscle, a vital organ for complex life activities and functional demands, has received limited attention regarding the effects of NPs. In this study, the effects of polystyrene NPs (PS-NPs) on skeletal muscle development were studied by oral administration of different sizes (1 mg/kg) of PS-NPs in mice. The findings revealed that PS-NPs resulted in skeletal muscle damage and significantly hindered muscle differentiation, exhibiting an inverse correlation with PS-NPs particle size. Morphological analysis demonstrated PS-NPs caused partial disruption of muscle fibers, increased spacing between fibers, and lipid accumulation. RT-qPCR and western blots analyses indicated that PS-NPs exposure downregulated the expression of myogenic differentiation-related factors (Myod, Myog and Myh2), activated PPARγ/LXRß pathway, and upregulated the expressions of lipid differentiation-related factors (SREBP1C, SCD-1, FAS, ACC1, CD36/FAT, ADIPOQ, C/EBPα and UCP-1). In vitro experiments, C2C12 cells were used to confirm cellular penetration of PS-NPs (0, 100, 200, 400 µg/mL) through cell membranes along with activation of PPARγ expression. Furthermore, to verify LXRß as a key signaling molecule, silencing RNA transfection experiments were conducted, resulting in no increase in the expressions of PPARγ, LXRß, SREBP1C, FAS, CD36/FAT, ADIPOQ, C/EBPα and UCP-1 even after exposure to PS-NPs. However, the expressions of SCD-1and ACC1 remained unaffected. The present study evidenced that exposure to PS-NPs induced lipid accumulation via the PPARγ/LXRß pathway thereby influencing skeletal muscle development.

Polystyrene microplastics induce myocardial inflammation and cell death via the TLR4/NF-κB pathway in carp.

Microplastics (MPs) have attracted widespread attention as an emerging environmental pollutant. Especially in aquatic ecosystems, the harm of MPs to aquatic animals has increasingly become a severe environmental problem. In this study, we constructed a carp polystyrene microplastics (PS-MPs) exposure model to explore the damage and mechanism of PS-MPs exposure to carp myocardial tissue. The results of H&E, TUNEL, and AO/EB staining showed that PS-MPs exposure could induce inflammation, apoptosis, and necrosis in carp myocardial tissue and cardiomyocytes. In addition, our study explored the targeting relationship between PS-MPs and TLR4 and found that PS-MPs exposure could significantly increase the expression of TLR4 pathway-related factors. As the concentration of PS-MPs increased, the NF-κB pathway and inflammation-related factors increased dose-dependent. In addition, myocardial injury induced by exposure to PS-MPs was predominantly apoptotic, accompanied by necrosis. In short, our data suggest that PS-MPs cause damage to myocardial tissue via the TLR4\NF-κB pathway. The above findings enrich the theory of toxicological studies on PS-MPs and provide an essential reference for aquaculture.

Polyethylene microplastics trigger cell apoptosis and inflammation via inducing oxidative stress and activation of the NLRP3 inflammasome in carp gills.

Microplastics cause varying degrees of damage to aquatic organisms. Exposure to microplastics contaminated water, the gills are among the first tissues, after the skin, to be affected by microplastics. As an essential immune organ, prolonged stimulation by microplastics disrupts immune function not only in the gills but throughout the body, yet the underlying mechanisms remain elusive. A model of gill injury from exposure to polyethylene (PE) microplastics was developed in this study. H&E staining revealed that polyethylene microplastics caused gill inflammation, vascular remodeling, and mucous cell proliferation. An increase in collagen indicates severe tissue damage. Additional analysis showed that polyethylene microplastics profoundly exacerbated oxidative stress in the gills. TUNEL assay demonstrated cell apoptosis induced by polyethylene microplastic. The mRNA levels were subsequently quantified using RT-PCR. The results showed that polyethylene microplastics increased the expression of the nuclear factor-κB (NF-κB) pathway (NF-κB p65, IKKα, IKKß) and apoptosis biomarkers (p53, caspase-3, caspase-9, and Bax). Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasomes, which is an influential component of innate immunity, were overactive. What's more, the pro-inflammatory factors (TNF-α, IFN-γ, IL-2, IL-6, IL-8, IL-1ß) that induce immune disorder also increased significantly, while the anti-inflammatory factors (IL-4, IL-10) decreased significantly. These results suggested that oxidative stress acted as an activation signal of apoptosis triggered by the NF-κB pathway and activating the NLRP3 inflammasome to promote inflammatory immune responses. The present study provided a different target for the prevention of toxin-induced gill injury under polyethylene microplastics.

Polystyrene microplastics induced inflammation with activating the TLR2 signal by excessive accumulation of ROS in hepatopancreas of carp (Cyprinus carpio).

Polystyrene microplastics (PS-MPs) affect the immune defense function on carp (Cyprinus carpio). The PS-MPs model of carp was established by feeding with PS-MPs particle size of 8 µm and concentration of 1000 ng/L water. Hepatopancreas function test revealed the activities of AKP, ALT, AST and LDH abnormal increase. PS-MPs induced tissue damage and lead to abnormal hepatopancreas function. The PS-MPs also induced a oxidative stress with the antioxidant enzymes SOD, CAT, GSH-PX, and T-AOC activities decreasing and reactive oxygen species (ROS) excessive accumulation. PS-MPs activated the Toll like receptor-2 (TLR2) signaling pathway. The mRNA and protein expressions of TLR2, Myeloid differentiation primary response 88 (MyD88), tumor necrosis factor receptor-associated factor 6 (TRAF6), NF-κB p65, Tumor necrosis factor (TNF-α), Interleukin-1ß (IL-1ß), Inducible Nitric Oxide Synthase (iNOS), and cycooxygenase 2(COX2) was revealed increased in both hepatopancreas and hepatocytes with the qPCR and Western blotting analysis mode. ELISA showed the expressions of TNF-α, IL-1ß, iNOS, and COX2 inflammatory molecule were increased in both hepatopancreas and hepatocytes. The results showed that PS-MPs caused a serious injure in the hepatopancreas and brought serious effects on the inflammatory response of carp. The present study displayed the harm caused by PS-MPs in freshwater fish, and provided some suggestions and references for toxicological studies of microplastics in freshwater environment.

Hierarchical Shish-Kebab Structures Functionalizing Nanofibers for Controlled Drug Release and Improved Antithrombogenicity.

The functionalization of the fibrous scaffolds including drug loading and release is of significance in tissue engineering and regenerative medicine. Our previous results have shown that the shish-kebab structure-modified fibrous scaffold shows a completely different microenvironment that mimics the topography of the collagen fibers, which interestingly facilitates the cell adhesion and migration. However, the functionalization of the unique structure needs to be further investigated. In this study, we modified the heparin-loaded fiber with a shish-kebab structure and tuned the kebab structure as the barrier for the sustained release of heparin. The introduction of the kebab structure increases the diffusion energy barrier by extending the diffusion distance. Moreover, the discontinued surface topography of the shish-kebab structure altered the surface chemistry from hydrophobic for the original poly(ε-caprolactone) (PCL) nanofibers to hydrophilic for the PCL nanofibers with the shish-kebab structure, which might have inhibited the activation of fibrinogen and thus improved the anticoagulant ability. This synergistic effect of heparin and the kebab structure significantly promotes the endothelial cell affinity and antithrombogenicity. This method might be a viable and versatile drug delivery strategy in vascular tissue engineering.

Inhibition of allogeneic islet graft rejection by VISTA-conjugated liposome.

The Ig superfamily member V-domain Ig-containing suppressor of T-cell activation (VISTA) is a negative regulator with broad-spectrum activities and has reported that blockade of VISTA or combination with other negative checkpoint receptors sufficiently break tumor tolerance. However, it remains unclear whether VISTA could induce allogeneic T-cell hyporesponsiveness and inhibit allograft rejection. Here we found VISTA treatment significantly inhibited lymphocyte proliferation and activation in allogeneic MLR assay through impairing SYK-VAV pathway. Interestingly, though neither VISTA protein nor VISTA-Fc fusion protein administration exerted satisfactory immunosuppressive effect on allograft survival due to their short half-life in circulation, this problem was solved by conjugating VISTA protein on liposome by biotin-streptavidin system, which markedly prolonged its circulating half-life to 60 h. With islet transplant model, administration of VISTA-conjugated liposome could markedly prolong allograft survival by inhibition of SYK-VAV pathway, thus maintained the normal blood glucose level of recipients during treatment period. The results indicate VISTA is a promising therapeutic target to treat allograft rejection of islet transplantation.

Preparation of core-shell magnetic molecularly imprinted polymer nanoparticle for the rapid and selective enrichment of trace diuron from complicated matrices.

A novel magnetic MIPs (DUMIPs) was prepared by surface molecular imprinting method using superparamagnetic core-shell nanoparticle (Fe3O4@SiO2) as the sacrificial support matrix, herbicide diuron as template, α-methacrylic acid as the functional monomer, trimethylolpropane trimethacrylate as the crosslinker, azobisisobutyronitrile as the initiator, and acetonitrile as the porogen. Highly cross-linked porous surface and excellent magnetic property were characterized by Fourier-transform infrared spectroscopy, transmission electron microscopy, and vibrating sample magnetometer, respectively. The adsorption capacity of DUMIPs was 8.1 mg g-1, 2.6-fold over its corresponding non-imprinted polymers (DUNIPs). The adsorption in DUMIPs was considered as multilayer adsorption and posed high affinity to diuron, due to the better fitting to Freundilich isotherm. Competitive recognition study demonstrated DUMIPs had highly selective binding diuron. DUMIPs, as an influential sorbent has been used for selective extraction of diuron from environmental samples (paddy field water, paddy soil and grain seedlings) and the elution was determined by high efficiency liquid chromatography (HPLC). In this analytical method, various factors affecting the extraction efficiency such as pH, sorbent dosage, utilization efficiency and volumes of eluent were simultaneously investigated. Under the optimal conditions, the linearity of the method obtained is in the range of 0.02-10.0 mg L-1. The limit of detection is 0.012 mg L-1. In four spiked levels (0.04, 0.2, 1.0, and 4.0 mg kg-1), the recoveries of diuron in real samples are in the range of 83.56%-116.10% with relative standard deviations in the range of 1.21-6.81%. Importantly, compared to C18-SPE column, the MMIPs exhibited convenient separation by external magnetic field, strong clean-up capacity, and selective enrichment for diuron. Thus, the DUMIPs-based method is great potential for efficient sample preparation in the determination of trace amounts of diuron residues in complex matrices.

Effectiveness of mandibular advancement devices in the treatment of obstructive sleep apnea and the impact of different body positions on treatment： A systematic review and meta-analysis.

OBJECTIVE: The meta-analysis aimed to evaluate the efficacy of mandibular advancement device (MAD) for the treatment of obstructive sleep apnea (OSA) and explore the effect of different positions on MAD for OSA. METHODS: The Embase, PubMed, Medline, and Cochrane Library databases were searched for relevant studies evaluating the effect of MAD on the treatment of OSA from database inception to November 2022. The Bayesian random-effects mode was used to calculate the pooled outcome. Subgroup analysis and sensitivity analysis were applied to investigate the heterogeneity. RESULTS: A total of 6 studies enrolling 643 patients were eligible for further analysis. MAD treatment led to improvements in total apnea-hypopnea index (AHI) for both positional OSA(POSA) and Non-POSA groups, but there was no significant difference in the effect of MAD on Non-POSA and POSA (MD = -1.46,95%CI [-4.89,1.97], P = 0.40). In the supine position, AHI improvement after MAD treatment in POSA group was more than that in Non-POSA group by 15 events/hour in average (MD = 14.82, 95%CI [11.43,18.22], P＜0.00001), while in the non-supine position, the change of AHI in Non-POSA group was significantly better than that in POSA group by approximately 8 events/hour (MD = -7.55,95%CI[-10.73,-4.38],p < 0.00001). CONCLUSION: MAD is more suitable for POSA compared to Non-POSA in patients with habitual sleep in the supine or supine predominant position. While for patients with habitual sleep in the non-supine position, MAD is an effective treatment option for Non-POSA.

Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice.

Microplastics (MPs) are ubiquitous environmental contaminants that have negative impacts on health and safety. The gut microbiota plays multiple roles as a newly discovered virtual metabolic organ. The objective of this study was to investigate the potential of MPs to cause liver injury by disrupting the balance of gut microbiota. The results indicated that exposure to MPs resulted in liver damage and disrupted the homeostasis of gut microbiota. MPs significantly reduced the liver organ coefficient, leading to liver cell injury and impaired function. Additionally, there was an increase in the expression of fibril-related proteins, which positively correlated with MPs concentration. Furthermore, MPs increased the relative abundances of Desulfovibrio, Clostridia, Enterorhabdus, Bacteroides, and Gemella while decreasing the abundance of Dubosoella. Different concentrations of MPs exhibited varying effects on specific bacterial groups, however, both concentrations resulted in an increase in pathogenic bacteria and a decrease in beneficial bacteria, as well as alterations in microbial structure. Moreover, MPs induced oxidative stress, inflammation, apoptosis and necrosis in liver cells. The study found that MPs disrupted gut microbiota homeostasis and activated TLR2/NF-κB/NLRP3 pathway in the liver, providing a new insight into the mechanism underlying MPs-induced liver injury. These findings serve as a warning regarding environmental pollution caused by MPs.

Zwitterion modified chitosan as a high-performance corrosion inhibitor for mild steel in hydrochloric acid solution.

Herein, a novel chitosan Schiff base (CS-FGA) as a sustainable corrosion inhibitor has been successfully synthesized via a simple amidation reaction by using an imidazolium zwitterion and chitosan (CS). The corrosion inhibition property of CS-FGA for mild steel (MS) in a 1.0 M HCl solution was studied by various electrochemical tests and physical characterization methods. The findings indicate that the maximum inhibition efficiency of CS-FGA as a mixed-type inhibitor for MS in 1.0 M HCl solution with 400 mg L-1 reaches 97.6 %, much much higher than the CS and the recently reported chitosan-based inhibitors. Scanning electron microscopy (SEM), atomic force microscopy (AFM), and water contact angle (WCA) results reveal that the CS-FGA molecules firmly adsorb on the MS surface to form a protective layer. The adsorption of CS-FGA on the MS surface belongs to the Langmuir adsorption isotherm containing both the physisorption and chemisorption. According to the X-ray photoelectron spectroscopy (XPS) and UV-vis spectrum, FeN bonds presented on the MS surface further prove the chemisorption between CS-FGA and Fe to generate the stable protective layer. Additionally, theoretical calculations from quantum chemical calculation (DFT) and molecular simulations (MD) were performed to reveal the inhibition mechanism of CS-FGA.

Corrosion inhibition activity of a natural polysaccharide from Dysosma versipellis using tailor-made deep eutectic solvents.

In this work, a total of 18 types of choline chloride, betaine, and L-proline-based deep eutectic solvents (DESs) were synthesized to determine the extraction yield of a natural polysaccharide (PSA) from Dysosma versipellis using an ultrasound-assisted extraction method. Results indicate that the choline-oxalic acid-based DES has the best extraction yield for PSA due to the proper physical-chemical properties between PSA and DES. To evaluate the optimal extraction conditions, a response surface methodology was carried out. Under the optimal conditions, the extraction yield of PSA reaches 10.37 % (± 0.03 %), higher than the conventional extraction methods. Findings from FT-IR and NMR suggest that the extracted PSA belongs to a neutral polysaccharide with (1 â†’ 6)-linked α-d-glucopyranose in the main chain. Interestingly, results from various electrochemical measurements show the extracted PSA exhibits excellent corrosion inhibition performance for mild steel (MS) in a 0.5 M HCl solution, with 90.8 % of maximum corrosion inhibition efficiency at 210 mg L-1. SEM and XPS measurements reveal the formation of a protective layer on the MS surface. The adsorption behaviour of extracted PSA well obeys the Langmuir adsorption isotherm containing the chemisorption and physisorption. Additionally, theoretical calculations validate the experimental findings.

[Effect of cement implantation and pressor agents in hip replacement on blood pressure].

OBJECTIVE: To discuss the change of blood pressure involved by pressor agents after the implantation of cement in hip replacement. METHODS: A total of 172 cases of femoral neck fracture underwent hip replacement in Department of Orthopedics and Trauma, Peking University People's Hospital between July 2008 and July 2013 were involved in this retrospective study. The blood pressure and usage of pressor agents were recorded before and after bone cement implantation. The data of blood pressure and usage of agents were collected according to anesthesia records. All the cases were divided into four groups by the application of pressor agents: Free of using agent group (Free-agent group), agents used before implantation of cement group (Pre-agent group), agents used after implantation of cement group (Post-agent group) and agent used before & after implantation of cement group (Pre and Post-agent group). Further statistic analysis was then performed. RESULTS: Free-agent group's mean systolic blood pressure decreased for (4.0 ± 10.3) mmHg. The decreasing was significant (t=3.660, P=0.000). Free-agent group's mean diastolic blood pressure decreased (1.3 ± 7.5) mmHg. The decreasing was not significant (t=2.286, P=0.149). Pre-agent group's mean systolic blood pressure decreased for (0.5 ± 20.2) mmHg. The decreasing was not significant (t=0.114, P=0.911). Pre-agent group's mean diastolic blood pressure increased (0.7 ± 10.2) mmHg. The increasing was not significant (t=-0.316, P=0.756). Post-agent group's mean systolic blood pressure decreased for (6.9 ± 15.0) mmHg. The decreasing was significant (t=3.195, P=0.002). Post-agent group's mean diastolic blood pressure decreased (3.6 ± 7.4) mmHg. The decreasing was significant (t=3.407,P=0.001). Pre & Post-agent group's mean systolic blood pressure decreased for (5.0 ± 12.2) mmHg. The decreasing was not significant (t=1.667, P=0.115). Pre & Post-agent group's mean diastolic blood pressure increased (1.3 ± 8.5) mmHg. The increasing was not significant (t=-0.656, P=0.521). CONCLUSION: Implantation of cement in hip replacement surgery causes blood pressure decreasing. The application of pressor agents before cement implantation can stabilize blood presure and shorten the period of hypotension.

Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp.

Microplastics (MPs), a new class of pollutant that threatens aquatic biodiversity, are becoming increasingly prevalent around the world. Fish growth may be severely inhibited by microplastics, resulting in severe mortality. Exposure to microplastics increases the likelihood of intestinal injuries, but the underlying mechanisms remain equivocal. The objective of this study was to investigate the potential toxic mechanisms underlying microplastic-induced intestinal injury in fish and to assist researchers in identifying novel therapeutic targets. In this study, a model of carp exposed to microplastics was established successfully. Histological observation showed that exposure to polyethylene microplastics caused damage to the intestinal mucosal surface and a significant increase in goblet cells, which aggregated on the surface of the mucosa. The mucosal layer was observed to fall off. Lymphocytes in the intestinal wall proliferated and aggregated. TUNEL staining showed that apoptosis occurred in the group exposed to microplastics. The qPCR results showed that the expression of Ferroptosis apoptotic factors COX-2 and ACSL4 was upregulated, while the expression of TFRC, FIH1, SLC7A11, and GPX4 was downregulated. The NF-κB pathway (p-p65, IκBα), inflammatory cytokines (TNF-α, IL-8, IL-6) and apoptosis genes (Bax, Caspase3) were upregulated. Semi-quantitative detection of related proteins by Western blotting was consistent with the gene expression results. In addition, the ELISA assay showed that lipid peroxidation and inflammatory cytokines (TNF-α, IL-1ß, IL-6) were increased in the microplastic exposed group. To conclude, lipid peroxidation induced by microplastics activates the NF-κB pathway and causes ferroptosis, ultimately resulting in intestinal damage and cellular apoptosis.

Polystyrene microplastics induce endoplasmic reticulum stress, apoptosis and inflammation by disrupting the gut microbiota in carp intestines.

Microplastics have been recognized as a widespread new pollutant in nature and have induced an increase in the occurrence of a variety of diseases in carp. An animal model of microplastic ingestion was successfully established in an aqueous environment. The gut microbiota was analysed using a metagenomic approach. The results showed a significant reduction in the relative abundances of Lactococcus garvieae, Bacteroides_paurosaccharolyticus, and Romboutsia_ilealis after PS-MPs treatment. The 16S Silva database was used to predict and analyse the known genes. Intestinal flora disorders related to infectious diseases, cancers, neurodegenerative diseases, endocrine and metabolic diseases, cardiovascular diseases, and other diseases were found. The intake of PS-MPs resulted in damage to carp intestinal tissue and apoptosis of intestinal epithelial cells. The levels of the inflammatory cytokines IL-1ß, IL-6, and TNF-α were significantly increased with the intake of PS-MPs. The gene and protein levels of GRP78, Caspase-3, Caspase-7, Caspase-9, Caspase-12, PERK, IRE1, and ATF6 were further examined in PS group. The occurrence of ERS and apoptosis in carp intestines was confirmed. These results suggest that the accumulation of PS-MPs in the aquatic environment can disturb the carp gut microbiota and induce ERS, apoptosis, and inflammation in the intestinal tissue.

Lactobacillus paracasei ET-22 Suppresses Dental Caries by Regulating Microbiota of Dental Plaques and Inhibiting Biofilm Formation.

Dental caries is a common and multifactorial biofilm disease that is associated with dietary habits and microbiota. Among the various pathogens inducing caries, S. mutans is the most extensively studied. Promoting oral health with probiotics has gained considerable attention. Lactobacillus paracasei (L. paracasei) strains were reported to modulate the gut microbiota and enhance host resistance to disease. Our previous research has found that L. paracasei ET-22 (ET-22) could inhibit S. mutans biofilms in vitro. However, the preventive effect in vivo and functional mechanism of ET-22 on dental caries were unclear. In this study, the preventive effects of ET-22 on dental caries in mice were checked. Meanwhile, the functional mechanism of ET-22 was further investigated. Results showed that the supplementation of ET-22 in drinking water significantly improved the caries scoring of mice. The microbiota of dental plaques revealed that the live and heat-killed ET-22 similarly regulated the microbial structure in plaque biofilms. Functional prediction of PICRUSt showed that the addition of live and heat-killed ET-22 may inhibit biofilm formation. By the in vitro trials, the live and heat-killed ET-22 indeed inhibited the construction of S. mutans biofilms and EPS productions of biofilms. This evidence suggests that ET-22 can restrain dental caries by regulating the microbiota of dental plaques and inhibiting biofilm formation, which may be partly mediated by the body components of ET-22.

Polyethylene microplastics cause apoptosis via the MiR-132/CAPN axis and inflammation in carp ovarian.

Microplastics (MPs) are widely distributed pollutants in the environment and accumulate in the aquatic environment due to human activities. Carp, a common edible aquatic organism, has been found to accumulate MPs in body. MicroRNA (miRNAs) is a non-coding short RNA that regulates protein expression by binding to target genes in various physiological processes such as proliferation, differentiation and apoptosis. The ovary is a crucial role in carp reproduction. In this study, we established a model of carp exposed to polyethylene microplastics (PE-MPs) in the aquatic environment to investigate the specific mechanism of PE-MPs causing ovarian injury and the involvement of miR-132/calpain (CAPN) axis. H&E stained sections revealed that PE-PMs induced inflammation in ovarian tissues and impaired oocyte development. TUNEL analysis showed an increased rate of apoptosis in ovarian cells treated with PE-PMs. RT-PCR and Western Blot assays confirmed that exposure to PE-MPs significantly decreased miR-132 expression while increasing CAPN expression at both mRNA and protein levels. The concentration of calcium ions was significantly increased in tissues, leading to CAPN enzyme activity increase. The expression of mitochondrial damage-related genes (bax, AIF, cyt-c, caspase-7, caspase-9, and caspase-3) was higher while the expression of anti-apoptotic genes (bcl-2 and bcl-xl) was lower. Protein levels of bax, AIF, caspase-3, bcl-2 and bcl-xl changed accordingly with the genetic alterations. Additionally, we discovered that PE-MPs can activate the p65 factor through the TRAF6/NF-kB pathway resulting in elevated production of pro-inflammatory factors IL-6, IL-1ß and TNF-a which contribute to ovarian inflammation development. This study investigates the impact of PE-MPs on carp ovarian function and provides insights into miRNAs' role and their target genes.

Dopamine modified natural glucomannan as a highly efficient inhibitor for mild steel: Experimental and theoretical methods.

In this work, Glucomannan was modified with dopamine to synthesize a new polysaccharide Schiff base (GAD). After confirmation of GAD by NMR and FT-IR spectroscopic methods, it was introduced as a sustainable corrosion inhibitor with excellent anti-corrosion action for mild steel in 0.5 M hydrochloric acid (HCl) solution. Employing electrochemical test, morphology measurement, and theoretical analysis, the anticorrosion performance of GAD on mild steel in 0.5 M HCl solution is determined. Maximum efficiency of GAD for suppressing the corrosion rate of mild steel at 0.12 g L-1 reaches 99.0 %. After immersion in HCl solution for 24 h, the results from scanning electron microscopy indicate that GAD is firmly attached to the mild steel surface by making a protective layer. According to the X-ray photoelectron spectroscopy (XPS), FeN bonds existed on the steel surface indicate the presence of chemisorption between GAD and Fe to form stable complexes attracted to the active position on the mild steel. The effects of Schiff base groups on the corrosion inhibition efficiencies were also investigated. Moreover, the inhibition mechanism of GAD was further illustrated by the free Gibbs energy, quantum chemical calculation and molecular dynamics simulation.

Immunological evaluation and comparison of different EV71 vaccine candidates.

Enterovirus 71 (EV71) and coxsackievirus A16 (CVA16) are major causative agents of hand, foot, and mouth diseases (HFMDs), and EV71 is now recognized as an emerging neurotropic virus in Asia. Effective medications and/or prophylactic vaccines against HFMD are not available. The current results from mouse immunogenicity studies using in-house standardized RD cell virus neutralization assays indicate that (1) VP1 peptide (residues 211-225) formulated with Freund's adjuvant (CFA/IFA) elicited low virus neutralizing antibody response (1/32 titer); (2) recombinant virus-like particles produced from baculovirus formulated with CFA/IFA could elicit good virus neutralization titer (1/160); (3) individual recombinant EV71 antigens (VP1, VP2, and VP3) formulated with CFA/IFA, only VP1 elicited antibody response with 1/128 virus neutralization titer; and (4) the formalin-inactivated EV71 formulated in alum elicited antibodies that cross-neutralized different EV71 genotypes (1/640), but failed to neutralize CVA16. In contrast, rabbits antisera could cross-neutralize strongly against different genotypes of EV71 but weakly against CVA16, with average titers 1/6400 and 1/32, respectively. The VP1 amino acid sequence dissimilarity between CVA16 and EV71 could partially explain why mouse antibodies failed to cross-neutralize CVA16. Therefore, the best formulation for producing cost-effective HFMD vaccine is a combination of formalin-inactivated EV71 and CAV16 virions.

The differences between surface degradation and bulk degradation of FEM on the prediction of the degradation time for poly (lactic-co-glycolic acid) stent.

The degradation time is a crucial factor in evaluating the performance of poly (lactic-co-glycolic acid) (PLGA) stents. Bulk degradation mode was commonly used to analyze the stent degradation behavior by finite element approach. However, the PLGA stents may present surface degradation more than bulk degradation under certain conditions, which will greatly affect the degradation time after implantation. In this study, the degradation processes of the poly (lactic-co-glycolic acid) stent were reproduced utilizing finite element analysis. Both bulk degradation and surface degradation modes were considered. The correlation between tensile stress and degradation rate was investigated. The degradation time was analyzed selectively. The stress distribution, fracture, and mass loss were also compared between bulk degradation mode and surface degradation mode. The simulation results showed that, in both evolution modes, the degradation began at the 'peak-valley' region and fracture occurred at the cross of links and rings. Additionally, high levels of Von-Mises stress were observed in these two regions. Compared with bulk degradation, the fracture time of the stent was delayed by 63% in the surface degradation mode. In conclusion, the mass loss rate and scaffolding period showed great differences between surface degradation and bulk degradation. Based on this study, it is suggested that bulk degradation mode is not applicable to the case of inadequate water uptake mode, such as the tracheal stent degradation process. More experimental research should be carried out to accurately predict the scaffolding period after implantation. The mechanical properties of the fracture zone should be strengthened.

Effects of SNPs in SOD2 and SOD3 interacted with fluoride exposure on the susceptibility of dental fluorosis.

A total of 649 children aged 7-13 years of age were recruited in a cross-sectional study in Tongxu County, China (2017) to assess the effects of interaction between single nucleotide polymorphisms (SNPs) in SOD2 and SOD3 gene and fluoride exposure on dental fluorosis (DF) status. Associations between biomarkers and DF status were evaluated. Logistic regression suggested that the risk of DF in children with rs10370 GG genotype and rs5746136 TT genotype was 1.89-fold and 1.72-fold than that in children with TT/CC genotype, respectively. Increased T-SOD activity was associated with a lower risk of DF (OR = 0.99). The rs2855262*rs10370*UF model was regarded as the optimal interaction model in generalized multifactor dimensionality reduction analyses. Our findings suggested that rs4880 and rs10370 might be useful genetic markers for DF, and there might be interactions among rs10370 in SOD2, rs2855262 in SOD3, and fluoride exposure on DF status.