Regulating Crystallinity Mismatch Between Donor and Acceptor to Improve Exciton/Charge Transport in Efficient Organic Solar Cells.

Achieving a more balanced charge transport by morphological control is crucial in reducing bimolecular and trap-assisted recombination and enhancing the critical parameters for efficient organic solar cells (OSCs). Hence, a facile strategy is proposed to reduce the crystallinity difference between donor and acceptor by incorporating a novel multifunctional liquid crystal small molecule (LCSM) BDTPF4-C6 into the binary blend. BDTPF4-C6 is the first LCSM based on a tetrafluorobenzene unit and features a low liquid crystal phase transition temperature and strong self-assembly ability, conducive to regulating the active layer morphology. When BDTPF4-C6 is introduced as a guest molecule into the PM6 : Y6 binary, it exhibits better compatibility with the donor PM6 and primarily resides within the PM6 phase because of the similarity-intermiscibility principle. Moreover, systematic studies revealed that BDTPF4-C6 could be used as a seeding agent for PM6 to enhance its crystallinity, thereby forming a more balanced and favourable charge transport with suppressed charge recombination. Intriguingly, dual Förster resonance energy transfer was observed between the guest molecule and the host donor and acceptor, resulting in an improved current density. This study demonstrates a facile approach to balance the charge mobilities and offers new insights into boosting the efficiency of single-junction OSCs beyond 20 %.

Baicalin Alleviate Apoptosis via PKC-MAPK Pathway in Porcine Peritoneal Mesothelial Cells Induced by Glaesserella parasuis.

Glaesserella parasuis (GPS), a causative agent of Glässer's disease, is thought to be the main fatal cause of peritonitis in swine, thus resulting in high mortality and morbidity and significant economic losses to the swine industry. However, the mechanisms of GPS infection-induced apoptosis and possible therapeutic pathway for GPS infection in peritonitis remain unclear. Baicalin has important biological functions during disease treatment, such as antiviral, bacterial inhibition, anti-apoptosis, and anti-inflammatory. However, whether baicalin has anti-apoptotic effects during the process of GPS infection in peritonitis is unclear. In the present study, the anti-apoptotic effect and mechanisms of baicalin in GPS infection-induced apoptosis were investigated in porcine peritoneal mesothelial cells (PPMC). The results showed that baicalin could inhibit the apoptosis rate occurrence of PPMC induced by GPS to various degrees and inhibit the expression of apoptosis-related genes and cleaved caspase-3. Meanwhile, baicalin significantly antagonized the expression of p-JNK, p-p38, and p-ERK induced by GPS in PPMC. These findings for the first time demonstrate that baicalin exerted the effect of antagonizing GPS induced apoptosis in PPMC by inhibiting the activation of the PKC-MAPK pathway and could be a therapeutic option in the management of GPS infection.

The effect of baicalin on microRNA expression profiles in porcine aortic vascular endothelial cells infected by Haemophilus parasuis.

Glässer's disease, caused by Haemophilus parasuis (H. parasuis), is associated with vascular damage and vascular inflammation in pigs. Therefore, early assessment and treatment are essential to control the inflammatory disorder. MicroRNAs have been shown to be involved in the vascular pathology. Baicalin has important pharmacological functions, including anti-inflammatory, antimicrobial and antioxidant effects. In this study, we investigated the changes of microRNAs in porcine aortic vascular endothelial cells (PAVECs) induced by H. parasuis and the effect of baicalin in this model by utilizing high-throughput sequencing. The results showed that 155 novel microRNAs and 76 differentially expressed microRNAs were identified in all samples. Subsequently, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the target genes of the differentially expressed microRNAs demonstrated that regulation of actin cytoskeleton, focal adhesion, ECM-receptor interaction, bacterial invasion of epithelial cells, and adherens junction were the most interesting pathways after PAVECs were infected with H. parasuis. In addition, when the PAVECs were pretreated with baicalin, mismatch repair, peroxisome, oxidative phosphorylation, DNA replication, and ABC transporters were the most predominant signaling pathways. STRING analysis showed that most of the target genes of the differentially expressed microRNAs were associated with each other. The expression levels of the differentially expressed microRNAs were negatively co-regulated with their target genes' mRNA following pretreatment with baicalin in the H. parasuis-induced PAVECs using co-expression networks analysis. This is the first report that microRNAs might have key roles in inflammatory damage of vascular tissue during H. parasuis infection. Baicalin regulated the microRNAs changes in the PAVECs following H. parasuis infection, which may represent useful novel targets to prevent or treat H. parasuis infection.

The effects of baicalin on piglets challenged with Glaesserella parasuis.

Glaesserella parasuis (G. parasuis) causes porcine vascular inflammation and damage. Baicalin is reported to have antioxidant and anti-inflammatory functions. However, whether baicalin protects piglets against G. parasuis challenge and the potential protective mechanism have not been investigated. Therefore, in this study, we comprehensively examined the protective efficacy of baicalin in piglets challenged with G. parasuis and the possible protective mechanism. Our results show that baicalin attenuated the release of the inflammation-related cytokines interleukin (IL) 1ß, IL6, IL8, IL10, and tumour necrosis factor α (TNF-α) and reduced high mobility group box 1 (HMGB1) production and cell apoptosis in piglets infected with G. parasuis. Baicalin also inhibited the activation of the mitogen-activated protein kinase (MAPK) signalling pathway and protected piglets against G. parasuis challenge. Taken together, our data suggest that baicalin could protect piglets from G. parasuis by reducing HMGB1 release, attenuating cell apoptosis, and inhibiting MAPK signalling activation, thereby alleviating the inflammatory response induced by the bacteria. Our results suggest that baicalin has utility as a novel therapeutic drug to control G. parasuis infection.

Effects of Baicalin on piglet monocytes involving PKC-MAPK signaling pathways induced by Haemophilus parasuis.

BACKGROUND: Haemophilus parasuis (HPS) is the causative agent of Glässer's disease, characterized by arthritis, fibrinous polyserositis and meningitis, and resulting in worldwide economic losses in the swine industry. Baicalin (BA), a commonly used traditional Chinese medication, has been shown to possess a series of activities, such as anti-bacterial, anti-viral, anti-tumor, anti-oxidant and anti-inflammatory activities. However, whether BA has anti-apoptotic effects following HPS infection is unclear. Here, we investigated the anti-apoptotic effects and mechanisms of BA in HPS-induced apoptosis via the protein kinase C (PKC)-mitogen-activated protein kinase (MAPK) pathway in piglet's mononuclear phagocytes (PMNP). RESULTS: Our data demonstrated that HPS could induce reactive oxygen species (ROS) production, arrest the cell cycle and promote apoptosis via the PKC-MAPK signaling pathway in PMNP. Moreover, when BA was administered, we observed a reduction in ROS production, suppression of cleavage of caspase-3 in inducing apoptosis, and inhibition of activation of the PKC-MAPK signaling pathway for down-regulating p-JNK, p-p38, p-ERK, p-PKC-α and PKC-δ in PMNP triggered by HPS. CONCLUSIONS: Our data strongly suggest that BA can reverse the apoptosis initiated by HPS through regulating the PKC-MAPK signaling pathway, which represents a promising therapeutic agent in the treatment of HPS infection.

Multi-Scale Vehicle Detection for Foreground-Background Class Imbalance with Improved YOLOv2.

Vehicle detection is a challenging task in computer vision. In recent years, numerous vehicle detection methods have been proposed. Since the vehicles may have varying sizes in a scene, while the vehicles and the background in a scene may be with imbalanced sizes, the performance of vehicle detection is influenced. To obtain better performance on vehicle detection, a multi-scale vehicle detection method was proposed in this paper by improving YOLOv2. The main contributions of this paper include: (1) a new anchor box generation method Rk-means++ was proposed to enhance the adaptation of varying sizes of vehicles and achieve multi-scale detection; (2) Focal Loss was introduced into YOLOv2 for vehicle detection to reduce the negative influence on training resulting from imbalance between vehicles and background. The experimental results upon the Beijing Institute of Technology (BIT)-Vehicle public dataset demonstrated that the proposed method can obtain better performance on vehicle localization and recognition than that of other existing methods.

Effect of Baicalin-Aluminum Complexes on Fecal Microbiome in Piglets.

The gut microbiome has important effects on gastrointestinal diseases. Diarrhea attenuation functions of baicalin (BA) is not clear. Baicalin-aluminum complexes (BBA) were synthesized from BA, but the BBA's efficacy on the diarrhea of piglets and the gut microbiomes have not been explored and the mechanism remains unclear. This study has explored whether BBA could modulate the composition of the gut microbiomes of piglets during diarrhea. The results showed that the diarrhea rate reduced significantly after treatment with BBA. BBA altered the overall structure of the gut microbiomes. In addition, the Gene Ontology (GO) enrichment analysis indicated that the functional differentially expressed genes, which were involved in the top 30 GO enrichments, were associated with hydrogenase (acceptor) activity, nicotinamide-nucleotide adenylyltransferase activity, and isocitrate lyase activity, belong to the molecular function. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that flagellar assembly, bacterial chemotaxis, lipopolysaccharide biosynthesis, ATP-binding cassette transporters (ABC) transporters, biosynthesis of amino acids, and phosphotransferase system (PTS) were the most enriched during BBA treatment process. Taken together, our results first demonstrated that BBA treatment could modulate the gut microbiomes composition of piglets with diarrhea, which may provide new potential insights on the mechanisms of gut microbiomes associated underlying the antimicrobial efficacy of BBA.

An Improved YOLOv2 for Vehicle Detection.

Vehicle detection is one of the important applications of object detection in intelligent transportation systems. It aims to extract specific vehicle-type information from pictures or videos containing vehicles. To solve the problems of existing vehicle detection, such as the lack of vehicle-type recognition, low detection accuracy, and slow speed, a new vehicle detection model YOLOv2_Vehicle based on YOLOv2 is proposed in this paper. The k-means++ clustering algorithm was used to cluster the vehicle bounding boxes on the training dataset, and six anchor boxes with different sizes were selected. Considering that the different scales of the vehicles may influence the vehicle detection model, normalization was applied to improve the loss calculation method for length and width of bounding boxes. To improve the feature extraction ability of the network, the multi-layer feature fusion strategy was adopted, and the repeated convolution layers in high layers were removed. The experimental results on the Beijing Institute of Technology (BIT)-Vehicle validation dataset demonstrated that the mean Average Precision (mAP) could reach 94.78%. The proposed model also showed excellent generalization ability on the CompCars test dataset, where the "vehicle face" is quite different from the training dataset. With the comparison experiments, it was proven that the proposed method is effective for vehicle detection. In addition, with network visualization, the proposed model showed excellent feature extraction ability.

Baicalin Inhibits Haemophilus Parasuis-Induced High-Mobility Group Box 1 Release during Inflammation.

Haemophilus parasuis (H. parasuis) can cause Glässer’s disease in pigs. However, the molecular mechanism of the inflammation response induced by H. parasuis remains unclear. The high-mobility group box 1 (HMGB1) protein is related to the pathogenesis of various infectious pathogens, but little is known about whether H. parasuis can induce the release of HMGB1 in piglet peripheral blood monocytes. Baicalin displays important anti-inflammatory and anti-microbial activities. In the present study, we investigated whether H. parasuis can trigger the secretion of HMGB1 in piglet peripheral blood monocytes and the anti-inflammatory effect of baicalin on the production of HMGB1 in peripheral blood monocytes induced by H. parasuis during the inflammation response. In addition, host cell responses stimulated by H. parasuis were determined with RNA-Seq. The RNA-Seq results showed that H. parasuis infection provokes the expression of cytokines and the activation of numerous pathways. In addition, baicalin significantly reduced the release of HMGB1 in peripheral blood monocytes induced by H. parasuis. Taken together, our study showed that H. parasuis can induce the release of HMGB1 and baicalin can inhibit HMGB1 secretion in an H. parasuis-induced peripheral blood monocytes model, which may provide a new strategy for preventing the inflammatory disorders induced by H. parasuis.

Transcriptional Profiling of Host Cell Responses to Virulent Haemophilus parasuis: New Insights into Pathogenesis.

Haemophilus parasuis is the causative agent of Glässer’s disease in pigs. H. parasuis can cause vascular damage, although the mechanism remains unclear. In this study, we investigated the host cell responses involved in the molecular pathway interactions in porcine aortic vascular endothelial cells (PAVECs) induced by H. parasuis using RNA-Seq. The transcriptome results showed that when PAVECs were infected with H. parasuis for 24 h, 281 differentially expressed genes (DEGs) were identified; of which, 236 were upregulated and 45 downregulated. The 281 DEGs were involved in 136 KEGG signaling pathways that were organismal systems, environmental information processing, metabolism, cellular processes, and genetic information processing. The main pathways were the Rap1, FoxO, and PI3K/Akt signaling pathways, and the overexpressed genes were determined and verified by quantitative reverse transcription polymerase chain reaction. In addition, 252 genes were clustered into biological processes, molecular processes, and cellular components. Our study provides new insights for understanding the interaction between bacterial and host cells, and analyzed, in detail, the possible mechanisms that lead to vascular damage induced by H. parasuis. This may lead to development of novel therapeutic targets to control H. parasuis infection.

Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection.

Haemophilus parasuis (H. parasuis) is the causative agent of Glässer's disease, a severe membrane inflammation disorder. Previously we showed that Baicalin (BA) possesses anti-inflammatory effects via the NLRP3 inflammatory pathway in an LPS-challenged piglet model. However, whether BA has anti-inflammatory effects upon H. parasuis infection is still unclear. This study investigated the anti-inflammatory effects and mechanisms of BA on H. parasuis-induced inflammatory responses via the NF-κB and NLRP3 inflammasome pathway in piglet mononuclear phagocytes (PMNP). Our data demonstrate that PMNP, when infected with H. parasuis, induced ROS (reactive oxygen species) production, promoted apoptosis, and initiated transcription expression of IL-6, IL-8, IL-10, PGE2, COX-2 and TNF-α via the NF-κB signaling pathway, and IL-1ß and IL-18 via the NLRP3 inflammasome signaling pathway. Moreover, when BA was administrated, we observed a reduction in ROS production, suppression of apoptosis, and inhibition of the activation of NF-κB and NLRP3 inflammasome signaling pathway in PMNP treated with H. parasuis. To our best knowledge, this is the first example that uses piglet primary immune cells for an H. parasuis infection study. Our data strongly suggest that BA can reverse the inflammatory effect initiated by H. parasuis and possesses significant immunosuppression activity, which represents a promising therapeutic agent in the treatment of H. parasuis infection.

Integrating network pharmacology and experimental validation to explore the mechanisms of luteolin in alleviating fumonisin B1-induced intestinal inflammatory injury.

Contamination with fumonisin B1 (FB1) represents a global health problem. FB1 exposure may also trigger intestinal injury by activating inflammatory responses, leading to a reduction in production performance and economic benefits. However, the mechanism of FB1-induced intestinal inflammatory injury is still unclear. At the same time, it is urgent to develop antibiotic alternatives and therapeutic targets to alleviate antibiotic resistance and to ensure effective treatment of intestinal inflammatory injury. We combined network pharmacology and in vitro experiments to explore the core therapeutic targets and potential mechanism of luteolin in FB1-induced intestinal inflammatory injury. Network pharmacology and molecular docking revealed that nuclear factor kappa B (NF-κB) p65, extracellular signal-regulated kinase (ERK), interleukin 6 (IL-6) and IL-1ß are the important targets, and the NF-κB and ERK signalling pathways are critical in FB1-induced intestinal inflammatory injury. Besides, in vitro experiments further demonstrated that luteolin can inhibit FB1-induced intestinal inflammatory injury by inhibiting activation of the NF-κB and ERK signalling pathways and reducing the expression of IL-6 and IL-1ß in IPEC-J2 cells. We have comprehensively illustrated the potential targets and molecular mechanism by which luteolin can alleviate FB1-induced intestinal inflammatory injury. Luteolin may be an effective antibiotic alternative to prevent intestinal inflammatory injury.

Characterization of dental light-curing resin composites incorporating multiple modified low-shrink monomers.

OBJECTIVE: Polymerization shrinkage poses a significant challenge in dental resin composites. The objective of this study is to introduce spiroorthocarbonate monomer 3,9-dimethylene-1,3,5,7-tetraoxa-spiro[5,5]undecane (BMSOC) and epoxy resin monomer 3,4-epoxycyclohexylmethyl-3,4-epoxycyclohexane carboxylate (ECHM-ECHC) into bisphenol-S-bis(3-methacrylato-2-hydroxy propyl)ether (BisS-GMA) based resin composites to develop composites with reduced shrinkage properties. METHODS: BMSOC and BisS-GMA were synthesized and thoroughly mixed with ECHM-ECHC, followed by inorganic fillers and photoinitiators. Based on the composition of the resin matrix, five groups of experimental composites were prepared, with traditional bisphenol A-dimethacrylate glycidyl ester (Bis-GMA)/triethylene glycol dimethacrylate (TEGDMA) based composite serving as the control. The polymerization properties, including degree of conversion (DC) and polymerization shrinkage (PS), as well as marginal microleakage, wettability, flexural strength (FS), flexural modulus (FM), and biocompatibility were evaluated. RESULTS: The results demonstrated that compared with the control group, the PS of BisS-GMA based composites containing BMSOC and ECHM-ECHC were significantly reduced (P < 0.05), and the lowest PS (0.96 ± 0.08 %) was observed when the ratio of BisS-GMA: (Epoxy + BMSOC) was 4:6. Additionally, the experimental composites also exhibited improved DC, minimal microleakage, low hydrophilicity, enhanced mechanical properties, qualified in vivo biocompatibility, and slight/moderate in vitro biocompatibility. SIGNIFICANCE: The resin composites incorporating multiple modified low-shrink monomers are promising for dental applications to prevent various clinical problems caused by PS and extend restoration longevity.

Using network pharmacology and molecular docking to uncover the mechanism by which quercetin alleviates deoxynivalenol-induced porcine intestinal injury.

Deoxynivalenol is a widespread feed contaminant that leads to vomit, which results in serious symptom such as increased intestinal permeability and even intestinal mucosal necrosis. Recent studies have reported the role of quercetin in alleviating deoxynivalenol-induced intestinal injury; however, the mechanisms and targets remain unclear. Thus, we aimed to identify the mechanisms of action by using a combination of network pharmacology and molecular docking. We identified 151 quercetin targets, 235 deoxynivalenol targets and 47 porcine intestinal injury targets by searching compound database and PubMed database, among which there were two common targets. The PPI network showed that the key proteins involved are NQO1 and PPAR-γ. The PPI network showed that the key proteins involved were NQO1 and PPARG. GO analysis found that genes were enriched primarily in response to oxidative stress. The PPI network showed that the key proteins involved are NQO1 and PPAR-γ. The genes are enriched primarily in response to oxidative stress. KEGG analysis showed enrichment of the HIF, reactive oxygen species and other signaling pathways. The molecular docking results indicated key binding activity between NQO1-quercetin and PPAR-γ-quercetin. By using network pharmacology, we have revealed the potential molecular mechanisms by which quercetin alleviates deoxynivalenol-induced porcine intestinal injury, which lays the foundation for the development of drugs to treat deoxynivalenol-induced intestinal injury in pigs.

Baicalin attenuates lipopolysaccharide-induced intestinal inflammatory injury via suppressing PARP1-mediated NF-κB and NLRP3 signalling pathway.

Bacterial lipopolysaccharide (LPS) exposure is a key inducer of intestinal inflammatory injury in weaned piglets, resulting in decreased growth performance of pigs and causing severe economic losses to the swine industry; however, the mechanism of intestinal inflammatory injury is still unclear. Baicalin is one of the main active ingredients extracted from the natural plant Scutellaria baicalensis that has biological functions, including anti-inflammatory activity. The aim of this study is to investigate the effect and mechanism of baicalin intervention on intestinal inflammatory injury caused by bacterial LPS exposure. In the present study, network pharmacology, molecular docking and DARTS results identified that baicalin has the potential to target PARP1, thereby potentially regulating a series of inflammation-related pathways, including the MAPK, NF-κB and Toll-like receptor signalling pathways, which play the role of antagonizing LPS-induced intestinal inflammatory injury. Further application of the LPS-induced IPEC-J2 cell model validated the finding that baicalin could alleviate LPS-induced intestinal inflammatory injury by inhibiting the PARP1-mediated NF-κB and NLRP3 signalling pathway. These findings demonstrate that baicalin can regulate the expression of PARP1 and that PARP1 has the potential to serve as an effective therapeutic target in the LPS-induced intestinal inflammatory injury.

Morphology-Based Prediction of Proliferation and Differentiation Potencies of Porcine Muscle Stem Cells for Cultured Meat Production.

Inconsistent efficiency of cell production caused by cellular quality variations has become a significant problem in the cultured meat industry. In our study, morphological information on passages 5-9 of porcine muscle stem cells (pMuSCs) from three lots was analyzed and used as input data in prediction models. Cell proliferation and differentiation potencies were measured by cell growth rate and average stained area of the myosin heavy chain. Analysis of PCA and heatmap showed that the morphological parameters could be used to discriminate the differences of passages and lots. Various morphological parameters were analyzed, which revealed that accumulating time-course information regarding morphological heterogeneity in cell populations is crucial to predicting the potencies. Based on the 36 and 60 h morphological profiles, the best proliferation potency prediction model (R2 = 0.95, RMSE = 1.1) and differentiation potency prediction model (R2 = 0.74, RMSE = 1.2) were explored. Correlation analysis demonstrated that morphological parameters selected in models are related to the quality of porcine muscle stem cells.

Bioactive Dental Resin Composites with MgO Nanoparticles.

Photoactivating dental resin composites have been the most prevailing material for repairing dental defects in various clinical scenarios due to their multiple advantages. However, compared to other restorative materials, the surface of resin-based composites is more susceptible to plaque biofilm accumulation, which can lead to secondary caries and restoration failure. This study introduced different weight fractions (1, 2, 5, 10, and 15%) of magnesium oxide nanoparticles (MgONPs) as antibacterial fillers into dental resin composites. Multifarious properties of the material were investigated, including antibacterial activity against a human salivary plaque-derived biofilm, cytotoxicity on human gingival fibroblasts, mechanical and physicochemical properties as well as the performance when subjected to thermocycling aging treatment. Results showed that the incorporation of MgONPs significantly improved the composites' anti-biofilm capability even at a low amount of 2 wt % without compromising the mechanical, physicochemical, and biocompatibility performances. The results of the thermocycling test suggested certain of aging resistance. Moreover, a small amount of MgONPs possibly made a difference in enhancing photoactivated polymerization and increasing the curing depth of experimental resin composites. Overall, this study highlights the potential of MgONPs as an effective strategy for developing antibacterial resin composites, which may help mitigating cariogenic biofilm-associated secondary caries.

18ß-Glycyrrhetinic Acid Alleviates P. multocida-Induced Vascular Endothelial Inflammation by PARP1-Mediated NF-κB and HMGB1 Signalling Suppression in PIEC Cells.

Background: At present, the treatment and prevention of Pasteurella multocida infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18ß-glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from Glycyrrhiza glabra L. root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by P. multocida infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections. Materials and Methods: Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were investigated using cell transfection and western blot. Results: Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates P. multocida-induced vascular endothelial inflammation by PARP1-mediated NF-κB and HMGB1 signalling suppression. Conclusion: These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by P. multocida infection.

Multifunctional dental resin composite with antibacterial and remineralization properties containing nMgO-BAG.

The inherent characteristics of resin composite can lead to micro-leakage after polymerization shrinkage. The bacteria invasion through edge micro-leakage and attachment onto the material surface can cause secondary caries, reducing the service life of resin composites. In this study, magnesium oxide nanoparticles (nMgO) as an inorganic antimicrobial agent and bioactive glass (BAG) as a remineralization agent were simultaneously incorporated into the resin composite. With the addition of both nMgO and BAG, the resin composite showed an excellent antimicrobial effect compared to the resin composite with nMgO or BAG only. The remineralization capacity of demineralized dentin increased with the increasing content of BAG. Vickers hardness, compressive strength, and flexural strength of the resin composite with nMgO-BAG were not significantly affected compared to the ones with the same total filler amount but with BAG only. The depth of cure and water sorption values of the resin composite showed an increasing trend with the increasing total amount of nMgO and BAG fillers. This developed multifunctional resin composite is expected to reduce bacterial invasion and promote remineralization of early caries damage.

Antibacterial and physical properties of resin cements containing MgO nanoparticles.

Cariogenic bacteria and dental plaque biofilm at prosthesis margins are considered a primary risk factor for failed restorations. Resin cement containing antibacterial agents can be beneficial in controlling bacteria and biofilm. This work aimed to evaluate the impact of incorporating magnesium oxide nanoparticles (MgONPs) as an antibacterial filler into dual-cure resin cement on bacteriostatic activity and physical properties, including mechanical, bonding, and physicochemical properties, as well as performance when subjected to a 5000-times thermocycling regimen. Experimental resin cements containing MgONPs of different mass fractions (0, 2.5%, 5%, 7.5% and 10%) were developed. Results suggested that the inclusion of MgONPs markedly improved the materials' bacteriostatic effect against Streptococcus mutans without compromising the physical properties when its addition reached 7.5 wt%. The mechanical properties of the specimens did not significantly decline after undergoing aging treatment, except for the flexural properties. In addition, the cements displayed good bonding performance and the material itself was not prone to cohesive fracture in the failure mode analysis. Furthermore, MgONPs possibly have played a role in decelerating material aging during thermocycling and enhancing bonding fastness in the early stage of cementation, which requires further investigation. Overall, developing MgONPs-doped resin cements can be a promising strategy to improve the material's performance in inhibiting cariogenic bacteria at restoration margins, in order to achieve a reduction in biofilm-associated secondary caries and a prolonged restoration lifespan.