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This article investigates the evolution of Chinese animation from 1949 to 1966, analyzing the complex interplay between politics and art during the ‘Seventeen Years’ period and its influence on the unique aesthetic of Chinese animation. During this time, Chinese animation served as both a showcase of artistic value and a political tool to advance the prevailing ideology, playing a key role in broadcasting political messages and shaping the depiction of socialist individuals. Through an examination of the themes, content, and artistic styles of animations, the study reveals how artists navigated political mandates to infuse their works with national identity and cultural meanings. Despite the political constraints that limited the diversity and creativity of animation, the period's animated works fulfilled an important social role and became a source of inspiration for subsequent projects, underscoring the distinctive appeal and growth potential of Chinese animation. The study contends that exploring Chinese animation within the ‘Seventeen Years’ framework not only sheds light on the importance of animation in specific historical contexts but also offers insights into the enduring relationship between art and politics, which continues to be significant in modern animation research and creation. [ABSTRACT FROM AUTHOR]

Selenium, in the form of selenoproteins, plays a pivotal role in anti-inflammatory processes and antioxidant defense system. The aim of this study was to examine the effects of selenium on lipopolysaccharide (LPS)-induced inflammatory responses in bovine mammary epithelial cells (bMEC) and to investigate the potential mechanism. bMEC viability was measured by MTT assay. TNF-α, IL-1β, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) expressions were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The activation of nuclear factor-kappa B (NF-κB) was determined by Western blotting. The results showed that the mRNA expressions of these inflammatory factors were significantly inhibited by selenium in a dose-dependent manner. At protein levels, Western blot analysis demonstrated that selenium dose-dependently decreased NF-κB p65 translocating from the cytoplasm to the nucleus. Taken together, these results suggest that the anti-inflammatory property of selenium in LPS-stimulated primary bMEC may be attributed to the downregulation of NF-κB activation. [ABSTRACT FROM AUTHOR]

The design of flexible phase change materials (FPCMs) with polyethylene glycol (PEG) as phase change components remains a great challenge due to high crystalline structure makes for high thermal energy storage ability yet deteriorates mechanical toughness. Herein, the preparation strategy of FPCMs was developed by introducing crystal structure regulators (CSRs) in PEG-based FPCM networks in a form of covalent linkages. The hydroquinone CSR had the strongest ability of crystal structure regulation over FPCMs compared to the three other used CSRs. The FPCMs had tuneable phase change temperatures (−2.0 °C–49.7 °C) and enthalpies (40.7 J g−1 to 109.3 J g−1) depending on the number-average molecular weight (M n = 4000 Da, 6000 Da) of PEGs used as well as the content and type of CSRs, further enabling tuneable mechanical stress (0.59–15.61 MPa) and strain (5.74%–505.86 %). Compared with the pristine PEGs, the FPCMs yielded excellent shape stability, thermal stability and thermal reliability. The flexibility and phase change properties endowed the FPCMs with excellent self-adaptability and shape memory function. The innovative strategy towards FPCMs highlights the application potential on individual wearable temperature-controlled devices. [Display omitted] • Flexible phase change materials were designed and synthesized. • Tuneable phase change properties were realized via the introduction of crystal structure regulators. • CSRs featuring enhanced performance was proved in the FPCMs. • Remarkable self-adaptability and shape memory function of FPCMs emphasized the potential applications. [ABSTRACT FROM AUTHOR]

Toxoplasma gondii (T. gondii) exhibits a significantly high prevalence of infection in goats, leading to adverse consequences such as abortion and stillbirth in ewes, thereby posing a substantial challenge to the goat farming industry. Neutrophil extracellular traps (NETs) have been shown to capture T. gondii in goats; however, the precise mechanisms underlying NET release in goats remain poorly understood. Therefore, the aim of our research was to elucidate the involved mechanism. We assessed the cytotoxicity of T. gondii on neutrophils using CCK-8 assay, visualized the structure of T. gondii-induced goat NETs through immunofluorescence, quantified ROS release during T. gondii-induced NET formation using fluorescence microplate analysis, and employed inhibitors targeting TLR 2, TLR4, NADPH oxidase, ERK1/2, and P38 MAPK signaling pathways as well as glycolysis to dissect the mechanisms underlying T. gondii-induced NET release. Within 1 h, T. gondii did not exhibit significant cytotoxicity towards neutrophils in our findings. The formation of typical NET structures induced by T. gondii involved DNA, citrullinated histone 3 (citH3), and neutrophil elastase (NE). Additionally, T. gondii significantly stimulated the release of NETs in goats. The process was accompanied by the production of reactive oxygen species (ROS) mediated through NADPH oxidase, p38, and ERK1/2 signaling pathways. Inhibition of these pathways resulted in a decrease in NET release. Moreover, inhibition of TLR 2, TLR4, and glycolysis also led to a reduction in T. gondii-induced NET release. Overall, our study demonstrates that T. gondii can induce characteristic NET structures and elucidates the involvement of various mechanisms including TLR2/TLR4 signaling pathway activation, NADPH oxidase activity modulation via ROS production regulation through p38 MAPK and ERK1/2 signaling pathways, and glycolysis regulation during the innate immune response against T. gondii infection in goats. [ABSTRACT FROM AUTHOR]

[Display omitted] • Multi-telechelic PEG-based multimers were designed and synthesized. • Multi-telechelic PEG-based multimers and curing agents constituted PCMs. • The multi-telechelic effect featuring enhanced performance was verified in the PCMs. • The reprocessing of PEG-based PCMs can be enabled by introducing dibutyltin dilaurate. Multi-telechelic polyethylene glycol (PEG)-based multimers with multiple reactive groups at both ends of the molecular chains can be used to prepare solid–solid phase change materials (PCMs) networks with enhanced mechanical strength, shape stability, PEG weight and adjustability in crosslink density, denoted as multi-telechelic effect in this report. Herein, multi-telechelic PEG-based PCMs networks were synthesized via the crosslinking reactions between designed hydroxyl-terminated multi-telechelic PEG-based multimers and curing agents, whose parameters can be readily tuned by the structure of multi-telechelic PEG-based multimers, for example, the number of PEG-derived structural units and the functionality of curing agents. Compared to conventional di-telechelic diethanolamine (DEA)-cured PCMs (DPCMs), the multi-telechelic tri-hexamethylene diisocyanate-cured PCMs (TPCMs) increase to 8–50 times in the storage modulus while decreasing only by 9.4 % in melting latent heat (Δ H m). The Δ H m of TPCMs increases by 58.2 % from 77.0 J/g to 121.8 J/g with increasing the number of PEG-derived structural units (y) from 1 to 4 when PEG with a number-average molecular weight of 4 kDa was used. TPCMs possess fine shape and thermal stability as well as thermal reliability while the reprocessability of PCMs is endowed by introducing a transcarbamoylation catalyst. The multi-telechelic PEG-based multimers can provide an alternative approach towards high-performance PCMs networks. [ABSTRACT FROM AUTHOR]

T-2 toxin, a highly toxic trichothecene mycotoxin widely found in food and feed, poses a significant threat to human health as well as livestock and poultry industry. Liver, being a crucial metabolic organ, is particularly susceptible to T-2 toxin induced damage characterized by inflammation and oxidative stress. Despite the role of Sirtuin 5 (SIRT5) in mitigating liver injury has been confirmed, its specific impact on T-2 toxin induced liver injury remains to be elucidated. The objective of this study was to investigate the protective role of SIRT5 against T-2 toxin induced liver injury in mice. Following the oral administration of 1 mg/kg.bw of T-2 toxin for 21 consecutive days to SIRT5 knockout (SIRT5−/−) and wild-type (WT) male mice, liver assessments were conducted. Our findings demonstrated that aggravated hepatic pathological injury was observed in SIRT5−/− mice, accompanied by elevated malondialdehyde (MDA) and Fe levels, as well as enhanced expression of glutathione peroxidase 4 (GPX4), NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, Gasdermin-D (GSDMD), tumour necrosis factor-alpha (TNF-α), and interleukin-1beta (IL-1β). These results indicated that SIRT5 alleviated hepatic structural damage and dysfunction, while inhibiting oxidative stress, iron accumulation, and NLRP3 inflammasome activation. Analysis revealed a positive correlation among NLRP3 inflammasome activation, iron accumulation, and oxidative stress. Overall, our study demonstrated that SIRT5 mitigated liver injury induced by T-2 toxin through inhibiting iron accumulation, oxidative stress, and NLRP3 inflammasome activation, providing novel insights into the management and prevention of T-2 toxin poisoning. [Display omitted] • SIRT5 alleviated liver dysfunction induced by T- 2 toxin. • SIRT5 mitigated histopathological damage to the liver. • SIRT5 mitigated T-2 toxin induced iron accumulation and oxidative stress. • SIRT5 inhibited NLRP3 inflammasome activation induced by T-2 toxin. [ABSTRACT FROM AUTHOR]

Neospora caninum (N. caninum) is an obligate intracellular Apicomplexa parasite that causes abortions in dairy cows and incurs substantial to significant economic losses in the global dairy farming industry. Cordycepin, a nucleoside antibiotic derived from Chinese medicine Cordyceps militaries, exhibits diverse biological activities. However, it remains unclear whether cordycepin possesses inhibitory effects against N. caninum infection. Therefore, this study aimed to establish both in vivo and in vitro models of N. caninum to investigate the potential impact of cordycepin against N. caninum infection. We successfully established an in vitro model of N. caninum infection in RAW264.7 cells, followed by qRT- PCR analysis to detect the content of N. caninum DNA within the cells. The effects of cordycepin on N. caninum was observed using the Giemsa method on RAW264.7, and the rate of cell infection was calculated. Cordycepin exhibited inhibitory effects on N. caninum tachyzoites in vitro , preserving cellular integrity and reducing the rate of cell infection. In mice, we established an in vivo model of N. caninum infection and detected N. caninum presence in tissues using. Real-time fluorescence quantitative PCR. Histopathological changes were observed through Hematoxylin-eosin staining. Liver function was assessed by using glutamic acid aminotransferase (ALT) and aspartic acid aminotransferase (AST) kits. Oxidative stress status was measured using catalase (CAT), malondialdehyde (MDA), and glutathione (GSH) kits. Compared with the model group, mice treated with cordycepin showed reduced clinical symptoms, increased food intake, and their body weight (P=0.0143, P=0.0068) was significantly higher than those in the model group. Furthermore, cordycepin treatment significantly alleviated hepatic cord disorders, hepatocellular swelling, detachment, and vacuolization; duodenal epithelial detachment and shortening of villi caused by N. caninum infection. Cordycepin administration reduced the increase in ALT (P=0.01, P=0.008) and AST (P<0.001) levels caused by N. caninum infection, while ameliorating hepatocyte swelling, necrosis, and detachment as well as inflammatory cell infiltration within mice liver; it also led to shortened or even disappeared duodenal villi along with and oedema of the submucosa. Analysis of oxidative stress showed that cordycepin ameliorated the damage caused by N. caninum by reducing MDA (P=0.03, P=0.02, P=0.005) and increasing CAT (P=0.004, P<0.001) and GSH (P=0.004, P<0.001) levels. In conclusion, this study reports for the first time on cordycepin's efficacy against N. caninum infection providing a potential candidate drug for neosporosis treatment. ● Neospora caninum infecting model of RAW264.7 cell was successfully established. ● Cordycepin inhibits the proliferation of N. caninum in RAW264.7 cells. ● Neospora caninum infecting model of mice was successfully established. ● Cordycepin exhibits pronounced in vivo reduction of Neospora caninum -induced damage. [ABSTRACT FROM AUTHOR]

• Linear PEG-based multimers and polyester network constituted semi-IPN-based PCMs. • The linear PEG-based multimers endowed semi-IPN-based PCMs with the multimerization effect. • The multimerization effect contributed to the enhanced latent heat, shape stability, mechanical strength. • The photothermal properties of semi-IPN-based PCMs can be enabled by introducing carbon black. Semi-interpenetrating polymer network (semi-IPN)-based phase change materials (PCMs) with linear polyethylene glycol (PEG)-based multimer intends to enhance the encapsulation fraction, shape stability and mechanical strength in a synergetic way relative to semi-IPN-based PCMs with linear PEG monomer. Herein, semi-IPN-based PCMs comprised of PEG-based multimers and covalent crosslinking polyester network were successfully synthesized via efficient esterification reaction between eco-friendly citric acid and multiple aziridine ring-containing species. The linear PEG-based multimers with various PEG unit number were formed by the reaction between polyethylene glycol and toluene diisocyanate in various molar ratio. With increasing PEG unit number of linear PEG-based multimers from 1 to 6, the PEG weight fraction of PCMs increases by 48.91% (from 60 wt% to 89.35 wt%) and the storage modulus (G′) of PCMs rises (from G′ = 12390 Pa for PCM-2–0.6 at 1 Hz at 90 °C while to G′ = 12780 Pa for PCM-6–0.6 at 1 Hz at 125 °C) when PEG weight fraction is nearly 60 wt%. The maximum latent heat reaches up to 141.0 J/g with the maximum PEG weight fraction of 89.35% in PCMs with linear PEG-based multimers encapsulated. The PCMs feature shape-stable form even at 140 °C, efficient photothermal effect by introducing carbon black and degradation ability resulting from hydrolysis effect of ester structure. The enhanced comprehensive performance of semi-IPN-based PCMs is due to the introduction of linear PEG-based multimers instead of pristine PEGs, which is denoted as multimerization effect, and the semi-IPN-based PCMs with multimerization effect will broaden the application of PCMs. [ABSTRACT FROM AUTHOR]

With the widespread use of copper oxide nanoparticles (CuO-NPs), their potential toxicity to the environment and biological health has attracted close attention. Heterophil extracellular traps (HETs) are an innate immune mechanism of chicken heterophils against adverse stimuli, but excessive HETs cause damage. Here, we explored the effect and mechanism of CuO-NPs on HETs formation in vitro and further evaluated the potential role of HETs in chicken liver and kidney injury. Heterophils were exposed to 5, 10, and 20 µg/mL of CuO-NPs for 2 h. The results showed that CuO-NPs induced typical HETs formation, which was dependent on NADPH oxidase, P38 and extracellular regulated protein kinases (ERK1/2) pathways, and glycolysis. In in vivo experiments, fluorescence microplate and morphological analysis showed that CuO-NPs elevated the level of HETs in chicken serum and caused liver and kidney damage. Meanwhile, CuO-NPs caused hepatic oxidative stress (MDA, SOD, CAT, and GSH–PX imbalance), and also induced an increase in mRNA expression of their inflammatory and apoptosis-related factors (IL-1β, IL-6, TNF-α, COX-2, iNOS, NLRP3, and Caspase-1, 3, 11). However, these results were significantly altered by DNase I (HETs degradation reagent). In conclusion, the present study demonstrates for the first time that CuO-NPs induce the formation of HETs and that HETs exacerbate pathological damage in chicken liver and kidney by promoting oxidative stress and inflammation, providing insights into immunotoxicity and potential prevention and treatment targets caused by CuO-NPs overexposure. [ABSTRACT FROM AUTHOR]

Zinc oxide nanoparticles (ZnO-NPs) are widely used in sunscreens, cosmetics, paint, construction materials, and other products. ZnO-NPs released into the environment can harm aquatic creatures and pose a health risk to humans through the food chain. ZnO-NPs are toxic to fish, but there are few reports on its immunotoxicity on crucian carp (Carassius carassius). In this study, ZnO-NPs increased the biochemical indexes of the liver in serum, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). In histopathological observation, many inflammatory cells were filled in the liver's central vein stimulated by ZnO-NPs. Furthermore, ZnO-NPs could increase malondialdehyde (MDA) level, lessen superoxide dismutase (SOD) level, and elevate the level of neutrophil extracellular traps (NETs). However, deoxyribonuclease I (DNase I) alleviated all biochemical indexes and histopathological changes. Immunofluorescence in vitro confirmed that NETs were composed of citrullinated histone 3, myeloperoxidase, and neutrophil elastase. ZnO-NPs-increased NETs were dependent on reactive oxygen species (ROS) and nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase and were also related to partial processes of glycolysis. Our study confirms that ZnO-NPS has a toxic effect on the liver of crucian carp. DNase I can prevent liver damage caused by ZnO-NPs, which provides a new insight into the immunotoxicity of ZnO-NPs to fish. [Display omitted] • Vivo experiment confirmed that ZnO-NPs caused Organ injury in crucian carp related to NETs. • Vitro experiment validated that ZnO-NPs induce NETs production in crucian carp neutrophils. • ZnO-NPs developed NETs in crucian carp to form ERK1/2 and p38 dependent signaling pathways. • The form of NETs in crucian carp induced by ZnO-NPs depended on NADPH oxidase and glycolysis. • DNase I is Promising for prevention of liver injury induced by ZnO-NPs. [ABSTRACT FROM AUTHOR]

Cyclopiazonic acid (CPA) is a secondary metabolite produced by Aspergillus and Penicillium, which is present in contaminated crops and food, causing severe toxicity to humans and animals. Heterophil extracellular traps (HETs) are a novel host innate immune mechanism of chicken heterophils against pathogen infection. However, whether CPA can cause immunotoxicity of heterophils on HETs release remains unclear. Here, we attempt to detect the effects of CPA on HETs release, and further investigate the molecular mechanisms underlying these processes. We exposed heterophils to 2.5, 5, 10 μM CPA for 90 min. The results showed that CPA induced the release of HETs in heterophils, consisting of DNA-modified citrullinated histone 3 and elastase. The quantitative analysis of HETs content was positively correlated with CPA concentration. CPA also promoted reactive oxygen species production and phosphorylation of ERK1/2 and p38. In addition, CPA-triggered HETs formation was reduced by NADPH oxidase, ERK1/2, and p38 signaling pathway and glycolysis inhibitors, indicating that CPA-induced HETs were related to the production of ROS dependent on NADPH oxidase, ERK1/2, and p38 signaling pathways, as well as glycolysis. Our study describes the underlying mechanism of CPA-induced HETs release, which may provide a further understanding of the immunotoxicology of CPA poisoning. [ABSTRACT FROM AUTHOR]

Pigeons are natural intermediate host of Neospora caninum (N. caninum). In comparison to ruminants, N. caninum causes milder clinical symptoms and less financial loss to pigeons. Natural infectious rates and high prevalence of N. caninum in pigeons, and death cases of N. caninum- infected pigeons under experimental conditions have been reported, but the detailed pathological characteristics and congenital immunological responses of pigeons-infected with N. caninum remain not well described. In this study, pigeons were infected intraperitoneally with 107 N. caninum tachyzoites. N. caninum in tissues was detected by qPCR. Pathological changes of tissues were examined by hematoxylin-eosin staining. Blood smears were prepared for counting eosinophils changes in blood. Heterophil extracellular traps (HETs) in vivo and in vitro were quantified by Pico Green. N. caninum- induced HETs structures were observed by immunofluorescence staining. The model of pigeons-infected with N. caninum was successfully established. Lung and duodenum were the main target organs of pigeons-infected with N. caninum. N. caninum caused hemorrhage, edema and inflammatory cell infiltration in liver, pulmonary congestion and hemorrhage, organizational destruction in lung, and shorter villi or even disappear in duodenum. N. caninum also increased the number of eosinophils in blood of pigeons. Moreover, N. caninum -induced HETs release in the congenital immunological system of pigeons were first demonstrated, and the HETs structures were consisted of DNA as the skeleton and modified with citH3 and elastase. N. caninum -induced HETs release was related with NADPH oxidase, TLR 2 and 4, ERK 1/2 and p38 MAPK signaling pathways, and glycolysis. In summary, it is the first report on the detailed pathological characteristics and congenital immunological responses of pigeons-infected with N. caninum , which may provide theoretical basis for the prevention and control of Neosporosis in pigeons. • Pathological characteristics and congenital immunological responses of pigeons infected with Neospora caninum. [ABSTRACT FROM AUTHOR]

Aspergillus fumigatus causes aspergillosis with high morbidity and mortality in the duck industry. As a vital virulence factor produced by A. fumigatus , gliotoxin (GT) is widely present in food and feed, threatening duck industry and human health. Quercetin is a polyphenol flavonoid compound from natural plants with anti-inflammatory and antioxidant functions. However, the effects of quercetin on ducklings with GT poisoning are unknown. The model of ducklings with GT poisoning was established, and the protective effects and molecular mechanisms of quercetin on ducklings with GT poisoning were investigated. Ducklings were divided into control, GT, and quercetin groups. A model of GT (2.5 mg/kg) poisoning in ducklings was successfully established. Quercetin protected GT-induced liver and kidney functions and alleviated GT-induced alveolar wall thickening in lungs, cell fragmentation, and inflammatory cell infiltration in liver and kidney. Quercetin decreased malondialdehyde (MDA) and increased superoxide dismutase (SOD) and catalase (CAT) after GT treatment. Quercetin significantly reduced GT-induced mRNA expression levels of inflammatory factors. Furthermore, quercetin increased GT-reduced heterophil extracellular traps (HETs) in serum. These results indicated that quercetin protected ducklings against GT poisoning by inhibiting oxidative stress, inflammation and increasing HETs release, which confirms the potential applicability of quercetin in treating GT-induced duckling poisoning. • Gliotoxin-induced tissue injury model in ducklings has been successful established. • Quercetin has significant healing effects against gliotoxin poisoning. • Quercetin can inhibit oxidative stress, inflammation and increase heterophil extracellular traps release. [ABSTRACT FROM AUTHOR]

Nanosilver is a metallic silver monomer with a diameter of <100 nm, which has excellent antibacterial activity and is widely used in the fields of medicine and sanitation, disinfection of drinking water in daily life and feed additives in livestock and poultry farming. Heterophil extracellular traps (HETs) are an important part of innate immunity in chickens and have an excellent antimicrobial effect, but their excessive release caused tissue damage. Nanosilver overdose caused toxic effects in chickens, while immunotoxic effects of nanosilver on chickens have not been reported. In this study, we explored the effects of nanosilver-induced HETs on chicken liver and kidney damage and further investigated the molecular mechanism of nanosilver-induced HETs release. The results showed that nanosilver significantly upregulated serum HETs and caused liver and kidney damage. The classical structure of nanosilver-induced HETs was also observed, and nanosilver-induced HETs were dependent on reactive oxygen species (ROS), extracellular regulatory protein kinase (ERK) 1/2 , p38 and glycolysis pathways. In summary, this research suggests that nanosilver induced HETs release, but excessive HETs release also caused damage to chicken. It also helps to understand the importance of moderate application of nanosilver, which may improve animal immunity but avoid negative effects in safeguarding the economic efficiency of poultry farming. Nanosilver stimulates heterophil extracellular traps (HETs) release through glycolysis, NADPH oxidase, extracellular regulatory protein kinase (ERK) 1/2 and p38 signaling pathways, leading to tissue damage. [Display omitted] • Nanosilver-stimulated heterophil extracellular trap consisted with DNA, histone 3 and elastase. • Nanosilver induces heterophil extracellular trap dependent on reactive oxygen species. • Nanosilver induced heterophil extracellular trap via NADPH oxidase and p38 signaling pathways. • Glycolysis provides energy for the induction of heterophil extracellular trap by nanosilver. • Nanosilver-stimulated heterophil extracellular traps promoted liver and kidney injury. [ABSTRACT FROM AUTHOR]

Widely used alumina nanoparticles (Al 2 O 3 NPs) exposed to the environment pose a serious threat to human and animal health. The formation of heterophil extracellular traps (HETs) is a mechanism of innate immune defense against infection, but excessive HETs cause pathological damage. Here, we aim to explore the influence and mechanism of Al 2 O 3 NPs on the formation of HETs in vitro , and further investigate the role of HETs release in histopathological damage after Al 2 O 3 NPs treatment. Immunofluorescence analysis showed that Al 2 O 3 NPs induced the formation of HETs, which was characterized by modified histones and elastase in the DNA backbone. Fluorescence microplate analysis showed that HETs formation was dependent on NADPH oxidase, P38, extracellular regulated protein kinases (ERK 1/2) pathways and glycolysis. In vivo investigation showed that Al 2 O 3 NPs significantly caused HETs release and liver damage. Biochemical analysis showed that Al 2 O 3 NPs inhibited the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX). Real-time fluorescence quantification results showed that Al 2 O 3 NPs caused the overexpression of inflammation-related molecules interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), caspase-1 and caspase-11. All these changes were significantly changed by DNase I (Degradation reagent for HETs). Together, these suggest that Al 2 O 3 NPs-induced HETs exacerbate liver injury by regulating oxidative stress and inflammatory responses, which provide a new perspective and potential prophylaxis and treatment targets for Al 2 O 3 NPs toxicological research. Alumina nanoparticles promote the formation of heterophil extracellular traps in chickens through glycolysis and reactive oxygen species production dependent on NADPH oxidase, extracellular regulated protein kinases (ERK 1/2), and P38 signaling pathways. [Display omitted] • Alumina nanoparticles (Al 2 O 3 NPs) triggered heterophil extracellular traps (HETs) formation. • HETs formation depended on NADPH oxidase, extracellular regulated protein kinase and P38. • HETs were associated with glycolysis. • Al 2 O 3 NPs induced serum HETs formation and caused liver and kidney damage. • Oxidative stress and inflammation aggravated chicken liver and kidney tissue damage. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AFB1) is a mycotoxin with strong toxicity and play a large proportion in aspergillosis. Heterophil extracellular traps (HETs) was considered as an innate immune response of chickens to resist pathogens. AFB1 has been reported to trigger macrophages extracellular traps (METs) in THP-1 cells and RAW264.7 cells, but whether AFB1 could also activate HETs release, and the mechanism underlying AFB1-activated HETs in chicken remains unclear. In this study, we confirmed that AFB1could induce HETs release, which was a network of DNA-based structures consist of citrullinated histone 3 (citH3) and elastase. Meanwhile, AFB1-activated HETs rely on the glycolytic process to provide energy, NADPH oxidase and p38 signaling pathway. Moreover, it has been verified that AFB1-activated HETs release could significantly increase the biochemical indexes of liver (ALT and AST) and kidney (CRE and BUN) in serum. In addition, histopathological observation showed that AFB1 caused swelling, necrosis and vacuolation of hepatocytes in liver, and necrosis, exfoliated of nephrocyte in kidney. Further investigation demonstrated that AFB1 significantly decreased the levels of SOD and GSH-PX but increased the level of MDA, and meanwhile induced the mRNA expressions of TNF-α, IL-6 and IL-1β, iNOS, COX-2, NLRP3, caspase-1, caspase-3 and caspase-11. However, all these AFB1-induced biochemical indexes and histopathological changes were effectively alleviated by DNase I (the standard degradant for HETs). In conclusion, it has preliminary confirmed that AFB1-activated HETs formation contributed to the immunotoxicity in chicken and provide new strategies for the therapy in aspergillosis. [Display omitted] • AFB1 induced the formation of heterophils extracellular traps (HETs) in chicken. • AFB1-induced HETs formation depends on ROS, NADPH oxidase and p38 signaling pathways. • AFB1-induced HETs formation depends on glycolytic pathways to provide energy. • HETs caused immunotoxicity to the liver and kidney damage through oxidative stress. [ABSTRACT FROM AUTHOR]

• The model of ZEA-induced liver injury in chicks was successfully established. • The ZEA-induced apoptosis of liver and kidney cells in chicks was confirmed. • The mechanism of baicalin in the injury induced by ZEA in chicks was revealed. Zearalenone (ZEA) is a secondary metabolite produced by fungi such as Fusarium and Fusarium flavum, which is classified as a mycotoxin. Crops and feed in a humid surrounding are widely polluted by ZEA, which further endangering the healthful aquaculture of poultry and even human health. Up to now, prevention and cure of mycotoxicosis is still a crucial subject of poultry husbandry. Baicalin (BAI) is a flavonoid refined from dried roots of Scutellaria baicalensis possessing the function of hepatoprotective, anti-inflammatory, anti-oxidant, and anti-atherosclerotic efficacies.etc. But whether Baicalin also has a protective effect against ZEA intoxication is unclear. Therefore, the aim of this study was to establish a model of ZEA-induced toxic injury in chicks, and then to investigate the way in which Baicalin plays a protective role in the mechanism of ZEA-induced liver and kidney injury in chicks. The results exhibit that Baicalin could not only significantly decrease aspartate aminotransferase (AST) , alanine aminotransferase (ALT) and creatinine (Cre) levels in serum, but also ameliorate ZEA-induced pathologic changes of liver and kidney. Baicalin could also significantly regulate ZEA-induced the changes of catalase (CAT) , malondialdehyde (MDA) , total sulfhydryl group , except for glutathione peroxidase (GSH-px) , and inhibit the mRNA levels of inflammatory cytokines tumor necrosis factor-α (TNF-α) , interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) with caspase-3 and caspase-11 in the caspase signaling pathway , meanwhile inhibit the cell apoptosis in immunohistochemistry. In summary, we successfully established a model of ZEA-induced liver injury in chicks, and confirm that Baicalin can reduce ZEA-induced liver and kidney injury in chicks. The mechanism of these effects is via inhibiting inflammation, oxidative stress and apoptosis, which also indicates the potential applicability of Baicalin for the prevention and treatment of ZEA-induced toxicity in chicks. [ABSTRACT FROM AUTHOR]

[Display omitted] • A novel SSPCM based on dynamic metal-ligand bonds was successfully prepared. • The devised DS-PCMs can be reprocessed in two simple and convenient ways. • The DS-PCMs have superior energy storage ability and thermoplastic performance. Thermal energy storage offers enormous potential for the development of modern energy technologies. Solid-solid phase-change materials (SSPCMs) have drawn great attention due to their efficient energy utilization and excellent thermal stability. However, it is still a challenge to synthesize SSPCMs capable of the intriguing properties of reprocessability and recyclability. Herein, we reported an effective strategy to construct dynamic cross-linked SSPCMs, namely DS-PCMs, through incorporating reversible metal-ligand coordination. The synthesized DS-PCMs can keep in a solid state during the phase change process with a high latent heat storage capacity of up to 99.3 J/g. Especially, the energy storage capacity, chemical structure and thermal stability of the reprocessed DS-PCMs can be consistent with that of original one after being reprocessed by hot pressing and ultrasound-assisted water solution casting. Additionally, these DS-PCMs have repeatable thermo-plasticity to manipulate permanent various 3D shapes without complex molds. Briefly, these designed DS-PCMs simultaneously have excellent stability, dual reprocessability, and reconfigurable thermoplastic performance. Our works provide a facile design strategy to prepare reprocessable SSPCMs, unlocking opportunities for the sustainable use of phase change materials. [ABSTRACT FROM AUTHOR]

Alongshan virus (ALSV) is a newly discovered pathogen in the Flaviviridae family, characterized by a unique multi-segmented genome that is distantly related to the canonical flaviviruses. Understanding the pathogenic mechanism of this emerging segmented flavivirus is crucial for the development of effective intervention strategies. In this study, we demonstrate that ALSV can infect various mammalian cells and induce the expression of antiviral genes. Furthermore, ALSV is sensitive to IFN-β, but it has developed strategies to counteract the host's type I IFN response. Mechanistically, ALSV's nonstructural protein NSP1 interacts with and degrades human STAT2 through an autophagy pathway, with species-dependent effects. This degradation directly inhibits the expression of interferon-stimulated genes (ISGs). Additionally, NSP1-mediated degradation of STAT2 disrupts mitochondrial dynamics, leading to mitophagy and inhibition of mitochondrial biogenesis. This, in turn, suppresses the host's innate immune response. Interestingly, we found that inhibiting mitophagy using 3-methyladenine and enhancing mitochondrial biogenesis with the PPARγ agonist pioglitazone can reverse NSP1-mediated inhibition of ISGs, suggesting that promoting mitochondrial mass could serve as an effective antiviral strategy. Specifically, the NSP1 methyltransferase domain binds to the key sites of F175/R176 located in the coiled-coil domain of STAT2. Our findings provide valuable insights into the intricate regulatory cross talk between ALSV and the host's innate immune response, shedding light on the pathogenesis of this emerging segmented flavivirus and offering potential intervention strategies.IMPORTANCEAlongshan virus (ALSV), a segmented flavivirus belonging to the Flaviviridae family, was first identified in individuals who had been bitten by ticks in Northeastern China. ALSV infection is responsible for causing Alongshan fever, a condition characterized by various clinical symptoms, including fever, headache, skin rash, myalgia, arthralgia, depression, and coma. There is an urgent need for effective antiviral therapies. Here, we demonstrate that ALSV is susceptible to IFN-β but has developed mechanisms to counteract the host's innate immune response. Specifically, the ALSV nonstructural protein NSP1 interacts with STAT2, leading to its degradation via an autophagy pathway that exhibits species-dependent effects. Additionally, NSP1 disrupts mitochondrial dynamics and suppresses mitochondrial biogenesis, resulting in a reduction in mitochondrial mass, which ultimately contributes to the inhibition of the host's innate immune response. Interestingly, we found that inhibiting mitophagy and promoting mitochondrial biogenesis can reverse NSP1-mediated suppression of innate immune response by increasing mitochondrial mass. These findings provide valuable insights into the molecular mechanisms of ALSV pathogenesis and suggest potential therapeutic targets against ALSV infection.

Enhancing or protecting sperm motility has always been a pivotal approach to improving the ewe pregnancy rate. Sperm motility is highly susceptible to the immune status of the reproductive tract. Neutrophil extracellular traps (NETs) have been demonstrated to capture sperm and impair its motility in human, swine, and goat species. Quercetin is a flavonoid derived from Cuscuta Chinensis Lam ., which can protect sperm from oxidative damage. In this study, we investigated whether inflammation decreases sperm motility and tried to clarify the potential protective mechanism of quercetin on goat sperm motility. Sperm-triggered NETs were analyzed by immunofluorescence analysis. Sperm acrosome integrity was detected by using giemsa staining. Quercetin exhibited no cytotoxicity towards sperm and PMNs within the concentration range of 20-80 μM. PMNs impaired both the survival rate and rapid linear motility of sperm, while quercetin significantly enhanced these parameters. PMNs captured sperm through NETs composed of DNA, citrullinated histone 3 (citH3), and neutrophil elastase (NE); however, quercetin effectively inhibited the release of sperm-stimulated NETs. The stimulation of PMNs with sperm resulted in a significant increase in levels of ROS and MDA, which decreased by quercetin. Moreover, PMNs caused integrity violation to both the plasma membrane and acrosome in sperm; this effect was significantly alleviated by quercetin. In conclusion, quercetin effectively ameliorated PMN-reduced sperm motility through the inhibition of NETs and oxidative stress, and preserving sperm plasma membrane and acrosome integrity, thereby providing preliminary insights into the underlying mechanisms and theoretical support for the development of potential sperm protectors.

Neospora caninum (N. caninum) is a protozoan parasite that poses a serious risk to livestock by infecting various domestic and wild animals. Loop-Mediated Isothermal Amplification (LAMP) offers a cost-effective, highly sensitive, and specific method for detecting protozoan parasites. This study aims to develop a precise, rapid, and visually assessable colorimetric LAMP method, improving on traditional techniques. We employed a rigorous screening process to identify the optimal primer set for this experiment. Subsequently, we fine-tuned the LAMP reaction at 65 °C for 40 min with 270 μmol/L neutral red. We then confirmed the specificity of primers for N. caninum through experimental validation. The LAMP method demonstrated a lower detection limit compared to traditional Polymerase Chain Reaction (PCR) techniques. While LAMP offers clear advantages, the prevalence of DNA detected in 89 sheep serum and 59 bovine serum samples using the nested PCR method was 3.37 % (3/89) and 1.69 % (1/59), respectively. In contrast, when the LAMP method was employed, the prevalence of detected DNA rose to 5.61 % (5/89) for sheep and 3.38 % (2 /59) for bovine. A comparison of two molecular assays using the intragroup correlation coefficient (ICC) resulted in a value of 0.999 (95 % CI: 0.993-0.996, p < 0.001), indicating the LAMP method is in the "better" range according to James Lee's categorization. The LAMP technique, optimized with specific primers of N. caninum and neutral red dye, not only exhibited higher sensitivity but also provided convenience over conventional PCR methods, highlighting its potential for on-site applications and cost-effective field detection., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Gliotoxin (GT) belongs to the epipolythiodioxopiperazine (ETP) family, which is considered a crucial virulence determinant among the secondary metabolites produced by Aspergillus fumigatus. The metabolites are commonly found in food and feed, contributing to the invasion and immune escape of Aspergillus fumigatus, thereby posing a significant threat to the health of livestock, poultry, and humans. Heterophil extracellular traps (HETs), a novel form of innate immune defense, have been documented in the chicken's innate immune systems for capturing and eliminating invading microbes. However, the effects and mechanisms of GT on the production of duck HETs in vitro remain unknown. In this study, we first confirmed the presence of HETs in duck innate immune systems and further investigated the molecular mechanism underlying GT-induced HETs release. Our results demonstrate that GT can trigger typical release of HETs in duck. The structures of GT-induced HETs structures were characterized by DNA decoration, citrullinated histones 3, and elastase. Furthermore, NADPH oxidase, glycolysis, ERK 1/2 and p38 signaling pathway were found to regulate GT-induced HETs. In summary, our findings reveal that gliotoxin activates HETs release in the early innate immune system of duck while providing new insights into the immunotoxicity of GT towards ducks., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)