The Missing Piece of the Puzzle: How Different Water-related Public Concerns Contribute to Water Governance in China.

Public participation is crucial to improving the performance of water governance systems, especially in a governance model dominated by a top-down hierarchical structure. Public concerns, as a vital form of public participation, have been acknowledged as an essential component in contributing to water governance. However, few studies explore the varying effects of diverse public concerns in leading to different water governance outcomes. This study addresses this gap by exploring the direct and indirect effects of water-related public concerns on water pollution control and governments' pollution mitigating actions, using citizens' water-related posts crawled from China's social media. Results show that public water-related concerns contribute to water governance both through its direct effects on reducing water pollution and indirect effects by promoting policy actions. Specifically, the concerns related to water pollution hazards, water pollution monitoring, prevention products, and water pollution control measures have more positive impacts on water pollution reduction compared to other types of concern. Meanwhile, public concerns demonstrate stronger effects in triggering economic-related and infrastructure-related water pollution mitigation actions. This study provides nuanced insights to understand the role of public participation in improving water governance, the findings of which are insightful to enhance accountability of water governance systems through a bottom-up approach.

Toward Integrating EBPR and the Short-Cut Nitrogen Removal Process in a One-Stage System for Treating High-Strength Wastewater.

Enhanced biological phosphorus removal (EBPR) is an economical and sustainable process for phosphorus removal from wastewater. Despite the widespread application of EBPR for low-strength domestic wastewater treatment, limited investigations have been conducted to apply EBPR to the high-strength wastewaters, particularly, the integration of EBPR and the short-cut nitrogen removal process in the one-stage system remains challenging. Herein, we reported a novel proof-of-concept demonstration of integrating EBPR and nitritation (oxidation of ammonium to nitrite) in a one-stage sequencing batch reactor to achieve simultaneous high-strength phosphorus and short-cut nitrogen removal. Excellent EBPR performance of effluent 0.8 ± 1.0 mg P/L and >99% removal efficiency was achieved fed with synthetic high-strength phosphorus wastewater. Long-term sludge acclimation proved that the dominant polyphosphate accumulating organisms (PAOs), Candidatus Accumulibacter, could evolve to a specific subtype that can tolerate the nitrite inhibition as revealed by operational taxonomic unit (OTU)-based oligotyping analysis. The EBPR kinetic and stoichiometric evaluations combined with the amplicon sequencing proved that the Candidatus Competibacter, as the dominant glycogen accumulating organisms (GAOs), could well coexist with PAOs (15.3-24.9% and 14.2-33.1%, respectively) and did not deteriorate the EBPR performance. The nitrification activity assessment, amplicon sequencing, and functional-based gene marker quantification verified that the unexpected nitrite accumulation (10.7-21.0 mg N/L) in the high-strength EBPR system was likely caused by the nitritation process, in which the nitrite-oxidizing bacteria (NOB) were successfully out-selected (<0.1% relative abundance). We hypothesized that the introduction of the anaerobic phase with high VFA concentrations could be the potential selection force for achieving nitritation based on the literature review and our preliminary batch tests. This study sheds light on developing a new feasible technical route for integrating EBPR with short-cut nitrogen removal for efficient high-strength wastewater treatment.

Effects of anti-stress agents on the growth performance and immune function in broiler chickens with vaccination-induced stress.

The aim of this study was to evaluate the effects of anti-stress agents on the growth performance and immune function of broilers under immune stress conditions induced by vaccination. A total of 128, 1-day-old Arbor Acres broilers were randomly divided into four groups. Group normal control (NC) was the control group. Group vaccination control (VC), T 0.5%, and T 1% were the treatment groups, which were nasally vaccinated with two doses of the Newcastle disease virus (NDV) vaccine. The chicks in groups T 0.5% and T 1% were fed conventional diets containing 0.5% and 1% anti-stress agents. Thereafter, these broilers were slaughtered on 1, 7, 14, and 21 days post-vaccination. The results indicated that anti-stress agents could significantly reduce serum adrenocorticotropic hormone (ACTH) (P < 0.01) and cortisol (CORT) (P < 0.05) levels, and improve the growth performance (P < 0.05) and immune function of broilers (P < 0.05); However, the levels of malondialdehyde (MDA) (P < 0.05) were decreased, and the decreased total antioxidant capacity (T-AOC) (P < 0.01) levels mediated by vaccination were markedly improved. In addition, anti-stress agents could attenuate apoptosis in spleen lymphocytes (P < 0.01) by upregulating the ratio of Bcl-2 to BAX (P < 0.01) and downregulating the expression of caspase-3 and -9 (P < 0.01), which might be attributed to the inhibition of the enzymatic activities of caspase-3 and -9 (P < 0.05). In conclusion, anti-stress agents may improve growth performance and immune function in broilers under immune-stress conditions.RESEARCH HIGHLIGHTS Investigation of effects and mechanism of immune stress induced by vaccination.Beneficial effect of anti-stress agents on growth performance, immune function, oxidative stress, and regulation of lymphocyte apoptosis.Demonstration of the effects of apoptosis on immune function in the organism.

Effect of thermal hydrolysis pretreatment on the stabilization of sludge with different solid contents during autothermal thermophilic aerobic digestion.

Sludge stabilization was affected by solid content during autothermal thermophilic aerobic digestion (ATAD). Thermal hydrolysis pretreatment (THP) could alleviate the issues of high viscosity, slow solubilization and low ATAD efficiency caused by increased solid content. The influence of THP on the stabilization of sludge with different solid contents (5.24%-17.14%) during ATAD was investigated in this study. The results demonstrated that stabilization was achieved with volatile solid (VS) removal of 39.0%-40.4% after 7-9 days of ATAD for sludge with solid content of 5.24%-17.14%. The solubilization of sludge with different solid contents reached 40.1%-45.0% after THP. The rheological analysis indicated that the apparent viscosity of sludge was obviously reduced after THP at different solid contents. The increase in fluorescence intensity of fulvic acid-like organics, soluble microbial by-products and humic acid-like organics in the supernatant after THP and the decrease in fluorescence intensity of soluble microbial by-products after ATAD were detected by excitation emission matrix (EEM). The molecular weight (MW) distribution in the supernatant elucidated that the proportion of 50 kDa < MW < 100 kDa increased to 16%-34% after THP and the proportion of 10 kDa < MW < 50 kDa decreased to 8%-24% after ATAD. High throughput sequencing showed that the dominant bacterial genera shifted from Acinetobacter, Defluviicoccus and Norank_f__norank_o__PeM15 to Sphaerobacter and Bacillus during ATAD. This work revealed that solid content of 13%-17% was appropriate for efficient ATAD and rapid stabilization under THP.

Medium-Low Temperature Conditions Induce the Formation of Environmentally Persistent Free Radicals in Microplastics with Conjugated Aromatic-Ring Structures during Sewage Sludge Pyrolysis.

Medium-low temperature pyrolysis is an effective method of retaining active components in sludge char. However, we found that incomplete cracking reactions resulted in residues of microplastics (MPs) remaining in the char; moreover, high levels of environmentally persistent free radicals (EPFRs) were detected in these MPs. Here, we investigated the temperature-dependent variations in the char-volatile products derived from sludge and MPs under different pyrolysis scenarios using multiple in situ probe coupling techniques and electron paramagnetic resonance spectroscopy, thereby identifying the sources of EPFRs and elucidating the corresponding formation-conversion mechanisms. The temperature was the key factor in the formation of EPFRs; in particular, in the 350-450 °C range, the abundance of EPFRs increased exponentially. Reactive EPFR readily formed in MPs with conjugated aromatic-ring structures (polyethylene terephthalate and polystyrene) at a temperature above 350 °C; EPFR concentrations were 5-17 times higher than those found in other types of polymers, and these radicals exhibited half-lives of more than 90 days. The EPFR formation mechanism could be summarized as solid-solid/solid-gas interfacial interactions between the polymers and the intermediate products from sludge pyrolysis (at 160-350 °C) and the homolytic cleavage-proton transfer occurring in the polymers themselves under the dual action of thermal induction and acid sites (at 350-450 °C). Based on the understanding of the evolution of EPFRs, temperature regulation and sludge components conditioning may be effective approaches to inhibit the formation of EPFRs in MPs, constituting reliable strategies to diminish the environmental risk associated with the byproducts of sludge pyrolysis.

Ameliorative effect of betulinic acid against zearalenone exposure triggers testicular dysfunction and oxidative stress in mice via p38/ERK MAPK inhibition and Nrf2-mediated antioxidant defense activation.

Zearalenone (ZEA) is a nonsteroidal estrogenic mycotoxin, which mainly contaminates grains and has estrogen-like effects on the reproductive system. Betulinic acid (BA), a natural lupane-type pentacyclic triterpene, has anti-oxidative and anti-inflammatory properties. This study aimed to investigate whether BA alleviates ZEA-induced testicular damage and explore the possible mechanism. Here, BA ameliorated testicular damage by mitigating the disordered arrangement of seminiferous tubules, the exfoliation of lumen cells, and the increase of cell apoptosis caused by ZEA. Meanwhile, BA alleviated ZEA-triggered testicular damage by restoring hormone levels and sperm motility, and reconstructing the blood-testis-barrier. Moreover, BA alleviated ZEA-exposed testicular oxidative stress by activating Nrf2 pathway. Furthermore, BA moderated ZEA-evoked testicular inflammation by inhibiting p38/ERK MAPK pathway. Overall, our results revealed that BA has a therapeutic protective effect on ZEA-induced testicular injury and oxidative stress via p38/ERK MAPK inhibition and Nrf2-mediated antioxidant defense activation, which provides a viable alternative to alleviate ZEA-induced male reproductive toxicology.

The role of ER stress and ATP/AMPK in oxidative stress meditated hepatotoxicity induced by citrinin.

Citrinin, a secondary metabolite, can pose serious risks to the environment and organisms, but its hepatotoxic mechanisms are still unclear. Histopathological and ultrastructural results showed that citrinin-induced liver injury in Kunming mice, and the mechanism of citrinin-induced hepatotoxicity was studied in L02 cells. Firstly, citrinin mades L02 cell cycle arrest in G2/M phase by inhibition of cyclin B1, cyclin D1, cyclin-dependent kinases 2 (CDK2), and CDK4 expression. Secondly, citrinin inhibits proliferation and promotes apoptosis of L02 cells via disruption of mitochondria membrane potential, increase Bax/Bcl-2 ration, activation of caspase-3, 9, and enhance lactate dehydrogenase (LDH) release. Then, citrinin inhibits superoxide dismutase (SOD) activity and increases the accumulation of malondialdehyde (MDA) and reactive oxygen species (ROS), resulting oxidative damage in L02 cells; upregulates the protein expression of binding immunoglobulin protein (Bip), C/EBP homologous protein (CHOP), PKR-like ER kinase (PERK) and activating transcription factor6 (ATF6), inducing ER stress in L02 cells; increases the phosphorylation of AMP-activated protein kinase (AMPK) and decreases the content of adenosine-triphosphate (ATP), activating AMPK pathway in L02 cells. Eventually, pretreatment with NAC, an ROS inhibitor, alleviates citrinin-induced cell cycle G2/M arrest and apoptosis by inhibiting ROS-mediated ER stress; pretreatment with 4-PBA, an ER stress inhibitor, reversed ER stress and p-AMPK; pretreatment with dorsomorphin, an AMPK inhibitor, decreases citrinin-induced cell cycle G2/M arrest and apoptosis. In summary, citrinin induces cell cycle arrest and apoptosis to aggravate liver injury by activating ROS-ER stress-AMPK signaling pathway.

Involvement of endoplasmic reticulum stress-activated PERK-eIF2α-ATF4 signaling pathway in T-2 toxin-induced apoptosis of porcine renal epithelial cells.

T-2 toxin is a highly toxic trichothecene that can induce toxic effects in a variety of organs and tissues, but the pathogenesis of its nephrotoxicity has not been elucidated. In this study, we assessed the involvement of protein kinase RNA-like ER kinase (PERK)-mediated endoplasmic reticulum (ER) stress and apoptosis in PK-15 cells cultured at different concentrations of T-2 toxin. Cell viability, antioxidant capacity, intracellular calcium (Ca2+) content, apoptotic rate, levels of ER stress, and apoptosis-related proteins were studied. T-2 toxin inhibited cell proliferation; increased the apoptosis rate; and was accompanied by increased cleaved caspase-3 expression, altered intracellular oxidative stress marker levels, and intracellular Ca2+ overloading. The ER stress inhibitor 4-phenylbutyrate (4-PBA) and PERK selective inhibitor GSK2606414 prevented the decrease of cell activity and apoptosis caused by T-2 toxin. The altered expression of glucose regulatory protein 78 (GRP78), C/EBP homologous protein (CHOP), and caspase-12 proved that ER stress was involved in cell injury triggered by T-2 toxin. T-2 toxin activated the phosphorylation of PERK and the alpha subunit of eukaryotic initiation factor 2 (eIF2α) and upregulated the activating transcription factor 4 (ATF4), thereby triggering ER stress via the GRP78/PERK/CHOP signaling pathway. This study provides a new perspective for understanding the nephrotoxicity of T-2 toxin.

Betulinic acid attenuates cyclophosphamide-induced intestinal mucosa injury by inhibiting the NF-κB/MAPK signalling pathways and activating the Nrf2 signalling pathway.

Betulinic acid (BA), a pentacyclic triterpenoid, has been associated with several biological effects, such as antioxidant, anti-inflammatory and antiviral activities. Previous studies have demonstrated that BA has the ability to alleviate intestinal mucosal damage, however, the potential mechanism associated with the effect has not been reported. This study aimed to investigate the possible protective mechanism of BA against cyclophosphamide (CYP)-induced intestinal mucosal damage. Here, we found that BA pretreatment prevented intestinal mucosal barrier dysfuction from CYP-challenged mice by repairing the intestinal physical, chemical, and immune barriers. Moreover, BA treatment suppressed the CYP-induced oxidative stress by activating the nuclear factor erythroid 2 [NF-E2]-related factor (Nrf2) pathway blocked reactive oxygen species (ROS) accumulation. In addition, BA inhibited CYP-triggered intestinal inflammation through down-regulating the nuclear transcription factor kappa B (NF-κB)/mitogen-activating protein kinase (MAPK) pathways. Furthermore, BA pretreatment reduced intestinal apoptosis by blocking ROS-activated mitochondrial apoptotic pathway. Overall, the current study demonstrated the protective effect of BA against CYP-caused intestinal mucosal damage by regulating the Nrf2 and NF-κB/MAPK signalling pathways, which may provide new therapeutic targets to attenuate intestinal impairment and maintain intestinal health.

Ganoderma lucidum Polysaccharides Prevent Palmitic Acid-Evoked Apoptosis and Autophagy in Intestinal Porcine Epithelial Cell Line via Restoration of Mitochondrial Function and Regulation of MAPK and AMPK/Akt/mTOR Signaling Pathway.

Ganoderma lucidum polysaccharide (GLP) extracted from Ganoderma lucidum (Leyss. ex Fr.) Karst, a traditional Chinese medicine, is a biologically active substance reported to possess anti-oxidative, anti-apoptotic, and neurological protection. However, it is unknown whether GLP have any protective effect against high-fat constituents-induced epithelial cell injury. The aim of this study was to investigate the protection and molecular mechanism of GLP on injury induced by palmitic acid (PA) in the intestinal porcine epithelial cell line (IPEC-J2). First, we tested whether the treatment of GLP attenuate PA-induced IPEC-J2 cell death. GLP markedly blocked PA-caused cytotoxicity and apoptosis in IPEC-J2 cells. Moreover, GLP recovered the decreased mitochondrial function and inhibited activation of caspase-dependent apoptotic pathway. Interestingly, PA promoted cell apoptosis and autophagy through stimulation of phosphorylation of mitogen-activated protein kinases (MAPKs), AMP-activated protein kinase (AMPK), and inhibition of phosphorylation of Akt and mammalian target of rapamycin (mTOR), which was reversed by GLP. Taken together, this study revealed a protective effect of GLP against PA-evoked IPEC-J2 cell death through anti-apoptotic and anti-autophagic properties.

Protective Effect of Koumine, an Alkaloid from Gelsemium Sempervirens, on Injury Induced by H2O2 in IPEC-J2 Cells.

Medicinal herbal plants have been commonly used for intervention in different diseases and improvement of health worldwide. Koumine, an alkaloid monomer found abundantly in Gelsemium plants, can be effectively used as an antioxidant. The purpose of this study was to evaluate the potential protective effect of koumine against hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in porcine intestinal epithelial cell line (IPEC-J2 cells). MTT assays showed that koumine significantly increased cell viability in H2O2-mediated IPEC-J2 cells. Preincubation with koumine ameliorated H2O2-medicated apoptosis by decreasing reactive oxygen species (ROS) production, and efficiently suppressed the lactate dehydrogenase (LDH) release and malondialdehyde (MDA) production. Moreover, a loss of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) activities was restored to normal level in H2O2-induced IPEC-J2 cells upon koumine exposure. Furthermore, pretreatment with koumine suppressed H2O2-mediated loss of mitochondrial membrane potential, caspase-9 and caspase-3 activation, decrease of Bcl-2 expression and elevation of Bax expressions. Collectively, the results of this study indicated that koumine possesses the cytoprotective effects in IPEC-J2 cells during exposure to H2O2 by suppressing production of ROS, inhibiting the caspase-3 activity and influencing the expression of Bax and Bcl-2. Koumine could potentially serve as a protective effect against H2O2-induced apoptosis.

T-2 Toxin Exposure Induces Apoptosis in TM3 Cells by Inhibiting Mammalian Target of Rapamycin/Serine/Threonine Protein Kinase(mTORC2/AKT) to Promote Ca2+Production.

Although mTOR (the mammalian target of rapamycin) can regulate intracellular free Ca2+concentration in normal cultured podocytes, it remains elusive as to how mTORC2/AKT-mediated Ca2+participates in the process of T-2 toxin-induced apoptosis. The potential signaling responsible for intracellular Ca2+ concentration changes was investigated using immunoblot assays in an in vitro model of TM3 cell injury induced by T-2 toxin. Changes in Ca2+ were assessed using the Ca2+-sensitive fluorescent indictor dye Fura 2-AM. The cytotoxicity of TM3 cells was assessed with an MTT bioassay, and apoptosis was measured using Annexin V-FITC staining. Following T-2 toxin treatment, the growth of cells, phospho-mTORSer2481, phospho-mTORSer2448, and phospho-AktSer473 were significantly decreased in a time-dependent manner, whereas Ca2+ and apoptosis were increased. T-2 toxin-induced apoptosis was prevented by BAPTA-AM (a Ca2+chelator) and MHY1485 (an mTOR activator), and the application of mTOR activator MHY1485 also prevented the increase of intracellular free Ca2+concentration in TM3 cells. Our results strongly suggest that T-2 toxin exposure induces apoptosis in TM3 cells by inhibiting mTORC2/AKT to promote Ca2+ production.

Koumine Attenuates Lipopolysaccaride-Stimulated Inflammation in RAW264.7 Macrophages, Coincidentally Associated with Inhibition of NF-κB, ERK and p38 Pathways.

Medicinal herbal plants have been commonly used for intervention of different diseases and health enhancement worldwide. Koumine, an alkaloid monomer found abundantly in Gelsemium plants, can be effectively used as an anti-inflammatory medication. In this study, the mechanisms associated with the preventative effect of koumine on lipopolysaccharide (LPS)-mediated inflammation in RAW264.7 macrophages were investigated. Koumine induced a decrease in the level of inducible nitric oxide synthase (iNOS) protein, concomitant reduction in the production of nitric oxide (NO) and reduction of the levels of interleukin (IL)-6, tumor necrosis factor-α (TNF-α) and IL-1ß. Furthermore, koumine decreased the phosphorylation of p65 and inhibited nuclear factor κ Bα (IκBα) proteins, resulting in lower production of nuclear factor (NF)-κB transactivation. Koumine also induced a decrease in the phosphorylation of extracellular-signal-regulated kinases (ERK) and p38 in RAW264 cells. In conclusion, these findings reveal that koumine decreases the productions of pro-inflammatory mediators though the suppression of p38 and ERK MAPK phosphorylation and the inhibition of NF-κB activation in RAW264.7 cells.

A Potential Mechanism for the Anti-Apoptotic Property of Koumine Involving Mitochondrial Pathway in LPS-Mediated RAW 264.7 Macrophages.

Koumine is a kind of alkaloid extracted from Gelsemium elegans (G. elegans). Benth, which has shown promise as an anti-tumor, anxiolytic, and analgesic agent. In our present study, the effect of koumine on lipopolysaccharide (LPS)-mediated RAW 264.7 cell apoptosis was evaluated. MTT assays showed that koumine obviously increased cell viability in LPS-mediated RAW 264.7 macrophages. Preincubation with koumine ameliorated LPS-medicated apoptosis by decreasing reactive oxygen species (ROS) production, which resulted in a significant decrease in the levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS). In addition, koumine-pretreated RAW 264.7 macrophages exhibited reduction of LPS-induced levels of TNF-α, IL-1ß, and IL-6 mRNA. Furthermore, pretreatment with koumine suppressed LPS-mediated p53 activation, loss of mitochondrial membrane potential, caspase-3 activation, decrease of Bcl-2 expression, and elevation of Bax and caspase-3 expressions, suggesting that koumine might act directly on RAW 264.7 cells to inhibit LPS-induced apoptosis. It seems as though the mechanism that koumine possesses is the anti-apoptotic effect mediated by suppressing production of ROS, activation of p53, and mitochondrial apoptotic pathways in RAW 264 cells. Koumine could potentially serve as a protective effect against LPS-induced apoptosis.

Latency-aware Unified Dynamic Networks for Efficient Image Recognition.

Dynamic computation has emerged as a promising strategy to improve the inference efficiency of deep networks. It allows selective activation of various computing units, such as layers or convolution channels, or adaptive allocation of computation to highly informative spatial regions in image features, thus significantly reducing unnecessary computations conditioned on each input sample. However, the practical efficiency of dynamic models does not always correspond to theoretical outcomes. This discrepancy stems from three key challenges: 1) The absence of a unified formulation for various dynamic inference paradigms, owing to the fragmented research landscape; 2) The undue emphasis on algorithm design while neglecting scheduling strategies, which are critical for optimizing computational performance and resource utilization in CUDA-enabled GPU settings; and 3) The cumbersome process of evaluating practical latency, as most existing libraries are tailored for static operators. To address these issues, we introduce Latency-Aware Unified Dynamic Networks (LAUDNet), a comprehensive framework that amalgamates three cornerstone dynamic paradigms-spatially-adaptive computation, dynamic layer skipping, and dynamic channel skipping-under a unified formulation. To reconcile theoretical and practical efficiency, LAUDNet integrates algorithmic design with scheduling optimization, assisted by a latency predictor that accurately and efficiently gauges the inference latency of dynamic operators. This latency predictor harmonizes considerations of algorithms, scheduling strategies, and hardware attributes. We empirically validate various dynamic paradigms within the LAUDNet framework across a range of vision tasks, including image classification, object detection, and instance segmentation. Our experiments confirm that LAUDNet effectively narrows the gap between theoretical and real-world efficiency. For example, LAUDNet can reduce the practical latency of its static counterpart, ResNet-101, by over 50% on hardware platforms such as V100, RTX3090, and TX2 GPUs. Furthermore, LAUDNet surpasses competing methods in the trade-off between accuracy and efficiency. Code is available at: https://www.github.com/LeapLabTHU/LAUDNet.

Viola yedoensis Makino alleviates heat stress-induced inflammation, oxidative stress, and cell apoptosis in the spleen and thymus of broilers.

ETHNOPHARMACOLOGICAL RELEVANCE: Viola yedoensis Makino (VYM) is a traditional Chinese herbal medicine widely distributed in China. It has many pharmacological effects such as anti-inflammatory, immune regulation and anti-oxidation. However, the protective effect of VYM on the spleen and thymus of broilers induced by heat stress has rarely been reported. AIM OF THE STUDY: We established a heat stress model of broilers to explore the protective effect of VYM on spleen and thymus of broilers. MATERIALS AND METHODS: In this experiment, a heat stress model was made by adjusting the feeding temperature of broilers. The protective effect of VYM on the spleen and thymus of heat-stressed broilers were evaluated by detecting immune organ coefficient, histological observation, Enzyme-Linked Immunosorbent Assay, production of antioxidant enzymes and peroxides, TUNEL Staining, Quantitative Real-time PCR. RESULTS: In this study, 60 healthy male AA broilers were divided into 6 groups: Control, 4.5% VYM, HS, HS + 0.5% VYM, HS + 1.5% VYM, HS + 4.5% VYM. After 42 days of feeding, serum, spleen and thymus were collected for detection and analysis. The study revealed that heat stress can lead to pathological damage in the spleen and thymus of broilers, reduce the content of immunoglobulin and newcastle disease (ND), infectious bursal disease (IBD) antibody levels, increase the expression of inflammatory factors IL-1ß, INF-γ, heat shock 70 kDa protein (HSP70), heat shock 90 kDa protein (HSP90). Heat stress inhibits the activity of antioxidant enzymes CAT and SOD, promotes the production of MDA, and then lead to oxidative damage of the spleen and thymus. In addition, apoptotic cells and the ratio of Bax/Bcl-2 was increased. However, the addition of VYM to the feed can alleviate the adverse effects of heat stress on the spleen and thymus of broilers. CONCLUSIONS: This study showed that the addition of VYM to the diet could inhibit oxidative stress and apoptosis, and reduce the inflammatory damage of heat stress on the spleen and thymus of broilers. This study provides a basis for further exploring the regulatory role of VYM in heat stress-induced immune imbalance in broilers. In addition, this study also provides a theoretical basis for the development of VYM as a feed additive with immunomodulatory effects.

Koumine inhibits IL-1ß-induced chondrocyte inflammation and ameliorates extracellular matrix degradation in osteoarthritic cartilage through activation of PINK1/Parkin-mediated mitochondrial autophagy.

Osteoarthritis (OA) is a degenerative joint disease, Increasingly, mitochondrial autophagy has been found to play an important regulatory role in the prevention and treatment of osteoarthritis. Koumine is a bioactive alkaloid extracted from the plant Gelsemium elegans. In previous research, Koumine was found to have potential in improving the progression of OA in rats. However, the specific mechanism of its action has not been fully explained. Therefore, the aim of this study was to investigate whether Koumine can alleviate OA in rats by influencing mitochondrial autophagy. In the in vitro study, rat chondrocytes (RCCS-1) were induced with IL-1ß (10 ng/mL) to induce inflammation, and Koumine (50 µg/mL) was co-treated. In the in vivo study, a rat OA model was established by intra-articular injection of 2% papain, and Koumine was administered orally (1 mg/kg, once daily for two weeks). It was found that Koumine effectively reduced cartilage erosion in rats with osteoarthritis. Additionally, it decreased the levels of inflammatory factors such as IL-1ß, IL-6, and extracellular matrix (ECM) components MMP13 and ADAMTS5 in chondrocytes and articular cartilage tissue, while increasing the level of Collagen II.Koumine inhibited the production of reactive oxygen species (ROS) in cartilage tissue and increased the number of autophagosomes in chondrocytes and articular cartilage tissue. Additionally, it upregulated the expression of mitochondrial autophagy proteins LC3Ⅱ/Ⅰ, PINK1, Parkin, and Drp1. The administration of Mdivi-1 (50 µM) reversed the enhanced effect of Koumine on mitochondrial autophagy, as well as its anti-inflammatory and anti-ECM degradation effects in rats with OA. These findings suggest that Koumine can alleviate chondrocyte inflammation and improve the progression of OA in rats by activating PINK1/Parkin-mediated mitochondrial autophagy.

Melatonin alleviates T-2 toxin-induced oxidative damage, inflammatory response, and apoptosis in piglet spleen and thymus.

T-2 toxin, an unavoidable contaminant in animal feeds, can induce oxidative stress and damage immune organs. Melatonin (MT), a natural and potent antioxidant, has shown promise as a detoxifier for various mycotoxins. However, the detoxifying effect of MT on T-2 toxin has not been previously reported. In order to investigate the protective effect of MT added to diets on the immune system of T-2 toxin-exposed piglets, twenty piglets weaned at 28d of age were randomly divided into control, T-2 toxin (1 mg/kg), MT (5 mg/kg), and T-2 toxin (1 mg/kg) + MT (5 mg/kg) groups(n = 5 per group). Our results demonstrated that MT mitigated T-2 toxin-induced histoarchitectural alterations in the spleen and thymus, such as hemorrhage, decreased white pulp size in the spleen, and medullary cell sparing in the thymus. Further research revealed that MT promoted the expression of Nrf2 and increased the activities of antioxidant enzymes CAT and SOD, while reducing the production of the lipid peroxidation product MDA. Moreover, MT inhibited the NF-κB signaling pathway, regulated the expression of downstream cytokines IL-1ß, IL-6, TNF-α, and TGF-ß1. MT also suppressed the activation of caspase-3 while down-regulating the ratio of Bax/Bcl-2 to reduce apoptosis. Additionally, MT ameliorated the T-2 toxin-induced disorders of immune cells and immune molecules in the blood. In conclusion, our findings suggest that MT may effectively protect the immune system of piglets against T-2 toxin-induced damage by inhibiting oxidative stress, inflammatory response, and apoptosis in the spleen and thymus. Therefore, MT holds the potential as an antidote for T-2 toxin poisoning.

Urban resilience to socioeconomic disruptions during the COVID-19 pandemic: Evidence from China.

The COVID-19 pandemic and the associated restrictions have raised the awareness of building pandemic-resilient cities. Prior studies often evaluated the resilience of one type of urban system while lacking a comparison across various urban subsystems. This study fills this gap by measuring and comparing the adaptive resilience to the pandemic of various urban subsystems in Chinese cities. We propose a novel outcome measurement of the pandemic's socioeconomic impacts on cities, i.e., the citizens' complaints data, and use its temporal changes to measure cities' adaptive resilience to the pandemic. We find a wide range of urban subsystems were severely shocked by the pandemic, including the urban economy, construction-and-housing sector, welfare system, and education system. Different urban subsystems exhibit divergent degrees of adaptive resilience to the pandemic. Using cluster analysis, we also identify three types of cities with different patterns of adaptive resilience: cities whose general economies were the least resilient, cities whose construction-and-housing system was the least resilient, and cities that were mostly affected by restriction measures. Our findings contribute to the understanding of the pandemic's socioeconomic costs and help identify the divergent resilience of different urban subsystems so as to develop targeted policy interventions to improve cities' resilience to the pandemic.

Identifying the fate of nitrogenous species during sewage sludge pyrolysis via in-situ tracing of protein-sludge inherent components interactions.

The effect of interactions between different components in sewage sludge on the thermochemical transformation of nitrogenous species is usually neglected, which is important to explain the generation mechanism of some key nitrogenous by-products. Here, we investigated the distribution, form, and chemical properties of the products from sludge-extracted protein (PR) under different pyrolysis scenarios using several in-situ probe techniques, to elucidate the critical role of typical sludge organics/inorganics on the evolution of nitrogenous intermediates and by-products. The results suggested that Ca/Fe/Si/Al-containing inorganics significantly affected the pyrolytic behavior of PR and the thermal transformation of nitrogenous species, while sludge organics, including humic acids and polysaccharides, had limited effects on the temperature-dependent evolution of nitrogenous species in PR. Among them, calcium oxide catalyzed the ring-opening reaction of heterocyclic-N with aromatic-like structures, resulting in a 21.1 %-68.8 % reduction in nitrogen fixation efficiency in the char. At lower temperatures (350-450 °C), calcium oxide caused more nitrogen to be transferred to the gas/tar phases in the form of NH3 and heterocyclic-N, and it also enhanced the conversion of nitrile-N → HCN → NO at temperatures above 450 °C. In contrast, polyferric salts inhibited the devolatilization of mono-heterocyclic-N and enhanced the thermal stability of poly-heterocyclic-N, resulting in a maximum increase of 18.5 mg·g-1 of nitrogen content in the char, while reducing the release of NH3 and HCN by 71.1 % and 32.0 %. This work elucidated the interaction between PR and inherent components in sludge, providing key information for the control of nitrogenous volatiles and NOx.