Adipose mesenchymal stem cell-derived exosomes (ADSC-Exo) have demonstrated therapeutic effects in liver diseases and injuries. The Augmenter of Liver Regeneration (ALR), a novel hepatic trophic growth factor, promotes hepatic structural and functional recovery. In this study, we constructed ALR-overexpressing ADSC-Exo (ADSC-ALR-Exo) by harnessing the messaging capacity of ADSC-Exo, and analyzed the effects of ADSC-ALR-Exo on hepatic ischemia-reperfusion injury (IRI) combined with partial hepatectomy in a minipig model. Our results indicated that, compared to the ADSC-Exo group, the ADSC-ALR-Exo group exhibited a significant reduction in reactive oxygen species (ROS) levels, alongside a notable increase in the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Furthermore, there was a marked decrease in malondialdehyde (MDA) content. Concurrently, the concentrations of pro-inflammatory factors in the blood (IL-1β, IL-18, and TNF-α) and liver tissue (IL-1β, IL-18, IL-6, and TNF-α) were significantly lower in the ADSC-ALR-Exo group, while the level of the anti-inflammatory factor IL-10 in the blood was significantly elevated. Additionally, ALR enrichment enhanced the inhibitory effect of ADSC-ALR-Exo on endoplasmic reticulum stress-related pathways, specifically ATF6, IRE1α, and PERK. Compared to ADSC-Exo, the ADSC-ALR-Exo intervention was also more effective in reducing the expression levels of NLRP3, caspase-1, and GSDMD, thereby decreasing the incidence of pyroptosis. In conclusion, ADSC-ALR-Exo mitigated liver injury by inhibiting endoplasmic reticulum stress and cellular pyroptosis induced by liver injury.

This study explored ultrastructural changes and the expression of oxidative stress-related genes and proteins in the laminar tissue of dairy cows with acute laminitis induced by oligofructose (OF) overload. Twelve clinically healthy, non-pregnant Chinese Holstein cows were randomly allocated into two groups: the OF-overload group (n = 6) and the control group (n = 6). 17 g/kg BW of oligofructose (OF) dissolved in 20 mL/kg BW of deionized water was provided to the OF-treated group, while the control group received 20 mL/kg BW of deionized water via a stomach tube. Laminar tissue samples were collected at 72 h post-OF administration. RT-qPCR revealed significantly increased Keap1 mRNA expression (p = 0.0097) and significantly decreased Nrf2 (p < 0.0001), Ho1 (p < 0.0001), and Nqo1 (p = 0.0101) mRNA expression in the OF group compared to the control group. Western blot analysis confirmed corresponding protein-level changes, with significantly increased Keap1 (p = 0.0062) and significantly decreased Nrf2 (p = 0.0008), Ho1 (p = 0.0297), and Nqo1 (p = 0.0004) in the OF group compared with the control group. Immunohistochemical analysis revealed significantly increased cytoplasmic Keap1 distribution (p = 0.0200) and significantly decreased nuclear Nrf2 localization (p = 0.0032) in the OF group than the control group. Ultrastructural examination revealed significant pathological changes in the OF group, including a reduced number of hemidesmosomes (p < 0.01), an increased distance from epidermal basal cells to the lamina densa (p < 0.01), thickened and damaged lamina densa with disorganized collagen fibers, and deformed basal cell nuclei with reduced chromatin relative to the control group. In conclusion, these findings demonstrate that OF-induced acute laminitis is associated with significant dysregulation of the Keap1-Nrf2 antioxidant pathway and severe ultrastructural damage to the dermal-epidermal interface, suggesting that oxidative stress contributes to laminar tissue injury in dairy cows.

IntroductionHepatic ischemia reperfusion injury is an important pathological factor leading to complications after hepatectomy and transplantation. Although cuproptosis has been reported as a new paradigm of programmed death triggered by copper homeostasis imbalance, its regulatory mechanisms and intervention strategies in liver IRI remain to be fully elucidated. The purpose of this study was to reveal the role of cuproptosis in liver IRI, and to elucidate the molecular mechanism by which adipose-derived stem cell exosomes (ADSC-Exos) exert therapeutic effects by regulating copper metabolism.MethodsRat IRI models were established to evaluate copper metabolism dysregulation and cuproptosis activation. Subsequently, miniature pig models underwent laparoscopic IRI induction to assess ADSC-Exos’s effects on copper homeostasis restoration over 7 days post-injury.ResultsWe found that liver IRI disrupts copper homeostasis through a dual pathway: it inhibits membrane transporters CTR1 and ATP7B to affect copper ion excretion, and down-regulates intracellular copper chaperones ATOX1, CCS and COX17 expression, resulting in intracellular copper metabolism disorders. Excessive copper ions will bind to the lipoylated protein DLAT, induce its oligomerization and mitochondrial Fe-S cluster protein depletion, eventually leading to cuproptosis in hepatocytes and aggravating IRI. The intervention of ADSC-Exos can effectively regulate the disorder of copper metabolism in hepatocytes, inhibit the occurrence of cuproptosis, and reduce liver IRI.DiscussionThis study first confirmed the damage mechanism of cuproptosis pathway caused by liver IRI, and revealed the regulatory mechanism of ADSC-Exos to hinder the process of cuproptosis by repairing the copper metabolism pathway of hepatocytes.

The link between neutrophil extracellular traps (NETs) and hepatocyte ferroptosis in liver ischemia–reperfusion injury (LIRI) is unclear. Adipose-derived mesenchymal stem cell exosomes (ADSCs-Exo) hold therapeutic potential for LIRI. This study employed miniature pigs to investigate the NETs’ role and ADSCs-Exo’s protection in LIRI. In vitro, established hepatocyte oxygen-glucose deprivation/reoxygenation (OGD/R) model and Transwell co-culture system with polymorphonuclear neutrophils (PMNs). In vivo, a laparoscopic minimally invasive LIRI model was constructed in miniature pigs, followed by ADSCs-Exo intervention. Results demonstrated that NETs exacerbate OGD/R-induced hepatocyte ferroptosis via myeloperoxidase. ADSCs-Exo inhibited NET formation via the NADPH/MAPK pathway, thereby mitigating ferroptosis, and ultimately improved liver histopathology and function. This study is the first to demonstrate in a large animal model that ADSCs-Exo alleviate LIRI by inhibiting NET formation via the NADPH/MAPK pathway, consequently attenuating hepatocyte ferroptosis. These findings provide novel insights into LIRI pathogenesis, support the translational potential of ADSCs-Exo as a cell-free therapeutic strategy, and highlight the value of the miniature pig model in liver research.

The ketogenic diet (KD), a high-fat, low-carbohydrate dietary regimen widely used for drug-resistant epilepsy and weight management, has been increasingly applied in adolescents. However, its long-term effects on juvenile cardiac development and functional homeostasis remain poorly understood. Here, juvenile mice (postnatal day 28–84) were fed a KD, and the underlying mechanisms were further investigated in β-hydroxybutyrate (OHB)-treated H9C2 cardiomyocytes. KD induced sustained ketosis, reduced body weight gain, and promoted a smaller cardiac phenotype accompanied by progressive alterations in ventricular functional parameters, including decreased LVEF/LVFS, septal thinning, and elevated BNP levels. Histological analyses revealed myocardial disorganization, myofibrillar disruption, mitochondrial abnormalities, and reduced cardiomyocyte area, together with decreased expression of proteins involved in cardiac contraction and calcium handling. Transcriptomic analysis identified Hopx as a key downregulated gene. Mechanistically, OHB exposure was associated with increased Ffar3 expression and reduced Hopx expression, while HOPX was found to interact with ACTC1. Hopx silencing recapitulated the OHB-induced alterations, whereas Hopx overexpression partially alleviated these effects. Collectively, long-term KD/OHB exposure impairs juvenile cardiac development and functional homeostasis through a candidate OHB-Ffar3-Hopx/ACTC1 regulatory pathway, highlighting potential cardiac risks associated with prolonged KD exposure during postnatal development.

Background Depression is one of the psychiatric disorders with the highest global disability rate. Dysfunction of the glutamatergic system is recognized as a core feature of stress-related psychiatric disorders. Previous studies have demonstrated that Higenamine (Hig) significantly ameliorates depressive-like phenotypes in rats. However, the underlying mechanism of its antidepressant effect, particularly whether it mitigates neuronal injury by modulating astrocyte-neuron crosstalk and inhibiting glutamate (Glu) excitotoxicity, remains unclear. Purpose This study aimed to investigate whether Hig exerts antidepressant effects by improving neuronal dysfunction via inhibiting excitotoxicity through the regulation of Glu transport between astrocytes and neurons. Study design The effects of Hig on depressive-like behaviors, Glu transport function and neuronal injury were evaluated in chronic unpredictable mild stress (CUMS) mice. Furthermore, a Glu-induced HT22 excitotoxicity model and a primary astrocyte-HT22 Transwell co-culture system were established for further pharmacodynamic validation and mechanistic exploration. Methods Mice were subjected to CUMS for 28 consecutive days. Hig (20 mg/kg) and fluoxetine (Flx, 10 mg/kg) were administered concurrently during the modeling period. Subsequently, sucrose preference test, open field test and forced swimming test were performed to assess depressive-like phenotypes in mice. Multiple assays were applied for in vitro and in vivo detection, including Western blot, immunofluorescence, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, Nissl staining, CCK-8 assay, viability/cytotoxicity staining and calcium fluorescence probes. Results Hig ameliorated Glu transport dysfunction in astrocytes, and alleviated neuroinflammation, neuronal apoptosis and synaptic impairment in CUMS-exposed mice. Consistently, in vitro, Hig preventedGlu-induced functional impairment in HT22 cells and attenuated excitotoxicity by modulating astrocyte-neuron interactions. Conclusion Hig exerts antidepressant effects by modulating astrocyte-neuron interactions to mitigate neuronal damage induced by Glu excitotoxicity.

Hepatic ischemia reperfusion injury is an important pathological factor leading to complications after hepatectomy and transplantation. Although cuproptosis has been reported as a new paradigm of programmed death triggered by copper homeostasis imbalance, its regulatory mechanism and intervention strategy in liver IRI are still blank. The purpose of this study was to reveal the role of cuproptosis in liver IRI, and to elucidate the molecular mechanism by which adipose-derived stem cell exosomes (ADSCs-Exo) exert therapeutic effects by regulating copper metabolism. Rat IRI models were established to evaluate copper metabolism dysregulation and cuproptosis activation. Subsequently, miniature pig models underwent laparoscopic IRI induction to assess ADSCs-Exo's effects on copper homeostasis restoration over 7 days post-injury. We found that liver IRI disrupts copper homeostasis through a dual pathway: it inhibits membrane transporters CTR1 and ATP7B to affect copper ion excretion, and down-regulates intracellular copper chaperones ATOX1, CCS and COX17 expression, resulting in intracellular copper metabolism disorders. Excessive copper ions will bind to the lipoylated protein DLAT, induce its oligomerization and mitochondrial Fe-S cluster protein depletion, eventually leading to copper death in hepatocytes and aggravating IRI. The intervention of ADSCs-Exo can effectively regulate the disorder of copper metabolism in hepatocytes, inhibit the occurrence of cuproptosis, and reduce liver IRI. This study first confirmed the damage mechanism of cuproptosis pathway caused by liver IRI, and revealed the regulatory mechanism of ADSCs-Exo to hinder the process of cuproptosis by repairing the copper metabolism pathway of hepatocytes.

Cattle diseases severely threaten the global agricultural economy. Traditional disease management, heavily reliant on manual observation, is inherently delayed and subjective. Artificial intelligence (AI) is driving a profound paradigm shift in veterinary diagnostics. By enabling proactive and scalable health monitoring, AI effectively mitigates the economic losses associated with delayed interventions. However, existing reviews primarily focus on individual diseases or specific scenarios, lacking a systematic analysis of cross-disease applications and technological evolution. Consequently, this paper provides a comprehensive review of AI applications in cattle disease diagnosis, with a focus on technological evolution, key challenges, and future directions. A systematic search across four databases (Web of Science, PubMed, Scopus, and EBSCOhost) yielded 316 studies for bibliometric and thematic analysis. Grounded in pathophysiological systems and veterinary clinical practice, the literature is systematically categorized into six core domains: locomotor and superficial anomalies, reproductive and lactation diseases, metabolic and digestive disorders, respiratory conditions, infectious disease prevention, and non-specific health monitoring. The analysis reveals a clear methodological transition from early contact-based sensing and traditional machine learning to non-contact techniques centered on computer vision and deep learning, with current advances toward multimodal data fusion. Vision-based methods are primarily applied to diseases with clear phenotypic traits, whereas multimodal approaches integrating physiological, behavioral, and environmental data demonstrate superior performance in identifying complex and subclinical conditions. Despite these advancements, real-world applications remain constrained by high data heterogeneity, insufficient standardization, multimodal alignment challenges, limited model interpretability, and high deployment costs. Furthermore, practical deployment is also constrained by ethical considerations and environmental complexity. In summary, AI provides valuable technical tools for the early identification, risk assessment, and intervention of cattle diseases. Future research should prioritize multimodal fusion and cloud-edge-device collaborative architectures, while improving deployment efficiency in complex environments through hierarchical computing, real-time decision-making, and advances in explainable AI.

Foot-and-Mouth Disease is a highly contagious transboundary animal disease. FMD has caused a significant economic impact globally due to direct losses and trade restrictions on animals and animal products. This study utilized multi-distance spatial cluster analysis, kernel density analysis, directional distribution analysis to investigate the spatial distribution patterns of historical FMD epidemics. A multi-algorithm ensemble model considering climatic, geographic, and social factors was developed to predict the suitability area for FMDV, and then risk maps of FMD for each species of livestock were generated in combination with the distribution of livestock. The results show that all serotypes of FMD exhibit significant clustering with a clear tendency toward a directional distribution. Serotypes A and O are widespread in Asia, Europe, Africa, and South America. Serotype Asia 1 is prevalent in Asia. Serotype SAT2 is prevalent in Africa and the Middle East, while Serotypes SAT1 and SAT3 are restricted to Africa. Ecological niche modeling reveals temperature, precipitation, wind speed, and vegetation are important factors influencing the occurrence of FMD. Except for buffaloes, the distribution of high-risk areas for FMD occurrence in other livestock species is quite widespread. The areas primarily include the southern region of North America, the northern, southern, and eastern regions of South America, the Mediterranean region, the eastern region of Europe, the central and southern regions of Africa, the central, eastern, and southern regions of Asia, and parts of Australia. These findings will provide valuable insights into the prevention and control of FMD.

Dairy cow laminitis leads to massive financial losses and animal health issues in the worldwide dairy sector. Apoptosis may be an important factor in the epidermal attachment failure. This study explored the laminar tissue apoptotic-related gene and protein status with oligofructose (OF)-induced laminitis in dairy cows. Twelve clinically healthy, non-pregnant Chinese Holstein cows were randomly divided into two groups of six cows each: the control group and the oligofructose overload group (OF group), respectively. At 0 h, 17 g/kg BW of OF dissolved in 20 mL/kg BW of warm deionized water was gavaged to the OF dairy cows through a stomach tube, while the control cows were given the same dose of deionized water in the same way. After 72 h, laminar tissue samples in both groups were collected to express genes and proteins. Compared with the control cows, the gene expression of Bcl2 significantly reduced in the OF cows laminar tissue. The gene expression of Bax and P53 significantly enhanced in the laminar tissue of OF cows compared to the control cows. The expression of Bcl2 protein significantly decreased, whereas the expression of Bax and Bif1, caspase3, caspase8, and caspase9/9p proteins significantly increased in the OF cows' laminar tissues than in the control cows. However, the distribution of Bax and P53 proteins significantly enhanced in the OF cows' laminar tissues relative to the control cows. In conclusion, imbalanced gene and protein status may represent the primary cause of the epidermal attachment failure, which confirmed the increased apoptosis in laminar tissue of sick cows.

Exosomes are rich in bioactive molecules. Their unique lipid bilayer structure gives them the advantages of protecting the contents from degradation, easy cellular uptake, and good passive targeting. MSC-derived exosomes, which are natural vesicles ideal for gene delivery, exhibit a broad spectrum of therapeutic benefits. In this study, which combines cell-free therapy with gene therapy, adipose mesenchymal stem cells (ADSCs) were genetically modified with augmenter of liver regeneration (ALR) to derive exosomes overexpressing ALR, which were used as therapeutic agents in a miniature porcine model of laparoscopic hepatic ischemia‒reperfusion injury (IRI) combined with partial hepatectomy injury. The findings of this study demonstrated that ALR-overexpressing adipose mesenchymal stem cell-derived exosomes (ADSC-Exo) ameliorate hepatic tissue injury, reduce apoptosis, promote hepatic regeneration, and protect the integrity of the cellular mitochondrial structure and function. In conclusion, ALR gene-modified ADSC-Exo strongly attenuate liver injury and promote liver tissue repair.

Extensive research has been conducted on mesenchymal stem cells (MSCs) regarding their ability to modify the immune response and reduce tissue damage. Many researchers have found that the regulatory capacity of MSCs primarily comes from their secretome. As a result, there has been much interest in utilizing “cell-free” therapies as alternatives to stem cell treatments. In this study, the secretome from adipose mesenchymal stem cells (ADSC-secretome) was extracted and injected into minipigs with established liver injury models. Blood and liver tissue samples were obtained prior to the procedure, as well as on days 1, 3, and 7 after surgery. It was found that ADSC-secretome effectively suppressed the synthesis of the NOD-like receptor protein 3 (NLRP3) inflammasome, leading to a downregulation of gasdermin-D (GSDMD) expression, and demonstrated a more prominent anti-pyroptosis effect compared to ADSCs. Furthermore, ADSC-secretome inhibited the high mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) inflammatory pathway. In summary, both ADSC-secretome and ADSCs inhibited pyroptosis in right hemihepatic ischemia–reperfusion combined with left hemihepatectomy injury, and ADSC-secretome exhibited a stronger therapeutic effect. ADSC-secretome exerted these therapeutic effects through the inhibition of the HMGB1/TLR4/NF-κB inflammatory pathway. In the future, “cell-free” therapy is expected to replace cell-based methods.

The skin functions as the body’s primary defense barrier; when compromised, it can lead to dehydration, infection, shock, or potentially life-threatening conditions. Miniature pigs exhibit skin characteristics and healing processes highly analogous to humans. Mesenchymal stem cells contribute to skin injury repair through a paracrine mechanism involving exosomes. This research examines whether adipose-derived MSC exosomes effectively enhance healing following autologous skin grafting in miniature pigs. It also compares the roles and distinctions of ADSCs and ADSC-Exos in inflammatory responses and tissue regeneration. This study found significantly reduced levels of oxidative stress products and pro-inflammatory factors, while antioxidant factors, anti-inflammatory factors, and pro-regenerative factors were elevated, and anti-regenerative factor levels decreased. Moreover, the expression levels of key markers—namely, PI3K, Akt, and mTOR—in the regeneration-associated signaling pathway were increased. The alterations in these indicators indicate that ADSC-Exos can regulate inflammatory responses and promote regeneration. This study provides a novel theoretical foundation for the implementation of acellular therapy in clinical settings.

Metformin(Met) and adipose-derived stem cell exosomes(ADSCs-Exo) both demonstrate therapeutic effects on mitochondrial dysfunction and pyroptosis. There is also a phenomenon of mutual promotion between these two pathological states. The synergistic effect of metformin-loaded exosomes (Met-Exo) via electroporation in a miniature pig liver ischemia-reperfusion injury (IRI) model remains unexplored. This study established a liver IRI model in miniature pigs to compare the effects of ADSCs-Exo and Met-Exo. We found that Met-Exo intervention better activated the Adenosine 5'-monophosphate activated protein kinase (AMPK)/NAD-dependent deacetylase sirtuin-1(SIRT1) axis, improved mitochondrial dynamics, promoted mitochondrial biogenesis, and inhibited the sustained excessive autophagy of mitochondria after liver IRI. It was then demonstrated that by improving mitochondrial dysfunction, ATP production in liver tissue could be ensured, and ROS generation could be suppressed. This also further inhibited the occurrence of pyroptosis and ensured that mitochondria were protected from gasdermin D-N(GSDMD-N) attack. Met-Exo inhibited the occurrence of pyroptosis through the above pathways, reducing the release of inflammatory factors such as IL-1β and IL-18, and alleviating inflammation. This provides a new therapeutic approach for clinical treatment of liver IRI and improving the success rate of liver transplantation.

OBJECTIVES:This study aimed to investigate the protective effect and mechanism of carvacrol hydrogel on the alveolar bone in rats with periodontitis. METHODS:A thermosensitive hydrogel supported by carvacrol was prepared using poloxamer and hydroxypropyl methyl cellulose as matrix. SD rats were randomly divided into blank group, periodontitis group, blank hydrogel group, and low-, medium-, and high-dose hydrogel groups. The periodontitis symptoms and the CT structure of the alveolar bone were observed. The changes in liver, spleen, kidney, and periodontal tissues were observed. The related indexes of bone metabolism in serum were detected. The expression of osteoprotegerin (OPG) and nuclear transcription factor-κB (NF-κB) pathway proteins was determined by Western blot. The levels of inflammatory factors were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). RESULTS:Carvacrol hydrogel had good slow release, biocompatibility, and cell adhesion. The periodontitis of rats in the carvacrol hydrogel group was significantly alleviated, the expression of OPG protein in gingival tissue was significantly increased (P<0.01), and the levels of receptor activator of NF-κB ligand (RANKL), receptor activator of NF-κB (RANK), NF-κB protein, and inflammatory factors were significantly decreased (P<0.01). CONCLUSIONS:Carvacrol hydrogel can regulate the OPG and NF-κB pathways, reduce alveolar bone absorption, and improve periodontal inflammation.

Against the backdrop of a global malaria epidemic that remains severe, China has eradicated indigenous malaria but still has to be alert to the risk of external importation. Understanding the distribution of vectors can provide an adequate and reliable basis for the development and implementation of vector control strategies. However, with the decline of malaria prevalence in recent years, the capacity of vector monitoring and identification has been greatly weakened. Here we have used new sampling records, climatic data, and topographic data to establish ecological niche models of the three main malaria vectors in China. The model results accurately identified the current habitat suitability areas for the three species of Anopheles and revealed that in addition to precipitation and temperature as important variables affecting the distribution of Anopheles mosquitoes, topographic variables also influenced the distribution of Anopheles mosquitoes. Anopheles sinensis is the most widespread malaria vector in China, with a wide region from the northeast (Heilongjiang Province) to the southwest (Yunnan Province) suitable for its survival. Suitable habitat areas for Anopheles lesteri are concentrated in the central, eastern, and southern regions of China. The suitable habitat areas of Anopheles minimus are the smallest and are only distributed in the border provinces of southern China. On this basis, we further assessed the seasonal variation in habitat suitability areas for these three major malaria vectors in China. The results of this study provide new and more detailed evidence for vector monitoring. In this new era of imported malaria prevention in China, regular reassessment of the risk of vector transmission is recommended.

Hepatic ischemia/reperfusion injury (IRI) is an important factor affecting liver regeneration and functional recovery postoperatively. Many studies have suggested that mesenchymal stem cells (MSCs) contribute to hepatic tissue repair and functional recovery through paracrine mechanisms mediated by exosomes. Minipigs exhibit much more similar characteristics of the liver to those of humans than rodents. This study aimed to explore whether exosomes from adipose-derived MSCs (ADSCs-exo) could actively promote liver regeneration after hepatectomy combined with HIRI in minipigs and the role they play in the cell proliferation process. This study also compared the effects and differences in the role of ADSCs and ADSCs-exo in the inflammatory response and liver regeneration. The results showed that ADSCs-exo suppressed histopathological changes and reduced inflammatory infiltration in the liver; significantly decreased levels of ALT, TBIL, HA, and the pro-inflammatory cytokines TNF-α, IL-6, and CRP; increased levels of the anti-inflammatory cytokine IL-10 and the pro-regeneration factors Ki67, PCNA, CyclinD1, HGF, STAT3, VEGF, ANG1, ANG2; and decreased levels of the anti-regeneration factors SOCS3 and TGF-β. These indicators above showed similar changes with the ADSCs intervention group. Indicating that ADSCs-exo can exert the same role as ADSCs in regulating inflammatory responses and promoting liver regeneration. Our findings provide experimental evidence for the possibility that ADSCs-exo could be considered a safe and effective cell-free therapy to promote regeneration of injured livers.

Equine Infectious Anemia (EIA) is a vector-borne persistent viral infection in equine animals. The EIA is characterized by recurrent fever, thrombocytopenia, depression, anemia, rapid weight loss, and lower body edema. Control of EIA is achieved through the elimination or isolation of infected animals, resulting in significant economic losses. In recent years, many countries in Europe have experienced outbreaks of EIA, which could potentially develop into a new wave of epidemic and pose a significant threat to the healthy development of the equine industry. This study utilized spatiotemporal analysis techniques and ecological niche modeling to investigate the spatiotemporal distribution characteristics of historical EIA outbreaks and predict risk areas for EIA occurrence in Europe. Spatiotemporal analysis results indicate that from 2005 to 2023, the EIA outbreaks in Europe exhibit five significant spatiotemporal clusters, with hotspots concentrated in southeastern France and northwestern Italy. Ecological niche modeling reveals that western, central, and southern Europe are high-risk areas for EIA outbreaks. Annual mean temperature, annual precipitation, and horse density are important variables that influence the occurrence of EIA. The results of this study can provide decision-makers with valuable insights, helping with EIA monitoring and resource allocation.

Phosphatidylcholine (PC) has garnered considerable attention due to its involvement in a wide array of crucial biological functions. However, there is still much to active explore regarding the precise mechanisms that underlie PC's actions in the context of high-fat diet. In this study, we found that both PC intervention and treatment significantly mitigated lipid accumulation, liver damage, and body weight gaining triggered by the high-fat diet. Untargeted and targeted metabolomic analyses uncovered substantial effects of PC on bile acid metabolism, especially led to a substantial reduction in elevated levels of free bile acids. 16S rRNA gene sequencing revealed that PC modulated the gut microbiota structures and compositions in high-fat diet mice, particularly exhibiting a positive association with Pseudoflavonifractor abundance, and a negative correlation with Olsenella, Parasutterella, and Allobaculum abundance. Our study suggested that PC held promise as a potential candidate for alleviating lipid metabolism injury, liver disease or obesity.

The purpose of this study was to analyze the characteristics of occurrence and spread of highly pathogenic avian influenza H5N1 (HPAI-H5N1) globally, understand its spatiotemporal characteristics, investigate the risk factors influencing outbreaks, and identify high-risk areas for disease occurrence. We collected the data on global poultry HPAI-H5N1 outbreaks from January 2005 to April 2023, and conducted a thorough analysis of the spatial and temporal characteristics of the disease through time series decomposition and directional distribution analysis. Additionally, an ecological niche model was established to explore the major factors influencing the occurrence of HPAI-H5N1 and to pinpoint high-risk areas. Our findings revealed that HPAI-H5N1 outbreaks were cyclical, and seasonal, exhibiting a rising trend, with a predominant northwest-southeast transmission direction. The ecological niche model highlighted that species factors and economic trade factors are critical in influencing the outbreak of HPAI-H5N1. Variables such as chicken and duck density, population density, isothermality, and road density, contributed to importantly risk of outbreaks. High-risk areas for HPAI-H5N1 occurrence were primarily identified in Europe, West Africa, Southeast Asia, and Southeast China. This study provided valuable insights into the spatial and temporal distribution characteristics and risk factors of global poultry HPAI-H5N1 outbreaks. The identification of high-risk areas provides essential information that can be used to develop more effective prevention and control policies.