Supercritical CO2 extrusion foaming of highly open-cell poly(lactic acid) foam with superior oil adsorption performance.

Addressing marine oil spills and industrial water pollution necessitates the development of eco-efficient oil-absorbing materials. With increasing concern for the environment, there is a consensus to decrease the use of petroleum-based polymers. Herein, lightweight poly(lactic acid) (PLA) blend foams with varying thermoplastic polyurethane (TPU) content were fabricated via a solvent-free, eco-friendly supercritical carbon dioxide (scCO2) extrusion foaming technology. The incorporation of TPU significantly enhanced the crystallization rate of PLA, with the semi-crystallization time of PT30 and PT50 blends at 105 °C exhibiting a reduction of 77.2 % and 47.9 %, respectively, compared to neat PLA. The resulting foams exhibited an open-cell structure with excellent selective oil adsorption capabilities. Notably, the PT30 foam achieved a remarkable maximum expansion ratio of 36.0, while the PT50 foam attained the highest open-cell content of 96.2 %. The PT50 foam demonstrated an outstanding adsorption capacity, spanning from 4.7 to 18.8 g/g for diverse oils and solvents, with rapid adsorption kinetics, reaching 94.9 % of the equilibrium adsorption capacity for CCl4 within just 1 min. Furthermore, the PT50 foam retained 95.2 % of its adsorption capacity for CCl4 over 10 adsorption-desorption cycles. This study presents a scalable and sustainable approach for large-scale production of high-performance, bio-based foams, facilitating efficient oil-water separation.

[3-Deazaadenosine (3-DAA) accelerates Japanese encephalitis virus replication and down-regulates levels of inflammatory factors in mouse and hamster cells].

Objective To investigate the effect of 3-deazaadenosine (3-DAA), an N6-methyladenosine (m6A) methylation modification inhibitor, on the replication of the Japanese encephalitis virus (JEV). Methods Neuro2a mouse neuroblastoma cells, N9 mouse microglial cells, and BHK baby hamster kidney cells were exposed to JEV and then treated with 3-DAA. JEV was also injected into the footpad of adult C57BL/6 mice, which were then administered 3-DAA intraperitoneally. Real-time quantitative PCR was utilized to measure mRNA expression levels of JEV, interleukin 1ß (IL-1ß), IL-6, tumor necrosis factor α (TNF-α), monocyte chemoattractant protein 1 (MCP-1), inducible nitric oxide synthase (iNOS), arginase 1 (Arg1), interferon (IFN)-α, IFN-ß, IFN-γ, and C-X-C motif chemokine ligand 10 (CXCL10) in the cells and mouse brain tissues. Western blot analysis was used to detect JEV protein expression in the cells and mouse brain tissues. Furthermore, the survival of the mice was monitored and pathological changes in mouse brains were observed via hematoxylin and eosin (HE) staining. Results 3-DAA had a dose-dependent effect on the replication of RNA and protein expression of JEV in both BHK, N9, Neuro 2α cells and mouse brain tissues, which resulted in rapid progression of JEV infection in mice and a decrease in their survival rate. Furthermore, 3-DAA suppressed the expression of inflammatory factors such as IL-6, TNF-α, CXCL10, IL-1ß and iNOS, thus weakening the immune response. Conclusion 3-DAA promotes JEV infection and hastens death of infected cells and mice, indicating that m6A modification may negatively regulate JEV replication.

N6-methyladenosine modification positively regulate Japanese encephalitis virus replication.

N6-methyladenosine (m6A) is present in diverse viral RNA and plays important regulatory roles in virus replication and host antiviral innate immunity. However, the role of m6A in regulating JEV replication has not been investigated. Here, we show that the JEV genome contains m6A modification upon infection of mouse neuroblast cells (neuro2a). JEV infection results in a decrease in the expression of m6A writer METTL3 in mouse brain tissue. METTL3 knockdown by siRNA leads to a substantial decrease in JEV replication and the production of progeny viruses at 48 hpi. Mechanically, JEV triggered a considerable increase in the innate immune response of METTL3 knockdown neuro2a cells compared to the control cells. Our study has revealed the distinctive m6A signatures of both the virus and host in neuro2a cells infected with JEV, illustrating the positive role of m6A modification in JEV infection. Our study further enhances understanding of the role of m6A modification in Flaviviridae viruses.

Overall Description and Predictors of Disruptive Behavior Toward Nurses in the Perioperative Arena.

PURPOSE: To investigate the prevalence, characteristics, causes, consequences, and predictors of and responses to disruptive behavior toward nurses in the perioperative arena. DESIGN: A cross-sectional design using a network questionnaire platform. METHODS: Nurses in the perioperative arena were recruited online in March 2020. Data on disruptive behavior toward nurses in the past 6 months and nurses' sociodemographic and environmental factors were collected. FINDINGS: Nurses (N = 496) responded validly to the survey. In total, 82.1% of participants experienced disruptive behavior. Assignment of overwhelming workloads and verbal aggression were the most common behaviors, and surgeons were the major perpetrators. Perpetrators' intrapersonal issues were the most commonly perceived causes. A positive strategy was the most common strategy adopted by participants. Further, 80.8% of participants recounted their negative experiences, and more than half of respondents (59.9%) talked with their nursing colleagues. Nearly half of respondents (45.9%) did not report disruptive behavior. Negative emotions as an immediate effect were reported by 53.1% of the participants, and the most common long-term impact was decreased passion for work. Middle age, job position, practice environment, and system help were risk factors for experiencing disruptive behavior. CONCLUSIONS: The prevalence of disruptive behavior toward nurses in the perioperative arena is high, and its ramifications should not be ignored. Health care institutions should urgently implement intervention strategies to reduce disruptive behavior toward nurses.

Biodegradable nanofibrillated microcellular PBS/PLA foams for selective oil absorption.

To address the challenges posed by spilled oil and oily wastewater, the development of clean oil-adsorption materials is crucial. However, traditional oil-adsorption materials suffer from the issue of secondary pollution. Herein, fully biodegradable nanofibrillated poly(butylene succinate)/poly(lactic acid) (PBS/PLA) foams with outstanding selective oil-adsorption performance were successfully fabricated via an eco-friendly supercritical CO2 foaming technology. The PBS/PLA composites, featuring nanofibrils with a diameter of approximately 100 nm, were prepared through a hot-stretching method subsequent to extrusion. Substantial improvements were observed in the crystallization rate and rheological properties of the fibrillated PBS/PLA composites. Furthermore, PLA nanofibrils enhanced foamability of the composite, achieving an impressive expansion ratio of up to 38.0, resulting in an outstanding oil-absorption performance (19.2-50.4 g/g) of the F-1 %-95 foam. Additionally, 20 adsorption-desorption cycles illustrated the prepared F-1 %-95 foam displayed recyclable oil-absorption characteristics. This work provides an eco-friendly strategy for preparing fully biodegradable foams intended for application as oil-adsorption materials.

Development of Eco-Friendly and High-Strength Foam Sensors Based on Segregated Elastomer Composites with a Large Work Range and High Sensitivity.

Achieving a high-strength piezoresistive foam with high sensitivity and a large workable range remains a major challenge. To realize these goals, we developed a facile, novel, and eco-friendly strategy for constructing segregated microcellular structures fabricated using coating, heat compression molding, and supercritical CO2 (ScCO2) foaming. The segregated poly(ether block amide) (PEBA)/carbon nanostructure (CNS) composites were fabricated via compression molding. This effectively improved the foamability and cell morphology of PEBA/CNS composites. Moreover, compared with the randomly distributed structure, the segregated structure also endowed the foams with better conductivity and sensing capability. Subsequently, the ScCO2 foaming was employed to fabricate segregated PEBA/CNS composite foams. The foaming gave composites a large compressibility and reduced their percolation threshold. Under 1 wt % CNS loading, via tuning the expansion ratio of foam from ∼2.1 to 4.1, the compression stress at 50% compression strain of foam varied from ∼3.3 to 0.5 MPa, and the conductivity changed from 4.89 × 10-3 to 1.93 × 10-6 s/m, implying a tunable conductivity. Additionally, the adjustable conductivity enabled the sensitivity of segregated composite foams to be regulated. The segregated PEBA/CNS foam (FCNS1-4.1) exhibited a good combination of high sensitivity (GF = 3.5), large work range (80% strain), and high compression strength (∼0.5 MPa at 50% strain) as well as a stable, reproducible, and durable sensing response under a low CNS content (∼0.11 vol %). Furthermore, the ΔI/I0 of FCNS1-4.1 (75.6% porosity) reached a high value of ∼810 and exhibited an ultrahigh sensitivity of ∼3706 (ΔI/I0ε) from 60 to 80% strain. Moreover, the foam sensor could be used as a sensing function sole for monitoring diverse human motions. Therefore, the segregated PEBA/CNS composite foams with outstanding piezoresistive performances show promising potential applications in monitoring human motions as wearable electronics and provides a new design strategy for a new generation of foam sensors with high performance.

Healthcare professionals' and patients' assessments of listed mobile health apps in China: a qualitative study.

Background: In recent years, mobile health (mHealth) has gradually developed in China, and intelligent medicine has become an important research topic. However, there are still significant problems in mHealth applications (apps). Although healthcare professionals and patients are the main users, few studies have focused on their perceptions of the quality of mHealth apps. Objective: This study aimed to (1) understand the respective perceptions of healthcare professionals and patients regarding mHealth apps, (2) assess what barriers exist that influence the user experience, and (3) explore how to improve the quality of mHealth apps and the development of the mHealth market in China. The study aims to promote the standardization of mHealth apps and provide effective information for the improvement and development of mHealth apps in the future. Methods: Semistructured interviews with 9 patients and 14 healthcare professionals were conducted from January 2022 to April 2022 in the Affiliated Hospital of Xuzhou Medical University. The participants used mHealth apps for more than 3 months, including the "Good Mood" and "Peace and Safe Doctors" apps and apps developed by the hospital that were popular in China. Interview transcripts were analysed using thematic analysis. Results: The following five themes were extracted: different concerns, hidden medical dangers, distance and insecurity, barriers for older people, and having positive perceptions of mHealth apps. Healthcare professionals prioritized simplicity in regard to mHealth apps, whereas patients rated effectiveness as the most crucial factor. The study also revealed several problems with mHealth apps, including insufficient information about physician qualifications, inaccurate medical content, nonstandard treatment processes, and unclear accountability, which led to a sense of distance and insecurity among participants. Older individuals faced additional obstacles when using mHealth apps. Despite these issues, the participants remained optimistic about the future of mHealth app development. Conclusion: The utilization, advantages, and obstacles of mHealth applications for healthcare professionals and patients were explored through semistructured interviews. Despite the promising prospects for mHealth apps in China, numerous issues still need to be addressed. Enhancing the safety monitoring system and developing user-friendly mHealth apps for older adult patients are essential steps to bridge the gap between healthcare providers and patients.

Metasurface-Enabled On-Chip Manipulation of Higher-Order Poincaré Sphere Beams.

An integrated way to generate and manipulate higher-order Poincaré sphere beams (HOPBs) is a sought-after goal in photonic integrated circuits for high-capacity communication systems. Here, we demonstrate a novel method for on-chip generation and manipulation of HOPBs through combining metasurface with optical waveguides on lithium niobate on insulator platform. With phase modulation by a diatomic geometric metasurface, guided waves are extracted into free space with a high signal-to-noise ratio in the form of two orthogonal circularly polarized optical vortices which are linearly superposed into HOPBs. Meanwhile, a dual-port waveguide crossing is established to reconfigure the output states into an arbitrary point on a higher-order Poincaré sphere based on in-plane interference of two guided waves. Our approach provides a promising solution to generate and manipulate the HOPBs in a compact manner, which would be further enhanced by employing the electro-optical modulation on a lithium niobate waveguide to access a fully tunable scheme.

Citrinin inhibits the function of Leydig cells in male rats in prepuberty.

Citrinin, a mycotoxin existing in fruits, has nephrotoxicity, hepatotoxicity and embryotoxicity. The effects of citrinin on Leydig cell development in prepuberty remains unclear. Male Sprague-Dawley rats were gavaged with 0, 1, 2.5, and 5 mg/kg citrinin from postnatal days 21-28. Citrinin at 5 mg/kg significantly decreased serum testosterone levels, while increasing serum LH and FSH levels. Citrinin at 1-5 mg/kg markedly downregulated Hsd17b3 and HSD17B3 expression, while upregulating Srd5a1 (SRD5A1) and Akr1c14 (AKR1C14) expression at 2.5 and/or 5 mg/kg. Citrinin at 5 mg/kg also significantly increased PCNA-labeling index in Leydig cells. Citrinin at 5 mg/kg significantly raised testicular MDA amount, whiling at 2.5 and 5 mg/kg downregulating SOD1 and SOD2 expression. Citrinin at 5 mg/kg markedly decreased the ratio of Bcl2 to Bax, in consistent with the increased apoptosis in Leydig cells judged by TUNEL assay. Enzymatic assay revealed that citrinin inhibited rat testicular HSD3B1 activity at 100 µM and HSD17B3 activity at 10-100 µM. Citrinin at 50 µM and higher also induced reactive oxygen species (ROS) and apoptosis of R2C cell line. In conclusion, citrinin inhibits Leydig cell development at multiple levels via different mechanisms and oxidative stress partially plays a role.

Pre-existing humoral immunity to low pathogenic human coronaviruses exhibits limited cross-reactive antibodies response against SARS-CoV-2 in children.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes asymptomatic or mild symptoms, even rare hospitalization in children. A major concern is whether the pre-existing antibodies induced by low pathogenic human coronaviruses (LPH-CoVs) in children can cross-react with SARS-CoV-2. To address this unresolved question, we analyzed the pre-existing spike (S)-specific immunoglobin (Ig) G antibodies against LPH-CoVs and the cross-reactive antibodies against SARS-CoV-2 in 658 serum samples collected from children prior to SARS-CoV-2 outbreak. We found that the seroprevalence of these four LPH-CoVs reached 75.84%, and about 24.64% of the seropositive samples had cross-reactive IgG antibodies against the nucleocapsid, S, and receptor binding domain antigens of SARS-CoV-2. Additionally, the re-infections with different LPH-CoVs occurred frequently in children and tended to increase the cross-reactive antibodies against SARS-CoV-2. From the forty-nine serum samples with cross-reactive anti-S IgG antibodies against SARS-CoV-2, we found that seven samples with a median age of 1.4 years old had detected neutralizing activity for the wild-type or mutant SARS-CoV-2 S pseudotypes. Interestingly, all of the seven samples contained anti-S IgG antibodies against HCoV-OC43. Together, these data suggest that children's pre-existing antibodies to LPH-CoVs have limited cross-reactive neutralizing antibodies against SRAS-CoV-2.

Tetramethyl bisphenol A stimulates proliferation but inhibits fetal Leydig cell function in male rats by targeting estrogen receptor α after in utero exposure.

Tetramethyl bisphenol A (TMBPA) is a widely used flame retardant. TMBPA has been a toxic to Leydig cells in puberty, but it remains unclear whether TMBPA has a similar inhibitor effect on fetal Leydig cells (FLCs). This study reported morphological and functional alterations of FLCs in the testes of male offspring at birth after in utero exposure to TMBPA. Pregnant Sprague Dawley rats were dosed via continuous gavage of TMBPA (0, 10, 50, and 200 mg/kg/day) from gestational day 14 to 21. TMBPA markedly raised serum total testosterone level, testicular volume, and FLC number of male offspring at 200 mg/kg dose. The up-regulation of Insl3, Star, and Cyp11a1 mRNAs was observed after 200 mg/kg TMBPA exposure. After normalization to the number of FLCs, TMBPA significantly reduced Lhcgr and Hsd3b1 expressions at 10 mg/kg, and Cyp17a1 at 200 mg/kg paralleling with their protein levels. TMBPA compromised the expression of Esr1, while increased the expression of Cdk2 and Cdk4 as well as their protein levels. TMBPA particularly increased the phosphorylation of AKT1 and AKT2 at 200 mg/kg. In conclusion, the present study suggests that TMBPA may promote FLC proliferation via ESR1-CDK2/4-AKT pathway, while inhibits the function of FLCs by reducing steroidogenic enzyme activity.

Serine active site containing protein 1 depletion alters lipid metabolism and protects against high fat diet-induced obesity in mice.

OBJECTIVE: Although the serine active site containing 1 (SERAC1) protein is essential for cardiolipin remodeling and cholesterol transfer, its physiological role in whole-body energy metabolism remains unclear. Thus, we investigated the role of SERAC1 in lipid distribution and metabolism in mice. METHODS: CRISPR/Cas9 was used to create homozygous Serac1 knockout mice. A range of methods, including electron microscopy, histological analysis, DNA sequencing, glucose and insulin tolerance tests, and biochemical analysis of serum lipid levels, were used to assess lipid distribution and rates of lipid synthesis in mice. RESULTS: We found that Serac1 depletion in mice prevented high-fat diet-induced obesity but did not affect energy expenditure. The liver was affected by Serac1 depletion, but adipose tissues were not. Serac1 depletion was shown to impair cholesterol transfer from the liver to the serum and led to an imbalance in cholesterol distribution. The livers from mice with Serac1 depletion showed increased cholesterol synthesis because the levels of cholesterol synthesis enzymes were upregulated. Moreover, the accumulation of hepatic lipid droplets in mice with Serac1 depletion were decreased, suggesting that SERAC1 depletion may decrease the risk for hepatic steatosis in high fat diet-induced mice. CONCLUSION: Our findings demonstrate that SERAC1 can serve as a potential target for the treatment or prevention of diet-induced hepatic lipid metabolic disorders.

Fluornen-9-bisphenol increases Leydig cell proliferation but inhibits maturation in pubertal male rats via interacting with androgen receptor as an antagonist and estrogen receptor α as an agonist.

Fluornen-9-bisphenol (BPFL) is used as one of the alternatives for bisphenol A. However, whether BPFL has deleterious effects to the male reproductive system and the underlying mechanism remain unknown. Here, we report the effects of BPFL on Leydig cell development in male rats in puberty. Male Sprague-Dawley (28 days old) rats were dosed with 0, 10, 100, 200 mg/kg/day BPFL via gavage for 28 days. BPFL significantly decreased serum testosterone levels at 200 mg/kg while increasing serum luteinizing hormone and follicle-stimulating hormone levels at 200 mg/kg. BPFL markedly increased Leydig cell number but down-regulated the expression of Cyp17a1 and its protein level in Leydig cells at 200 mg/kg. Further study showed that BPFL significantly increased Pcna and Cdk2 expression and increased Leydig cell proliferation at 200 mg/kg. BPFL treatment to immature Leydig cells isolated from 28-day-old male rats for 24 h significantly inhibited testosterone biosynthesis at 50 µM, which was completely reversed by the androgen receptor agonist 7α-methyl-nortestosterone and estrogen receptor α antagonist ICI 182,780. In conclusion, BPFL increases Leydig cell proliferation but inhibits its maturation in male rats in puberty by blocking androgen receptor and activating estrogen receptor α.

Tetramethyl bisphenol a inhibits leydig cell function in late puberty by inducing ferroptosis.

Tetramethyl bisphenol A (TMBPA) is a commonly used bisphenol analog, used as a fire retardant. However, whether it inhibits the function of Leydig cells in late puberty remains unclear. In this study, 35-day-old male Sprague-Dawley rats were gavaged with 0, 10, 100, and 200 mg/kg body weight TMBPA for 21 days. TMBPA significantly reduced serum testosterone levels at 10 mg/kg and higher doses without altering serum luteinizing hormone and follicle-stimulating hormone levels. TMBPA significantly increased serum iron concentraion while reducing the ratio of serum glutathione (GSH) and GSH/GSSG (oxidized glutathione disulfide). In addition, TMBPA significantly increased testicular iron amount at 10 mg/kg and higher doses and malondialdehyde level at 200 mg/kg. TMBPA down-regulated the expression of Leydig cell genes, including Nr5a1, Star, Scarb1, Insl3, Cyp11a1, Cyp17a1, Hsd17b3, and Hsd11b1, and their proteins. In addition, TMBPA markedly down-regulated the expression of genes in the ferroptosis pathway (Tp53, Slc7a11, Sod1, Sod2, Cat, Sqstm1, Keap1, and Hmox1). TMBPA significantly reduced the levels of ferroptosis pathway proteins (TP53, SLC7A11, GPX4, SQSTM1, KEAP1, NRF2, and HMOX1) in Leydig cells in vivo. Immature and adult Leydig cell culture in vitro also showed that TMBPA significantly reduced testosterone concentrations in the medium, which can be reversed by a ferroptosis inhibitor. After 24 h of culture in primary Leydig cells at 10 and 50 µM, TMBPA significantly induced reactive oxygen species and lowered the mitochondrial membrane potential. TMBPA also altered protein levels in the ferroptosis pathway in Leydig cells in vitro. In conclusion, TMBPA directly inhibits the activity of rat Leydig cell steroidogenic enzymes and induces the ferroptosis of Leydig cells, thereby inhibiting the testosterone synthesis of Leydig cells in the late puberty.

SERAC1 is a component of the mitochondrial serine transporter complex required for the maintenance of mitochondrial DNA.

SERAC1 deficiency is associated with the mitochondrial 3-methylglutaconic aciduria with deafness, (hepatopathy), encephalopathy, and Leigh-like disease [MEGD(H)EL] syndrome, but the role of SERAC1 in mitochondrial physiology remains unknown. Here, we generated Serac1-/- mice that mimic the major diagnostic clinical and biochemical phenotypes of the MEGD(H)EL syndrome. We found that SERAC1 localizes to the outer mitochondrial membrane and is a protein component of the one-carbon cycle. By interacting with the mitochondrial serine transporter protein SFXN1, SERAC1 facilitated and was required for SFXN1-mediated serine transport from the cytosol to the mitochondria. Loss of SERAC1 impaired the one-carbon cycle and disrupted the balance of the nucleotide pool, which led to primary mitochondrial DNA (mtDNA) depletion in mice, HEK293T cells, and patient-derived immortalized lymphocyte cells due to insufficient supply of nucleotides. Moreover, both in vitro and in vivo supplementation of nucleosides/nucleotides restored mtDNA content and mitochondrial function. Collectively, our findings suggest that MEGD(H)EL syndrome shares both clinical and molecular features with the mtDNA depletion syndrome, and nucleotide supplementation may be an effective therapeutic strategy for MEGD(H)EL syndrome.

Oncostatin M stimulates immature Leydig cell proliferation but inhibits its maturation and function in rats through JAK1/STAT3 signaling and induction of oxidative stress in vitro.

BACKGROUND: Oncostatin M (OSM) is a member of the interleukin-6 group of cytokines, which can regulate cell proliferation, growth, and function. Immature Leydig cells have the ability to proliferate and differentiate, and adult Leydig cells have the function of testosterone synthesis. However, the role and underlying mechanisms of OSM on the proliferation and function of Leydig cells remain unclear. METHODS: The effects of OSM on the proliferation, apoptosis, and function of immature Leydig cells isolated from 35-day-old rats and the function of adult Leydig cells isolated from 63-day-old rats in vitro. RESULTS: OSM stimulated immature Leydig cell proliferation after up-regulating the expression of Ccnd1 and Cdk4 to drive the transition of G1 phase to M2 phase in the cell cycle at 10 and 100 ng/ml. OSM did not affect the apoptosis of immature Leydig cells up to 100 ng/ml. OSM inhibited testosterone production in immature and adult Leydig cells by down-regulating the expression of Lhcgr, Star, Cyp11a1, Hsd3b1, and Cyp17a1 at 1-100 ng/ml. OSM induced reactive oxygen species and down-regulated the expression of antioxidant genes and lowered mitochondrial membrane potential at 10 and 100 ng/ml in both Leydig cells. Janus kinase 1 (JAK1) antagonist filgotinib and signal transducer and activator of transcription 3 (STAT3) antagonist S3I-201 reversed the effect of OSM, indicating that it acts on JAK1/STAT3 signaling. CONCLUSION: Oncostatin M stimulates immature Leydig cell proliferation while inhibiting the function of immature and adult Leydig cells.

Host-Adaptive Signatures of H3N2 Influenza Virus in Canine.

Wild aquatic birds are the primary natural reservoir of influenza A viruses (IAVs), although a small number of viruses can spill over to mammals and circulate. The focus of IAV infection in mammals was largely limited to humans and swine variants, until the emergence of H3N2 canine influenza viruses (CIVs), which provides new perspective for interspecies transmission of the virus. In this study, we captured 54 canine-adaptive signatures in H3N2 CIVs through entropy computation, which were largely concentrated in the interaction region of polymerase proteins on ribonucleoprotein complex. The receiver operating characteristic curves of these sites showed >95% accuracy in distinguishing between the hosts. Nine of the 54 canine-adaptive signatures were shared in avian-human/equine or equine-canine (PB2-82; PB1-361; PA-277; HA-81, 111, 172, 196, 222, 489), suggesting their involvement in canine adaptation. Furthermore, we found that IAVs can establish persistent transmission in lower mammals with greater ease compared to higher mammals, and 25 common adaptation signatures of H3 IAVs were observed in diverse avian-mammals comparison. There were few human-like residues in H3N2 CIVs, which suggested a low risk of human infection. Our study highlights the necessity of identifying and monitoring the emerging adaptive mutations in companion animals by enhanced surveillance and provides a basis for mammal adaptation of avian influenza viruses.