Development and application of a cycleave dual-probe fluorescence quantitative PCR method for simultaneous detection of Mycoplasma gallisepticum ts-11 vaccine strain and non-ts-11 strains.

An attenuated vaccine against the Mycoplasma gallisepticum ts-11 strain has become an effective prevention and control method against MG infection. However, the ts-11 strain is usually difficult to distinguish from the non-ts-11 strain (including field isolates and other vaccine strains (F and 6/85)). Therefore, it is critical to establish a rapid and effective method to distinguish ts-11 strains from non-ts-11 strains. The gene sequences of the ts-11 strain (CP044225.1) and the non-ts-11 strain (including the wild-type (CP006916.3), 6/85 (CP044224.1), and F strains (NC_017503.1) were used to construct a conserved region containing a single point mutation in the potC gene in the ts-11 strain, after which a primer-probe combination method was designed. The primer-probe method was able to accurately and efficiently identify the ts-11 and non-ts-11 strains with minimum detection limits of 2.43 copies/µL and 1.65 copies/µL, respectively. Moreover, it could simultaneously distinguish the ts-11 strain from a non-ts-11 strain, and amplifications of avian influenza virus, infectious bronchitis virus, Newcastle disease virus, fowl adenovirus, infectious laryngotracheitis virus, infectious bursal disease virus, chicken anemia virus, Marek's disease virus, Mycoplasma synoviae, and Ornithobacter rhinotracheale were negative. The detection of clinical samples revealed that the established dual-probe fluorescence quantitative PCR method could be used to screen for mixed and single infections of the ts-11 strain and non-ts-11 strains effectively, with lower variation coefficients for intra- and interbatch repetition. The established cycleave dual-probe fluorescence quantitative PCR method showed good specificity, sensitivity, and repeatability and provides powerful technical support for the rapid and efficient differential diagnosis of the MG ts-11 strain from non-ts-11 strains.

Vesicle-associated membrane protein 8 knockdown exerts anti-proliferative, pro-apoptotic, anti-autophagic, and pro-ferroptotic effects on colorectal cancer cells by inhibition of the JAK/STAT3 pathway.

Vesicle-associated membrane protein 8 (VAMP8), a soluble n-ethylmaleimide-sensitive factor receptor protein, acts as an oncogenic gene in the progression of several malignancies. Nevertheless, the roles and mechanisms of VAMP8 in colorectal cancer (CRC) progression remain unknown. The expression and prognostic significance of VAMP8 in CRC samples were analyzed through bioinformatics analyses. Cell proliferation was detected using CCK-8 and EdU incorporation assays and apoptosis was evaluated via flow cytometry. Western blot analysis was conducted to examine the protein expression. Ferroptosis was evaluated by measurement of iron metabolism, lipid peroxidation, and glutathione (GSH) content. VAMP8 was increased in CRC samples relative to normal samples on the basis of GEPIA and HPA databases. CRC patients with high level of VAMP8 had a worse overall survival. VAMP8 depletion led to a suppression of proliferation and promotion of apoptosis in CRC cells. Additionally, VAMP8 knockdown suppressed beclin1 expression and LC3-II/LC3-I ratio, elevated p62 expression, increased Fe2+, labile iron pool, lipid reactive oxygen species, and malondialdehyde levels, and repressed GSH content and glutathione peroxidase activity. Moreover, VAMP8 knockdown inhibited the activation of janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway in CRC cells. Mechanistically, activation of the JAK/STAT3 pathway by JAK1 or JAK2 overexpression attenuated VAMP8 silencing-mediated anti-proliferative, pro-apoptotic, anti-autophagic, and pro-ferroptotic effects on CRC cells. In conclusion, VAMP8 knockdown affects the proliferation, apoptosis, autophagy, and ferroptosis by the JAK/STAT3 pathway in CRC cells.

Molecular mechanisms of artificial light at night affecting circadian rhythm disturbance.

Artificial light at night (ALAN) pollution has been regarded as a global environmental concern. More than 80% of the global population is exposed to light pollution. Exacerbating this issue, artificially lit outdoor areas are growing by 2.2% per year, while continuously lit areas have brightened by 2.2% each year due to rapid population growth and expanding urbanization. Furthermore, the increasing prevalence of night shift work and smart device usage contributes to the inescapable influence of ALAN. Studies have shown that ALAN can disrupt endogenous biological clocks, resulting in a disturbance of the circadian rhythm, which ultimately affects various physiological functions. Up until now, scholars have studied various disease mechanisms caused by ALAN that may be related to the response of the circadian system to light. This review outlines the molecular mechanisms by which ALAN causes circadian rhythm abnormalities in sleep disorders, endocrine diseases, cardiovascular disease, cancer, immune impairment, depression, anxiety and cognitive impairments.

Hepatitis C virus infection is associated with high risk of breast cancer: a pooled analysis of 68,014 participants.

Introduction: Breast cancer is the most common malignancy among women. Previous studies had shown that hepatitis C virus (HCV) infection might serve as a risk factor for breast cancer, while some studies failed to find such an association. Methods: In this study, we presented a first attempt to capture and clarify this clinical debate via a cumulative analysis (registration ID: CRD42023445888). Results: After systematically searching and excluding the irrelevant publications, five case-control or cohort studies were finally included. The synthetic effect from the eligible studies showed that patients with HCV infection had a significantly higher prevalence of breast cancer than non-HCV infected general population (combined HR= 1.382, 95%CI: 1.129 to 1.692, P=0.002). There was no evidence of statistical heterogeneity during this pooled analysis (I2 = 13.2%, P=0.33). The sensitivity analyses confirmed the above findings. No significant publication bias was observed among the included studies. The underlying pathophysiological mechanisms for this relationship might be associated with persistent infection/inflammation, host immune response, and the modulation of HCV-associated gene expression. Discussion: Though the causal association between HCV infection and breast cancer did not seem quite as strong, screening for HCV might enable the early detection of breast cancer and help to prevent the progression of the disease. Since the topic of this study remains a matter of clinical debate, further studies are still warranted to validate this potential association. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42023445888.

Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11.

Programed cell death plays a key role in promoting human development and maintaining homeostasis. Ferroptosis is a recently identified pattern of programmed cell death that is closely associated with the onset and progression of neurodegenerative diseases. Ferroptosis is mainly caused by the intracellular accumulation of iron-dependent lipid peroxides. The cysteine/glutamate antibody Solute carrier family 7 member 11 (SLC7A11, also known as xCT) functions to import cysteine for glutathione biosynthesis and antioxidant defense. SLC7A11 has a significant impact on ferroptosis, and inhibition of SLC7A11 expression promotes ferroptosis. Moreover, SLC7A11 is also closely associated with neurodegenerative diseases. In this paper, we summarize the relationship between ferroptosis and neurodegenerative diseases and the role of SLC7A11 during this process. The various regulatory mechanisms of SLC7A11 are also discussed. In conclusion, we are looking forward to a theoretical basis for further understanding the occurrence and development of ferroptosis in SLC7A11 and neurodegenerative diseases, and to seek new clues for the treatment of neurodegenerative diseases.

Methylmercury promotes oxidative stress and autophagy in rat cerebral cortex: Involvement of PI3K/AKT/mTOR or AMPK/TSC2/mTOR pathways and attenuation by N-acetyl-L-cysteine.

Methylmercury (MeHg) is a potent neurotoxicant that could induce oxidative stress and autophagy. However, the underlying mechanisms through which MeHg affects the central nervous system have not been fully elucidated, and little has been known of the interaction between oxidative stress and autophagy. Therefore, rats were administrated with different MeHg concentrations to evaluate the neurotoxic effects and autophagy in cerebral cortex. Moreover, we have investigated the neuroprotective role of N-acetyl-L-cysteine (NAC) against MeHg-induced neurotoxicity in order to estimate the regulation effects of oxidative stress on autophagy. A total of 64 rats, 40 of which were randomly divided into control and MeHg-treated (4, 8 and 12 µ mol/kg) groups. The remaining 24 rats were divided into control, NAC control (1 mmol/kg), 12 µ mol/kg MeHg, and NAC pretreatment. Administration of 12 µ mol/kg MeHg significantly increased behavioral and pathological abnormalities, and autophagy levels. In addition, the oxidative stress levels increased, together with abnormal expression of autophagy-related molecules. Pretreatment with NAC significantly prevented MeHg-induced oxidative stress and PI3K/AKT/mTOR or AMPK/TSC2/mTOR-mediated autophagy. In conclusion, the present study suggested that oxidative stress can regulate autophagy through PI3K/AKT/mTOR or AMPK/TSC2/mTOR pathways. This study provides a theoretical basis for the study and treatment of MeHg-induced neurotoxicity.

Indoor solid fuel use and incident arthritis among middle-aged and older adults in rural China: A nationwide population-based cohort study.

BACKGROUND: Many households in developing countries, including China, rely on the traditional use of solid fuels for cooking and heating. Arthritis is highly prevalent in middle-aged and older adults and is a major cause of disability. However, evidence linking indoor solid fuel use with arthritis is scarce in this age group (≥45 years) in developing countries. OBJECTIVES: To investigate whether exposure to indoor solid fuel for cooking and heating is associated with arthritis in middle-aged and older adults in rural China. METHODS: Data for the present study were extracted from the China Health and Retirement Longitudinal Study (CHARLS), a longitudinal national prospective study of adults aged 45 years and older enrolled in 2010 and followed up through 2015. We included 7807 rural participants without arthritis at baseline, of whom 1548 living in a central heating area in winter were included in the heating analysis (taking the Qinling-Huaihe line as the heating boundary). Cox proportional hazards models were used to examine the association between indoor solid fuel use and arthritis, controlling for age, sex, education, marital status, smoking status, drinking status, self-reported socioeconomic status, BMI, sleep time, napping time, independent cooking, hypertension, diabetes, dyslipidemia, heart problems and stroke. We also investigated the effect of switching primary fuels and using solid fuels for both cooking and heating on arthritis risk. RESULTS: The mean (SD) age of the study participants was 59.2 (10.0) years old, and 48.0% of participants were women. A total of 64.8% and 63.0% of the participants reported primarily using solid fuel for cooking and heating, respectively. Arthritis incidence rates were lower among clean fuel users than solid fuel users. Compared to those using clean fuels, cooking and heating solid fuel users had a higher risk of arthritis, with hazard ratios (HRs) of 1.22 (95% confidence interval (CI): 1.01, 1.49) and 1.76 (95% CI: 1.07, 2.89), respectively. Switching from clean fuels to solid fuels for heating (HR: 3.28, 95% CI: 1.21, 7.91) and using solid fuels for both cooking and heating (HR, 1.71, 95% CI, 1.01-2.79) increased the risk of arthritis. CONCLUSIONS: Long-term solid fuel use for indoor cooking and heating is associated with an increased risk of arthritis events among adults aged 45 years and older in rural China. The potential benefits of reducing indoor solid fuel use in groups at high risk for arthritis merit further exploration.

lncRNA OTUD6B-AS1 Exacerbates As2O3-Induced Oxidative Damage in Bladder Cancer via miR-6734-5p-Mediated Functional Inhibition of IDH2.

Arsenic trioxide (As2O3) is a promising effective chemotherapeutic agent for cancer treatment; however, how and through what molecular mechanisms the oxidative damage of As2O3 is controlled remains poorly understood. Recently, the involvement of dysregulated long noncoding RNA ovarian tumor domain containing 6B antisense RNA1 (lncRNA OTUD6B-AS1) in tumorigenesis is established. Here, for the first time, we characterize the regulation of As2O3 in the oxidative damage against bladder cancer via lncRNA OTUD6B-AS1. As2O3 could activate lncRNA OTUD6B-AS1 transcription in bladder cancer cells, and these findings were validated in a xenograft tumor model. Functional assays showed that lncRNA OTUD6B-AS1 dramatically exacerbated As2O3-mediated oxidative damage by inducing oxidative stress. Mechanistically, As2O3 increased levels of metal-regulatory transcription factor 1 (MTF1), which regulates lncRNA OTUD6B-AS1, in response to oxidative stress. Further, lncRNA OTUD6B-AS1 inhibited mitochondrial NADP+-dependent isocitrate dehydrogenase 2 (IDH2) expression by stabilizing miR-6734-5p, which contributed to cytotoxicity by enhancing oxidative stress. Together, our findings offer new insights into the mechanism of As2O3-induced oxidative damage and identify important factors in the pathway, As2O3/lncRNA OTUD6B-AS1/miR-6734-5p/IDH2, expanding the knowledge of activity of As2O3 as cancer treatment.

miR-222 expression is correlated with the ATA risk stratifications in papillary thyroid carcinomas.

BACKGROUND: miR-222 is one of the most consistently overexpressed miRNAs in papillary thyroid carcinoma (PTC). Previous studies demonstrated that miR-222 overexpression conferred high-risk features in PTC patients, suggesting its value in risk-stratification. However, studies in term of miR-222's utility on stratifying PTCs are lacking. METHODS: One hundred patients including 10 with multinodular goiter and 90 with PTC were enrolled. Formalin-fixed paraffin-embedded samples were exploited for miR-222 quantitative reverse transcriptase- polymerase chain reaction (RT-PCR) analysis. Correlations between miR-222 expression and different clinicopathological features, Tumor-node-metastasis (TNM) staging and ATA risk level were analyzed. RESULTS: miR-222 expression of the PTC group was significantly higher than that of the goiter group (P < .001). Furthermore, miR-222 expression was significantly higher in PTCs with advanced features like larger tumor, capsular invasion, vascular invasion and lymph nodes metastasis. The majority of patients (61%) were in stage I group (similar to ATA low-risk) by TNM staging system. As to the ATA system, the majority (73%) were in intermediate-risk group (similar to TNM stage II and III roughly). Contrary to previous report, here we found that miR-222 expression was correlated with the ATA risk level (P < .001), but not with the TNM staging (P = .122). CONCLUSION: In the present study, we demonstrated that miR-222 overexpression was correlated with advanced features like capsular invasion, vascular invasion, larger tumor size and lymph node metastasis in PTCs. Most importantly, miR-222 expression was correlated with ATA risk levels, suggesting its potential value in PTC risk-stratification.

The role S-nitrosylation in manganese-induced autophagy dysregulation in SH-SY5Y cells.

Overexposure to manganese (Mn) has been known to induce nitrosative stress. The dysregulation of autophagy has implicated in nitric oxide (NO) bioactivity alterations. However, the mechanism of Mn-induced autophagic dysregulation is unclear. The protein of Bcl-2 was considered as a key role that could participate to the autophagy signaling regulation. To further explore whether S-nitrosylation of Bcl-2 involved in Mn-induced autophagy dysregulation, we treated human neuroblastoma (SH-SY5Y) cells with Mn and pretreated cells with 1400 W, a selective iNOS inhibitor. After cells were treated with 400 µM Mn for 24 h, there were significant increases in production of NO, inducible NO synthase (iNOS) activity, the mRNA and protein expressions of iNOS. Interestingly, autophagy was activated after cells were treated with Mn for 0-12 h; while the degradation process of autophagy-lysosome pathway was blocked after cells were treated with Mn for 24 h. Moreover, S-nitrosylated JNK and Bcl-2 also increased and phospho-JNK and phospho-Bcl-2 reduced in Mn-treated cells. Then, the affinity between Bcl-2 and Beclin-1 increased significantly in Mn-treated cells. We used the 1400 W to neutralize Mn-induced nitrosative stress. The results showed that S-nitrosylated JNK and Bcl-2 reduced while their phosphorylation were recovered to some extent. The findings revealed that NO-mediated S-nitrosylation of Bcl-2 directly affected the interaction between Beclin-1 and Bcl-2 leading to autophagy inhibition.

Alpha-lipoic acid reduces methylmercury-induced neuronal injury in rat cerebral cortex via antioxidation pathways.

Methylmercury (MeHg), an extremely dangerous environmental pollutant, accumulating preferentially in central nervous system, causes a series of cytotoxic effects. The present study explored the mechanisms which contribute to MeHg-induced neurotoxicity focusing on the oxidative stress in rat cerebral cortex. In addition, the protective effects of alpha-lipoic acid (LA), a potent antioxidant on MeHg-mediated neuronal injury, was also investigated in current study. A MeHg poisoning model was established as 64 rats randomly divided into 4 groups of which saline control group, MeHg-treated groups (4 and 12 µmol kg-1 ), and LA pretreatment (35 µmol kg-1 ) group, respectively. After administration of 12 µmol kg-1 MeHg for 4 weeks, it was found that obvious pathological changes and apoptosis in neuronal cells. Meanwhile, total Hg levels elevated significantly, superoxide dismutase (SOD) and gluthathione peroxidase (GSH-Px) activities were inhibited, and ROS formation elevated, which might be critical to aggravate oxidative stress in cerebral cortex. In addition, NF-E2-related factor 2 (Nrf2) pathways were activated, as heme oxygenase-1 (HO-1) and γ-glutamylcysteine synthetase heavy subunit (γ-GCSh) expressions were up-regulated obviously by MeHg exposure. Moreover, activities of Na+ -K+ -ATPase and Ca2+ -ATPase were inhibited, leading to intracellular calcium (Ca2+ ) overload. LA pre-treatment partially reduced MeHg neurotoxic effects via anti-oxidation pathways. In conclusion, these findings clearly indicated that MeHg aggravated oxidative stress and Ca2+ overload in cerebral cortex. LA possesses the ability to prevent MeHg neurotoxicity through its anti-oxidative properties. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 931-943, 2017.

Tea Polyphenols Protect Against Methylmercury-Induced Cell Injury in Rat Primary Cultured Astrocytes, Involvement of Oxidative Stress and Glutamate Uptake/Metabolism Disorders.

Methylmercury (MeHg) is an extremely dangerous environmental contaminant, accumulating preferentially in CNS and causing a series of cytotoxic effects. However, the precise mechanisms are still incompletely understood. The current study explored the mechanisms that contribute to MeHg-induced cell injury focusing on the oxidative stress and Glu uptake/metabolism disorders in rat primary cultured astrocytes. Moreover, the neuroprotective effects of tea polyphenols (TP), a natural antioxidant, against MeHg cytotoxicity were also investigated. Astrocytes were exposed to 0, 2.5, 5, 10, and 20 µM MeHgCl for 6-30 h, or pretreated with 50, 100, 200, and 400 µM TP for 1-12 h; cell viability and LDH release were then determined. For further experiments, 50, 100, and 200 µM of TP pretreatment for 6 h followed by 10 µM MeHgCl for 24 h were performed for the examination of the responses of astrocytes, specifically addressing NPSH levels, ROS generation, ATPase activity, the expressions of Nrf2 pathway as well as Glu metabolism enzyme GS and Glu transporters (GLAST and GLT-1). Exposure of MeHg resulted in damages of astrocytes, which were shown by a loss of cell viability, and supported by high levels of LDH release, morphological changes, apoptosis rates, and NPSH depletion. In addition, astrocytes were sensitive to MeHg-mediated oxidative stress, a finding that is consistent with ROS overproduction; Nrf2 as well as its downstream genes HO-1 and γ-GCSh were markedly upregulated. Moreover, MeHg significantly inhibited GS activity, as well as expressions of GS, GLAST, and GLT-1. On the contrary, pretreatment with TP presented a concentration-dependent prevention against MeHg-mediated cytotoxic effects of astrocytes. In conclusion, the findings clearly indicated that MeHg aggravated oxidative stress and Glu uptake/metabolism dysfunction in astrocytes. TP possesses some abilities to prevent MeHg cytotoxicity through its antioxidative properties.

Antioxidative effects of schidandrin B and green tea polyphenols against mercuric chloride-induced hepatotoxicity in rats.

In the present study, we investigated the hepatoprotective effects of schisandrin B (Sch B) and green tea polyphenols (GrTP), two natural antioxidants, against Hg hepatotoxicity. Fifty-six rats were randomly divided into four groups of fourteen animals in each group: control group, Hg-treated group, Sch B pretreated group, and GrTP pretreated group. HgCl2 injection increased Hg accumulation, pathological and ultrastructural injury, lactate dehydrogenase (LDH) level, alanine transaminase (ALT) level, apoptosis, reactive oxygen species (ROS) level, glutathione (GSH) level, and malondialdehyde (MDA) level. HgCl2 injection decreased glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities. Sch B and GrTP protected against Hg-induced dysfunction and liver injury by enhancing the antioxidant defense system. Our results indicate that Sch B and GrTP exert antioxidative effects against Hg-induced hepatotoxicity in rats.

Exploring cross-talk between oxidative damage and excitotoxicity and the effects of riluzole in the rat cortex after exposure to methylmercury.

Methylmercury (MeHg) is a ubiquitous environmental toxin that causes neurologic and developmental diseases. Oxidative damage and excitotoxicity are putative mechanisms, which underlie MeHg-induced neurotoxicity. In this study, the cross-talk between the oxidative damage and excitotoxicity pathways and the protective effects of riluzole in the rat cortex were explored. Rats were injected with MeHg and/or riluzole, and cold vapor atomic fluorescence spectrometry, hematoxylin and eosin staining, flow cytometry, fluorescence assays, spectrophotometry, real-time PCR, and Western blotting were used to evaluate neurotoxicity. The present study showed that (1) MeHg accumulated in the cerebral cortex and caused pathology. (2) MeHg caused oxidative damage by inducing glutathione (GSH) depletion, reactive oxygen species (ROS) production, inhibition of antioxidant enzyme activity, and alteration of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. (3) MeHg disrupted the glutamate transporters (GluTs), glutamate-glutamine cycle, and N-methyl-D-aspartate receptor expression and induced excitotoxicity. (4) Excitotoxicity resulted in disruption of GSH synthesis, calcium overloading, oxidative damage, and excessive ROS production. (5) Pretreatment with riluzole antagonized MeHg neurotoxicity by down regulating cross-talk between the oxidative damage and excitotoxicity pathways. In conclusion, the cross-talk between the oxidative damage and excitotoxicity pathways caused by MeHg exposure was linked by GluTs and calcium and inhibited by riluzole treatment.

Oxidative stress involvement in manganese-induced alpha-synuclein oligomerization in organotypic brain slice cultures.

Overexposure to manganese (Mn) has been known to induce neuronal damage. However, little is known of the role that reactive oxygen species (ROS) play in protein aggregation resulting from Mn exposure. The current study investigated whether oxidative stress is involved in manganese-induced alpha-synuclein oligomerization in organotypic brain slices. After application of Mn (0-400µM) for 24h, there was a dose-dependent increase in average percentage of propidium iodide positive (PI(+)) nuclei in slices and levels of lactate dehydrogenase (LDH) in the culture medium. Moreover, the treatment with Mn resulted in a dose-dependent increase in neurocyte apoptosis, ROS level, and decrease in superoxide dismutase (SOD) activity. Mn also caused oxidative damage in cell lipid and protein. At the same time, the exposure of Mn leaded to significantly increase in the expression of alpha-synuclein mRNA and protein. Alpha-synuclein oligomerization occurred in Mn-treated slices, especially on membrane-bound form. It indicated that alpha-synuclein oligomers were more likely to combination cell membranes and resulting in membrane damage. Mn-induced neurocyte damage and alpha-synuclein oligomerization were also partially alleviated by the pretreatment with GSH and aggravated by H2O2 pretreatment. The findings revealed Mn might exert its neurotoxic effects by oxidative stress-mediated alpha-synuclein oligomerization in organotypic brain slices.

Development of an inflammation-inducible gene expression system using helper-dependent adenoviral vectors.

BACKGROUND: Clinical studies have shown that gene therapy is a promising approach for treating such genetic diseases as the eye disease, Leber's congenital amaurosis. Development of gene therapy approaches for treating chronic inflammatory diseases is, however, more challenging because it requires the production of anti-inflammatory molecules at the diseased tissues only when they are needed. METHODS: We designed such a system by modifying the human interleukin (IL)-6 gene promoter to direct transgene expression and delivered the system into cultured cells as well as mouse lungs using a helper-dependent adenoviral vector. RESULTS: We have demonstrated both in vitro and in vivo that the reporter LacZ or human IL-10 gene can be induced by inflammatory stimuli. CONCLUSIONS: The results obtained indicate that the inflammation inducible gene expression system based on the modified human IL-6 gene promoter has the potential to be used for developing gene therapy for treating inflammatory diseases.

cDNA cloning, genomic structure and expression analysis of the goose (Anser cygnoides) MHC class I gene.

To provide data for studies on avian disease resistance, goose MHC class I cDNA (Ancy-MHC I) was cloned from a goose cDNA library, it's genomic structure and expression analysis were investigated. The mature peptides of Ancy-MHC I cDNA encoded 333 amino acids. The genomic organization is composed of eight exons and seven introns. Based on the genetic distance, six Ancy-MHC I genes from six individuals can be classified into four lineages. A total of nineteen amino acid positions in peptide-binding domain showed high scores by Wu-kabat index analysis. The Ancy-MHC I amino acid sequence displayed seven critical HLA-A2 amino acids that bind with antigen polypeptides, and have an 85.4-98.9% amino acid homology with each genes, and a 59.8-66.0% amino acid homology with chicken MHC class I. Expression analyses using Q-RT-PCR to detect the tissue-specific expression of Ancy-MHC I mRNA in an adult goose. The result appeared that Ancy-MHC I cDNA was expressed in the liver, spleen, intestine, kidney, lung, pancreas, heart, brain, and skin. The phylogenetic tree appears to branch in an order consistent with accepted evolutionary pathways.