BACKGROUND:Severe thrombocytopenia and coagulation dysregulation remain major barriers to survival in pig-to-primate liver xenotransplantation models. METHODS:Porcine livers with five genetic modifications (GTKO, CMAHKO, β4GalNT2KO, hCD55, and hTBM) were orthotopically transplanted into four Tibetan macaques under two conventional immunosuppressive protocols. Longitudinal monitoring included graft and multi-organ function, hematology, coagulation, and immune responses. Histopathological and immunohistochemical analyses were performed to characterize graft and recipient pathology. RESULTS:High expression of human thrombomodulin (hTBM) in donor livers effectively prevented early rapid and severe thrombocytopenia, with three of four recipients maintaining platelets >100 × 109/L. Thrombotic microangiopathy (TMA) was absent in grafts and recipient organs despite transient hypercoagulability. No spontaneous bleeding occurred in three of four cases. However, porcine livers failed to synthesize functional coagulation factor II, protein C, and protein S, contributing to progressive coagulopathy. While early graft function and coagulation remained stable for four posttransplant days, late dysfunction ensued, characterized by impaired coagulation factor synthesis and progressive graft failure. Antibody-mediated rejection, accompanied by IgM/IgG/C4b deposition, anti-TKO antibody increase, and pvWF upregulation, triggered injury that was amplified by innate and T cell-mediated responses. CONCLUSIONS:GTKO/CMAHKO/β4GalNT2KO/hCD55/hTBM donor liver transplantation was associated with an absence of early severe thrombocytopenia, transfusion requirement, and TMA, but long-term survival was limited by immune-mediated rejection and cross-species incompatibilities in coagulation factor synthesis. Optimizing (i) donor genetic modifications and (ii) immunosuppressive therapy, with (iii) replacement of targeted coagulation factors will be crucial for achieving durable survival in pig liver xenotransplantation.

Following the publication of the above paper, the following areas of concern associated with the western blot data featured in Figs. 3, 4 and 5 were drawn to the Editor's attention by a concerned reader, essentially involving the apparent incorrect assembly of blots within these figures and duplications of data: i) Control blots were shared between Figs. 3A and 5A, where the experimental conditions were reported to be different; ii) MDM2 blots may have been featured incorrectly in Figs. 4B and 5A, as the control blots/reported experimental conditions featured in these figure parts appeared to be the same; and iii) there was also the probable duplication of protein bands of interest comparing Fig. 5A and B. A subsequent analysis of the data in this paper performed by the Editorial Office also revealed the potential re‑use of data in a paper that was published a year later, also in the journal Molecular Medicine Reports, albeit no authors were held in common comparing these papers, and that paper has since been retracted on account of the re‑use of data with another article: Given the identification of the above problems associated with the assembly of data in three of the figures in this paper, the Editor has decided that it should be retracted from the Journal on account of a lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 15: 442‑450, 2017; DOI: 10.3892/mmr.2016.5999].

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic condition with an incompletely understood pathogenesis. In this study, five candidate genes-RAG1, CKAP2, CENPK, TYMS, and BUB1-were identified as being associated with NAFLD progression through integrative bioinformatics analyses. A predictive model incorporating these genes demonstrated strong robustness and diagnostic accuracy. Single-nucleus RNA sequencing analysis further revealed that RAG1 plays a potential role in hepatocytes of NAFLD patients. Functional experiments using RNA interference to suppress RAG1 expression in HepG2 cells treated with oleic and palmitic acids showed reduced total glyceride and cholesterol levels, mitigated lipid accumulation, and alterations in pathways related to lipid metabolism, inflammation, and fibrosis. Furthermore, adeno-associated virus-specific knockdown of RAG1 in hepatocytes attenuated hepatic steatosis in high-fat diet-fed mice. These findings suggest that investigating the molecular mechanisms of hub genes like RAG1 may advance our understanding of NAFLD pathogenesis and inform therapeutic development.

BACKGROUND:Immune dysregulation and metabolic derangement have been recognized as key factors that contribute to the progression of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF). However, the mechanisms underlying immune and metabolic derangement in patients with advanced HBV-ACLF are unclear. AIM:To identify the bioenergetic alterations in the liver of patients with HBV-ACLF causing hepatic immune dysregulation and metabolic disorders. METHODS:Liver samples were collected from 16 healthy donors (HDs) and 17 advanced HBV-ACLF patients who were eligible for liver transplantation. The mitochondrial ultrastructure, metabolic characteristics, and immune microenvironment of the liver were assessed. More focus was given to organic acid metabolism as well as the function and subpopulations of macrophages in patients with HBV-ACLF. RESULTS:Compared with HDs, there was extensive hepatocyte necrosis, immune cell infiltration, and ductular reaction in patients with ACLF. In patients, the liver suffered severe hypoxia, as evidenced by increased expression of hypoxia-inducible factor-1α. Swollen mitochondria and cristae were observed in the liver of patients. The number, length, width, and area of mitochondria were adaptively increased in hepatocytes. Targeted metabolomics analysis revealed that mitochondrial oxidative phosphorylation decreased, while anaerobic glycolysis was enhanced in patients with HBV-ACLF. These findings suggested that, to a greater extent, hepa-tocytes used the extra-mitochondrial glycolytic pathway as an energy source. Patients with HBV-ACLF had elevated levels of chemokine C-C motif ligand 2 in the liver homogenate, which stimulates peripheral monocyte infiltration into the liver. Characterization and functional analysis of macrophage subsets revealed that patients with ACLF had a high abundance of CD68+ HLA-DR+ macrophages and elevated levels of both interleukin-1β and transforming growth factor-β1 in their livers. The abundance of CD206+ CD163+ macrophages and expression of interleukin-10 decreased. The correlation analysis revealed that hepatic organic acid metabolites were closely associated with macrophage-derived cytokines/chemokines. CONCLUSION:The results indicated that bioenergetic alteration driven by hypoxia and mitochondrial dysfunction affects hepatic immune and metabolic remodeling, leading to advanced HBV-ACLF. These findings highlight a new therapeutic target for improving the treatment of HBV-ACLF.

BackgroundsNon-alcoholic fatty liver disease (NAFLD) presents as a common liver disease characterized by an indistinct pathogenesis. Disulfidptosis is a recently identified mode of cell death. This study aimed to investigate the potential role of disulfidptosis-related genes (DRGs) in the pathogenesis of NAFLD.MethodsGene expression profiles were obtained from the bulk RNA dataset GSE126848 and the single-cell RNA dataset GSE136103, both associated with NAFLD. Our study assessed the expression of DRGs in NAFLD and normal tissues. Weighted gene co-expression network analysis (WGCNA) and differential expression analysis were employed to identify the key NAFLD-specific differentially expressed DRGs (DE-DRGs). To explore the biological functions and immune regulatory roles of these key DE-DRGs, we conducted immune infiltration analysis, functional enrichment analysis, consensus clustering analysis, and single-cell differential state analysis. Finally, we validated the expression and biological functions of DRGs in NAFLD patients using histology and RNA-sequencing transcriptomic assays with human liver tissue samples.ResultsThrough the intersection of WGCNA, differentially expressed genes, and DRGs, two key DE-DRGs (DSTN and MYL6) were identified. Immune infiltration analysis indicated a higher proportion of macrophages, T cells, and resting dendritic cells in NAFLD compared to control liver samples. Based on the key DE-DRGs, Two disulfidptosis clusters were defined in GSE126848. Cluster 1, with higher expression of the key DE-DRGs, exhibited increased immune infiltration abundance and was closely associated with oxidative stress and immune regulation compared to cluster 2. High-resolution analysis of mononuclear phagocytes highlighted the potential role of MYL6 in intrahepatic M1 phenotype Kupffer cells in NAFLD patients. Our transcriptome data revealed that the expression levels of the majority of DRGs were significantly increased in NAFLD patients. NAFLD patients exhibit elevated MYL6 correlating with inflammation, oxidative stress, and disease severity, offering promising diagnostic specificity.ConclusionThis comprehensive study provides evidence for the association between NAFLD and disulfidptosis, identifying potential target genes and pathways in NAFLD. The identification of MYL6 as a possible treatment target for NAFLD provided a novel understanding of the disease’s development.

非酒精性脂肪性肝病(NAFLD)是目前最常见的慢性肝病,可进展为肝硬化及肝癌,是世界范围内的一个严重健康问题.NAFLD与代谢因素联系紧密,是代谢综合征的一个主要肝脏表现,常合并有肥胖、糖尿病、心血管疾病和其他代谢紊乱等疾病.为了更准确地反映其发病机制,2020年国际肝脏专家小组将NAFLD更名为代谢相关脂肪性肝病(MAFLD).迄今为止,其病理生理学机制尚无明确理论可以阐明,其典型特征是肝细胞的过度脂质蓄积.随着肝细胞的损伤和纤维化的产生,NAFLD将逐渐发展为终末期肝病.早期NAFLD的治疗主要提倡饮食和生活方式的改变.NAFLD药物治疗主要以发病关键环节及相关代谢紊乱为靶点,但仍然缺乏特效药.肥胖相关的NAFLD以及NAFLD相关的终末期肝病患病率逐年递增.这些患者对饮食变化和运动无反应,或无法通过改变生活方式减重,从而导致疾病的恶化,因此手术治疗成为此类患者的新选择.减重手术可以改善肝脏组织学、降低转氨酶水平及心血管疾病的发病率等.常见的手术方式包括胃袖状切除术(SG)、可调节胃束带术(ABG)以及Roux-en-Y胃旁路术(RYGB),其中SG是NAFLD相关肝硬化患者最常用的术式.但减重手术也存在一定的局限性,包括患者耐受程度、术者的技术水平以及围术期并发症的发生等,需要慎重考虑,其临床疗效和安全性还需要进一步研究,以使其适用于NAFLD患者.肝脏移植术是NAFLD相关终末期肝病患者唯一可能的治愈手段.近年来,随着移植技术和免疫抑制剂的成熟发展,肝移植术在终末期肝病的治疗中取得较为可观的成绩,但在NAFLD患者的治疗中仍存在诸多问题.边缘供肝的使用、等肝期的延长、移植术前评估与管理以及移植术后复发均影响着移植物存活率及患者生存率.本文主要综述了 NAFLD的概况、一般治疗及手术治疗进展,以期为临床工作提供参考.

目的:了解医学专业学生对器官移植认知情况,为提高器官移植教学质量探讨相应的策略.方法:采用调查的形式与自愿填写的原则对中南大学湘雅二医院临床医学专业医学生进行了问卷调查,并统计分析.结果:尽管医学生对器官捐献及移植有着相对积极的态度,但是他们捐献器官的意愿相对较低,对移植的认知相对不足,移植伦理学知识欠缺.结论:需要加强移植伦理学的教学,强化"脑死亡"的概念,提高器官移植教学内容的比重,增加器官捐献的教学内容.

Objective:To explore the feasibility of a stable pig-to-monkey orthotopic liver transplantation (LT) model and provide a favorable experimental tool for preclinical studies of xenotransplantation.Methods:In this retrospective analysis, the authors reviewed the perioperative conditions and outcomes of 7 pig-to-monkey orthotopic liver transplants performed by a xenotransplantation research team of Second Xiangya Hospital.Gene-edited Banna miniature pigs were selected as donors and rhesus monkeys with similar anatomical characteristics, physiology, biochemistry and immune mechanism to humans were selected as recipients for pig-monkey xenogeneic orthotopic LT.Based upon classic transplantation procedures, whole liver xenogeneic orthotopic transplantation was performed.Surgical processes were modified for minimizing intraoperative hemorrhage and shortening anhepatic period.A bile duct drainage tube was implanted for observing bile secretion.ATG + anti-CD20 + snake venom factor and FK-506 were utilized for immunoinduction pre-operation while tacrolimus, mycophenolate mofetil (MMF) and methyl prednisolone for postoperative immunomaintenance therapy.Antibiotics and antiviral agents were also applied and thrombin complex for improving coagulation functions.Results:All procedures were successfully completed.After the stability and maturity of our model, in case No.7, donor's acquisition operative duration was 42 min without heat ischemic time, donor's trimming time 87 min, donor cold retention time 128 min, recipient's operative duration 123 min and anhepatic phase 27 min.Subhepatic inferior vena cava was occluded for 38 min.Blood loss was around 10 ml.And 4/7 models survived post-operation and the longest survival time was 27 h. Among 3 non-survival cases, the causes were anesthesia accident (n=1) and immaturity of early operation (n=2). Model No.7 had a biliary secretion volume of 86 ml post-operation.Conclusions:Qualified donor acquisition, high-quality vascular anastomosis, intraoperative reduction of blood loss, shortening of anhepatic period, strict fluid replenishing and careful monitoring are essential for boosting the success rate of pig-monkey liver xenotransplantation model.Optimization of donor gene combination and advanced immunosuppression protocol help to further achieve the long-term survival of pig-monkey liver xenotransplantation model.

Metabolic-associated fatty liver disease (MAFLD) affects approximately a quarter of the global population. Identification of the key genes and pathways involved in hepatic lipid metabolism is of the utmost importance for the diagnosis, treatment, and prevention of MAFLD. In this study, differentially expressed genes were identified through whole-genome transcriptional analysis of liver tissue from MAFLD patients and healthy controls, and a series of lipid metabolism-related molecules and pathways were obtained through pathway analysis. Subsequently, we focused on Iroquois homeobox protein 3 ( IRX3 ), one of 13 transcription factors that were screened from the 331 differentially expressed genes. The transcription factor IRX3 was significantly decreased in the liver tissue of patients with MAFLD when compared with healthy controls. Pearson’s correlation analysis showed that the expression levels of IRX3 in liver tissue were negatively correlated with serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, and uric acid levels. The overexpression and interference of IRX3 induced the increased and decreased lipid droplet accumulation in vitro , respectively. Moreover, interference of IRX3 expression increased mitochondrial fragmentation and reduced the activity of the mitochondrial respiratory chain complex IV. In summary, the study demonstrated that IRX3 regulated hepatic lipid metabolism of MAFLD, and also revealed the effect of IRX3 on mitochondria might be an important mechanism by which IRX3 regulated hepatic lipid metabolism of MAFLD.

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder with abnormal lipid metabolism. The present study was to identify regulatory genes related to lipid droplets (LDs) abnormal accumulation in NAFLD. Methods transcriptomic analysis and bioinformatics analysis (GEO database) were used to identify potential genes in abnormal lipid metabolism of NAFLD. A candidate gene MAP3K4 expression were detected by immunohistochemistry staining in NAFLD and controls. RNA interference and immunoblotting were used to verify the roles of MAP3K4 in the formation of hepatic LDs. Results A total of 134 candidate genes were screened, including 44 up-regulated genes and 90 down-regulated genes. 29 genes in the protein–protein interaction (PPI) were selected as hub genes, including MAP3K4. The expression levels of MAP3K4 were positively correlated with NAFLD activity score (r = 0.702, p = 0.002). Furthermore, we found a positive correlation of MAP3K4 expression with serum total cholesterol (r = 0.564, p = 0.023), uric acid levels (r = 0.520, p = 0.039), and body mass index (r = 0.574, p = 0.020). Downregulation of MAP3K4 decreased LDs accumulation in HepG2 cells and reduced the expression of CGI-58 and Plin-2 by imbibition of JNK and group IVA cytosolic phospholipase A2 (cPLA2) activation. Conclusion The study revealed a number of regulatory genes related to hepatic lipid metabolism of NAFLD, and demonstrated that MAP3K4 played a pivotal role in the hepatic lipogenesis of NAFLD.

OBJECTIVES Hepatitis B virus-related acute-on-chronic liver failure remains a life-threatening syndrome, and transplant is the definitive treatment. Early allograft dysfunction is a postoperative complication and affects morbidity and mortality. We studied the risk factors associated with early allograft dysfunction in livertransplantrecipients with hepatitis B virus-related acute-on-chronic liver failure. MATERIALS AND METHODS This single-center retrospective study of early allograft dysfunction is based on data from January 2015 to June 2020 for 323 recipients with hepatitis B virus-related acute-on-chronic liver failure and 445 with only hepatitis B virus infection (control group). Data that correlated with early allograft dysfunction and outcome were analyzed. RESULTS Incidence of early allograft dysfunction in patients with hepatitis B virus-related acute-on-chronic liver failure was significantly higher versus the control group (39.3% vs 21.1%; P < .001). Transplant recipients with hepatitis B virus-related acute-onchronic liver failure who developed early allograft dysfunction had lower 90-day, 180-day, and 360-day patient survival rates versus patients with no early allograft dysfunction (89.0% vs 98.0%, 82.7% vs 97.5%, and 80.3% vs 96.4%, respectively; P < .001). Pretransplant kidney failure (odds ratio, 2.644; 95% CI, 1.019-6.864; P = .046), pretransplant coagulation failure (odds ratio, 2.162; 95% CI, 1.291-3.621; P = .003), and operative time (odds ratio, 1.005; 95% CI, 1.002-1.008; P = .003) were independent risk factors for early allograft dysfunction in liver transplant recipients with hepatitis B virus-related acute-onchronic liver failure. There was a synergistic effect of early allograft dysfunction and preoperative kidney/coagulation failure on survival rates of liver transplant recipients with hepatitis B virus-related acute-on-chronic liver failure. CONCLUSIONS Preoperative kidney/coagulation failure and operative time were independent risk factors of early allograft dysfunction in deceased donor liver transplant recipients with hepatitis B virus-related acute-on-chronic liver failure. The combination of early allograft dysfunction and preoperative kidney/coagulation failure was significantly associated with lower survival of these recipients.

Objectives . Factors prognostic of survival in liver transplant (LT) recipients with hepatitis B virus related acute-on-chronic liver failure (HBV-ACLF) remain unclear. This study evaluated risk factors for survival in LT recipients with HBV-ACLF and determined the scoring system optimal for assessing patient prognosis. Methods . This retrospective study included 323 HBV-ACLF related patients undergoing LT, including 112, 146, and 65 patients with HBV-ACLF grades 1, 2, and 3, respectively. Overall survival (OS) was estimated by the Kaplan–Meier method, and factors associated with survival were analysed by multivariate Cox proportional hazards models. Pretransplant prognostic scoring systems were compared by receiver operating characteristic (ROC) curve analysis. Results . The one-year survival rate was significantly lower in HBV-ACLF grade 3 (80.0%) than in grades 1 (93.8%) and 2 (91.8%) recipients ( p = 0.0063). Cox multivariate analysis showed that age >53 years (hazard ratio (HR) 3.731; 95% confidence interval (CI) 1.640–8.407), WBC count >8.6 × 10 9 /L (HR 4.544; 95% CI 1.140–18.107), HBV-ACLF 3 (HR 2.729; 95% CI 1.050–7.096), and cold ischaemia time >8.5 hours (HR 2.867; 95% CI, 1.38–5.921) were independently prognostic of 1-year survival. Comparisons of pretransplant scoring systems showed that chronic liver failure-consortium ACLF score (CLIF-C ACLFs) was superior to COSSH-ACLF, MELD-Na, and MELD scores in predicting 1-year OS in these patients. Conclusions . Age >53 years, WBC counts >8.6 × 10 9 /L, HBV-ACLF grade 3, and cold ischaemia time >8.5 hours are independently prognostic of OS in LT recipients with HBV-ACLF. CLIF-C ACLFs is superior to other scoring methods in predicting 1-year OS in these patients.

Recently, attentions have come to the alleviatory effect of protein inhibitor of activated STAT1 (PIAS1) in hepatic ischemia-reperfusion injury (HIRI), but the underlying molecular mechanistic actions remain largely unknown, which were illustrated in the present study. Microarray-based analysis predicted a possible regulatory mechanism involving the PIAS1/NFATc1/HDAC1/IRF-1/p38 MAPK signaling axis in HIRI. Then, growth dynamics of hypoxia/reoxygenation- (H/R-) exposed hepatocytes and liver injury of HIRI-like mice were delineated after the alteration of the PIAS1 expression. We validated that PIAS1 downregulation occurred in H/R-exposed hepatocytes and HIRI-like mice, while the expression of NFATc1, HDAC1, and IRF-1 and phosphorylation levels of p38 were increased. PIAS1 inactivated p38 MAPK signaling by inhibiting HDAC1-mediated IRF-1 through NFATc1 SUMOylation, thereby repressing the inflammatory response and apoptosis of hepatocytes in vitro, and alleviated liver injury in vivo. Collectively, the NFATc1/HDAC1/IRF-1/p38 MAPK signaling axis is highlighted as a promising therapeutic target for potentiating hepatoprotective effects of PIAS1 against HIRI.

Additional file 6: Table S6. Results of GO enrichment on differentially expressed genes from GSE159676 datasets.

Hepatic encephalopathy (HE) is a brain dysfunction associated with poor quality of life, increased morbidity and mortality. The pathogenesis of HE is still not fully clarified and effective therapeutic strategies are imperative. Among multiple factors that contribute to the pathophysiological process of HE, ammonia neurotoxicity is thought to be central in the pathogenesis of HE. Therefore, in this study, we subjected SH-SY5Y cells to ammonia insult and performed a pooled genome-wide CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 (CRISPR-associated protein 9) knockout screen to unveil the underlying molecular mechanisms of ammonia neurotoxicity and discover new potential therapeutic targets for HE. We found that EGLN3 (egl-9 family hypoxia-inducible factor 3) UCP3,GTPBP5, OR4D11 and SDR9C7 with 6 unique sgRNAs may contribute to protection against ammonia injury, while EGLN3 may be most related to ammonia resistance. We knocked down EGLN3 by transfecting neurons with specific shRNA lentivirus and confirmed that EGLN3 knockdown decreased ammonia-induced caspase-3 activation and apoptosis. We also demonstrated that EGLN3 knockdown ameliorated ammonia induced decreased expression of Bcl-2, increased expression of Bax and inhibited release of cytochrome c into the cytosol in neurons, suggesting that EGLN3 inhibition protected against ammonia induced apoptosis through mitochondrial dependent apoptosis pathway. Future therapeutic strategies regulating EGLN3 may be applied to the management of HE.

The lateral part of the bed nucleus of the stria terminalis (BSTL) is a component of the subpallial amygdala located near the ventral sulcus of the lateral ventricle, but its limits have not been well defined in birds. In this study, we analyzed the expression patterns of a number of neurochemical markers: GABA, calbindin (CB), calretinin (CR), or neuronal nitric oxide synthase (nNOS), in the embryonic and adult chicken brain, to further characterize the organization of the avian BSTL. From embryonic day 16, it was possible to distinguish three different regions within BSTL on the basis of cytoarchitectonic and immunohistochemical features. A central region, referred to as lateral bed nucleus of the stria terminalis pars densocellularis (BSTLdc), is characterized by numerous tightly packed cell bodies, most of which are GABA-immunoreactive (ir), and two peripheral regions with lower cellular density displaying a moderate GABA expression, referred to as lateral bed nucleus of the stria terminalis, plexiform part 1 (BSTLp1) and plexiform part 2 (BSTLp2), respectively. In contrast to BSTLdc, both plexiform parts are characterized by the presence of many fibers and terminals immunoreactive for nNOS and CR, as well as some CR-ir scattered cells. A distinctive feature of BSTLp2 is a population of CB-ir cells embedded in a slightly CB-ir neuropil. Comparison of our immunohistochemical data with gene expression data suggests that BSTLdc and BSTLp1 are pallidal in nature, whereas BSTLp2 receives important contributions from the entopeduncular/preoptic area.

Non-alcoholic fatty liver disease (NAFLD) is the highest incidence of chronic liver disease worldwide characterized by lipid accumulation in the liver. The full understanding of the lipogenesis of NAFLD is extreme importance. Here, whole-genome transcriptome analysis was performed on liver tissues of NAFLD patients and healthy controls to identify the differentially expressed genes and find new pathways and target genes related to the lipogenesis of NAFLD. Combined with the Gene Expression Omnibus (GEO) database, we found 86 overlapping genes, many of which are related to lipid metabolism of NAFLD. ECHDC1 is one of 86 overlapping genes, and its role in NAFLD has not been reported. The expression of ECHDC1 was significantly increased in liver tissue of patients with NAFLD than that of healthy controls, and oil Red O intensity was positively correlated with the expression levels of ECHDC1. Inhibition of ECHDC1 expression in HepG2 cells by RNAi significantly reduced intracellular lipid droplet number in vitro. In summary, this study analyzed pathogenic factors related to NAFLD at the whole-genome level and demonstrated that ECHDC1 may be involved in the occurrence and development of NAFLD by regulating hepatic lipid metabolism.

Additional file 4: Table S4. The top 20 significantly KEGG pathways of RNA-seq data.

目的 了解中南大学湘雅二医院临床医学硕士专业学位研究生(简称"专硕")科研能力培养的现状,探讨相应的策略.方法 采用网络调查的形式与自愿填写的原则对2020年12月至2021年2月中南大学湘雅二医院临床医学专硕进行了问卷调查,进行统计分析.结果 调查结果显示,79.69％(102/128)的专硕认为科研比较重要,59.38％(76/128)的专硕科研时间4～8 h/周,57.81％(74/128)的专硕文献阅读量4～8篇/月,42.97％(55/128)的专硕以第一作者身份发表了论文,7.03％(9/128)的专硕申报过课题,90.63％(116/128)的专硕认为科研培训课程缺乏并希望加强科研方面的培训,65.63％(84/128)的专硕希望医院和导师能提供更多的临床研究资源.结论 专硕的科研能力培养还有待进一步加强,需要完善培养标准、调动专硕的积极性、加强专硕导师队伍建设、优化专硕科研课程体系及增加临床科研资源,培养出具有过硬临床技能与科研能力的高水平医学人才.