The global population is aging at an unprecedented rate, significantly increasing the burden of age-related liver diseases. While the mechanisms of liver aging remain incompletely understood, immune senescence within the hepatic microenvironment has emerged as a pivotal, yet underexplored, contributing factor. With advancing age, the liver undergoes profound remodeling of its immune landscape, encompassing dysfunction in both innate and adaptive immunity. This immunosenescence heightens susceptibility to infectious liver diseases, accelerates the progression of metabolic liver conditions, increases the risk of drug-induced liver injury (DILI), and promotes hepatocellular carcinoma (HCC) through compromised immune surveillance. In conclusion, aging-driven reorganization of the hepatic immune microenvironment elevates disease risk and undermines treatment efficacy. Targeting these age-related immune alterations therefore represents a promising therapeutic strategy for improving liver health in the elderly.

Background/AimsAcute-on-chronic liver failure (ACLF) is associated with high short-term mortality, and early prediction is critical to reduce the deaths of ACLF patients. To date, however, the prognostic accuracy of current models for ACLF is unsatisfactory, particularly, in patients with hepatitis B virus (HBV) infection. This study aims to develop novel prognostic models based on the dynamic changes in variables to predict the short-term mortality of HBV-associated ACLF (HBV-ACLF).MethodsA retrospective cohort study was conducted, with the population comprised in whom ACLF was confirmed.319 patients were enrolled and their clinical data were collected on Days 1 and 7 following hospital admission. Univariate and multivariate analyses were performed to identify risk factors for 28 and 90-day mortality. The dynamic alterations in the risk factors were further analyzed, and Days 1 and 7 prognostic models were constructed. Receiver operating characteristic (ROC) analysis were used to identify and compared the predictors of prognosis among our model.ResultsUnivariate and multivariate analyses revealed significant risk factors at Days 1 and 7, which when combined with the clinically important parameters, were used to establish the Days 1 and 7 prognostic models. For 28-day mortality, the predictive accuracy of the Day 1 prognostic model was significantly higher than that of the albumin-bilirubin (ALBI) model. For 90-day mortality, the predictive accuracy of the Days 1 and 7 prognostic models was significantly higher than that of the Model of End-Stage Liver Disease (MELD), MELD-sodium (MELD-Na), and ALBI prognostic models.ConclusionsThe prognostic models established in this study were superior to the existing prognostic scoring systems to accurately predict short-term mortality, and therefore, could be potential novel prognostic tools for HBV-ACLF.

The characteristics of HBV-positive HCC patients in the prognostic analysis

Locations of APOBEC-signature HBV mutations in the preS and the enhancer II/basal core promoter/precure regions

Effects of APOBEC3B and UNG expression on the prognosis of HCC patients in different cohorts

Study design for the stratification analyses

Characteristics of HBV-infected participants with/without successfully sequenced HBV regions

Characteristics of participants in the case-control study

Associations of APOBEC3 and UNG polymorphisms with the risk of HCC in genotype C and B HBV-infected patients

Demographic characteristics of hepatocellular carcinoma patients in LIHC and GSE14520 cohort

Primers for the genotyping of APOBEC3 and UNG genetic polymorphisms, PCR, and quantitative RT-PCR

The locations and linkage disequilibrium of APOBEC3B single nucleotide polymorphisms

Multivariate Cox regression analysis for the disease specific survival of patients with HCC

Supplementary methods and figure legends for supplementary figures

Objective: To investigate and establish the related factors of non-invasive score model for prediction of non-alcoholic fatty liver disease in chronic hepatitis B patients with normal or mildly elevated alanine aminotransferase (ALT). Methods: A total of 128 cases with chronic hepatitis B who had undergone liver biopsy were included. According to the presence or absence of hepatocyte steatosis on the pathological results of liver biopsy, they were divided into a fatty infiltration and a non-fatty infiltration group. Patients' demographic characteristics, laboratory test indexes, and pathological test results were collected. Univariate and multivariate logistic regression analysis combined with clinical screening variables were used to establish a predictive model. The prediction efficiency of the new model was evaluated by the receiver operating curve, and the difference between the accuracy of the new model and ultrasound in the diagnosis of fatty liver was compared by Delong's-test. Result: Multivariate regression analysis showed that serum triglyceride, serum uric acid and platelets were highly correlated with intrahepatic steatosis (P<0.05). The regression equation triglyceride-uric acid-platelet (TUP)-1=-8.195+0.011×uric acid+1.439×triglyceride+0.012×platelet count was established by combining the above variables. Tthe equation TUP-2=-7.527+0.010×uric acid+1.309×triglyceride+0.012×platelet count+1.397×fatty liver (ultrasound) was established (yes=1; no=0) after incorporating the results of abdominal ultrasound. The diagnostic value of TUP-1 and TUP-2 models for fatty liver was better than that of ultrasound alone and there was no statistically significant difference in diagnostic value between TUP-1 and TUP-2 models (Z=1.453, P=0.146). Conclusion: Compared with abdominal ultrasonography alone, the new model is more effective in diagnosing fatty liver and has good application value.

Objective:To analyze the risk factors for the progression of acute kidney injury (AKI) in decompensated cirrhosis patients with acute kidney injury.Methods:The basic data and laboratory results of decompensated cirrhosis patients with AKI hospitalized in the Department of Infectious Diseases, The First Affiliated Hospital of Naval Medical University from May 2016 to November 2021 were collected. Treatment and intervention were performed according to the International Club of Ascites guidelines. According to the outcome of AKI during hospitalization, patients were divided into the progression group and the non-progression group. Two independent sample rank sum test, two independent sample or approximate t test, chi-square test and binary logistic regression analysis were used for statistical analysis. Results:A total of 263 decompensated cirrhosis AKI patients were enrolled, including 50 in the progressive group and 213 in the non-progressive group. Univariate analysis showed that there were statistically significant differences in baseline total bilirubin, alanine aminotransferase, prothrombin time, serum sodium, white blood cell count, model for end-stage liver disease score, proportion of patients with infection, proportion of patients with upper gastrointestinal hemorrhage, and proportion of patients with primary AKI stage between the two groups ( Z=-6.49, -3.53, t=-3.06, 3.40, -3.55, -8.19 and χ2=14.64, 8.40, 103.98, respectively, all P<0.050). Binary logistic regression analysis showed that primary AKI stage (stage two odds ratio ( OR)=33.176, 95% confidence interval ( CI) 11.294 to 97.458, P<0.001; stage three OR=114.139, 95% CI 25.321 to 514.515, P<0.001), upper gastrointestinal hemorrhage ( OR=3.850, 95% CI 1.238 to 11.971, P=0.020) and total bilirubin ( OR=1.009, 95% CI 1.005 to 1.012, P<0.001) were the risk factors for the progression of AKI in patients with decompensated cirrhosis. Conclusions:Decompensated cirrhosis patients with AKI stage two or three, high baseline total bilirubin value or gastrointestinal hemorrhage have a high risk of AKI progression. It is necessary to strengthen the assessment and take targeted intervention measures at early stage in the clinical practice.

肝细胞癌的早期诊断和有效治疗对提高生存率和改善预后至关重要.甲胎蛋白是目前应用最广的诊断肝细胞癌的生物学标志物,但临床中发现甲胎蛋白易受一些非肝细胞癌疾病的影响[1],对于早期肝细胞癌和小肝细胞癌,其诊断能力较低,并且有30％～40％的肝细胞癌患者甲胎蛋白阴性或低于临界值,为了弥补甲胎蛋白的缺点,提高诊断的敏感性和特异度,国内外学者对甲胎蛋白阴性肝细胞癌患者早期筛查和诊断进行了大量的研究,本文对有望用于甲胎蛋白阴性肝细胞癌患者早期辅助诊断的生物学标志物做一综述.

不同微生物空间结构承其相应的生长繁殖、释放毒素、感染机体等病理生理机制.教材中的微生物结构、作用机制及感染人体过程等内容通常以文字描述和简易二维图示的固定形式呈现.学员只能凭借想象建立微生物形态及作用人体的过程.目前,国内外有些课堂采用具体的3D打印实物模型进行讲解,但受到时间及空间的制约,无法模拟微生物活动的动态过程,更无法让学员线下自学.近年来,随着科技的高速发展,互联网技术已经在各行各业中发挥着重要的作用.为了更好的开展微生物教学,笔者探索性的对传统的教学方法和手段进行改革,笔者将互联网三维仿真模型与课堂相结合,通过常见的肠道微生物为切入点,建立可视化程度较高的数字化三维肠道微生物模型及其作用于人体的动效过程插入学员课堂教学教案中.结合病例分析、临床事件探讨以及如何诊治等教学节点,创建一个打破空间和时间限制的互动性较好的教学平台,以改善教学质量,帮助学员积极思考,增强学习兴趣.

目的 了解新型冠状病毒肺炎(COVID-19)疫情期间军校医学生的健康意识、职业意识及心理健康情况.方法 2020年2月17日至2月20日,采用电子问卷调查的方法对COVID-19疫情期间某军校医学生对隔离与延迟开学的态度及应对方式、对网络授课的态度、卫生防护意识、职业意识等进行调查,并采用90项症状自评量表(SCL-90)对其心理健康状况进行评分.结果 共收到有效调查数据2736份.COVID-19疫情期间学生对隔离、延迟开学措施基本表示理解和赞成,70.83％(1938/2736)的学生支持网络授课.隔离期间85.31％(2334/2736)的学生选择听音乐、看剧作为放松方式,64.69％(1770/2736)的学生坚持学习/看文献/写论文.学生基本做到了勤洗手和戴口罩,卫生防护意识较疫情前提升.疫情期间军校医学生普遍能坚定自己的职业信念和决心,不少学生希望投身抗击疫情行动.调查发现12.94％(354/2736)的学生出现SCL-90因子阳性,在各因子中排名前3位的分别为强迫症状(78.53％,278/354)、人际关系敏感(64.12％,227/354)、抑郁(44.07％,156/354).结论 军校医学生能普遍适应COVID-19疫情时期的困难环境,并提升自我.疫情期间军校医学生的心理健康问题有其自身特点,应给予关注,同时还要加强医学生的人文素质教育.

目的 探讨免疫抑制剂或化疗药物治疗后HBsAg阳性或抗-HBc阳性人群发生HBV再激活(hepatitis B virus reactivation,HBVr)的危险因素.方法 回顾性分析2010年1月至2017年1月上海市长海医院HBsAg阳性或HBsAg阴性而抗-HBc阳性238例患者的临床资料,接受免疫抑制剂治疗后,根据随访结果分为发生HBVr组与未发生HBVr组,分析HBVr发生的危险因素.结果 238例患者中,发生HBVr的患者为33例(13.87％).logistic回归模型提示:有无抗病毒治疗(OR=0.022,95％CI:0.001～0.34),HBV DNA基线水平(OR=15.352,95％CI:3.809～86.160),化疗方案(OR=0.361,95％CI:0.068～1.929),为发生HBVr的独立危险因素.根据变量筛选的结果,建立了预判HBVr风险的回归方程:-4.78×抗病毒干预(有=1,无=0)+2.731×HBV DNA(≥104=1,<104=0)+3.272×化疗方案(A=3,B=2,C=1)+3.355,以及相应的评分系统.结论 HBVr的发生与有无抗病毒治疗、HBV DNA基线水平以及化疗方案的选择等因素有关,建立模型有助于对HBVr进行预测.