BACKGROUND:The association between hepatitis B virus (HBV) exposure (anti-HBc+) and metabolic dysfunction-associated steatotic liver disease (MASLD) constitutes a critical public health dilemma. Emerging evidence reveals paradoxical epidemiological patterns, with observational studies demonstrating lower NAFLD/MAFLD prevalence among individuals with HBV exposure despite its hepatotropic nature-contradicting conventional pathophysiological frameworks. Under the 2023 AASLD criteria requiring concurrent cardiometabolic risk factors with hepatic steatosis for MASLD diagnosis, understanding HBV-MASLD interactions across diverse populations becomes imperative. Current evidence predominantly derives from Asian cohorts, leaving U.S. population-level associations underexplored. OBJECTIVE:To investigate the population-level HBV-MASLD association among U.S. adults using nationally representative data. METHODS:We analyzed 2017-2020 NHANES data (n=6,342 adults, representing 181.71 million residents) through complex survey-weighted analyses. MASLD required hepatic steatosis (controlled attenuation parameter ≥285 dB/m) plus ≥1 CMRF. HBV exposure was diagnosed as HBcAb (+). Weighted multivariable logistic regression adjusted for demographic and metabolic confounders (R 4.2.2 and FreeStatistics v1.9.2; two-tailed α=0.05). RESULTS:The retrospective cross-sectional study (mean age 51.1±17.4 years; 52.5% female) included 509 HBV-exposed individuals (8.03%) and 1,712 MASLD cases (26.99%). HBV-exposed individuals demonstrated: 1) lower MASLD prevalence (21.6% vs. 27.5%); 2) persistently inverse association after full adjustment (OR 0.57, 95% CI 0.40-0.81); 3) consistent patterns across subgroups without significant interactions by demographics (all P > 0.05). Sensitivity analyses in the complete-case subset (n=5,355) confirmed robustness (OR 0.58, 95% CI 0.40-0.85). CONCLUSIONS:This observational U.S. study identifies an inverse association between HBV exposure and MASLD, suggesting the need for further investigation into metabolic assessment in this population.

BACKGROUND:Hepatocellular ballooning degeneration distinguishes metabolic dysfunction-associated steatohepatitis (MASH) from metabolic dysfunction-associated steatotic liver (MASL), yet specific biomarkers are lacking. METHODS:The spatial transcriptomes of liver sections from human MASL and MASH patients and single-cell data were used to examine hepatocyte ballooning. AKR1B10 and CK8/18 expression in 20 human liver samples were analysed by H&E staining and immunofluorescence. Serum AKR1B10 levels were quantified in 284 patients with various liver aetiologies to assess its differential expression across liver disease types and its diagnostic performance. RESULTS:Spatial and single-cell transcriptomic analyses revealed significant AKR1B10 enrichment in the ballooned hepatocytes. The proportions of T cells and fibroblasts were significantly greater in ballooning regions than in steatotic regions. Immunostaining confirmed the localization of AKR1B10 in ballooning regions, along with the cytoplasm and cell membrane. This expression pattern was consistent with areas of cytokeratin CK8/18 loss; moreover, their combined application improved the ballooning diagnostic rate and accuracy. Serum AKR1B10 levels were markedly higher in patients with MASH than in individuals with other liver diseases (p < 0.01) and correlated with ballooning severity (R = 0.624). Ordinal logistic regression analysis indicated that the serum AKR1B10 level was strongly positively correlated with liver tissue ballooning severity (OR = 1.541 per unit, p = 0.003). The constructed model demonstrated significant discriminatory ability for identifying MASH patients with ballooning (AUC = 0.863). CONCLUSIONS:AKR1B10 is a potential diagnostic and therapeutic biomarker for hepatocyte ballooning in MASH patients with strong spatial specificity and clinical value for noninvasive diagnosis, disease stratification, and treatment monitoring.

Introduction Our goal was to explore the differences in clinical characteristics, including laboratory biochemical parameters, age, and sex, between overweight and nonoverweight children. Method In this study, 140 participants were 3- to 6-year-old children. Data were obtained from Chinese children at South China Normal University Affiliated Kindergarten from March 10 to 12, 2025. Weight, height, laboratory biochemical parameters, and liver elastography were measured. We divided the participants into 3 different groups according to their BMI, age, and sex. Results Compared with that in the nonoverweight group, HDL-C was significantly lower in the overweight group. The laboratory biochemical parameters TC, TG, and LDL-C were significantly greater in females than in males. The weight and height at baseline were significantly greater in the 5–6-year-old group than in the 3–4-year-old group, and HGB, GGT, TP, TC, and CREA were significantly greater in the laboratory biochemical parameters in the 5–6-year-old group than in the 3–4-year-old group. Conclusion We found that among preschool children aged 3-6 in Guangzhou, China, the prevalence of overweight was 22%, and the detection rate of NAFLD (assessed by CAP ≥225 dB/m) was 2.9%, and revealed significant differences in metabolic indicators and liver health parameters among children of different weight, sex, and age groups. In conclusion, this study emphasizes significant differences in metabolic indicators and liver health parameters during the preschool period and adopting targeted early health screening and prevention strategies addressing overweight, sex, and age-specific factors to curb the further development of childhood obesity and its related metabolic complications. Future research should incorporate longitudinal designs and expand the sample size to more comprehensively elucidate the dynamic developmental trajectory of liver and metabolic health in children.

Background:In view of the established role of endothelial dysfunction in the pathophysiology of chronic obstructive pulmonary disease (COPD), the Endothelial Activation and Stress Index (EASIX), a validated biomarker of endothelial injury, warrants investigation as a potential prognostic tool. We therefore investigated its association with outcomes in critically ill COPD patients. Methods:This retrospective cohort study analyzed data from critically ill patients with COPD in the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The exposure was log2(EASIX) (continuous or tertiles). The outcomes were 28‑, 60‑, and 90‑day all‑cause mortality. Cox regression was primarily used to assess the association, and multiple additional approaches were employed to verify its robustness. Results:A total of 1534 patients were included. Kaplan‑Meier survival curves showed significantly lower survival probabilities in higher EASIX tertiles (log‑rank p < 0.01 for all comparisons). Multivariable Cox regression confirmed that higher log2(EASIX) was independently associated with increased 28‑, 60‑, and 90‑day all‑cause mortality, with adjusted hazard ratios (HRs) of 1.87 (95% CI: 1.31-2.58), 1.83 (95% CI: 1.33-2.52), and 1.84 (95% CI: 1.36-2.50), respectively (all p < 0.01). Restricted cubic spline analysis indicated a linear relationship, and the association was robust across clinical subgroups. Sensitivity analyses in the fully imputed cohort confirmed linearity at 28 and 60 days but revealed a U‑shaped relationship at 90 days, with a nadir at log2(EASIX) = 0.56 (original EASIX = 1.47) and a HR of 0.74 (95% CI: 0.58-0.96). The E‑value of 2.96 (lower confidence bound 1.88) indicates robustness to unmeasured confounding. Conclusion:Higher EASIX is independently associated with 28-day and 60-day mortality in critically ill COPD patients, whereas the 90-day relationship appears more complex. These findings suggest that EASIX may aid early risk assessment, pending external validation.

Sepsis is a systemic inflammatory response that often leads to multiple-organ dysfunction, particularly intestinal injury, which worsens prognosis. This study aims to explore the effects of exosomes derived from mesenchymal stem cells (MSCs) on intestinal injury in sepsis and their underlying mechanisms. Bioinformatics analyses of sequencing data from mouse models of spesis and lipopolysaccharide-treated intestinal epithelial cells were conducted to identify candidate genes and pathways involved in intestinal damage. Human umbilical cord MSCs were isolated, and their exosomes were administered to mouse models of spesis. Various assays were conducted to evaluate the protective role of MSC-derived exosomes. The bioinformatics analyses revealed upregulation of miR-218-5p and downregulation of Chromobox homolog 8 (Cbx8) in mouse models of spesis. Experimental results showed that exosome treatment significantly reduced intestinal inflammation, necrosis, cytokine levels (e.g., IL-1β, IL-6), and apoptosis-related proteins (e.g., caspase-3, Bax). Exosomes also restored the miR-218-5p-Cbx8 axis, confirming the bioinformatics findings. Overall, this study highlights that MSCs-derived exosomes offer a promising therapeutic strategy for sepsis-induced intestinal injury by reducing inflammation and apoptosis while modulating the miR-218-5p-Cbx8 axis, demonstrating their potential application in sepsis and other inflammatory diseases.

Non‑alcoholic fatty liver disease (NAFLD) is characterized by excessive hepatic fat accumulation and is closely associated with inflammation and metabolic dysregulation. The C‑reactive protein–albumin–lymphocyte (CALLY) index, a composite marker of inflammation, immunity, and nutritional status, remains understudied in relation to NAFLD. A crosssectional analysis was conducted using data from 7,271 U.S. adults in NHANES 2017–2020. NAFLD was defined by vibrationcontrolled transient elastography with a controlled attenuation parameter (CAP) > 274 dB/m. Weighted logistic regression, restricted cubic spline (RCS) modeling, and twopiecewise logistic regression were applied to assess linear and nonlinear associations between the CALLY index and NAFLD prevalence. Subgroup and sensitivity analyses were performed to evaluate the consistency and robustness of the findings. The mean CALLY index was 8.08 (SD 12.42). Higher CALLY levels were inversely associated with NAFLD prevalence ( OR = 0.96; 95

Objective: To elucidate the regional distribution of metabolic dysfunction-associated steatohepatitis (MASH) fibrosis within the liver and to identify potential therapeutic targets for MASH fibrosis. Methods: Liver sections from healthy controls, patients with simple steatosis and MASH patients were analysed using spatial transcriptomics integrated with single-cell RNA-seq. Results: Spatial transcriptomics analysis of liver tissues revealed that the fibrotic region (Cluster 9) was primarily distributed in lobules, with some fibrosis also found in the surrounding area. Integration of the single-cell-sequencing data set (GSE189175) showed a greater proportion of inflammatory cells (Kupffer cells and T cells) and myofibroblasts in MASH. Six genes, showing high- or low-specific expression in Cluster 9, namely, ADAMTSL2, PTGDS, S100A6, PPP1R1A, ASS1 and G6PC, were identified in combination with pathology. The average expression levels of ADAMTSL2, PTGDS and S100A6 on the pathological HE staining map were positively correlated with the increase in the degree of fibrosis and aligned strongly with the distribution of fibrosis. ADAMTSL2+ myofibroblasts play a role in TNF signalling pathways and in the production of ECM structural components. Pseudotime analysis indicated that in the early stages of MASH, infiltration by T cells and Kupffer cells triggers a significant inflammatory response. Subsequently, this inflammation leads to the activation of hepatic stellate cells (HSCs), transforming them into myofibroblasts and promoting the development of liver fibrosis. Conclusion: This study is the first to characterise lineage-specific changes in gene expression, subpopulation composition, and pseudotime analysis in MASH fibrosis and reveals potential therapeutic targets for this condition.

BACKGROUND:Accompanied by the growing prevalence of nonalcoholic fatty liver disease (NAFLD), the coexistence of chronic hepatitis B (CHB) and NAFLD has increased. In the context of CHB, there is limited understanding of the factors that influence the development of NASH. METHODS:We enrolled CHB combined NAFLD patients who had liver biopsy and divided them to NASH vs. non-NASH groups. A whole transcriptome chip was used to examine the expression profiles of long noncoding RNAs (lncRNAs) and mRNA in biopsied liver tissues. The function analysis of HIGD1A were performed. We knocked down or overexpressed HIGD1A in HepG2.2.15 cells by transient transfection of siRNA-HIGD1A or pcDNA-HIGD1A. In vivo investigations were conducted using hepatitis B virus (HBV) transgenic mice. RESULTS:In 65 patients with CHB and NAFLD, 28 were patients with NASH, and 37 were those without NASH. After screening 582 differentially expressed mRNAs, GO analysis revealed differentially expressed mRNAs acting on nicotinamide adenine dinucleotide phosphate (NADPH), which influenced redox enzyme activity. KEGG analysis also shown that they were involved in the NAFLD signaling pathway. The function analysis revealed that HIGD1A was associated with the mitochondrion. Then, both in vivo and in vitro CHB model, HIGD1A was significantly higher in the NASH group than in the non-NASH group. HIGD1A knockdown impaired mitochondrial transmembrane potential and induced cell apoptosis in HepG2.2.15 cells added oleic acid and palmitate. On the contrary, hepatic HIGD1A overexpression ameliorated free fatty acids-induced apoptosis and oxidative stress. Furthermore, HIGD1A reduced reactive oxygen species (ROS) level by increasing glutathione (GSH) expression, but Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/Acetyl-CoA carboxylase (ACC) pathway was not involved. CONCLUSION:Both in vivo and in vitro CHB model, an upward trend of HIGD1A was observed in the NASH-related inflammatory response. HIGDIA played a protective role in cells against oxidative stress. Our data suggested that HIGD1A may be a positive regulator of NASH within the CHB context.

BackgroundTuberculosis (TB) persists as a global health challenge, with its treatment hampered by the side effects of long-term combination drug therapies and the growing issue of drug resistance. Therefore, the development of novel therapeutic strategies is critical. This study focuses on the role of immune checkpoint molecules (ICs) and functions of CD8+ T cells in the search for new potential targets against TB.MethodsWe conducted differential expression genes analysis and CD8+ T cell functional gene analysis on 92 TB samples and 61 healthy individual (HI) samples from TB database GSE83456, which contains data on 34,603 genes. The GSE54992 dataset was used to validated the findings. Additionally, a cluster analysis on single-cell data from primates infected with mycobacterium tuberculosis and those vaccinated with BCG was performed.ResultsThe overexpression of LAG-3 gene was found as a potentially important characteristic of both pulmonary TB (PTB) and extrapulmonary TB (EPTB). Further correlation analysis showed that LAG-3 gene was correlated with GZMB, perforin, IL-2 and IL-12. A significant temporal and spatial variation in LAG-3 expression was observed in T cells and macrophages during TB infection and after BCG vaccination.ConclusionLAG-3 was overexpressed in TB samples. Targeting LAG-3 may represent a potential therapeutic target for tuberculosis.

Introduction: The prevalence of non-alcoholic fatty liver disease (NAFLD) in non-lean patients is significantly increased, and obesity significantly increases the risk of cirrhosis and HCC in NAFLD patients. However, whether there is a difference in clinical manifestations of NAFLD between overweight and obesity remains unclear. The objective of this study was to assess the clinical and histological features of NAFLD among a non-lean population. Methods: Current study enrolled consecutive non-lean (body mass index [BMI] >23 kg/m2) patients with NAFLD and available liver biopsy results. Patients were stratified by BMI into two groups for the comparison of their clinical and histological variables, which included the overweight (BMI 23∼<28 kg/m2) and the obese (BMI ≥28 kg/m2). Risk factors for moderate to severe fibrosis (stage >1) were also analyzed through the logistic regression model. Results: Among 184 non-lean patients with metabolic-associated fatty liver disease enrolled, 65 and 119 were overweight and obese, respectively. Patients in the obesity group had a significantly lower level of gamma-glutamyl transpeptidase, higher levels of platelet, glucose, prothrombin time, and more common of moderate to severe inflammatory activity when compared to those in the overweight group. However, a significant low frequency of moderate to severe fibrosis was found in the obesity group versus the overweight group (19.33% vs. 40.00%, p = 0.002). Binary logistics regression analysis of fibrosis found that aspartate transaminase (AST), BMI, alanine transaminase (ALT), and cholesterol (CHOL) were independent predictors for moderate to severe fibrosis in non-lean patients with NAFLD. Compared with the traditional fibrosis-4 (AUC = 0.77) and aminotransferase to platelet ratio index (AUC = 0.79) indexes, the combined index based on AST, BMI, ALT, and CHOL was more accurate in predicting moderate to severe fibrosis in non-lean patients with NAFLD (AUC = 0.87). Conclusions: Clinical and histological features differed between obesity and overweight patients with NAFLD. When compared to the traditional serum markers, the combination index including AST, BMI, ALT, and CHOL provided a better model to predict moderate to severe fibrosis in non-lean patients with NAFLD.

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most prevalent chronic liver disorder worldwide, with liver fibrosis (LF) serving as a pivotal juncture in NAFLD progression. Natural products have demonstrated substantial antifibrotic properties, ushering in novel avenues for NAFLD treatment. This study provides a comprehensive review of the potential of natural products as antifibrotic agents, including flavonoids, polyphenol compounds, and terpenoids, with specific emphasis on the role of Baicalin in NAFLD-associated fibrosis. Mechanistically, these natural products have exhibited the capacity to target a multitude of signaling pathways, including Hedgehog, Wnt/β-catenin, TGF-β1, and NF-κB. Moreover, they can augment the activities of antioxidant enzymes, inhibit pro-fibrotic factors, and diminish fibrosis markers. In conclusion, this review underscores the considerable potential of natural products in addressing NAFLD-related liver fibrosis through multifaceted mechanisms. Nonetheless, it underscores the imperative need for further clinical investigation to authenticate their effectiveness, offering invaluable insights for future therapeutic advancements in this domain.

Immune checkpoint inhibitors (ICIs) are widely used to treat a variety of cancers and common infectious diseases with high efficacy. During the coronavirus disease 2019 (COVID-19) pandemic, studies suggested that COVID-19 patients may benefit from ICI immunotherapy. However, clinical studies on the safety and efficacy of ICI in COVID-19 patients are still being conducted. Currently, it is not clear whether cancer patients undergoing ICI immunotherapy should adjust their treatment strategy after infection with SARS-CoV-2 and whether ICI can reduce the viral load of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this study, reports of patients with different types of tumors infected with SARS-CoV-2 under ICI immunotherapy were classified and sorted, including lung cancer, melanoma, squamous cell carcinoma of the head and neck, and hematologic malignances. The safety and efficacy of ICI in antitumor and anti-SARS-CoV-2 therapies were compared and further discussed to provide more reference materials for the application of ICI treatment. In a word, COVID-19 has changed the ICI treatment strategy for cancer patients indeed, and ICI treatment may be a "double-edged sword" for cancer patients complicated with COVID-19.

Abstract Objective To assess the clinical and histological features of metabolic associated fatty liver disease (MAFLD) in non-lean population. Methods Current study enrolled consecutive non-lean (Body Mass Index (BMI) > 23 kg/m2) patients with MAFLD and available liver biopsy results. Patients were stratified by BMI into two groups for the comparison of their clinical and histological variables, which included the overweight (BMI 23 ~ < 28 kg/m2) and the obese (BMI ≥ 28 kg/m2). Risk factors for moderate to severe fibrosis (stage > 1) were also analysed through the logistic regression model. Results Among 184 non-lean patients with MALFD enrolled, 65 and 119 were overweight and obese, respectively. Patients in the obesity group had a significantly lower level of gamma-Glutamyl transpeptidase (GGT), higher levels of platelet (PLT), Glucose (Glu), prothrombin time (PT), and more common of moderate to severe inflammatory activity when compared to those in the overweight group. However, a significant low frequency of moderate to severe fibrosis was found in the obesity group vs the overweight group (19.33% vs 40.00%, P = 0.002). Multivariate logistic regression analysis of fibrosis found that aspartate transaminase (AST), BMI, alanine transaminase (ALT) and cholesterol (CHOL) were independent predictors for moderate to severe fibrosis in non-lean patients with MAFLD. Compared with the traditional FIB-4 (AUC = 0.77) and APRI (AUC = 0.79) indexes, the combined index based on AST, BMI, ALT and CHOL was more accurated in predicting moderate to severe fibrosis in non-lean patients with MAFLD (AUC = 0.87). Conclusions Clinical and histological features differed between obesity and overweight patients with MAFLD. When compared to the traditional serum markers, the combination index including AST, BMI, ALT and CHOL provides a better model to predictor moderate to severe fibrosis in non-lean patients with MAFLD.

目的:在新型冠状病毒肺炎(COVID-19)疫情爆发的早期阶段,通过优化氧疗资源的措施,使所有患者得到合适的氧疗,观察对患者病情的改善和预后的影响.方法:观察对象为COVID-19确诊患者,共有127例患者入组.以优化氧疗措施的实施日期为分界点,各取前后15 d内入院的患者(患者相对最多的时间段).将患者分为两组:(1)优化氧疗措施前入院的患者,这些患者无论轻重,主要通过中心供氧系统供氧,共52例;(2)优化氧疗措施后入院的患者,这些患者分为轻症、普通、重症和危重症患者,轻症患者予以中心供氧系统吸氧,普通患者予以家用制氧机吸氧,重症患者予以氧气筒吸氧,危重症患者予以机械通气,共75例.观察指标为生命体征、血常规和凝血功能、心脏、肝脏和肾脏功能等指标,同时观察对住院时间和死亡率的影响.结果:两组患者的基本临床资料比较无统计学的差异.优化氧疗措施后入院的患者生命体征得到改善,尤其是血氧饱和度(SpO2)明显好转(P<0.01).凝血功能紊乱减轻,表现为D-二聚体升高减轻(P<0.01).患者的炎症反应得到一定程度的抑制,表现为C反应蛋白(CRP)的降低(P<0.05).经过对年龄、性别和病情危重程度等危险因素的调整,优化氧疗后患者死亡率明显下降(P<0.01).结论:在COVID-19疫情大规模爆发期间,尽快使氧疗资源优化是重要的措施,使所有患者得到尽可能有效的氧疗,从而提高氧合而改善患者病情及其预后.

Background/aims: To identify the inflammatory damage caused by chronic hepatitis B (CHB) in patients of chronic hepatitis B virus (HBV) infection complicated with non-alcoholic fatty liver disease (NAFLD), then guiding clinicians to carry out antiviral treatment. Methods: According to the pathological features of liver biopsy, treatment-na?ve obese patients of chronic HBV infection complicated with NAFLD who had elevated alanine transaminase (ALT) were divided into CHB group and NASH group. Transcriptome chips were used to analyze the expression profiles of long non-coding RNA (lncRNA) and mRNA in liver puncture tissues from the two groups. The chip data of CHB and NASH groups were analyzed for differential expression analysis, gene function analysis, signal pathway analysis, target gene prediction and competing endogenous RNAs (ceRNA) network analysis. Results: By comparing CHB group with NASH group, a total of 44 differentially expressed lncRNAs and 567 differentially expressed mRNAs were screened. GO analysis predicted that the differentially expressed mRNAs may affect monooxygenase activity and oxidoreductase activity. KEGG analysis predicted that the differentially expressed mRNAs may be related to signaling pathways involved in oxidative phosphorylation, phagosomes, and NAFLD. Differential analysis of lncRNA shown that the expression of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) in CHB group was significantly upregulated. Subsequently, through target gene prediction and ceRNA network analysis, we found thioredoxin interacting protein (TXNIP), which was significantly upregulated in the CHB group and had a ceRNA relationship with MALAT1. It is predicted that there may be a ceRNA regulation relationship of MALAT1/hsa-miR- 20b-5p/TXNIP. Conclusion: The MALAT1/hsa-miR-20b-5p/TXNIP axis may mediate CHB-induced inflammatory damage in chronic HBV infection complicated with NAFLD, and the mechanism may be related to the activation of NLRP3 inflammatory bodies and downstream inflammatory responses.

目的:探索LINC00092在肝性脑病(HE)的发生发展中的作用机制.方法:从基因表达数据库(GEO)下载芯片GSE57193的数据,并使用R-limma包筛选出HE组和健康对照组中的差异表达基因,接着利用R-clusterProfiler包对差异表达基因进行京都基因和基因组百科全书(KEGG)分析.从miRcode数据库预测差异表达长链非编码RNA(LncRNA)靶向的miRNA,然后使用Targetscan、miRdb和miRTarBase预测miRNA靶向的mRNA,与差异表达mRNA取交集得到目标mRNA,Cytoscape用于构建lncRNA-miRNA-mRNA ceRNA网络.通过RNA结合蛋白数据库预测LINC00092的结合蛋白,根据表达的相关性和RNA结合蛋白,提出LINC00092在肝性脑病中的机制假说.结果:从正常脑组织中筛选出HE的9个特异的LncRNA和728个特异的mRNA,其中LINC00092相对健康对照组在HE中特异性高表达.差异表达基因的KEGG富集分析显示它们主要集中在脂肪酸降解、过氧化物酶体增殖物激活受体(PPAR)信号通路、矿物质的吸收、缬氨酸、亮氨酸和异亮氨酸的降解、β-丙氨酸新陈代谢、脂肪酸代谢通路上.结合ceRNA网络和LINC00092的结合蛋白,LINC00092在HE中可能存在3个调控路径:(1)LINC00092/hsa-miR206/GJA1轴介导谷氨酸的神经兴奋性毒性损伤;(2)LINC00092/hsa-miR184/LRRC8A轴介导星形胶质细胞的溶胀激活和ATP诱导的兴奋性氨基酸释放;(3)LINC00092-A2BP1轴介导的谷氨酸再摄取.结论:LINC00092在HE中特异性高表达,一方面通过半通道和体积调节阴离子通道介导谷氨酸的释放,同时使细胞内线粒体Ca2+超载而造成神经元功能障碍和细胞死亡,另一方面LINC00092-A2BP1轴介导的谷氨酸-谷氨酰胺循环障碍,导致谷氨酸的细胞外蓄积,两方面共同导致神经元的兴奋性毒性.

目的 分析初治慢性HBV感染者血清标志物(HBsAg、HBcAb)定量水平与其他指标的相关性,研究血清标志物的临床意义.方法 717例初治慢性HBV感染者根据HBeAg状态分为2组:HBeAg阳性与HBeAg阴性组.对2组患者的血常规、肝功能、HBV DNA、HBsAg定量、HBcAb定量等进行检测比较.结果 HBeAg阳性慢性HBV感染者血清HBsAg水平与HBV DNA呈中等相关(r=0.42,P<0.001);血清HBcAb水平与ALT(r=0.36,P<0.001)、AST(r=0.37,P<0.001)呈中等相关,当ALT>120 U/L,HBcAb水平不再随之升高.HBeAg阴性慢性HBV感染者血清HBsAg水平与HBV DNA(r=0.14,P=0.08)仅弱相关.HBeAg阴性者血清HBcAb水平ALT(r=0.37,P=0.01)、AST(r=0.39,P<0.001)呈中等相关,ALT高水平者(>120 U/L)HBcAb定量显著高于ALT低水平者(≤120 U/L).结论 初治HBeAg阳性慢性HBV感染者血清HBsAg水平与HBV DNA呈中等正相关,HBeAg阴性者血清HBsAg水平与HBV DNA呈弱相关.HBeAg阳性与阴性慢性HBV感染者血清HBcAb水平与ALT均呈正相关.

An epidemic caused by SARS-Coronavirus-2 (SARS-CoV-2) infection has appeared in Wuhan City in December 2019. The disease has shown a "clustering epidemic" pattern, and family-clustered onset has been the main characteristic. We collected data about 130 cases from 35 cluster-onset families (COFs) and 41 cases from 16 solitary-onset families (SOFs). The incidence of 2019 coronavirus disease (COVID-19) in COFs was significantly higher than that of SOFs. Our study also showed that patients with exposure to high-risk factors (respiratory droplets and close contact), advanced age, and comorbidities were more likely to develop COVID-19 in the COFs. In addition, advanced age and elevated neutrophil/lymphocyte ratio (NLR) were risk factors for death in patients with SARS-CoV-2 infection in the COFs.