目的 分析长链非编码RNA LINC02038的表达与子宫内膜癌发生、发展的关联性,并探讨其潜在的生物学调控机制,为子宫内膜癌的精准诊治提供科学线索。方法 采用荧光定量PCR技术检测LINC02038 在2019年—2020年期间于我院收集的42例子宫内膜癌标本及相应癌旁正常组织中的表达差异。构建LINC02038过表达载体并转染子宫内膜癌Ishikawa 细胞系,通过CCK-8、Transwell等功能实验验证其对肿瘤细胞增殖、侵袭能力的影响。利用TCGA公共数据库分析LINC02038与子宫内膜癌预后的相关性,并通过基因本体论（GO）、京都基因组百科全书（KEGG）及基因集富集分析（GSEA）等生物信息学方法预测其潜在的下游调控机制。结果 LINC02038在子宫内膜癌组织中的表达高于癌旁正常组织（P<0.001）。过表达LINC02038可促进子宫内膜癌细胞Ishikawa的增殖和迁移。生物信息学分析提示LINC02038可能通过调控细胞分化、激素分泌、细胞外基质重塑等过程,激活NF-κB、细胞外基质受体等信号通路影响子宫内膜癌的发生。结论 LINC02038的异常表达与子宫内膜癌的发生、发展相关联,可作为评估子宫内膜癌发病风险的候选生物标志物。

Objective To analyze the expression of long non-coding RNA LINC02038 and its relationship with the occurrence and development of endometrial carcinoma（EC）,explore its potential biological mechanisms,and provide potential biomarkers for targeted therapy of EC．Methods Quantitative real-time PCR was used to detect the expression levels of LINC02038 in 42 EC tissues and their adjacent tissues．The LINC02038 overexpressin vector was constructed and transfected into EC Ishikawa cells．CCK-8,Transwell migration and invasion assays were performed to examine the effects of LINC02038 overexpression on cancer cell proliferation,migration and invasion．Public TCGA data were analyzed to investigate the associations between LINC02038 and EC pathogenesis and prognosis．GO,KEGG and GSEA enrichment analyses were conducted to elucidate the potential biological mechanisms of LINC02038．Results LINC02038 expression was significantly upregulated in EC tissues compared to adjacent non-tumor tissues（P<0.001）．Overexpression of LINC02038 markedly promoted the proliferation and migration of Ishikawa cells．Bioinformatics analysis suggested that LINC02038 may participate in regulating cell differentiation,hormone secretion,extracellular matrix remodeling and other processes,as well as activating NF-κB,extracellular matrix receptor and other signaling pathways involved in endometrial carcinogenesis．Conclusions The aberrant expression of LINC02038 is associated with EC occurrence and may serve as a potential biomarker for assessing the risk of this cancer．

腺苷至肌苷RNA编辑（AIRE）是指转录前体RNA在腺苷酸脱氨酶的作用下,某些位点的腺苷发生脱氨反应转变成肌苷的过程,在碱基配对时,肌苷被识别作鸟苷,导致转录组重编写。随着高通量测序技术的不断进步,大量异常的AIRE被发现可导致氨基酸编码改变、RNA剪切异常以及microRNA-mRNA重定向等过程,从而参与肿瘤的发生发展。绝大部分的AIRE位点均位于基因非编码区,解析它们的生物学功能仍存在一定的挑战。本综述旨在描述AIRE的生物学机制和AIRE位点在不同肿瘤发生发展作用的进展,为AIRE与肿瘤的研究提供思路。

Adenosine-to-inosine RNA editing（AIRE）is catalysed by adenosine deaminases acting on RNA（ADARs）,which converts adenosine to inosine in nascent RNA．Since inosine is recognized as guanosine in post-transcriptional process,AIRE is functionally approximate to an A-to-G mutation and results in transcriptome recoding．With the continuous advancement of high-throughput sequencing technology,a large number of abnormal AIRE events have been found to exert different biological mechanisms such as amino acid changes,RNA splicing abnormalities and microRNA-mRNA redirection,which plays an important role in the development of human tumorigenesis．Most of AIRE sites are located in non-coding region,which brings challenges in analyzing their biological functions．This review aims to describe the biological mechanisms of AIRE and the relationship between AIRE sites and the development of different tumor types,providing ideas for the study of AIRE and tumors．

目的 通过多种生物信息学方法分析MAML1在GC患者中的表达及与临床特征、预后和免疫治疗疗效的相关性。方法 利用TCGA数据库分析胃癌组织与正常胃黏膜组织中的MAML1表达水平;Kaplan-Meier在线工具对胃癌数据集GSE15459进行分析,阐明MAML1与患者临床特征及分期、治疗疗效的相关性;STRING软件预测与MAML1表达相关的基因,并用FUNRICH软件评估其富集的分子生物学功能和信号通路;TIMER和GEPIA数据库探索MAML1表达水平与肿瘤浸润免疫细胞及其相应基因标记集之间的关系。结果 MAML1在GC组织中的表达水平高于正常组织(P<0.001),且其表达水平与III期、有淋巴结转移、无远处转移的患者生存期相关(P<0.05),而与I、II和IV期、无淋巴结转移和有远处转移的患者生存期无相关性(P>0.05)。MAML1的相关作用基因主要分布在细胞核、参与转录调控,并且主要富集在雄激素受体、C-MYB转录因子和HIF-2α转录调控等相关的信号通路。MAML1表达水平与B细胞、CD4⁺ T细胞、巨噬细胞的表达水平存在正相关关系(P<0.05),但与肿瘤纯度、CD8⁺ T细胞、中性粒细胞、树突状细胞无相关性(P>0.05)。结论 MAML1有可能成为GC患者较差的临床预后标志物之一,其潜在分子机制可能与转录调控调节肿瘤微环境有关。

Objective To investigate the expression of MAML1 and its relationship with clinical characteristics, prognosis and the efficiency of immunotherapy in patients with GC. Methods MAML1 expression profile was observed by TCGA database. Kaplan-Meier survival analysis was applied to evaluate the correlation between the expression of MAML1 and clinical characteristics, prognosis and treatment efficiency of patients in GSE15459 dataset. MAML1-associated genes were predicted by STRING and were enriched in GO and KEGG by FUNRICH software. The relationship between MAML1 expression and markers of tumor infiltrated cells were explored by TIMER and GEPIA database. Results MAML1 was abnormally upregulated in GC tissues compared to normal gastric tissues (P<0.001). MAML1 expression was significantly associated with the overall survival of patients in stage III, with lymph node metastasis and without distant metastasis (P<0.001). There was no significant difference between MAML1 expression and the overall survival of patients in stage I, II, IV, without lymph node metastasis and with distant metastasis (P>0.05). MAML1-assoicated genes were mainly located at the nucleus, mediating transcriptional regulation and mainly enriching in androgen receptor, C-MYB transcription factor and HIF-2α transcription regulation and other related signaling pathways. MAML1 expression was positively related with the expression of B cell, CD4⁺ T cell and macrophages (P<0.05), but without significant difference with tumor purity, CD8⁺ T cell, neutrophils and dendritic cells (P>0.05). Conclusions MAML1 could be used as a marker of clinical prognosis of patients with GC. The potential molecular mechanism might be associated with its function in transcriptional regulation and changes in tumor microenvironment.

帕金森病（PD）是一种常见的与年龄相关的神经退行性疾病,其特点是黑质致密部内多巴胺能神经元的进行性丢失以及路易小体的积累。多巴胺能神经元的退化导致纹状体的多巴胺水平降低,最终出现静息性震颤、运动迟缓、肌肉僵硬和姿势不稳等运动症状,以及认知能力下降、嗅觉功能受损、精神异常和睡眠障碍等非运动症状。由于人口结构转变和全球老龄化,PD的不断增加对患者、家庭和社会构成重大负担。尽管广泛的研究已阐明了PD的病因学和潜在机制,但现有治疗主要集中在症状管理,无法阻止疾病的进展。小胶质细胞作为脑内重要的免疫细胞,对维持中枢神经系统的稳态具有关键作用。本文综述了PD研究,包括其病因学因素、分子机制和现有治疗策略。此外,审视了在PD样模型中涉及小胶质细胞的研究,深入探讨了小胶质细胞在疾病进展中的动态,并探究了小胶质细胞在促进或减轻疾病进展方面所扮演的错综角色。通过这样的探讨,本综述旨在为PD复杂的发病机制提供新的洞见和观点,激发出针对性治疗干预的创新思路。

Parkinson's disease（PD）,a prevalent age-related neurodegenerative disorder,is characterized by the progressive loss of dopaminergic neurons within the substantia nigra compacta（SNc）and the accumulation of Lewy bodies．The degeneration of dopaminergic neurons leads to diminished striatal dopamine levels,culminating in motor symptoms such as resting tremors,bradykinesia,muscle rigidity and postural instability,alongside non-motor manifestations encompassing cognitive decline,impaired olfactory function,psychological abnormalities and sleep disturbances．The escalating incidence of PD due to shifting demographics and global aging poses substantial burdens on patients,families and society．Although extensive research has elucidated the etiology and underlying mechanisms of PD,available treatments largely focus on symptom management and lack the capacity to halt disease progression．Microglia,as integral immune cells within the brain,wield pivotal influence over central nervous system homeostasis．This review presents a comprehensive synthesis of PD,encompassing its etiological factors,molecular mechanisms,and existing therapeutic strategies．Furthermore,we scrutinized research involving microglia in PD-like models,delving into the dynamics of microglia in disease progression and probing into the intricate roles that microglia assume in either fostering or mitigating disease advancement．By doing so,this review aims to furnish novel insights and perspectives that shed light on the intricate pathogenesis of PD,potentially sparking innovative concepts for targeted therapeutic interventions．

目的 通过生物信息分析途径,从分子水平揭示非酒精性脂肪性肝病（NAFLD）的发病发展机制,为NAFLD研究提供新的思路。方法 从公共数据库GEO中下载NAFLD相关的基因芯片数据GSE48452,利用Transcriptome Analysis Console软件筛选差异表达基因,FunRich软件和STRING在线分析工具对差异基因进行下一步的生物信息学分析。结果 正常组与NAFLD组差异基因52个,正常组与非酒精性脂肪性肝炎（NASH）基因64个,共同差异基因15个。这些差异表达基因参与脂质转运、胆汁酸合成、脂质和脂蛋白代谢、生物氧化等过程。通过通路分析及蛋白质相互作用分析进一步筛选出与NAFLD发病发展密切相关的18个差异表达基因。结论 通过生物信息学分析筛选出MSN、CDC45、ANXA5、PIK3CG和DTL基因可能为研究乃至阻断NAFLD发展进程的重要靶点,需进一步验证。

Objective To explore the molecular mechanism of nonalcoholic fatty liver disease （NAFLD） with bioinformatics analysis. Methods The microarray data of NAFLD were downloaded from the Gene Expression Omnibus （GEO） database and analyzed using Transcriptome Analysis Console （TAC） for screening differentially expressed genes. The further analysis of differentially expressed genes was conducted by FunRich software and the online tool STRING. Results For the comparison of control group vs. NAFLD group,52 genes have differentially expressed,while control groups vs. nonalcoholic steatohepatitis （NASH） group,64 genes have differentially expressed. 15 differentially expressed genes were found in both comparisons. These genes were involved in the biological pathway of lipid transport,bile acid biosynthesis,metabolism of lipids and lipoproteins and biological oxidations. With biological pathway analysis and protein-protein interaction analysis,18 differentially expressed genes were found closely associated with the progression of NAFLD. Conclusion MSN、CDC45、ANXA5、PIK3CG and DTL may be the important target for study the progression of NAFLD,which needs a further study to confirm.