2025年 · 第138卷第13期

出版日期 2025-07-05电子版￥0.00元

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Editorial

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肠道微生物群：脓毒症治疗的新靶点

Weifeng Shang, Sheng Zhang, Lechen Yang, Jiao Liu, Dechang Chen

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003630

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急性呼吸窘迫综合征：反思与研究重点

Hui Chen, Haibo Qiu

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003643

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脓毒症的免疫监测：当前和未来问题

Hui Zhang, Fenghua Yao, Yongming Yao

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003657

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心脏移植的全球挑战与发展：武汉方案开发与临床实施

Yixuan Wang, Fei Li, Weihua Qiao, Jing Zhang, Nianguo Dong

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003715

摘要

Consensus Statement

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中欧关于子宫副空化畸形的共识

Lan Zhu, Zichen Zhao, Attilio Di Spiezio Sardo, Maribel Acién, Joel Naftalin, Thierry Van den Bosch, Charleen Sze-yan Cheung, Dabao Xu, Xiaowu Huang, Grigoris Grimbizis

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003717

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Review Article

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CAR NK细胞在结直肠癌中的工程和靶向潜力

Muhammad Babar Khawar, Ali Afzal, Shuangshuang Dong, Yue Si, Haibo Sun

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003346

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癌症与神经递质受体

Xiaoqiang Wang, Muyan Shi, Jie Tian, Weifeng Yu

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003656

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肺癌在线自适应放疗的关键技术与挑战

Baiqiang Dong, Shuohan Zheng, Kelly Chen, Xuan Zhu, Sijuan Huang, Xiaobo Jiang, Wenchao Diao, Hua Li, Lecheng Jia, Feng Chi 等

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003299

摘要

Meta Analysis

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对于单室骨关节炎，单室膝关节置换术比全膝关节置换术是更好的选择吗？随机对照试验的系统综述和荟萃分析

Kuanyu Xia, Lang Min, Wenqing Xie, Guang Yang, Dong Keon Yon, Seung Won Lee, Ai Koyanagi, Louis Jacob, Lee Smith, Jae Il Shin 等

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003193

摘要

Background: The choice of unicompartmental knee arthroplasty (UKA) vs. total knee arthroplasty (TKA) in the surgical treatment of knee osteoarthritis (KOA) remains controversial. This study aimed to perform a systematic review and meta-analysis of randomized controlled trials (RCTs) to compare the clinical results of UKA and TKA for treating unicompartmental KOA. Methods: PubMed, Embase, and the Cochrane Library were systematically searched for articles published up to January 2, 2023. The literature was rigorously screened to include only RCTs comparing UKA and TKA for unicompartmental KOA. A systematic review and meta-analysis were performed to calculate the mean difference (MD), relative risk (RR), and 95% confidence interval (CI) according to the Cochrane standards. Results: Thirteen publications involving 683 UKAs and 683 TKAs were analyzed. Except for one study with a follow-up period of 15 years, all outcome measures reported were within 5 years of follow-up. Meta-analysis showed better knee recovery (MD: 1.23; 95% CI: 1.01–1.45; P <0.001), greater knee function (MD: 1.78; 95% CI: 0.34–3.22; P = 0.020), less pain (MD: 0.75; 95% CI: 0.43–1.06; P <0.001), and better health status (MD: 3.75; 95% CI: 0.81–6.69; P = 0.010) after UKA than TKA. However, considering the minimal clinically important difference values for these variables, the findings were not clinically relevant. Moreover, UKA patients had fewer complications (RR: 0.59; 95% CI: 0.45–0.78; P <0.001) and shorter hospital stays (MD: –0.89; 95% CI: –1.57 to –0.22; P = 0.009) than did TKA patients. There were no statistically significant differences in terms of postoperative range of movement, revision, failure, operation time, and patient satisfaction. Conclusions: In terms of clinical efficacy, there was no obvious advantage of UKA over TKA in the surgical treatment of knee OA when considering the minimal clinically important difference. The main advantage of UKA over TKA is that it leads to fewer complications and a shorter length of hospital stay. It is ideal to perform prospective studies with longer follow-up periods to fully evaluate the long-term efficacy and safety of the two procedures in the future.

Original Article

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严重缺血性卒中的临床病程、恶化原因和预后：一项前瞻性多中心队列研究

Simiao Wu, Yanan Wang, Ruozhen Yuan, Meng Liu, Xing Hua, Linrui Huang, Fuqiang Guo, Dongdong Yang, Zuoxiao Li, Bihua Wu 等

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003556

摘要

Background: Severe stroke has high rates of mortality and morbidity. This study aimed to investigate the clinical course, causes of worsening, and outcomes of severe ischemic stroke. Methods: This prospective, multicenter cohort study enrolled adult patients admitted ≤30 days after ischemic stroke from nine hospitals in China between September 2017 and December 2019. Severe stroke was defined as a score of ≥15 on the National Institutes of Health Stroke Scale (NIHSS). Clinical worsening was defined as an increase of 4 in the NIHSS score from baseline. Unfavorable functional outcome was defined as a modified Rankin scale score ≥3 at 3 months and 1 year after stroke onset, respectively. We performed Logistic regression to explore baseline features and reperfusion therapies associated with clinical worsening and functional outcomes. Results: Among 4201 patients enrolled, 854 patients (20.33%) had severe stroke on admission. Of 3347 patients without severe stroke on admission, 142 (4.24%) patients developed severe stroke in hospital. Of 854 patients with severe stroke on admission, 33.95% (290/854) experienced clinical worsening (median time from stroke onset: 43 h, Q1–Q3: 20–88 h), with brain edema (54.83% [159/290]) as the leading cause; 24.59% (210/854) of these patients died by 30 days, and 81.47% (677/831) and 78.44% (633/807) had unfavorable functional outcomes at 3 months and 1 year respectively. Reperfusion reduced the risk of worsening (adjusted odds ratio [OR]: 0.24, 95% confidence interval [CI]: 0.12–0.49, P <0.01), 30-day death (adjusted OR: 0.22, 95% CI: 0.11–0.41, P <0.01), and unfavorable functional outcomes at 3 months (adjusted OR: 0.24, 95% CI: 0.08–0.68, P <0.01) and 1 year (adjusted OR: 0.17, 95% CI: 0.06–0.50, P <0.01). Conclusions: Approximately one-fifth of patients with ischemic stroke had severe neurological deficits on admission. Clinical worsening mainly occurred in the first 3 to 4 days after stroke onset, with brain edema as the leading cause of worsening. Reperfusion reduced the risk of clinical worsening and improved functional outcomes.

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中国社区人群慢性腹泻患病率及其与肥胖的关系

Ke Han, Xiangyao Wang, Yan Wang, Xiaotong Niu, Jingyuan Xiang, Nan Ru, Chunxu Jia, Hongyi Sun, Zhengting He, Yujie Feng 等

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003190

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FLT3配体通过Notch途径调节从肠相关淋巴组织分离的调节性树突状细胞诱导的调节性T细胞的扩增

Na Li, Jingwei Mao, Haiying Tang, Xiaoyan Tan, Jian Bi, Hao Wu, Xiuli Chen, Yingde Wang

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003493

摘要

Background: Regulatory dendritic cell (DCreg) subset exhibits a unique capacity for inducing immune tolerance among the variety subsets of dendritic cells (DCs) within gut-associated lymphoid tissues (GALTs). Fms-like tyrosine kinase 3 ligand (FLT3L) is involved in the differentiation of DCregs and the subsequent expansion of regulatory T-cells (Tregs) mediated by DCregs, though the precise mechanism remains poorly understood. This study aimed to explore the expansion mechanism of Treg induced by DCreg and the role of FLT3L in this process. Methods: DCregs were distinguished from other DC subsets isolated from GALTs of BALB/c mice through a mixed lymphocyte reaction assay. The functions and mechanisms by which FLT3L promoted Treg expansion via DCregs were investigated in vitro through co-culture experiments involving DCregs and either CD4+CD25- T-cells or CD4+CD25+ T-cells. Additionally, an in vivo experiment was conducted using a dextran sulfate sodium (DSS)-induced colitis model in mice. Results: CD103+CD11b+ DC exhibited DCreg-like functionality and was identified as DCreg for subsequent investigation. Analysis of Foxp3+Treg percentages within a co-culture system of CD4+CD25- T-cells and DCregs, with or without FLT3L, demonstrated the involvement of the FLT3/FLT3L axis in driving the differentiation of precursor T-cells into Foxp3+ Tregs induced by DCregs. Cell migration and co-culture assays revealed that the FLT3/FLT3L axis enhanced DCreg migration toward Tregs via the Rho pathway. Additionally, it was observed that DCregs could promote Treg proliferation through the Notch pathway, as inhibition of Notch signaling by DAPT (N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester) suppressed Treg expansion within the co-culture system of DCregs and CD4+ T-cells or CD4+CD25+ T-cells. Furthermore, the FLT3/FLT3L axis influenced JAG1 expression in DCregs, indirectly modulating Treg expansion. In vivo experiments further established that FLT3L promoted DCreg expansion and restored Treg balance in DSS-induced colitis models, thereby ameliorating colitis symptoms in mice. Conclusion: The FLT3/FLT3L axis is integral to the maintenance of DCreg function in Treg expansion.

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SAMSN1通过诱导巨噬细胞表达通过Keap1-Nrf2信号引起T细胞耗竭的共抑制分子而引起脓毒症免疫抑制

Yao Li, Tingting Li, Fei Xiao, Lijun Wang, Xuelian Liao, Wei Zhang, Yan Kang

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003606

摘要

Background: Immunosuppression is closely related to the pathogenesis of sepsis, but the underlying mechanisms have not yet been fully elucidated. In this study, we aimed to examine the role of the Sterile Alpha Motif, Src Homology 3 domain and nuclear localization signal 1 (SAMSN1) in sepsis and elucidate its potential molecular mechanism in sepsis induced immunosuppression. Methods: RNA sequencing databases were used to validate SAMSN1 expression in sepsis. The impact of SAMSN1 on sepsis was verified using gene knockout mice. Flow cytometry was employed to delineate how SAMSN1 affects immunity in sepsis, focusing on immune cell types and T cell functions. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated gene editing in RAW264.7 macrophages enabled interrogation of SAMSN1’s regulatory effects on essential macrophage functions, including cell proliferation and phagocytic capacity. The mechanism of SAMSN1 in the interaction between macrophages and T cells was investigated using the RAW264.7 cell line and primary cell lines. Results: SAMSN1 expression was significantly increased in patients with sepsis and was positively correlated with sepsis mortality. Genetic deletion of Samsn1 in murine sepsis model improved T cell survival, elevated T cell cytolytic activity, and activated T cell signaling transduction. Concurrently, Samsn1 knockout augmented macrophage proliferation capacity and phagocytic efficiency. In macrophage, SAMSN1 binds to Kelch-like epichlorohydrin-associated protein 1 (KEAP1), causing nuclear factor erythroid 2-related factor 2 (NRF2) to dissociate from the KEAP1–NRF2 complex and translocate into the nucleus. This promotes the transcription of the coinhibitory molecules CD48/CD86/carcinoembryonic antigen related cell adhesion molecule 1 (CEACAM1), which bind to their corresponding receptors natural killer cell receptor 2B4/CD152/T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) on the surface of T cells, inducing T-cell exhaustion. Conclusions: SAMSN1 deletion augmented adaptive T cell immunity and macrophage phagocytic-proliferative dual function. Furthermore, it mediates the KEAP1–NRF2 axis, which affects the expression of coinhibitory molecules on macrophages, leading to T-cell exhaustion. This novel immunosuppression mechanism potentially provides a candidate molecular target for sepsis immunotherapy.

Correspondence

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全身炎症反应指数对冠状动脉非阻塞性心肌梗死患者预后的影响

Yanwen Fang, Haihua Zhang, Sizhuang Huang, Mengyue Yu

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003523

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中国新诊断子宫内膜癌患者的真实世界特征和治疗模式

Aijun Yin, Dong Wang, Yanlin Luo, Ruifang An, Shuzhong Yao, Yufei Shen, Li Sun, Cuirong Lei, Yan Tian, Li Wang 等

中华医学杂志英文版2025年 138卷 13期

DOI: 10.1097/CM9.0000000000003562