2026年 · 第139卷第06期

出版日期 2026-03-20电子版￥0.00元￥100.00元

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Consensus Statement

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基于RNA的下一代测序检测非小细胞肺癌融合基因的临床实践专家共识

Hua Zhong, Baohui Han, The Consensus Expert Panel

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003967

摘要

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机器人辅助上颈椎内固定临床循证指南（2026版）

Smart Orthopaedics Group of Chinese Association of Orthopaedic Surgeons, Spine Trauma Group of Chinese Association of Orthopaedic Surgeons

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003961

摘要

Review Article

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健康与脑疾病中的肠脑轴

Oluwatayo Israel Olasunkanmi, Luqi Zheng, Peng Zheng

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003920

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儿科疾病中的宿主遗传变异和肠道微生物组

Yi Meng, Hua Wang, Dezhi Mu, Shuqin Zeng, Shaopu Wang

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003959

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胰腺导管腺癌进展和治疗中的微生物群：隐藏的参与者

Xiulin Hu, Fanyang Kong, Jiayu Chen, Zhaoshen Li, Zhenzhai Cai, Xiangyu Kong

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003986

摘要

Original Article

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脑白质病变改变大型缺血性核心卒中血管内治疗结果：ANGEL-ASPECT试验的二次分析

Zan Wang, Chenhui Liu, Mengxing Wang, Shuning Cai, Ximing Nie, Liping Liu, Xiaochuan Huo, Yuesong Pan, Zhongrong Miao, Yilong Wang

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003993

摘要

Background: Severe white matter lesions (WMLs) have been linked to poorer functional outcomes following endovascular therapy (EVT) in patients with acute ischemic stroke (AIS) due to large-vessel occlusion (LVO). However, the absence of a control group in previous studies has limited the ability to determine the benefit of EVT to patients with severe WMLs. Methods: This work is a secondary analysis of the Endovascular Therapy in Acute Anterior Circulation Large Vessel Occlusive Patients with a Large Infarct Core (ANGEL-ASPECT) trial, a multicenter, randomized controlled trial conducted at 46 comprehensive stroke centers across China, which enrolled 456 patients with AIS with anterior-circulation LVO and large ischemic cores between October 2020 and May 2022. WML severity was graded using the van Swieten Scale on pretreatment noncontrast computed tomography (CT). For supplementary analyses, WML severity was further assessed using T2 fluid-attenuated inversion recovery (T2-FLAIR) magnetic resonance imaging (MRI) and graded according to the Fazekas scale, with WMLs categorized into periventricular and deep subtypes. Treatment effect on the primary outcome (90-day modified Rankin Scale [mRS] score) was assessed using multivariable ordinal logistic regression, and a treatment-by-WML interaction term was tested to evaluate effect modification. Results: In patients with absent-to-moderate WMLs, EVT was associated with a favorable shift in the distribution of 90-day mRS scores (adjusted common odds ratio [cOR] 2.15, 95% confidence interval [CI, 1.48-3.13], P <0.001). However, this benefit was less pronounced in those with severe WMLs (adjusted cOR 2.25, 95% CI [0.95-5.30], P = 0.065). No significant interaction between WML severity and treatment effect was detected (Pinteraction = 0.888). Similarly, only among patients with absent-to-moderate WMLs, EVT significantly increased rates of mRS scores of 0-2 (adjusted OR 4.86, 95% CI [2.66-8.86], P <0.001), the rates of mRS scores of 0-3 (adjusted OR 2.23, 95% CI [1.39-3.57], P = 0.001), and the rates of early neurological improvement (adjusted OR 5.22, 95% CI [1.31-20.79], P = 0.019) compared to medical management alone. Supplementary analyses using T2-FLAIR MRI to stratify patients by WML burden yielded results consistent with those of the primary analyses. Conclusions: EVT significantly improved functional outcomes in patients with LVO-AIS with absent-to-moderate WMLs, while the benefit in those with severe WMLs appeared less pronounced. However, estimates within subgroups were underpowered. Future pooled analyses of randomized clinical trials with adequate statistical power are needed to clarify the impact of WML severity on EVT outcomes and to refine patient selection criteria.

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硫化氢通过Sirt3/SOD2信号通路减轻慢性阻塞性肺疾病氧化应激诱导的细胞衰老

Sha Liao, Dian Chen, Huanyu Long, Simin Jiang, Jing Fan, Shurun Li, Yongfen Qi, Lixiang Xue, Yanling Ding, Yahong Chen

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003452

摘要

Background: Senescence significantly participates in shaping the pathobiological process underlying chronic obstructive pulmonary disease (COPD). Currently, the mechanisms underlying the anti-aging effects of hydrogen sulfide (H2S) in COPD are not fully illustrated. Methods: Immunohistochemistry (IHC) staining was performed on human lung tissue to detect the expression levels of sirtuin 3 (Sirt3), cyclin-dependent kinase 4 inhibitor (P16), and cystathionin gamma lyase (CTH). An animal COPD model including wild-type (WT) and Sirt3 knockout (KO) mice was established by exposing them to cigarette smoking (CS) for 24 weeks, with or without intraperitoneal injection of sodium hydrosulfide (NaHS, 50 µmol·L-1·kg-1) 30 min prior to CS exposure. Lung function was assessed. The expression levels of P16, cyclin-dependent kinase inhibitor 1A (P21), Sirt3, manganese superoxide dismutase (SOD2), manganese acetylated superoxide dismutase (ac-SOD2), interleukin-6 (IL-6), IL-8, malondialdehyde (MDA), and glutathione (GSH), as well as the activity of SOD2 and Sirt3, were evaluated. Human bronchial epithelial BEAS-2B cells were subjected to diverse cigarette smoking extract (CSE) concentrations for 48 h with or without sodium hydrosulfide (NaHS). Subsequently, the levels of total intracellular reactive oxygen species (T-ROS), mitochondrial reactive oxygen species (mitoROS), mitochondrial membrane potential (MMP), senescence-associated β-galactosidase (SA-β-gal) staining positive cells, and related marker proteins and cytokines were assessed. Furthermore, the Sirt3-specific inhibitor 3-TYP and small interfering RNAs (siRNAs) of Sirt3 were used to examine the mechanisms whereby H2S inhibits oxidative stress and senescence in COPD. Results: IHC showed a significant reduction of CTH and Sirt3 protein levels in the lung tissue of COPD with smoking patients and smokers without COPD compared to non-smokers. Furthermore, the expression of the aging marker protein P16 was notably elevated in the COPD with smoking group compared to the smokers without COPD and non-smoker groups. Furthermore, our results demonstrated that exposure to CS resulted in imbalanced oxidative and cellular senescence, including elevated mitoROS, T-ROS, MDA, and ac-SOD2, along with increased proportions of SA-β-gal staining positive cells and the increased expression levels of IL-6, IL-8, P21, and P16, as well as decreased GSH levels, SOD2 and Sirt3 activities, and Sirt3 expression, which ultimately contribute to emphysema development and impaired lung function. However, pretreatment with NaHS effectively reversed these detrimental effects. Nevertheless, the protective effect of NaHS was alleviated in Sirt3 KO mice and in cellular models treated with Sirt3 siRNA and 3-TYP. Conclusion: Our study indicates that H2S inhibits oxidative stress and cellular senescence by modulating the Sirt3/SOD2 signaling pathway, therefore attenuating the emphysema and impaired lung function induced by CS.

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LncRNAH19过表达通过激活Pink1/Parkin介导的线粒体自噬保护体外循环后急性肾损伤

Mingru Zhang, Min Liu, Tianlong Wang, Yingjie Du, Yimeng Chen, Yafan Bai, Yue Zhang, Dinghao Xue, Bingyang Ji, Guyan Wang

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003552

摘要

Background: Cardiopulmonary bypass-associated acute kidney injury (CPB-AKI) is a serious and common complication following cardiopulmonary bypass (CPB), leading to worse outcomes and higher mortality. However, the underlying pathological mechanisms of CPB-AKI remain largely unknown. This study aimed to investigate the role of long non-coding RNA H19 (H19) in regulating CPB-AKI. Methods: We examined the expressions of H19 and mitophagy-related proteins in a CPB-AKI rat model and HK-2 cells following oxygen-glucose deprivation/reperfusion (OGD/R). In vivo, lentiviral-mediated overexpression of H19 was induced in the kidney through tail vein injection. We then evaluated renal functions, kidney pathological damage, levels of inflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and IL-10), neutrophil infiltration, and the activation of PTEN-induced putative kinase 1 (Pink1)/Parkin-mediated mitophagy following CPB-AKI. In vitro, small interfering RNA (siRNA) was used to downregulate H19 expression in HK-2 cells. We also examined cell viability, apoptosis, inflammation, and Pink1/Parkin-mediated mitophagy after OGD/R. Results: We demonstrated an increase in H19 expression and activation of Pink1/Parkin-mediated mitophagy in the rat model of CPB-AKI and HK-2 cells following OGD/R. In the rat models of CPB-AKI, lentivirus-mediated overexpression of H19 significantly attenuated renal injury, characterized by better renal function, reduced tissue damage, decreased neutrophil infiltration, and lower inflammatory cytokine release (P <0.05). Notably, overexpression of H19 significantly activated Pink1/Parkin-mediated mitophagy. Furthermore, in vitro, downregulation of H19 by specific siRNA in HK-2 cells significantly decreased cell viability, worsened HK-2 injury after OGD/R, increased inflammatory cytokine release, and decreased Pink1/Parkin-mediated mitophagy activity, promoting cell apoptosis (P <0.05). Conclusions: These findings suggest that H19 overexpression may protect against CPB-AKI by activating Pink1/Parkin-mediated mitophagy and decreasing inflammatory responses and cellular apoptosis. Thus, H19 overexpression might be a promising therapeutic target for treating CPB-AKI.

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“一石三鸟”：穿心莲-衍生的外泌体样纳米颗粒减轻葡聚糖硫酸钠诱导的结肠炎

Minzheng Zhu, Shimin Wang, Ningning Yue, Hailan Zhao, Yuan Zhang, Chengmei Tian, Chen Kong, Zhiliang Mai, Longbin Huang, Qianjun Luo 等

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003651

摘要

Background: Ulcerative colitis (UC), a chronic inflammatory bowel disease, is characterized by a multifactorial etiology and limited therapeutic options. Recent advancements in plant-derived exosome-like nanoparticles (PDENs) have demonstrated promising potential for UC treatment. This study explored the therapeutic efficacy of Andrographis paniculata-derived exosome-like nanoparticles (APELNs) in alleviating dextran sodium sulfate (DSS)-induced colitis. Methods: APELNs were isolated and purified using sucrose gradient centrifugation and subsequently characterized through visualization techniques. Their stability was assessed under simulated stomach-like and intestine-like conditions. The therapeutic potential of APELNs was evaluated through both in vivo and in vitro experiments. In addition, the biosafety of APELNs was comprehensively analyzed in these settings. Results: APELNs exhibited excellent stability and biosafety, with a targeted accumulation in inflamed colonic tissues under gastrointestinal conditions. The nanoparticles displayed a desirable size (about 180 nm) and a negative zeta potential (-40 mV). Treatment with APELNs significantly ameliorated colonic pathologies in vivo and suppressed the expression of pro-inflammatory cytokines in vitro. Mechanistically, APELNs enhanced gut microbiota richness and diversity, fostering the growth of the probiotic Lactobacillus murinus. Moreover, APELNs reduced intestinal permeability and preserved intestinal barrier integrity by upregulating tight junction proteins, including Claudin-1, zonula occludens-1, Mucin2, and anti-occludin. Importantly, oral administration of APELNs shifted macrophage polarization in the colon, inhibiting the pro-inflammatory M1 subset while promoting the anti-inflammatory M2 subset. This polarization was mediated through the activation of the phosphatidylinositol 3 kinase-protein kinase B (PI3K-AKT) and Janus tyrosine kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways and the upregulation of interleukin-4 receptor expression. Conclusion: These findings highlighted the potential of APELNs as a novel therapeutic strategy for UC, offering a promising alternative for effective disease management.

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钠-葡萄糖协同转运蛋白2抑制剂通过激活糖尿病小鼠中的PPARGC1 α促进α细胞通过祖细胞向β细胞的细胞表型转化

Yafei Jiang, Dandan Wang, Ming Tao, Xiaona Cui, Jian Li, Tianjiao Wei, Jin Yang, Tianpei Hong, Rui Wei

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003859

摘要

Background: Sodium-glucose cotransporter 2 inhibitor (SGLT2i) improves beta-cell function in animals and humans with diabetes. Herein, we aimed to investigate the effects of SGLT2i on beta-cell regeneration, trace the origin of regenerated beta cells, and reveal the potential mechanism. Methods: Type 2 and type 1 diabetic mice were treated with canagliflozin (10 mg/kg), dapagliflozin (1 mg/kg), or vehicle. Islet morphology was evaluated to investigate beta-cell regeneration. Inducible pancreatic neurogenin 3 (Ngn3)+ progenitor lineage-tracing mice and alpha-cell lineage-tracing mice were used to trace the origin of regenerated cells. Mouse and human islets, alpha cells, and beta cells were incubated with dapagliflozin (12.5 µmol/L) or vehicle. Insulin and glucagon-like peptide-1 (GLP-1) release, gene expression, and RNA sequencing analysis were performed to clarify the direct actions of SGLT2i and to screen potential targets. Alpha cells were transfected with peroxisome proliferator-activated receptor-γ coactivator 1α (Ppargc1α) plasmid or with Ppargc1α siRNA, followed by incubation with or without dapagliflozin to confirm the effects of Ppargc1α in alpha-cell phenotype conversion. Results: SGLT2i increased islet and beta-cell areas in type 2 diabetic mice and showed a similar trend in type 1 diabetic mice. SGLT2i induced alpha-cell dedifferentiation into Ngn3+ progenitors and promoted progenitor differentiation toward beta cells. In cultured diabetic mouse and human islets and in stressed alpha cells, SGLT2i increased supernatant insulin and active GLP-1 levels, downregulated alpha-cell-specific marker expression, and upregulated the expression of endocrine progenitor- and beta-cell-specific markers, including prohormone convertase 1/3. Although dapagliflozin did not affect beta cells directly, it affected alpha cells (457 upregulated and 235 downregulated genes). Ppargc1α, a coactivator participating in oxidative phosphorylation, was identified as a potential target. By using overexpression and knockdown, we confirmed that Ppargc1α participated in SGLT2i-induced regulation of alpha-cell phenotype conversion. Conclusion: Alpha-cell regression to progenitors and progenitor differentiation toward beta cells represent a novel pathway for beta-cell neogenesis induced by SGLT2i in diabetes, with Ppargc1α playing a role in this process.

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视觉状态对健康年轻人步行相关脑功能影响的静息态功能磁共振成像研究

Mingxin Ao, Ruilan Dai, Xiaoming Shi, Yunan Zhou, Mingxuan Gao, Yingfang Ao

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000004040

摘要

Background: Visual input supports locomotion through sensorimotor integration. However, the neural mechanisms underlying how the brain adapts to degraded vision are not well understood. This study investigated the effects of visual occlusion on interactions between regions within the sensorimotor network. Methods: Twelve healthy young adults (8 males, 4 females; mean age 24.0 ± 2.1 years) were recruited from the Department of Ophthalmology at Peking University Third Hospital between December 2024 and September 2025. Pattern-reversal visual evoked potentials were recorded under both normal vision and visual occlusion condition (Snellen 20/60 acuity). We acquired resting-state functional magnetic resonance imaging (rs-fMRI) data to calculate the amplitude of low-frequency fluctuations (ALFF) and seed-based functional connectivity (FC) focused on visuomotor integration regions. A one-way repeated-measures analysis of variance was conducted with three within-subject conditions: seated rest, level walking with normal vision, and level walking with visual occlusion. Results: Stimuli consisted of checkerboard patterns with large (1°) and small (15′) checks. Under 1° visual stimulation, visual occlusion prolonged binocular P100 latency (117.00 ± 8.55 ms vs. 111.81 ± 5.12 ms; 116.78 ± 9.79 ms vs. 110.96 ± 4.28 ms; all P <0.05) and reduced N75-P100 amplitude (5.798 ± 2.372 µV vs. 8.613 ± 3.949 µV; 6.230 ± 2.459 µV vs. 7.453 ± 2.692 µV, all P <0.05). For 15′ stimulation, occlusion decreased both binocular N75-P100 (5.935 ± 3.500 µV vs. 10.794 ± 5.249 µV; 3.991 ± 1.585 µV vs. 10.361 ± 3.143 µV, all P <0.001) and P100-N135 amplitudes (6.218 ± 3.516 µV vs. 12.499 ± 4.236 µV; 4.427 ± 2.218 µV vs. 10.767 ± 4.904 µV, all P <0.001). Rs-fMRI analysis showed reduced ALFF in the right paracentral lobule after walking (peak Montreal Neurological Institute [MNI] coordinates: 3, -39, 66; P <0.001, F = 14.009). Walking activated multiple visuomotor pathways (all P <0.001), including the bilateral calcarine and middle temporal gyri, the right calcarine and middle frontal gyri, the bilateral supplementary motor area and right cuneus, and the bilateral precentral gyrus and right cerebellar lobule VI. The visual occlusion strengthened FC between the right precentral and the right middle frontal gyri (peak MNI: 27, 57, 27; F = 16.456, P <0.001). Conclusions: Basic visuomotor pathways demonstrate consistent activation to maintain locomotion. Increased functional connectivity between the right precentral and middle frontal gyri serves as a compensatory mechanism for reduced visual input.

Correspondence

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化疗单独或联合免疫检查点抑制剂作为晚期患者一线治疗的疗效和安全性HER2-突变非小细胞肺癌：一项多中心回顾性研究

Chenyi Ren, Nan Jiang, Guixian Wu, Lei Zhang, Wenjia Sun, Zhengwei Dou, Jing Zheng, Jianya Zhou

中华医学杂志英文版2026年 139卷 06期

DOI: 10.1097/CM9.0000000000003928

摘要