Volume 139 · Issue 05 · 2026

结直肠癌是中国第二大常见恶性肿瘤和第四大死亡率，^[1]随着疾病负担逐年增加。^[2]关于右侧结肠癌的临床研究不断产生支持右侧结肠癌手术标准化的证据，尤其是在高质量研究之后，例如右侧结肠癌淋巴结切除术范围的临床试验。几项手术原则已被纳入国家和国际结直肠癌诊断和治疗指南。^[3,4]然而，这些共识声明和指南仅为结肠直肠癌患者提供一般技术说明，而不是专门为解决右侧结肠癌患者而设计的。2022年，来自18个国家的55名专家就完全结肠切除术(CME)达成了共识。该共识涵盖的大部分主题是继续医学教育的解剖策略以及培训计划和绩效评估的临床问题。然而，该共识不包括关于右半结肠切除术相关手术策略的指南，包括关于开放和腹腔镜手术之间的决定或淋巴结清扫范围的指南。此外，由于缺乏系统的搜索结果和对现有证据的描述，共识受到限制。

Cardiometabolic risk encompasses the interconnected conditions of cardiovascular diseases (CVDs), type 2 diabetes (T2D), and other metabolic diseases, which are leading global health challenges. The American Heart Association (AHA) has introduced "Life’s Essential 8" (LE8), a framework emphasizing eight key lifestyle and health factors, including diet, physical activity, smoking, sleep health, body weight, blood glucose, blood lipids, and blood pressure to optimize cardiovascular health and reduce the burden of cardiometabolic risk. This review examined the associations between individual and combined lifestyle factors and the development and progression of cardiometabolic risk, using CVD and T2D as representative conditions. Evidence highlighted that adherence to healthy lifestyle behaviors, such as maintaining a balanced diet, engaging in physical activity, avoiding smoking, and achieving a healthy weight, significantly reduced the risks of CVD, T2D, and hypertension. Studies showed that adherence to 3–4 healthy lifestyle factors lowers the risk of transition from baseline to diabetes, complications, and mortality. Despite the proven benefits, barriers such as limited access to healthy food and safe environments for physical activity hinder widespread adoption. Addressing these challenges requires innovative public health interventions and personalized strategies targeting high-risk populations. This review underscored the importance of promoting and adhering to LE8 principles to reduce the global burden of cardiometabolic risk and improve overall health outcomes.

Leucine-rich repeat kinase 2 (LRRK2) is a critical target for the treatment of Parkinson’s disease (PD) and potentially other diseases. LRRK2 is involved in intracellular signaling, immune response, and inflammation, with key roles in both the central nervous system and peripheral tissues. LRRK2 mutations are linked to cellular dysfunction including mitochondrial and neuronal damage and can disrupt signaling pathway balance, thereby contributing to PD and other disorders. Inhibiting LRRK2 kinase activity shows potential for treating PD by correcting cellular imbalances and reducing neuronal damage. However, risks associated with regulating a multifunctional protein must be addressed. Further research on the molecular partners and tissue-specific functions of LRRK2 is essential for developing targeted therapies and improving treatment options for related diseases. This review offers a comprehensive analysis of LRRK2, with a focus on its physiological functions, disease involvement, and emerging therapeutic strategies.

Heart failure (HF) is a chronic condition characterized by high morbidity and mortality worldwide, imposing a substantial burden on healthcare systems. In recent years, artificial intelligence (AI) technologies, including machine learning, deep learning, and large language models, have demonstrated great potential in HF management. By integrating multimodal data, such as electronic health records and medical imaging, AI models address limitations in risk prediction, phenotyping, diagnosis, treatment, and prognosis, offering novel insights to improve the quality of life for HF patients. However, several challenges remain before AI can be reliably implemented in clinical practice, including model selection, model generalization, interpretability, and limited reliability in real-world settings. In this review, we systematically summarize recent advances in application of AI in HF management across multiple domains, including inspection, monitoring, treatment, and integration. We further discuss key real-world challenges to implementation, and outline future directions for the development of intelligent HF management. In addition, representative application cases are presented to illustrate how AI technologies can be developed and translated into clinical practice, with the aim of providing practical insights and methodological guidance for researchers.

Glucocorticoids are widely used for managing acute exacerbations of chronic obstructive pulmonary disease (AECOPD); however, limited studies have described the comparative effectiveness of inhaled corticosteroids (ICS), systemic corticosteroids administered orally or intravenously (oral/intra), and a combination of ICS and oral/intra for AECOPD treatment in China. Thus, we aimed to explore the effects of different glucocorticoid administration routes during hospitalization on both short- and long-term patient prognosis in AECOPD.

Data were collected from the Acute Exacerbations of Chronic Obstructive Pulmonary Disease Inpatient Registry study, a nationwide multicenter, prospective, observational study conducted in China from September 2017 to November 2021. The study involved 179 hospitals. The patients were categorized into three groups according to their treatment profiles as follows: (1) ICS alone, (2) ICS combined with oral/intra, and (3) oral/intra. Propensity score-matching was utilized to minimize potential bias, using a caliper value <0.1. Competing risk models were used to calculate the relative risks for short- (30 days) and long-term (12 months) severe exacerbations, COPD-specific readmission, and all-cause readmission.

After propensity score matching, each group included 572 patients. In the ICS group, the cumulative incidence of short-term severe exacerbations, COPD-specific readmission, and all-cause readmission was 2.4%, 2.2%, and 2.7%, respectively, which was comparable to that in the ICS + oral/intra group (3.7%, 3.4%, and 4.2%, respectively). However, the incidence in the ICS + oral/intra group was significantly lower than that in the oral/intra group (5.4% for short-term severe exacerbations, 5.2% for COPD-specific readmission, and 5.7% for all-cause readmission). The 12-month incidence did not significantly differ among the groups. Compared with the ICS group, the short- or long-term risks did not differ in the ICS + oral/intra group, whereas the short-term risk was higher in the oral/intra group (severe exacerbations: hazards ratio [HR] = 2.29, 95% confidence interval [CI]: 1.09–4.82; COPD-specific readmission: HR = 2.44, 95% CI: 1.12–5.30; and all-cause readmission: HR = 2.18, 95% CI: 1.07–4.45).

The use of systemic corticosteroids alone during hospitalization for AECOPD increases the short-term risk of outcomes but does not affect the long-term prognosis.

Triple-negative breast cancer (TNBC) is a highly aggressive and treatment-resistant subtype of breast cancer, characterized by high rates of metastasis and mortality. This study aimed to identify and evaluate the therapeutic potential of blestriarene C (BC), a novel diphenanthrene compound, in the treatment of TNBC. The study also sought to explore the underlying mechanisms and signaling pathways involved in BC’s antitumor effects.

A multiomics analysis was conducted to identify key genes and pathways involved in TNBC treatment. We performed experiments related to cell viability, ferroptosis, and mitophagy to explore the effects of BC in the treatment of TNBC, utilizing the TNBC cell lines BT-549 and 4T1 cells. The impact of sestrin 2 (SESN2) knockout on BC’s effects was also studied. We also conducted in vivo experiments using the patient-derived xenograft (PDX) model in zebrafish to assess the antitumor effects of BC.

The results of RNA sequencing and proteomics showed that ferroptosis and mitophagy may be the main mechanisms of BC acting on TNBC cells. BC could inhibit cell proliferation by modulating the phosphoinositide 3-kinase/protein kinase B/forkhead box O4 and SESN2/mechanistic target of rapamycin signaling pathways, and inducing ferroptosis and mitophagy. SESN2 and microtubule-associated protein 1 light chain 3 beta (MAP1LC3B), as hub genes, participated in regulating the therapeutic effect of BC on TNBC. TNBC tumors in zebrafish treated with BC were smaller and lighter, indicating that BC had antitumor effect.

BC emerges as a promising therapeutic agent for TNBC by targeting SESN2 and MAP1LC3B, modulating associated signaling pathways, and inducing ferroptosis and mitophagy. These findings provide the basis for further investigation of BC’s potential as a targeted therapy for TNBC.

There is a growing demand for fertility-sparing treatment among young patients with early-stage endometrial cancer (EC) and endometrial atypical hyperplasia (EAH). This study aims to evaluate the efficacy of a regimen that combines anti-estrogen therapy with treatments targeting glucose, lipid, and calcium metabolism in EC and EAH patients.

We conducted a retrospective analysis of patients with EC and EAH who were treated at Peking University People’s Hospital between January 2018 and November 2023. The study investigated the clinical profiles of the patients and assessed the efficacy of different treatment strategies.

A total of 285 patients were enrolled in the study, with 149 receiving anti-estrogen monotherapy and 136 receiving a combination therapy (including metformin, statins, calcium channel blockers [CCBs]). The combination therapy group showed a significantly higher proportion of patients with elevated body mass index, insulin resistance, diabetes, and hypertension compared to anti-estrogen group (P <0.05), and both groups had similar complete response (CR) time and CR rate. Pathological type of EAH and metformin regimen were protective factors for shorter complete response time (P <0.05). Subsequent stratified analysis revealed that combination therapy with metformin significantly benefited patients with insulin resistance (hazard ratio [HR] = 1.888, 95% confidence interval [CI]: 1.313–2.713) and diabetes mellitus (HR = 2.749, 95% CI: 1.046–7.299).

Fertility-sparing treatments for patients with metabolic risk factors may have poor efficacy. However, the integration of anti-estrogen therapy with the metabolic-targeting interventions, like metformin, appears to improve the outcomes of fertility-preserving strategies in this patient population.

Psoriasis is a systemic disease that brings enormous mental pressure and economic burden to patients and has a significant impact on patients’ quality of life (QoL). This study aimed to explore factors affecting the dermatology life quality index (DLQI) in patients with psoriasis.

This retrospective cross-sectional study used data sourced from the Psoriasis Diagnosis and Treatment Real-world Database, and 8839 patients with psoriasis (recruited between June 24, 2020 and September 2, 2021) were included. Demographic and clinical characteristics and DLQI scores were retrospectively analyzed, and correlations between DLQI score and age, disease course, psoriasis area and severity index (PASI) score were calculated. Regression analysis was conducted to explore the factors affecting the DLQI scores of patients with psoriasis.

The average DLQI scores were significantly higher in young (8.58 ± 7.22) and middle-aged individuals (8.09 ± 6.61) than those in juveniles (6.00 ± 5.79) and older individuals (7.39 ± 6.29) (P = 1.70E-15). The average DLQI scores gradually decreased among individuals whose work status were unemployment (10.4 ± 7.83), part-time (9.02 ± 6.83), full-time (8.43 ± 6.90), retired (7.93 ± 6.07), and students (7.10 ± 6.31) (P = 9.82E-23). Except for those with disease course ≥20 years, DLQI scores increased gradually with prolongation of the disease course (P = 4.72E-22). The higher the severity of psoriasis, the higher the average DLQI score (P = 3.79E-113). The presence of psoriatic lesions at the exposed sites significantly affected DLQI scores (P <0.001). The average DLQI scores were significantly higher among individuals with nail holes, joint pain, and comorbidities than among those without these conditions (P <0.05). Correlation analysis indicated that the PASI scores were positively correlated with the DLQI scores (r = 0.26, P = 4.19E-134). Multinomial logistic regression analysis showed significant influencing factors (excluding comorbidity) with different degrees of impact based on the DLQI score (P <0.05).

Physicians should focus on significant factors, such as sex, age, marital status, education, work status, sub-types, disease course, PASI score, joint pain, and nail holes, to improve the QoL of patients with psoriasis.

Autologous chimeric antigen receptor T (CAR-T) cell therapy has demonstrated efficacy in the treatment of acute myeloid leukemia (AML). Nevertheless, the intrinsic characteristics of autologous therapy, such as extended manufacturing timelines and patient-specific limitations, contribute to delays in treatment availability. More critically, relapse due to antigen escape following single-targeted CAR-T therapy constitutes a significant clinical obstacle. To address the dual challenges of delayed treatment accessibility and antigen escape relapse, this study proposes the development of universal tandem CAR-T cells. These cells, engineered to target CD123 and B7-H3 through clustered regularly interspaced short palindromic repeats (CRISPR) gene editing technology, represent an innovative therapeutic strategy for AML.

In this study, an immune phage display nanobody library was developed for the purpose of screening CD123-specific nanobodies. The CRISPR/CRISPR-associated protein 9 (CRISPR/Cas9) gene editing system was utilized to disrupt the T-cell receptor alpha chain (TRAC) and B2M genes present in T cells, resulting in the generation of universal CD123/B7-H3 bispecific universal CAR-T (UCAR-T) cells. The efficacy of these dual-specific UCAR-T cells in combating tumors was subsequently assessed through in vitro and in vivo experiments.

Through four rounds of panning against CD123 from an immunized camelid VHH library, we identified 21 antigen-specific nanobodies. Tandem bispecific UCAR-T engineered with these binders demonstrated CAR transduction efficiencies ranging from 82% to 87%. In vitro functional profiling revealed a significantly enhanced cytotoxicity of bispecific UCAR-Ts against CD123⁺/B7-H3⁺ AML cell lines when compared to single-target constructs, while effectively regulating the secretion of effector cytokines (IL-2, IFN-γ, TNF-α). In AML xenograft models, treatment with bispecific UCAR-T notably inhibited tumor progression, extended the survival of tumor-bearing mice with recurrence-free persistence throughout the observation period, and did not result in significant body weight loss or cytokine release syndrome.

The findings of the study address the issue of tumor antigen evasion in the treatment of AML, circumvent certain constraints associated with autologous CAR-T cell therapy, and offer novel insights and strategies for managing AML.

Glioma is a common malignant brain tumor with poor prognosis. Choline kinase α (CHKA) has been implicated in glioma progression, but its regulatory mechanisms remain unclear.

Single-cell ribonucleic acid (RNA) sequencing was performed to assess the coexpression of CHKA and epidermal growth factor receptor (EGFR) in glioma subpopulations. Public datasets were analyzed to evaluate their clinical relevance, which was verified in a cohort from Ningxia Medical Hospital (November 2019–October 2024). Immunohistochemical staining confirmed their expression and subcellular localization. The interaction between CHKA and EGFR was examined using mass spectrometry, coimmunoprecipitation, polymerase chain reaction, and Western blotting. The effects of the CHKA/EGFR axis on the mitogen-activated protein kinase (MAPK) pathway were explored using polymerase chain reaction and Western blotting. Cell Counting Kit-8 (CCK-8), transwell, and wound-healing assays were conducted in glioma cell lines following CHKA knockdown and EGFR rescue. Finally, a nude mouse xenograft model was established to validate in vivo tumorigenicity and MAPK pathway activation.

CHKA was highly coexpressed with EGFR in specific glioma subpopulations, and their expression levels were positively correlated. Both genes were associated with advanced tumor grade and poor prognosis. CHKA interacted with EGFR and promoted its expression and phosphorylation. Silencing CHKA reduced EGFR levels and suppressed MAPK signaling. Functionally, CHKA enhanced glioma cell proliferation, migration, and invasion through EGFR upregulation. Moreover, CHKA knockdown inhibited tumor growth and MAPK activation in vivo, while EGFR overexpression restored tumorigenesis.

CHKA drives glioma malignancy by regulating EGFR and activating the MAPK pathway. The CHKA/EGFR/MAPK axis represents a potential therapeutic target for glioma treatment.

The objective of this study is to delineate the differential gene expression patterns of neutrophils in bronchoalveolar lavage fluid (BALF) from patients with sepsis and those experiencing progression to sepsis-induced acute respiratory distress syndrome (SI-ARDS). Additionally, we aim to comprehensively profile the transcriptomic landscape of neutrophils in BALF from patients with sepsis and SI-ARDS, particularly focusing on cases caused by specific bacterial pathogens.

Patients with confirmed sepsis (n = 14) or SI-ARDS (n = 11) were recruited. Besides, a control group consisting of patients with unrelated diseases (n = 7) who required bronchoscopy was also included (cohort 1). We collected the neutrophils in BALF from participants in cohort 1. To validate the identified differentially expressed genes (DEGs) and evaluate neutrophil apoptosis, an additional cohort (cohort 2) was recruited, consisting of 5 healthy controls, 10 patients with sepsis, and 10 patients with SI-ARDS. Peripheral blood neutrophils were collected from participants in cohort 2 for further analysis. DEGs between SI-ARDS patients and controls, sepsis patients and controls, as well as SI-ARDS patients and sepsis patients were identified. And, publicly available datasets were downloaded to compare with local results. Additionally, the DEGs were also identified between patients infected with drug-resistant Klebsiella pneumoniae and those infected with other bacterial pathogens. Furthermore, a third cohort (cohort 3) consisting of 57 sepsis patients and 46 SI-ARDS patients was recruited for investigating the prognostic significance of neutrophils in SI-ARDS.

In cohort 1, 8/14 of the septic patients and 6/11 of the SI-ARDS patients were affected by drug-resistant Klebsiella pneumonia. There were 9921 DEGs between sepsis patients and controls, 10,252 DEGs between SI-ARDS patients and controls, and 24 DEGs between SI-ARDS and sepsis patients in neutrophils from BALF. Notably, fatty acid-binding protein 4 (FABP4) exhibited significant downregulation in SI-ARDS patients. In cohort 2, peripheral blood analysis confirmed consistent trends, demonstrating that FABP4 expression was decreased, which contributed to the attenuation of neutrophil apoptosis. And FABP4 inhibitor-induced apoptosis resistance was reversed by a phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) inhibitor. Furthermore, survival analysis revealed that SI-ARDS patients with low levels of neutrophil FABP4 expression exhibited poor survival. Additionally, 520 overlapping DEGs were identified between the sepsis and control group comparisons and the SI-ARDS and sepsis group comparisons. Among these overlapping DEGs, 85% were downregulated, predominantly targeting immune-related pathways, whereas a smaller subset was upregulated, mainly associated with metabolism. DEGs in neutrophils in BALF of SI-ARDS and controls notably overlapped with those in neutrophils in peripheral blood. Importantly, DEGs in sepsis/SI-ARDS caused by drug-resistant Klebsiella pneumoniae differed from DEGs in sepsis/SI-ARDS caused by other bacteria. Additionally, FABP4 expression consistently decreased, attenuating neutrophil apoptosis.

The downregulation of FABP4 in neutrophils was found to inhibit apoptosis through the activation of the PI3K/AKT signaling pathway. Importantly, the expression level of FABP4 in neutrophil emerged as a prognostic indicator for sepsis and SI-ARDS patients, suggesting its potential utility in clinical decision-making to address the challenges posed by this condition.

致编辑：慢性术后疼痛（CPSP）是手术后最常见的并发症之一。根据风险因素，多达5-58%的患者在手术后经历慢性疼痛。^[1]CPSP的机制复杂且不确定；目前的理解表明，持续的外周炎症和伤害性超敏反应起着至关重要的作用。

致编辑：基于即刻植入物的乳房重建（IBBR）已成为乳房切除术后重建的首选。^[1]采用回顾性研究，通过问卷调查的方式调查了中国乳腺癌术后即刻行IBBR患者的管理现状及并发症。本研究经中国医科大学第一医院伦理委员会批准（No.[2024]579）。本问卷包含两部分：（I）参与医院概况及2022年1月1日至2022年5月31日期间进行的乳房重建手术的整体情况。（II）各医院即刻IBBR手术详情。数据收集截止日期为2023年12月12日，中位随访时间为17个月。总结研究设计和患者选择过程的详细问卷和流程图可在补充文件和补充图1中找到，http://links.lww.com/CM9/C693。统计学显著性设定为P<0.05.Theχ²采用检验、Fisher精确检验和逻辑回归。

致编辑：卵巢癌（OC）是一种高度侵袭性的恶性肿瘤，对女性健康构成重大威胁，并且由于诊断晚和化疗耐药性而导致高死亡率。^[1]贝伐珠单抗是一种血管生成抑制剂，是美国食品药品监督管理局（FDA）批准的晚期OC疗法，当与化疗联合使用或用作维持疗法时，可改善无进展生存期（PFS）和总生存期（OS）。^[2]然而，挑战依然存在。识别预测性生物标志物和优化贝伐单抗治疗持续时间和时机至关重要。由血管生成途径的再激活和肿瘤微环境的变化驱动的对贝伐单抗的耐药性导致治疗失败。^[3]由于其成本、潜在毒性和有限的患者益处，迫切需要开发新的预测方法。早期诊断是改善OC预后的关键。组织病理学是诊断和预后预测的金标准，但复杂且耗时。最近，基于病理组学特征的深度学习已被用于构建预测模型，提供了一种更快的替代方案。^[4,5]在这项研究中，我们使用癌症基因组图谱卵巢癌（TCGA-OV）数据集、癌症成像档案（TCIA）队列和东南大学中大医院（中大队列）中OC患者的全载玻片图像（WSIs），通过深度学习和软件Cell-profiler（英国马萨诸塞州剑桥布罗德研究所）开发了一个预测模型。该模型准确地识别了肿瘤区域，并评估了贝伐单抗对患者预后的影响。我们还尝试根据患者的治疗反应对患者进行聚类，以分析基因组差异并指导患者预后。

致编辑：经导管主动脉瓣置换术（TAVR）是一种在所有手术风险类别中治疗严重主动脉瓣狭窄（AS）的成熟方法，患有二叶主动脉瓣（BAV）狭窄的候选人比例不断增加。^[1,2,3]BAV解剖结构以椭圆环、不对称尖、严重钙化和可变冠状动脉起源为特征，给TAVR手术带来了独特的挑战。尽管经导管心脏瓣膜（THV）技术取得了进步，但这些解剖特征导致了更高的并发症发生率，如卒中、瓣周反流（PVR）和永久性起搏器植入（PPI）。^[4]在并发症中，即使对于轻度病例，显著的PVR也与更差的临床结局相关，而TAVR后新发传导障碍（NOCDs）与死亡率增加和心室恢复受损相关。^[5,6]为了降低PVR和NOCD，THV的最佳尺寸至关重要。然而，目前的尺寸指南仍然有限，特别是对于BAV患者，并且环形过大比（OSr）策略的影响仍然存在争议。为了解决这个问题，我们研究了基于计算机断层扫描（CT）的环形OSr与接受自扩张瓣膜（SEV）植入的患者PVR和NOCD发生率之间的关系，旨在确定平衡二叶和三叶主动脉瓣（TAV）解剖结构中PVR和NOCD风险的最佳OSr策略。

致编辑：与妊娠期糖尿病不同，2型糖尿病（T2DM）控制不佳的孕妇在整个妊娠期间都会经历高血糖，^[1]在妊娠早期可能会干扰正常的胎盘形成。控制不良的T2DM更容易导致严重的母体和胎儿并发症，如重大畸形、不明原因的胎儿死亡、巨大儿和小于胎龄儿。^[1,2]胎盘位于胎儿和母亲之间，是高血糖暴露与母体和胎儿并发症之间的重要介质。在这里，我们利用10 ×基因组学平台生成从T2DM控制不良的孕妇和正常孕妇获得的足月胎盘绒毛的单细胞转录组谱。在T2DM胎盘中，巨噬细胞增加_S100A8/9^高的(Macro_S100A8/9^高的）在绒毛部位，并发现合胞体滋养层（STB）中的营养转运缺陷。我们在T2DM绒毛中发现了从巨噬细胞到胎盘滋养细胞的促炎调节信号升高，包括S100A8/9-TLR4和IL1B-IL1R1/IL1RAP发现其干扰滋养细胞的正常功能。

致编辑：银屑病是一种以表皮角质形成细胞（KC）过度增殖和免疫失调为特征的慢性炎症性皮肤病。KCs通过细胞因子/趋化因子产生驱动病理细胞扩增和炎症，细胞因子/趋化因子产生激活树突状细胞、T细胞和中性粒细胞以维持炎症级联反应。^[1]角蛋白17(K17)是对表皮稳态至关重要的I型上皮角蛋白，在细胞因子如血管内皮生长因子(VEGF)、白细胞介素(IL)-17A、干扰素-γ(IFN-γ)和IL-22诱导下，在银屑病病变中显示出显著上调。^[2,3]除了其结构作用之外，K17还通过K17/T细胞/细胞因子自身免疫环促进疾病进展。^[4,5]这项研究表明，K17通过C-X-C基序趋化因子配体1（CXCL1）上调触发中性粒细胞趋化性，促进中性粒细胞微脓肿形成和炎症扩增。这些发现提供了新的证据，证明K17是调节KCs免疫反应的关键分子。方法和数据可用性可在补充文本http：//links.lww中找到。com/CM9/C733。

致编辑：成人弥漫性胶质瘤是最常见的原发性恶性脑肿瘤，其特点是死亡率高。^[1]异柠檬酸脱氢酶（IDH）是一种关键的分子标志物，目前正用于成人弥漫性胶质瘤的诊断和预后分层。^[2]传统上，IDH状态已通过免疫组织化学或测序技术鉴定。然而，这些侵入性程序具有一定的风险。磁共振成像(MRI)是一种非侵入性成像技术，可用于评估IDH术前突变状态。研究表明，卷积神经网络（CNN）在基于MR的深度学习中的使用越来越多，用于非侵入性预测IDH神经胶质瘤的突变。^[3]没有进行全面的比较来确定哪种方法在大型和多样化的数据集上最有效。我们研究的目的是使用包括从多个中心收集的数据的大型数据集，对二维（2D）、2.5 D和3D CNN方法预测IDH状态的预测性能进行详细比较。

致编辑亨廷顿病(HD)是一种遗传性常染色体显性神经退行性疾病，由胞嘧啶-腺嘌呤-鸟嘌呤(CAG)重复扩增引起HTT基因。^[1]目前没有针对HD的有效疾病缓解疗法；因此，研究可能影响HD发病和进展的可改变因素是至关重要的。脂质在正常脑功能的维持中起着至关重要的作用，包括充当膜结构的结构成分、参与能量代谢和信号转导。脂质代谢紊乱参与了HD的发病机制，但循环脂质在HD中的作用尚未阐明。我们的目的是研究血脂是否与HD患者的疾病进展相关。