Translational Research最新文献_第6页

Modeling diabetic epitheliopathy using 3D-Organotypic corneal epithelium 利用3d器官型角膜上皮建立糖尿病上皮病变模型。

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-05-17 DOI: 10.1016/j.trsl.2025.05.003

Grazia Maugeri , Agata Grazia D’Amico , Salvatore Saccone , Francesca Bruno , Elisabetta Pricoco , Davide Scollo , Teresio Avitabile , Antonio Longo , Velia D’Agata

Diabetic keratopathy (DK) is a degenerative corneal disease occurring in more than 50 % of diabetic patients. DK is correlated with the hyperglycemic state causing morphological and functional changes in corneal layers. Currently, most studies on the cornea are performed on two-dimensional (2D) cultures in vitro or animal models. Although 2D culture models can provide large amounts of data at low cost, they poorly represent the complex pathophysiology of the human cornea and hardly predict in vivo responses that can be achieved with animal model studies. However, the use of the latter presents ethical problems. Therefore, it is necessary to identify new strategies and models that can integrate the information validly and effectively, to reduce the number of animals used. Here, we used human corneal epithelial cells (hCECs) derived from donor cornea differentiated into three-dimensional (3D)-organotypic air-liquid interface (ALI), which resemble the features of the corneal epithelium. The 3D-organotypic ALI corneal epithelium was subjected to high-glucose conditions to generate a model of diabetic epitheliopathy. Our model showed well-established molecular and cellular characteristics of this pathology, such as epithelial defects and inflammation, with increased expression of IL-1β, TNF-

α

, p-NF-kB, COX-2, MMP-2 and MMP-9. The data provided highlight the utility of 3D-organotypic corneal epithelium in modeling diabetic epitheliopathy, offering new avenues in drug screening, as well as in precision and personalized medicine.

糖尿病性角膜病变（DK）是一种退行性角膜疾病，发生在50%以上的糖尿病患者中。DK与高血糖状态引起的角膜层形态和功能改变有关。目前，大多数关于角膜的研究都是在体外二维培养或动物模型上进行的。尽管2D培养模型可以以低成本提供大量数据，但它们很难代表人类角膜复杂的病理生理，并且很难预测动物模型研究可以实现的体内反应。然而，后者的使用带来了伦理问题。因此，有必要确定新的策略和模型，可以有效地整合信息，以减少动物的使用数量。在这里，我们使用来自供体角膜的人角膜上皮细胞（hCECs）分化成三维(3D)-器官型气液界面（ALI），其特征与角膜上皮相似。将3d器官型ALI角膜上皮置于高糖条件下，生成糖尿病上皮病模型。我们的模型显示了这种病理的分子和细胞特征，如上皮缺陷和炎症，IL-1β、TNF-α、p-NF-kB、COX-2、MMP-2和MMP-9的表达增加。所提供的数据强调了3d器官型角膜上皮在糖尿病上皮病变建模中的效用，为药物筛选以及精确和个性化医疗提供了新的途径。

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引用次数: 0

Abundance of dopamine and its receptors in the brain and adipose tissue following diet-induced obesity or caloric restriction 饮食引起的肥胖或热量限制后大脑和脂肪组织中多巴胺及其受体的丰度

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-05-08 DOI: 10.1016/j.trsl.2025.05.001

Fleur W Hukema , Susanne Hetty , Christakis Kagios , Sofia Zelleroth , Giovanni Fanni , Maria J Pereira , Maria K Svensson , Magnus Sundbom , Anna Nilsson , Per E Andrén , Erika Roman , Jan W Eriksson

While obesity and type 2 diabetes (T2D) are associated with altered dopaminergic activity in the central nervous system and in adipose tissue (AT), the directions and underlying mechanisms remain inconclusive. Therefore, we characterized changes in the abundance of dopamine, its metabolites, and receptors DRD1 and DRD2 in the brain and AT upon dietary intervention or obesity. Male Wistar rats were fed either a standard pellet diet, a cafeteria diet inducing obesity and insulin resistance, or a calorie-restricted diet for 12 weeks. Abundance of dopamine and its receptors DRD1 and DRD2 were examined in brain regions relevant for feeding behavior and energy homeostasis. Furthermore, DRD1 and DRD2 protein levels were analyzed in rat inguinal and epidydimal AT and in human subcutaneous and omental AT from individuals with or without obesity. Rats with diet-induced obesity displayed higher dopamine levels, as well as DRD1 or DRD2 receptor levels in the caudate putamen and the nucleus accumbens core. Surprisingly, caloric restriction induced similar changes in DRD1 and DRD2, but not in dopamine levels, in the brain. Both diets reduced DRD1 abundance in inguinal and epidydimal AT, but upregulated DRD2 levels in inguinal AT. Furthermore, in human obesity, DRD1 protein levels were elevated only in omental AT, while DRD2 was upregulated in both omental and subcutaneous AT. These findings highlight dopaminergic responses to changes in energy balance, occurring both in the brain and AT. We propose that dopaminergic pathways are involved in tissue crosstalk during the development of obesity and T2D.

虽然肥胖和2型糖尿病（T2D）与中枢神经系统和脂肪组织（AT）中多巴胺能活性的改变有关，但其方向和潜在机制尚不明确。因此，我们表征了饮食干预或肥胖后大脑和AT中多巴胺、多巴胺代谢物以及受体DRD1和DRD2丰度的变化。雄性Wistar大鼠被喂食标准颗粒饮食、导致肥胖和胰岛素抵抗的自助餐厅饮食或限制卡路里饮食，为期12周。多巴胺及其受体DRD1和DRD2的丰度在与摄食行为和能量稳态相关的大脑区域被检测。此外，还分析了肥胖或非肥胖个体大鼠腹股沟和附睾AT以及人皮下和网膜AT中DRD1和DRD2蛋白水平。饮食诱导肥胖的大鼠显示出更高的多巴胺水平，以及尾状壳核和伏隔核核心的DRD1或DRD2受体水平。令人惊讶的是，热量限制引起了大脑中DRD1和DRD2的类似变化，但没有引起多巴胺水平的变化。两种饮食均降低了腹股沟和附睾AT中DRD1的丰度，但上调了腹股沟AT中DRD2的水平。此外，在人类肥胖中，DRD1蛋白水平仅在网膜AT中升高，而DRD2在网膜和皮下AT中均上调。这些发现强调了多巴胺能对能量平衡变化的反应，发生在大脑和AT中。我们认为多巴胺能通路在肥胖和T2D的发展过程中参与了组织串扰。

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引用次数: 0

Information for Readers 读者资讯

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-05-01 DOI: 10.1016/S1931-5244(25)00045-3

引用次数: 0

Editorial Advisory Board 编辑顾问委员会

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-05-01 DOI: 10.1016/S1931-5244(25)00043-X

引用次数: 0

Author Guidelines 作者指导方针

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-05-01 DOI: 10.1016/S1931-5244(25)00044-1

引用次数: 0

Cardioprotective effects of PARP Inhibitors: A meta-analysis of animal studies PARP抑制剂的心脏保护作用：动物研究的荟萃分析

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-04-30 DOI: 10.1016/j.trsl.2025.04.004

Seong Kyung Kim , Jae Hyun Kim , Inyeong Moon , Jiwon Min , Jieun Park , Myeong Gyu Kim

Poly(adenosine diphosphate [ADP] ribose) polymerase (PARP) inhibitors are expected to provide benefits to the cardiovascular system. However, the cardioprotective effect of PARP inhibitors has not been systematically reviewed or quantitatively analyzed. This study aimed to assess the cardioprotective effects of PARP inhibitors through a meta-analysis of animal studies. Three databases PubMed, Web of Sciences, and Embase were searched until September 1, 2023. The risk of bias was assessed using SYRCLE’s Risk of Bias. A total of 74 animal studies that investigated the cardiac function of PARP inhibitors compared to placebo or vehicle, were included. Outcome measures were hemodynamic indexes, cardiac contractility, and biomarkers of myocardial injury. Pooled effect size was estimated using a random-effects model with RevMan 5.4. PARP inhibitors were associated with enhanced hemodynamic indexes, including cardiac output (standardized mean difference, 0.86 [95 % CI, 0.54 to 1.17]; p < 0.00001) and stroke volume (0.42 [0.07 to 0.76]; p = 0.02). PARP inhibitors were associated with increased cardiac contractility, including ejection fraction (0.71 [0.42 to 1.01]; p < 0.00001) and fractional shortening (0.96 [0.62 to 1.31]; p < 0.00001). PARP inhibitors were associated with decreased troponin І (-1.42 [-2.16 to -0.68]; p = 0.0002), plasma B-type natriuretic peptide (-0.95 [-1.56 to -0.33]; p = 0.003), creatine kinase (-1.81 [-2.63 to -0.99]; p < 0.0001), and infarct size (-1.58 [-2.01 to -1.14]; p < 0.00001). PARP inhibitors improve cardiac functions and attenuate myocardial injury in animals, which indicate the cardioprotective effects. Further human studies are necessary.

聚二磷酸腺苷[ADP]核糖)聚合酶（PARP）抑制剂有望为心血管系统提供益处。然而，PARP抑制剂的心脏保护作用尚未系统回顾或定量分析。本研究旨在通过动物研究的荟萃分析来评估PARP抑制剂的心脏保护作用。检索了PubMed、Web of Sciences和Embase三个数据库，直到2023年9月1日。偏倚风险采用sycle的偏倚风险评估。共纳入74项动物研究，研究了PARP抑制剂与安慰剂或对照剂的心功能。结果测量血液动力学指标、心脏收缩力和心肌损伤的生物标志物。使用RevMan 5.4的随机效应模型估计合并效应大小。PARP抑制剂与血流动力学指标增强相关，包括心输出量(标准化平均差，0.86 [95% CI， 0.54至1.17]；p & lt;0.00001)和行程体积(0.42 [0.07 ~ 0.76]；P = 0.02)。PARP抑制剂与心脏收缩力增加相关，包括射血分数(0.71 [0.42 ~ 1.01]；p & lt;0.00001)和分数缩短(0.96[0.62至1.31]；p & lt;0.00001)。PARP抑制剂与肌钙蛋白降低І相关(-1.42[-2.16至-0.68]；p = 0.0002)，血浆b型利钠肽(-0.95 [-1.56 ~ -0.33]；P = 0.003)，肌酸激酶(-1.81 [-2.63 ~ -0.99]；p & lt;0.0001)，梗死面积(-1.58[-2.01至-1.14]；p & lt;0.00001)。PARP抑制剂可改善动物心功能，减轻心肌损伤，表明其具有心脏保护作用。进一步的人体研究是必要的。

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引用次数: 0

tiRNA-HAR contributes to ischemic myocardial injury via facilitating HuR-mediated stability of p53 tiRNA-HAR通过促进hr介导的p53稳定性参与缺血性心肌损伤

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-04-17 DOI: 10.1016/j.trsl.2025.04.002

Changhao Wang , Yuelin Gao , Kuiwu Liu , Yaozhi Zhang , Zhiyong Sun , Min Huang , Zhezhe Qu , Shuting Yu , Jiaqi Han , Zhongting Mei , Shunkang Dou , Jianhao Jiang , Ying Li , Na Li , Chuanhao Huang , Yuechao Dong , Baofeng Yang , Weijie Du

Cardiomyocyte death due to heart occlusion of coronary artery is the main driver to myocardial infarction (MI) and subsequent heart failure progression. tsRNA, a small RNA fragment from tRNA, has been shown to be implicated in many physiological and pathological processes by exerting different biological functions, but the roles of tsRNA in ischemic cardiac injury remain to be determined. The present study identified a hypoxia responsive-tiRNA (tiRNA-HAR) was markedly upregulated in ischemic mouse myocardium and hypoxic cardiomyocytes, respectively. Enforced expression of tiRNA-HAR by transfecting its mimic caused and aggravated, while knockdown of tiRNA-HAR mitigated cardiomyocyte apoptosis upon hypoxia. Cardiac specific knockdown of tiRNA-HAR mediated by AAV9 (adeno-associated virus 9) harboring an antisense oligonucleotide reduced cardiomyocytes apoptosis and improved cardiac function after MI. Mechanistically, tiRNA-HAR directly bound to HuR and enhanced the binding capacity of HuR and p53, thereby increasing the stability of p53. Silencing of HuR partially reversed the aggravative effects of tiRNA-HAR overexpression on cardiomyocyte apoptosis in the context of hypoxia. Collectively, our study reveals that tiRNA-HAR play a critical role in regulating cardiomyocytes apoptosis and cardiac injury via targeting HuR/p53 signaling axis after MI, and tiRNA-HAR might be a novel therapeutic target for treatment of ischemic heart disease.

冠状动脉心脏闭塞引起的心肌细胞死亡是心肌梗死（MI）和随后的心力衰竭进展的主要驱动因素。tsRNA是来自tRNA的一个小RNA片段，已被证明通过发挥不同的生物学功能参与许多生理和病理过程，但tsRNA在缺血性心脏损伤中的作用仍有待确定。本研究发现缺氧反应性的tirna （tiRNA-HAR）分别在缺血小鼠心肌和缺氧心肌细胞中显著上调。通过转染tiRNA-HAR模拟物，增强tiRNA-HAR的表达可引起并加重心肌细胞缺氧后的凋亡，而tiRNA-HAR的敲低可减轻心肌细胞缺氧后的凋亡。含有反义寡核苷酸的腺相关病毒9 （AAV9）介导的心脏特异性敲低tiRNA-HAR可减少心肌细胞凋亡，改善心肌功能。在机制上，tiRNA-HAR可直接与HuR结合，增强HuR与p53的结合能力，从而提高p53的稳定性。在缺氧环境下，HuR的沉默部分逆转了tiRNA-HAR过表达对心肌细胞凋亡的加重作用。综上所述，我们的研究表明，tiRNA-HAR在心肌梗死后通过靶向HuR/p53信号轴调控心肌细胞凋亡和心脏损伤中发挥了关键作用，tiRNA-HAR可能成为治疗缺血性心脏病的新靶点。

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引用次数: 0

Loss of peptidylarginine deiminase 4 mitigates maladaptive cardiac remodeling after myocardial infarction through inhibition of inflammatory and profibrotic pathways 肽精氨酸脱亚胺酶4的缺失通过抑制炎症和纤维化途径减轻心肌梗死后不适应的心脏重构

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-04-17 DOI: 10.1016/j.trsl.2025.04.003

Michelle Holthaus , Xiaolin Xiong , Kaveh Eghbalzadeh , Clara Großmann , Simon Geißen , Fabian Piontek , Martin Mollenhauer , Ali T. Abdallah , Thomas Kamphausen , Markus Rothschild , Thorsten Wahlers , Adnana Paunel-Görgülü

Inflammation and progressive fibrosis represent predictive risk factors for heart failure (HF) development following myocardial infarction (MI). Peptidylargininine deiminase 4 (PAD4) catalyzes the citrullination of arginine residues in polypeptides and has recently been identified as a contributor to HF pathogenesis. This study aimed to evaluate the role of PAD4 in monocytes / macrophages (Mo/Mφ) and cardiac fibroblasts (CFs) for cardiac repair following MI and HF progression. Cardiac Padi4 expression significantly increased in mice subjected to MI by permanent coronary artery ligation as well as in humans who died from MI. Transcriptome analysis revealed marked downregulation of inflammation-related genes in infarcted hearts and cardiac Mo/Mφ from global PAD4 knockout (PAD4^−/−) mice on day 7 post-MI accompanied by increased frequency of reparative CD206⁺ macrophages. Mechanistically, pharmacological and genetic PAD4 inhibition abrogated nuclear NF-κB translocation and inflammatory gene expression in bone marrow-derived macrophages (BMDM). Simultaneously, reduced inflammation and diminished cardiac levels of transforming growth factor-β (TGF-β) along with impaired IL-6 / TGF-β signaling in PAD4^−/− CFs were associated with decreased expression of fibrotic genes, reduced collagen deposition, improved cardiac function, and enhanced 28-day survival in PAD4^−/− mice. Strikingly, whereas pharmacological PAD inhibition in the acute phase after MI exacerbated cardiac damage, treatment starting on day 7 ameliorated cardiac remodeling and improved long-term survival in mice. Collectively, we here identified PAD4 as a critical regulator of inflammatory genes in Mo/Mφ and of profibrotic pathways in CFs. Thus, therapeutic approaches directed against PAD4 are promising interventions to alleviate adverse cardiac remodeling and subsequent HF development.

炎症和进行性纤维化是心肌梗死（MI）后心力衰竭（HF）发展的预测危险因素。肽精氨酸脱亚胺酶4 （PAD4）催化多肽中精氨酸残基的瓜氨酸化，最近被确定为HF发病机制的一个贡献者。本研究旨在评估PAD4在心肌梗死和心衰进展后单核/巨噬细胞（Mo/Mφ）和心脏成纤维细胞（CFs）心脏修复中的作用。永久性冠状动脉结痂导致心肌梗死的小鼠以及心肌梗死死亡的人心脏中Padi4的表达显著增加。转录组分析显示，心肌梗死后第7天，PAD4全基因敲除（PAD4−/−）小鼠的梗死心脏和心脏Mo/Mφ中炎症相关基因显著下调，并伴有修复性CD206+巨噬细胞频率增加。在机制上，药物和基因PAD4抑制可消除骨髓源性巨噬细胞（BMDM）的核NF-κB易位和炎症基因表达。同时，PAD4−/−CFs中炎症的减少和心肌转化生长因子-β (TGF-β)水平的降低以及IL-6 / TGF-β信号的受损与纤维化基因表达的降低、胶原沉积的减少、心功能的改善以及PAD4−/−小鼠28天生存率的提高有关。引人注目的是，尽管心肌梗死后急性期的PAD药物抑制加重了心脏损伤，但从第7天开始的治疗改善了小鼠的心脏重塑并提高了长期存活率。总之，我们在这里确定了PAD4是Mo/Mφ中炎症基因和cf中纤维化途径的关键调节因子。因此，针对PAD4的治疗方法有望缓解不良的心脏重构和随后的HF发展。

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引用次数: 0

Kv1.3 expression on CD4 (+) T cells promotes interleukin-17A-associated airway inflammation and airway remodeling in asthma Kv1.3在CD4 (+) T细胞上的表达可促进哮喘患者白细胞介素- 17a相关的气道炎症和气道重塑

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-04-10 DOI: 10.1016/j.trsl.2025.04.001

Bingqing Sun , Jiangtao Lin

Background

Different types of T helper cells play an important role in disease severity and treatment response in patients with asthma. The potassium channel Kv1.3 is a type of potentially therapeutic target in T-cell-mediated inflammatory diseases.

Objective

This study aimed to explore the potential of Kv1.3 as a therapeutic target for asthma and to assess the efficacy of the Kv1.3 inhibitor PAP-1 in the treatment of asthma.

Methods

Kv1.3 expression on CD4⁺T cells was determined using data from public databases. CD4⁺T cells were isolated from peripheral blood samples obtained from healthy individuals and patients with asthma. The mouse models of OVA-induced asthma and Kv1.3 knockout were established. The underlying mechanism was investigated using mouse splenic CD4⁺T cells and BEAS-2B cells. OVA-induced asthmatic mice were treated with the Kv1.3 selective blocker PAP-1.

Results

Based on public data, we determined the distribution of Kv1.3 on CD4⁺T cells, its up-regulation in asthma, and its correlation with Th17/Treg balance. Upregulation of Kv1.3 in CD4⁺T cells was associated with enhanced activation of these cells and airway inflammation in patients and mice with asthma, accompanied by increased IL-17A levels in alveolar lavage fluid. Conversely, Kv1.3 deficiency significantly attenuated airway inflammation, lowered IL-17A levels in bronchoalveolar lavage fluid, and inhibited airway epithelial-mesenchymal transition in asthmatic mice. Furthermore, treatment with the Kv1.3 selective blocker PAP-1 attenuated inflammation in lung tissues and prevented airway remodeling in OVA-induced asthmatic mice.

Conclusions

Kv1.3 expression on CD4⁺ T cells was correlated with IL-17A-associated airway inflammation and remodeling in asthma, which may be regarded as a potential diagnostic marker and therapeutic target for asthma.

Translational significance

Based on our study, Kv1.3 expression on CD4⁺T cells was correlated with IL-17A-associated airway inflammation and remodeling in asthma, which may be regarded as a potential diagnostic marker and therapeutic target for asthma. The treatment with the Kv1.3 selective blocker PAP-1 attenuated inflammation in lung tissues and prevented airway remodeling in OVA-induced asthmatic mice. Our discoveries offer novel perspectives for a better understanding of IL-17A-associated airway remodeling in asthma. The development of drugs targeting Kv1.3 holds application value for IL-17A-associated asthma.

不同类型的辅助性T细胞在哮喘患者的疾病严重程度和治疗反应中起重要作用。钾通道Kv1.3是t细胞介导的炎症性疾病的一种潜在治疗靶点。目的探讨Kv1.3作为哮喘治疗靶点的潜力，评估Kv1.3抑制剂PAP-1治疗哮喘的疗效。方法利用公共数据库数据检测CD4+T细胞中skv1.3的表达。从健康个体和哮喘患者的外周血样本中分离出CD4+T细胞。建立ova致哮喘小鼠模型和Kv1.3基因敲除模型。利用小鼠脾CD4+T细胞和BEAS-2B细胞研究其潜在机制。用Kv1.3选择性阻断剂PAP-1治疗ova诱导的哮喘小鼠。结果基于公开数据，我们确定了Kv1.3在CD4+T细胞上的分布、哮喘患者Kv1.3的上调及其与Th17/Treg平衡的相关性。在哮喘患者和小鼠中，CD4+T细胞中Kv1.3的上调与这些细胞的激活增强和气道炎症有关，并伴有肺泡灌洗液中IL-17A水平升高。相反，Kv1.3缺乏可显著减轻哮喘小鼠气道炎症，降低支气管肺泡灌洗液中IL-17A水平，抑制气道上皮-间质转化。结论skv1.3在CD4+ T细胞上的表达与il - 17a相关的哮喘气道炎症和气道重构相关，可作为哮喘的潜在诊断标志物和治疗靶点。根据我们的研究，Kv1.3在CD4+T细胞上的表达与il - 17a相关的哮喘气道炎症和重塑相关，可作为哮喘的潜在诊断标志物和治疗靶点。Kv1.3选择性阻滞剂PAP-1可减轻ova诱导的哮喘小鼠肺组织炎症，阻止气道重塑。我们的发现为更好地理解il - 17a相关的哮喘气道重塑提供了新的视角。靶向Kv1.3的药物开发对il - 17a相关哮喘具有应用价值。

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引用次数: 0

Optical coherence tomography for the qualitative analysis of thyroid tissue images: Feasibility, features, and clinical potential 用于甲状腺组织图像定性分析的光学相干断层扫描：可行性、特征和临床潜力。

IF 6.4 2区医学 Q1 MEDICAL LABORATORY TECHNOLOGY

Translational Research

Pub Date : 2025-03-25 DOI: 10.1016/j.trsl.2025.03.003

Yun Shao , Qianru Xu , Cuixia Feng , Yang Liu , Baolei Jia , Yuning Song , Yuxuan Qiu , Qing Xu , Yanhong Tai , Feng Liang

The most important steps in thyroid surgery include distinguishing benign from malignant lesions and identifying the parathyroid glands. Optical coherence tomography (OCT) provides technical support for intraoperative guidance owing to its real-time, three-dimensional imaging capability. Benign and malignant diagnoses can be confirmed with intraoperative frozen sections; however, current approaches are time-consuming and labor-intensive and do not allow comprehensive, nondestructive tissue assessments. This study aimed to explore the use of OCT for imaging the thyroid tissue by verifying its clinical feasibility and qualitatively analyzing the OCT imaging characteristics of pathological thyroid glands. A customized swept-source OCT (SS-OCT) system was used to collect OCT data corresponding to the pathologies of 61 freshly excised tissue blocks containing either benign or malignant lesions from 45 patients. The OCT images were highly consistent with the H&E histological images, verifying the feasibility of OCT in producing suitable images for analysis. The OCT-derived characteristics of the thyroid tissue were as follows: normal thyroid follicles presented with regularly arranged honeycomb structures; follicular nodular disease (FND) was characterized by heterogeneous nodules composed of follicles of different sizes, with multiple nodules also differing in size and consisting of varied reticular structures and a focally solid appearance; lymphocyte aggregation led to a gray‒black appearance in Hashimoto's thyroiditis tumors; and papillary thyroid carcinoma lesions were characterized by a heterogeneous texture and a low penetration depth. These results demonstrate the imaging capabilities of OCT for thyroid tissue with different pathological conditions and its broad prospects for clinical application.

甲状腺手术中最重要的步骤包括区分良性和恶性病变以及识别甲状旁腺。光学相干断层扫描（OCT）以其实时、三维成像能力为术中引导提供技术支持。术中冷冻切片可确诊良恶性；然而，目前的方法是耗时和劳动密集型的，不允许全面的，非破坏性的组织评估。本研究旨在通过验证OCT对甲状腺组织成像的临床可行性，定性分析病理甲状腺的OCT成像特征，探讨其应用价值。使用定制的扫描源OCT （SS-OCT）系统收集来自45例患者的61个新鲜切除的组织块的病理对应的OCT数据，这些组织块包含良性或恶性病变。OCT图像与H&E组织学图像高度一致，验证了OCT生成适合分析的图像的可行性。oct衍生的甲状腺组织特征如下：正常甲状腺滤泡呈规则排列的蜂窝状结构；卵泡结节病（FND）的特征是由不同大小的卵泡组成的异质性结节，多个结节大小不一，由不同的网状结构组成，局部呈实性外观；淋巴细胞聚集导致桥本甲状腺炎肿瘤呈灰黑色外观；甲状腺乳头状癌病变具有质地不均、浸润深度低的特点。这些结果显示了OCT对不同病理条件下甲状腺组织的成像能力和临床应用的广阔前景。

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引用次数: 0