Experimental and molecular pathology最新文献_第2页

Influence of diet and exercise on leukocyte telomere length, markers of oxidative stress and inflammation in rats 饮食和运动对大鼠白细胞端粒长度、氧化应激和炎症标志物的影响

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104947

Mehmet Mustafa Tilekli , Ali Kerim Yılmaz , Yavuz Yasul , Nurhan Çon , Sevcan Mercan , Nilüfer Tek

Telomere length is an important biomarker of biological aging and is affected by nutrition and physical activity. This study investigated the effects of diets with different fat contents and increased physical activity on certain pro/anti-inflammatory and oxidative stress markers and aging. The study is performed in a randomized, experimental, and controlled design with 48 rats, 8 weeks old, divided into 6 different groups (Control (C), exercise (E), unsaturated fat diet (USF), saturated fat diet (SF), unsaturated fat diet + exercise (USF + E), and saturated fat diet + exercise (SF + E)). The rats performed aerobic swimming exercise for 50 days and were fed a diet with different fat content. TAS, TOS, and MDA levels were determined by colorimetric analysis while 8-OHdG, IL-10, and TNF-α were determined by ELISA. Additionally, leukocyte telomere length is determined by the PCR method. Weight changes were also recorded. Plasma TOS, OSI, and TNF-α were lowest in the USF group and highest in the SF and SF + E groups. MDA, 8-OHdG and TG levels were highest in the SF group. The lowest IL-10 level was detected in group C. TL level was the highest in the USF group. There was also a moderate, negative, and significant correlation between telomeres and TOS, OSI, and TNF-α. The groups with the highest body weight gain were C, SF, and SF + E. Diets low in saturated fat or high in unsaturated fat, and physical activity were associated with leukocyte telomere length and alteration of oxidative and pro/anti-inflammatory markers.

端粒长度是生物衰老的重要生物指标，受营养和体力活动的影响。本研究探讨了不同脂肪含量的饮食和增加体力活动对某些促/抗炎和氧化应激标志物以及衰老的影响。研究采用随机、实验和对照设计，将48只8周龄大鼠分为6个不同组(对照组(C)、运动组（E)、不饱和脂肪饮食（USF）、饱和脂肪饮食（SF）、不饱和脂肪饮食+运动组（USF + E）和饱和脂肪饮食+运动组（SF + E））。大鼠进行有氧游泳运动50天，并喂食不同脂肪含量的饮食。比色法测定TAS、TOS、MDA水平，ELISA法测定8-OHdG、IL-10、TNF-α水平。此外，白细胞端粒长度由PCR方法确定。体重变化也被记录下来。血浆TOS、OSI、TNF-α在USF组最低，SF和SF + E组最高。SF组MDA、8-OHdG和TG水平最高。c组IL-10水平最低，USF组IL-10水平最高。端粒与TOS、OSI和TNF-α之间也存在中度、负和显著相关。体重增加最多的组是C组、SF组和SF + e组。低饱和脂肪或高不饱和脂肪的饮食，体力活动与白细胞端粒长度以及氧化和促/抗炎标志物的改变有关。

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引用次数: 0

Corrigendum to “Anti-tumor effect of antibody-drug conjugate targeting cell adhesion molecule 1 on GIST cells representing small intestinal GIST” [Experimental and Molecular Pathology 139 (2024) 104922] 以细胞粘附分子 1 为靶点的抗体-药物共轭物对小肠 GIST 细胞的抗肿瘤作用》[实验与分子病理学 139 (2024) 104922] 勘误。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104934

Makoto Yoshida , Jiayin Yuan , Takako Kihara , Neinei Kimura , Takashi Yamasaki , Mizuka Ohkouchi , Yuka Hashikura , Koji Isozaki , Man Hagiyama , Akihiko Ito , Seiichi Hirota

引用次数: 0

Corrigendum to “Suppression of miR-143-3p contributes to the anti-fibrosis effect of atorvastatin on myocardial tissues via the modulation of Smad2 activity” [Experimental and Molecular Pathology 112 (2020) 104346] “抑制miR-143-3p通过调节Smad2活性有助于阿托伐他汀对心肌组织的抗纤维化作用”[实验与分子病理学112(2020)104346]的勘误。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104945

Bo Yu , Ming Yu , Hongli Zhang, Di Xie, Wei Nie, Kaiyao Shi

引用次数: 0

Pathobiology of myocardial and cardiomyocyte injury in ischemic heart disease: Perspective from seventy years of cell injury research 缺血性心脏病心肌和心肌细胞损伤的病理生物学：七十年细胞损伤研究的视角。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-11-21 DOI: 10.1016/j.yexmp.2024.104944

L. Maximilian Buja

This review presents a perspective on the pathobiology of acute myocardial infarction, a major manifestation of ischemic heart disease, and related mechanisms of ischemic and toxic cardiomyocyte injury, based on advances and insights that have accrued over the last seventy years, including my sixty years of involvement in the field as a physician-scientist-pathologist. This analysis is based on integration of my research within the broader context of research in the field. A particular focus has been on direct measurements in cardiomyocytes of electrolyte content by electron probe X-ray microanalysis (EPXMA) and Ca²⁺ fluxes by fura-2 microspectrofluorometry. These studies established that increased intracellular Ca²⁺ develops at a transitional stage in the progression of cardiomyocyte injury in association with ATP depletion, other electrolyte alterations, altered cell volume regulation, and altered membrane phospholipid composition. Subsequent increase in total calcium with mitochondrial calcium accumulation can occur. These alterations are characteristic of oncosis, which is an initial pre-lethal state of cell injury with cell swelling due to cell membrane dysfunction in ATP depleted cells; oncosis rapidly progresses to necrosis/necroptosis with physical disruption of the cell membrane, unless the adverse stimulus is rapidly reversed. The observed sequential changes fit a three-stage model of membrane injury leading to irreversible cell injury. The data establish oncosis as the primary mode of cardiomyocyte injury in evolving myocardial infarcts. Oncosis also has been documented to be the typical form of non-ischemic cell injury due to toxins. Cardiomyocytes with less energy impairment have the capability of undergoing apoptosis and autophagic death as well as oncosis, as is seen in pathological remodeling in chronic heart failure. Work is ongoing to apply the insights from experimental studies to better understand and ameliorate myocardial ischemia and reperfusion injury in patients. The perspective and insights in this review are derived from basic principles of pathology, an integrative discipline focused on mechanisms of disease affecting the cell, the organizing unit of living organisms.

急性心肌梗死是缺血性心脏病的一种主要表现形式，本综述基于过去七十年（包括我作为一名医生、科学家和病理学家参与该领域研究的六十年）积累的进展和见解，从病理生物学的角度阐述了急性心肌梗死的病理生理以及缺血性和毒性心肌细胞损伤的相关机制。这一分析的基础是将我的研究与该领域更广泛的研究相结合。我的研究重点之一是通过电子探针 X 射线显微分析法（EPXMA）直接测量心肌细胞中的电解质含量，以及通过呋喃-2 微谱荧光测定法测量 Ca2+ 通量。这些研究证实，细胞内 Ca2+ 的增加发生在心肌细胞损伤进展的过渡阶段，与 ATP 消耗、其他电解质改变、细胞体积调节改变和膜磷脂成分改变有关。随后会出现总钙增加和线粒体钙积聚。这些变化是细胞坏死的特征。细胞坏死是一种细胞损伤的初始致死前状态，由于 ATP 贫竭细胞的细胞膜功能失调而导致细胞肿胀；除非迅速逆转不良刺激，否则细胞坏死会迅速发展为细胞膜物理破坏的坏死/坏死。观察到的连续变化符合膜损伤导致不可逆细胞损伤的三阶段模型。这些数据确立了瘤变是演变性心肌梗死中心肌细胞损伤的主要模式。据文献记载，瘤变也是毒素导致的非缺血性细胞损伤的典型形式。能量损伤较小的心肌细胞有能力发生凋亡和自噬死亡以及肿瘤病变，这在慢性心力衰竭的病理重塑中可以看到。目前正在努力应用实验研究的见解，以更好地理解和改善患者的心肌缺血和再灌注损伤。本综述的观点和见解来自病理学的基本原理，病理学是一门综合性学科，重点研究影响细胞（生物体的组织单位）的疾病机制。

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引用次数: 0

Diagnostic criteria and therapeutic implications of rapid-onset demyelinating polyneuropathies 速发型脱髓鞘性多发性神经病的诊断标准和治疗意义

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-11-04 DOI: 10.1016/j.yexmp.2024.104942

Wiktoria Rałowska-Gmoch , Magdalena Koszewicz , Beata Łabuz-Roszak , Sławomir Budrewicz , Edyta Dziadkowiak

Guillain-Barré syndrome (GBS) and acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) are the most common autoimmune polyneuropathies. Their aetiology is unclear. The pathomechanism includes damage mainly to the myelin sheath and, in the long-term process, secondary axonal loss. Both inflammatory polyneuropathies involve different combinations of motor, sensory and autonomic fibres in the peripheral nerves. The differential diagnosis should be based on clinical and neurophysiological features, and laboratory tests. Numerous studies aim to demonstrate the most common errors in the diagnosis of Guillain-Barré syndrome and acute-onset CIDP. Misdiagnosis can result in the wrong treatment. We still do not have reliable markers to help diagnose the disease or to monitor the effectiveness of the therapy.

吉兰-巴雷综合征（GBS）和急性发作性慢性炎症性脱髓鞘多发性神经病（A-CIDP）是最常见的自身免疫性多发性神经病。它们的病因尚不清楚。其病理机制主要包括髓鞘受损，以及在长期过程中继发的轴突丢失。这两种炎症性多发性神经病都涉及周围神经中运动、感觉和自主神经纤维的不同组合。鉴别诊断应基于临床和神经生理学特征以及实验室检查。大量研究旨在证明吉兰-巴雷综合征和急发性 CIDP 诊断中最常见的错误。误诊会导致错误的治疗。我们仍然没有可靠的标记物来帮助诊断疾病或监测治疗效果。

引用次数: 0

Irisin and neuroinflammation: Challenges and opportunities 鸢尾素与神经炎症：挑战与机遇

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-10-28 DOI: 10.1016/j.yexmp.2024.104941

Erika Yolanda Hernández Sandoval, Zulma Janeth Dueñas Gómez

Irisin is a myokine that is cleaved from 5-domain type III fibronectin (FNDC5), and is known for its metabolic functions as it stimulates browning of white adipose tissue; similarly, effects on the central nervous system have been described, specifically in neurodevelopmental and neuroprotection processes. The purpose of this review is to describe recent information on the effects of irisin on neuroinflammation to contribute to the knowledge about the mechanisms by which irisin and exercise could generate benefits for some neurological diseases. The review conducted found several studies describing the effect of irisin on pathways such as STAT3, p38, cAMP/PKA/CREB, as well as effects on GFAP protein expression or apoptosis processes in both in vitro and in vivo models; likewise, these pathways are associated with better BDNF expression. Despite increasing information on this topic, it is still necessary to clarify the mechanisms by which irisin has effects on neuroinflammation and this could represent an opportunity to generate more treatments for diseases such as Alzheimer's, Parkinson's or Diabetes Mellitus.

鸢尾素是一种肌动素，由 5-结构域 III 型纤维粘连蛋白（FNDC5）裂解而成，因其刺激白色脂肪组织褐变的代谢功能而闻名；同样，它对中枢神经系统的影响也有描述，特别是在神经发育和神经保护过程中。本综述旨在描述鸢尾素对神经炎症影响的最新信息，以帮助人们了解鸢尾素和运动对某些神经系统疾病产生益处的机制。综述发现，有几项研究描述了鸢尾素对 STAT3、p38、cAMP/PKA/CREB 等通路的影响，以及在体外和体内模型中对 GFAP 蛋白表达或细胞凋亡过程的影响；同样，这些通路与更好的 BDNF 表达相关。尽管有关这一主题的信息越来越多，但仍有必要阐明鸢尾素对神经炎症产生影响的机制，这可能是为阿尔茨海默氏症、帕金森氏症或糖尿病等疾病提供更多治疗方法的机会。

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引用次数: 0

Assessing pathogenicity of mismatch repair variants of uncertain significance by molecular tumor analysis 通过肿瘤分子分析评估意义不明的错配修复变体的致病性。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-10-21 DOI: 10.1016/j.yexmp.2024.104940

Anne-Sophie van der Werf't Lam , Noah C. Helderman , Arnoud Boot , Diantha Terlouw , Hans Morreau , Hailian Mei , Rebecca E.E. Esveldt-van Lange , Inge M.M. Lakeman , Christi J. van Asperen , Emmelien Aten , Nandy Hofland , Pia A.M. de Koning Gans , Emily Rayner , Carli Tops , Niels de Wind , Tom van Wezel , Maartje Nielsen

Functional analyses are the main method to classify mismatch repair (MMR) gene variants of uncertain significance (VUSs). However, the pathogenicity remains unclear for many variants because of conflicting results between clinical, molecular, and functional data. In this study, we evaluated whether whole exome sequencing (WES) could add another layer of evidence to elucidate the pathogenicity of MMR variants with conflicting interpretations. WES was performed on formalin-fixed paraffin-embedded tumor tissue of eight patients with a constitutional MMR VUS (seven families), including eight colorectal and two endometrial carcinomas and one ovarian carcinoma. Cell-free CIMRA assays were performed to assign Odds of Pathogenicity to these VUSs. In four families, seven tumors showed MMR deficiency-associated mutational signatures, supporting the pathogenicity of the VUS. Moreover, somatic (second) MMR hits identified in the WES data were found to explain MMR staining patterns when the MMR staining was discordant with the reported germline MMR gene variant. In conclusion, WES did not significantly reclassify VUS in these cases but clarified some phenotypic aspects such as age of onset and explanations in case of discordant MMR stainings.

功能分析是对意义不确定的错配修复（MMR）基因变异进行分类的主要方法。然而，由于临床、分子和功能数据之间的结果相互矛盾，许多变异的致病性仍不明确。在本研究中，我们评估了全外显子组测序（WES）能否为阐明存在解释冲突的 MMR 变异的致病性提供另一层证据。我们对八名MMR VUS患者（七个家族）的福尔马林固定石蜡包埋肿瘤组织进行了全外显子组测序，其中包括八例结直肠癌、两例子宫内膜癌和一例卵巢癌。进行了无细胞 CIMRA 检测，以确定这些 VUS 的致病几率。在四个家族中，七个肿瘤显示出与 MMR 缺乏相关的突变特征，支持了 VUS 的致病性。此外，当MMR染色与报告的种系MMR基因变异不一致时，WES数据中发现的体细胞（第二）MMR命中可解释MMR染色模式。总之，在这些病例中，WES 并没有对 VUS 进行明显的重新分类，但澄清了一些表型方面的问题，如发病年龄和 MMR 染色不一致时的解释。

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引用次数: 0

Impaired immunoproteasomal function exacerbates renal ischemia-reperfusion injury 免疫保护体功能受损会加剧肾缺血再灌注损伤

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-10-18 DOI: 10.1016/j.yexmp.2024.104939

Yasushi Ishii , Aya Fukui-Miyazaki , Sari Iwasaki , Takahiro Tsuji , Kiyohiko Hotta , Hajime Sasaki , Shimpei Nakagawa , Takuma Yoshida , Eri Murata , Koji Taniguchi , Nobuo Shinohara , Akihiro Ishizu , Masanori Kasahara , Utano Tomaru

Oxidative stress caused by reactive oxygen species (ROS) is involved in the pathogenesis of renal ischemia-reperfusion injury (I/R injury), a major cause of acute kidney injury and delayed graft function (DGF). DGF is an early transplant complication that worsens graft prognosis and patient survival, but the underlying molecular changes are unclear. The proteasome is a multicatalytic enzyme complex that degrades both normal and damaged proteins, and recent studies have revealed that the immunoproteasome, a specific proteasome isoform whose proteolytic activity enhances the generation of antigenic peptides, plays critical roles in the cellular response against oxidative stress. In this study, we demonstrate the impact of the immunoproteasome in human DGF and in a mouse model of I/R injury. In patients with DGF, the expression of β5i, a specific immunoproteasome subunit, was decreased in vascular endothelial cells. In a mouse model, β5i knockout (KO) exacerbated renal I/R injury. KO mice showed greater inflammation, oxidative stress, and endothelial damage compared with wild-type mice. Impaired immunoproteasomal activity also caused increased cell death, ROS production, and expression of inflammatory factors in mouse renal vascular endothelial cells under conditions of hypoxia and reoxygenation. In conclusion, reduced expression of the immunoproteasomal catalytic subunit β5i exacerbates renal I/R injury in vivo, potentially increasing the risk of DGF. Further research targeting β5i expression in DGF could lead to the development of novel therapeutic strategies and biomarkers.

活性氧（ROS）引起的氧化应激参与了肾缺血再灌注损伤（I/R 损伤）的发病机制，而I/R 损伤是急性肾损伤和移植物功能延迟（DGF）的主要原因。DGF 是一种早期移植并发症，会恶化移植物预后和患者存活率，但其潜在的分子变化尚不清楚。蛋白酶体是一种多催化酶复合物，可降解正常蛋白质和受损蛋白质，最近的研究发现，免疫蛋白酶体是一种特殊的蛋白酶体异构体，其蛋白水解活性可增强抗原肽的生成，在细胞应对氧化应激的过程中发挥着关键作用。在本研究中，我们证明了免疫蛋白酶体在人类 DGF 和小鼠 I/R 损伤模型中的影响。在 DGF 患者中，血管内皮细胞中特异性免疫蛋白酶体亚基 β5i 的表达减少。在小鼠模型中，β5i基因敲除（KO）会加重肾脏I/R损伤。与野生型小鼠相比，KO 小鼠表现出更严重的炎症、氧化应激和内皮损伤。在缺氧和复氧条件下，免疫保护体活性受损也会导致小鼠肾血管内皮细胞的细胞死亡、ROS 生成和炎症因子表达增加。总之，免疫蛋白酶体催化亚基β5i的表达减少会加重体内肾脏I/R损伤，可能会增加DGF的风险。针对 DGF 中 β5i 表达的进一步研究可能会开发出新型治疗策略和生物标志物。

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引用次数: 0

Histomorphological scoring of murine colitis models: A practical guide for the evaluation of colitis and colitis-associated cancer 小鼠结肠炎模型的组织形态学评分：评估结肠炎和结肠炎相关癌症的实用指南

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-10-16 DOI: 10.1016/j.yexmp.2024.104938

Marianne Remke , Tanja Groll , Thomas Metzler , Elisabeth Urbauer , Janine Kövilein , Theresa Schnalzger , Jürgen Ruland , Dirk Haller , Katja Steiger

Background and aims

Histomorphology is a powerful and cost-efficient tool for evaluating inflammatory and neoplastic conditions. Inflammatory bowel disease (IBD) is a widespread condition with globally rising incidences, and a lot of research is done to better understand the pathogenesis of IBD and to identify potential therapeutic approaches. However, standardized and reproducible scores for the histomorphological evaluation of murine IBD models are lacking. Therefore, we aimed to develop an easy-to-use and reproducible score for standardized assessment of colitis and associated cancer models.

Methods

In this study, samples from three different colitis models with and without associated cancer formation were analyzed to develop a universal, robust, and reproducible score for the grading of murine colitis models using the following three parameters: 1. Extent of leucocyte infiltration, 2. Tissue damage, 3. Architectural disruption of the mucosa.

Results

A scoring system was established for different kinds of colitis models (genetically induced enterocolitis, genetically induced metabolic injury, and chemically induced colitis-associated cancer) and all stages of the disease, from mild inflammatory changes to severe inflammation with neoplastic changes as the extreme extent of IBD. The scoring scheme is easy to use, can easily be learned, and proves to have a high interrater reliability.

Conclusions

We propose a robust histological scoring system for the assessment of murine colitis and colitis-associated cancer models, giving more researchers access to conclusive and reliable histological assessment.

背景和目的组织形态学是评估炎症和肿瘤性疾病的一种强大而经济的工具。炎症性肠病（IBD）是一种广泛存在的疾病，其发病率在全球范围内呈上升趋势，为了更好地了解 IBD 的发病机制并确定潜在的治疗方法，人们进行了大量的研究。然而，小鼠 IBD 模型的组织形态学评估缺乏标准化和可重复的评分标准。因此，我们旨在开发一种易于使用且可重复的评分方法，用于对结肠炎和相关癌症模型进行标准化评估。方法在本研究中，我们分析了三种不同结肠炎模型的样本，包括伴有和不伴有癌症形成的结肠炎模型，并利用以下三个参数开发了一种通用、稳健且可重复的评分方法，用于对小鼠结肠炎模型进行分级：1.结果针对不同类型的结肠炎模型（基因诱导的肠炎、基因诱导的代谢损伤和化学诱导的结肠炎相关癌症）和疾病的各个阶段（从轻度炎症变化到重度炎症并伴有新生物变化，即 IBD 的极端程度）建立了一套评分系统。结论我们提出了一种用于评估小鼠结肠炎和结肠炎相关癌症模型的强大的组织学评分系统，让更多的研究人员能够获得确凿可靠的组织学评估。

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引用次数: 0

A weighted and cumulative point system for accurate scoring of intestinal pathology in a piglet model of necrotizing enterocolitis 用于在仔猪坏死性小肠结肠炎模型中对肠道病理学进行准确评分的加权累积积分系统。

IF 2.8 4区医学 Q2 PATHOLOGY

Experimental and molecular pathology

Pub Date : 2024-10-03 DOI: 10.1016/j.yexmp.2024.104936

Simone Margaard Offersen, Nicole Lind Henriksen, Anders Brunse

Necrotizing enterocolitis (NEC) is a serious condition in premature infants, in which a portion of the intestine undergoes inflammation and necrosis. The preterm pig develops NEC spontaneously, making it a suitable model for exploring novel NEC treatments. We aimed to revise the intestinal scoring system to more accurately describe the diversity of NEC lesions in the preterm piglet model. We included 333 preterm piglets from four experiments, each delivered via cesarean section. The piglets were fed either a gently processed (GP) or harshly processed (HP) milk formula for 96 h before euthanasia. At necropsy, the gastrointestinal tract was assessed with 1) an established 6-grade score and 2) a descriptive approach focusing on the distribution and severity of hyperemia, hemorrhage, pneumatosis intestinalis (intramural gas), and necrosis. Subsequently, the descriptive registrations were converted into a weighted and cumulative point (WCP) score. Compared to the 6-grade score, the WCP score enabled a greater segregation of severity levels, especially among organs with more prominent NEC lesions. IL-1β in small intestinal lesions and both IL-8 and IL-1β in colon lesions correlated positively with the WCP scale. A histopathological grade system (0–8) was established and revealed mucosal pathology in lesion biopsies, which were not recognized macroscopically. Finally, the WCP score showed a higher NEC-promoting effect of the HP formula compared to the GP formula. The descriptive registrations and extended score range of this revised intestinal scoring system enhance the accuracy of describing NEC lesions in preterm pigs. This approach may increase the efficiency of preclinical NEC experiments.

坏死性小肠结肠炎（NEC）是早产儿的一种严重疾病，部分肠道会发生炎症和坏死。早产猪会自发发生坏死性小肠结肠炎，因此是探索新型坏死性小肠结肠炎治疗方法的合适模型。我们旨在修订肠道评分系统，以便更准确地描述早产猪模型中 NEC 病变的多样性。我们纳入了四次实验中的 333 头早产仔猪，每头仔猪都是通过剖腹产分娩的。这些仔猪在安乐死前被喂食温和处理（GP）或苛刻处理（HP）配方奶 96 小时。尸体解剖时，采用以下方法对胃肠道进行评估：1）既定的 6 级评分；2）描述性方法，重点是充血、出血、肠道积气（肠道内气体）和坏死的分布和严重程度。随后，将描述性登记转换为加权累积分（WCP）。与 6 级评分相比，WCP 评分能更好地划分严重程度，尤其是在 NEC 病变较突出的器官之间。小肠病变中的IL-1β以及结肠病变中的IL-8和IL-1β与WCP评分呈正相关。组织病理学分级系统（0-8 级）的建立揭示了病变活组织切片中的粘膜病变，而这些病变在宏观上是无法识别的。最后，WCP评分显示，与GP配方相比，HP配方的NEC促进效果更高。该修订版肠道评分系统的描述性注册和扩展的评分范围提高了早产猪 NEC 病变描述的准确性。这种方法可提高临床前 NEC 实验的效率。

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引用次数: 0