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Paternity testing for crab-eating macaques and rhesus macaques using microsatellite markers 利用微卫星标记对食蟹猕猴和恒河猕猴进行亲子鉴定。
IF 3.4 Q1 Health Professions Pub Date : 2025-09-14 DOI: 10.1002/ame2.70072
Yiming Yuan, Tianqi Sun, Lu Zhang, Wensheng Zhang, Teng Meng, Jianhua Zheng, Rui Zhang, Lei Lu, Zirong Pu, Yan Li, Yefeng Qiu

Accurate macaque paternity identification is of great significance in various fields, yet relevant research remains scarce. Our study aimed to screen effective microsatellite markers for macaque paternity testing. Initially, 300 microsatellite markers were randomly selected from the genome of the crab-eating macaque (Macaca fascicularis), and 12 highly polymorphic tetra-nucleotide repeat markers were identified. These markers' genetic parameters and exclusion probabilities in both crab-eating and rhesus macaque (Macaca mulatta) populations were calculated, meeting the paternity testing requirements for both species. To validate the markers, 16 crab-eating macaque and 10 rhesus macaque families with known pedigrees were randomly chosen for testing. The genotypes of the 12 markers in the macaques' offspring could be traced back to their parents, confirming the accuracy and applicability of the marker combination for paternity identification in both macaque species.

准确的猕猴父权鉴定在各个领域都具有重要意义,但相关的研究还很少。本研究旨在筛选有效的猕猴亲子鉴定微卫星标记。首先,从食蟹猕猴(Macaca fascicularis)基因组中随机选择300个微卫星标记,鉴定出12个高度多态性的四核苷酸重复标记。计算了这些标记在食蟹和恒河猴(Macaca mulatta)种群中的遗传参数和排除概率,满足了这两个物种的亲子鉴定要求。为了验证这些标记,随机选择了16只食蟹猕猴和10个已知血统的恒河猕猴家族进行测试。子代12个标记的基因型均可追溯到其亲本,证实了标记组合在两种猕猴父系鉴定中的准确性和适用性。
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引用次数: 0
Molecular dynamics of the host response to Streptococcus pneumoniae pneumonia in baboons 宿主对狒狒肺炎链球菌肺炎反应的分子动力学。
IF 3.4 Q1 Health Professions Pub Date : 2025-09-14 DOI: 10.1002/ame2.70079
Bryan D. Kraft, Ashlee M. Valente, Ephraim L. Tsalik, Micah T. McClain, Marshall Nichols, Thomas W. Burke, Ricardo Henao, Erik J. Soderblom, J. Will Thompson, M. Arthur Moseley, Lori L. Hudson, Timothy Veldman, Olga M. Better, Mert Aydin, Anna Mazur, Karen E. Welty-Wolf, Claude A. Piantadosi, Geoffrey S. Ginsburg, Christopher W. Woods

Background

Bacterial pneumonia remains a leading cause of morbidity and mortality worldwide despite the widespread availability of antibiotics. Novel pneumonia therapies and biomarkers are urgently needed to improve outcomes and advance personalized therapy. Using an established baboon model of S. pneumoniae pneumonia, we sought to characterize the temporal dynamics of pneumonia host responses to identify novel potential diagnostic and therapeutic molecular targets.

Methods

We performed whole blood transcriptomics, unbiased proteomics, and peripheral cytokine measurements serially in baboons inoculated with S. pneumoniae (n = 23) or saline (n = 10) and modeled the peripheral blood host response using principal components analysis and complex sparse logistic regression. Differentially expressed genes were analyzed for pathway analysis.

Results

Inoculated animals developed characteristic signs and symptoms of pneumonia. A 39-gene signature was derived that classified S. pneumoniae infection with high accuracy (auROC 0.9 and 0.99 at 24 and 48 h post-inoculation, respectively). Similar performance was observed for 48-h biomarker signatures derived from peripheral blood plasma proteomic and cytokine measurements (both auROC >0.9). The gene signature retained strong diagnostic performance (auROC = 0.88) when transformed to human orthologs and applied to patients with acute respiratory illness (n = 34) or healthy controls (n = 20). Pathway analysis at 48 h identified down-regulation of mitophagy and glucocorticoid signaling in peripheral blood.

Conclusions

We report novel peripheral blood gene and protein expression signatures of S. pneumoniae pneumonia that could improve pneumonia diagnosis and found distinct pathways that may be amenable to modulation. Our findings illustrate how non-human primate models of bacterial pneumonia can successfully translate biomarker discoveries to patients.

背景:尽管抗生素广泛使用,细菌性肺炎仍然是世界范围内发病率和死亡率的主要原因。迫切需要新的肺炎疗法和生物标志物来改善预后和推进个性化治疗。利用已建立的肺炎链球菌肺炎狒狒模型,我们试图表征肺炎宿主反应的时间动态,以确定新的潜在诊断和治疗分子靶点。方法:我们对接种肺炎链球菌(n = 23)或生理盐水(n = 10)的狒狒进行了全血转录组学、无偏蛋白质组学和外周血细胞因子测量,并使用主成分分析和复杂稀疏逻辑回归模拟了外周血宿主的反应。对差异表达基因进行通路分析。结果:接种动物出现肺炎的特征性体征和症状。获得了39个基因标记,对肺炎链球菌感染进行了高精度分类(接种后24和48 h的auROC分别为0.9和0.99)。从外周血血浆蛋白质组学和细胞因子测量中获得的48小时生物标志物特征也有类似的表现(均为auROC >0.9)。当转化为人类同源物并应用于急性呼吸系统疾病患者(n = 34)或健康对照(n = 20)时,该基因标记保留了很强的诊断性能(auROC = 0.88)。48 h通路分析发现外周血有丝分裂和糖皮质激素信号通路下调。结论:我们报道了肺炎链球菌肺炎的新的外周血基因和蛋白表达特征,可以改善肺炎的诊断,并发现了可能适合调节的独特途径。我们的研究结果说明了细菌性肺炎的非人类灵长类动物模型如何成功地将生物标志物发现转化为患者。
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引用次数: 0
Brief introduction in phenotypic and genetic differences of C57BL/6 and BALB/c mice substrains C57BL/6和BALB/c小鼠亚株表型和遗传差异的简要介绍。
IF 3.4 Q1 Health Professions Pub Date : 2025-09-03 DOI: 10.1002/ame2.70067
Lan Zhao, Jie Wei, Bingfei Yue

Experimental mice play a critical role in biomedical research. The phenotype and application of different substrains vary due to genetic differentiation and variation. To ensure validity and reliability of results, it is imperative to adhere to standardized experiments and controls. This paper objectively reviews the origin, differentiation, and phenotypic and genetic differences between the C57BL/6 and BALB/c mouse substrains. Furthermore, an optimal selection strategy is proposed based on the genetic quality control technology to facilitate the precise application of these two mouse substrains.

实验小鼠在生物医学研究中发挥着关键作用。不同亚株的表型和应用因遗传分化和变异而异。为了确保结果的有效性和可靠性,必须坚持标准化的实验和控制。本文客观回顾了C57BL/6和BALB/c小鼠亚株的起源、分化、表型和遗传差异。同时,提出了一种基于遗传质量控制技术的最佳选择策略,以促进这两个小鼠亚品系的精确应用。
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引用次数: 0
Development, validation, and preliminary phenotypic characterization of a Col6a3 knockout mouse model targeting exon 3 Col6a3外显子3敲除小鼠模型的开发、验证和初步表型表征
IF 3.4 Q1 Health Professions Pub Date : 2025-08-12 DOI: 10.1002/ame2.70063
Michel ElChoueiry, Harsimran Sidhu, Maude Lévesque, Dominique Lévesque, Jean-François Jacques, Otman Sarrhini, Jean-François Beaudoin, Molly Caron, Brenda Gaudette, Roger Lecomte, Xavier Roucou, François-Michel Boisvert, Jean-Philippe Brosseau

Background

Most mutations in the COL6A3 gene lead to collagen VI-related myopathies. This is due to a reduced expression or mislocalization of the COL6A3 protein. Therefore, studying the consequence of knocking out the Col6a3 gene in mouse models is relevant, but the Col6a3 mouse models reported so far do not entirely abolish COL6A3 protein expression.

Methods

Here, we present the development, validation and preliminary phenotypic characterization of a novel CRISPR-based knockout mouse model targeting Col6a3 exon 3 (Col6a3d3/d3).

Results

In this mouse model, Col6a3 mRNA is still expressed at a similar level to wild-type littermates, although the expected protein is undetectable by mass spectrometry. Histological analysis of Col6a3d3/d3 quadriceps revealed an abnormally high frequency of muscle cells with internally nucleated muscle cells, consistent with a myopathy phenotype. Interestingly, Col6a3d3/d3 mice are smaller in size, with their fat, muscle, and bone kept proportional compared to wild-type littermates.

Conclusions

In summary, we performed the validation and preliminary phenotypic characterization of a novel Col6a3 knockout mouse model that could be further characterized and used to study COL6A3 biology and model collagen VI-associated diseases.

背景:COL6A3基因的大多数突变导致vi型胶原相关的肌病。这是由于COL6A3蛋白的表达减少或定位错误。因此,研究敲除Col6a3基因在小鼠模型中的结果是有意义的,但目前报道的Col6a3小鼠模型并没有完全消除Col6a3蛋白的表达。方法:在这里,我们提出了一种新的基于crispr的Col6a3外显子3 (Col6a3d3/d3)敲除小鼠模型的开发、验证和初步表型表征。结果:在该小鼠模型中,Col6a3 mRNA的表达水平与野生型窝鼠相似,尽管质谱法无法检测到预期的蛋白质。Col6a3d3/d3股四头肌的组织学分析显示,肌细胞与内核肌细胞的频率异常高,与肌病表型一致。有趣的是,Col6a3d3/d3小鼠的体型更小,脂肪、肌肉和骨骼与野生型小鼠保持比例。综上所述,我们对Col6a3敲除小鼠模型进行了验证和初步表型表征,该模型可进一步表征并用于Col6a3生物学研究和胶原vi相关疾病模型。
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引用次数: 0
Research progress on traditional Chinese medicine animal models of post-stroke depression and pathological insights 脑卒中后抑郁中药动物模型的研究进展及病理意义。
IF 3.4 Q1 Health Professions Pub Date : 2025-08-11 DOI: 10.1002/ame2.70068
Jielin Wang, Wenlu Ma, Wei Wu, Yujuan Fu, Hui Li

Post-stroke depression (PSD) is a common psychiatric complication affecting nearly one-third of stroke survivors, leading to increased disability, mortality, and cognitive decline. Traditional Chinese Medicine (TCM) has proven effective in treating PSD through syndrome differentiation, yet existing animal models primarily reflect Western medical concepts and fail to incorporate the TCM principle of “同病异治” (treating the same disease with different methods). This paper provides a review of the current methods for constructing animal models of post-stroke depression (PSD) from the perspective of Traditional Chinese Medicine (TCM) syndrome differentiation and proposes multi-dimensional assessment indicators. By integrating TCM theories with modern biomedical techniques, this study offers a comprehensive framework for deepening the understanding of the pathogenesis and therapeutic evaluation of PSD. This approach not only contributes to advancing PSD research but also paves the way for innovative treatment strategies that combine traditional and modern medicine.

中风后抑郁(PSD)是一种常见的精神并发症,影响了近三分之一的中风幸存者,导致残疾、死亡率增加和认知能力下降。中医通过辨证论治PSD已被证明是有效的,但现有的动物模型主要反映的是西方医学概念,未能融入中医“同病异法”的原则。本文从中医辨证角度综述了目前脑卒中后抑郁动物模型的构建方法,并提出了多维度评价指标。本研究将中医理论与现代生物医学技术相结合,为加深对PSD发病机制的认识和治疗评价提供了一个全面的框架。这种方法不仅有助于推进PSD研究,而且为结合传统和现代医学的创新治疗策略铺平了道路。
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引用次数: 0
Establishment of a patient-derived drug-resistant oral squamous cell carcinoma animal model 患者源性口腔鳞癌耐药动物模型的建立。
IF 3.4 Q1 Health Professions Pub Date : 2025-08-08 DOI: 10.1002/ame2.70066
Chuanni Feng, Hao Liu, Yalan Lu, Yanfeng Xu, Xinghan Wu, Jinlong Wang, Chuan Qin, Binbin Li, Yanhong Li

Oral squamous cell carcinoma (OSCC) constitutes 90% of oral tumors. Advanced cases severely impair patients' life quality of life due to anatomical location and limited therapies. Conventional treatments often induce drug resistance or recurrence. Patient-derived xenograft (PDX) models are widely used to simulate tumor progression and drug responses, serving as translational tools for precision medicine. This study aimed to establish drug-resistant OSCC PDX models. Human OSCC tissues were transplanted into immunodeficient mice and passaged (P1–P2). At P2 (tumor volume: 40–80 mm3), mice received cisplatin (1 mg/kg, three times/week) with cetuximab (1 mg/kg, weekly), GSK690693 (10 mg/kg, five times/week), or rapamycin (4 mg/kg, five times/week). PDX tissues from groups with less-therapeutic response (manifested as larger tumor volumes) were serially passaged to assess treatment efficacy. Tumor tissues with diminished drug sensitivity underwent histopathological analysis and identified stability of their tumor characteristics using hematoxylin–eosin (HE) and immunohistochemical staining after one additional passage and retreatment. Results demonstrated that successive passaging accelerates tumor growth. First-generation treatments showed universal sensitivity. At P2, cisplatin–cetuximab and rapamycin groups remained sensitive, whereas GSK690693 efficacy declined. Continued passaging of GSK690693-treated tumors confirmed resistance, as evidenced by exhibiting enhanced malignant characteristics at histological level. The GSK690693-resistant model was established first, whereas resistant models of other treatment groups were established according to similar protocols. These findings suggest that sequential passaging and drug exposure in PDX models recapitulated clinical tumor evolution, enabling the development of drug-resistant OSCC models. This study can offer methodological insights for precision therapy of OSCC.

口腔鳞状细胞癌(OSCC)占口腔肿瘤的90%。晚期病例由于解剖位置和治疗方法有限,严重影响患者的生活质量。常规治疗往往会引起耐药性或复发。患者源性异种移植(PDX)模型被广泛用于模拟肿瘤进展和药物反应,作为精准医学的转化工具。本研究旨在建立耐药的OSCC PDX模型。将人OSCC组织移植到免疫缺陷小鼠体内传代(P1-P2)。在P2(肿瘤体积:40-80 mm3)时,小鼠接受顺铂(1 mg/kg, 3次/周)联合西妥昔单抗(1 mg/kg,每周)、GSK690693 (10 mg/kg, 5次/周)或雷帕霉素(4 mg/kg, 5次/周)治疗。治疗反应较差(表现为肿瘤体积较大)组的PDX组织连续传代以评估治疗效果。对药物敏感性降低的肿瘤组织进行组织病理学分析,并在一次额外传代和再治疗后使用苏木精-伊红(HE)和免疫组织化学染色确定其肿瘤特征的稳定性。结果表明,连续传代可促进肿瘤生长。第一代治疗显示出普遍的敏感性。在P2时,顺铂-西妥昔单抗和雷帕霉素组仍然敏感,而GSK690693组的疗效下降。继续传代gsk690693治疗的肿瘤证实了耐药性,在组织学水平上表现出增强的恶性特征。先建立gsk690693耐药模型,其他治疗组均按类似方案建立耐药模型。这些发现表明,PDX模型中的顺序传代和药物暴露重现了临床肿瘤的演变,从而促进了耐药OSCC模型的发展。本研究可为OSCC的精准治疗提供方法学见解。
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引用次数: 0
Insight into pericytes in glioblastoma angiogenesis: In vivo tracking by two-photon microscopy and proteomic profiling 胶质母细胞瘤血管生成中的周细胞:双光子显微镜和蛋白质组学分析的体内跟踪。
IF 3.4 Q1 Health Professions Pub Date : 2025-08-07 DOI: 10.1002/ame2.70073
Qinghong Wang, Chengyan Ma, Xinpei Wang, Mengyuan Li, Xingjiu Yang, Ran Gao

Background

Glioblastoma (GBM) is a highly aggressive brain tumor characterized by aberrant angiogenesis and an immunosuppressive microenvironment. Pericytes are aberrantly recruited but their spatiotemporal roles and molecular changes remain unclear. This study investigated platelet-derived growth factor receptor beta-positive (Pdgfrb+) pericyte dynamics and reprogramming in GBM vasculature.

Methods

We generated GL261-Luc and GL261-CFP glioblastoma cells via lentiviral transduction and established two transgenic models. (1) For pericyte labeling, Ai14 reporter mice was crossed with PDGFRβ-P2A-CreERT2 mice for tdTomato-specific lineage tracing (PT mice). (2) For conditional ablation, we generated inducible Pdgfrb-expressing cell ablation models (PT mice was crossed with ROSA-DTA mice). An intravital imaging platform (FITC-dextran/CFP/tdTomato + two-photon microscopy) tracked pericytes, vessels, and tumor cells, while FACS-sorted Pdgfrb+ cells from GBM and normal brain were analyzed by LC–MS/MS proteomics.

Results

Cre-mediated ablation of Pdgfrb-expressing cells revealed stage-dependent effects on GBM growth: early ablation inhibited progression while late ablation promoted it. Pericytes undergo dual spatial reorganization in GBM: regional enrichment with pre-sprouting accumulation at the tumor-brain interface, and focal positioning with preferential localization at vascular branch points. Concurrently, GBM vasculature displayed simplified branching, dilation, and pericyte remodeling (shorter processes, higher density). Proteomics revealed 1426 altered proteins, with upregulated proliferation pathways (e.g., matrix metallopeptidase 14 [Mmp14], lysyl oxidase like 2 [Loxl2]) and downregulated homeostasis functions (e.g., transforming growth factor beta 1 [Tgfb1]), validated by scRNA-seq in human GBM.

Conclusions

This study demonstrates that during early GBM progression, pericytes actively drive tumor angiogenesis through molecular reprogramming toward proliferative and pro-angiogenic phenotypes, with the integrated imaging-proteomics framework revealing potential therapeutic targets for disrupting pericyte-mediated vascular remodeling.

背景:胶质母细胞瘤(GBM)是一种高度侵袭性的脑肿瘤,其特征是异常血管生成和免疫抑制微环境。周细胞异常募集,但其时空作用和分子变化尚不清楚。本研究探讨了血小板衍生生长因子受体β阳性(Pdgfrb+)周细胞动力学和重编程在GBM血管系统中的作用。方法:采用慢病毒转导法制备GL261-Luc和GL261-CFP胶质母细胞瘤细胞,建立两种转基因模型。(1)为了进行周细胞标记,将Ai14报告小鼠与PDGFRβ-P2A-CreERT2小鼠杂交进行tdtomato特异性谱系追踪(PT小鼠)。(2)对于条件消融,我们建立了可诱导的表达pdgfrb的细胞消融模型(PT小鼠与ROSA-DTA小鼠杂交)。活体成像平台(fitc -葡聚糖/CFP/tdTomato +双光子显微镜)跟踪周细胞、血管和肿瘤细胞,而facs分选的GBM和正常脑Pdgfrb+细胞通过LC-MS/MS蛋白质组学分析。结果:cre介导的pdgfrb表达细胞消融对GBM生长的影响显示出分期依赖性:早期消融抑制进展,而晚期消融促进进展。在GBM中,周细胞经历了双重空间重组:在肿瘤-脑界面的区域富集和芽前积累,以及在血管分支点优先定位的局灶定位。同时,GBM血管系统分支简化,扩张,周细胞重塑(过程更短,密度更高)。蛋白质组学发现1426个蛋白发生改变,增殖途径上调(如基质金属肽酶14 [Mmp14]、赖氨酸氧化酶样2 [Loxl2]),体内平衡功能下调(如转化生长因子β 1 [Tgfb1]),经scRNA-seq在人GBM中证实。结论:本研究表明,在GBM早期进展过程中,周细胞通过分子重编程向增殖型和促血管生成表型积极推动肿瘤血管生成,整合成像-蛋白质组学框架揭示了破坏周细胞介导的血管重塑的潜在治疗靶点。
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引用次数: 0
Building a Culture of Care in Laboratory Animal Science through practicing “remembrance”: A reflection on local practices in Sri Lanka 通过实践“记忆”在实验动物科学中建立关怀文化:对斯里兰卡当地实践的反思。
IF 3.4 Q1 Health Professions Pub Date : 2025-07-29 DOI: 10.1002/ame2.70070
A. D. D. S. Amarasekara, K. A. A. U. Karunarathna, W. M. K. M. Ratnayake, A. A. I. Senevirathne, P. Yapa, M. Gunatilake

Remembrance activities can support the Culture of Care (CoC) in Laboratory Animal Science (LAS) not only by promoting a culture of respect, gratitude and thankfulness for animal life but also by helping the emotional processing and healing of lab animal researchers and animal facility staff. Even though remembrance activities are practiced in many parts of the world, we did not come across any reported cases in Sri Lanka before 2022. Therefore, here, we report on the various remembrance activities and practices observed within our local scientific community.

纪念活动可以支持实验动物科学(LAS)中的关怀文化(CoC),不仅可以促进尊重、感激和感谢动物生命的文化,还可以帮助实验动物研究人员和动物设施工作人员处理和治愈情感。尽管世界许多地方都有纪念活动,但我们在2022年之前没有在斯里兰卡发现任何报告的病例。因此,在这里,我们报告了在我们当地科学界观察到的各种纪念活动和实践。
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引用次数: 0
A potential strategy for improving offspring behavior in maternal immune activation: Amantadine-mediated suppression of neuroinflammation 在母体免疫激活中改善后代行为的潜在策略:金刚烷胺介导的神经炎症抑制。
IF 3.4 Q1 Health Professions Pub Date : 2025-07-23 DOI: 10.1002/ame2.70059
Jianfei Wu, Yu Liu, Binglong Wang, Yilin Wang, Bo Liu, Youguo Tan, Duanfang Cai, Kezhi Liu, Daixu Wei

Background

Maternal viral infection during pregnancy can lead to maternal immune activation (MIA), increasing the risk of neurodevelopmental disorders in offspring. Amantadine (AMA) exhibits antiviral activity and is widely employed in the management of neurologic conditions. Nevertheless, the efficacy of AMA in treating MIA is currently not established.

Methods

MIA was induced by polyinosinic acid–polycytidylic acid (poly(I:C)); AMA was administered from embryonic (E) day 11.5 for 3 days. BV-2 cells were stimulated using poly(I:C) and treated with AMA. Behavior was assessed via open field test, elevated plus maze test, three-chamber sociability test, and marble burying test. Neuronal morphology was vizualized using Nissl stain; apoptosis via TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) stain; protein expression (Iba1, NeuN, CD68, TNF-α [tumor necrosis factor-alpha], IL-1β [interleukin-1β]) using immunofluorescence (IF); interleukin-6 (IL-6) levels using enzyme-linked immunosorbent assay; reactive oxygen species using staining; Iba1, NeuN, Bcl-2, Bax, and cleaved caspase 3 using Western blot; and gene expression changes using RNA-seq.

Results

AMA treatment reduced the levels of IL-6 in maternal blood, improved autism-like behaviors in MIA offspring, and effectively prevented neuronal damage and neuroinflammation. In vitro cellular studies have demonstrated that AMA effectively downregulates the expression levels of pro-inflammatory cytokines, including IL-6, TNF-α, and IL-1β. RNA-seq analysis indicated that AMA mitigates abnormal activation of microglia by modulating inflammatory pathways associated with IL-6.

Conclusion

AMA can prevent the development of neuropsychiatric disorders in MIA offspring. This effect may be related to its ability to attenuate neuronal damage, reduce neuronal apoptosis, and inhibit neuroinflammation, indicating that the antiviral drug AMA may be a potential treatment for MIA.

背景:怀孕期间母体病毒感染可导致母体免疫激活(MIA),增加后代神经发育障碍的风险。金刚烷胺(AMA)具有抗病毒活性,被广泛应用于神经系统疾病的治疗。然而,AMA治疗MIA的疗效目前尚未确定。方法:用多肌苷酸-多胞苷酸(poly(I:C))诱导MIA;从胚胎(E)第11.5天开始给药,持续3天。用poly(I:C)刺激BV-2细胞,并用AMA处理。行为评估方法为野外测试、升高迷宫测试、三室社交能力测试和弹珠掩埋测试。尼氏染色观察神经元形态;TUNEL(末端脱氧核苷酸转移酶dUTP镍端标记)染色法检测细胞凋亡;免疫荧光(IF)蛋白表达(Iba1, NeuN, CD68, TNF-α[肿瘤坏死因子α], IL-1β[白细胞介素1β]);酶联免疫吸附法检测白细胞介素-6 (IL-6)水平;活性氧染色法;Iba1, NeuN, Bcl-2, Bax和cleaved caspase 3使用Western blot;利用RNA-seq分析基因表达变化。结果:AMA治疗降低了母亲血液中IL-6水平,改善了MIA后代的自闭症样行为,有效预防了神经元损伤和神经炎症。体外细胞研究表明,AMA有效下调促炎细胞因子的表达水平,包括IL-6、TNF-α和IL-1β。RNA-seq分析表明,AMA通过调节与IL-6相关的炎症通路来减轻小胶质细胞的异常激活。结论:AMA可预防MIA子代神经精神障碍的发生。这种作用可能与其减轻神经元损伤、减少神经元凋亡和抑制神经炎症的能力有关,这表明抗病毒药物AMA可能是治疗MIA的潜在药物。
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引用次数: 0
Strategies for optimization of hypoglycemia rat models 低血糖大鼠模型的优化策略。
IF 3.4 Q1 Health Professions Pub Date : 2025-07-21 DOI: 10.1002/ame2.70045
Lee Yeong Zher, Eason Kong Qi Zheng, Rayneshia Elaura Raymond, Ye Zhen Jie, Christina Gertrude Yap

This review focuses on rat models for studying the short-term and long-term effects of mild and severe hypoglycemia. We explored the physiological mechanisms to understand the consequences of hypoglycemia in rat experimental models. This study aims to investigate the therapeutic potential of phytotherapeutic agents and their efficacy in mitigating the adverse effects of hypoglycemia. Insights from our planned research will be beneficial in improving quality of life for individuals at risk of episodes of low blood sugar. Optimizing hypoglycemic rat models for research requires selecting a suitable experimental model that will be susceptible to hypoglycemia induction, effective monitoring of blood glucose levels, and maintaining a high survival rate throughout the required experimental duration.

本文综述了用于研究轻度和重度低血糖短期和长期影响的大鼠模型。我们在大鼠实验模型中探讨了低血糖的生理机制。本研究旨在探讨植物治疗药物的治疗潜力及其在减轻低血糖不良反应方面的疗效。从我们计划的研究中获得的见解将有助于改善有低血糖发作风险的个体的生活质量。优化低血糖大鼠模型进行研究需要选择合适的易诱导低血糖的实验模型,有效监测血糖水平,并在所需的实验时间内保持较高的存活率。
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Animal models and experimental medicine
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