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American journal of obstetrics and gynecology最新文献

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Key actions to improve linkage to care for pregnant and postpartum women with hepatitis C. 改善孕妇和产后妇女丙型肝炎护理链接的关键行动。
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-03-01 Epub Date: 2024-10-18 DOI: 10.1016/j.ajog.2024.10.018
Neil Gupta, Lindsey Hiebert, John W Ward
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引用次数: 0
Should we focus on endometrial-free closure technique? 我们是否应该关注无子宫内膜闭合技术?
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-03-01 Epub Date: 2024-10-19 DOI: 10.1016/j.ajog.2024.10.012
Carry Verberkt, Sanne I Stegwee, Judith A F Huirne
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引用次数: 0
Commentary on distinct obstetrical characteristics and maternal mortality in patients with HELLP syndrome vs severe preeclampsia. 评论:HELLP 综合征与重度子痫前期患者不同的产科特征和孕产妇死亡率。
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-03-01 Epub Date: 2024-10-18 DOI: 10.1016/j.ajog.2024.10.015
Supreet K Raina, Keisha Callins
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引用次数: 0
Key points for analyzing Longitudinal Twin Growth Discordance Patterns and Adverse Perinatal Outcomes.
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-25 DOI: 10.1016/j.ajog.2025.02.034
Xin Li, Xue Xiao, Tianjiao Liu
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引用次数: 0
Optimizing patient selection and technique for occiput posterior vacuum extraction.
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-25 DOI: 10.1016/j.ajog.2025.02.036
Daniel J Kiely
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引用次数: 0
Methodological Approach to Twin Growth Discordance Trajectories: Choice of clustering algorithm.
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-25 DOI: 10.1016/j.ajog.2025.02.035
Smriti Prasad, Erkan Kalafat, Asma Khalil
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引用次数: 0
Information for readers
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-20 DOI: 10.1016/S0002-9378(25)00035-3
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引用次数: 0
AJOG GR Table of Contents
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-20 DOI: 10.1016/S0002-9378(25)00037-7
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引用次数: 0
Impaired Fertility and Perinatal Outcomes in Adenomyosis: Insights from a Novel Murine Model and Uterine Gene Profile Alterations During Implantations.
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-20 DOI: 10.1016/j.ajog.2025.02.033
Hanxi Zheng, Meng Liu, Qiaolian Su, Hong Li, Fuxin Wang
<p><strong>Background: </strong>Adenomyosis is a uterine disorder closely linked to infertility and adverse pregnancy outcomes. Despite its clinical significance, the mechanisms by which adenomyosis impairs embryo implantation and perinatal outcomes remain incompletely defined. Previous studies have indicated that alterations in the uterine microenvironment may contribute to these reproductive challenges.</p><p><strong>Aim: </strong>To investigate the effects of adenomyosis on fertility and perinatal outcomes using a novel murine model and to identify molecular pathways involved in implantation failure and pregnancy loss.</p><p><strong>Study design: </strong>A mechanically induced adenomyosis model was established in female BALB/c mice through endometrial-myometrial interface disruption (EMID) to closely simulate the clinical condition observed in humans. Mice were randomly assigned to either the adenomyosis group or a sham-operated control group. Reproductive outcomes were systematically assessed at multiple gestational time points, focusing on embryo implantation site distribution, implantation rates, pregnancy loss, fetal growth parameters, and postnatal uterine recovery. In parallel, uterine tissues collected from implantation sites and inter-implantation regions at 4.5 days post coitus were subjected to RNA sequencing. Differential gene expression analyses were performed, and enriched pathways were identified using Gene Ontology and KEGG enrichment tools.</p><p><strong>Results: </strong>Mice in the adenomyosis group demonstrated significant disruptions in the uterine microenvironment compared to controls. Notably, the adenomyosis group exhibited irregular distribution of implantation sites with reduced inter-embryo distances, leading to compromised spatial organization of the developing conceptuses. Although the total number of embryos at early gestation did not differ significantly between groups, a marked increase in pregnancy loss was observed during mid-gestation, accompanied by a reduction in the size of surviving embryos. Histological evaluation revealed extensive architectural disruptions in the uterine muscle layers and increased local inflammatory responses in adenomyotic uteri. RNA sequencing further revealed that adenomyosis was associated with the dysregulation of multiple genes involved in immune modulation, apoptotic regulation, and metabolic processes. In particular, significant enrichment of the PI3K-Akt, MAPK, and TNF signaling pathways was observed, suggesting that variation in these cascades may underlie the impaired uterine receptivity and embryo development seen in adenomyosis.</p><p><strong>Conclusion: </strong>Our findings indicate that adenomyosis exerts a adverse effect on fertility and perinatal outcomes by disrupting the uterine environment and interfering with critical molecular pathways essential for proper embryo implantation and development. The results of this study not only enhance our understanding of adenom
背景:子宫腺肌症是一种与不孕和不良妊娠结局密切相关的子宫疾病。尽管子宫腺肌症具有重要的临床意义,但其影响胚胎着床和围产期结局的机制仍未完全明确。目的:使用一种新型小鼠模型研究子宫腺肌症对生育能力和围产期结局的影响,并确定参与植入失败和妊娠丢失的分子途径:研究设计:通过子宫内膜-子宫肌层界面破坏(EMID)在雌性BALB/c小鼠中建立机械诱导的子宫腺肌症模型,以近似模拟人类的临床症状。小鼠被随机分配到子宫腺肌症组或假手术对照组。在多个妊娠时间点对生殖结果进行系统评估,重点是胚胎植入部位分布、植入率、妊娠损失、胎儿生长参数和产后子宫恢复情况。同时,对同房后 4.5 天从着床部位和着床间区域采集的子宫组织进行了 RNA 测序。进行了差异基因表达分析,并使用基因本体论和 KEGG 富集工具确定了富集通路:结果:与对照组相比,子宫腺肌症组小鼠的子宫微环境明显受到破坏。值得注意的是,子宫腺肌症组的植入点分布不规则,胚胎间距离缩短,导致发育中的胚胎空间组织受损。虽然妊娠早期各组的胚胎总数没有显著差异,但妊娠中期观察到的妊娠损失明显增加,同时存活胚胎的大小也有所减少。组织学评估显示,腺肌症子宫的子宫肌层结构广泛破坏,局部炎症反应加剧。RNA 测序进一步显示,子宫腺肌症与涉及免疫调节、细胞凋亡调节和代谢过程的多个基因失调有关。特别是,我们观察到 PI3K-Akt、MAPK 和 TNF 信号通路明显丰富,这表明这些级联的变化可能是子宫腺肌症导致子宫接受能力和胚胎发育受损的原因:我们的研究结果表明,子宫腺肌症会破坏子宫环境,干扰胚胎正常着床和发育所必需的关键分子通路,从而对生育能力和围产期结果产生不利影响。这项研究的结果不仅加深了我们对子宫腺肌症病理生理学的了解,还指出了潜在的分子靶点--如 PI3K-Akt、MAPK 和 TNF 通路--以进行治疗干预。这些见解为开发旨在逆转与子宫腺肌症相关的不良生殖影响的治疗方法提供了有希望的靶点。
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引用次数: 0
AJOG MFM Table of Contents
IF 8.7 1区 医学 Q1 OBSTETRICS & GYNECOLOGY Pub Date : 2025-02-20 DOI: 10.1016/S0002-9378(25)00036-5
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引用次数: 0
期刊
American journal of obstetrics and gynecology
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