胎儿生长迟缓胎儿脐血中一种新的抗氧化标记物：人源蛋白。

IF 0.7 4区医学 Q4 PATHOLOGY

Fetal and Pediatric Pathology Pub Date : 2023-10-01 Epub Date: 2023-06-27 DOI:10.1080/15513815.2023.2229432

Caner Kose, Busra Korpe, Kadriye Yakut Yucel, Ozgur Arat, Mevlut Bucak, Yaprak Engin Ustun

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引用次数: 0

摘要

目的：本研究调查了晚期胎儿生长受限（FGR）胎儿脐带血中人源蛋白水平，并评估了其与围产期结局的关系。材料和方法：共包括95例32-41周的单胎妊娠（45例晚期FGR，50例对照）。评估了多普勒参数、出生体重和新生儿重症监护室（NICU）入院需求。分析人源蛋白水平与这些参数之间的相关性。结果：与对照组相比，FGR晚期胎儿的人源蛋白水平较高（p p 结论：在患有晚期FGR的胎儿中，具有统计学意义的较高水平的人源蛋白可能提示人源蛋白作为晚期FGR指标的潜力。还需要进一步的研究来探索人源蛋白的临床应用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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A New Antioxidant Marker in Cord Blood of Fetuses with Late Fetal Growth Restriction: Humanin.

Purpose: This study investigated the Humanin levels in the umbilical cord blood of fetuses with late fetal growth restriction (FGR) and -evaluated their association with perinatal outcomes. Materials and Methods: A total of 95 single pregnancies between 32-41 wk (45 with late FGR and 50 controls) were included. Doppler parameters, birth weight and the need for neonatal intensive care unit admission (NICU) were assessed. Correlations between Humanin levels and these parameters were analyzed. Results: Higher Humanin levels were found in fetuses with late FGR compared to the control group (p < 0.05). No significant correlation was observed between Humanin levels and Doppler parameters. Elevated Humanin levels were associated with an increased need for NICU (p < 0.05). Conclusions: The statistically higher levels of Humanin in fetuses with late FGR may suggest the potential of Humanin as an indicator of late FGR. Further research is needed to explore the clinical utility of Humanin.

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.