The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2016
Variable effect of maternal oral glucose load on circulating cell-free placental mRNAs.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
MacDonald Teresa Mary, Kaitu'u-Lino Tu'uhevaha Joy, Walker Susan Philippa, Dane Kirsten Margaret, Lockie Elizabeth Beatrice, Tong Stephen, Whitehead Clare Louise, Hui Lisa
Аннотация
BACKGROUND: It is not known whether fasting affects levels of circulating placenta-specific transcripts.
OBJECTIVE: To assess whether a glucose load affects circulating placenta-specific transcripts.
METHOD: RNA was extracted from paired blood samples (fasting and 1-h post 75 g oral glucose) from 22 women. Placenta-specific genes were measured by RT-qPCR.
RESULTS: There was no change in ADM, CSH1, PAPPA2, PSG1 or TAC3 expression between fasting and post-glucose states. However, HTRA1 decreased after glucose load.
CONCLUSION: Maternal fasting state does not influence expression of the majority of placenta-specific genes but may need to be accounted for when validating biomarkers of placental disease.
OBJECTIVE: To assess whether a glucose load affects circulating placenta-specific transcripts.
METHOD: RNA was extracted from paired blood samples (fasting and 1-h post 75 g oral glucose) from 22 women. Placenta-specific genes were measured by RT-qPCR.
RESULTS: There was no change in ADM, CSH1, PAPPA2, PSG1 or TAC3 expression between fasting and post-glucose states. However, HTRA1 decreased after glucose load.
CONCLUSION: Maternal fasting state does not influence expression of the majority of placenta-specific genes but may need to be accounted for when validating biomarkers of placental disease.