Pub Date : 2021-12-16DOI: 10.1097/FM9.0000000000000136
Yuanyuan Liu, Lu Gao
Abstract Preterm labor (before 37 weeks’ gestation) is the leading cause of neonatal mortality and morbidity, which can be divided into iatrogenic preterm labor, infectious preterm labor, and spontaneous preterm labor (sPTL). Up to now, there continue to be great difficulties in prediction and prevention of sPTL, owing to multiple risk factors, pathogenesis, and pathologic processes contributing to the event, which have not been fully clarified. Pregnancy maintenance and parturition is a complicated process with continuous maternal-fetal dialogue, in which both maternal and fetal factors participate and affect the outcome of pregnancy, including sPTL. Besides, external factors can also participate in sPTL, individually or through the interaction with internal factors. In this article, we summarize recent studies regarding sPTL from our and other groups, and discuss the risk factors and pathogenesis of preterm birth from both external and internal (maternal and fetal) aspects, so as to provide theoretical evidences for the diagnosis, prevention, and treatment of sPTL in the future.
{"title":"Preterm Labor, a Syndrome Attributed to the Combination of External and Internal Factors","authors":"Yuanyuan Liu, Lu Gao","doi":"10.1097/FM9.0000000000000136","DOIUrl":"https://doi.org/10.1097/FM9.0000000000000136","url":null,"abstract":"Abstract Preterm labor (before 37 weeks’ gestation) is the leading cause of neonatal mortality and morbidity, which can be divided into iatrogenic preterm labor, infectious preterm labor, and spontaneous preterm labor (sPTL). Up to now, there continue to be great difficulties in prediction and prevention of sPTL, owing to multiple risk factors, pathogenesis, and pathologic processes contributing to the event, which have not been fully clarified. Pregnancy maintenance and parturition is a complicated process with continuous maternal-fetal dialogue, in which both maternal and fetal factors participate and affect the outcome of pregnancy, including sPTL. Besides, external factors can also participate in sPTL, individually or through the interaction with internal factors. In this article, we summarize recent studies regarding sPTL from our and other groups, and discuss the risk factors and pathogenesis of preterm birth from both external and internal (maternal and fetal) aspects, so as to provide theoretical evidences for the diagnosis, prevention, and treatment of sPTL in the future.","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41965122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-12-15DOI: 10.1097/FM9.0000000000000137
Tingting Xu, Daijuan Chen, X. Deng, Yongchi Zhan, F. Zhou, Xiaodong Wang
Supplemental Digital Content is available in the text Abstract Objective: To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model. Methods: Pregnant rats (n = 60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups), and were studied on the 17th, 19th, and 21st gestational days (GD) (n = 5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons. Results: A significant difference was found in placenta weight (F = 8.10, P < 0.05), fetal rat weight (F = 40.86, P < 0.05), fetal rat length (F = 61.61, P < 0.05), and fetal rat tail length (F = 55.63, P < 0.05) among four groups on the 17th ,19th , and 21st GD.What's more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant (F = 2.48, P < 0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46 ± 0.15 vs. 0.24 ± 0.09, P < 0.05), EE (0.46 ± 0.15 vs. 0.17 ± 0.04, P > 0.05), and IR (0.46 ± 0.15 vs. 0.22 ± 0.15, P > 0.05) groups at 19th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42 ± 0.05 vs. 0.58 ± 0.12, P < 0.05), UCN (0.43 ± 0.01 vs. 0.47 ± 0.16, P > 0.05), and WFS1 (0.57 ± 0.07 vs. 0.74 ± 0.12, P > 0.05) protein in the EE-IR group was subsided compared to the IR group at 17th GD. Conclusion: Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.
{"title":"Impaired Compensatory Vasodilatory Effect Mediated by Wolfram Syndrome 1 and Corticotropin-Releasing Hormone Family Peptides in 17α-Ethynylestradiol-Induced Intrahepatic Cholestasis Pregnant Rats When Under Additional Acute Hypoxia Stress","authors":"Tingting Xu, Daijuan Chen, X. Deng, Yongchi Zhan, F. Zhou, Xiaodong Wang","doi":"10.1097/FM9.0000000000000137","DOIUrl":"https://doi.org/10.1097/FM9.0000000000000137","url":null,"abstract":"Supplemental Digital Content is available in the text Abstract Objective: To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model. Methods: Pregnant rats (n = 60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups), and were studied on the 17th, 19th, and 21st gestational days (GD) (n = 5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons. Results: A significant difference was found in placenta weight (F = 8.10, P < 0.05), fetal rat weight (F = 40.86, P < 0.05), fetal rat length (F = 61.61, P < 0.05), and fetal rat tail length (F = 55.63, P < 0.05) among four groups on the 17th ,19th , and 21st GD.What's more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant (F = 2.48, P < 0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46 ± 0.15 vs. 0.24 ± 0.09, P < 0.05), EE (0.46 ± 0.15 vs. 0.17 ± 0.04, P > 0.05), and IR (0.46 ± 0.15 vs. 0.22 ± 0.15, P > 0.05) groups at 19th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42 ± 0.05 vs. 0.58 ± 0.12, P < 0.05), UCN (0.43 ± 0.01 vs. 0.47 ± 0.16, P > 0.05), and WFS1 (0.57 ± 0.07 vs. 0.74 ± 0.12, P > 0.05) protein in the EE-IR group was subsided compared to the IR group at 17th GD. Conclusion: Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44667806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-12-14DOI: 10.1097/FM9.0000000000000138
H. Tang, M. Zheng
Abstract In the last few years, the introduction of cell-free DNA has rapidly altered prenatal screening regimens and is increasingly offered as the second- or, at times, even the first-tier screening test. Should an early anomaly scan also be part of an up-to-date screening policy? This paper reappraises the value of fetal first-trimester ultrasonography. The primary aims of the first-trimester scan are to establish gestational age based on the measurement of fetal crown-rump length, to detect multiple pregnancy and chorionicity, and to measure fetal nuchal translucency thickness as part of a combined screening test for chromosomal abnormalities. With recent advancements in ultrasound technology, there is compelling evidence that a majority of fetuses with major structural abnormalities and almost half of them without chromosomal abnormalities can be detected in the first trimester. We focused on the first-trimester screening of fetal major defects, especially including fetal congenital heart disease and cleft lip and palate by ultrasound markers and views. Moreover, it is critical to highlight that after a detailed anomaly scan in the first trimester without major structural anomalies and positive genetic tests, the residual chance of favorable outcome in fetuses with isolated increased nuchal translucency is relatively high. The discussion on the role of cell-free DNA in prenatal screening is still ongoing. Even in the event of it becoming a first-line screening test for aneuploidies, the importance of a first-trimester fetal scan, including assessment of markers for other anomalies, remains undisputed.
{"title":"Reappraising the Value of Fetal First-Trimester Ultrasonography","authors":"H. Tang, M. Zheng","doi":"10.1097/FM9.0000000000000138","DOIUrl":"https://doi.org/10.1097/FM9.0000000000000138","url":null,"abstract":"Abstract In the last few years, the introduction of cell-free DNA has rapidly altered prenatal screening regimens and is increasingly offered as the second- or, at times, even the first-tier screening test. Should an early anomaly scan also be part of an up-to-date screening policy? This paper reappraises the value of fetal first-trimester ultrasonography. The primary aims of the first-trimester scan are to establish gestational age based on the measurement of fetal crown-rump length, to detect multiple pregnancy and chorionicity, and to measure fetal nuchal translucency thickness as part of a combined screening test for chromosomal abnormalities. With recent advancements in ultrasound technology, there is compelling evidence that a majority of fetuses with major structural abnormalities and almost half of them without chromosomal abnormalities can be detected in the first trimester. We focused on the first-trimester screening of fetal major defects, especially including fetal congenital heart disease and cleft lip and palate by ultrasound markers and views. Moreover, it is critical to highlight that after a detailed anomaly scan in the first trimester without major structural anomalies and positive genetic tests, the residual chance of favorable outcome in fetuses with isolated increased nuchal translucency is relatively high. The discussion on the role of cell-free DNA in prenatal screening is still ongoing. Even in the event of it becoming a first-line screening test for aneuploidies, the importance of a first-trimester fetal scan, including assessment of markers for other anomalies, remains undisputed.","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48332687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-12-09eCollection Date: 2022-01-01DOI: 10.1097/FM9.0000000000000132
Yan Li, Baoshi Han, Alejandra Garcia Salmeron, Jin Bai, Dong-Bao Chen
Normal pregnancy is associated with dramatically increased estrogen biosynthesis whose role is believed to raise uterine blood flow to facilitate the bi-directional maternal-fetal exchanges of gases (O2 and CO2), to deliver nutrients, and exhaust wastes to support fetal development and survival. Constrained uterine blood flow in pregnancy is a leading cause of preeclampsia with fetal growth restriction, rendering investigations of uterine hemodynamics to hold a high promise to inform pathways as targets for therapeutic interventions for preeclampsia. The mechanisms of estrogen-induced uterine vasodilation in pregnancy have long been attributed to enhanced endothelium production of nitric oxide, but clinical trials targeting this pathway that dominates uterine hemodynamics have achieved no to little success. Emerging evidence has recently shown a novel proangiogenic vasodilatory role of hydrogen sulfide in regulating uterine hemodynamics in pregnancy and preeclampsia, provoking a new field of perinatal research in searching for alternative pathways for pregnancy disorders especially preeclampsia and intrauterine growth restriction. This minireview is intended to summarize the nitric oxide pathway and to discuss the emerging hydrogen sulfide pathway in modulating estrogen-induced uterine vasodilation in pregnancy and preeclampsia.
{"title":"Estrogen-Induced Uterine Vasodilation in Pregnancy and Preeclampsia.","authors":"Yan Li, Baoshi Han, Alejandra Garcia Salmeron, Jin Bai, Dong-Bao Chen","doi":"10.1097/FM9.0000000000000132","DOIUrl":"https://doi.org/10.1097/FM9.0000000000000132","url":null,"abstract":"<p><p>Normal pregnancy is associated with dramatically increased estrogen biosynthesis whose role is believed to raise uterine blood flow to facilitate the bi-directional maternal-fetal exchanges of gases (O<sub>2</sub> and CO<sub>2</sub>), to deliver nutrients, and exhaust wastes to support fetal development and survival. Constrained uterine blood flow in pregnancy is a leading cause of preeclampsia with fetal growth restriction, rendering investigations of uterine hemodynamics to hold a high promise to inform pathways as targets for therapeutic interventions for preeclampsia. The mechanisms of estrogen-induced uterine vasodilation in pregnancy have long been attributed to enhanced endothelium production of nitric oxide, but clinical trials targeting this pathway that dominates uterine hemodynamics have achieved no to little success. Emerging evidence has recently shown a novel proangiogenic vasodilatory role of hydrogen sulfide in regulating uterine hemodynamics in pregnancy and preeclampsia, provoking a new field of perinatal research in searching for alternative pathways for pregnancy disorders especially preeclampsia and intrauterine growth restriction. This minireview is intended to summarize the nitric oxide pathway and to discuss the emerging hydrogen sulfide pathway in modulating estrogen-induced uterine vasodilation in pregnancy and preeclampsia.</p>","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f0/04/mfm-4-52.PMC8772435.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39854732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-12-09eCollection Date: 2022-01-01DOI: 10.1097/FM9.0000000000000133
Wenzhe Yu, Xiaoqian Hu, Bin Cao
Viral infections during pregnancy are associated with adverse pregnancy outcomes, including maternal and fetal mortality, pregnancy loss, premature labor, and congenital anomalies. Mammalian gestation encounters an immunological paradox wherein the placenta balances the tolerance of an allogeneic fetus with protection against pathogens. Viruses cannot easily transmit from mother to fetus due to physical and immunological barriers at the maternal-fetal interface posing a restricted threat to the fetus and newborns. Despite this, the unknown strategies utilized by certain viruses could weaken the placental barrier to trigger severe maternal and fetal health issues especially through vertical transmission, which was not fully understood until now. In this review, we summarize diverse aspects of the major viral infections relevant to pregnancy, including the characteristics of pathogenesis, related maternal-fetal complications, and the underlying molecular and cellular mechanisms of vertical transmission. We highlight the fundamental signatures of complex placental defense mechanisms, which will prepare us to fight the next emerging and re-emerging infectious disease in the pregnancy population.
{"title":"Viral Infections During Pregnancy: The Big Challenge Threatening Maternal and Fetal Health.","authors":"Wenzhe Yu, Xiaoqian Hu, Bin Cao","doi":"10.1097/FM9.0000000000000133","DOIUrl":"10.1097/FM9.0000000000000133","url":null,"abstract":"<p><p>Viral infections during pregnancy are associated with adverse pregnancy outcomes, including maternal and fetal mortality, pregnancy loss, premature labor, and congenital anomalies. Mammalian gestation encounters an immunological paradox wherein the placenta balances the tolerance of an allogeneic fetus with protection against pathogens. Viruses cannot easily transmit from mother to fetus due to physical and immunological barriers at the maternal-fetal interface posing a restricted threat to the fetus and newborns. Despite this, the unknown strategies utilized by certain viruses could weaken the placental barrier to trigger severe maternal and fetal health issues especially through vertical transmission, which was not fully understood until now. In this review, we summarize diverse aspects of the major viral infections relevant to pregnancy, including the characteristics of pathogenesis, related maternal-fetal complications, and the underlying molecular and cellular mechanisms of vertical transmission. We highlight the fundamental signatures of complex placental defense mechanisms, which will prepare us to fight the next emerging and re-emerging infectious disease in the pregnancy population.</p>","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7b/ec/mfm-4-72.PMC8843053.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39940720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-10-22DOI: 10.1097/fm9.0000000000000131
N. Melamed, L. Hiersch
{"title":"Fetal Growth in Twin Pregnancies and the Choice of Growth Chart","authors":"N. Melamed, L. Hiersch","doi":"10.1097/fm9.0000000000000131","DOIUrl":"https://doi.org/10.1097/fm9.0000000000000131","url":null,"abstract":"","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49142284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-10-04DOI: 10.1097/FM9.0000000000000125
Mohammad Salameh, O. Oniya, Reem S Chamseddine, J. Konje
Abstract Gestational diabetes mellitus (GDM) is a well-established risk factor for fetal macrosomia. A significant number of patients with GDM also suffer from obesity, a factor associated with fetal macrosomia. An important question is whether GDM is independently associated with fetal macrosomia, or whether this relationship is merely the result of maternal obesity acting as a confounder. In this review of the literature, we attempt to further elucidate the relationship between GDM, maternal obesity, and fetal macrosomia.
{"title":"Maternal Obesity, Gestational Diabetes, and Fetal Macrosomia: An Incidental or a Mechanistic Relationship?","authors":"Mohammad Salameh, O. Oniya, Reem S Chamseddine, J. Konje","doi":"10.1097/FM9.0000000000000125","DOIUrl":"https://doi.org/10.1097/FM9.0000000000000125","url":null,"abstract":"Abstract Gestational diabetes mellitus (GDM) is a well-established risk factor for fetal macrosomia. A significant number of patients with GDM also suffer from obesity, a factor associated with fetal macrosomia. An important question is whether GDM is independently associated with fetal macrosomia, or whether this relationship is merely the result of maternal obesity acting as a confounder. In this review of the literature, we attempt to further elucidate the relationship between GDM, maternal obesity, and fetal macrosomia.","PeriodicalId":74121,"journal":{"name":"Maternal-fetal medicine (Wolters Kluwer Health, Inc.)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49645639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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