cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.27710579.v1
title: Interobserver agreement of intrapartum cardiotocography interpretation by midwives using current FIGO and physiology-based guidelines

description: To investigate the interobserver agreement among midwives for the interpretation of intrapartum CTG traces, using both the 2015 FIGO guidelines and the physiology-based guidelines. Retrospective, single-center, observational study conducted at the Maternity Hospital of the University of Parma, Italy, between November 2022 and July 2023. We selected 100 nonconsecutive intrapartum CTG traces from women undergoing operative delivery (cesarean or instrumental vaginal delivery). Participating midwives received the last 60 min of CTG recording prior to the decision for an operative delivery was made. Five midwives with different professional experience classified the CTG tracing according to the 2015 FIGO guidelines and the physiology-based guidelines at the time of the decision for the operative delivery. Each midwife was categorized as senior or junior if her clinical experience was equal or more or less than 5 years. All participating midwives were blinded to the demographic and clinical variables of each case, as well as to the labor and neonatal outcome. The main outcome of the study was the interobserver agreement among the 5 midwives with either guideline. The secondary outcome was the interobserver agreement based on clinical experience. The agreement between the observers was estimated through the Krippendorff’s alpha statistics. The interobserver agreement for the interpretation of intrapartum CTG traces according to the 2015 FIGO guideline was in the upper limit of the “unacceptable” classification, with a Krippendorff’s alpha of 0.632 (95% CI, 0.545–0.723). The interobserver agreement of the physiology-based CTG guideline was classified as “unacceptable” with a Krippendorff’s alpha of 0.359 (95% CI, 0.125–0.582). The interobserver agreement among senior midwives according to the 2015 FIGO guidelines was considered as “tentative acceptable agreement” with a Krippendorff’s alpha of 0.724 (95% CI, 0.636–0.805). Among junior midwives, the interobserver agreement according to the latter guideline was classified as “unacceptable” with a Krippendorff’s alpha of 0.569 (95% CI, 0.359–0.751). Using the physiology-based guideline, the interobserver agreement of the senior midwives – Krippendorff’s alpha 0.493 (95% CI, 0.320–0.623) – and “junior” midwives – Krippendorff’s alpha 0.359 (95% CI, 0.100–0.581) – were considered both “unacceptable”. Our study showed that intrapartum CTG interpretation is characterized by an overall unacceptable level of interobserver agreement among midwives, with the 2015 FIGO guidelines showing better agreement compared to physiology-based guidelines. The interpretation of intrapartum CTG by “senior” midwives using the 2015 FIGO guidelines showed the highest, interobserver agreement, indicating a “tentative acceptable agreement”.
DOI: 10.6084/m9.figshare.24970600
title: Upregulation of hepatic nuclear receptors in extremely preterm ovine fetuses undergoing artificial placenta therapy

description: Extremely preterm infants have low Nuclear Receptor (NR) expression in their developing hepatobiliary systems, as they rely on the placenta and maternal liver for compensation. NRs play a crucial role in detoxification and the elimination of both endogenous and xenobiotic substances by regulating key genes encoding specific proteins. In this study, we utilized an Artificial Placenta Therapy (APT) platform to examine the liver tissue expression of NRs of extremely preterm ovine fetuses. This fetal model, resembling a “knockout placenta,” lacks placental and maternal support, while maintaining a healthy extrauterine survival. Six ovine fetuses at 95 ± 1 d gestational age (GA; term = ∼150 d)/∼600 g delivery weight were maintained on an APT platform for a period of 120 h (APT Group). Six age-matched, <i>in utero</i> control fetuses were delivered at 99–100 d GA (Control Group). Fetal liver tissue samples and blood samples were collected at delivery from both groups and assessed mRNA expression of NRs and target transporters involved in the hepatobiliary transport system using quantitative PCR. Data were tested for group differences with ANOVA (<i>p</i> &lt; .05 deemed significant). mRNA expression of NRs was identified in both the placenta and the extremely preterm ovine fetal liver. The expression of <i>HNF4α</i>, <i>LRH1</i>, <i>LXR</i>, <i>ESR1</i>, <i>PXR</i>, <i>CAR</i>, and <i>PPARα/γ</i> were significantly elevated in the liver of the APT Group compared to the Control Group. Moreover, target transporters <i>NTCP</i>, <i>OATP1B3</i>, <i>BSEP</i>, and <i>MRP4</i> were upregulated, whereas <i>MRP2</i> and <i>MRP3</i> were unchanged. Although there was no evidence of liver necrosis or apoptotic changes histologically, there was an impact in the fetal liver of the ATP group at the tissue level with a significant increase in <i>TNFα</i> mRNA, a cytokine involved in liver inflammation, and blood elevation of transaminases. A number of NRs in the fetal liver were significantly upregulated after loss of placental-maternal support. However, the expression of target transporter genes appeared to be insufficient to compensate role of the placenta and maternal liver and avoid fetal liver damage, potentially due to insufficient excretion of organic anions.
DOI: 10.6084/m9.figshare.24970600.v1
title: Upregulation of hepatic nuclear receptors in extremely preterm ovine fetuses undergoing artificial placenta therapy

description: Extremely preterm infants have low Nuclear Receptor (NR) expression in their developing hepatobiliary systems, as they rely on the placenta and maternal liver for compensation. NRs play a crucial role in detoxification and the elimination of both endogenous and xenobiotic substances by regulating key genes encoding specific proteins. In this study, we utilized an Artificial Placenta Therapy (APT) platform to examine the liver tissue expression of NRs of extremely preterm ovine fetuses. This fetal model, resembling a “knockout placenta,” lacks placental and maternal support, while maintaining a healthy extrauterine survival. Six ovine fetuses at 95 ± 1 d gestational age (GA; term = ∼150 d)/∼600 g delivery weight were maintained on an APT platform for a period of 120 h (APT Group). Six age-matched, <i>in utero</i> control fetuses were delivered at 99–100 d GA (Control Group). Fetal liver tissue samples and blood samples were collected at delivery from both groups and assessed mRNA expression of NRs and target transporters involved in the hepatobiliary transport system using quantitative PCR. Data were tested for group differences with ANOVA (<i>p</i> &lt; .05 deemed significant). mRNA expression of NRs was identified in both the placenta and the extremely preterm ovine fetal liver. The expression of <i>HNF4α</i>, <i>LRH1</i>, <i>LXR</i>, <i>ESR1</i>, <i>PXR</i>, <i>CAR</i>, and <i>PPARα/γ</i> were significantly elevated in the liver of the APT Group compared to the Control Group. Moreover, target transporters <i>NTCP</i>, <i>OATP1B3</i>, <i>BSEP</i>, and <i>MRP4</i> were upregulated, whereas <i>MRP2</i> and <i>MRP3</i> were unchanged. Although there was no evidence of liver necrosis or apoptotic changes histologically, there was an impact in the fetal liver of the ATP group at the tissue level with a significant increase in <i>TNFα</i> mRNA, a cytokine involved in liver inflammation, and blood elevation of transaminases. A number of NRs in the fetal liver were significantly upregulated after loss of placental-maternal support. However, the expression of target transporter genes appeared to be insufficient to compensate role of the placenta and maternal liver and avoid fetal liver damage, potentially due to insufficient excretion of organic anions.
DOI: 10.6084/m9.figshare.25974353
title: Single-cell RNA sequencing reveals heterogeneity and differential expression of the maternal–fetal interface during ICP and normal pregnancy

description: Intrahepatic cholestasis of pregnancy (ICP) can cause adverse perinatal outcomes. Previous studies have demonstrated that the placenta of an ICP pregnancy differs in morphology and gene expression from the placenta of a normal pregnancy. To date, however, the genetic mechanism by which ICP affects the placenta is poorly understood. Therefore, the aim of this study was to investigate the differences in main cell types, gene signatures, cell ratio, and functional changes in the placenta between ICP and normal pregnancy. Single-cell RNA sequencing (scRNA-seq) technology was used to detect the gene expression of all cells at the placental maternal–fetal interface. Two individuals were analyzed – one with ICP and one without ICP. The classification of cell types was determined by a graph-based clustering algorithm. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the R software <i>phyper</i> () function and DAVID website. The differentially expressed genes (DEGs) encoding transcription factors (TFs) were identified using getorf and DIAMOND software. We identified 14 cell types and 22 distinct cell subtypes that showed unique functional properties. Additionally, we found differences in the proportions of fibroblasts 1, helper T (Th) cells, extravillous trophoblasts, and villous cytotrophoblasts, and we observed heterogeneity of gene expression between ICP and control placentas. Furthermore, we identified 263 DEGs that belonged to TF families, including zf-C2H2, HMGI/HMGY, and Homeobox. In addition, 28 imprinted genes were preferentially expressed in specific cell types, such as <i>PEG3</i> and <i>PEG10</i> in trophoblasts as well as <i>DLK1</i> and <i>DIO3</i> in fibroblasts. Our results revealed the differences in cell-type ratios, gene expression, and functional changes between ICP and normal placentas, and heterogeneity was found among cell subgroups. Hence, the imbalance of various cell types affects placental activity to varying degrees, indicating the complexity of the cell networks that form the placental tissue system, and this alteration of placental function is associated with adverse events in the perinatal period.
DOI: 10.6084/m9.figshare.25974353.v1
title: Single-cell RNA sequencing reveals heterogeneity and differential expression of the maternal–fetal interface during ICP and normal pregnancy

description: Intrahepatic cholestasis of pregnancy (ICP) can cause adverse perinatal outcomes. Previous studies have demonstrated that the placenta of an ICP pregnancy differs in morphology and gene expression from the placenta of a normal pregnancy. To date, however, the genetic mechanism by which ICP affects the placenta is poorly understood. Therefore, the aim of this study was to investigate the differences in main cell types, gene signatures, cell ratio, and functional changes in the placenta between ICP and normal pregnancy. Single-cell RNA sequencing (scRNA-seq) technology was used to detect the gene expression of all cells at the placental maternal–fetal interface. Two individuals were analyzed – one with ICP and one without ICP. The classification of cell types was determined by a graph-based clustering algorithm. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the R software <i>phyper</i> () function and DAVID website. The differentially expressed genes (DEGs) encoding transcription factors (TFs) were identified using getorf and DIAMOND software. We identified 14 cell types and 22 distinct cell subtypes that showed unique functional properties. Additionally, we found differences in the proportions of fibroblasts 1, helper T (Th) cells, extravillous trophoblasts, and villous cytotrophoblasts, and we observed heterogeneity of gene expression between ICP and control placentas. Furthermore, we identified 263 DEGs that belonged to TF families, including zf-C2H2, HMGI/HMGY, and Homeobox. In addition, 28 imprinted genes were preferentially expressed in specific cell types, such as <i>PEG3</i> and <i>PEG10</i> in trophoblasts as well as <i>DLK1</i> and <i>DIO3</i> in fibroblasts. Our results revealed the differences in cell-type ratios, gene expression, and functional changes between ICP and normal placentas, and heterogeneity was found among cell subgroups. Hence, the imbalance of various cell types affects placental activity to varying degrees, indicating the complexity of the cell networks that form the placental tissue system, and this alteration of placental function is associated with adverse events in the perinatal period.
DOI: 10.6084/m9.figshare.27823172
title: Exploring the relationship between maternal Continuous Glucose Monitoring “time in range” and fetal abdominal circumference in pregnant women with Type 1 Diabetes

description: To explore the relationship between maternal glycaemic control and fetal abdominal circumference in pregnancies complicated by T1D. This is a retrospective cohort study of 81 pregnant women with T1D using CGM. Inclusion criteria were T1D, CGM use, ≥2 in-house ultrasounds, and the birth of a live singleton neonate between 1st December 2019 and 1st December 2022. Linear regression analysis was used to assess the cross-sectional relationships between estimated fetal abdominal circumference (AC) on ultrasound and time in range (TIR) at matched time-points in the third trimester of pregnancy. Linear regression analysis was also used to examine whether first trimester TIR and HbA1c predicts third trimester fetal AC. At baseline, the mean ± standard deviation (SD) of the first trimester HbA1c was 7.0 ± 1.4% and mean ± SD total daily dose (TDD) insulin was 46.6 ± 21.0 units. The mean ± SD birthweight was 3367.0 ± 861.3 grams. There was no cross-sectional relationship between TIR and fetal AC at 28-, 32- or 36-week’ gestation. The results of the regression analysis indicate a significant relationship between first trimester TIR (independent predictor) and fetal AC (dependent variable) at 32- and 36-weeks’ gestation while controlling for maternal age, BMI, pump use, and TDD insulin (Adj<i>β=</i> −0.42, 95%CI −0.80 to −0.03 and Adj<i>β = −</i>0.57, 95%CI −1.02 to −0.12 at 32- and 36-weeks respectively). Although there was a significant relationship between first trimester HbA1c and fetal AC at 32-weeks’ gestation (<i>β =</i> 3.81, 95%CI 0.29 to 7.33), the relationship was not significant after adjustment for confounders. There was no cross-sectional relationship between TIR and fetal AC in the third trimester of pregnancy but first trimester TIR did predict fetal AC in late pregnancy.
DOI: 10.6084/m9.figshare.27823172.v1
title: Exploring the relationship between maternal Continuous Glucose Monitoring “time in range” and fetal abdominal circumference in pregnant women with Type 1 Diabetes

description: To explore the relationship between maternal glycaemic control and fetal abdominal circumference in pregnancies complicated by T1D. This is a retrospective cohort study of 81 pregnant women with T1D using CGM. Inclusion criteria were T1D, CGM use, ≥2 in-house ultrasounds, and the birth of a live singleton neonate between 1st December 2019 and 1st December 2022. Linear regression analysis was used to assess the cross-sectional relationships between estimated fetal abdominal circumference (AC) on ultrasound and time in range (TIR) at matched time-points in the third trimester of pregnancy. Linear regression analysis was also used to examine whether first trimester TIR and HbA1c predicts third trimester fetal AC. At baseline, the mean ± standard deviation (SD) of the first trimester HbA1c was 7.0 ± 1.4% and mean ± SD total daily dose (TDD) insulin was 46.6 ± 21.0 units. The mean ± SD birthweight was 3367.0 ± 861.3 grams. There was no cross-sectional relationship between TIR and fetal AC at 28-, 32- or 36-week’ gestation. The results of the regression analysis indicate a significant relationship between first trimester TIR (independent predictor) and fetal AC (dependent variable) at 32- and 36-weeks’ gestation while controlling for maternal age, BMI, pump use, and TDD insulin (Adj<i>β=</i> −0.42, 95%CI −0.80 to −0.03 and Adj<i>β = −</i>0.57, 95%CI −1.02 to −0.12 at 32- and 36-weeks respectively). Although there was a significant relationship between first trimester HbA1c and fetal AC at 32-weeks’ gestation (<i>β =</i> 3.81, 95%CI 0.29 to 7.33), the relationship was not significant after adjustment for confounders. There was no cross-sectional relationship between TIR and fetal AC in the third trimester of pregnancy but first trimester TIR did predict fetal AC in late pregnancy.
DOI: 10.6084/m9.figshare.25712645
title: Prenatal identification of a pathogenic maternal <i>FGFR1</i> variant in two consecutive pregnancies with fetal forebrain malformations

description: Holoprosencephaly (HPE) is the most common aberration of forebrain development, and it leads to a wide spectrum of developmental and craniofacial anomalies. HPE etiology is highly heterogeneous and includes both chromosomal abnormalities and single-gene defects. Here, we report an <i>FGFR1</i> heterozygous variant detected by prenatal exome sequencing and inherited from the asymptomatic mother, in association with recurrent neurological abnormalities in the HPE spectrum in two consecutive pregnancies. Individuals with germline pathogenic variants in <i>FGFR1</i> (MIM: 136350) show extensive phenotypic variability, which ranges from asymptomatic carriers to hypogonadotropic hypogonadism, arhinencephaly, Kallmann’s syndrome with associated features such as cleft lip and palate, skeletal anomalies, isolated HPE, and Hartsfield syndrome. The presented case supports the role of exome sequencing in prenatal diagnosis when fetal midline structural anomalies are suggestive of a genetic etiology, as early as the first trimester of gestation. The profound heterogeneity of <i>FGFR1</i> allelic disorders needs to be considered when planning prenatal screening even in asymptomatic carriers.
DOI: 10.6084/m9.figshare.25712645.v1
title: Prenatal identification of a pathogenic maternal <i>FGFR1</i> variant in two consecutive pregnancies with fetal forebrain malformations

description: Holoprosencephaly (HPE) is the most common aberration of forebrain development, and it leads to a wide spectrum of developmental and craniofacial anomalies. HPE etiology is highly heterogeneous and includes both chromosomal abnormalities and single-gene defects. Here, we report an <i>FGFR1</i> heterozygous variant detected by prenatal exome sequencing and inherited from the asymptomatic mother, in association with recurrent neurological abnormalities in the HPE spectrum in two consecutive pregnancies. Individuals with germline pathogenic variants in <i>FGFR1</i> (MIM: 136350) show extensive phenotypic variability, which ranges from asymptomatic carriers to hypogonadotropic hypogonadism, arhinencephaly, Kallmann’s syndrome with associated features such as cleft lip and palate, skeletal anomalies, isolated HPE, and Hartsfield syndrome. The presented case supports the role of exome sequencing in prenatal diagnosis when fetal midline structural anomalies are suggestive of a genetic etiology, as early as the first trimester of gestation. The profound heterogeneity of <i>FGFR1</i> allelic disorders needs to be considered when planning prenatal screening even in asymptomatic carriers.
DOI: 10.15468/dl.zcduzj
title: Occurrence Download

description: A dataset containing 653 species occurrences available in GBIF matching the query:
{"type":"and","predicates":[{"type":"within","geometry":"POLYGON ((-78.73999999999999 1.918181, -78.81030199999999 1.912612, -78.878872 1.896045, -78.944019 1.868886, -79.004141 1.831805, -79.057754 1.785716, -79.10354 1.731754, -79.140371 1.671248, -79.16734099999999 1.605689, -79.183786 1.536692, -79.18930400000001 1.465955, -79.183758 1.39522, -79.167288 1.326228, -79.140298 1.260679, -79.103454 1.200186, -79.057664 1.146238, -79.00405499999999 1.100162, -78.94394699999999 1.063094, -78.87881899999999 1.035945, -78.81027400000001 1.019384, -78.73999999999999 1.013817, -78.669726 1.019384, -78.601181 1.035945, -78.536053 1.063094, -78.475945 1.100162, -78.422336 1.146238, -78.376546 1.200186, -78.339702 1.260679, -78.312712 1.326228, -78.29624200000001 1.39522, -78.290696 1.465955, -78.29621400000001 1.536692, -78.312659 1.605689, -78.339629 1.671248, -78.37645999999999 1.731754, -78.422246 1.785716, -78.475859 1.831805, -78.53598100000001 1.868886, -78.601128 1.896045, -78.669698 1.912612, -78.73999999999999 1.918181))"},{"type":"equals","key":"CLASS_KEY","value":"212","matchCase":false},{"type":"greaterThanOrEquals","key":"YEAR","value":"2015","matchCase":false},{"type":"not","predicate":{"type":"in","key":"BASIS_OF_RECORD","values":["MATERIAL_CITATION","MATERIAL_SAMPLE","PRESERVED_SPECIMEN"],"matchCase":false}},{"type":"lessThanOrEquals","key":"COORDINATE_UNCERTAINTY_IN_METERS","value":"10000","matchCase":false},{"type":"equals","key":"LICENSE","value":"CC BY 4.0","matchCase":false}]}

 The dataset includes 653 records from 2 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002335-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.28071074
title: Causal associations of metabolic dysfunction-associated steatotic liver disease with gestational hypertension and preeclampsia: a two-sample Mendelian randomization study

description: Hypertensive disorders of pregnancy (HDPs), which include gestational hypertension (GH) and preeclampsia (PE), are the primary causes of maternal morbidity and mortality worldwide. Recent studies have found a correlation between metabolic dysfunction-associated steatotic liver disease (MASLD) and HDPs, but the causality of this association remains to be identified. Therefore, this study aims to evaluate the causal relationship between MASLD and HDPs through Mendelian randomization (MR) analysis. The summary statistics from genome-wide association studies were employed to conduct a two-sample MR analysis. Five complementary MR methods, including inverse variance weighting (IVW), MR-Egger, weighted median, simple mode and weighted mode were performed to assess the causality of MASLD on GH and PE. Furthermore, we conducted various sensitivity analyses to ensure the stability and reliability of the results. Genetically predicted MASLD significantly increased the risk of GH (IVW: OR = 1.138, 95% CI: 1.062–1.220, <i>p</i> &lt; 0.001), while there was little evidence of a causal relationship between MASLD and PE (IVW: OR = 0.980, 95% CI: 0.910–1.056, <i>p</i> = 0.594). The sensitivity analyses indicated no presence of heterogeneity and horizontal pleiotropy. This MR study provided evidence supporting the causal effect of MASLD on GH. Our findings underscore the significance of providing more intensive prenatal care and early intervention for pregnant women with MASLD to prevent potential adverse obstetric outcomes.