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Anke de Haan Markus A. Landolt Eiko I. Fried Kristian Kleinke Eva Alisic Richard Bryant Karen Salmon Sue-Huei Chen Shu-Tsen Liu Tim Dalgleish Anna McKinnon Alice Alberici Jade Claxton Julia Diehle Ramón Lindauer Carlijn de Roos Sarah L. Halligan Rachel Hiller Christian H. Kristensen Beatriz O.M. Lobo Nicole M. Volkmann Meghan Marsac Lamia Barakat Nancy Kassam-Adams Reginald D.V. Nixon Susan Hogan Raija-Leena Punamäki Esa Palosaari Elizabeth Schilpzand Rowena Conroy Patrick Smith William Yule Richard Meiser-Stedman 《Journal of child psychology and psychiatry, and allied disciplines》2020,61(1):77-87
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Alessio Coi Michele Santoro Ester Garne Anna Pierini Marie‐Claude Addor Jean‐Luc Alessandri Jorieke E. H. Bergman Fabrizio Bianchi Ljubica Boban Paula Braz Clara Cavero‐Carbonell Miriam Gatt Martin Haeusler Kari Klungsøyr Jennifer J. Kurinczuk Monica Lanzoni Nathalie Lelong Karen Luyt Olatz Mokoroa Carmel Mullaney Vera Nelen Amanda J. Neville Mary T. O'Mahony Isabelle Perthus Judith Rankin Anke Rissmann Florence Rouget Bruno Schaub David Tucker Diana Wellesley Katarzyna Wisniewska Nataliia Zymak‐Zakutnia Ingeborg Barišić 《American journal of medical genetics. Part A》2019,179(9):1791-1798
Achondroplasia is a rare genetic disorder resulting in short‐limb skeletal dysplasia. We present the largest European population‐based epidemiological study to date using data provided by the European Surveillance of Congenital Anomalies (EUROCAT) network. All cases of achondroplasia notified to 28 EUROCAT registries (1991–2015) were included in the study. Prevalence, birth outcomes, prenatal diagnosis, associated anomalies, and the impact of paternal and maternal age on de novo achondroplasia were presented. The study population consisted of 434 achondroplasia cases with a prevalence of 3.72 per 100,000 births (95%CIs: 3.14–4.39). There were 350 live births, 82 terminations of pregnancy after prenatal diagnosis, and two fetal deaths. The prenatal detection rate was significantly higher in recent years (71% in 2011–2015 vs. 36% in 1991–1995). Major associated congenital anomalies were present in 10% of cases. About 20% of cases were familial. After adjusting for maternal age, fathers >34 years had a significantly higher risk of having infants with de novo achondroplasia than younger fathers. Prevalence was stable over time, but regional differences were observed. All pregnancy outcomes were included in the prevalence estimate with 80.6% being live born. The study confirmed the increased risk for older fathers of having infants with de novo achondroplasia. 相似文献
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Garnier Y Kadyrov M Gantert M Einig A Rath W Huppertz B 《European journal of obstetrics, gynecology, and reproductive biology》2008,140(2):152-157
OBJECTIVES: Antenatal infections are associated with an increased risk of perinatal morbidity and mortality. Systemic application of endotoxins to the fetus results in an increase in placental vascular resistance and chronic reduction in umbilical blood flow. We studied morphological alterations of the placenta in response to fetal inflammation in the preterm sheep. STUDY DESIGN: Therefore, 14 fetal sheep were chronically instrumented at a mean gestational age of 107+/-1 days (term is 147 days). Four days after surgery fetuses received 100 ng lipopolysaccharide (LPS; n=8) or saline (control; n=6) intravenously. Fetal heart rate and arterial blood pressure were monitored continuously while blood gases and acid-base balance were measured at time points 0, +1, +3, +6, +12, +24, +48 and +72 h. Three days after LPS application placental cotyledons were analyzed by immunohistochemistry and morphometry. Different primary antibodies like AE 1 and AE 3 against cytokeratins were used. Secondary antibodies were visualized with 3-amino-9-ethylcarbazole (AEC) or using the Vectastain kit (Vector Laboratories, Burlingame, CA). Double staining was carried out first by utilizing Vectastain kit (black), followed by AEC staining (red). Counterstaining was performed with haematoxylin. RESULTS: Fetal tachycardia and hypertension were induced transiently during the first 12h after LPS application. Fetuses suffered from mild hypoxaemia while acidemia was absent. Morphometry revealed a non-significant shift in the relation of maternal and fetal placental compartments towards the maternal parts in response to LPS treatment. Endotoxin induced an increased proliferation in both compartments of the placenta with a 3.2-fold increase on the maternal and a 1.8-fold increase on the fetal side. CONCLUSIONS: Systemic endotoxin exposure of the preterm fetal sheep leads to a change in the gross organization of the placenta and changes in the proliferation patterns in both placental compartments. These rearrangements inside the placenta may disturb its organ function and subsequently lead to fetal morbidity associated with the fetal inflammatory response syndrome and chronic placental dysfunction, respectively. 相似文献
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Hajer El Oussini Hanna Bayer Jelena Scekic-Zahirovic Pauline Vercruysse Jérôme Sinniger Sylvie Dirrig-Grosch Stéphane Dieterlé Andoni Echaniz-Laguna Yves Larmet Kathrin Müller Jochen H. Weishaupt Dietmar R. Thal Wouter van Rheenen Kristel van Eijk Roland Lawson Laurent Monassier Luc Maroteaux Anne Roumier Philip C. Wong Leonard H. van den Berg Albert C. Ludolph Jan H. Veldink Anke Witting Luc Dupuis 《Acta neuropathologica》2016,131(3):465-480
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