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[PMID]: 29523277
[Au] Autor:Vasku M; Kleine-Eggebrecht N; Rath W; Mohaupt MG; Escher G; Pecks U
[Ad] Address:Department of Obstetrics and Gynecology, University Hospital RWTH Aachen, Aachen, Germany; Department of Obstetrics and Gynecology, Florence-Nightingale Hospital, Duesseldorf, Germany. Electronic address: vasku@kaiserswerther-diakonie.de.
[Ti] Title:Apparent systemic 11ß-dehydroxysteroid dehydrogenase 2 activity is increased in preeclampsia but not in intrauterine growth restriction.
[So] Source:Pregnancy Hypertens;11:7-11, 2018 Jan.
[Is] ISSN:2210-7797
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The enzyme 11ß-dehydroxysteroid dehydrogenase 2 (11ß-HSD2) converts active cortisol (F) to inactive cortisone (E). A reduced 11ß-HSD2 activity in the placenta has been demonstrated for prematurity, low birth weight, and preeclampsia. We hypothesized that disturbed placental function rather than a maternal response contributes to decreased 11ßHSD2 activity as reflected by a diminished conversion of F to E. Hence, the aim of the present study was to estimate the systemic activity of 11ß-HSD2 throughout gestation and in pregnancies complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR) by calculating maternal serum F/E ratios. METHODS: A total of 188 maternal serum samples were analyzed for nine glucocorticoid metabolites by gas chromatography-mass spectrometry (GC-MS) and F/E ratios were calculated. Study Group A: In a longitudinal set 33 healthy pregnant women were analyzed at three different time points throughout gestation and one postpartum. Study Group B: Cross-sectionally additional 56 patients were enrolled. We compared patients with PE (N = 14) and IUGR (N = 14) with gestational age matched healthy controls (CTRL = 28). RESULTS: Group A: The apparent 11ß-HSD2 activity dropped in the second trimester being restored to first trimester levels (P value = 0.016). Group B: The 11ß-HSD2 activity was high in PE (P value < 0.05) but not in the IUGR group as compared to CTRL. CONCLUSION: The increased apparent serum 11ß-HSD2 activity observed with advancing gestation in normal pregnancy may reflect an elevated general increase in enzyme activity due to a higher placental mass. The high systemic 11ß-HSD2 activity in PE but not in IUGR however suggests an increased F deactivation in maternal tissue in PE rather than in the placenta since placental insufficiency in the absence of PE does not significantly alter F/E ratio.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  2 / 3160 MEDLINE  
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[PMID]: 29377939
[Au] Autor:Budzyn M; Iskra M; Turkiewicz W; Krasinski Z; Gryszczynska B; Kasprzak MP
[Ad] Address:Department of General Chemistry, Chair of Chemistry and Clinical Biochemistry, Poznan University of Medical Sciences, Poznan, Poland.
[Ti] Title:Plasma concentration of selected biochemical markers of endothelial dysfunction in women with various severity of chronic venous insufficiency (CVI)-A pilot study.
[So] Source:PLoS One;13(1):e0191902, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Although the endothelial dysfunction is considered to be implicated in the pathogenesis of chronic venous insufficiency (CVI) the endothelial status in patients with venous disorders is still not fully evaluated. Therefore the aim of the study was to measure the concentration of selected markers of endothelial dysfunction: von Willebrand factor (vWf), soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM) and soluble VE-cadherin (sVE-cadherin) in CVI women who constitute the most numerous group of patients suffering from venous disease. MATERIALS AND METHODS: Forty four women with CVI were involved in the study and divided into subgroups based on CEAP classification. Concentration of vWf, sP-selectin, sTM and sVE-cadherin were measured and compared with those obtained in 25 healthy age and sex-matched women. RESULTS: It was found that the concentration of sTM increased and sVEcadherin decreased along with disease severity in CVI women. A significant rise of sTM was observed especially in CVI women, with the highest inflammation status reflected by hsCRP or elastase concentration, and in CVI women with a high oxidative stress manifested by an increased plasma MDA. A significant fall of circulating sVE-cadherin was reported in CVI women with moderate to highest intensity of inflammation and oxidative stress. There was no change in vWF and sP-selectin concentration at any stage of CVI severity. CONCLUSIONS: The results of the present study demonstrate the presence of endothelial dysfunction in women suffering from CVI which seems to progress with the disease severity and may be associated with inflammation and enhanced oxidative stress.
[Mh] MeSH terms primary: Biomarkers/blood
Endothelium, Vascular/physiopathology
Venous Insufficiency/blood
[Mh] MeSH terms secundary: Adult
Antigens, CD/blood
Cadherins/blood
Chronic Disease
Female
Humans
Middle Aged
P-Selectin/blood
Pilot Projects
Severity of Illness Index
Thrombomodulin/blood
von Willebrand Factor/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD); 0 (Biomarkers); 0 (Cadherins); 0 (P-Selectin); 0 (Thrombomodulin); 0 (cadherin 5); 0 (von Willebrand Factor)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191902

  3 / 3160 MEDLINE  
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[PMID]: 29272530
[Au] Autor:Lappas M; McCracken S; McKelvey K; Lim R; James J; Roberts CT; Fournier T; Alfaidy N; Powell KL; Borg AJ; Morris JM; Leaw B; Singh H; Ebeling PR; Wallace EM; Parry LJ; Dimitriadis E; Murthi P
[Ad] Address:Mercy Perinatal Research Centre, Mercy Hospital for Women, Heidelberg, Victoria 3079, Australia.
[Ti] Title:Formyl peptide receptor-2 is decreased in foetal growth restriction and contributes to placental dysfunction.
[So] Source:Mol Hum Reprod;24(2):94-109, 2018 Feb 01.
[Is] ISSN:1460-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:STUDY QUESTION: What is the association between placental formyl peptide receptor 2 (FPR2) and trophoblast and endothelial functions in pregnancies affected by foetal growth restriction (FGR)? SUMMARY ANSWER: Reduced FPR2 placental expression in idiopathic FGR results in significantly altered trophoblast differentiation and endothelial function in vitro. WHAT IS KNOWN ALREADY: FGR is associated with placental insufficiency, where defective trophoblast and endothelial functions contribute to reduced feto-placental growth. STUDY DESIGN, SIZE, DURATION: The expression of FPR2 in placental tissues from human pregnancies complicated with FGR was compared to that in gestation-matched uncomplicated control pregnancies (n = 25 from each group). Fpr2 expression was also determined in placental tissues obtained from a murine model of FGR (n = 4). The functional role of FPR2 in primary trophoblasts and endothelial cells in vitro was assessed in diverse assays in a time-dependent manner. PARTICIPANTS/MATERIALS, SETTING, METHODS: Placentae from third-trimester pregnancies complicated by idiopathic FGR (n = 25) and those from gestation-matched pregnancies with appropriately grown infants as controls (n = 25) were collected at gestation 27-40 weeks. Placental tissues were also collected from a spontaneous CBA/CaH × DBA/2 J murine model of FGR. Placental FPR2/Fpr2 mRNA expression was determined by real-time PCR, while protein expression was examined by immunoblotting and immunohistochemistry. siRNA transfection was used to silence FPR2 expression in primary trophoblasts and in human umbilical vein endothelial cells (HUVEC), and the quantitation of cytokines, chemokines and apoptosis was performed following a cDNA array analyses. Functional effects of trophoblast differentiation were measured using HCGB/ß-hCG and syncytin-2 expression as well as markers of apoptosis, tumour protein 53 (TP53), caspase 8, B cell lymphoma 2 (BCL2) and BCL associated X (BAX). Endothelial function was assessed by proliferation, network formation and permeability assays. MAIN RESULTS AND THE ROLE OF CHANCE: Placental FPR2/Fpr2 expression was significantly decreased in FGR placentae (n = 25, P < 0.05) as well as in murine FGR placentae compared to controls (n = 4, P < 0.05). FPR2 siRNA (siFPR2) in term trophoblasts significantly increased differentiation markers, HCGB and syncytin-2; cytokines, interleukin (IL)-6, CXCL8; and apoptotic markers, TP53, caspase 8 and BAX, but significantly reduced the expression of the chemokines CXCL12 and its receptors CXCR4 and CXCR7; CXCL16 and its receptor, CXCR6; and cytokine, IL-10, compared with control siRNA (siCONT). Treatment of HUVECs with siFPR2 significantly reduced proliferation and endothelial tube formation, but significantly increased permeability of HUVECs. LARGE SCALE DATA: N/A. LIMITATIONS, REASONS FOR CAUTION: Reduced expression of placental FPR2/Fpr2 was observed in the third trimester at delivery after development of FGR, suggesting that FPR2 is associated with FGR pregnancies. However, there is a possibility that the decreased placental FPR2 observed in FGR may be a consequence rather than a cause of FGR, although our in vitro functional analyses using primary trophoblasts and endothelial cells suggest that FPR2 may have a direct or indirect regulatory role on trophoblast differentiation and endothelial function in FGR. WIDER IMPLICATIONS OF THE FINDINGS: This is the first study linking placental FPR2 expression with changes in the trophoblast and endothelial functions that may explain the placental insufficiency observed in FGR. STUDY FUNDING/COMPETING INTERESTS: P.M. and P.R.E. received funding from the Australian Institute of Musculoskeletal Science, Western Health, St. Albans, Victoria 3021, Australia. M.L. is supported by a Career Development Fellowship from the National Health and Medical Research Council (NHMRC; Grant no. 1047025). Monash Health is supported by the Victorian Government's Operational Infrastructure Support Programme. The authors declare that there is no conflict of interest in publishing this work.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1093/molehr/gax067

  4 / 3160 MEDLINE  
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[PMID]: 29509436
[Au] Autor:Spradley FT; Smith JA; Alexander BT; Anderson CD
[Ad] Address:Surgery, University of Mississippi Medical Center, United States.
[Ti] Title:Developmental origins of non-alcoholic fatty liver disease as a risk factor for exaggerated metabolic and cardiovascular-renal disease.
[So] Source:Am J Physiol Endocrinol Metab;, 2018 Mar 06.
[Is] ISSN:1522-1555
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Intrauterine growth restriction (IUGR) is linked to increased risk for chronic disease. Placental ischemia and insufficiency in the mother are implicated in predisposing IUGR offspring to metabolic dysfunction, including hypertension, insulin resistance, abnormalities in glucose homeostasis, and non-alcoholic fatty liver disease (NAFLD). Whether these metabolic disturbances contribute to the developmental origins of exaggerated cardiovascular-renal disease (CVRD) risk accompanying IUGR is unclear. IUGR impacts the pancreas, adipose tissue, and liver, which are hypothesized to program for hepatic insulin resistance and subsequent NAFLD. NAFLD is projected to become the major cause of chronic liver disease and contributor to uncontrolled Type 2 Diabetes Mellitus (T2DM), which is a leading cause of chronic kidney disease. While NAFLD is increased in experimental models of IUGR, lacking is a full comprehension of the mechanisms responsible for programming of NAFLD and whether this potentiates susceptibility to liver injury. The use of well-established and clinically relevant rodent models, which mimic the clinical characteristics of IUGR, metabolic disturbances, and increased blood pressure in the offspring, will permit investigation into mechanisms linking adverse influences during early life and later chronic health. The purpose of this review is to propose mechanisms, including those pro-inflammatory in nature, whereby IUGR exacerbates the pathogenesis of NAFLD and how these adverse programmed outcomes contribute to exaggerated CVRD risk. Understanding the etiology of the developmental origins of chronic disease will allow investigators to uncover treatment strategies to intervene in the mother and her offspring to halt the increasing prevalence of metabolic dysfunction and CVRD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1152/ajpendo.00394.2017

  5 / 3160 MEDLINE  
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[PMID]: 28454692
[Au] Autor:Bustamante Helfrich B; Chilukuri N; He H; Cerda SR; Hong X; Wang G; Pearson C; Burd I; Wang X
[Ad] Address:Center on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States; Department of Clinical and Applied Science Education (Pathology), University of the Incarnate Word School of Osteopath
[Ti] Title:Maternal vascular malperfusion of the placental bed associated with hypertensive disorders in the Boston Birth Cohort.
[So] Source:Placenta;52:106-113, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The associations of maternal conditions, before or during pregnancy, with placental lesions have not been adequately studied in populations. METHODS: In the Boston Birth Cohort, we evaluated associations between three maternal medical conditions (hypertensive disorders [HDs], gestational/pre-gestational diabetes and obesity), and placental histological findings, using a standardized classification system proposed by the Amsterdam Placental Workshop Group. Placental pathology diagnoses and clinical data from 3074 mothers with clinical indications who delivered singleton live births at the Boston Medical Center between October 1998 and November 2013 were evaluated. Associations between each maternal condition and maternal vascular malperfusion (MVM) of the placental bed and its standardized subgroups were examined using multivariate logistic and multinomial regressions. RESULTS: Women with HDs (chronic hypertension, eclampsia, preeclampsia, HELLP syndrome) had significantly increased odds of MVM lesions when compared to women with no HD (aOR 2.08 95% CI 1.74-2.50), after adjusting for demographics, substance use, diabetes and body mass index. No significant differences in frequencies or aORs were seen in women with and without diabetes, or across body mass index categories. Co-morbid condition patterns that included HDs were more likely to be associated with MVM than those without. DISCUSSION: Using a standardized classification system, we showed that MVM is strongly and specifically associated with maternal HDs, but not other maternal conditions. Additional studies are needed to confirm and validate our findings, and evaluate the role of maternal vascular lesions of the placental bed in relation to postnatal growth and development of the offspring and effect modifiers.
[Mh] MeSH terms primary: Diabetes, Gestational/pathology
Hypertension, Pregnancy-Induced/pathology
Obesity/complications
Placenta/blood supply
Placental Insufficiency/etiology
[Mh] MeSH terms secundary: Adult
Body Mass Index
Female
Humans
Obesity/pathology
Placenta/pathology
Placental Insufficiency/pathology
Pregnancy
Retrospective Studies
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:170430
[St] Status:MEDLINE

  6 / 3160 MEDLINE  
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[PMID]: 28454690
[Au] Autor:Spiel M; Salahuddin S; Pernicone E; Zsengeller Z; Wang A; Modest AM; Karumanchi SA; Hecht JL
[Ad] Address:Department of Obstetrics & Gynecology, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave, Boston, MA 02215, USA.
[Ti] Title:Placental soluble fms-like tyrosine kinase expression in small for gestational age infants and risk for adverse outcomes.
[So] Source:Placenta;52:10-16, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Soluble fms-like tyrosine kinase 1 (sFLT-1) is an anti-angiogenic factor implicated in the pathogenesis of preterm preeclampsia. We evaluated sFLT-1 expression and placental pathology in pregnancies complicated by small for gestational age (SGA) infants (<10th percentile), without evidence of preeclampsia. METHODS: Clinical and histologic data were compared between groups with high or low sFLT-1 expression determined by immunohistochemistry on archived placentas. RESULTS: Nineteen of 69 placentas showed high sFLT-1 expression. The high sFLT-1 group had higher predelivery median systolic blood pressure (BP); 140 (interquartile range (IQR) 133-152) vs. 126 (118-139) mm Hg (p = 0.003), and median diastolic BP; 87 (78-94) vs. 77.5 (71-86) mm Hg (p = 0.02). Abnormal umbilical Doppler abnormalities were more prevalent; 89.5% vs. 46% (p = 0.001). These pregnancies delivered earlier; 31.9 weeks (28.3-34.7 weeks) vs. 37.1 weeks (33.7-38.7 weeks) (p < 0.001), and infants had lower birthweight; 980 grams (520-1545 grams) vs. 2087.5 grams (1455-2340 grams) (p < 0.001). Placental-weight to fetal-weight ratios, a marker of vascular insufficiency, was increased in the high sFlt-1 group: 0.18 (0.14-0.28) vs 0.15 (0.13-0.18), p = 0.03. Placentas with high sFLT-1 showed more decidual vasculopathy; 42.1% vs. 10.0% (p = 0.005), infarction; 36.8% vs. 14.0% (p = 0.048), distal villous hypoplasia; 78.9% vs. 36.0% (p = 0.001), and fetal thrombotic vasculopathy; 47.4% vs. 16.0% (p = 0.01). DISCUSSION: Placental sFLT-1 expression is upregulated in approximately 28% of non-preeclamptic pregnancies complicated by SGA infants. These pregnancies showed increased placental vascular pathology, more umbilical Doppler abnormalities, and earlier delivery with lower birthweight. A subgroup of non-preeclamptic fetal growth restriction with upregulated sFlt-1 expression may share a common pathogenic pathway with preterm preeclampsia. This subgroup is worthy of additional study.
[Mh] MeSH terms primary: Infant, Small for Gestational Age/metabolism
Placenta/metabolism
Placental Insufficiency/metabolism
Up-Regulation
Vascular Endothelial Growth Factor Receptor-1/metabolism
[Mh] MeSH terms secundary: Adult
Female
Gestational Age
Humans
Infant, Newborn
Placenta/diagnostic imaging
Placenta/pathology
Placental Insufficiency/diagnostic imaging
Placental Insufficiency/pathology
Pregnancy
Ultrasonography, Doppler
Ultrasonography, Prenatal
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170430
[St] Status:MEDLINE

  7 / 3160 MEDLINE  
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[PMID]: 29273273
[Au] Autor:Wilson SL; Robinson WP
[Ad] Address:BC Children's Hospital Research, 950 W 28th Ave, Vancouver, BC, V5Z 4H4, Canada; Dept. of Medical Genetics, University of British Columbia, C201-4500 Oak St, Vancouver, BC, V6H 3N1, Canada. Electronic address: swils6@alumni.ubc.ca.
[Ti] Title:Utility of DNA methylation to assess placental health.
[So] Source:Placenta;, 2017 Dec 14.
[Is] ISSN:1532-3102
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:DNA methylation (DNAm), a mitotically stable epigenetic mark, can influence as well as reflect gene expression. DNAm has been gaining interest for use as a biomarker for many conditions including placental insufficiency, specifically preeclampsia (PE) and intrauterine growth restriction (IUGR). Additionally, DNAm may retain a "memory" of earlier in utero exposures and hence provide insight into pathogeneses occurring earlier in gestation. This review will discuss the placental DNA methylome, the uses of DNAm to assess placental health, and considerations and limitations to understand in epigenome-wide association studies (EWAS).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher

  8 / 3160 MEDLINE  
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[PMID]: 29466434
[Au] Autor:Gumus HG; Illa M; Pla L; Zamora M; Crispi F; Gratacos E
[Ad] Address:Fetal i+D Fetal Medicine Research Center, BCNatal -Barcelona Center for Maternal-Fetal and Neonatal Medicine (Hospital Clinic and Hospital San Juan de Deu), Institut Clinic de Ginecologia, Obstetricia i Neonatalogia, Institut d'Investigacions Biomediques August Pi i Sunyer, University of Barcelona,
[Ti] Title:Nutritional intra-amniotic therapy increases survival in a rabbit model of fetal growth restriction.
[So] Source:PLoS One;13(2):e0193240, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To evaluate the perinatal effects of a prenatal therapy based on intra-amniotic nutritional supplementation in a rabbit model of intrauterine growth restriction (IUGR). METHODS: IUGR was surgically induced in pregnant rabbits at gestational day 25 by ligating 40-50% of uteroplacental vessels of each gestational sac. At the same time, modified-parenteral nutrition solution (containing glucose, amino acids and electrolytes) was injected into the amniotic sac of nearly half of the IUGR fetuses (IUGR-T group n = 106), whereas sham injections were performed in the rest of fetuses (IUGR group n = 118). A control group without IUGR induction but sham injection was also included (n = 115). Five days after the ligation procedure, a cesarean section was performed to evaluate fetal cardiac function, survival and birth weight. RESULTS: Survival was significantly improved in the IUGR fetuses that were treated with intra-amniotic nutritional supplementation as compared to non-treated IUGR animals (survival rate: controls 71% vs. IUGR 44% p = 0.003 and IUGR-T 63% vs. IUGR 44% p = 0.02), whereas, birth weight (controls mean 43g ± SD 9 vs. IUGR 36g ± SD 9 vs. IUGR-T 35g ± SD 8, p = 0.001) and fetal cardiac function were similar among the IUGR groups. CONCLUSION: Intra-amniotic injection of a modified-parenteral nutrient solution appears to be a promising therapy for reducing mortality among IUGR. These results provide an opportunity to develop new intra-amniotic nutritional strategies to reach the fetus by bypassing the placental insufficiency.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0193240

  9 / 3160 MEDLINE  
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[PMID]: 29463784
[Au] Autor:Turrini I; Sorbi F; Ghizzoni V; Mannini L; Fambrini M; Terreni A; Projetto E; Castiglione F; Noci I
[Ad] Address:Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy.
[Ti] Title:Severe Fetal Distress and Placental Damage might be Associated with High Troponin I (cTnI) Levels in Mothers.
[So] Source:Am J Case Rep;19:194-198, 2018 Feb 21.
[Is] ISSN:1941-5923
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND Troponin I is the gold standard for the diagnosis of adult acute coronary syndrome. Although it is known that a hypoxic fetus may produce cTnI, fetal cTnI passage in maternal blood has never been documented. CASE REPORT We report a case where the rise of cTnI in the blood of a pregnant woman was not related to maternal heart disease. Instead, it might be suggestive of a fetal cardiac origin, as there was a severe placental insufficiency with a fetal intrauterine growth restriction. CONCLUSIONS This study suggests that the rise of cTnI in maternal blood in a cardiovascular healthy pregnant woman might have a fetal origin. After having excluded any maternal causes, cTnI elevation could be explained with the transfer of fetal cTnI through an injured placenta.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Process

  10 / 3160 MEDLINE  
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[PMID]: 29373603
[Au] Autor:Guo MY; Wang H; Chen YH; Xia MZ; Zhang C; Xu DX
[Ad] Address:Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
[Ti] Title:N-acetylcysteine alleviates cadmium-induced placental endoplasmic reticulum stress and fetal growth restriction in mice.
[So] Source:PLoS One;13(1):e0191667, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cadmium (Cd) is a developmental toxicant that induces fetal growth restriction (FGR). Placental endoplasmic reticulum (ER) stress is associated with FGR. This study investigated the effects of N-acetylcysteine (NAC) on Cd-induced placental ER stress and FGR. Pregnant mice were intraperitoneally injected with CdCl2 daily from gestational day (GD)13 to GD17. As expected, Cd reduced fetal weight and crown-rump length. Cd decreased the internal space of blood vessels in the placental labyrinth layer and inhibited placental cell proliferation. Several genes of growth factors, such as Vegf-a, placental growth factor, Igf1 and Igf1r, and several genes of nutrient transport pumps, such as Glut1, Fatp1 and Snat2, were down-regulated in placenta of Cd-treated mice. Moreover, Cd evoked placental ER stress. Of interest, NAC alleviated Cd-induced FGR. Additional experiment showed that NAC inhibited Cd-induced impairment of placental development and placental ER stress. Therefore, NAC may be exploited for prevention of Cd-induced placental insufficiency and FGR.
[Mh] MeSH terms primary: Acetylcysteine/pharmacology
Cadmium/toxicity
Endoplasmic Reticulum Stress/drug effects
Fetal Growth Retardation/prevention & control
Placenta/drug effects
[Mh] MeSH terms secundary: Animals
Down-Regulation/drug effects
Female
Mice
Pregnancy
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:00BH33GNGH (Cadmium); WYQ7N0BPYC (Acetylcysteine)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191667


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