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Sökning: WFRF:(Vinnars Marie Therese)

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  • Björvang, Richelle D., et al. (författare)
  • Mixtures of persistent organic pollutants are found in vital organs of late gestation human fetuses
  • 2021
  • Ingår i: Chemosphere. - : Elsevier. - 0045-6535 .- 1879-1298. ; 283
  • Tidskriftsartikel (refereegranskat)abstract
    • Persistent organic pollutants (POPs) are industrial chemicals with long half-lives. Early life exposure to POPs has been associated with adverse effects. Fetal exposure is typically estimated based on concentrations in maternal serum or placenta and little is known on the actual fetal exposure. We measured the concentrations of nine organochlorine pesticides (OCPs), ten polychlorinated biphenyl (PCB) congeners, and polybrominated diphenyl ether (PBDE) congeners by gas chromatography – tandem mass spectrometry in maternal serum, placenta, and fetal tissues (adipose tissue, liver, heart, lung and brain) in 20 pregnancies that ended in stillbirth (gestational weeks 36–41). The data were combined with our earlier data on perfluoroalkyl substances (PFASs) in the same cohort (Mamsen et al. 2019). HCB, p,p’-DDE, PCB 138 and PCB 153 were quantified in all samples of maternal serum, placenta and fetal tissues. All 22 POPs were detected in all fetal adipose tissue samples, even in cases where they could not be detected in maternal serum or placenta. Tissue:serum ratios were significantly higher in later gestations, male fetuses, and pregnancies with normal placental function. OCPs showed the highest tissue:serum ratios and PFAS the lowest. The highest chemical burden was found in adipose tissue and lowest in the brain. Overall, all studied human fetuses were intrinsically exposed to mixtures of POPs. Tissue:serum ratios were significantly modified by gestational age, fetal sex and placental function. Importantly, more chemicals were detected in fetal tissues compared to maternal serum and placenta, implying that these proxy samples may provide a misleading picture of actual fetal exposures.
  • Mamsen, Linn Salto, et al. (författare)
  • Concentrations of perfluoroalkyl substances (PFASs) in human embryonic and fetal organs from first, second, and third trimester pregnancies
  • 2019
  • Ingår i: Environment International. - : Elsevier. - 0160-4120 .- 1873-6750. ; 124, s. 482-492
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The persistent environmental contaminants perfluoroalkyl substances (PFASs) have gained attention due to their potential adverse health effects, in particular following early life exposure. Information on human fetal exposure to PFASs is currently limited to one report on first trimester samples. There is no data available on PFAS concentrations in fetal organs throughout all three trimesters of pregnancy. Methods: We measured the concentrations of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), and perfluorohexane sulfonic acid (PFHxS) in human embryos and fetuses with corresponding placentas and maternal serum samples derived from elective pregnancy terminations and cases of intrauterine fetal death. A total of 78 embryos and fetuses aged 7–42 gestational weeks were included and a total of 225 fetal organs covering liver, lung, heart, central nervous system (CNS), and adipose tissue were analyzed, together with 71 placentas and 63 maternal serum samples. PFAS concentrations were assayed by liquid chromatography/triple quadrupole mass spectrometry. Results: All evaluated PFASs were detected and quantified in maternal sera, placentas and embryos/fetuses. In maternal serum samples, PFOS was detected in highest concentrations, followed by PFOA > PFNA > PFDA = PFUnA = PFHxS. Similarly, PFOS was detected in highest concentrations in embryo/fetal tissues, followed by PFOA > PFNA = PFDA = PFUnA. PFHxS was detected in very few fetuses. In general, PFAS concentrations in embryo/fetal tissue (ng/g) were lower than maternal serum (ng/ml) but similar to placenta concentrations. The total PFAS burden (i.e. the sum of all PFASs) was highest in lung tissue in first trimester samples and in liver in second and third trimester samples. The burden was lowest in CNS samples irrespective of fetal age. The placenta:maternal serum ratios of PFOS, PFOA and PFNA increased across gestation suggesting bioaccumulation in the placenta. Further, we observed that the ratios were higher in pregnancies with male fetuses compared to female fetuses. Conclusions: Human fetuses were intrinsically exposed to a mixture of PFASs throughout gestation. The compounds were detected in all analyzed tissues, suggesting that PFASs reach and may affect many types of organs. Collectively, our results demonstrate that PFASs pass the placenta and deposit to embryo and fetal tissues, calling for risk assessment of gestational exposures.
  • Vinnars, Marie-Therese, et al. (författare)
  • Association between placental pathology and neonatal outcome in preeclampsia : a large cohort study
  • 2014
  • Ingår i: Hypertension in Pregnancy. - 1064-1955 .- 1525-6065. ; 33:2, s. 145-158
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To study associations between placental histopathology and neonatal outcome in preeclampsia (PE). Study design: The cohort consisted of 544 singleton pregnancies complicated by PE and managed at Karolinska University Hospital, Stockholm, Sweden during 2000-2009. Evaluation of placental histopathology was made by one senior perinatal pathologist, blinded to outcome. Clinical outcome was obtained from prospectively collected medical registry data and medical records. Main outcome measures were intrauterine fetal death, smallness for gestational age, admission to neonatal unit, major neonatal morbidity (defined as presence of intraventricular hemorrhage >= grade 3, retinopathy of prematurity >= grade 3, necrotizing enterocolitis, cystic periventricular leucomalacia and/or severe bronchopulmonary dysplasia) and neonatal mortality. Logistic regression analyses including gestational age were performed. Results: Abnormal placental weight, both low (adjusted odds ratio (OR) [95% confidence interval] 5.2 [1.1-24], p = 0.03) and high (adjusted OR 1048 [21-51 663], p < 0.001) for gestational age, was associated with major neonatal morbidity in preterm infants. Accelerated villous maturation was less prevalent in intrauterine fetal death pregnancies (adjusted OR 0.18 [0.04-0.77], p = 0.02). Decidual arteriopathy increased the odds for admission to neonatal care (adjusted OR 2.7 [1.1-6.5], p = 0.03). Infarction involving >= 5% of the placenta was associated with intrauterine fetal death and small for gestational age infants (adjusted OR's 75 [5.5-1011], p = 0.001 and 3.2 [1.7-5.9], p < 0.001; respectively). No relations between histological variables and neonatal mortality could be found. Conclusion: Placental pathology in PE reflects adverse perinatal events and deviant placental weight predicts adverse neonatal outcome in preeclamptic women delivering preterm. Placental investigation without delay can contribute to neonatal risk assessment.
  • Vinnars, Marie-Therese, et al. (författare)
  • Enhanced Th1 and inflammatory mRNA responses upregulate NK cell cytotoxicity and NKG2D ligand expression in human pre-eclamptic placenta and target it for NK cell attack
  • 2018
  • Ingår i: American Journal of Reproductive Immunology. - : John Wiley & Sons. - 1046-7408 .- 1600-0897. ; 80:1
  • Tidskriftsartikel (refereegranskat)abstract
    • ProblemPre-eclampsia (PE), a severe human pregnancy disorder, is associated with exaggerated systemic inflammation, enhanced cytokine production, and increased shedding of microvesicles leading to endothelial dysfunction, coagulopathy, and extensive placenta destruction. The cause of PE is still unclear. Evidence suggests that its origin lies in the placenta and that the maternal immune system is involved. A shift in cytokine production in PE pregnancy promotes NK cell activation, suggested to be important in PE pathogenesis. In line with this suggestion, we studied NK cell cytotoxicity in peripheral blood of PE patients and controls and the mRNA expression of cytokines and of the NKG2D receptor and its ligands MICA/B and ULBP1-3 in PE- and normal placenta. Method of studyThe cytotoxic capacity of peripheral blood NK cells was analyzed using K562 target cells. The cytokine mRNA profiles and the mRNA expression of the NKG2D receptor and its ligands MICA/B and ULBP 1-3 in PE placenta were assessed and compared to those in normal placenta using real-time quantitative RT-PCR. ResultsThe cytotoxicity of peripheral blood NK cells was upregulated in PE cases. Further, we found an enhanced inflammatory cytokine mRNA response combined with a dysregulated regulatory response and a significant mRNA overexpression of NKG2D receptor and its ligands MICA/B and ULBP in PE placenta. ConclusionThe destruction of chorionic villi observed in PE placenta might be conveyed by an enhanced local cytotoxic response through the NKG2D receptor-ligand pathway, which in turn might be promoted by an intense inflammatory response not counteracted by regulatory cytokine responses.
  • Vinnars, Marie-Therese, et al. (författare)
  • Placental pathology in relation to stillbirth and neonatal outcome in an extremely preterm population : a prospective cohort study
  • 2015
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - 0001-6349 .- 1600-0412. ; 94:6, s. 584-590
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To study associations between placental histopathology and stillbirth as well as neonatal outcome in a population born extremely preterm. Design: Prospective cohort study. Setting: Stockholm, Sweden. Population: 167 infants born <27 gestational weeks during 2004-2007. Methods: One senior perinatal pathologist, blinded to outcome data, evaluated all placental slides. Main outcome measures: Intrauterine fetal death, small-for-gestational age, major neonatal morbidity (intraventricular hemorrhage grade 3, retinopathy of prematurity grade 3, necrotizing enterocolitis, cystic periventricular leukomalacia or severe bronchopulmonary dysplasia) and neonatal mortality. Additional outcome variables were Apgar score at 5min, sepsis, and treated patent ductus arteriosus. Results: Accelerated villous maturation was associated with a decreased risk for Apgar score <7 at 5min (p=0.041). Fetal thrombosis and low placental weight were associated with an increased risk for both intrauterine fetal death (p<0.001 and p=0.011, respectively) and small-for-gestational age (p<0.001 and p<0.001, respectively). Conclusion: Placental histology may have prognostic value as it appears to be associated with intrauterine fetal death, as well as with being small-for-gestational age and assignment of a low Apgar score at birth.
  • Björk, Emma, et al. (författare)
  • Enhanced local and systemic inflammatory cytokine mRNA expression in women with endometriosis evokes compensatory adaptive regulatory mRNA response that mediates immune suppression and impairs cytotoxicity
  • 2020
  • Ingår i: American Journal of Reproductive Immunology. - : John Wiley & Sons. - 1046-7408 .- 1600-0897. ; 84:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Problem: Endometriosis is a disease characterized by ectopic implantation of endometrium and impaired immune responses. To explore its pathogenic mechanisms, we studied the local and systemic cytokine mRNA profiles and their role in the immunity of patients with endometriosis and healthy controls.Method of Study: mRNA for eleven cytokines defining cytotoxic Th1, humoral Th2, regulatory Tr1/Th3, and inflammatory cytokine profiles was characterized locally in endometriotic tissue and endometrium, and systemically in PBMCs from women with endometriosis and healthy controls, using real‐time qRT‐PCR. In addition, immunohistochemical stainings with monoclonal antibodies were performed looking for T regulatory cells in endometriotic lesions.Results: We found a downregulation of mRNA for cytokines mediating cytotoxicity and antibody response and an upregulation of inflammatory and T‐regulatory cytokines in the endometriotic tissues and endometrium from the patients with endometriosis, suggesting enhanced local inflammation and priming of an adaptive regulatory response. Consistent with those findings, there was an abundancy of T regulatory cells in the endometriotic lesions.Conclusions: The ectopic implantation seen in endometriosis could be possible as a consequence of increased inflammation and priming of adaptive T regulatory cells, resulting in impaired cytotoxicity and enhanced immune suppression.
  • Lindberg, Richard, et al. (författare)
  • Polyunsaturated Fatty Acids and Their Metabolites in Hyperemesis Gravidarum
  • 2020
  • Ingår i: Nutrients. - : MDPI. - 2072-6643 .- 2072-6643. ; 12:11
  • Forskningsöversikt (refereegranskat)abstract
    • Polyunsaturated fatty acids (PUFAs) have been studied in relation to pregnancy. However, there is limited knowledge on PUFAs and their metabolites in relation to hyperemesis gravidarum (HG), a pregnancy complication associated with nutritional deficiencies and excessive vomiting. In order to survey the field, a systematic review of the literature was performed, which also included nausea and vomiting of pregnancy (NVP) due to its close relationship with HG. In the very few published studies found, the main subjects of the research concerned free fatty acids (four records), lipid profiles (three records), and bioactive lipids (one article about prostaglandin E2 and one about endocannabinoids). The authors of these studies concluded that, although no cause-and-effect relationship can be established, HG is linked to increased sympathetic responsiveness, thermogenic activity and metabolic rate. In addition, NVP is linked to a metabolic perturbance (which lasts throughout pregnancy). The low number of retrieved records underlines the need for more research in the area of PUFAs and HG, especially with regard to the underlying mechanism for the detected effects, potentially involving growth differentiation factor 15 (GDF15) since evidence for GDF15 regulation of lipid metabolism and the role for GDF15 and its receptor in nausea and vomiting is emerging.
  • Vinnars, Marie-Therese (författare)
  • Placental histopathology in preeclampsia and outcome of the offspring
  • 2013
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Preeclampsia (PE) is a major cause of maternal and fetal morbidity and mortality. The maternal symptoms are diverse and the neonates are often born premature and growth-restricted. Today the survival of premature infants has increased, but the neonatal complications including morbidity and long-term developmental deficits are still common. The etiology and pathophysiological mechanisms in PE are still not known, but it seems as if a central part of the pathogenesis is associated with an unsuccessful implantation of the placenta into the uterus. The only cure is to deliver the mother, which is often a difficult decision in regard to prematurity of the fetus, when the disease has begun early in pregnancy. In our first and second studies, we examined the placental pathology in relation to the maternal symptoms and severity of disease. The first study showed that there was a correlation between the severity of symptoms and the placental pathology. Further, the pathological picture was similar in mild and severe PE, but differed in relation to controls. To summarize, mild PE seems to be part of the PE spectrum, and not a normal physiological development of pregnancy, in contrast to what has previously been claimed. The second study showed that placental pathology differed in severe PE with and without HELLP syndrome (hemolysis, elevated liver enzymes and low platelets), which is a disease regarded as a PE subtype, although the clinical picture is different from classical PE. This indicates that other mechanisms might be involved in the HELLP syndrome. In the third and fourth studies, we examined the placental pathology in relation to perinatal, neonatal and childhood outcome. In the third study, we investigated the relation between placental pathology and perinatal and neonatal outcome in a cohort of PE patients and found that placental pathology was associated with adverse outcome. In the fourth study, in which we studied infants born extremely premature, we also found correlations between placental pathology and perinatal and neonatal outcome. In the fourth study, we also explored possible relations between placental pathology and neurologic and developmental outcome of the child at the age of 2.5 years. We found a significant association between placental infarction and cerebral palsy (CP), and tendencies between several pathological findings and developmental outcome. Overall, we have shown that the underlying pathologies in mild and severe PE probably are similar, whereas HELLP syndrome might have a different etiology. In addition, we have found associations between placental pathology and outcome of the offspring.
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  • Resultat 1-8 av 8

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