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Placental Abnormalities (placental + abnormality)
Selected AbstractsUnderreporting of placental abnormalitiesHISTOPATHOLOGY, Issue 4 2009Francis E Sharkey No abstract is available for this article. [source] Placental thickness in the first half of pregnancyJOURNAL OF CLINICAL ULTRASOUND, Issue 5 2004Theera Tongsong MD Abstract Purpose This study was conducted to establish normal values of placental thickness during the first half of pregnancy. Methods Normal pregnant women with singleton pregnancies between 8 and 20 weeks of gestation were recruited into the study. All the newborns were normal at birth. Placental thickness was measured perpendicularly through the thickest part of the placenta on transabdominal scans. The placental thickness data were analyzed for mean, standard deviation, 95% confidence interval, and 2.5th, 5th, 50th, 95th, and 97.5th percentile for each week of gestational age. The best-fit mathematical model was derived by regression analysis. Results The total number of measurements was 333 and the number of measurements for each week of gestational age ranged from 9 to 37. Regression analysis yielded the following linear equation of the relationship: placental thickness (in mm) = gestational age (in weeks) × 1.4,5.6 (r = 0.82). Conclusion We have established a nomogram for placental thickness. This resource may be a useful aid in the early detection of placental abnormalities, such as hydropic placenta secondary to hemoglobin Bart's disease. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:231,234, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/jcu.20023 [source] PRE-ECLAMPSIA: CONTRIBUTION OF MATERNAL CONSTITUTIONAL FACTORS AND THE CONSEQUENCES FOR CARDIOVASCULAR HEALTHCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2006Anne Barden SUMMARY 1Pre-eclampsia is a serious complication of pregnancy that is potentially life threatening for both the mother and baby. It encompasses a number of abnormalities that may be present in other clinical conditions. 2A placenta is essential for the development of pre-eclampsia and can be important in the pathogenesis of pre-eclampsia. Normal pregnancy is associated with remodelling of the maternal spiral arteries, which deliver blood to the placental villous space. Remodelling involves invasion by placental cytotrophoblasts that cause the maternal spiral arteries to lose their smooth muscle and become capacitance vessels; this process, known as placentation, is complete by 20 weeks of pregnancy. Poor placentation is associated with small-for-gestational-age fetuses and some cases of pre-eclampsia. It is thought that poor placentation can result in a hypoxic placenta that releases ,toxic substances' into the maternal circulation, contributing to the maternal syndrome. A number of candidate ,toxic substances' have been proposed, but none is universally raised in pre-eclampsia. 3Although the placenta is necessary for the development of pre-eclampsia, the extent to which placental abnormalities contribute to the condition varies. It is becoming apparent that maternal constitutional factors may also be important in this syndrome. Underlying hypertension, diabetes and obesity strongly predispose to pre-eclampsia. However, a continuum of risk may exist for blood pressure, bodyweight, glucose and lipids, which, in combination with each other and some degree of placental abnormalities, may lead to the development of pre-eclampsia. 4The present review will focus on the maternal constitutional factors that define the metabolic syndrome and examine their contribution to pre-eclampsia and the long-term consequences for cardiovascular health. [source] Placental endothelial nitric oxide synthase localization and expression in normal human pregnancy and pre-eclampsiaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2003SJ Orange Summary 1.,The aim of the present study was to investigate whether pre-eclampisa, a state of placental hypoxia, is associated with placental abnormalities in the amount, distribution and expression of enothelial nitric oxide synthase (eNOS). 2.,Localization and intensity of eNOS was determined by immunohistochemistry using an antibody specific for eNOS. The amount of eNOS mRNA expression was determined by reverse transcription,polymerase chain reaction (RT-PCR) and the densitometry of gel bands was expressed as a ratio of the band density of the housekeeping gene ,2 -microglobulin. 3.,Endothelial NOS staining was localized to syncytiotrophoblast cells within the villi and decidual trophoblast cells. It was not present in the endothelium of terminal villous vessels. There was no significant difference in eNOS villous or decidual staining intensity between normal pregnancy (NP; n = 12), pre-eclampsia (n = 14), or gestational hypertension (GH; n = 4). Staining for eNOS was not significantly different in the decidua compared with the villi in NP, GH or pre-eclampsia. Within the decidua, the depth of eNOS staining was similar in NP, pre-eclampisa and GH. 4.,There was no significant difference in eNOS mRNA expression between NP (0.70 ± 0.11), pre-eclampsia (0.5 ± 0.07) or GH (0.69 ± 0.26). 5.,These findings suggest that the amount of eNOS in the placenta is not deficient in pre-eclampsia, excluding a possible pathogenic role for eNOS in this disease. Furthermore, placental hypoxia, which is associated with pre-eclampsia, did not induce an upregulation of eNOS [source] Abnormal Expression of TIMP-2, SOD, Vimentin and PAI Proteins in Cloned Bovine PlacentaeREPRODUCTION IN DOMESTIC ANIMALS, Issue 4 2009H-R Kim Contents Cloned mammals suffer from high rates of placental abnormality and foetal loss during pregnancy. We previously used 2-D gel electrophoresis and mass spectrometry for global proteomic analysis of cloned and normal bovine placentae to identify differential protein expression patterns. Here, we used Western blot analysis to confirm the expression levels of several pregnancy-related proteins putatively identified as being differentially expressed in somatic cell nuclear transfer (SCNT) vs normal bovine placentae. The expression levels of tissue inhibitor of metalloproteinase-2 (TIMP-2), its downstream protein, matrix metalloproteinase-2 (MMP-2), superoxide dismutase (SOD), vimentin and plasminogen activator inhibitor-1 (PAI) were analysed in the placentae of SCNT cloned Korean native cattle that died immediately after birth and in normal placentae obtained by AI. Our results revealed that TIMP-2 and SOD were up-regulated in SCNT placenta compared with normal placenta, whereas MMP-2 levels were comparable in cloned and normal placentae, and vimentin and PAI were significantly down-regulated in SCNT compared with normal placentae. Our results suggest that key proteins of placental development are abnormally expressed in SCNT cloned bovine placentae, probably resulting in abnormal placental function and clonal mortality. [source] | ||||||||||