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    ABSTRACT: We assessed whether placental morphology is affected by placental storage before fixation. Fresh tissue from uncomplicated pregnancies (n = 10) was fixed immediately and further samples were stored dry, in PBS or culture medium for 24, 48 or 72 h at 4 °C. Placental morphology quantified using image analysis software found no difference in syncytial nuclear aggregates, cytokeratin 7, CD45 or Ki67 immunostaining irrespective of duration or mode of storage. The number of blood vessels per villus (CD31) was reduced in all conditions after 72 h (p < 0.05). Distal villous hypoplasia increased after 72 h (p < 0.05). Ideally, storage time should be minimised to ≤48 h prior to morphological or qualitative analysis.
    No preview · Article · Aug 2013 · Placenta
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    ABSTRACT: Villitis of unknown etiology (VUE) is an inflammatory condition reported to occur in up to 15% of term placentas. It has been reported in association with fetal growth restriction and antepartum stillbirth. This study aimed to investigate the strength of these associations by completing a systematic review using established guidelines. 618 potentially relevant studies were identified. After exclusion of studies that were not relevant or of insufficient quality, a total of 24 case-control and cohort studies were included in the review. Studies were grouped according to whether their main focus was VUE, fetal growth restriction or stillbirth. A methodological quality assessment carried out for each group demonstrated significant heterogeneity in study design. VUE occurs more frequently in placentas of growth restricted infants. A significant link between VUE and stillbirth could not be reliably established because there were too few published studies. Further research into the pathological effects of VUE using robust protocols and reporting methods is required.
    No preview · Article · Jul 2013 · Placenta
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    ABSTRACT: The potency of adult-derived circulating progenitor Endothelial Colony Forming Cells (ECFCs) is drastically surpassed by their fetal counterparts. Human pregnancy is associated with robust intensification of blood flow and vascular expansion in the uterus, crucial for placental perfusion and fetal supply. Here we investigate whether fetal ECFCs transmigrate to maternal bloodstream and home to locations of maternal vasculogenesis, primarily the pregnant uterus. In the first instance, endothelial-like cells, originating from mouse fetuses expressing paternal eGFP, were identified within uterine endothelia. Subsequently, LacZ or eGFP-labelled human fetal ECFCs, transplanted into immuno-deficient (NOD/SCID) fetuses on D15.5 pregnancy, showed similar integration into the mouse uterus by term. Mature endothelial controls (HUVECs), similarly introduced, were unequivocally absent. In humans, SRY was detected in 6/12 myometrial microvessels obtained from women delivering male babies. The copy number was calculated at 175 [IQR 149-471] fetal cells/mm(2) endothelium, constituting 12.5% of maternal vessel lumina. Cross-sections of similar human vessels, hybridized for Y-chromosome, positively identified endothelial-associated fetal cells. It appears that through ECFC donation, fetuses assist maternal uterine vascular expansion in pregnancy; potentiating placental perfusion and consequently their own fetal supply. In addition to fetal growth, this cellular mechanism holds implications for materno-fetal immune-interactions and long-term maternal vascular health.
    Full-text · Article · Jul 2013 · Stem Cells
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