INTRODUCTION It is widely debated whether fetal membranes possess a genuine microbiome, and if bacterial presence and load is linked to inflammation. Chorioamnionitis is an inflammation of the fetal membranes. This research focussed on inflammatory diagnosed histological chorioamnionitis (HCA) and aimed to determine whether the bacterial load in fetal membranes correlates to inflammatory response, including histological staging and inflammatory markers in HCA. METHODS Fetal membrane samples were collected from patients with preterm spontaneous labour and histologically phenotyped chorioamnionitis (HCA; n = 12), or preterm (n = 6) and term labour without HCA (n = 6). The bacterial profile of fetal membranes was analysed by sequencing the V4 region of the 16S rRNA gene. Bacterial load was determined using qPCR copy number/mg of tissue. The association between bacterial load and bacterial profile composition was assessed using correlation analysis. RESULTS Bacterial load was significantly greater within HCA amnion (p = 0.002) and chorion (p = 0.042), compared to preterm birth without HCA. Increased bacterial load was positively correlated with increased histological staging (p = 0.001) and the expression of five inflammatory markers; IL8, TLR1, TLR2, LY96 and IRAK2 (p= less then 0.050). Bacterial profiles were significantly different between membranes with and without HCA in amnion (p = 0.012) and chorion (p = 0.001), but no differences between specific genera were detected. DISCUSSION Inflammatory HCA is associated with infection and increased bacterial load in a dose response relationship. Bacterial load is positively correlated with HCA severity and the TLR signalling pathway. Further research should investigate the bacterial load threshold required to generate an inflammatory response in HCA. INTRODUCTION Abnormally invasive placenta (AIP, aka placenta accreta spectrum; PAS) is an increasingly common pregnancy pathology, which, despite significant morbidity risk to the mother, is often undiagnosed prior to delivery. We tested several potential biomarkers in plasma from PAS mothers to determine whether any were sufficiently robust for a formal, diagnostic accuracy study. METHODS We examined hyperglycosylated hCG (h-hCG), decorin and IL-8, based on biological plausibility and literature indications that they might be altered in PAS. These analytes were assayed by ELISA in maternal plasma from five groups, comprising (1) normal term controls, (2) placenta previa controls, and cases of (3) placenta increta/percreta without placenta previa, (4) placenta previa increta/percreta and (5) placenta previa accreta. RESULTS There were no differences in h-hCG, ß-hCG or the h-hCG/ß-hCG ratio between the groups. Mean decorin levels were increased in previa controls (Group 2) compared to the other groups, but there was substantial overlap between the individual values. While an initial multiplex assay showed a greater value for IL-8 in the placenta previa increta/percreta group (Group 4) compared to placenta previa controls (Group 2), the subsequent validation ELISA for IL-8 showed no differences between the groups. DISCUSSION We conclude that the absence of differences and the extent of overlap between cases and controls does not justify further assessment of these biomarkers. INTRODUCTION Chronic histiocytic intervillositis (CHI) is a placental disease that has been associated with unfavorable obstetric outcomes in small, noncomparative series. The objective was to measure the excess risk of adverse obstetric outcomes associated with the discovery of CHI after birth. METHODS Retrospective single-center case-control study from 2000 through 2016. The case patients had a CHI diagnosis after a pathology analysis of the placenta. Two types of controls were defined for each case low-risk control women were those who gave birth in our hospital immediately before each case patient, and the high-risk controls were the next women after each case for whom microscopic examination of the placenta was indicated. RESULTS We observed 111 cases of CHI during the study period. Compared with the 111 low-risk controls, the cases had a significantly higher frequency of late miscarriages (5.4 vs 0.0%, p  less then  .03), small for gestational age (SGA) babies less then 3rd centile (70.4 vs 0.9%, p  less then  .001, OR 140, 95% CI, 19.9-2800), and in utero deaths (35.1 vs 0.9%, p  less then  .001, OR 59.6, 95% CI 8.5-1192), with significantly fewer children surviving to discharge (54.9 vs 99.1%, p  less then  .001, OR 0.01, 95% CI, 0.00-0.08). All of these factors also differed significantly compared with the high-risk women (severe SGA OR 3.7, 95% CI 1.9-7.0; in utero death OR 4.1, 95% CI 1.9-8.7; children surviving to discharge OR 0.27, 95% CI, 0.14-0.52). DISCUSSION Even compared with high-risk pregnancies, CHI is a severe placental disease associated with a substantial excess rate of late miscarriages, severe SGA and in utero death. INTRODUCTION Recently, Delta-like homolog 1 (DLK1) was identified as a potential marker of small-for-gestational-age (SGA; less then 10th centile) fetuses; mouse studies suggest reduced levels may represent a fetal stress signal. We sought to measure DLK1 in a large independent cohort of maternal blood samples, correlate levels with measures of placental insufficiency and assess whether DLK1 might be placental derived.  https://www.selleckchem.com/products/aminoguanidine-hydrochloride.html  METHODS The Fetal Longitudinal Assessment of Growth (FLAG) study was a prospective blood collection from 2000 women. We assessed a case-control cohort at 28 and 36 weeks from the first 1000 FLAG women, before validating changes in the entire second 1000. A subgroup of FLAG participants underwent ultrasound examinations, and 137 neonates, body composition assessment (PEAPOD). DLK1 secretion was assessed from human placentas ex vivo. RESULTS Circulating DLK1 was significantly reduced at 28 and 36 weeks' gestation in women destined to deliver a SGA fetus and associated with birthweight centile (n = 999, p  less then  0.0001), and placental weight (n = 96, p = 0.0064). Ex vivo, DLK1 was abundantly released from human placenta and significantly reduced under hypoxia (n = 7, p  less then  0.05). We found no relationship between circulating DLK1 and estimated fetal weight, cerebroplacental ratio, uterine artery or umbilical artery pulsatility index. Nor was there a relationship between DLK1 and neonatal fat or lean mass (n = 137). CONCLUSION We confirmed circulating DLK1 is reduced at both 28 and 36 weeks' gestation preceding delivery of a SGA infant, shown that it is not significantly associated with clinical measures of placental insufficiency, and provide new data demonstrating it may be placenta-derived in humans.