We tested whether placentalmorphology criteria predicted toddler internalizing, externalizing and total prob- lems using linear regression. We present B and 95% CI from unadjusted models, models adjusted for toddler age and sex, gestation length, maternal age, education, BMI, diabetes and hypertension in pregnancy, and models adjusted for maternal depressive symptoms concurrent to rating toddler’s psychiatric problems. To specify any possible effects of toddler psychiatric problems, we examined the syndrome- and DSM-IV-oriented CBCL as sec- ondary outcomes for those placental criterion that showed significant associations with the main scales. The asso- ciations with these CBCL subscales were examined with tobit regressions, since these scales are left-censored 51 . Data Availability. The datasets generated during and/or analysed during the current study are not publicly available due to prohibitions by national laws since the data include patient report data. However, the datasets generated during and/or analysed during the current study are available from the corresponding author on rea- sonable request in completely anonymized form. Due to the sensitive nature of the patient report data, data requests may require further approval by the PREDO Study Board, that also enables collaboration in PREDO data analysis through specific study proposals 55 .
In our series, all the studied factors showed a signi ﬁcantly lower expression in complicated pregnancies than uncomplicated ones. This result appears even more interesting if we consider that the expression of these molecules gradually decreases after about 30 weeks with placental aging, and thus it should have been higher in cases (mean gestational age = 32 weeks) than in controls (mean gestational age = 39 weeks). Also the placentalmorphology showed important differences between the two groups: cases showed a disorder of villous development as a distal villous hypoplasia with placental undergrowth, while the controls showed no abnormalities. Placenta with distal villous hypoplasia is unable to absorb oxygen. This pathologic aspect could result in placental dysfunction and abnormal feto-maternal ﬂows [ 19 ].
Diet controlled placentae were significantly different from normal placentae as they showed villous immaturity, infarction, chorangiosis and syncytial knots formation when compared to normal control. Verma et al. 2016 has documented that in GDM treated with diet only, placentae showed fibrosis and ischemic changes, more syncytial knots, mild edema and fibrinoid necrosis, which is similar to our results. 19 Placentae treated with Metformin revealed non-significant results when compared to normal control in gross placentalmorphology except for cord width. All remaining gross and microscopic hypoxic parameters were non- significant between the groups, making it near to control. Metformin treated placenta had significantly less thickness, chorangiosis and syncytial knot formation as compared to diet controlled placentae when light microscopic results were evaluated. Remaining microscopic hypoxic parameters were also numerically lowered in metformin group than diet control group. Using multiple related key words and utilizing search such as engines google.com, Google scholar, PubMed, Science direct, Wiley.com from 1980 till Dec 2015, no documentation was found on the details of placentalmorphology with Metformin in GDM. Except a single case documented by Campbell in 2009 in which a GDM patient with preeclampsia on Metformin had intrauterine death and the placentalmorphology showed pronounced changes such as villous dysmaturity, chorioamniotis, villi fibrosis. 20 However it was not clarified that the placental changes were purely because of gestational diabetes or the combination of GDM with hypertension had produced them.
Objective: To evaluate the effects of diet control and Metformin on placentalmorphology in gestational diabetes mellitus (GDM). Methods: After written informed consent 62 GDMs were enrolled. According to WHO criteria, 30 cases of GDMs with blood sugar level <130 mg/dl, were assigned Group B (2000-2500Kcal/day and 30 minute walk thrice weekly were kept on diet control and 32 cases of GDM with blood sugar level >130 mg/dl, assigned Group C were kept on diet with tablet Metformin,(500mg TDS) Finally 25 normal pregnant females were kept in Group A as control. After delivery placentae were preserved and evaluated for morphology. Results: Heavy placentae with abundant villous immaturity, chorangiosis and syncytial knots in group B and fibrinoid necrosis and calcification in group C were seen. In group B versus A placental and cord width while in Group C versus A only cord width in gross morphology showed significant results. In group B versus A villous immaturity, chorangiosis, infarction and syncytial knots in light microscopy were present; similarly in B versus C placental width, chorangiosis and syncytial knots showed significant results, while in C versus A results were non-significant.
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Background: Placentalmorphology and cellular arrangement can be altered in maternal diseases. Rheumatic heart
disease (RHD) is a chronic heart condition that can lead to death in pregnant women. The aim of this study is to determine the histological changes of the placenta in pregnant women suffering from RHD. Methods: Placentae were collected from 10 healthy pregnant women, and 31 pregnant women with heart conditions (26 with RHD and 5 with NRHD) who had been admitted to the Baghdad Teaching Hospital. Placental tissues were fixed in 10% formal-saline and were processed for light microscopy. Measurements including the placental weight and diameter of the chorionic villi capillaries were recorded. Results: The results indicate that there are many histological changes in pregnant women with RHD such as hyalinisation, fibrosis of the chorionic villi, proliferation of trophoblastic cells, and thickening of its membrane. Additionally, expectant mothers with RHD experience a reduction in capillary diameter and thickening of the capillary walls, and decreased size and weight of their placenta when compared with the control.
Here we describe the first report of targeted delivery of miRNA inhibitor to placental tissue, resulting in a clinically relevant enhancement of placental weight in healthy mice and enhanced CTB proliferation in human first trimester placental explants. We demonstrate expression of miR-145 in mouse placenta for the first time, propose that this molecule controls placental weight gain and validate a previous report that miR-675 is a negative regulator of murine placental growth . The data also show that the PNA conjugates were successfully internalised into their target cells and that the presence of the targeting sequence did not interfere with miRNA inhibitor function. Indeed, the miRNA inhibitor PNA and targeting peptide were conjugated using a disulphide linkage, so that the targeting element would be hydrolysed and released upon internalisation, and not impair binding of the inhibitor to endogenous cellular miRNAs. The CCGKRK peptide was chosen due to its effective cell penetrating properties, as well as for its ability to selectively target placental tissue . The conjugates retained their function in vivo, likely due to the inherent resistance of these synthetic sequences to digestion by proteases and nucleases . They were also well tolerated; no pathological effects were noted in dams or fetuses in this study and the lack of effect on gross placentalmorphology, litter size or number of pregnancy losses suggests that no overt immune response was stimulated by the conjugates. A more extensive investigation will be needed to screen for any subtle effects that may not have been detected in our pilot study; however, our current data highlights the favourable therapeutic profile of peptide-PNA conjugates in pregnancy.
Thompson, 1993; Thompson and Stewart, 1994; Thompson et al., 1999) and that of species with simple chorio–allantoic placentae (Table 6), as implied by the placentalmorphology. It seems that certain nutrients such as potassium and sodium, most probably protein and possibly certain lipid components, are not provided in sufficient quantities to meet the demands of the developing embryo and must be supplemented across the placenta. Hence, the yolks of N. metallicus are not merely smaller versions of the yolks expected in the oviparous ancestors of N. metallicus, but are at least partly modified. The details of how individual nutrients are transported across the placenta of lizards are completely unknown, but an understanding of these mechanisms is required to explain modifications to yolk composition during the evolution of viviparity.
preeclampsia in the current pregnancy; and (3) giving birth to a normally formed infant without proven chromosomal aberrations at gestational week (GW) ≥ 36. SGA was diagnosed in neonates with birthweight less than the 10 th percentile corrected by maternal parity (nulliparous or multiparous), GW at birth, and gender for Japanese infants. 19 Determination of GW and diagnoses of DM, GDM, and HDP were based on Japanese guidelines for obstetric practice. 20 Both birthweight and placental weight were transformed to z-score using data specific for Japanese infants. 19,21
Placentas were reviewed by a single observer, a perinatal anatomic pathol- ogist (Dr Sandra Viero), according to a standardized technique. Gross exami- nation was performed after ﬁxation in 10% formalin. Cord abnormalities were described, and 2 sections of cord, 1 including the placental inser- tion site, were sampled. An extrapla- cental membrane roll including de- cidua was sampled. The trimmed disk weight was recorded. The placental disk was sectioned at 1-cm intervals with at least 2 random sections sam- pled and any lesions sampled. Sec- tions were submitted for routine pro- cessing, parafﬁn embedding, and staining with hematoxylin and eosin. Gross and histologic characteristics were noted and additionally classiﬁed according to subcategories estab- lished by Redline. 21 Placental lesions
placenta. Transfer of cimetidine from maternal to fetal compartments showed no saturation kinetics and was not inhibited by putative carrier competitors. Cimetidine did not accumulate against a drug concentration gradient. Fetal clearance of cimetidine was similar to maternal clearance. Studies with placental apical vesicles confirmed lack of saturability of cimetidine transport and of its concentration within vesicles. Thus, (a) cimetidine is transported across the human placenta bidirectionally at a rate about one third that of antipyrine, (b) the drug is not metabolized by the placenta, and (c) the transport is a passive one.
thereafter declining to be virtually absent at term (Hamperl and Hellweg, 1958; Dallenbach-Hellweg and Nette, 1964). This distri- bution was confirmed for pregnancy in phloxine tartrazine staining of pregnancy hysterectomies from 8 weeks to term (Bulmer and Lash, 2005); granulated leukocytes were rare after 20 weeks gestation. Immunostaining for CD56 has largely confirmed this distribution, although CD56+ cells are present in the proliferative and early secretory phase, albeit in small numbers (Bulmer et al., 1991; King et al., 1989a). Numbers increase in the late secretory phase of the menstrual cycle and even higher numbers are observed in early pregnancy. Several studies have recorded a reduction in CD56+ cells in third trimester decidua. However, we have noted that substantial numbers of CD56+ cells remain in both decidua basalis and decidua parietalis in third trimester placental bed biopsies (Scaife et al., 2003). Reports from others of lower numbers of CD56+ cells in term decidua (Haller et al., 1993; Vargas et al., 1993) may be due to the use of different tissues, some studies being based on decidua attached to the placental membranes and delivered placenta, while others have studied decidua in placental bed biopsies. The possibility that there is a population of agranular CD56+ cells in proliferative and early secretory phase endometrium and in decidua in the second half of pregnancy has not been analysed in detail.
The subplacenta, or accessory organ to the placenta, in two animals, the C. porcellus (guinea pig) and the Brazilian porcupine (C. prehensilis), both hystrichomorphous rodents . The chorioallantoic placentation of the G. spixii and the subplacenta as a component of the placenta that served as a point of origin of invasive tro- phoblasts . The placenta of the red-rumped agouti Dasyprocta leporina and that the subplacenta is related to the production of hormones secreted in the fetal blood but not on maternal tissues . Evolutionary transfor- mations of the chorioallantoic placenta in hystricognath rodents and found macroscopic changes in these ani- mals, primarily the formation of a ring-shaped arrangement of placental regions with maternal arteries situated centrally with a subplacenta .
Evidence for transcriptionally distinct subtypes of late-onset preeclampsia. Recently, Redman and colleagues have suggested that there are two main placental causes for preeclampsia. PE caused by poor placentation in early pregnancy is frequently accompanied with fetal growth restriction, whereas at term PE may also develop when placental growth reaches its functional limits and is often linked to macrosomy 26 . To further dissect the relationship between LO-PE and fetal growth we divided the PE study sample according to the presence of concomitant intrauterine growth restriction (IUGR). The two subgroups (n = 4/group) were separately tested for the differential placental gene expression compared to the normal gestation group (n = 8). We identified 199 and 98 differentially expressed genes in PE without IUGR and PE with IUGR, respectively (Supplementary Data S3). Only 20 genes overlapped between the two LO-PE subtypes with statistically significant alternations in transcript levels. Still, examination of the top 200 highest ranked genes in both analyses revealed substantial correlation in their expressional changes compared to normal pregnancy (R 2 = 0.62; P = 7.82 × 10 −77 ; 36 shared genes among the top-200; Fig. 6a–b). Notably, placental transcriptome profile in cases of LO-PE with IUGR showed the highest correlation with SGA group (R 2 = 0.67; P = 2.81 × 10 −85 ; 42 shared genes; Fig. 6a–b), whereas the LO-PE without IUGR bears the closest similarity to LGA cases (R 2 = 0.62; P = 1.24 × 10 −70 ; 53 shared genes; Fig. 6a–b). Hierarchical clustering analysis based on all 283 genes matching the statistical significance criteria across study groups also separated the transcriptome profiles of LO-PE with and without IUGR, supporting their distinct molecular signatures (Fig. 6c).
placental function. As we utilized macrophages exosomes, this current study has particular implications for con- veyance of signals from maternal immune cells to the placenta. Given the macrophage origin of our exosomes, and the ability of trophoblast to respond to inflammatory milieu, we examined the production of cytokines by the placenta. Initially we utilised BeWo cells, and found a sig- nificant induction of IL-6 by macrophage exosomes (data not shown). However, we also found that our BeWo cells did not respond well to our positive control (1–100 ng/ml LPS), similar to previous studies which show that, despite expressing TLR-4, BeWos do not respond as expected to LPS (33). Therefore, all subsequent functional experiments were performed only in the more relevant human placental explant model.
In 1984 the first fetal placental volumes studied by USG were constructed by Brinkley at el. After the development of 3 dimensional USG imaging assisted by computer technology it is possible to measure and calculate fetal & placental volume quickly & accurately ,measuring and monitoring the fetal and placental volume at different gestational ages may improve our understanding about pathophysiological mechanisms of fetal & placental growth. Fetal and placental volumes can be used in screening of fetuses with chromosomal anomalies ,IUGR , preeclampsia. Some reports in literatures says that increase in placental volume preceding preeclampsia & decrease in placental volume preceding IUGR & decrease in fetal volume in fetuses with chromosomal anomaly.
methodological strength of this approach is that disclosure of the scan results could have led to differential treatment of the women based on the information from the scans, which could have biased the results. Another strength of this study is the consistency of the measurements of placental size and shape achieved by using a Matlab code. Evaluation of intra-observer reproducibility and reliability showed a high level of consistency between two sets of blinded measurements. The present study could be criticised on the grounds that it was confined to nulliparous women who were largely of white European ancestry. While this fact somewhat limits the external validity of the study, the analysis of a homogeneous population has some
Placental impression smears were fixed in methanol and together with thick films stained for 20 mins with 5% Giemsa (Sigma). Fixed placental biopsies were transferred to the Anatomy and Pathology (ANAPATH) Laboratory, University of Yaoundé I Teaching Hospital (CHU), Yaoundé, Cameroon, where they were processed, embed- ded in paraffin wax and sectioned onto slides by standard techniques. Sections were later stained with haematoxy- lin-eosin stain for detection of active and past infections. Microscopic examination of blood smears was done under oil immersion for parasite detection and 200 high power fields were examined before the smear was consid- ered negative. Parasites were counted against 200 leuco- cytes assuming an average leucocyte count of 8,000 per microlitre of blood . To determine the percentage of malaria parasitaemia from placental impression smears, malaria parasite-infected red cells were counted against 1,000 erythrocytes.
abruption, matched by maternal age, parity, multiplicity, year of birth, and hospital district area. If all controls were not found, the age criteria were loosened by ±1 year to achieve 3 controls for each case. The hospital discharge data were then linked to the MBR by using the mother’s unique personal identification number to identify all births with placental abruption. Multiple pregnancies were excluded from the final study sample. We identified 4190 women with a singleton birth and placental abruption and 12 570 matched referent women with a singleton birth without placental abruption. After excluding stillbirths, the final study population comprised 3888 children born after placental abruption (later referred to as index children) and 12 530 referent children.