Journal articles on the topic 'Placenta Blood-vessels'
To see the other types of publications on this topic, follow the link: Placenta Blood-vessels.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Placenta Blood-vessels.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Konkov, Dmitro G., Alina O. Piskun, Oksana A. Taran, and Galyna V. Kostur. "SPECIALTIES OF HYSTOMORPHOMETRICAL CHANGES IN PLACENTA OF WOMEN WITH EARLY AND LATE PREECLAMPSIA." Wiadomości Lekarskie 73, no. 1 (January 2020): 151–55. http://dx.doi.org/10.36740/wlek202001129.
Full textAbstract:
The aim: To find out typical pathomorphological differences in placenta of women with early and late preeclampsia. Materials and methods: Investigation includes 40 placentas from deliveries in women with preeclampsia (main group) and 40 placentas from physiological delivery in somatically healthy women, who had no complications during pregnancy (control group). Placentas in the main group were devided into two sub-groups (20 in each) – with early and late preeclampsia. Specialties of the blood vessels in normal pregnancy were investigated, and their structural transformation with the developement of preeclampsia, according to the appearence of perinatal pathology. Morphometrical data of the blood stream was investigated with the help of eyepiece and program Image Tools 3,6. Results: Significant decrease of weight (p<0,05), square and volume of placenta was common to early preeclampsia, comparing to the same characteristics in late Preeclampsia (PE). Specific gravity of villi without vessels, hardened blood vessels, hardened villi and fibrinoid altered vessels was increased statistically significantly (p<0,05) in placenta of women with early PE, comparing to women with late PE. The number of effective blood vessels crossings was determined mostly in late PE, comparing to the early form (p<0,05). Found out significant defferences (p<0,05) in changes of hystovasoarchitecture of placenta in early preeclampsia, according to the number of immature villi and villi with no signs of compensatory angiomatosis. Conclusions: Increased number of hypoplasia of placenta, breach of effective placental blood stream and significant decrease of compensatory and adaptive changes in placenta are more common to early PE, comparing to late PE.
2
Abdelghany Hassan Abdelghany, Ahmed Abdelghany Hassan, Sarah Abdelghany Hassan, and Rania Mohamed Fawzy. "Ultrastructural changes of the placenta in cases of preeclampsia." Magna Scientia Advanced Research and Reviews 3, no. 2 (November 30, 2021): 047–60. http://dx.doi.org/10.30574/msarr.2021.3.2.0080.
Full textAbstract:
The placenta plays vital roles during fetal development and growth. The ultrastructure of the placenta together with remodeling of the uterine spiral arteries are very important to maintain the utero-placental blood flow. Preeclampsia (PE) is a multifactorial disorder with abnormal placentation affecting the mother and fetus. The aim of this study was to study the ultrastructural abnormalities of the placenta in cases of PE. The placentas of 10 PE women and 10 controls were studied. Women of PE group were delivered by caesarian section while seven control women were delivered vaginally, and three by caesarian section. Placental samples were studied both morphologically and histologically by light and transmission electron microscopy. Light microscopic study of control placentas showed numerous microvilli, few syncytial knots, thin-walled blood vessels. PE placentas showed reduced number of microvilli with numerous syncytial knots, thick-walled vessels, edematous spaces, fibrotic areas and fibrinoid degeneration. Electron microscopic study of the control placentas showed a thick layer of syncytiotrophoblast (Sy), numerous microvilli and a thin layer of cytotrophoblast (Cy). PE placenta showed hypertrophy of Cy with atrophy of Sy and scarce microvilli. The trophoblast showed edematous vacuoles and glycogen storage areas. The villous core had congested capillaries, edematous spaces, glycogen storage areas and widespread areas of fibrosis. All the changes in PE placentas were attributed to hypoxia and oxidative stress and reduced utero-placental flow due to abnormal remodeling of the uterine spiral arteries that was aggravated by the thick placental barrier and the presence of edema, fibrosis and glycogen storage areas.
3
Kiran, Nazma, Nadia Aslam, Tahira Tabassum, Saadia Kanwal, and Tanveer Zia. "MORPHOLOGICAL FINDINGS IN INTRAUTERINE GROWTH RESTRICTION (IUGR) PLACENTAS VERSUS NORMAL PLACENTAS IN PREGNANT WOMEN OF DISTRICT RAWALPINDI, PAKISTAN." Gomal Journal of Medical Sciences 17, no. 3 (June 10, 2020): 65–69. http://dx.doi.org/10.46903/gjms/17.03.2021.
Full textAbstract:
Background: Intrauterine growth restriction (IUGR) is a principal cause of fetal and neonatal morbidity and mortality. The placenta, as a vector for maternal-fetal nutrient and oxygen exchange has major influence on birthweight. The objectives of this study were to compare the placental weight (grams), number of syncytial knots and number of blood vessels in villi of IUGR placentas versus normal placentas. Materials & Methods: This cross-sectional study was carried out at Rai Medical College, Sargodha, Pakistan in collaboration with Zainab Memorial Hospital, Rawalpindi, Pakistan from December 2016 to November 2018. Study group included 45 IUGR placentas and control group included 25 normal placentas. Placental weight in grams, number of syncytial knots and number of blood vessels in villi of placentas were three research variables. These were described by mean, minimum, maximum, range and standard deviation for each group separately and were compared between the two groups through independent-samples t-test. Results: Descriptively the mean placental weight in grams in IUGR group (423.35±64.13g) was lower than control group placentas (535.92±44.57g). The number of syncytial knots in IUGR group placentas (22.04±5.21) was more than control group placentas (13.84±4.41). The number of blood vessels in IUGR placentas was lower than control group placentas. All three null hypothesis for research variables between the two groups were rejected (p=
4
Giri, Tusar K., and Douglas M. Tollefsen. "Placental dermatan sulfate: isolation, anticoagulant activity, and association with heparin cofactor II." Blood 107, no. 7 (April 1, 2006): 2753–58. http://dx.doi.org/10.1182/blood-2005-09-3755.
Full textAbstract:
AbstractPregnancy is associated with hemostatic challenges that may lead to thrombosis. Heparin cofactor II (HCII) is a glycosaminoglycan-dependent thrombin inhibitor present in both maternal and fetal plasma. HCII activity increases during pregnancy, and HCII levels are significantly decreased in women with severe pre-eclampsia. Dermatan sulfate (DS) specifically activates HCII and is abundant in the placenta, but the locations of DS and HCII in the placenta have not been determined. We present evidence that DS is the major anticoagulant glycosaminoglycan in the human placenta at term. DS isolated from human placenta contains disaccharides implicated in activation of HCII and has anticoagulant activity similar to that of mucosal DS. Immunohistochemical studies revealed that DS is associated with fetal blood vessels and stromal regions of placental villi but is notably absent from the syncytiotrophoblast cells in contact with the maternal circulation. HCII colocalizes with DS in the walls of fetal blood vessels and is also present in syncytiotrophoblast cells. Our data suggest that DS is in a position to activate HCII in the fetal blood vessels or in the stroma of placental villi after injury to the syncytiotrophoblast layer and thereby inhibit fibrin generation in the placenta.
5
Starks, Rebekah R., Rabab Abu Alhasan, Haninder Kaur, Kathleen A. Pennington, Laura C. Schulz, and Geetu Tuteja. "Transcription Factor PLAGL1 Is Associated with Angiogenic Gene Expression in the Placenta." International Journal of Molecular Sciences 21, no. 21 (November 6, 2020): 8317. http://dx.doi.org/10.3390/ijms21218317.
Full textAbstract:
During pregnancy, the placenta is important for transporting nutrients and waste between the maternal and fetal blood supply, secreting hormones, and serving as a protective barrier. To better understand placental development, we must understand how placental gene expression is regulated. We used RNA-seq data and ChIP-seq data for the enhancer associated mark, H3k27ac, to study gene regulation in the mouse placenta at embryonic day (e) 9.5, when the placenta is developing a complex network of blood vessels. We identified several upregulated transcription factors with enriched binding sites in e9.5-specific enhancers. The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. We then performed several experiments using mouse placenta and a human trophoblast cell line to understand the role of PLAGL1 in placental development. In the mouse placenta, Plagl1 is expressed in endothelial cells of the labyrinth layer and is differentially expressed in placentas from mice with gestational diabetes compared to placentas from control mice in a sex-specific manner. In human trophoblast cells, siRNA knockdown significantly decreased expression of genes associated with placental vasculature development terms. In a tube assay, decreased PLAGL1 expression led to reduced cord formation. These results suggest that Plagl1 regulates overlapping gene networks in placental trophoblast and endothelial cells, and may play a critical role in placental development in normal and complicated pregnancies.
6
Zakurina, Anna N., and Natalia G. Pavlova. "Intraplacental blood flow in third trimester of placental insufficiency pregnancy." Journal of obstetrics and women's diseases 63, no. 5 (December 15, 2014): 51–57. http://dx.doi.org/10.17816/jowd63551-57.
Full textAbstract:
Background. Serious perinatal, most of all, neurological consequences of placental insufficiency condition necessity further search it’s markers for optimal delivery time. Methods. At third term of pregnancy we examined 16 singleton physiological pregnant women (first group) and 27 placental insufficiency patients (second group). We standard obstetrical examined, ultrasound fetometry, basic arteries of functional system mother-placenta-fetus Doppler and three-dimensional power Doppler in central, two paracentral and two periphery placenta areas. We processing images by VOCAL and analyzed vascularisation (VI), flow (FI) and vascularisation-flow indexes (VFI). Results. In placentae correlated groups FI differ in size reliable in central (t=4,03; p<0,001 и U=240,00; p<0,001) and paracentral (t=2,61; p<0,05 и U=348,00; p<0,05) areas. Patients second group indexes were relative on 17% and 8% less than patients first group indexes. Patients second group VFI was on 35% less than patients first group VFI (t=2,08; p<0,05 и U=337,00; p<0,05). We described results of comparison three-dimensional power Doppler intraplacental blood flow indexes from patients second group with different degree hemodynamic disorder. Conclusion. In placental insufficiency presence reduction blood circulation, particular in central placenta area, conditioned by reduction blood flow in initial vessels number. Central placenta area FI may be regarded new additional criterion of placental insufficiency at third term of pregnancy.
7
Van Handel, Benjamin J., Sacha Prashad, Andy Huang, Eija Hamalainen, Angela Chen, and Hanna K. A. Mikkola. "The First Trimester Human Placenta Is a Site of Primitive Red Blood Cell Maturation." Blood 110, no. 11 (November 16, 2007): 2224. http://dx.doi.org/10.1182/blood.v110.11.2224.2224.
Full textAbstract:
Abstract Embryonic hematopoiesis occurs in multiple anatomic sites and is generally divided into two waves, primitive and definitive. The primitive wave produces mostly red blood cells in the yolk sac, while the definitive wave generates hematopoietic stem cells (HSCs) that provide lifelong blood homeostasis. Definitive erythropoiesis, occurring first in the fetal liver and eventually the bone marrow, is an orchestrated process in which erythroblasts cluster around a central macrophage. These functional units, termed erythroblast islands, facilitate the maturation of nucleated erythroblasts to enucleated erythrocytes. It has long been thought that primitive red cells maintain their nucleus until undergoing apoptosis; however, the enucleation of primitive erythroblasts has been recently documented in mice, although the site at which this occurs is unknown. We have recently identified the placenta as a major hematopoietic organ that promotes the development of HSCs in mice; preliminary data suggests that the first trimester human placenta also supports definitive hematopoiesis. Surprisingly, our most recent findings indicate a novel, unexpected role for the human placenta in primitive hematopoiesis: the promotion of terminal maturation of primitive erythroblasts. Analysis of placental sections revealed a striking tendency of primitive red blood cells to extravasate from blood vessels in the villi and migrate out into the stroma. Furthermore, once out in the stroma, primitive erythroblasts mature: they lose expression of CD43 and enucleate. The finding that human primitive red blood cells enucleate is undocumented; interestingly, the developmental timing of erythroblast enucleation in humans parallels that in mice. At three weeks, nascent vessels in the placenta are empty, but starting at about 4 weeks, placental circulation begins and fills these vessels with large, nucleated primitive erythroblasts generated in the yolk sac. The migration of primitive erythroblasts into the stroma occurs between 4.5 and 7 weeks. Enucleation mirrors this process, with a large enrichment of enucleated cells in the stroma versus in the vessels at early developmental ages, suggesting that primitive erythroblasts enucleate in the placental stroma. This phenomenon is restricted to placental villi and does not occur in the chorionic plate. Strikingly, extravasated erythroblasts are often in close proximity to placental macrophages, reminiscent of the macrophage-erythroblast associations seen in fetal liver and bone marrow erythropoiesis at later developmental stages. Fetal liver-derived definitive erythrocytes enter circulation at around 8 weeks. After 9–10 weeks, most red blood cells can be observed in vessels, and almost all are enucleated. The concerted processes of extravasation and maturation of primitive erythroblasts in placental stroma nominate the placenta as an important site in primitive hematopoiesis. Furthermore, the association between placental macrophages and primitive erythroblasts suggests that primitive and definitive erythropoiesis share common mechanisms of terminal maturation.
8
Madhu, L., S. L. Karthavya, and B. G. Lepakshi. "HISTOMORPHOLOGICAL AND MORPHOMETRICAL CHANGES OF PLACENTAL TERMINAL VILLI OF NORMOTENSIVE AND HYPERTENSIVE MOTHERS." International Journal of Medical Sciences and Pharma Research 1, no. 3 (June 15, 2015): 5–14. http://dx.doi.org/10.22270/ijmspr.v1i3.8.
Full textAbstract:
Background & Objectives: Placental examination has clinical value in preeclampsia (PE) and IUGR. The luminal diameter of the uterine spiral arterioles in women with PE is narrowed leading to placental ischemia thus causing fetal hypoxia and pathological changes in placenta. The main objective of the present study is to compare morphological and histomorphometrical changes in placentas of preeclamptic and normotensive mothers. Methods: 50 placentas from both vaginal and LSCS delivery were collected at Dept. of OBG in a tertiary care center, half of them from normotensive pregnancies and the rest from preeclamptic mothers. An inclusion criterion for control was normal blood pressure and no proteinuria. Exclusion criteria for both control and study group was DM, obesity, severe anemia or any systemic disorders. Placental thickness, weight, diameter and surface area were recorded. Histopathological sections stained with H&E were observed for surface area and diameter of TV. Results: The mean placental weight in PE was 430 g. The placental diameter was decreased in PE (16 cm) compared to controls (19 cm). Neonatal weight followed the same trend. Histologically, the changes in the TV and blood vessels was significant; there was decrease in the diameter of villi in PE cases(0.01 μm) when compared to controls (0.05 μm). There was significant decrease in the diameter of blood vessels in PE (0.0049 μm) than in controls (0.01 mm). Conclusion: This study has revealed that there are significant changes in the placenta in cases of PE both morphologically and histologically. There is also a need for further studies to prove the molecular and genetic factors involved in preeclampsia.
9
V. K., Shantha, Priyadarshini M., Priya Dharshini A., and Litty Mariyam Jacob. "Effectiveness of ligation of uterine vessels prior to uterine incision for major placenta previa on reducing maternal morbidity without increasing neonatal morbidity." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 7 (June 27, 2018): 2891. http://dx.doi.org/10.18203/2320-1770.ijrcog20182902.
Full textAbstract:
Background: Placenta previa causes massive obstetric haemorrhage and severe maternal morbidity. The objective is to analyse the effectiveness of uterine vessels (artery and vein) ligation before uterine incision in reducing blood loss and hysterectomy during caesarean section for major placenta previa without increasing morbidity in the newborn.Methods: A retrospective analysis of caesarean section for major placenta previa from 2002 to 2017 was done. Uterine vessels ligation before uterine incision was done in 52 patients. In 19 patients unilateral and in 33 patients bilateral uterine vessels ligation was done before uterine incision. In control group, 12 patients with major placenta previa uterine vessels were ligated after the removal of the placenta. The blood loss, blood transfusion, maternal morbidity and NICU admission of the newborns were compared.Results: The mean blood loss was 1002 ml in unilateral, 793 ml in bilateral uterine vessels ligation group, compared to 2191 ml in the control group. The mean blood transfusion volume 0.89 units in unilateral 0.60 units in bilateral ligation group while 2.33 units in the control group. The difference in blood loss and blood transfusion were statistically significant. Out of 52 babies, only 6 babies were admitted in NICU for mild depression with stay less than 3 days.Conclusions: Uterine vessels ligation before uterine incision reduces blood loss and hysterectomy during caesarean section for placenta previa without increasing the morbidity in the newborns.
10
Baran, Özlem, Mehmet Tuncer, Yusuf Nergiz, Murat Akkuş, Mahmut Erdemoğlu, and H. Büyükbayram. "An increase of elastic tissue fibers in blood vessel walls of placental stem villi and differences in the thickness of blood vessel walls in third trimester pre-eclampsia pregnancies." Open Medicine 5, no. 2 (April 1, 2010): 227–34. http://dx.doi.org/10.2478/s11536-009-0025-6.
Full textAbstract:
AbstractThis study has goals of examining whether pre-eclampsia may lead to an increase of elastic tissue fibers in blood vessel walls of placental stem villi or whether there are differences in the thickness of blood vessel walls within these villi when compared to normotensive pregnant women. Non-infarcted placental tissue samples from 28 participants with uncomplicated pregnancies and 26 patients with pre-eclampsia were obtained. After routine histological procedures, the sections were processed either for conventional Verhoeff staining for the demonstration of elastic fiber system. Paraffine sections from placenta biopsies prepared for light microscopic examination were gathered. In uncomplicated pregnancies, terminal villi blood vessels were observed with no stained elastic tissue fibers in most areas. In the pre-eclampsia pregnancy of human placenta, the elastic fibers significiantly increased in terminal villi blood vessel walls which were dark in color, using Verhoeff’s tissue stain, when comparing with the uncomplicated pregnancy group. Our results indicate that an increase of elastic tissue fibers in blood vessels of placental stem villus and terminal villi, and also an increase of wall thickness during pre-eclampsia.
11
Gorikov, I. N. "Pathomorphological characteristics of cotyledons with weak contrasting of the blood flow in the placenta of women who have undergone exacerbation of cytomegalovirus infection during the second trimester of pregnancy." Bulletin Physiology and Pathology of Respiration, no. 85 (September 23, 2022): 100–107. http://dx.doi.org/10.36604/1998-5029-2022-85-100-107.
Full textAbstract:
Aim. To give pathomorphological characteristics of placental cotyledons with weakly contrasted bloodstream in women who had an exacerbation of cytomegalovirus infection (CMVI) in the second trimester of pregnancy.Materials and methods. A study was made of involutive-destructive processes in 153 cotyledons of the placenta with well and weakly contrasted bloodstream in women with pregnancy, uncomplicated and complicated by exacerbation of CMVI at 21-24 weeks of gestation. The first group included 36 cotyledon placentas from women with CMV-seronegative uncomplicated pregnancy with well contrasted blood vessels; the second group – 67 cotyledon placentas from patients with chronic compensated placental insufficiency (CCPI) and poorly contrasted vascular network; the third group – 30 cotyledon placentas from women with chronic subcompensated placental insufficiency (CSPI) with indistinctly visualized blood vessels; the fourth group – 20 cotyledon placentas from patients with chronic decompensated placental insufficiency (CDPI). Dosed introduction of red lead on drying oil (1:3) into the blood vessels of the placenta was carried out through the umbilical cord vein. Obtaining X-ray images of cotyledons with well and weakly contrasted blood vessels in the marginal part of the organ was carried out on the apparatus RUM-20M with X-ray image intensifier Sapphire (Russia). Cotyledon biopsy specimens for histometry and histochemical analysis were taken before their contrasting, and for survey microscopy – after injection of the contrast mass.Results. In the first group, the amount of fibrinoid in the stroma of the villi was 1.35±0.09%, perivillous fibrinoid − 1.02±0.08% in the absence of pseudonecrosis and calcifications. In the second group, unlike the first one, cotyledons prevailed, in which in 40-50% of cases weakly expressed contours of blood vessels were found, an increase in the specific volume of stromal fibrinoid by 1.82 times was observed (p<0.001), and fibrinoid around villi by 2.04 times (p<0.001); pseudonecrosis accounted for 2.29±0.13%, and calcificates − 1.50±0.12%. In the third group, in comparison with the second one, cotyledons were more common with 50-70% of indistinctly contoured vessels, villi with edematous changes and stromal collagenization; the concentration of stromal fibrinoid increased by 1.47 times (p<0.001), the proportion of perivillous fibrinoid – 1.46 times (p<0.001), pseudonecrosis – 1.41 times (p<0.001) and the accumulation of calcium salt – 1.57 times (p<0.001). In the fourth group, compared to the third one, cotyledons were more common, in which more than 70% of weakly contrasted blood vessels were determined, while the number of collagen fibers and acid glycosaminoglycans increased in the villi; there was an increase in the amount of fibrinoid around the villi by 1.24 times (p<0.01), pseudonecrosis – by 1.23 times (p<0.05) and calcificates – by 1.32 times (p<0.01).Conclusion. In women with an exacerbation of CMVI in the second trimester of gestation and CSPI, in contrast to patients with a similar infectious disease and CCPI, a decrease in the flow of contrast into the bloodstream of cotyledons is due to more pronounced edema, the formation of collagen fibers, fibrinoid and calcium salts in the stroma of the villi, as well as perivillous fibrinoid. In CDPI of cytomegalovirus etiology, compared with CSPI, weak contrasting of the vascular bed of cotyledons is associated with increasing changes in the stroma involved in the regulation of the resistance of draining veins and intracotyledon blood vessels.
12
Ljubojević, Vesna, Sanja Jovičić, Dragica Draganović, Ljiljana Amidžić, Biljana Vatreš, and Nataša Vojinović. "Analysis of CD31 expression and vascular parameters in human placentas from pregnant women with intrauterine growth restriction." Биомедицинска истраживања 13, no. 2 (2022): 146–54. http://dx.doi.org/10.5937/bii2202146l.
Full textAbstract:
Introduction. Placental dysfunction is underlying cause in most of the intrauterine growth restriction and the pregnancy complications where the fetus does not achieve its genetically determined potential for growth. The critical process for the development of the placenta is angiogenesis. CD31 is an important endothelial adhesion protein that enables angiogenesis. The study aimed to analyze the CD31 expression and vascular parameters in normal placentas and IUGR placentas. Methods. Thirty placental samples, fifteen IUGR placentas, and fifteen term normal placental samples were analyzed. The hematoxylin-eosin method and immunohistochemical method with anti CD31 antibody were used for the staining of the tissue sections. The analyzed vascular parameters were: capillary number density (CND), capillary area density (CAD), and capillary surface density (CSD). Results. Between normal placentas and IUGR placentas there was no determined difference in CD31 expression. Positive intensive staining of CD31 was found in the endothelium of all blood vessels and no staining was observed in cytotrophoblast and syncytiotrophoblast cells. In IUGR placentas, CND of 2.55 capillary/1000 µm2 villous area was significantly decreased compared to normal placentas of 3.49 capillary/1000 µm2 villous area. CAD in IUGR placentas of 30.49 % was significantly decreased compared to normal placentas of 52.80 % villous area. CSD in IUGR placentas (92.81 µm/1000µm2) was significantly reduced compared to CSD in normal placentas (145.51 µm/1000µm2). Conclusion. The localization and intensity of CD31 expression were not different between the IUGR and normal placentas. Histological vascular parameters of placental villi are decreased in the IUGR placenta. In case of intrauterine growth restriction, there is a reduced vascularization of the terminal villi of the placenta.
13
Siemieniuch, Marta J., Ewelina Jursza, Anna Z. Szóstek, Lina Zschockelt, Alois Boos, and Mariusz P. Kowalewski. "Placental Origin of Prostaglandin F2αin the Domestic Cat." Mediators of Inflammation 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/364787.
Full textAbstract:
In the present study, the question was addressed whether the feline placenta can synthesize prostaglandin F2α(PGF2α). The PGFS protein was elevated, particularly at 2.5–3 weeks of pregnancy compared to 7-8 (P<0.05) and 8.5–9 weeks (P<0.001). Transcripts for PGFS were significantly upregulated at 2.5–3 weeks of pregnancy and then gradually declined towards the end of gestation (P<0.001). Transcripts for PTGS2 were only upregulated in placentas from queens close to term (P<0.001) compared with earlier phases. Staining of PTGS2 showed distinct positive signals in placentas obtained during the last week before labor, particularly in the strongly invading trophoblast surrounding blood vessels, and also in decidual cells. Shortly after implantation, signals for PGFS were localized in the trophoblast cells. Near term, PGFS staining was seen mainly in decidual cells. Both placental PGF2αand plasma PGFM were elevated towards the end of pregnancy (P<0.001) compared with earlier weeks of pregnancy. The content of PGF2αin extracted placenta mirrored the PGFM level in plasma of pregnant females. During late gestation there is a significant increase in PGFM levels in maternal blood and of PGF2αlevels in placental tissue concomitant with an upregulation of placental PTGS2.
14
Sawa, Hiroki, Hiroyuki Ukita, Minoru Fukuda, Hajime Kamada, Isamu Saito, and Björn öbrink. "Spatiotemporal Expression of C-CAM in the Rat Placenta." Journal of Histochemistry & Cytochemistry 45, no. 7 (July 1997): 1021–34. http://dx.doi.org/10.1177/002215549704500711.
Full textAbstract:
We investigated the expression of the immunoglobulin superfamily cell adhesion molecule, C-CAM, in developing and mature rat placenta. By immunohistochemical staining at the light microscopic level, no C-CAM-expression was seen before Day 9 of gestation, when it appeared in the trophoblasts of ectoplacental cones. On Day 10.5, spongiotrophoblasts and invasive trophoblasts around the maternal vessels of the decidua basalis were stained positively. On Day 12.5, C-CAM was detected in the spongiotrophoblasts of the junctional layer, but labyrinth trophoblasts and secondary giant trophoblasts were not stained. On Day 17.5, C-CAM was found only in the labyrinth and lacunae of the junctional layer. At this stage, both the labyrinth cytotrophoblasts of the maternal blood vessels and the endothelial cells of the embryonic capillaries were strongly stained. Placental tissues from gestational Days 12.5 and 17.5 were analyzed by immunoelectron microscopy to determine the location of C-CAM at the subcellular level. On Day 12.5, positive staining of the spongiotrophoblasts was observed, mainly on surface membranes and microvilli between loosely associated cells. On Day 17.5, staining was found primarily on the microvilli of the maternal luminal surfaces of the labyrinth cytotrophoblasts, and both on the luminal surface and in the cytoplasm of endothelial cells of the embryonic vessels. RT-PCR analysis and Southern blotting of the PCR products revealed expression of mRNA species for both of the major isoforms, C-CAM1 and C-CAM2. Immunoblotting analysis of C-CAM isolated from 12.5-day and 14.5-day placentae showed that it appeared as a broad band with an apparent molecular mass of 110–170 kD. In summary, C-CAM was strongly expressed in a specific spatiotemporal pattern in trophoblasts actively involved in formation of the placental tissue, suggesting an important role in placental development. In the mature placenta, C-CAM expression was confined to the trophoblastic and endothelial cells lining the maternal and embryonic vessels, respectively, suggesting important functions in placental physiology.
15
Pringle, K. G., and C. T. Roberts. "210. Localisation of insulin-like growth factor-II (IGF-II) and its receptor in early murine pregnancy: a role in placentation and angiogenesis in the decidua?" Reproduction, Fertility and Development 17, no. 9 (2005): 80. http://dx.doi.org/10.1071/srb05abs210.
Full textAbstract:
The highly invasive activity of the human placenta is tightly regulated by a variety of growth factors and other molecules. Contrary to the dominant view, recent data suggests that IGF-II, upon binding to the IGF2R, can stimulate an intracellular signalling pathway.1 Evidence in humans and mice suggests that IGF-II and the IGF2R are important regulators of placental growth; however, to date they have not yet been localised to early murine implantation sites. This study provides a photo micrographic account of early placental development and the decidual vasculature in the mouse, and localises IGF-II and the IGF2R from days 5.5 to 10.5 of pregnancy. During early pregnancy, the decidua displays a paucity of blood vessels, which appear to undergo angiogenesis, so that by day 10.5 the decidua has become a highly vascularized structure, with an extensive network of dilated vessels that presumably enable maximal blood supply to the placenta. Unlike humans, murine trophoblast cells do not invade the endometrium individually, but remain in close contact with the main giant cell layer. The trophoblast giant cells (TGCs) are the outermost cell type of the murine placenta and maternal blood spaces beneath this layer are not lined by endothelium. Due to their location, TGCs appear to play a direct role in displacing this endothelium and therefore may play a role in the transformation into trophoblast lined maternal blood spaces. IGF-II and its receptor were present throughout early pregnancy in the conceptus and maternal decidua supporting their role as regulators of fetal and placental development. Most interesting, however, was their association with the developing maternal blood vessels in the mesometrial decidua. It seems likely that in mice the maternal vessels are remodelled by a variety of locally derived molecules. By association, IGF-II and its receptor are likely candidates. (1)McKinnon T, et al. (2001). Stimulation of human extravillous trophoblast migration by IGF-II is mediated by IGF type 2 receptor involving inhibitory G protein(s) and phosphorylation of MAPK. J. Clin. Endocrinol. Metab. 86(8), 3665–3674.
16
Schreiber, Jörg, Eva Riethmacher-Sonnenberg, Dieter Riethmacher, Elisabeth E. Tuerk, Janna Enderich, Michael R. Bösl, and Michael Wegner. "Placental Failure in Mice Lacking the Mammalian Homolog of Glial Cells Missing, GCMa." Molecular and Cellular Biology 20, no. 7 (April 1, 2000): 2466–74. http://dx.doi.org/10.1128/mcb.20.7.2466-2474.2000.
Full textAbstract:
ABSTRACT The GCM family of transcription factors consists ofDrosophila melanogaster GCM, an important regulator of gliogenesis in the fly, and its two mammalian homologs, GCMa and GCMb. To clarify the function of these mammalian homologs, we deleted GCMa in mice. Genetic ablation of murine GCMa (mGCMa) is embryonic lethal, with mice dying between 9.5 and 10 days postcoitum. At the time of death, no abnormalities were apparent in the embryo proper. Nervous system development, in particular, was not impaired, as might have been expected in analogy to Drosophila GCM. Instead, placental failure was the cause of death. In agreement with the selective expression of mGCMa in labyrinthine trophoblasts, mutant placentas did not develop a functional labyrinth layer, which is necessary for nutrient and gas exchange between maternal and fetal blood. Only a few fetal blood vessels entered the placenta, and these failed to thrive and branch normally. Labyrinthine trophoblasts did not differentiate. All other layers of the placenta, including spongiotrophoblast and giant cell layer, formed normally. Our results indicate that mGCMa plays a critical role in trophoblast differentiation and the signal transduction processes required for normal vascularization of the placenta.
17
Maliar, Volodymyr, Tunzala Ibadova, Vitalii Maliar, and Vasyl Maliar. "MORPHOFUNCTIONAL PECULIARITIES OF THE PLACENTA IN WOMEN WITH UNDIFFERENTIATED CONNECTIVE TISSUE DYSPLASIA SYNDROME." Wiadomości Lekarskie 75, no. 10 (2022): 2467–70. http://dx.doi.org/10.36740/wlek202210128.
Full textAbstract:
The aim: The impact of undifferentiated connective tissue dysplasia on the formation of the placenta. Materials and methods: The morphostructure of 50 placentas with the undifferentiated connective tissue syndrome and 50 placentas of women with physiological pregnancy and absence of connective tissue pathology was studied. Results: The results of morphological studies have shown that the main pathogenetic link of placental dysfunction with highly resistant blood flow in the umbilical arteries in pregnant women with undifferentiated connective tissue dysplasia syndrome is a disorder of functional differentiation of the villous tree.In these cases the dominats were large and medium-sized villi with narrowed lumen in arterial, venular and capillary vessels and arterial spasm and venous plethora, as well as with numerous chaotically sclerosed villi, indicating stage I and II of placental. There is a large amount of fibrins in intervillous space which narrows it and leads to violation of microcirculation and placenta tissue hypoxia. Conclusions: The morphological basis of high flow resistance in the umbilical artery with the undifferentiated connective tissue dysplasia syndrome in pregnant women is a pathological immaturity of the placental villous tree. Morphological study of the architecture of the stem and intermediate placental villi revealed a violation of the structure of collagen fibers in the form of lack of crosslinks of bundles of collagen fibers.
18
Amer, S., J. Yin, and H. Hennawy. "Two Giant Placental Chorangiomas Discovered at 34 week’s Gestation: A Case Report." American Journal of Clinical Pathology 158, Supplement_1 (November 1, 2022): S89—S90. http://dx.doi.org/10.1093/ajcp/aqac126.187.
Full textAbstract:
Abstract Introduction/Objective Chorangioma is a benign vascular tumor of the placenta, likely hamartoma, occurring in 1% of all examined placentas and arising from the primitive chorionic mesenchyme. The clinical significance is related to the size of the tumor. Most chorangiomas are small and asymptomatic; however, those larger than 4 cm are associated with intrauterine growth restriction (IUGR), polyhydramnios, preterm delivery, arteriovenous shunting, hydrops, and fetal thrombocytopenia. Methods/Case Report Herein, we present a case report of a placenta with two chorangiomas that are prenatally detected in a 25-year-old G2P1 female patient by ultrasound which showed a placental mass and mild polyhydramnios. The patient also developed hypertension and preeclampsia so she was referred for early induction of labor. The patient was elected for caesarian section and the placenta was delivered at 35 weeks of gestation. Grossly, two tan soft well-circumscribed lobulated placental masses were identified and measured 9.5 x 9.1 x 3.3 cm and 5.5 x 4.5 x 1.9 cm, respectively. The two masses were joined together by a thick blood vessel. The larger 9.5 cm mass was connected to the placental disc at the umbilical cord insertion site and is associated with blood vessel thrombosis. Microscopically the mass showed proliferation of capillary-sized vessels with surrounding stroma consistent with chorangioma. Clinical, radiological, and microscopic profiles support the diagnosis of placental chorangioma. Results (if a Case Study enter NA) N/A Conclusion To our knowledge, this is the first case report of two giant placental chorangiomas connected together by a thick blood vessel. Although both are giant (more than 4 cm), early diagnosis and timely intervention led to good maternal and neonatal outcomes aided with neonatal intensive care unit management.
19
Clark, A. R., M. Lin, M. Tawhai, R. Saghian, and J. L. James. "Multiscale modelling of the feto–placental vasculature." Interface Focus 5, no. 2 (April 6, 2015): 20140078. http://dx.doi.org/10.1098/rsfs.2014.0078.
Full textAbstract:
The placenta provides all the nutrients required for the fetus through pregnancy. It develops dynamically, and, to avoid rejection of the fetus, there is no mixing of fetal and maternal blood; rather, the branched placental villi ‘bathe’ in blood supplied from the uterine arteries. Within the villi, the feto–placental vasculature also develops a complex branching structure in order to maximize exchange between the placental and maternal circulations. To understand the development of the placenta, we must translate functional information across spatial scales including the interaction between macro- and micro-scale haemodynamics and account for the effects of a dynamically and rapidly changing structure through the time course of pregnancy. Here, we present steps towards an anatomically based and multiscale approach to modelling the feto–placental circulation. We assess the effect of the location of cord insertion on feto–placental blood flow resistance and flow heterogeneity and show that, although cord insertion does not appear to directly influence feto–placental resistance, the heterogeneity of flow in the placenta is predicted to increase from a 19.4% coefficient of variation with central cord insertion to 23.3% when the cord is inserted 2 cm from the edge of the placenta. Model geometries with spheroidal and ellipsoidal shapes, but the same volume, showed no significant differences in flow resistance or heterogeneity, implying that normal asymmetry in shape does not affect placental efficiency. However, the size and number of small capillary vessels is predicted to have a large effect on feto–placental resistance and flow heterogeneity. Using this new model as an example, we highlight the importance of taking an integrated multi-disciplinary and multiscale approach to understand development of the placenta.
20
Koukoulas, Irene, Tomris Mustafa, Rebecca Douglas-Denton, and E. Marelyn Wintour. "Angiotensin II receptor (type 1 and 2) expression peaks when placental growth is maximal in sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 4 (October 1, 2002): R972—R982. http://dx.doi.org/10.1152/ajpregu.00070.2002.
Full textAbstract:
In sheep, placental size is maximal by midgestation, but blood flow continues to increase until term. No nerves are present and ANG II is thought to be a major regulator of vascular tone. We hypothesized that angiotensin type 2 receptors (AT2) would predominate over type 1 (AT1) until late in gestation and be primarily expressed in the vasculature. Real-time PCR, hybridization histochemistry, and ligand-binding studies were performed on placentae and fetal membranes at 27, 45, 66 ± 1, 100 ± 4, 130, and 140 days of gestation (term ≈ 150 days) to determine quantitative changes and localization. The maximum level of AT1 expression occurred in the 45-day placenta and was located predominantly in the maternal stromal cells. AT1receptors were expressed in the endothelial cells of the chorion in the first half of pregnancy, where later in gestation, both AT1and AT2 receptors were predominant in blood vessels. These results suggest that ANG II, via the AT1 receptor, may have hitherto unsuspected important roles in the growth/function on the ovine placenta during the maximal growth phase.
21
Khan, Nahid Ahmed, Nuzaira Nahid, Melia Choudhury, Khaleda Islam, and Shafinaz Mehzabin. "Morphological study of placenta in selected normotensive and pre-eclamptic women in Bangladesh." Journal of Dhaka Medical College 29, no. 2 (January 10, 2021): 171–77. http://dx.doi.org/10.3329/jdmc.v29i2.51299.
Full textAbstract:
Pre – Eclampsia is a disorder of 2nd half of pregnancy, which is characterized by a combination of hypertension, proteinuria and edema, secondary to decreased placental perfusion. Clinical studies suggest that there are morphological changes in the placenta of pre-eclamptic women, compared to normotensive pregnant women. In developing countries, pre-eclampsia causes an estimated 50,000 maternal deaths per year. Only a small number of studies have however, been conducted in Bangladesh.
Objective: To compare the morphology of placenta in selected pre-eclamptic and normotensive pregnant women.
Methods: 220 pregnant women were selected with inclusion and exclusion criteria from 3 different medical colleges and divided into 2 groups – A study group, consisting of 110 pre-eclamptic women and a control group consisting of 110 normotensive pregnant women. Dietary information was collected by 7 days food frequency questionnaire and food score was determined. Anthropometric and biochemical tests were performed. To measure the weight of the placentas, the decidual part of the placentas were removed. The umbilical cords were then cut, nearest to the placenta, to drain the blood from the placental vessels, and the weight was recorded upto nearest gram with weighing machine. The diameters of placentas were measured by taking the average of two maximum diameters of placentas with measuring tape (cm).The cotyledons were counted from maternal side after removal of deciduas basalis. Number of placental infarcts were counted from fetal side.
Results: The mean weights, diameters, number of cotyledons were found to be significantly lower in the study group, compared to the control group. The number of infarcted areas was significantly higher in the placentas of pre-eclamptic women
Conclusion: Therefore, weight, diameter and number of cotyledons are decreased and number of infarcted areas are increased in the placenta of pre-eclamptic women, compared to normotensive pregnant women.
J Dhaka Medical College, Vol. 29, No.2, October, 2020, Page 171-177
22
E. S. Al-Allaf, E. R. Al-Kennany, M. A. Rahawy and. "Clinical and pathological study of retained placenta in Iraqi buffaloes." Al-Qadisiyah Journal of Veterinary Medicine Sciences 9, no. 1 (June 20, 2010): 6. http://dx.doi.org/10.29079/vol9iss1art86.
Full textAbstract:
The present study was conducted to explore the clinical signs and pathological changes might occur with retained placenta. Sixty-three placenta examined Iraqi buffaloes in Ninevah province during the period from February 2005 to February 2006, were collected after 24 hr postpartum, Result showed variable gross lesions in those examined placenta. Some retained placenta showed severe congestion associated with the presence of focal areas of necrosis and, others suffer from thickening with congested some of the cotyledons. Histologically, the lesions characterized by thickening in wall of maternal blood vessels and, coagulative necrosis appeared in placental plates, maternal caruncles and fetal cotyledon. Infiltration and proliferation of macrophages and binucleated cells, desquamation of syncytiotrophoblast were quite obvious. Moreover, most Retained Placenta sections have revealed dystrophic calcification association with fatty infiltration.
23
Chhabra, Akanksha, Andrew J. Lechner, Asha Acharya, Masaya Ueno, Ben Van Handel, Michelle Tallquist, and Hanna Mikkola. "Essential Function of PDGF-B Signaling In the Placental Microenvironment In Protecting Hematopoietic Progenitors From Erythroid Differentiation." Blood 116, no. 21 (November 19, 2010): 1559. http://dx.doi.org/10.1182/blood.v116.21.1559.1559.
Full textAbstract:
Abstract Abstract 1559 The goals of hematopoiesis during embryogenesis are two-fold, to rapidly produce red blood cells to support the survival and development of the embryo, and to establish a pool of undifferentiated hematopoietic stem cells (HSC) for postnatal life. These goals are achieved by segregation of fetal hematopoiesis in multiple waves that are executed in distinct anatomical sites and microenvironmental niches. However, the microenvironmental cues that promote “stemness” vs. differentiation remain poorly understood. The placenta is a recently discovered hematopoietic organ that supports HSC generation and expansion without promoting their differentiation. The placental HSC pool is thought to reside in the placental labyrinth, which is comprised of an intricate vascular network surrounded by trophoblasts. So far, it has been unknown how a disruption of the integrity of the placental vascular labyrinth affects fetal hematopoiesis. The structure of the placental labyrinth is compromised in embryos that lack components of PDGF-B signaling. PDGF-B-/- and PDGF-Rβ-/- (receptor for PDGF-B) embryos display dilation of fetal blood vessels and reduction of trophoblast cells in the placental labyrinth. Our studies revealed that loss of PDGF-B signaling alters the unique placental hematopoietic microenvironment, resulting in active erythropoiesis in the placenta. The unexpected erythropoiesis in the placenta exhibited the same hallmarks of normal definitive erythropoiesis observed in the fetal liver as confirmed by flow cytometry for erythroid markers, morphological analysis and association of erythroblasts with macrophages. Interestingly, deletion of PDGF-Rβ in hematopoietic cells by using a Tie2-Cre strain did not induce the differentiation of placental hematopoietic progenitors into erythroid cells, implying that the ectopic definitive erythropoiesis results from the lack of PDGF-B signaling in the placental microenvironment rather than in the hematopoietic cells themselves. Our studies revealed that the erythroid differentiation in placentas of PDGF-B-/- embryos was induced by marked upregulation of Epo in placental trophoblasts. Strikingly, lentiviral overexpression of Epo specifically in the placental trophoblasts was sufficient to convert the placenta into an ectopic erythropoietic organ. These data reveal a critical function of PDGF-B signaling in protecting the integrity of the placental microenvironment that is required for preventing hematopoietic progenitors from differentiation during their residence in the placenta. Furthermore, these studies highlight the placenta as a versatile hematopoietic organ that supports HSC development during normal pregnancy but can be recruited as a site for definitive erythropoiesis during pathological conditions. Disclosures: No relevant conflicts of interest to declare.
24
Psarris, Alexandros, Michail Sindos, Ploutarchos Kourtis, Andreas Pampanos, Panagiotis Antsaklis, Marianna Theodora, Maria Eleni Chondrogianni, Georgios Morphopoulos, Dimitrios Loutradis, and Georgios Daskalakis. "Placental Mesenchymal Dysplasia: Ultrasound Characteristics and Diagnostic Pitfalls." Ultrasound International Open 06, no. 01 (June 2020): E2—E3. http://dx.doi.org/10.1055/a-1180-9571.
Full textAbstract:
Placental mesenchymal dysplasia (PMD) is a rare, benign developmental anomaly with a reported prevalence of 0.02% (Arizawa and Nakayama, 2002). It is characterized by placentomegaly with multiple cystic lesions of the stem villi and vascular anomalies (Pawoo and Heller, 2014). Early detection of PMD has been described during routine prenatal ultrasound (Vaisbuch et al., 2009). The sonographic characteristics of PMD include increased placental thickness and multiple cystic areas within the placenta with either an absence of blood flow or with low venous Doppler signals (Vaisbuch et al., 2009). The differential diagnosis of multicystic placental lesions with the presence of a live fetus include partial molar pregnancy, multiple hematomas, chorioangioma Beckwith-Wiedemann syndrome and PMD. Chorioangiomas are well circumscribed masses within the placenta and they are characterized by the presence of a single feeding vessel with the same pulse rate as the umbilical cord (Zalel et al., 2002). Invasive prenatal testing is required for the exclusion of partial molar pregnancy and Beckwith-Wiedemann Syndrome (Vaisbuch et al., 2009). Definitive diagnosis of PMD is based on the pathologic examination of the placenta. Histology reveals aneurysm or dilated blood vessels that may be thrombosed. The stem villi are edematous and enlarged with thick-walled vessels, without trophoblastic proliferation (Pawoo and Heller, 2014). This case report highlights the significance of the early detection of PMD, illustrates the pitfalls in differential diagnosis and provides valuable insights regarding PMD management in a clinical setting.
25
Paterson, P. G., B. Sarkar, and S. H. Zlotkin. "The effect of zinc levels in fetal circulation on zinc clearance across the in situ perfused guinea pig placenta." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1401–6. http://dx.doi.org/10.1139/y90-213.
Full textAbstract:
Although zinc is essential for normal fetal growth and development, little is known about factors that influence its transfer across the placenta. The in situ perfused guinea pig placenta model was used to study the influence of the zinc concentration of fetal circulation on maternofetal placental zinc transfer. A placenta of the anaesthetized sow was perfused (on the fetal side) with a physiological perfusate via the umbilical vessels, with the fetus excluded. The sow was infused intravenously with 65zinc as a tracer of placental Zn clearance, and with antipyrine as an indirect indicator of maternal placental blood flow. Maternal plasma and placental effluent samples collected at intervals were counted for 65zinc by gamma counter, and the absorbance of nitrosated antipyrine was measured at 350 nm. Varying the mean zinc concentration in the perfusate from 0.176 to 1.87 mg/L had no effect on relative zinc clearance calculated as zinc clearance/antipyrine clearance (mean ± SEM; 0.085 ± 0.010 vs. 0.114 ± 0.018; n = 6; p > 0.05). The results suggest that short-term changes in fetal zinc status do not influence placental zinc transfer.Key words: placenta, zinc, transport, trophoblast.
26
Carter, A. M., M. A. Miglino, C. E. Ambrosio, T. C. Santos, F. C. W. Rosas, J. A. d'Affonseca Neto, S. M. Lazzarini, A. F. Carvalho, and V. M. F. da Silva. "Placentation in the Amazonian manatee (Trichechus inunguis)." Reproduction, Fertility and Development 20, no. 4 (2008): 537. http://dx.doi.org/10.1071/rd08009.
Full textAbstract:
Evidence from several sources supports a close phylogenetic relationship between elephants and sirenians. To explore whether this was reflected in similar placentation, we examined eight delivered placentae from the Amazonian manatee using light microscopy and immunohistochemistry. In addition, the fetal placental circulation was described by scanning electron microscopy of vessel casts. The manatee placenta was zonary and endotheliochorial, like that of the elephant. The interhaemal barrier comprised maternal endothelium, cytotrophoblasts and fetal endothelium. We found columnar trophoblast beneath the chorionic plate and lining lacunae in this region, but there was no trace in the term placenta of haemophagous activity. The gross anatomy of the cord and fetal membranes was consistent with previous descriptions and included a four-chambered allantoic sac, as also found in the elephant and other afrotherians. Connective tissue septae descended from the chorionic plate and carried blood vessels to the labyrinth, where they gave rise to a dense capillary network. This appeared to drain into shorter vessels near the chorionic plate. The maternal vasculature could not be examined in the same detail, but maternal capillaries ran rather straight and roughly parallel to the fetal ones. Overall, there is a close resemblance in placentation between the manatee and the elephant.
27
Moser, Guettler, Forstner, and Gauster. "Maternal Platelets of the Human Placenta: Friend or Foe?" International Journal of Molecular Sciences 20, no. 22 (November 11, 2019): 5639. http://dx.doi.org/10.3390/ijms20225639.
Full textAbstract:
Human pregnancy relies on hemochorial placentation, including implantation of the blastocyst and deep invasion of fetal trophoblast cells into maternal uterine blood vessels, enabling direct contact of maternal blood with placental villi. Hemochorial placentation requires fast and reliable hemostasis to guarantee survival of the mother, but also for the neonates. During human pregnancy, maternal platelet count decreases gradually from first, to second, and third trimester. In addition to hemodilution, accelerated platelet sequestration and consumption in the placental circulation may contribute to a decline of platelet count throughout gestation. Local stasis, turbulences, or damage of the syncytiotrophoblast layer can activate maternal platelets within the placental intervillous space and result in formation of fibrin-type fibrinoid. Perivillous fibrinoid is a regular constituent of the normal placenta which is considered to be an important regulator of intervillous hemodynamics, as well as having a role in shaping the developing villous trees. However, exaggerated activation of platelets at the maternal-fetal interface can provoke inflammasome activation in the placental trophoblast, and enhance formation of circulating platelet-monocyte aggregates, resulting in sterile inflammation of the placenta and a systemic inflammatory response in the mother. Hence, the degree of activation determines whether maternal platelets are a friend or foe of the human placenta. Exaggerated activation of maternal platelets can either directly cause or propagate the disease process in placenta-associated pregnancy pathologies, such as preeclampsia.
28
Saghian, Rojan, Gib Bogle, Joanna L. James, and Alys R. Clark. "Establishment of maternal blood supply to the placenta: insights into plugging, unplugging and trophoblast behaviour from an agent-based model." Interface Focus 9, no. 5 (August 16, 2019): 20190019. http://dx.doi.org/10.1098/rsfs.2019.0019.
Full textAbstract:
The ability of the baby to receive nutrients and oxygen in utero depends on the healthy development of the placenta. For maternal blood to adequately perfuse the placenta, it dramatically alters the arteries in the uterus that supply it with nutrient-rich blood right from the start of pregnancy. Placental cells (trophoblasts) invade both into the tissue of the uterus and into the maternal blood vessels nearest to the site of implantation (the spiral arteries (SAs)) and transform these allowing a relatively high and steady flow of nutrient-rich blood to perfuse the placenta. Trophoblasts also form plugs that occlude SAs, preventing maternal blood flow to the placenta until the late first trimester, at which point these plugs dislodge or disintegrate. Here we present an agent-based model of trophoblast migration within plugged SAs to tease apart the impact of chemical signals and mechanical factors on trophoblast behaviour. The model supports our previous in vitro hypothesis that plugging of the maternal arteries in early pregnancy can act to promote trophoblast invasion by providing a ‘low flow’ environment and extends our understanding by suggesting ‘weak spots’ in plug structure can lead to plug degeneration, allowing increased blood flow through the materno-fetal circulation.
29
Gauster, M., U. Hiden, A. Blaschitz, S. Frank, U. Lang, G. Alvino, I. Cetin, G. Desoye, and C. Wadsack. "Dysregulation of Placental Endothelial Lipase and Lipoprotein Lipase in Intrauterine Growth-Restricted Pregnancies." Journal of Clinical Endocrinology & Metabolism 92, no. 6 (June 1, 2007): 2256–63. http://dx.doi.org/10.1210/jc.2006-2403.
Full textAbstract:
Abstract Context: Fetal supply of maternally derived fatty acids requires lipase-mediated hydrolysis of lipoprotein-borne triglycerides and phospholipids at the placental surface. Objective: The objective of the study was to test the hypothesis that members of the triglyceride lipase gene (TLG) family are expressed in the human placenta at the maternoplacental (syncytiotrophoblast) and fetoplacental (endothelial cells) interface and that their expression is altered in pregnancy pathologies. Design and Setting: Expression of TLG family members in primary placental cells (trophoblast and endothelial cells) and tissues of first-trimester and term human placenta was analyzed by microarrays, RT-PCR, Western blotting, and immunohistochemistry. Their expression was compared between normal pregnancies and those complicated with intrauterine growth restriction (IUGR). Participants: Participants included women with uncomplicated pregnancies and pregnancies complicated by IUGR. Results: Endothelial lipase (EL) and lipoprotein lipase (LPL) were the only lipases among the TLG family expressed in key cells of the human placenta. In first trimester, EL and LPL were expressed in trophoblasts. At term, EL was detected in trophoblasts and endothelial cells, whereas LPL was absent in these cells. Both lipases were found at placental blood vessels, EL in vascular endothelial cells and LPL in the surrounding smooth muscle cells. In total placental tissue EL expression prevails in first trimester and at term. Compared with normal placentas, EL mRNA was decreased (30%; P < 0.02), whereas LPL mRNA expression was increased (2.4-fold; P < 0.015) in IUGR. Conclusion: EL is the predominant TLG family member in the human placenta present at both interfaces. EL and LPL are dysregulated in IUGR.
30
Al-Rawaf, Sara A., Enas T. Mousa, and Noora M. Kareem. "Correlation between Pregnancy Outcome and Placental Pathology in COVID-19 Pregnant Women." Infectious Diseases in Obstetrics and Gynecology 2022 (August 21, 2022): 1–5. http://dx.doi.org/10.1155/2022/8061112.
Full textAbstract:
Background. Vertical transmission of several viruses during pregnancy has been shown to cause adverse fetal outcomes. The question about the possibility of a similar outcome in association with SARS-CoV-2 has been raised in recently published articles. Indeed, the rate of transmission through the placenta to the fetus reported in women with COVID-19 has been shown to form a minority. The aim of this study was to explore the possible histopathological changes in the placenta of pregnant women with COVID-19 after delivery and those changes in the umbilical cord. Methods. A case-control study including a total of 50 full-term pregnant women with COVID-19 and 60 control pregnant females. Histopathological evaluation of placental tissues and umbilical cords were reported. Results. The main findings in the umbilical cord were increased thickness of vessels, thrombus formation, endothelins, and narrow lumen; except for the increased thickness of blood vessels, these findings were more frequently seen in women with COVID-19, in comparison with control women in a significant manner ( p < 0.05 ). Increased thickness of blood vessels was more significantly observed in the control group compared to the COVID-19 group ( p < 0.01 ). Findings of the placenta included avascular villi, fibrin, thrombosis, and meconium macrophage in various combinations. Except for fibrin as the sole findings, all other findings including combinations were more frequently encountered in the study group in comparison to the control group ( p < 0.05 ). Conclusion. Pregnant women with COVID-19 have significant pathological alterations in the placenta and umbilical cord. These findings reflect the capability of SARS-CoV-2 in causing immunological reactions to the placenta, either directly or indirectly, and these pathologies may be linked to the higher rate of adverse neonatal outcomes and maternal admission to the intensive care unit.
31
Husiev, Viacheslav M., Daria S. Khapchenkova, Serhii O. Dubyna, and Stanislav V. Bondarenko. "MORPHOLOGICAL AND IMMUNOHISTOCHEMICAL SIGNS OF PLACENTAL DISORDERS OF WOMEN AFTER SYPHILITIC INFECTION." Wiadomości Lekarskie 75, no. 12 (2022): 2958–64. http://dx.doi.org/10.36740/wlek202212111.
Full textAbstract:
The aim: To define morphological and immunohistochemical signs of placental disorders of women after syphilitic infection. Materials and methods: The prospective study of 60 pregnant women with history of syphilitic infection (main group) and 57 pregnant patients without syphilis (control group) was conducted. The morphological and immunohistochemical study of the afterbirth was performed. Results: In the placentas of women of the main group the following phenomena were found out: circulatory disorders in the form of hemorrhages into the intervillous space and the stroma of villi; accumulation of fibrinoid around villi with dystrophically altered stroma, compensatory-adaptive reactions resulted in hyperplasia of terminal villi and vessels in them, which provoked narrowing of the intervillous space and disruption of blood supply in it. Pathogenic immune complexes containing Ig G, M and C3 of the complement fraction were located in the central part of the placenta – 45.00% of cases, 16.67% – in the regional, 8.33% – in both parts. Immune complexes with Ig M content occurred in 38.33% of cases. The content of pathogenic immune complexes was the most concentrated in the placentas of women with latent forms and secondary recurrent syphilis – 60.00% of cases. Conclusions: changes in morphohistological and immunohistochemical examination of the placenta of this group of women confirmed the detrimental effect of syphilitic infection in the anamnesis on the structure of placenta during the next pregnancies.
32
Antonson, Per, Gertrud U. Schuster, Ling Wang, Björn Rozell, Elin Holter, Per Flodby, Eckardt Treuter, Lars Holmgren, and Jan-Åke Gustafsson. "Inactivation of the Nuclear Receptor Coactivator RAP250 in Mice Results in Placental Vascular Dysfunction." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1260–68. http://dx.doi.org/10.1128/mcb.23.4.1260-1268.2003.
Full textAbstract:
ABSTRACT Coactivators constitute a diverse group of proteins that are essential for optimal transcriptional activity of nuclear receptors. In the past few years many coactivators have been identified but it is still unclear whether these proteins interact indiscriminately with all nuclear receptors and whether there is some redundancy in their functions. We have previously cloned and characterized RAP250 (ASC-2/PRIP/TRBP/NRC), an LXXLL-containing coactivator for nuclear receptors. In order to study its biological role, Rap250 null mice were generated by gene targeting. Here we show that genetic disruption of Rap250 results in embryonic lethality at embryonic day (E) 13.5. Histological examination of placentas revealed a dramatically reduced spongiotrophoblast layer, a collapse of blood vessels in the region bordering the spongiotrophoblast, and labyrinthine layers in placentas from Rap250−/− embryos. These findings suggest that the lethality of Rap250−/− embryos is the result of obstructed placental blood circulation. Moreover, the transcriptional activity of PPARγ is reduced in fibroblasts derived from Rap250−/− embryos, suggesting that RAP250 is an essential coactivator for this nuclear receptor in the placenta. Our results demonstrate that RAP250 is necessary for placental development and thus essential for embryonic development.
33
Feng, Xueqin, Yingying Zhang, Yumeng Zhang, Xiaojun Yang, Dongmei Man, Likui Lu, Ting Xu, et al. "Prostaglandin I2 mediates weak vasodilatation in human placental microvessels." Biology of Reproduction 103, no. 6 (September 9, 2020): 1229–37. http://dx.doi.org/10.1093/biolre/ioaa156.
Full textAbstract:
Abstract Human placental vessels (HPVs) play important roles in the exchange of metabolites and oxygen in maternal-fetal circulation. Endothelial-derived prostacyclin (prostaglandin I2, PGI2) is a critical endothelial vasodilator in the body. However, the physiological and pharmacological functions of endothelial PGI2 in the human placenta are still unclear. Human, sheep, and rat blood vessels were used in this study. Unlike non-placental vessels (non-PVs), the PGI2 synthesis inhibitor tranylcypromine (TCP) did not modify 5-hydroxytryptamine (5-HT)-induced vascular contraction, indicating that endothelial-derived PGI2 was weak in PVs. Vascular responses to exogenous PGI2 showed slight relaxation followed by a significant contraction at a higher concentration in HPV, which was inhibited by the thromboxane-prostanoid (TP) receptors antagonist SQ-29,548. Testing PVs and non-PVs from sheep also showed similar functional results. More TP receptors than PGI2 (IP) receptors were observed in HPVs. The whole-cell K+ current density of HPVs was significantly weaker than that of non-PVs. This study demonstrated the specific characteristics of the placental endogenous endothelial PGI2 system and the patterns of placental vascular physiological/pharmacological response to exogenous PGI2, showing that placental endothelial PGI2 does not markedly contribute to vascular dilation in the human placenta, in notable contrast to non-PVs. The results provide crucial information for understanding the endothelial roles of HPVs, which may be helpful for further investigations of potential targets in the treatment of diseases such as preeclampsia.
34
Sharma, Deepak Kumar, and Eva Garg. "Twin-to-Twin Transfusion Syndrome." Journal of Nepal Paediatric Society 33, no. 2 (October 7, 2013): 157. http://dx.doi.org/10.3126/jnps.v33i2.8379.
Full textAbstract:
TTTS is a specific condition that only occurs in multiple pregnancies of monozygotic (monochorionic) twins. When twins share a single placenta, the blood vessels become mutually interconnected in the placenta, so that blood flows back and forth between both twins. DOI: http://dx.doi.org/10.3126/jnps.v33i2.8379 J Nepal Paediatr Soc. 2013; 33(2):157
35
Ibba-Manneschi, L., M. Manetti, A. F. Milia, I. Miniati, G. Benelli, S. Guiducci, F. Mecacci, G. Mello, S. Di Lollo, and M. Matucci-Cerinic. "Severe fibrotic changes and altered expression of angiogenic factors in maternal scleroderma: placental findings." Annals of the Rheumatic Diseases 69, no. 2 (March 30, 2009): 458–61. http://dx.doi.org/10.1136/ard.2009.107623.
Full textAbstract:
Objective:Pregnant women with systemic sclerosis (SSc; scleroderma) have an increased risk of premature delivery and small full-term infants. During placental development, angiogenesis and vascular remodelling are essential for a successful pregnancy outcome. An analysis was made of the pathological changes and expression of angiogenic factors in SSc placentas.Methods:Placenta biopsies were obtained from three patients with SSc and four healthy uncomplicated pregnancies after delivery at 34–38 weeks of gestation. The sections were stained with Masson’s trichrome and phosphotungstic-acid-haematoxylin and immunostained for connective tissue growth factor (CTGF), α-smooth muscle actin (α-SMA), vascular endothelial growth factor (VEGF), placenta growth factor (PlGF) and receptors VEGFR-1 and VEGFR-2.Results:The pathological findings were signs of decidual vasculopathy, increased syncytiotrophoblast knotting, placental infarcts and villous hypoplasia. Severe and diffuse perivascular and stromal fibrosis of decidua and chorionic villi, and extensive deposition of fibrinoid material around decidual vessels and in intervillous spaces were observed. Strong CTGF expression in the vessel wall, decidual cells and fibroblasts and α-SMA+ myofibroblasts were found. VEGF and VEGFR-2 expression was stronger in SSc than in healthy placentas, while VEGFR-1 expression was similar to controls. PlGF immunopositivity was weaker in SSc.Conclusion:In SSc placentas, severe fibrosis and abnormal vascular remodelling were detected. This may result in reduced blood flow leading to deep sufferance of maternal placenta and possible premature delivery.
36
Gorikov, I. N. "Anatomical characteristics of the placental cotyledon bloodstream in women with exacerbation of cytomegalovirus infection during the second trimester of gestation." Bulletin Physiology and Pathology of Respiration, no. 83 (April 23, 2022): 66–71. http://dx.doi.org/10.36604/1998-5029-2022-83-66-71.
Full textAbstract:
Aim. To give an anatomical description of the placental cotyledon bloodstream in women who had an exacerbation of cytomegalovirus infection (CMVI) in the second trimester of gestation. Materials and methods. A study was conducted on 117 placentas, of which 101 were from women with full-term pregnancy and 16 from women with premature birth. In all cases, CMVI led to the development of chronic compensated (CCPI), subcompensated (CSPI) and decompensated placental insufficiency (CDPI). 5 groups were identified: the first group consisted of 30 placentas from women with full-term pregnancy seronegative for cytomegalovirus (CMV); the second – 27 placentas from patients who had an acute phase of chronic CMVI, initiating the development of CCPI; the third – 23 placentas from women with exacerbation of CMVI, leading to the formation of CSPI; the fourth – 21 placentas from patients with an exacerbation of CMVI, which caused the development of CDPI and prolongation of pregnancy to the term of delivery; the fifth – 16 placentas from women with an acute phase of chronic CMVI, initiating the formation of CDPI and miscarriage. The assessment of the bloodstream of cotyledons of the placenta was carried out by injection of contrast (red lead-paint on dryingoil) through the vein of the umbilical cord. To obtain X-ray phlebograms, the apparatus RUM-20M “Sapphire” was used. Results. It was shown that the total number of cotyledons did not differ in the studied groups. In the first group, anatomical forms with a well-contrasted bloodstream were 21.4±2.17, with weakly contrasted vessels – 9.3±0.47, and with no contrast in the veins, arteries and capillaries of the villi – 2.9±0.22. In the placentas of the second group, in comparison with the first one, no differences were found in the number of cotyledons, in which blood vessels were clearly visualized and not detected. However, the number of anatomical forms with poorly contrasted vessels increased by 1.51 times (p<0.05). The placentas of the third group in comparison with the second one were characterized by a decrease by 1.97 times (p < 0.001) in the proportion of cotyledons with a clear contouring of the vascular network and an increase in anatomical forms with a poorly contrasted bloodstream by 2.34 times (p<0.001). In the fourth group, in comparison with the third group, the number of cotyledons with clear visualization of vessels decreased by 2.05 times (p<0.001), and the number of anatomical forms increased by 1.44 times (p<0.01), in which X-ray phlebography did not determine the vasculature. In the fifth group compared to the fourth one, cotyledons with a well-contrasted bloodstream were found 2.83 times less frequently (p < 0.01). Conclusion. With an exacerbation of CMVI in the second trimester of gestation, leading to the formation of CDPI, in comparison with CCPI and CSPI in the placenta, a reduction of blood flow in cotyledons is more often detected as a result of direct endotheliotropic and mediated effects of CMV. This is the anatomical basis of placental ischemia and one of the pathogenetic mechanisms for the development of miscarriage.
37
Hitzerd, Emilie, Michelle Broekhuizen, Rugina I. Neuman, Katrina M. Mirabito Colafella, Daphne Merkus, Sam Schoenmakers, Sinno H. P. Simons, Irwin K. M. Reiss, and A. H. Jan Danser. "Human Placental Vascular Reactivity in Health and Disease: Implications for the Treatment of Pre-eclampsia." Current Pharmaceutical Design 25, no. 5 (June 3, 2019): 505–27. http://dx.doi.org/10.2174/1381612825666190405145228.
Full textAbstract:
Adequate development of the placenta is essential for optimal pregnancy outcome. Pre-eclampsia (PE) is increasingly recognized to be a consequence of placental dysfunction and can cause serious maternal and fetal complications during pregnancy. Furthermore, PE increases the risk of neonatal problems and has been shown to be a risk factor for cardiovascular disease of the mother later in life. Currently, there is no adequate treatment for PE, mainly because its multifactorial pathophysiology remains incompletely understood. It originates in early pregnancy with abnormal placentation and involves a cascade of dysregulated systems in the placental vasculature. To investigate therapeutic strategies it is essential to understand the regulation of vascular reactivity and remodeling of blood vessels in the placenta. Techniques using human tissue such as the ex vivo placental perfusion model provide insight in the vasoactive profile of the placenta, and are essential to study the effects of drugs on the fetal vasculature. This approach highlights the different pathways that are involved in the vascular regulation of the human placenta, changes that occur during PE and the importance of focusing on restoring these dysfunctional systems when studying treatment strategies for PE.
38
Rojas, Mariana, and Ángel Rodríguez. "Embryonic Annexes." International Journal of Medical and Surgical Sciences 1, no. 4 (October 26, 2018): 301–9. http://dx.doi.org/10.32457/ijmss.2014.037.
Full textAbstract:
In vertebrates, depending on the environment in which an embryo develops, different types of extraembryonic membranes are formed. In placental mammals the following extraembryonic membranes are formed: amnion, yolk sac, allantois, chorion and placenta. Extraembryonic membranes perform functions vital to the embryo. The amnion protects the embryo from drying, the mechanical trauma, temperature changes and adhesions which can distort it. The yolk sac is present in all vertebrates. In mammals allows the formation of the first blood vessels and the first blood, home to the primordial germ cells for some time; however, in fish and birds these have nutritional importance. In birds and mammals such as cattle, sheep and pig the allantois receives urinary wastes; this structure also contributes part of the bladder and at the time of birth becomes the suspensory ligament, urachus. The chorion form chorionic villus, which can produce hormones such as chorionic gonadotropin and human placental lactogen. A portion of the chorionic sac helps form the placenta.
39
Holmgren, L., A. Glaser, S. Pfeifer-Ohlsson, and R. Ohlsson. "Angiogenesis during human extraembryonic development involves the spatiotemporal control of PDGF ligand and receptor gene expression." Development 113, no. 3 (November 1, 1991): 749–54. http://dx.doi.org/10.1242/dev.113.3.749.
Full textAbstract:
We have examined the role of platelet-derived growth factor (PDGF) ligand and receptor genes in the angiogenic process of the developing human placenta. In situ hybridization analysis of first trimester placentae showed that most microcapillary endothelial cells coexpress the PDGF-B and PDGF beta-receptor genes. This observation indicates that PDGF-B may participate in placental angiogenesis by forming autostimulatory loops in capillary endothelial cells to promote cell proliferation. Endothelial cells of macro blood vessels maintained high PDGF-B expression, whereas PDGF beta-receptor mRNA was not detectable. In contrast, PDGF beta-receptor mRNA was readily detectable in fibroblast-like cells and smooth muscle cells in the surrounding intima of intermediate and macro blood vessels. Taken together, these data suggest that the PDGF-B signalling pathway appears to switch from an autocrine to a paracrine mechanism to stimulate growth of surrounding PDGF beta-receptor-positive mesenchymal stromal cells. Smooth muscle cells of the blood vessel intima also expressed the PDGF-A gene, the protein product of which is presumably targeted to the fibroblast-like cells of the mesenchymal stroma as these cells were the only ones expressing the PDGF alpha-receptor. PDGF-A expression was also detected in columnar cytotrophoblasts where it may have a potential role in stimulating mesenchymal cell growth at the base of the growing placental villi. We discuss the possibility that the regulation of the PDGF-B and beta-receptor gene expression might represent the potential targets for primary angiogenic factors.
40
Han, Yiping W., Raymond W. Redline, Mei Li, Lihong Yin, Gale B. Hill, and Thomas S. McCormick. "Fusobacterium nucleatum Induces Premature and Term Stillbirths in Pregnant Mice: Implication of Oral Bacteria in Preterm Birth." Infection and Immunity 72, no. 4 (April 2004): 2272–79. http://dx.doi.org/10.1128/iai.72.4.2272-2279.2004.
Full textAbstract:
ABSTRACT Fusobacterium nucleatum is a gram-negative anaerobe ubiquitous to the oral cavity. It is associated with periodontal disease. It is also associated with preterm birth and has been isolated from the amniotic fluid, placenta, and chorioamnionic membranes of women delivering prematurely. Periodontal disease is a newly recognized risk factor for preterm birth. This study examined the possible mechanism underlying the link between these two diseases. F. nucleatum strains isolated from amniotic fluids and placentas along with those isolated from orally related sources invaded both epithelial and endothelial cells. The invasive ability may enable F. nucleatum to colonize and infect the pregnant uterus. Transient bacteremia caused by periodontal infection may facilitate bacterial transmission from the oral cavity to the uterus. To test this hypothesis, we intravenously injected F. nucleatum into pregnant CF-1 mice. The injection resulted in premature delivery, stillbirths, and nonsustained live births. The bacterial infection was restricted inside the uterus, without spreading systemically. F. nucleatum was first detected in the blood vessels in murine placentas. Invasion of the endothelial cells lining the blood vessels was observed. The bacteria then crossed the endothelium, proliferated in surrounding tissues, and finally spread to the amniotic fluid. The pattern of infection paralleled that in humans. This study represents the first evidence that F. nucleatum may be transmitted hematogenously to the placenta and cause adverse pregnancy outcomes. The results strengthen the link between periodontal disease and preterm birth. Our study also indicates that invasion may be an important virulence mechanism for F. nucleatum to infect the placenta.
41
Gorikov, I. N. "Morphological structure of cotyledons with non-contrasted blood vessels in the placenta of women who had an exacerbation of mono- and mixed-cytomegalovirus infection in the second trimester of pregnancy." Bulletin Physiology and Pathology of Respiration 1, no. 86 (December 23, 2022): 80–90. http://dx.doi.org/10.36604/1998-5029-2022-86-80-90.
Full textAbstract:
Aim. To assess the morphological structure of cotyledons with non-contrasted blood vessels in the placentas in women who had an exacerbation of mono- and mixed cytomegalovirus infection (CMVI) in the second trimester of pregnancy.Materials and methods. The histometric parameters of the villi were studied with different visualization on X-ray phlebograms of blood vessels in 112 cotyledons of placentas in women with pregnancy, uncomplicated and complicated by mono- and mixed-CMVI (combination of CMVI and reactivation of chronic herpes virus infection type 1 HSV). The first group (control) included 36 cotyledons with a clear contrasting of the vascular bed in the placentas from women with an uncomplicated gestational period. The main group was represented by 76 cotyledons: subgroup 2a - 24 cotyledons, in which the bloodstream was not detected, in placentas from patients with exacerbation of mono-CMVI associated with chronic subcompensated placental insufficiency (CSPI); subgroup 2b - 16 cotyledons with blood vessels not diagnosed by X-ray phlebography, in placentas from women with mixed CMVI infection, initiating the development of CSPI; subgroup 3a - 21 cotyledons with non-contrasted bloodstream in placentas from patients with exacerbation of mono-CMVI and chronic decompensated placental insufficiency (CDPI); subgroup 3b - 15 cotyledons with a similar angiographic picture in placentas from women who had an exacerbation of mixed CMVI in the second trimester of gestation and CDPI. Identification of cotyledons with a clear visualization of blood vessels and with a non-contrasted vascular bed in the marginal part of the placenta was carried out by dosed administration of minium on linseed oil (1:3) through the vein of umbilical cord and assessment of the angiographic picture on X-ray, which were obtained using the RUM-20M apparatus with X-ray image amplifier Sapphire (Russia). For histological analysis, tissue pieces were taken in the same places before and after injection of the contrast mass into the bloodstream of the organ, on the damaged areas of which clamps were applied.Results. In the first group, the cotyledons had clear contours of the blood vessels and the vein draining them. Avascular villi (AV) accounted for 2.05±0.22%, villi with syncytiocapillary membranes (SCM) - 33.5±2.41%, villi with one (1) SCM - 77.1±2.07%, with two (2) SCM - 20.9±1.98% and with three (3) SCM - 1.42±0.09%. In subgroup 2a, compared with the first group, there was a deformation of the lumen of the vein of the stem villi of the I and II order, in which erythrocyte aggregates, single leukocytes and rarely thrombi were determined, as well as signs of edema and partial desquamation of endotheliocytes, fibrinoid and inflammatory changes in the vessel wall. The number of AV increased (by 6.87 times, p<0.001) and the number of villi with SCM decreased (by 2.05 times, p<0.001) with no significant differences between villi with 1, 2, and 3 SCM. In subgroup 2b, in comparison with subgroup 2a, moderate folding of the endothelium, areas of its partial desquamation, AV (1.39 times, p<0.01) and villi with 2 SCMs (1.44 times, p<0.05) were more common against the background of a decrease in the concentration of villi with 1 SCM (by 1.19 times, p<0.05). In subgroup 3b, a greater number of vessels were found that did not provide outflow of blood from cotyledons (12, p<0.001) and had an arcuate shape (10, p<0.001) compared with subgroup 3a, where their number was, respectively, 3 (p<0.001) and 2 (p<0.001). A more pronounced folding of the endothelial lining was determined, as well as aggregates, neutrophils, lymphocytes and thrombi in the lumen of the vessels. There was an increase in the percentage of villi with 1 SCM (by 1.13 times, p<0.05), as well as a decrease in the frequency of occurrence of villi with 2 SCM (by 1.67 times, p<0.05) and 3 SCM (by 2.13 times, p<0.001). In cotyledons of subgroup 3b, in contrast to those of subgroup 2b, blindly ending vessels were more common (2 times, p<0.05), arcuate course of veins (2.5 times, p<0.05), lumen deformity, hyperchromia of the nucleus and total desquamation of cells, thrombi with calcification, complete and partial obliteration of the arterial lumen, inflammation, fibrinoid degradation of the muscular layer of vessels and the deposition of calcium salts in it, as well as AV (1.29 times, p<0.05) and villi with 1 SCM (1.40 times, p<0.001); less often villi were detected with SCM (1.35 times, p<0.05), with 2 SCM (2.78 times, p<0.001) and 3 SCM (1.57 times, p<0.05).Conclusion. In women with exacerbation of mixed CMVI in the second trimester of gestation and CDPI, in contrast to patients with reactivation of mono-CMVI leading to CDPI, angiodestructive and angioobstructive processes, as well as inhibition of angiogenesis, are more pronounced in cotyledons with non-visualized blood vessels. This increases vascular resistance and blocks the flow of the contrast mass during its dosed injection into the vascular bed of the placenta.
42
Sastry, BV. "Placental toxicology: tobacco smoke, abused drugs, multiple chemical interactions, and placental function." Reproduction, Fertility and Development 3, no. 4 (1991): 355. http://dx.doi.org/10.1071/rd9910355.
Full textAbstract:
There are increasing numbers of reports on the tobacco smoking and ingestion of abused drugs (e.g. morphine, cocaine) by pregnant women and the effects of the substances on the developing fetus and newborn infant. The passage of drugs and chemicals from the mother to the fetus is influenced by the placental transport and metabolism of the substances. Further, these drugs and chemicals affect the nutrient transport systems in the placenta. The three major drugs of abuse-nicotine, morphine and cocaine-depress both active amino-acid uptake by human placental villi and transplacental amino-acid transport by reason of the drugs' influence on placental cholinergic and opiate systems. Part of this depression (10-16%) is not reversible. Nicotine blocks the cholinergic receptor and thus blocks acetylcholine (ACh)-facilitated amino-acid transport. Morphine stimulates opiate kappa receptors and depresses ACh release. Cocaine blocks Ca2+ influx and thus blocks ACh release. ACh causes dilation of blood vessels and maintains placental blood flow by the activation of endothelial muscarinic receptors. By interfering with ACh release and placental blood flow, the three drugs of abuse may depress the diffusion of amino acids and other nutrients from the trophoblast into the placental circulation. Three regulatory systems are delineated for amino-acid uptake by the placenta: placental ACh, phospholipid N-methyltransferase, and the gammaglutamyl cycle. These systems operate in concert with one another and are dependent on cellular formation of adenosine 5'-triphosphate (ATP). Placental hypoxia induced by carbon monoxide and other tobacco gases depresses the energy-dependent processes and thus the ATP levels of placental cells. Maternal tobacco smoking and drug abuse cause placental insufficiencies for amino-acid transport, which may partially explain the fetal intrauterine growth retardation caused by these substances. Part of the amino-acid deficits may be compensated for by the induction of new amino-acid transport systems. Specific receptors or drug-binding proteins for the three drugs of abuse are present in the placenta. A DNA adduct selective for maternal smoking has been demonstrated in the placenta. DNA adducts selective for cocaine, morphine and other environmental chemicals have yet to be demonstrated ins the placenta.
43
Frolova, N. A., Y. V. Tezikov, and I. S. Lipatov. "Justification of the choice of diosmin vasoprotective as a preventive agent of pre-eclampsia." Reproductive health of woman 1 (February 26, 2021): 40–43. http://dx.doi.org/10.30841/2708-8731.1.2021.229710.
Full textAbstract:
In this study, the effectiveness of vasoprotective Diosmin for the prevention of pre-eclampsia in pregnant women of high-risk group with severe forms of placental insufficiency was evaluated. The choice of prophylactic agent in the clinical group is justified by close pathogenetic relationship between placental insufficiency and pre-eclampsia on the one hand, and proved fetoprotective action of Diosmin in case of placental insufficiency on the other hand. It is shown that a normalizing effect on the uterine-placental- fetal blood flow, the functional state of the endothelium of blood vessels, the production of growth factors, the induction of apoptosis of immunocompetent cells by trophoblasts, metabolism and angiogenesis in the placenta, contributes to clinically significant reduction in the frequency of implementation of fetoplacental complex pathology and pre-eclampsia.
44
Lumbanraja, Sarma, M. Rizki Yaznil, Andre M. Siahaan, and Bancin Berry Eka Parda. "Soluble FMS-Like Tyrosine Kinase: Role in placenta accreta spectrum disorder." F1000Research 10 (July 21, 2021): 618. http://dx.doi.org/10.12688/f1000research.54719.1.
Full textAbstract:
Background: Placenta accreta is a pregnancy condition where the placenta's blood vessels attach too deeply to the uterine wall. Incidence of placenta accreta is increasingly seen today as the rate of cesarean section increases, however, the exact pathophysiology of this condition is still not fully understood. Soluble fms-like tyrosine kinase-1 (sflt-1) as a protein produced by the placenta was found to be decreased in placenta accreta, Therefore we aim to see if sflt-1 has a role in the development of placenta accreta. Methods: This study involved 40 samples from patients that had been diagnosed with placenta accreta spectrum disorder (case group), and 40 samples from patients with normal pregnancies (control group) at Rumah Skit Umum Pusat H.Adam Malik (RSUP) Haji Adam Malik Medan, in Indonesia. Diagnosis of placenta accreta syndrome was based on Placenta Accreta Spectrum Score (PAS), and International Federation of Gynecology and Obstetrics (FIGO) classification of placenta accreta spectrum disorder.Analyses were performed by independent t-test, man Whitney U test, and Kruskal-Wallis analysis test, with a P-value <0.05 considered as statistically significant (95%CI). Results: Based on this study, we found that the sFlt-1 level in the case group was lower than the control group. Data analysis using the Kruskal-Wallis test showed that there was a difference in sFlt-1 levels in this study group (p = 0.02), which was further evaluated with post hoc analysis using Mann. Whitney U test. The results indicated that there were significant differences between the control and PAS 0, PAS1, and PAS 2 (p = 0.043; p = 0.002; p = 0.03). Conclusion: sFlt-1 levels decreased in placental invasive pregnancies compared to normal pregnancies, however, this still needs to be investigated further in a multi-center study, considering that sFlt-1 levels are also influenced by ethnicity and other conditions that cannot be excluded in this study.
45
Yeboah, D., M. Sun, J. Kingdom, D. Baczyk, S. J. Lye, S. G. Matthews, and W. Gibb. "Expression of breast cancer resistance protein (BCRP/ABCG2) in human placenta throughout gestation and at term before and after labor." Canadian Journal of Physiology and Pharmacology 84, no. 12 (December 2006): 1251–58. http://dx.doi.org/10.1139/y06-078.
Full textAbstract:
Breast cancer resistance protein, BCRP, is a multidrug resistance protein that is highly expressed in the human placenta. In cancer tissues, this protein actively extrudes a wide variety of chemically and structurally unrelated chemotherapeutic drugs and other compounds. Studies in mice have shown that in the absence of BCRP activity in the placenta, there is a 2-fold increase in the uptake in BCRP substrates into fetus. This suggests that in the placenta, BCRP extrudes compounds that would otherwise cross the syncytiotrophoblast cells into fetal circulation. The purpose of this study was to examine the expression and localization of BCRP in the human placenta throughout gestation. Tissues from 6–13, 16–19, 24–29, 32–35, and 38–41 weeks of gestation were used. Real time RT-PCR analysis demonstrated that the mRNA levels of BCRP in the placenta do not change significantly as gestation progressed. However, Western blot analysis revealed that the protein levels increased towards the end of gestation. We demonstrated that BCRP is localized to the syncytiotrophoblast of the placenta and in some fetal blood vessels within the placenta. Tissues from the early stages of pregnancy (6–13 weeks) showed fewer BCRP positive blood vessels than term tissues (38–41 weeks).
46
Островская, Ольга, Olga Ostrovskaya, Ольга Кожарская, Ol'ga Kozharskaya, Стефания Супрун, Stefaniya Suprun, Денис Мусатов, et al. "MORPHOMETRIC FEATURES OF TERMINAL VILLI IN PRETERM PLACENTA." Bulletin physiology and pathology of respiration 1, no. 70 (December 29, 2018): 68–73. http://dx.doi.org/10.12737/article_5c1269c4350159.55377375.
Full textAbstract:
In this study, morphometric features of terminal villi in term and preterm placentas were compared. Placentas of 13 patients whose pregnancy ended in premature birth and placentas of 35 women with physiological pregnancy and delivery at term were studied. Morphometric assessment was made with Carl Zeiss Axio Imager microscope using an image analysis software package. The number of capillaries in terminal villi of preterm placentas was found to be decreased, while the vessels-to-syncytiotrophoblast distance was found to be increased. These result in a decreased gas exchange between maternal blood and placental tissue, hypoxia and can cause early termination of pregnancy. Mean values of cross-sectional area, vertical dimension and perimeter of terminal villi in preterm placentas are found to be greater than those in term placentas, which contributed to an increase in gas exchange area and can be regarded as a compensatory reaction at a tissue level.
47
Karimov, A. Kh, and D. M. Davletova. "Possibilities of the correction of placental dysfunction in women with preeclampsia." Infusion & Chemotherapy, no. 3.1 (October 11, 2020): 38–39. http://dx.doi.org/10.32902/2663-0338-2020-3.1-31.
Full textAbstract:
Objective. To study the possibilities of diagnosing placental dysfunction and its correction in women with preeclampsia.
Materials and methods. 72 women with preeclampsia in the 2nd and 3rd trimesters of pregnancy were examined at the multidisciplinary clinic of the Tashkent Medical Academy from 2017 to 2019. All women underwent: clinical, laboratory, echography, color Doppler mapping of the vessels of the uteroplacental-fetal system with Doppler analysis of blood flow velocity.
Results and discussion. Diagnostic criteria for placental dysfunction: the placenta acquires its echographic picture at the beginning of the 2nd trimester of pregnancy. During the 2nd and 3rd trimesters of pregnancy, the thickness of the placenta corresponds to 2-3.6 cm. A decrease of <2 cm is regarded as hypoplasia, an increase >4 cm as hyperplasia. Premature aging of the placenta was detected in 77.3 % of cases, the presence of cysts of the placental tissue – in 4.5 %, turbid amniotic fluid – 59.09 %, oligohydramnios – in 27.3 %. At 24th week, the fetal thigh length lag was less by 9.04 % (p<0.05). Doppler criteria for placental dysfunction: in almost equal proportions there are circulatory disorders in the uteroplacental and fetal-placental blood flow (28.2 and 27.7 %). Treatment of placental dysfunction in compensated form: was carried out according to the generally accepted method according to the national guidelines; 4.2 g of L-arginine (Tivortin, “Yuria-Pharm”, Ukraine) was added to the complex therapy in the hospital in dosage 100 ml per day for 7 days. Then Tivortin aspartate was continued on an outpatient basis, orally, 20 ml (1 table spoon 4 times per day, 20 days). The effectiveness of therapy was monitored again after 2 weeks.
Conclusions. Timely initiation of therapy for uterine-fetal-placental blood flow disorders in the 2nd trimester was more effective than in the 3rd.
48
Ramaesh, Thayalini, James J. Logie, Antonia K. Roseweir, Robert P. Millar, Brian R. Walker, Patrick W. F. Hadoke, and Rebecca M. Reynolds. "Kisspeptin-10 Inhibits Angiogenesis in Human Placental Vessels ex Vivo and Endothelial Cells in Vitro." Endocrinology 151, no. 12 (October 6, 2010): 5927–34. http://dx.doi.org/10.1210/en.2010-0565.
Full textAbstract:
Recent studies suggest that kisspeptin (a neuropeptide central to the regulation of gonadotrophin secretion) has diverse roles in human physiology, including a putative role in implantation and placental function. Kisspeptin and its receptor are present in human blood vessels, where they mediate vasoconstriction, and kisspeptin is known to inhibit tumor metastasis and trophoblast invasion, both processes involving angiogenesis. We hypothesized that kisspeptin contributes to the regulation of angiogenesis in the reproductive system. The presence of the kisspeptin receptor was confirmed in human placental blood vessels and human umbilical vein endothelial cells (HUVEC) using immunochemistry. The ability of kisspeptin-10 (KP-10) (a shorter biologically active processed peptide) to inhibit angiogenesis was tested in explanted human placental arteries and HUVEC using complementary ex vivo and in vitro assays. KP-10 inhibited new vessel sprouting from placental arteries embedded in Matrigel and tube-like structure formation by HUVEC, in a concentration-dependent manner. KP-10 had no effect on HUVEC viability or apoptosis but induced concentration-dependent inhibition of proliferation and migration. In conclusion, KP-10 has antiangiogenic effects and, given its high expression in the placenta, may contribute to the regulation of angiogenesis in this tissue.
49
Hermans, Sammy, Jacob Pilon, Dennis Eschweiler, Johannes Stegmaier, Carmen A. H. Severens–Rijvers, Salwan Al-Nasiry, Marc van Zandvoort, and Dimitrios Kapsokalyvas. "Definition and Quantification of Three-Dimensional Imaging Targets to Phenotype Pre-Eclampsia Subtypes: An Exploratory Study." International Journal of Molecular Sciences 24, no. 4 (February 7, 2023): 3240. http://dx.doi.org/10.3390/ijms24043240.
Full textAbstract:
Pre-eclampsia is a severe placenta-related complication of pregnancy with limited early diagnostic and therapeutic options. Aetiological knowledge is controversial, and there is no universal consensus on what constitutes the early and late phenotypes of pre-eclampsia. Phenotyping of native placental three-dimensional (3D) morphology offers a novel approach to improve our understanding of the structural placental abnormalities in pre-eclampsia. Healthy and pre-eclamptic placental tissues were imaged with multiphoton microscopy (MPM). Imaging based on inherent signal (collagen, and cytoplasm) and fluorescent staining (nuclei, and blood vessels) enabled the visualization of placental villous tissue with subcellular resolution. Images were analysed with a combination of open source (FIJI, VMTK, Stardist, MATLAB, DBSCAN), and commercially (MATLAB) available software. Trophoblast organization, 3D-villous tree structure, syncytial knots, fibrosis, and 3D-vascular networks were identified as quantifiable imaging targets. Preliminary data indicate increased syncytial knot density with characteristic elongated shape, higher occurrence of paddle-like villous sprouts, abnormal villous volume-to-surface ratio, and decreased vascular density in pre-eclampsia compared to control placentas. The preliminary data presented indicate the potential of quantifying 3D microscopic images for identifying different morphological features and phenotyping pre-eclampsia in placental villous tissue.
50
Taga, Shigeki, Junko Haraga, Mari Sawada, Aya Nagai, Dan Yamamoto, and Ryoji Hayase. "A Case of Placental Mesenchymal Dysplasia." Case Reports in Obstetrics and Gynecology 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/265159.
Full textAbstract:
Placental mesenchymal dysplasia (PMD) rarely complicates with pregnancy. A 30-year-old woman, gravida 3, para 3, presenting with placentomegaly, was referred to our department at 18 weeks of gestation. An ultrasonography revealed a normal fetus with a large multicystic placenta, measuring 125 × 42 × 80 mm. The border between the lesion and normal region was not clear. Color doppler revealed little blood flow in the lesion. Magnetic resonance imaging revealed normal fetus and a large multicystic placenta. Serum human chorionic gonadotropin level was 20124.97 U/L, which was normal at 20 weeks of gestation. Thus, placental mesenchymal dysplasia rather than hydatidiform mole with coexistent fetus was suspected. Then, routine checkup was continued. Because she had the history of Cesarean section, an elective Cesarean section was performed at 37 weeks of gestation, and 2520 g female infant with apgar score 8/9 was delivered. The baby was normal with no evidence of Beckwith-Wiedemann syndrome. Placenta of 20 × 16 × 2 cm, weighing 720 g, was bulky with grape like vesicles involving whole placenta. Microscopic examination revealed dilated villi and vessels with thick wall which was lacking trophoblast proliferation. Large hydropic stem villi with myxomatous struma and cistern formation were seen. PMD was histopathologically confirmed.