Relevant bibliographies by topics / Placenta Blood-vessels

Academic literature on the topic 'Placenta Blood-vessels'

Author: Grafiati
Published: 10 December 2022
Last updated: 20 February 2023

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Journal articles on the topic "Placenta Blood-vessels"

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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.

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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.
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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.

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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.
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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.

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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=
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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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.

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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.
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Dissertations / Theses on the topic "Placenta Blood-vessels"

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Wilcox, Gavin Rutledge. "Haematological processes occurring in the fetus with Doppler-defined placental insufficiency." Thesis, The University of Sydney, 1991. https://hdl.handle.net/2123/26400.

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Doppler-defined placental insufficiency may be diagnosed by measurement of the systolic: diastolic ratio of the umbilical artery flow velocity waveform and is associated with a number of perinatal complications including perinatal mortality, intrauterine growth retardation, pregnancy-induced hypertension and fetal distress in labour. It is known that the changes seen in the umbilical artery waveform are caused by a reduction in the number of arterioles and small arteries in the tertiary placental villi but the processes that precede and accompany these placental vascular changes remain obscure. The aim of the work described in this thesis is to extend current knowledge of the pathophysiology of placental insufficiency by examining various haematological processes that may cause or accompany the placental vascular changes seen in this disease. Infants with placental insufficiency were categorised as moderately or severely affected according to the degree that their umbilical artery waveforms differed from normal. A control group of infants with normal umbilical artery waveforms was also defined. Fetal blood was collected from the umbilical cord or the placenta at the time of delivery. The following haematological parameters were assessed and compared in the three groups of infants: erythrocyte number, size and related parameters, platelet number, the plasma glycocalicin concentration which may be used to estimate platelet lifespan, the coagulation status and the plasma concentration of 6keto-prostaglandin Fla, a major hydrolytic product of prostacyclin. In addition an immunoradiometric assay for glycocalicin was developed and characterised and the effects of maternal ingestion of low-dose aspirin on the production of thromboxane 82 by fetal platelets and on the placental production of thromboxane B2 and 6-keto-prostaglandin Fla were measured.
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Books on the topic "Placenta Blood-vessels"

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Nadirashvili, S. A. Iskusstvennoe plat͡s︡entarnoe krovoobrashchenie ploda. Tbilisi: "Met͡s︡niereba", 1986.

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International Conference on Placenta (1990 Tokyo, Japan). Placenta: Basic research for clinical application. Edited by Soma H. Basel: Karger, 1991.

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Doppler blood flow measurement in uteroplacental and fetal vessels: Pathophysiological and clinical significance. Berlin: Springer-Verlag, 1990.

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1942-, Kaufmann Peter, Miller Richard K. 1946-, European Placenta Group Meeting, and Rochester Trophoblast Conference (11th : 1986 : Rolduc Monastery, Netherlands), eds. Placental vascularization and blood flow: Basic research and clinical applications. New York: Plenum Medical Book Co., 1988.

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Bonnet, Marie-Pierre, and Anne Alice Chantry. Placenta and uteroplacental perfusion. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0003.

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The placenta is a complex and changing organ necessary for normal fetal growth and development and for maintenance of a healthy pregnancy. It has three major functions: a protective function of the fetus, an endocrine function, and a metabolic function. The main functional unit of the placenta is the chorionic villous, responsible for the majority of the fetal–maternal exchanges. Migration of trophoblastic cells induces a remodelling of the uterine arteries, with vasodilatated and compliant vessels, unresponsive to maternal vasomotor control. Therefore, any significant change in maternal blood pressure, in particular in the context of general or regional anaesthesia, can directly impact on uteroplacental perfusion. Most anaesthetic drugs cross the placental barrier, but without significant consequences on the fetal well-being.
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(Editor), R. K. Miller, and H. A. Thiede (Editor), eds. Trophoblast Research: Volume 3: Placental Vascularization and Blood Flow: Basic Research and Clinical Applications (TROPHOBLAST RESEARCH). Springer, 1988.

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The placenta from implantation to trophoblastic disease: Apoptosis, proliferation, invasion, and pathology. Rochester, NY: University of Rochester Press, 1999.

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(Editor), Masaomi Takayama, ed. The Placenta from Implantation to Trophoblastic Disease:: Apoptosis, Proliferation, Invasion, and Pathology (Trophoblast Research). University of Rochester Press, 1999.

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1948-, Morrish Donald, Miller Richard K. 1946-, Rochester Trophoblast Conference (13th : 1996 : Banff, Alta.), and Thomas G. Wegmann Memorial Symposium on Reproductive Immunology (1996 : Banff, Alta.), eds. Genetic regulation of placental development, and immunology. Rochester, N.Y: University of Rochester Press, 1998.

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Book chapters on the topic "Placenta Blood-vessels"

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Obladen, Michael. "Hepar uterinum." In Oxford Textbook of the Newborn, edited by Michael Obladen, 11–16. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198854807.003.0002.

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The means of fetal nutrition has been debated for over two millennia, with the controversy of oral versus parenteral nutrition already in the Corpus Hippocraticum. In 1587, Aranzio rejected connections between maternal and fetal blood vessels, and coined the term hepar uterinum for the placenta. From the 16th to 18th century, fervent debate focused on the type and extent of connection between maternal and fetal vessels. But up to the middle of the 19th century, an important nutritive function was attributed to amniotic fluid. When with the discovery of oxygen the placenta’s respiratory function became understood, its nutritional function fell from grace. Most scientists realized reluctantly that the organ had numerous functions. As late as the 19th century, the advent of microscopy allowed cell theory to develop, and analytical chemistry furthered the understanding of the transport of nutrients across the placenta. The identification of the syncytiotrophoblast made passive diffusion unlikely. Radioisotopes, molecular biology, and the fluid mosaic model of the cell membrane revealed active transport mechanisms for nearly all macronutrients.
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Conference papers on the topic "Placenta Blood-vessels"

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Martin, John T., and Virginia L. Ferguson. "Regional Similarities in the Mechanical Properties of the Human Umbilical Artery." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206800.

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The human umbilical cord (UC) bridges the blood flow gap between baby and mother, protecting the blood supply in a way that allows the fetus freedom to move within the amniotic sac. Once the blood supply has been oxygenated by the maternal blood pool via the placenta, the umbilical vein (UV) provides a transport pathway to the fetus. Two umbilical arteries (UA) return the blood supply to the pool to eliminate CO2 and other metabolic wastes [1]. The walls of the UA’s and UV are made up of an intima composed a single layer of large, elongated endothelial cells [2], and a media composed of randomly distributed smooth muscles cells, collagen, elastin, and ground substance. These vessels are unique in that their adventitia is absent and substituted by Wharton’s jelly, a mucoid connective tissue.
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Kowalski, William J., Berk M. Yigit, David J. R. Hutchon, and Kerem Pekkan. "Transition From the Fetal to Neonatal Circulation: Modeling the Effect of Umbilical Cord Clamping." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14431.

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The transition from fetal to neonatal circulation requires a concert of events to transfer gas exchange function from the placenta to the lungs and separate the pulmonary and systemic pathways. Pulmonary vascular resistance (PVR) rapidly decreases within the first minutes of extrauterine life and continues to gradually decrease during the first week, increasing pulmonary blood flow and reducing pulmonary pressure [1, 2]. Umbilical vessels constrict, removing the placental circulation and leading to closure of the ductus venosus (DV) [2]. The increased left atrial filling and reduced right atrial filling results in permanent closure of the flap of the foramen ovale, removing the R→L interatrial shunt. Closure of the ductus arteriosus (DA) completes the separation of the pulmonary and systemic circulations by 48 hours in 82% of term newborns and by 96 hours in 100% [3]. Removal of the placental circulation is routinely achieved by umbilical cord clamping (UCC) immediately after birth. This practice, however, has been called into question by many studies, which suggest that continued umbilical flow in the early neonate is beneficial, and immediate UCC can lead to infant anemia [4, 5]. Due to routine UCC, the effects of this practice on transitional flow patterns are largely unknown [1, 6]. We therefore developed a lumped parameter model (LPM) to study the role of UCC in the fetal to neonatal transition. Our model includes time-varying resistance functions that allow us to simulate the opening of the PVR and closure of the DA and umbilical vessels. This model demonstrates that UCC can lead to an earlier onset of DA flow reversal and slightly reduced cardiac output (CO).
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