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Gotowa bibliografia na temat „Rat placenta”

Autor: Grafiati

Data publikacji: 6 września 2023

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Artykuły w czasopismach na temat "Rat placenta"

Trifunović, Svetlana, Branka Šošić Jurjević, Nataša Ristić, Nataša Nestorović, Branko Filipović, Ivana Stevanović, Vesna Begović-Kuprešanin i Milica Manojlović-Stojanoski. "Maternal Dexamethasone Exposure Induces Sex-Specific Changes in Histomorphology and Redox Homeostasis of Rat Placenta". International Journal of Molecular Sciences 24, nr 1 (29.12.2022): 540. http://dx.doi.org/10.3390/ijms24010540.

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As the mediator between the mother and fetus, the placenta allows the most appropriate environment and optimal fetal growth. The placenta of one sex sometimes has a greater ability over the other to respond to and protect against possible maternal insults. Here, we characterized sex differences in the placenta’s morphological features and antioxidant status following dexamethasone (Dx) exposure. Pregnant rats were exposed to Dx or saline. The placenta was histologically and stereologically analyzed. The activity of the antioxidant enzymes, lipid peroxides (TBARS), superoxide anion and nitric oxide (NO) was measured. The decrease in placental zone volumes was more pronounced (p < 0.05) in female placentas. The volume density of PCNA-immunopositive nuclei was reduced (p < 0.05) in both sexes. The reduced (p < 0.05) antioxidant enzyme activities, enhanced TBARS and NO concentration indicate that Dx exposure triggered oxidative stress in the placenta of both fetal sexes, albeit stronger in the placenta of female fetuses. In conclusion, maternal Dx treatment reduced the size and volume of placental zones, altered placental histomorphology, decreased cell proliferation and triggered oxidative stress; however, the placentas of female fetuses exerted more significant responses to the treatment effects. The reduced placental size most probably reduced the transport of nutrients and oxygen, thus resulting in the reduced weight of fetuses, similar in both sexes. The lesser ability of the male placenta to detect and react to maternal exposure to environmental challenges may lead to long-standing health effects.

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Achur, Rajeshwara N., Sean T. Agbor-Enoh i D. Channe Gowda. "Rat Spongiotrophoblast-specific Protein Is Predominantly a Unique Low Sulfated Chondroitin Sulfate Proteoglycan". Journal of Biological Chemistry 281, nr 43 (5.09.2006): 32327–34. http://dx.doi.org/10.1074/jbc.m605841200.

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We have previously demonstrated that the human placenta contains a uniquely low sulfated extracellular aggrecan family chondroitin sulfate proteoglycan (CSPG). This CSPG is a major receptor for the adherence of Plasmodium falciparum-infected red blood cells (IRBCs) in placentas, causing pregnancy-specific malaria. However, it is not known whether such low sulfated CSPGs occur in placentas of other animals and, if so, whether IRBCs bind to those CSPGs. In this study, we show that rat placenta contains a uniquely low sulfated extracellular CSPG bearing chondroitin sulfate (CS) chains, which comprise only ∼2% 4-sulfated and the remainder nonsulfated disaccharides. Surprisingly, the core protein of the rat placental CSPG, unlike that of the human placental CSPG, is a spongiotrophoblast-specific protein (SSP), which is expressed in a pregnancy stage-dependent manner. The majority of rat placental SSP is present in the CSPG form, and only ∼10% occurs without CS chain substitution. Of the total SSP-CSPG in rat placenta, ∼57% is modified with a single CS chain, and ∼43% carries two CS chains. These data together with the previous finding on human placental CSPG suggest that the expression of low sulfated CSPG is a common feature of animal placentas. Our data also show that the unique species-specific difference in the biology of the rat and human placentas is reflected in the occurrence of completely different CSPG core protein types. Furthermore, the rat SSP-CSPG binds P. falciparum IRBCs in a CS chain-dependent manner. Since IRBCs have been reported to accumulate in the placentas of malaria parasite-infected rodents, our results have important implications for exploiting pregnant rats as a model for studying chondroitin 4-sulfate-based therapeutics for human placental malaria.

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Clifton, Vicki L., Phillip C. Owens, Phillip J. Robinson i Roger Smith. "Identification and characterization of a corticotrophin-releasing hormone receptor in human placenta". European Journal of Endocrinology 133, nr 5 (listopad 1995): 591–97. http://dx.doi.org/10.1530/eje.0.1330591.

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Clifton VL, Owens PC, Robinson PJ, Smith R. Identification and characterization of a corticotrophinreleasing hormone receptor in human placenta. Eur J Endocrinol 1995;133:591–7. ISSN 0804–4643 Corticotrophin-releasing hormone (CRH) causes vasodilatation in the human fetal–placental circulation and has paracrine actions in placental tissue, suggesting that CRH receptors may be present in the human placenta. We have now identified and characterized placental CRH binding sites and compared them to those described previously in human myometrium and rat pituitary. Radiolabelled ovine CRH binding to placental membranes was pH-, time-, temperature- and divalent cation-dependent and was reversible in the presence of 1 μmol/l unlabelled ovine CRH. Scatchard analysis of placentae delivered vaginally or by elective caesarean section revealed dissociation constants (Kd) of 214.5 ± 84 pmol/l (N = 8) and 45.4 ± 23.9 pmol/l (N = 9), respectively. The Kd for caesarean placental binding sites was similar to that of human myometrium (59.6 pmol/l, N = 3) and rat pituitary (82.5 pmol/l, N = 3) receptors. However, in vaginally delivered placentae the CRH binding sites had a much lower affinity (p < 0.05). The receptor densities (Bmax) of vaginally delivered and caesarean-delivered placentae were 28.6 ± 9.6 and 6.1 ± 2.8 fmol/mg, respectively (p < 0.05). Chemical cross-linking studies using disuccinimidyl suberate indicated that the molecular weight of the CRH receptor in the placenta and rat pituitary is 75 kD. We conclude that there is a high-affinity population of CRH binding sites in the human placenta that are physicochemically similar to pituitary and myometrial CRH receptors. The CRH receptor properties in the placenta change in response to labour, when CRH levels in maternal blood are highest, suggesting that placental CRH may regulate its receptor. R Smith, Endocrinology Unit, John Hunter Hospital, Locked Bag 1, Hunter Regional Mail Centre, Newcastle, NSW 2310, Australia

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Charest, Phanie L., Vanessa Vrolyk, Pauline Herst, Maryse Lessard, Deborah M. Sloboda, Mathieu Dalvai, Julius Haruna, Janice L. Bailey i Marie-Odile Benoit-Biancamano. "Histomorphologic Analysis of the Late-term Rat Fetus and Placenta". Toxicologic Pathology 46, nr 2 (luty 2018): 158–68. http://dx.doi.org/10.1177/0192623318755135.

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Histological examination of the rat placenta and fetus is uncommon. Toxicological studies mainly rely on gross examination of the fetus and on fetal and placental weights. These are often insufficient to assess the fetal and placental toxicity of xenobiotics. The small size of the fetus makes its dissection labor-intensive. Thus, our objective was to develop a simple and accurate technique to evaluate the rat fetus and placenta. Sprague-Dawley rat fetuses at gestational day 19.5 ( n = 18) and their placentas ( n = 32) were fixed in formalin. Placentas were cut transversally in the center. Fetuses were cut following a freehand whole-body serial sectioning diagram adapted from Wilson’s method. Sections were stained with hematoxylin–eosin–phloxine–saffron, and histomorphometry was used to measure the area of the fetal placental region (27.2 ± 1.7 mm2), including the labyrinth (22.2 ± 1.0 mm2) and the basal zone (4.8 ± 0.8 mm2). Our whole-fetus serial sectioning technique resulted in 12 precise cutting planes that fit on 3 histological slides, enabling the examination of most organs without labor-intensive dissection. Quantitative analysis of placental areas improves the understanding of the pathogenesis of treatment-related changes. This technique provides a standardized method for future research in pertinent fields such as developmental biology and toxicology.

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Borke, James L., Ariel Caride, Anil K. Verma, Lucky K. Kelley, Carl H. Smith, John T. Penniston i Rajiv Kumar. "Calcium pump epitopes in placental trophoblast basal plasma membranes". American Journal of Physiology-Cell Physiology 257, nr 2 (1.08.1989): C341—C346. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c341.

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The syncytiotrophoblast represents the primary cellular barrier between maternal and fetal circulations in the placenta. Large amounts of Ca2+ are transported across this barrier by mechanisms that are not clearly understood. To further understand this phenomenon, we examined rat and human placenta by immunohistochemical and protein blotting techniques with a monoclonal antibody raised against the human erythrocyte plasma membrane Ca2+ pump. Immunohistochemistry with this antibody showed specific staining in the human placenta of the basal (fetal facing) surface of the syncytiotrophoblast. In the rat placenta, immunohistochemistry also showed specific staining of the innermost (fetal facing) layer of the trophoblast and the basal surface of the endoderm of the intraplacental yolk sac. In Western blots of placental homogenates and membranes, the monoclonal antibody bound to a 140,000-mol wt band, characteristic of Ca2+ pumps in other tissues. Western blots of isolated basal membranes showed more intense staining than isolated microvillous membranes, confirming the results of the immunohistochemistry. In addition, Ca2+ transport in basal membrane vesicles from human placenta was inhibited by polyclonal antibodies prepared against the erythrocyte Ca2+ pump. We conclude that basal (fetal facing) layers of human and rat placentas contain a high-affinity Ca2+ pump situated to transport Ca2+ from the maternal to the fetal circulation. calcium-magnesium-adenosinetriphosphatase; calcium transport; immunohistochemistry; rat and human placenta Submitted on November 14, 1988 Accepted on March 27, 1989

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Lacroix, MC, H. Jammes i G. Kann. "Occurrence of a growth hormone-releasing hormone-like messenger ribonucleic acid and immunoreactive peptide in the sheep placenta". Reproduction, Fertility and Development 8, nr 3 (1996): 449. http://dx.doi.org/10.1071/rd9960449.

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Growth hormone releasing factor (GHRH) has been described in the rat, mouse and human placentae. This study reports the presence of an immunoreactive GHRH activity (IR-GHRH) in the ovine placenta. This activity was detected by radioimmunoassay from day 50 (D50) until the end of pregnancy. Higher IR-GHRH concentration in placental tissue was observed on days 100 (543 +/- 123 pg/g) and 140 (550 +/- 62 pg/g) and, when compared with the GHRH content of the ovine hypothalamus (1.2 ng/hypothalamus), represents a considerable amount of GHRH per placenta (a mean of 200 ng). Perifused placenta explants released IR-GHRH in vitro at a mean rate of 200 pg/g/h. Depolarization by 55 mM KCl increased the IR-GHRH concentration of the perifusion media 1.7 times over basal values. The elution position of GHRH immunoreactivity in the gel filtration chromatography profiles was the same for placenta and hypothalamus extracts and lay very near to the molecular weight of bovine GHRH. Northern blot hybridization analysis revealed the existence of a placental transcript whose size (0.75 kb) was comparable to the size of the ovine hypothalamus and rat placenta GHRH transcripts. Hybridization signal was observed at each stage studied from D50 until D120 of pregnancy. This study demonstrated the existence of a IR-GHRH peptide in the ovine placenta.

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Shearman, Lauren P., Alison M. McReynolds, Feng C. Zhou i Jerrold S. Meyer. "Relationship between [125I]RTI-55-labeled cocaine binding sites and the serotonin transporter in rat placenta". American Journal of Physiology-Cell Physiology 275, nr 6 (1.12.1998): C1621—C1629. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1621.

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We investigated the characteristics of cocainelike binding sites in rat placenta using [125I]RTI-55. [3H]paroxetine binding and immunocytochemical staining for serotonin [5-hydroxytryptamine (5-HT)] and for the 5-HT transporter were also used to obtain evidence for rat placental 5-HT uptake. [125I]RTI-55 saturation analyses with membranes from normal gestational day 20 placentas yielded curvilinear Scatchard plots that were resolved into high- and low-affinity components (mean dissociation constants of 0.29 and 7.9 nM, respectively). Drug competition studies with various monoamine uptake inhibitors gave rise to complex multiphasic displacement curves, although the results obtained with the selective 5-HT uptake inhibitor citalopram suggest that the 5-HT transporter is an important component of placental high-affinity [125I]RTI-55 binding. The presence of a rat placental 5-HT uptake system was additionally supported by the [3H]paroxetine binding experiments and by the presence throughout the placenta of immunoreactivity for 5-HT and the 5-HT transporter. Immunostaining with both antibodies was most intense in the junctional zone, whereas the density of [125I]RTI-55 binding sites was greater in the placental labyrinth. This discrepancy may be due to the fact that [125I]RTI-55 appears to be labeling additional cellular components besides the 5-HT transporter. The presence of cocaine- and antidepressant-sensitive 5-HT transporters in the placenta has important implications for the possible effects of these compounds on pregnancy and fetal development.

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White, Elizabeth A., Joffre B. Baker, Michael McGrogan i Paul A. Kitos. "Protease Nexin 1 Is Expressed in the Human Placenta". Thrombosis and Haemostasis 69, nr 02 (1993): 119–23. http://dx.doi.org/10.1055/s-0038-1651566.

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SummaryProtease nexin 1 (PN1), a serine protease inhibitor that inactivates thrombin, urokinase, and plasmin, is produced abundantly in cultures of human fibroblasts and rat and human glioma cells. The major sites of PN1 synthesis in vivo and the specific physiological function(s) of this serpin are unknown. Using Northern blot analysis and a full-length PN1 cDNA probe we demonstrated the presence of PN1 mRNA in human term placentas. In situ hybridization of placental tissue with a PN1 riboprobe showed that PN1 mRNA is present throughout the placenta and is also abundant in the placental membranes. Immunohistochemical analysis with an anti-PN1 antibody showed co-localization of PN1 and its mRNA within the placenta.

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Vaswani, Kanchan, Hsiu-Wen Chan, Hassendrini N. Peiris, Marloes Dekker Nitert, Ryan J. Wood Bradley, James A. Armitage, Gregory E. Rice i Murray D. Mitchell. "Gestation Related Gene Expression of the Endocannabinoid Pathway in Rat Placenta". Mediators of Inflammation 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/850471.

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Mammalian placentation is a vital facet of the development of a healthy and viable offspring. Throughout gestation the placenta changes to accommodate, provide for, and meet the demands of a growing fetus. Gestational gene expression is a crucial part of placenta development. The endocannabinoid pathway is activated in the placenta and decidual tissues throughout pregnancy and aberrant endocannabinoid signaling during the period of placental development has been associated with pregnancy disorders. In this study, the gene expression of eight endocannabinoid system enzymes was investigated throughout gestation. Rat placentae were obtained at E14.25, E15.25, E17.25, and E20, RNA was extracted, and microarray was performed. Gene expression of enzymesFaah, Mgll, Plcd4, Pld1, Nat1, Daglα, andPtgs2was studied (cohort 1, microarray). Biological replication of the results was performed by qPCR (cohort 2). Four genes showed differential expression (Mgll, Plcd4, Ptgs2, and Pld1), from mid to late gestation. Genes positively associated with gestational age werePtgs2, Mgll, and Pld1, whilePlcd4was downregulated. This is the first comprehensive study that has investigated endocannabinoid pathway gene expression during rat pregnancy. This study provides the framework for future studies that investigate the role of endocannabinoid system during pregnancy.

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Sobočan, Nikola, Marta Himelreich-Perić, Ana Katušić-Bojanac, Jure Krasić, Nino Sinčić, Željka Majić, Gordana Jurić-Lekić i in. "Extended Prophylactic Effect of N-tert-Butyl-α-phenylnitron against Oxidative/Nitrosative Damage Caused by the DNA-Hypomethylating Drug 5-Azacytidine in the Rat Placenta". International Journal of Molecular Sciences 23, nr 2 (6.01.2022): 603. http://dx.doi.org/10.3390/ijms23020603.

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Antioxidant N-tert-Butyl-α-phenylnitron (PBN) partly protected embryos from the negative effects of a DNA demethylating drug 5-azacytidine during pregnancy. Our aim was to investigate PBN’s impact on the placenta. Fischer rat dams were treated on gestation days (GD) 12 and 13 by PBN (40 mg/kg), followed by 5azaC (5 mg/kg) after one hour. Global methylation was assessed by pyrosequencing. Numerical density was calculated from immunohistochemical expression in single cells for proliferating (PCNA), oxidative (oxoguanosine) and nitrosative (nitrotyrosine) activity. Results were compared with the PBN-treated and control rats. PBN-pretreatment significantly increased placental weight at GD15 and GD20, diminished by 5azaC, and diminished apoptosis in GD 20 placentas caused by 5azaC. Oxoguanosine expression in placentas of 5azaC-treated dams was especially high in the placental labyrinth on GD 15, while PBN-pretreatment lowered its expression on GD 15 and GD 20 in both the labyrinth and basal layer. 5azaC enhanced nitrotyrosine level in the labyrinth of both gestational stages, while PBN-pretreatment lowered it. We conclude that PBN exerted its prophylactic activity against DNA hypomethylating agent 5azaC in the placenta through free radical scavenging, especially in the labyrinthine part of the placenta until the last day of pregnancy.

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Rozprawy doktorskie na temat "Rat placenta"

Robinson, N. R. "Calcium transfer across the rat placenta". Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234186.

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Freitas, Murilo Rodrigues Barbosa de. "O efeito do selênio em ratas Wistar prenhas infectadas pela cepa Y de Trypanosoma cruzi". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-31102014-102620/.

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O selênio (Se) é um micronutriente importante na dieta de mamíferos e tem sido descrito com importante papel na função imune. É constituinte de mais de 25 selenoproteínas na forma do aminoácido selenocisteína, sendo este elemento crítico na manutenção do sistema de defesa antioxidante. Uma dieta complementar com Se pode ser benéfica no tratamento de doenças correlacionadas com altos níveis de estresse oxidativo, como a doença de Chagas, enfermidade negligenciada causada por Trypanosoma cruzi. O objetivo deste estudo foi avaliar os efeitos do Se em ratas Wistar prenhas infectadas pela cepa Y de T. cruzi. O tratamento com Se desencadeou aumento no peso e comprimento fetal, bem como no diâmetro e peso placentário. Também foi observada diminuição da parasitemia. Não ocorreram alterações significativas nas concentrações de NO e no número de ninhos de amastigotas no coração. A avaliação histológica das placentas mostrou elevado número de ninhos de amastigotas nos animais do grupo infectado e tratado. A redução da concentração de citocinas pró-inflamatórias e de populações de células T desencadeou uma resposta voltada ao padrão Th-2, característico da gestação, fato que provavelmente contribuiu no aumento do parasitismo placentário encontrado nos animais tratados com Se. Assim, é possível que a administração de Se, durante a prenhez, poderia alterar a resposta imune placentária local, favorecendo a instalação do parasita. Mais estudos são necessários para avaliar a interação entre o Se e a doença de Chagas durante a prenhez.
The selenium (Se) is an essential micronutrient in the diet ofmammals and has an important role in the immune function. A range of 25 selenoproteinshas Sein its structure and most of them in the form of amino acid selenocysteine, being this element involved in the in maintenance of the antioxidant defense. Diet with Se is beneficial in the treatment of diseases correlated with high levels of oxidative stress, like Chagas\' disease, a neglected illness caused by Trypanosoma cruzi. The objective of this study was to evaluate the effects of selenium in the immune response of pregnant Wistar rats infected withtheY strain of T. cruzi. Se treatment triggered enhanced fetal weight and length and placental diameter and weight. It was observed decreased parasitemia. No significant alterations in NO concentrations and amastigote nests in heart were observed. The histological evaluation of placenta displayed an enhanced number of amastigote nests in infected and Se treated animals. The reduction of pro-inflammatory cytokines and T cell populations triggered a Th-2 immune response, which is the hallmark of the gestation period. This fact probably led to the raise in parasite nests in placenta of infected and Se treated animals. So it is possible that the Se supplementation during pregnancy could impair the local placental immune response. Further studies are needed to assess the interaction between selenium and the acute Chagas\' disease during pregnancy.

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Taylor, Louise. "Comparative analyses of ABC transporters and metabolising enzymes in human and rat placental models". Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/comparative-analyses-of-abc-transporters-and-metabolising-enzymes-in-human-and-rat-placental-models(3daff296-0364-4e4b-89f8-337dac6dbf10).html.

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The placenta provides a protective barrier for the developing foetus during gestation. Physiological barriers including the placenta, liver, kidney, intestine and blood-brain barrier are known to express ATP-Binding cassette transporters (ABC transporters) and metabolising enzymes. These specialised proteins have the ability to transport or metabolise xenobiotics. There is evidence to suggest that ABC transporters and metabolising enzymes are located at the interface between the maternal and foetal blood supplies (a cell layer referred to as the syncytiotrophoblast) and therefore may help protect the foetus from harmful xenobiotics. During new compound development prenatal developmental toxicity testing forms an important part of safety assessment. In order to predict potential toxicity of a new chemical entity to humans, rodent and non-rodent species are currently used. This thesis investigates the rat and human placental barrier properties in order to help facilitate our knowledge of species differences and contribute to our understanding of the limitations of these surrogate models. The approaches taken include: genomic analyses using microarray data to compare the overall expression of ABC transporters and metabolising enzymes throughout gestation in both species, immunohistochemical techniques to localise transporters and metabolising enzymes in the rat placenta, and in vitro functionality assays of selected transporters performed in rat and human placental cell line models. The main findings have shown a similar mRNA expression level of ABCG2/BCRP (breast cancer resistance protein) throughout gestation in the rat and human, however different mRNA expression levels of other transporters (slco4a1/oatp4a1 in particular) and metabolising enzymes were also highlighted. Immunohistochemistry localised selected transporters to the syncytiotrophoblast region of the rat placenta (the interface of maternal and foetal circulations). Functional in vitro assays were successfully utilised in rat and human placental cell lines which showed functional ABCB1/P-gp in both species. Overall, these findings provide a genomic characterisation of the rat and human protective placental barrier properties and show transporter functionality in in vitro cell-based assays which will prove useful in prenatal and developmental toxicity tests. Alternatives to using animals have been explored by using functional in vitro assays which could potentially be implored during the new compound discovery phase. This could help to make animal testing more selective for given compounds and ensures the new chemical entity is being tested in the model closest resembling the human.

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Carter, Wayne Grant. "Site specificity and purification of an insulin receptor associated serine kinase from human placenta and rat liver". Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295913.

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Cisse, Ouma. "Conséquences transgénérationnelles d'une programmation fœtale par dénutrition maternelle et d'un régime hyperlipidique chez le rat : focus sur le placenta". Phd thesis, Université du Droit et de la Santé - Lille II, 2013. http://tel.archives-ouvertes.fr/tel-01064268.

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Le concept de DOHaD (Developmental Origins of Health and Disease) qui découle de la théorie de Barker, replace l'origine des maladies métaboliques de l'adulte au moment du développement fœtal et/ou périnatal. De nombreuses données épidémiologiques indiquent qu'une dysnutrition maternelle (dénutrition, surnutrition) a des répercussions sur la croissance fœtale qui se traduisent par une anomalie du poids à la naissance (retard de croissance intra utérin : RCIU / gros poids de naissance : Macrosomie) et prédisposent l'individu au développement des maladies métaboliques. Afin de mieux comprendre les mécanismes susceptibles de transmettre de génération en génération cette vulnérabilité métabolique, nous avons développé un modèle transgénérationnel chez le rat associant la programmation fœtale chez la F0 par dénutrition maternelle (modèle FR30) et une dysnutrition chez la F1 avec un régime alimentaire hyperlipidique.Nos résultats montrent qu'une restriction alimentaire de 70% durant toute la grossesse (modèle FR30) contribue à une sensibilité accrue chez la descendance F1 femelle au développement de traits de syndrome métabolique. Les femelles F1 issues de mères dénutries présentent à l'âge adulte une intolérance au glucose et une hyperleptinémie. Les femelles de la F1 soumises à un régime hyperlipidique " high fat " (HF) ne présentent pas d'obésité que ce soit celles issues de mères contrôle que de mères dénutries. La faible appétence du régime, et la carence en hydrates de carbone qui l'accompagnent ne permettent pas le développement de l'obésité. En revanche, ce régime accentue les perturbations métaboliques chez des animaux sensibilisés par la programmation.Lorsque les femelles F1 sont mises en reproduction, on observe qu'en réponse à la programmation fœtale (FR) et/ou au régime alimentaire (Standard ou HF) la trajectoire de croissance dans la descendance F2 conduit à des phénotypes différents à la naissance. Les nouveau-nés de mères F1 issues de mères C ou FR et ayant suivi un régime HF en prégestation et en gestation (C HF-HF et FR HF-HF) ont un RCIU. A l'inverse, les nouveau-nés issus de mères F1 issues de mères dénutries et ayant eu un régime HF en prégestation puis un régime standard durant la gestation (FR HF-S) ont une macrosomie. Les perturbations métaboliques et hormonales des mères F1 ne pouvant expliquer à elles seules la survenue de ces phénotypes, nous nous sommes intéressés à l'organe situé à l'interface entre les compartiments maternels et fœtaux permettant le dialogue entre la mère et le fœtus : le placenta.L'analyse morphologique et moléculaire du placenta nous indique que cet organe est non seulement sensible aux modifications métaboliques de la mère, mais s'adapte à la demande du fœtus. On observe de fortes variations géniques qui se traduisent par une surexpression ou sous expressions géniques selon le phénotype observé RCIU ou macrosomie. Il est important de noter que les variations présentent un dimorphisme sexuel. Nos travaux suggèrent donc que les phénotypes de RCIU ou macrosomie sont le résultat d'anomalies métaboliques et hormonales maternelles mais également de l'adaptation génique placentaire sexe-spécifique.

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Cisse, Ouma. "Conséquences transgénérationnelles d’une programmation fœtale par dénutrition maternelle et d’un régime hyperlipidique chez le rat : focus sur le placenta". Thesis, Lille 2, 2013. http://www.theses.fr/2013LIL2S005/document.

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Le concept de DOHaD (Developmental Origins of Health and Disease) qui découle de la théorie de Barker, replace l’origine des maladies métaboliques de l’adulte au moment du développement fœtal et/ou périnatal. De nombreuses données épidémiologiques indiquent qu’une dysnutrition maternelle (dénutrition, surnutrition) a des répercussions sur la croissance fœtale qui se traduisent par une anomalie du poids à la naissance (retard de croissance intra utérin : RCIU / gros poids de naissance : Macrosomie) et prédisposent l’individu au développement des maladies métaboliques. Afin de mieux comprendre les mécanismes susceptibles de transmettre de génération en génération cette vulnérabilité métabolique, nous avons développé un modèle transgénérationnel chez le rat associant la programmation fœtale chez la F0 par dénutrition maternelle (modèle FR30) et une dysnutrition chez la F1 avec un régime alimentaire hyperlipidique.Nos résultats montrent qu’une restriction alimentaire de 70% durant toute la grossesse (modèle FR30) contribue à une sensibilité accrue chez la descendance F1 femelle au développement de traits de syndrome métabolique. Les femelles F1 issues de mères dénutries présentent à l’âge adulte une intolérance au glucose et une hyperleptinémie. Les femelles de la F1 soumises à un régime hyperlipidique « high fat » (HF) ne présentent pas d’obésité que ce soit celles issues de mères contrôle que de mères dénutries. La faible appétence du régime, et la carence en hydrates de carbone qui l’accompagnent ne permettent pas le développement de l’obésité. En revanche, ce régime accentue les perturbations métaboliques chez des animaux sensibilisés par la programmation.Lorsque les femelles F1 sont mises en reproduction, on observe qu’en réponse à la programmation fœtale (FR) et/ou au régime alimentaire (Standard ou HF) la trajectoire de croissance dans la descendance F2 conduit à des phénotypes différents à la naissance. Les nouveau-nés de mères F1 issues de mères C ou FR et ayant suivi un régime HF en prégestation et en gestation (C HF-HF et FR HF-HF) ont un RCIU. A l’inverse, les nouveau-nés issus de mères F1 issues de mères dénutries et ayant eu un régime HF en prégestation puis un régime standard durant la gestation (FR HF-S) ont une macrosomie. Les perturbations métaboliques et hormonales des mères F1 ne pouvant expliquer à elles seules la survenue de ces phénotypes, nous nous sommes intéressés à l’organe situé à l’interface entre les compartiments maternels et fœtaux permettant le dialogue entre la mère et le fœtus : le placenta.L’analyse morphologique et moléculaire du placenta nous indique que cet organe est non seulement sensible aux modifications métaboliques de la mère, mais s’adapte à la demande du fœtus. On observe de fortes variations géniques qui se traduisent par une surexpression ou sous expressions géniques selon le phénotype observé RCIU ou macrosomie. Il est important de noter que les variations présentent un dimorphisme sexuel. Nos travaux suggèrent donc que les phénotypes de RCIU ou macrosomie sont le résultat d’anomalies métaboliques et hormonales maternelles mais également de l’adaptation génique placentaire sexe-spécifique
The concept of DOHaD (Developmental Origins of Health and Disease) which derives from the theory of Barker, replace the origin of metabolic diseases in adults during fetal development and / or perinatal period. Many epidemiological data indicate that maternal dysnutrition (undernutrition, overnutrition) affects fetal growth showing abnormal birth weight (intrauterine growth retardation : IUGR / large birth weight macrosomia) and predispose individuals to development of metabolic diseases. To better understand the mechanisms invovle in transmission of the metabolic vulnerability from one generation to another, we have developed a model combining transgenerational rat fetal programming in the F0 by maternal undernutrition (model FR30) and dysnutrition in F1 with an hyperlipidic diet.Our results show that dietary restriction of 70% throughout pregnancy (FR30 model) contributes to emphasize development of metabolic syndrome traits into female F1 progeny. F1 females from undernourished mothers have an adult glucose intolerance and hyperleptinemia. These metabolic disturbances will be increase by a high fat diet (HF) but will not lead to obesity in female F1 regardless of the mother (F0) diet/statut. This can be explain by the low palatability of the diet, and the lack of carbohydrates largely involve in the development of obesity. These F1 phenoypes conduce to different F2 phenotypes at birth depending of fetal growth trajectory.Newborns from F1 mothers C or FR with HF diet during pregestation and gestation (C HF-HF and FR HF-HF) present IUGR. In contrast, infants born from F1 undernourished mothers with HF diet during pregestation following by standard diet during pregnancy (FR HF-S) show macrosomia. Like metabolic and hormonal disturbances into F1 mothers can not explain themselves the occurrence of these phenotypes, we studied the organ at the interface between maternal and fetal compartments in charge of the crosstalk between mother and fetus : the placenta. Morphological and molecular analysis indicate that placenta is not only sensitive to metabolic changes in the mother, but also able to adapt to the fetus needs. We observe strong correlation between gene expression (decrease or increase) and phenotype (IUGR/macrosomia) with gender specificity.Our work therefore suggests that IUGR or macrosomia phenotypes are not only depending on maternal hormonal and metabolic abnormalities but also in the sex-specific placental gene response to these exposure

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Hering, Lydia. "Die Bedeutung des Renin-Angiotensin-Systems im Tiermodell für Präeklampsie". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16550.

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Das Renin-Angiotensin-System ist nachweislich in die Entwicklung der schwangerschaftsspezifischen Erkrankung Präeklampsie involviert. Ziel der Arbeit ist die Charakterisierung der Effekte des zirkulierenden sowie uteroplazentaren Renin-Angiotensin-Systems im Rattenmodell. Wurden weibliche Ratten, transgen für humanes Angiotensinogen, mit männlichen Ratten, transgen für humanes Renin verpaart, so entwickelten sie während der Schwangerschaft Bluthochdruck und Proteinurie, während die umgekehrte Kreuzung diese Hauptsymptome der Präeklampsie nicht zeigte. Weiterhin wurde mit einer Kontrollgruppe sowie einer Angiotensin II behandelten Gruppe gearbeitet. Chronisch, systemische Angiotensin II Infusion (1000 ng/kg/min) erhöhte zirkulierendes Angiotensin II während in der umgekehrten, Präeklampsie-negativen Kreuzung uteroplazentares Angiotensin II erhöht war. In der Präeklampsie-positiven Gruppe war Angiotensin II zirkulär und uteroplazentar erhöht. Bluthochdruck und Albuminurie waren alleinig in den Tiermodellen mit erhöhtem zirkulierendem Angiotensin II nachweisbar. In der Kontrollgruppe kam es während der Schwangerschaft zu einer physiologischen Herzhypertrophie, während in der Präeklampsie-positiven Gruppe Anzeichen einer pathologischen Herzhypertrophie nachweisbar waren. Weiterhin unterstützte uteroplazentares Angiotensin II die tiefe Invasion von Trophoblasten in plazentafernen Spiralarterien, während zirkulierendes Angiotensin II die Trophoblasteninvasion im gesamten mesometrialen Dreieck diffus förderte. In Zellkulturexperimenten konnte gezeigt werden, dass Angiotensin II die Mobilität und die Invasion einer Trophoblastenzelllinie förderte. Ebenso erhöhte Angiotensin II die Migration von Trophoblasten in Plazentakulturen. Diese Ergebnisse verdeutlichen den unterschiedlichen Einfluss des zirkulierenden und uteroplazentaren Renin-Angiotensin-Systems auf die Schwangerschaft und tragen damit zum Verständnis pathologischer Prozesse bei, die zu Präeklampsie führen.
Dysregulation of the renin-angiotensin-system is important in preeclampsia, a pregnancy specific disorder, characterized by high blood pressure and albuminuria. Aim of this study is to characterize the effects of circulation and uteroplacental renin-angiotensin-system during pregnancy in a rat model. Female rats transgenic for the human angiotensinogen gene crossed with males transgenic for the human renin gene develop preeclampsia, whereas those of the opposite cross do not. We used this model to study the role of angiotensin II in trophoblast invasion, which is shallow in human preeclampsia but deeper in this model. We investigated the following groups: preeclampsia rats, opposite-cross rats, angiotensin II–infused rats and control rats. Angiotensin II infusion increased only circulating angiotensin II levels, opposite cross influenced only uteroplacental angiotensin II and preeclampsia rats showed increased circulating and uteroplacental angiotensin II. Blood pressure and albuminuria occurred in the models with high circulating angiotensin II but not in other models. Control rats showed physiological heart hypertrophy during pregnancy whereas pathological heart hypertrophy occurred in preeclampsia rats. High uteroplacental angiotensin II influenced deep trophoblast invasion in distant spiral arteries whilst the effect of circulating angiotensin II was more diffuse. We then studied human trophoblast cell line and villous explants derived from first-trimester pregnancy. Local angiotensin II dose-dependently increased migration, invasion and motility. The data suggest that angiotensin II stimulates trophoblast invasion in vivo in the rat and in vitro in human cells, a hitherto fore unrecognized function.

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Chartrel, Nicolas. "Identification de quelques facteurs impliqués dans l'induction de l'hypotrophie foetale chez la rate rendue expérimentalement diabétique". Rouen, 1989. http://www.theses.fr/1989ROUES016.

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Etude réalisée pendant la gestation chez la rate rendue diabétique par injection de streptozotocine, dans le but d'identifier quelques facteurs impliqués dans le développement de l'hypotrophie foetale: sont évalués le rôle des perturbations hémodynamiques utéroplacentaires, et l'hypertonie du myomètre, avec les facteurs neuro-endocriniens impliqués dans ces modifications

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Nash, Peppi. "Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7717.

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Impaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of pre-eclampsia (PE). It has recently been pointed out that PE might be more than one disease and may have several different pathogeneses. This thesis describes a new animal model for PE and examines the role of oxidative stress in early respective late onset PE.

The effects of Suramin injections on day 10 and 11 of pregnancy were investigated in normal and diabetic rats of two strains (U and H), with or without additional vitamin E treatment. Suramin caused placental dysfunction in both rat strains: foetal growth restriction, increased resorption rate, reduced placental blood flow, and decreased maternal blood volume in the placenta. In the U strain Suramin also caused maternal hypertension and reduced renal blood flow. Oxidative stress in the Suramin treated rats was indicated by increased levels of isoprostane 8-iso-PGF_2α in the placenta. Antioxidative treatment with vitamin E partly protected against the effects of Suramin. Streptozotocin-induced diabetes seemed to cause similar placental effects as Suramin, and in the diabetic rats the additional effects of Suramin were only moderate. In conclusion, Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction (U and H rats) and PE (U rats).

Oxidative stress was estimated in women with early onset (≤ 32 weeks) or late onset (≥ 35 weeks) PE, in normotensive pregnant women of respective gestational length, and in healthy non-pregnant women. The ratio of PAI-1/PAI-2 was measured in serum, and the amount of isoprostane 8-iso-PGF_2α was measured in placenta, serum, and urine. The ratio of PAI-1/PAI-2 and placental isoprostane levels were higher in women with early onset PE compared with all other groups. Serum levels of isoprostane were similar between groups. Urinary levels of isoprostane were similar in all pregnant women, but lower in non-pregnant women. These data indicate that pregnancy increases general oxidative stress, and that early onset, but not late onset PE, causes increased oxidative stress also in placental tissue. The pathogeneses of early and late onset PE are, therefore, not likely to be identical.

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Lippi, Luciana Lucinio. "Estudo da toxicidade da Ipomoea carnea em ratas durante o período perinatal. Avaliação dos possíveis efeitos lesivos no tecido placentário". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-17122009-173640/.

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A Ipomoea carnea é uma planta tóxica amplamente distribuída no Brasil e em outros países tropicais. Durante os períodos de seca esta planta se mantém verde, podendo servir como fonte de alimento para os animais de produção. A intoxicação natural é de caráter crônico e ocorre quando ruminantes particularmente, caprinos ingerem a planta, estes animais desenvolvem, principalmente, sintomatologia de origem nervosa. Dois tipos de princípios ativos tóxicos foram isolados desta planta, um alcalóide nortropânico, as calisteginas B1, B2, B3 e C1 e principalmente o alcalóide indolizidínico, a suainsonina, cujo mecanismo de ação tóxico se estabelece por inibição de duas enzimas a α-manosidase lisossomal, levando ao acúmulo de oligossacarídeos não metabolizados no interior de lisossomos, promovendo a degeneração vacuolar intracitoplasmática, perda de função e até mesmo morte celular e a manosidase II do Complexo de Golgi, causando alterações na síntese, no processamento e no transporte de glicoproteínas. Histologicamente esta intoxicação é caracterizada pela presença de vacúolos lisossomais no sistema nervoso central (SNC), tireóide, fígado, pâncreas e rins. Recentemente, pesquisas, relativas à toxicidade perinatal desta planta, vêm mostrando que a Ipomoea carnea possui efeitos teratogênicos, em ratos, caprinos e coelhos, porém até o momento não se sabe se a placenta poderia estar envolvida na gênese desta patologia ou se os efeitos deletérios no feto seriam devidos diretamente à passagem transplacentária do princípio ativo tóxico. Portanto o principal objetivo desta pesquisa foi verificar o possível efeito placentotóxico da planta. Assim, o resíduo aquoso final da planta (RAF) foi administrado, via oral, por gavage para ratas Wistar gestantes, nas doses de 1,0; 3,0 e 7,0 g/kg no período do 6º ao 19º dias de gestação, já os animais do grupo controle e peer-feeding, receberam apenas água pela mesma via e período que os animais tratados. Durante o período de tratamento estes animais foram inspecionados diariamente e o consumo de água e ração, bem como o ganho de peso mensurados à cada 3 dias. No final da gestação parte dos animais foram, destinados a secção cesariana, para principalmente avaliação do tecido placentário e os outros animais seguiram a gestação até o nascimento a termo para análise das proles. Dos animais provenientes da secção cesariana, foram coletados os fetos e suas respectivas placentas, sendo estas encaminhadas para análise anatomopatológica, histoquímica (lectinas e TUNEL) e morfométrica, assim como os fetos mensurados quanto ao seu tamanho e peso e avaliados para malformações externas e análise óssea e visceral e realizado o desempenho reprodutivo destas fêmeas. As gestantes que seguiram até o nascimento de suas prole, as quais foram avaliadas quanto ao seu desenvolvimento físico e reflexológico diariamente e nos dias 4, 8, 15 e 22 de lactação, um filhote de cada mãe foi eutanasiado para coleta de fragmentos representativos do fígado, rim, SNC e pâncreas para avaliação histopatológica, este procedimento também foi realizado naquelas mães submetidas a secção cesariana no 20º dia de gestação, bem como nas mães lactantes no 22º dia de lactação. Os resultados obtidos evidenciam claramente o potencial teratogênico produzido pela Ipomoea carnea, visto que tanto os fetos quanto os filhotes apresentaram algumas anomalias congênitas, diminuição do peso ao nascimento e também o retardo na geotaxia negativa. No fígado e nos rins das mães e dos filhotes foi observada a degeneração vacuolar, evidenciando a toxicidade materna e fetal promovida pela planta expostos durante o período gestacional. Um dado importante aqui observado se refere à avaliação do tecido placentário, o qual apresentou algumas alterações histopatológicas, como o espessamento da zona de labirinto e a redução de espessura da zona juncional, porém a degeneração vacuolar não fora observada neste órgão, porém quando realizada a técnica de lectina-histoquímica, foi possível observar o acúmulo de alguns açúcares nas células em diversas regiões da placenta, evidenciando desta forma que este tecido também sofreu injúria promovida pela ação da planta, não sendo mais possível considerar este órgão apenas como um local de passagem para estes princípios ativos tóxicos.
Ipomoea carnea is a toxic plant widely distributed in Brazil and other tropical countries. During periods of drought, animals graze on this plant which grows even in the presence of adverse climatic conditions. After prolonged periods of plant intake, the animals exhibit a variety of clinical signs as depression, general weakness, body weight loss, staggering gait, muscle tremors, ataxia, posterior paresis, and paralysis. Two kinds of toxic principles were isolated from the plant, the nortropane alkaloids calystegines B1, B2, B3 and C1 and mainly the indolizidine alkaloid swainsonine. The latter alkaloid is a potent inhibitor of two distinct intracellular enzymes, the lysosomal α-mannosidase which results in lysosomal accumulation of incompletely processed oligosaccharides moieties inside vacuoles, which progresses to cellular function loss and, ultimately, to cell death and the Golgi mannosidase II enzyme causes alteration of the N-linked glycoprotein process, modifying the glycoprotein synthesis, processing and carrier. Histologically, cellular vacuolization of Purkinje cells, thyroid follicles, exocrine pancreas, liver and kidney cells have been observed. Recently, many studies in our laboratory have shown that Ipomoea carnea have teratogenic effects in rats, goats and rabbits. However, it is not known yet if the alterations observed in the fetuses are due to alterations in the placenta or if they can be directly related to the transplacental transfer of the active principle. The present study was performed to evaluate the effects of Ipomoea carnea in the placental tissue and in the litter of female rats treated during. Pregnant rats of the experimental groups were treated orally by gavage, once a day from GD6 to GD19, with 1,0; 3,0; 7,0 g/kg of Ipomoea carnea AF. The control and peer-feeding group received tap water by gavage. Total body weight gain, water and food consumption were measured each three days during the experimental period. At the end of pregnancy period some animals were, for cesarean section, mainly for evaluation of placental tissue and the other animals followed the pregnancy until the birth to the term analysis of offspring. From the animals that came from the cesarean section, were collected the fetuses and their placental, those being collected for anatomopathological, histochemistry (lectins and TUNEL) and morphometric analysis, as the fetuses measured about their sizes and weight and assessed to external malformation and bone and visceral analysis and performed the reproductive performance of those females. The pregnants that followed up to the birth of their offspring, which were assessed regarding their physical and reflexology development daily and at days 4, 8, 15 e 22 of lactation, an offspring of each mother was euthanized so representatives fragments of the liver, kidney, SNC and pancreas could be collected for a histopathological assessment, this procedure was also performed at those mothers submitted to the cesarean section at the 20th pregnancy day, as well as at the breastfeeding at the 22nd lactation day. The obtained results clearly show the teratogenic potential produced by the Ipomoea carnea, because both the fetuses as the pups had some congenital anomalies, decrease in birth weight and the delayed negative geotaxis. At both the mother and offsprings liver and kidneys was observed a vacuolar degeneration, showing the maternal and fetal toxicity promoted by the plant exposed during the pregnancy period. An important data noted here refers to the placental tissue assessment, which showed some histopathological alterations, as the labirinth zone thickening and the reduction of the junctional zone thickness, however the vacuolar degeneration was not observed in this organ, although when performed the lectin-histochemistry technique, it was possible to observe the accumulation of some sugars in some cells located at several regions of the placenta, this way showing that this tissue has also suffered some injury promoted by the plant action, not being possible anymore to consider this organs just as a plac of passage for these toxic active principle.

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Książki na temat "Rat placenta"

Husain, Shahid Masud. Tr ansport of calcium and magnesium across the placenta of the diabetic rat. Manchester: University of Manchester, 1996.

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Hudson, Lionel. The Rats of Rangoon: The inside story of the 'fiasco' that took placeat the end of the war in Burma. London: Arrow Bks., 1989.

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Rizzuto, Gabrielle A., i Anna I. Bakardjiev. Listeria monocytogenes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0020.

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Listeria monocytogenes is a intracellular bacterial pathogen that causes serious foodborne illness in humans. Among all infectious diseases caused by gastrointestinal pathogens, listeriosis has the highest mortality rate, likely because of its ability to cross the gastrointestinal barrier and cause sepsis and infection of other organs such as the brain and placenta. Infection of the placenta leads to fetal infection, and otherwise healthy pregnant women have a significantly increased incidence of listeriosis than the general population, likely due to changes in the maternal cell-mediated immune response during pregnancy. Clinical manifestations include miscarriage, stillbirth, preterm labor, and neonatal infection and death. Neonates develop early-onset sepsis or late-onset meningitis. Physicians must evaluate pregnant women and neonates with febrile illnesses for listeriosis, since prompt treatment with antibiotics can cure it. It is important to note that L. monocytogenes is resistant to cephalosporins. Ampicillin is the treatment of choice in patients without penicillin allergy.

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Koo, Paul. The regulation of placental glutathione S-transferase (GST-P or -7-7) expression in rat liver in relation to chemical hepatocarcinogenesis. 1992.

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Części książek na temat "Rat placenta"

Ogle, T. F., T. M. Nosek i T. M. Mills. "Action of Progesterone and RU38486 on Protein Synthesis in Rat Placenta". W Advances in Experimental Medicine and Biology, 689–92. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5395-9_43.

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Gambling, L., W. Bruce-Johnson, R. G. Lea, M. J. Bingham i H. J. McArdle. "Ceruloplasmin Oxidase Expression in the Rowett Hooded rat and Human Placenta During Pregnancy". W Trace Elements in Man and Animals 10, 383–84. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_119.

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Miatello, R. M., M. C. Lama, E. S. González i H. L. Nolly. "Kallikrein-Like Activity in Nonpregnant and Pregnant Rat Uterus, Fetal Membranes, Placenta and Amniotic Fluid". W Recent Progress on Kinins, 106–13. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7321-5_14.

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Wang, Shoou-Lih, Mohan K. Raizada i Kathleen T. Shiverick. "Alteration of Insulin Receptor Binding and Protein Kinase Activity in Rat Liver and Placenta by ß-Naphthoflavone". W Insulin, Insulin-like Growth Factors, and Their Receptors in the Central Nervous System, 93–106. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5380-5_7.

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Masuda, Ryuichi, Michihiro C. Yoshida i Motomichi Sasaki. "Chromosomal Mapping of the Placental Glutathione S-Transferase Gene and Its Expression in Livers of LEC Rats". W The LEC Rat, 341–48. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68153-3_37.

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Meyer, R. K. "Enzymes in the Placentoma of the Rat". W Ciba Foundation Symposium - Steroid Hormones and Enzymes (Book II of Colloquia on Endocrinology, Vol. 1), 266–70. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718742.ch7.

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Duckworth, Mary Lynn, May C. Robertson, Ingo C. Schroedter, Claude Szpirer i Henry G. Friesen. "Molecular Genetics and Biology of the Rat Placental Prolactin Family". W Trophoblast Cells, 169–90. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4612-2718-2_12.

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Wierman, Margaret E., Wei Sun, Chun Wang, David F. Gordon i William W. Wood. "Control of Rat Gonadotropin Releasing Hormone Promoter Activity in Placental Cells". W Modes of Action of GnRH and GnRH Analogs, 106–15. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2916-2_7.

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Sato, Sanai, Susan Old, Deborah Carper i Peter F. Kador. "Purification and Characterization of Recombinant Human Placental and Rat Lens Aldose Reductases Expressed in Escherichia Coli". W Advances in Experimental Medicine and Biology, 259–68. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1965-2_32.

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Hazelhoff Roelfzema, W., A. M. Roelofsen, J. H. J. Copius Peereboom-Stegemann i R. F. M. Herber. "ZINC AND CADMIUM CONCENTRATIONS IN LIVER AND PLACENTAS OF RATS: ARE THEY INTERRELATED?" W Proceedings of the 4. International Workshop, Neuherberg, F. R. G., April 1986, redaktor Peter Brätter, 301–10. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783111692449-025.

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Streszczenia konferencji na temat "Rat placenta"

Novell, Anthony, Vanda Mendes, Arthuis Chloe, Ayache Bouakaz i Franck Perrotin. "Notice of Removal: Evaluation of utero-placental perfusion in intrauterine growth restriction rat model using CEUS". W 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8092965.

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Lukovnikova, L. V., L. A. Lelbiks i E. E. Lesiovskaya. "EFFECT OF NICKEL AND ITS INSOLUBLE INORGANIC COMPOUNDS ON REPRODUCTIVE FUNCTION OF WHITE RATS". W The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-326-329.

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Abstract. Introduction. The problem of women's health protection in enterprises producing and using nickel and its compounds is particularly relevant, since women make up a significant contingent of workers at some stages of production. Nickel and its compounds are used in the production of high-alloy steels, alloys with copper, chromium, aluminum, as a catalyst in the processes of hydrogenation of fats, in the production of batteries, nickel-plating of metal products. In case of violations of the technological process, labor protection conditions, workers may be exposed to nickel aerosol and its oxides. Purpose. To study the effect of nickel and its insoluble compounds on the reproductive function of white rats. Method of research. The studies were carried out on sexually mature female white rats weighing 180-200 g with a stable estrous cycle lasting 4-6 days. Experimental studies were conducted in accordance with national and international regulatory requirements ensuring humane treatment of animals used in experiments: Directive 2010/63/EU of the European Parliament and of the Council of the European Union of September 22, 2010 on the protection of animals used in scientific purposes, Order of the Ministry of Health of the Russian Federation of 01.04.2016 No. 199n «On approval of the Rules of good laboratory Practice». The industrial conditions for the action of aerosol of insoluble nickel compounds were simulated in a special chamber with an individual intake of aerosol into the breathing zone at a concentration of 0.2 mg / m3 daily for 4 hours during the entire gestation period. The animals were assessed for the dynamics of body weight on the 1st, 8th, 14th and 20th days of pregnancy. On the 20th day of pregnancy, the number of yellow bodies of pregnancy, placentas and fetuses was determined, pre-, post-implantation and total intrauterine death, average length and weight of fetuses, and average placenta weight were calculated. The total number of pregnant females and fetuses was recorded with the subsequent calculation of the number of fetuses per female. Results. The action of an aerosol of insoluble nickel compounds at a concentration of 0.2 mg / m3 in this mode did not lead to a violation of the reproductive function of white rats in all the studied parameters. Conclusion. The experimental data obtained indicate that insoluble nickel compounds at the level of the maximum permissible concentrations for the air of the working area will not pose a risk of developing reproductive health pathology in working women.

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Godal, H. C., F. Brosstad i B. Holm. "CONGENITAL HYPOFIBRINOGENEMIA, DEEP VEIN THROMBOSIS AND RECURRENT PLACENTAL ABRUPTION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644279.

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A patient with hypofibrinogenemia, deep vein thrombosis and recurrent placental abruption is reported. The persistently low plasma fibrinogen concentration strongly suggested that the condition was inherited, and this was supported by low fibrinogen levels and thrombosis tendency in the patient's brother. The exact nature of the condition is not known, but the close agreement between the clottable and immunologic fibrinogen -indicates the presence of a hyperfibrinogenemia sensu stricte rather than dysfibrinogenemia, and this was supported by uniformly negative tests to detect fibrinogen abnormalitied.Up to now, less than 50 cases of congenital hypofibrinogenemia have been reported. It is not entirely clear whether hypofibrinogenemia represents the heterozygous form of afibrinogenemia or whether itrepresents some sort- of dysfibrinogenemia with abnormal rate of biosynthesis but normal clotting and crosslinking functions. Four of the reported patients with hypofibrinogenemia had placental abruption, a complication which occursin less than of pregnancies. In addition, a relatively high proportion of patients withcongenital hypofibrinogenemiahad increased tendency to thrombosis. On this background it is tempting to speculate that the elevated fibrinogen during pregnancy serves other functions than to facilitate the formation of haemostatic plugs. Thus, during pregnancy and other socalled "acute phase" situations, minute amounts of fibrin may be generatedwithin the circulating blood. Since, moreover, the solvent for these fibrin molecules isfibrinogen, the possibility exists that hyperfibrinogenemia contributes to the prevention of thromboembolism by keeping trace amounts of fibrin in solution.

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Yadav, Sushma. "Unusual clinical presentation of chriocarcinoma in young patients – Neulological meatastasis". W 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685389.

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Introduction: Choriocarcinoma is a malignant trophoblastic tumor, usually of placenta and characterized by ‘early hematogenous spread’ to lungs. Choriocarcinoma of placenta is preceded by – H. Mole (50%), spontaneous abortion (20%), ectopic pregnancy (2%) and normal term pregnancy (20%-30%). It is chemosensitive tumor and even in metastatic lesion cure rate is 90%-95%. Most common site of metastasis is lung and vagina, vulva, kidney, liver, ovaries, brain and intestine. If tumor is not diagnosed and managed timely, because of its vascularity, it bleeds profusely leading to death. Cases: We encountered 2 rare cases, with age of 25 and 27 years respectively with choriocarcinoma with unusual clinical presentation. Both patients presented with neurological symptoms of brain metastasis and succumbed to death within a short span of time. In both cases histopathological report failed to detect chorio-carcinoma but b-HCG and radiological findings were suggestive of choriocarcinoma. Conclusion: If b–HCG level are unusually high with radiological findings, the patients should be considered for chemotherapy even if HPE is inconclusive. Without chemotherapy chorio-carcinoma has a rapid progression and mortality which can be prevented by early suspicion and timely management.

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Philips, M., A. G. Juul, S. Thorsen, J. Selmer i L. Thim. "PURIFICATION AND CHARACTERIZATION OF REACTIVE AND NON-REACTIVE PLASMINOGEN ACTIVATOR INHIBITOR-1 (PAI-1) FROM HUMAN PLACENTA". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642806.

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Reactive and non-reactive forms of PAI-1 have been identified in various biological materials. The structural differences between these forms remain to be determined.A monoclonal antibody specific for a non-reactive PAI-1 and a monoclonal antibody reacting with both the reactive and nonreactive form of the inhibitor were obtained by immunization with a tissue-type plasminogen activator (t-PA)-PAI-1 complex (Philips et al., Thromb Haemostas 1986; 55:213-7). These antibodies were used for the isolation of reactive and non-reactive PAI-1 by solid-phase immunoadsorption from extracts of human placenta. The inhibitor preparations were further purified by HPLC. Reactive and non-reactive PAI-1 both migrated with a Mr ∼ 52,000 when analyzed by SDS-PAGE. Furthermore, the two inhibitor forms were indistinguishable by N-terminal sequence analysis. Two N-terminal sequences were found in about equal ammounts for both the reactive and non-reactive PAI-1. They were Ser-Ala-Val-His-His-Pro-Pro- and a two residues shorter sequence (Val-His-His-Pro-Pro-). These sequences are in agreement with the published cDNA sequence of PAI-1 and shows that the inhibitor is N-terminally heterogeneously processed. The second order rate constant (ki) for the reaction between reactive PAI-1 and single-chain t-PA was about 6 106 M-1s-1. Treatment with 4 M guanidinium-HCl partially converted the non-reactive PAI-1 to a reactive form exhibiting a similar k1 for inhibition of single-chain t-PA. SDS-PAGE showed that the t-PA-PAI-1 complex could be dissociated by 1,5 M NH4OH/ 39 mM SDS resulting in the release of a PAI-1 with approximately the same Mr as native PAI-1. This indicates either that t-PA does not cleave the inhibitor or that it cleaves a peptide bond close to the C-terminus.In conclusion a non-reactive and a reactive form of PAI-1 can be purified from placenta. The two forms are distinguishable by monoclonal antibodies but they show similar Mr′ls and the same N-terminal sequences.

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Rayer, Debby Jacqueline Jochebed, i dan Jacklin Stella Salome Manoppo. "Production of Superior Pigs as Breeding Stocks by Improving Maternal Uterus and Placental Environment during Pregnancy". W Unima International Conference on Science and Technology 2022. Switzerland: Trans Tech Publications Ltd, 2023. http://dx.doi.org/10.4028/p-x30och.

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An experiment was conducted to study the inheritance of improved growth phenotypes in pigs born to sows injected with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (HCG) prior to mating. Twelve sows were assigned into a randomized design with 3 groups and each group consisted of 4 sows as replications. The first group consisted of sows without PMSG and HCG injection prior to mating as a control group (NSO). The second group consisted of sows injected with PMSG and HCG prior to mating to improve endogenous secretion of pregnant hormones that improve prenatal growth of the piglets (SO). The third group consisted of female pigs born to PMSG and HCG-injected mother in SO group that were mated after maturity without PMSG and HCG injection (F1SO). The number of sows used in each group consisted of 2 sows with 11 litter size and 2 sows with 12 litter size at parturition and total of born pigs observed in this study was 138 pigs. The results of experiment showed that injection of the sows with PMSG and HCG prior to mating improved body weight, body length and leg heights and decreased within-litter variation that finally increased total weight of live born pigs per sow. Sows injected with PMSG and HCG prior to mating produced pigs with higher pre-weaning growth rate and higher survival rate with a higher weaning weight and total weaned pigs per sow. The female pigs born to SO sows produced piglets with similar growth phenotypes as their mothers that was significantly higher and better that the growth phenotypes of the pigs born to NSO sows. The results of this experiment strongly confirm that the improvement of uterine and placental environment by improving endogenous secretion of pregnant hormones during pre-implantation and during the whole pregnancy by injecting the mothers with PMSG and HCG prior to mating improve prenatal and postnatal growth phenotypes of pigsand the improved growth phenotypes are inherited to their offspring. It was concluded that this simple and relatively cheap technique could be used to improve growth genotype expression to produce a superior pigs either as a finisher or as a parent stock.

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Bajaj, Kanika. "Poster Abstract". W 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685361.

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Tuberous sclerosis (TS) is a genetic disorder that is inherited in an autosomal dominant fashion with variable clinical manifestations including seizures, mental retardation, renal failure and pneumothorax. The literature on TS in pregnancy is largely based upon case reports which have shown a 43% complication rate including oligohydramnios, polyhydramnios, IUGR, hemorrhage from ruptured renal tumors, PPROM, renal failure, placental abruption and perinatal demise. We reporting a case of 33 yr old female with gravida 3 para 2 and live 2 with period of gestation 9 months with tuberous sclerosis, with severe oligohydramnios with fetal cardiomegaly and mild pericardial effusion and pleural effusion. She had facial angiofibromas along with bilateral renal angiomyolipomas. The previous fetal outcomes were normal, with facial angiofibroma. We report such a unique case having all clinically diagnostic physical sings of tuberous sclerosis with good fetal outcomes.

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Shipkova, L. N., N. V. Shipkov, S. V. Kalmanovich i A. K. Cherednichenko. "TOXOPLASMOSIS AMONG THE POPULATION OF THE KRASNODAR TERRITORY". W THEORY AND PRACTICE OF PARASITIC DISEASE CONTROL. All-Russian Scientific Research Institute for Fundamental and Applied Parasitology of Animals and Plant – a branch of the Federal State Budget Scientific Institution “Federal Scientific Centre VIEV”, 2023. http://dx.doi.org/10.31016/978-5-6048555-6-0.2023.24.544-548.

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The existing interest in the problem of toxoplasmosis is largely due to the fact that Toxoplasma gondii plays a significant role in human pathology. Toxoplasmas enter the human body in many ways: through the mouth when eating raw meat; with contaminated products, vegetables or fruits; with dirty hands, after contact with infected animals; through damaged skin, mucous membranes, when removing skins from infected animals or dividing carcasses; in medical procedures in patients with toxoplasmosis; and prenatally, from mother to fetus. Toxoplasmosis is more common in children, while adults may remain asymptomatic carriers of the pathogen. The reliability of invasion in humans is only established by the detection of toxoplasma in the blood, sputum, cerebrospinal fluid, puncture samples of lymph nodes, remnants of fetal membranes, placenta, etc. Therefore, the purpose of our study is to determine the occurrence of toxoplasmosis in the Krasnodar Territory for 5 years (2018–2022) and to identify organ systems that are affected most often. Toxoplasmosis is widespread in the Krasnodar Territory. This is due to climatic and geographical features. The study used data from outpatient medical records of people with diagnosed toxoplasmosis who seek medical advice in infectious diseases hospitals of the Krasnodar Territory.

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Cherkashova, Elvira, Veronika Burunova, Daria Namestnikova, Ilya Gubskiy, Tatiana Bukharova, Diasna Salikhova, Georgy Leonov i in. "THE EFFECTIVENESS AND DISTRIBUTION OF INTRAVENOUS TRANSPLANTATION OF MESENCHYMAL STEM CELLS DERIVED FROM HUMAN PLACENTA AND NEURAL PROGENITOR CELLS DERIVED FROM INDUCED PLURIPOTENT STEM CELLS IN RATS WITH FOCAL CEREBRAL ISCHEMIA". W XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2398.sudak.ns2021-17/417-418.

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"Gestational choriocarcinoma after term pregnancy: A case report". W 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685341.

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Choriocarcinoma coexisting with or after a “normal” pregnancy has an incidence of one per 1,60,000 pregnancies. In case of choriocarcinoma after term pregnancy, early diagnosis by histopathological examination of the placenta is very important, the precocity of the diagnosis influencing the prognosis and tumor response to chemotherapy. In, this paper we report the case of a 28-year-old woman parity 2 with metastatic choriocarcinoma after term pregnancy, diagnosed at four months after the delivery of a healthy baby. An episode of abundant vaginal bleeding occurred after four months from delivery. The local examination revealed a vaginal tumor whose pathological examination on biopsy sample was inconclusive. Subsequently, she was admitted in our hospital with abundant vaginal bleeding, severe anemia and fever. Abdominal ultrasonography revealed an intracavitary uterine tumoral mass with signe of myometrial invasion to the uterine serosa, strong Doppler signal and moderate ascites. Pulmonary X-Ray and computed tomography scan excluded extrapelvic tumoral masses. The pretreatment human chorionic gonadotropin (HCG) level was 310300 Miu/ml and her FIGO risk factor score was 8 (high–risk group). Total hysterectomy with bilateral salpingo-oophorectomy and omentectomy was performed as an optimal cytoreduction. Postoperative remaining presented by the metastasis located in the lower two-thirds of vagina. Histopatholgical examination revealed uterine choriocarcinoma. Postoperative was initiated four courses of polychemotherapy. Case evaluation was favorable, with the normalization of the Beta-HCG value in two months postoperative and complete remission of vaginal metastasis in six weeks posteoperative.

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Raporty organizacyjne na temat "Rat placenta"

Sophia Johnson, Sophia Johnson. Human placentophagy: What is the microbial composition of raw and processed placental tissue? Experiment, maj 2018. http://dx.doi.org/10.18258/11227.

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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska i Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, marzec 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.

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