Rozprawy doktorskie: „Rat placenta”

1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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Dunton, Anne. "The 'giant' yolk sac : an in vitro model for studying early placental transport". Thesis, University of Leicester, 1988. http://hdl.handle.net/2381/34333.

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In the rat, before the establishment of the chorioallantoic placenta, the nutritional requirements of the post-implantation embryo, are met solely by the visceral yolk sac and therefore a study of its structure and functions is essential to a full understanding of early embryonic nutrition. A method has been developed for maintaining the rat visceral yolk sac in organ culture over a prolonged period, having first removed the embryo by microsurgery at 9.5 days or alternatively allowing it to die within its own amnion. The yolk sac continues to grow as a closed vesicle, and can reach a diameter of 2cm. The system has been called the 'giant' yolk sac. The 'giant' yolk sac and in vivo yolk sac have been compared using various criteria. A detailed morphological study was made, including a quantitative analysis of the vacuolar compartment. The endocytic capacity of both systems was studied using three different substrates; those used were 125I-polyvinylpyrrolidone (PVP), a non-degradable macromolecule, taken up in the fluid phase and accumulated within the yolk sac tissue, 125I-bovine serum albumin (BSA) taken up by adsorptive pinocytosis and digested within the lysosomes and 125I-IgG (and colloidal gold-IgG) taken up with great efficiency by specific receptor mediated endocytosis. Also a preliminary study of 14C-amino acid uptake was made. In many instances the 'giant' yolk sac functioned very similarly to the in vivo yolk sac and therefore seems an ideal model for studying transport across an epithelial sheet. It is particularly useful as its continuous epithelium separates the exocoelom from the external culture medium. The fluid maintained within the exocoelom of the 'giant' yolk sac should be an excellent source of processed histiotroph essential for embryonic nutrition during organogenesis. Experiments carried out indicate that some of the trophic factors necessary for growth are present in this fluid.

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Cooper, Andrea Claire. "The renin angiotensin system in the human placenta throughout gestation". Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312204.

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Matos, Marcelo Alexandre de. "Efeitos do ciclamato de sódio na placenta de ratas: estudo morfométrico". Faculdade de Medicina de São José do Rio Preto, 2006. http://bdtd.famerp.br/handle/tede/8.

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Made available in DSpace on 2016-01-26T12:51:10Z (GMT). No. of bitstreams: 1 marceloalexandrematos_dissert.pdf: 295732 bytes, checksum: b602897faf078224a99d93671326e504 (MD5) Previous issue date: 2006-05-24
Objective: To evaluate the effects of sodium cyclamate on the rat placenta by its administration in the period of embryogenesis. Method: The sodium cyclamate was administered by intraperitoneal route in rats of the treated group at the dose of 60 mg/kg, from the tenth to fourteenth day of gestation, while the equivalent volume of saline solution was given to the control group, by the same route. On the twentieth day of pregnancy, 10 fetuses (5 from each group) were chosen at random for study. The technique of cariometry was utilized for evaluation of nuclear parameters of cells in deciduous and spongy layers, and of chorionic villi in the rat placenta. Results: The weights of treated fetuses and their placentas were less than those of the control group, while umbilical-cord length in the treated group was shorter than that in control fetuses. There were no alterations in the deciduous layer. In the placental spongy layer were found alterations of the following parameters: major diameter, mean diameter, perimeter, area, volume, the volume/area ratio and eccentricity. The altered parameters in chorionic villi were the following: mean diameter, perimeter, area, volume, the volume/area ratio. Conclusions: This study demonstrated placental alteration with the use of cyclamate by the pregnancy rat, and its repercussion in fetal weight and umbilical-cord length.
Objetivo: Avaliar os efeitos do ciclamato de sódio na placenta de ratas com sua administração no período da embriogênese. Método: Foi administrado por via intraperitoneal nas ratas do grupo tratado a dose de 60 mg / Kg de ciclamato de sódio, do décimo ao décimo quarto dia de gestação, e volume equivalente de solução salina no grupo controle, pela mesma via. No vigésimo dia de prenhez, 10 fetos (5 de cada grupo) foram escolhidos ao acaso para estudo. Foi utilizada a técnica de cariometria para avaliação dos parâmetros nucleares das células das camadas decídua, esponjosa e das vilosidades coriônicas da placenta de ratas. Resultados: O peso dos fetos tratados e de suas placentas foi menor que os do grupo controle, assim como o comprimento do cordão umbilical do grupo tratado foi mais curto que o dos fetos controles. Não houveram alterações na camada decídua. Na camada esponjosa placentária ocorreram alterações dos seguintes parâmetros: diâmetro maior, diâmetro médio, perímetro, área, volume, relação volume / área e excentricidade. Os parâmetros alterados nas vilosidades coriônicas foram os seguintes: diâmetro médio, perímetro, área, volume e relação volume / área. Conclusões: Este estudo demonstrou alteração placentária com o uso de ciclamato pela rata grávida, e sua repercussão no peso fetal e comprimento do cordão umbilical

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Hassanein, Mohamed. "Biochemical and functional characterization of a novel placental protease, cathepsin P, in rat trophoblasts". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 148 p, 2007. http://proquest.umi.com/pqdweb?did=1654487491&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Kaihola, Helena. "The Effects of SSRI Treatment on Human Placenta and Embryo". Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-248527.

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During pregnancy, 4 - 7% of women suffer from major depressive disorder. When antidepressive treatment is needed, selective serotonin reuptake inhibitors (SSRIs) are the most commonly used. Although severe complications from SSRI treatment are rare, association with a number of adverse pregnancy and fetal outcomes has been found. Also, antenatal depression per se has been shown to affect pregnancy outcomes. The overall aim of this thesis was to examine the effects of SSRIs on human placenta and embryo. In the first study, gene expression was investigated in placenta from depressed, SSRI-treated and healthy pregnant women, using microarray analysis. Antenatal depression and SSRI treatment induced alterations in gene expression, but only 20 genes in common were noted. Validation with qRT-PCR showed that six out of seven selected genes were altered in SSRI-treated women compared with controls, and two genes were altered between depressed women and controls. In study two, the protein levels in placenta from depressed, SSRI-treated and healthy pregnant women were investigated, focusing on the NGF signaling pathway. NGF, phosphorylated Raf-1, ROCK2 and phosphorylated ROCK2, were altered in both SSRI-treated and depressed women, although the proteins were regulated differently in the two groups. In the third study, human embryos were treated with fluoxetine. Embryo development and protein expression were studied. Fluoxetine had some effect on the timing of embryo developmental stages. Also, several proteins were uniquely found in fluoxetine-treated embryos compared with untreated embryos. Fluoxetine also altered the levels of proteins secreted from the embryo. In the fourth study, the human neuroblastoma cell line SH-SY5Y/TrkA was treated with TPA and NGF. The activation of Raf-1 was investigated and the involvement of Ras and PKC was studied. Both NGF and TPA activated Raf-1, but to a different extent and via different pathways. The NGF-induced activation of Raf-1 was mediated via Ras, while TPA induced signaling via PKC. In conclusion, SSRI treatment and antenatal depression influence placental gene and protein expression. These findings may affect placental development and function, which in turn could affect fetal development. Also, direct exposure of embryos to fluoxetine has some effects on embryo development and protein expression, which may affect the development of the fetus.

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Chura, Lindsay R. "The effect of chronic and acute maternal stress on expression of placental barrier genes in the rat /". Connect to online version, 2006. http://ada.mtholyoke.edu/setr/websrc/pdfs/mhc/2006/143.pdf.

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Leone, Francesca Marie. "Placental restriction impairs glucose homeostasis in the adult rat, independently of adiposity and circulating free fatty acids /". Title page and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09HS/09hsl583.pdf.

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Bojja, Aruna Sri. "Functional characterization of placental cathepsins". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 81 p, 2009. http://proquest.umi.com/pqdweb?did=1885754561&sid=4&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Binsalamah, Ziyad. "Intramyocardial sustained delivery of Placental growth factor using nanoparticles as a vehicle for delivery in the rat infarct model". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104785.

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Background: Acute myocardial ischemia results in scar formation with ventricular dilatation and eventually heart failure. Placental growth factor (PlGF) is reported to stimulate angiogenesis and improve cardiac function. In this study, we hypothesized that intramyocardial injection of PlGF contained in nanoparticles can be released at the site of action for an extended time period as a sustained slow-release protective mechanism that accelerates myocardial recovery in a rat model of ischemic cardiomyopathy. Methods: The study was conducted on 35 Lewis rats. The rats were randomized into the following four groups: control group I (n=10) received empty chitosan-alginate nanoparticles; treatment group II (n=10) received PlGF, and treatment group III (n=10) received PlGF contained in chitosan–alginate nanoparticles; all of which had coronary ligation and injection of the material into the peri-infarcted area; and finally a sham operated group (n=5). Transthoracic echocardiography was performed for each rat as a baseline before the surgery, after ligation at 2 days, one week, 4 weeks, and at 8 weeks. Left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) were measured at these time intervals. ELISA was used to measure the serum level of TNF-α, IL-6 and IL-10 at 8 weeks. Hearts were stained with Masson's trichrome for scar area analysis. Results: At 8 weeks post coronary ligation, group I had LVEF of 27.6±7.5%, versus 47.1±2.6% in group II, and 56.6±3.7% in group III. Groups II and III had a statistically significant (P < 0.01) improvement in LVEF and LVFS compared to group I. The difference between groups II and III was also statistically significant (P < 0.01). The percentage of scarred left ventricle at mid-papillary cross-section was 32.7±4% in group I, versus 28.4±3% in group II, and 24.5±2.6% in Group III. The difference between group I versus group II, and group II versus III was statistically significant (P < 0.05). This effect was associated with a significant decrease in pro-inflammatory cytokines (TNF-α, IL-6) and an increase in the anti-inflammatory cytokine (IL-10) in group III as opposed to group II. Conclusion: The use of nanoparticles as a vehicle for PlGF delivery as opposed to the direct application of the growth factor post acute myocardial infarction resulted in a significant increase in LV function, a decrease in scar area formation, a decrease in pro-inflammatory cytokines (TNF-α, IL-6) and an increase in the anti-inflammatory cytokine (IL-10). Thus, nanoparticles can be used to provide a sustained slow-release protective mechanism of PlGF therapy enhancing the positive effects of the growth factor in the setting of myocardial ischemia.
Contexte: Les résultats de l'ischémie myocardique aiguë dans la formation de cicatrices avec dilatation ventriculaire et l'insuffisance cardiaque par la suite. Le facteur de croissance placentaire (PlGF) est signalé pour stimuler l'angiogenèse et améliorer la fonction cardiaque. Dans cette étude, nous avons émis l'hypothèse que l'injection intramyocardique de PlGF contenus dans des nanoparticules peuvent être libérés sur le site d'action pour une période prolongée en tant que mécanisme durable à libération lente de protection qui accélère la récupération du myocarde dans un modèle de rat de cardiomyopathie ischémique. Méthodes: L'étude a été menée sur 35 rats Lewis. Les rats ont été répartis au hasard en quatre groupes: le groupe de contrôle I (n=10) a reçu des nanoparticules de chitosan-alginate vides; le groupe de traitement II (n=10) a reçu le PlGF, et le groupe de traitement III (n=10) a reçu le PlGF contenu dans les nanoparticules de chitosan-alginate; qui avaient tous la ligature coronaire et l'injection de la matière dans la zone péri-infarctus, et enfin un groupe fictif utilisé (n=5). L'échocardiographie transthoracique a été réalisée pour chaque rat comme base de référence avant la chirurgie, après la ligature à 2 jours, une semaine, 4 semaines, et à 8 semaines. Le raccourcissement du ventricule gauche fractionné (FRVG) et la fraction d'éjection ventriculaire gauche (FEVG) ont été mesurés à ces intervalles de temps. ELISA a été utilisé pour mesurer le taux sérique de TNF-α, IL-6 et IL-10 à 8 semaines. Les cœurs ont été colorés au trichrome de Masson pour l'analyse de la surface de cicatrice. Résultats: 8 semaines après la ligature coronaire, le groupe I avait une FEVG de 27.6±7.5%, contre 47.1±2.6% dans le groupe II, et 56.6±3.7% dans le groupe III. Les groupes II et III ont montré une amélioration statistiquement significative (P < 0.01) de la FEVG et FRVG par rapport au groupe I. La différence entre les groupes II et III a également été statistiquement significative (P < 0.01). Le pourcentage du ventricule gauche marqué à la section mi-papillaire était 32.7±4% dans le groupe I, contre 28.4±3% dans le groupe II, et 24.5±2.6% dans le groupe III. La différence entre le groupe I par rapport au groupe II, et le groupe II versus III était statistiquement significative (P < 0.05). Cet effet a été associé à une diminution significative des cytokines pro-inflammatoires (TNF-α, IL-6) et une augmentation de la cytokine anti-inflammatoire (IL-10) dans le groupe III par opposition au groupe II. Conclusion: L'utilisation de nanoparticules en tant que véhicule pour la livraison du PlGF par opposition à l'application directe du facteur de croissance post-infarctus aigu du myocarde a entraîné une augmentation significative de la fonction ventriculaire gauche, une diminution de la zone de cicatrice, une diminution des cytokines pro-inflammatoires (TNF-α, IL-6) et une augmentation de la cytokine anti-inflammatoires (IL-10). Ainsi, les nanoparticules peuvent être utilisées pour fournir un mécanisme de protection soutenu à libération lente de la thérapie PlGF, renforçant les effets positifs du facteur de croissance dans le cadre de l'ischémie myocardique.

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Rhodes, Katrin Elisabeth. "Hematopoietic stem cell development in placental vasculature". Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1997626891&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Chang, Miao. "Cell type specific regulation of human placenta growth factor gene transcription /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1597612421&sid=3&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (Ph.D.)--Southern Illinois University Carbondale, 2008.
"Department of Molecular Biology, Microbiology and Biochemisty." Includes bibliographical references (p. 123-150). Also available online.

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Sun, Yuxiang. "Identification and characterization of cis- and trans-acting factors involved in the expression of the rat placental lactogen II gene". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0027/NQ51670.pdf.

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Weis, Simone Nardin. "Efeitos de compostos orgânicos de selênio sobre o desenvolvimento intra-uterino da prole de ratas wistar". Universidade Federal de Santa Maria, 2007. http://repositorio.ufsm.br/handle/1/11081.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Selenium (Se) is an essential trace element for man and is known for its role in regulating growth and development of the fetus and newborn. It is well known that Se deficiency is related to miscarriages and pre-term deliveries. However, it is established that Se compounds, depending of dose, can be highly toxic to several species of animals. The organoselenium compounds, diphenyl diselenide [(PhSe)2] and 3 3- ditrifluoromethyldiphenyl diselenide [(F3CPhSe)2] were the target of this study since they present important pharmacological properties. Therefore, it is necessary to dtudy the effects of these compounds on the embryofetal development. The purpose of the present study was to evaluate the effects of (PhSe)2 and (F3CPhSe)2 administration during the organogenesis period of intrauterine development of Wistar rats. Dams were subcutaneously exposed to (PhSe)2 (1.5, 3.0 or 6.0 mg/kg) or only vehicle (canola oil), from days 6 to 15 of gestation (Article). External and internal fetal examination was performed at gestational day 20. No mortality was observed in fetuses or dams at any (PhSe)2 treatment. A decrease in maternal body weight gain (corrected) was found in all (PhSe)2 groups and also an increase in the liver relative weight were observed in these dams, indicating maternal toxicity. Exposure to (PhSe)2 produced significant changes in fetal body weight and biometry. Furthermore, we verify an increase in the incidence of skeletal alterations of fetuses of all (PhSe)2 doses tested, however, these alterations were considered variations that are generally reversible and is unlikely to adversely affect survival or health. (PhSe)2 was capable to cause some morphological modifications on placentas such as vascular congestion, an increase in leucocyte infiltration and phagocytosis. These effects might have contributed with adverse reproductive outcomes observed in the progeny. In the second work presented in this dissertation (Manuscript), pregnant rats were given, via intragastric intubation, 1, 5 or 10 mg/kg of (F3CPhSe)2 or vehicle (canola oil), from days 6 to 15 of gestation. The parameters evaluated were the same of the first study. Administration of 5 and 10 mg/kg of (F3CPhSe)2 decreased maternal weight gain during pregnancy and this was accompanied by a reduced food consumption in the higher dose. Furthermore, there was an increase in liver absolute and relative weight of dams given the higher dose. These data confirm the liver as the primary target organ for Se compounds exposition. Differently from (PhSe)2 exposure, (F3CPhSe)2 administration did not alter fetal body weight and biometry. However, the compound caused embryolethality in the higher dose tested. This effect seems to be all or none since it led to totally resorption of some litters and the others were not affected by the compound. In this dose level, it was also observed a number of skeletal variations that, equally to (PhSe)2 study, seems unlikely represent survival risks. The placentas morphological analysis revealed that exposure to (F3CPhSe)2 was able to alter placental morphology. On the basis of results mentioned above, we conclude that maternal exposure to (PhSe)2 and (F3CPhSe)2 did not cause externally visible malformations but they were able to increase fetuses skeletal alterations incidence, without affecting fetuses survival. Organoselenium compounds also alter placental morphology that could contribute with adverse reproductive outcomes observed on the progeny.
O selênio (Se) é um elemento traço essencial para humanos e desempenha importante função no crescimento e desenvolvimento de fetos e recém-nascidos. Sabese que a deficiência desse elemento pode ocasionar abortos e nascimentos prematuros. Entretanto, os compostos de Se, dependendo da dose, podem ser tóxicos para diversas espécies de animais. Os compostos orgânicos de selênio, disseleneto de difenila [(ØSe)2] e disseleneto de 3'3-ditrifluormetildifenila [(F3CØSe)2], foram os alvos deste estudo, visto que possuem importantes propriedades farmacológicas. Com isso, faz-se necessário o estudo dos efeitos destes compostos sobre o desenvolvimento embriofetal. O objetivo deste estudo foi avaliar os efeitos da administração de (ØSe)2 e (F3CØSe)2 durante o período da organogênese do desenvolvimento intra-uterino de ratas Wistar. No primeiro trabalho, as ratas prenhas foram expostas ao (ØSe)2 (1,5; 3,0 ou 6,0 mg/kg) ou ao seu veículo (óleo de canola) via injeção subcutânea, do 6º ao 15º dia de gestação (Artigo). No 20° dia de gestação foi realizada uma laparotomia para a retirada dos fetos e a observação do aparecimento de malformações morfológicas externas e esqueléticas. Não foram observadas mortes maternas e fetais nos grupos expostos ao (ØSe)2. A exposição causou uma diminuição do ganho de peso corporal materno (corrigido) nas duas maiores doses testadas, além de um aumento no peso relativo do fígado destas ratas, indicando que o composto causou toxicidade materna. A exposição ao ( Se)2 alterou significativamente os parâmetros de desenvolvimento avaliados (peso e medidas corporais fetais). Além disso, verificou-se um aumentou de incidência de alterações na ossificação do esqueleto desses fetos, em todas as doses avaliadas, porém, estas alterações são consideradas variações que são geralmente reversíveis e parecem não apresentar riscos à vida. Observou-se também que as placentas das ratas que foram expostas ao (ØSe)2 apresentavam alterações na morfologia, tais como, congestão vascular, aumento da infiltração leucocitária e uma intensa atividade fagocítica. Estes efeitos parecem ter contribuído para os efeitos adversos encontrados nas proles analisadas. No segundo trabalho apresentado nesta dissertação, as ratas prenhas foram expostas ao (F3CØSe)2 (1; 5 ou 10 mg/kg) ou ao seu veículo (óleo de canola) através de entubação gástrica, do 6º ao 15º dia de gestação (Manuscrito). Foram avaliados os mesmos parâmetros do primeiro trabalho. A administração das doses de 5 e 10 mg/kg de (F3CØSe)2 causou uma diminuição de ganho de peso corporal materno, acompanhada de uma diminuição de consumo de alimento na maior dose administrada. Além disso, as ratas que receberam a maior dose do composto tiveram um aumento do peso do fígado (absoluto e relativo). Estes dados confirmam que o fígado é o órgão alvo da exposição a compostos de Se. Diferentemente da exposição ao (ØSe)2, a administração de (F3CØSe)2 não alterou o peso e as medidas corporais fetais. Entretanto, o composto causou embrioletalidade na maior dose testada. Este efeito parece ser do tipo tudo-ounada, uma vez que levou à reabsorção total de metade das ninhadas estudadas, sendo que a outra metade não foi afetada pelo composto. Nesta dose também foram observadas variações esqueléticas, que igualmente ao estudo com (ØSe)2 parecem não apresentar riscos à vida. A análise morfológica das placentas também revelou que a exposição ao (F3CØSe)2 foi capaz de alterar de forma significativa a morfologia da placenta. Portanto, com base nos resultados encontrados, concluímos que a exposição materna ao (ØSe)2 e ao (F3CØSe)2 não provocou o aparecimento de malformações externas visíveis, porém, aumentou a incidência de alterações esqueléticas nos fetos, alterações essas que não afetam a sobrevivência dos mesmos. A exposição aos organocalcogênios também modificou a morfologia das placentas o que pode ter contribuído para o atraso no desenvolvimento intra-uterino observado nas proles.

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Leandro, Sandra Márcia. "Sobrecarga e restrição de sal na dieta durante a gestação em ratas Wistar: efeitos sobre o sistema renina-angiotensina, função renal, resistência à insulina e pressão arterial". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-08012007-172716/.

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Diversos estudos epidemiológicos têm relacionado doenças na vida adulta, como diabetes tipo-2 e hipertensão, e ambiente inadequado durante a vida fetal. Fatores distintos relacionados aos hábitos alimentares, como ingestão de sal na dieta, podem ter impacto importante no período perinatal. Recentemente, demonstramos que dieta hipossódica (HO) durante a gestação está associada com baixo peso ao nascimento e alterações na vida adulta. O objetivo do presente estudo foi avaliar o efeito da dieta HO e hipersódica (HR) durante gestação em ratas. Ratas Wistar foram alimentadas com dieta HO, dieta normossódica ou HR desde a 8ª semana e foram acasaladas com 12 semanas de idade. Estes animais foram estudados na terceira semana de gestação e um grupo adicional de ratas virgens foi estudado como controle para o efeito da gestação. O peso da placenta e o do feto e o fluxo sangüíneo uterino foram menores e a resistência vascular periférica foi maior no grupo HO. Maior peroxidação lipídica e expressão gênica do receptor AT1 na placenta foram observadas no grupo HR. Em conclusão, peso do feto, peso da placenta e fluxo sangüíneo uterino são influenciados pelo consumo de sal durante a gestação.
Many epidemiological studies have linked diseases in adulthood, such as type-2 diabetes and hypertension, to adverse intrauterine environment during fetal life. Distinct factors related to dietary habits, such as salt intake, may have a major impact on the perinatal period. Recently, we have demonstrated that low-salt diet (LSD) during pregnancy is associated with low birth weight and diseases during adulthood. The aim of this study was to evaluate the effect of LSD and high-salt diet (HSD) during pregnancy in rats. Female Wistar rats were fed with LSD, normal-salt diet or HSD since 8 weeks of age and matted with 12 weeks of age. These animals were studied at the third week of gestation and one additional group of virgin rats was evaluated as a control for the gestation effect. Placenta and fetus weight and uterine blood flow were lower and peripheral vascular resistance was higher in the LSD group. In the placenta from HSD rats, higher lipid peroxidation and AT1 receptor mRNA were observed. In conclusion, fetal weight, placenta weight and uterine blood flow are influenced by the degree of salt consumption during pregnancy.

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Maheshwari, Vatsala. "Potential role of NF-[kappa]B in regulation of human placenta growth factor (PlGF) in trophoblast /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1650513211&sid=4&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (M.S.)--Southern Illinois University Carbondale, 2008.
"Department of Molecular Biology, Microbiology and Biochemisty." Includes bibliographical references (p. 98-113). Also available online.

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Johnson, Gabriel Paul. "Early embryology of Ceratopteris richardii and immunocytochemistry of placental transfer cell wall ingrowths /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1597619681&sid=11&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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De, Blasio Miles Jonathon. "Placental restriction of fetal growth increases growth rate and sensitivity to insulin and insulin-like growth factor 1 (IGF-1) after birth in sheep /". Title page and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09SB/09sbd286.pdf.

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Thesis (B.Sc.(Hons.))--University of Adelaide, Dept. of Physiology, 1999.
Spine title: Fetal gowth restriction increases insulin and IGF-1 sensitivity in neonatal sheep. Bibliography: leaves 21-24.

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Arnold, Daniel Robert. "Regulation of trophoblast development in the bovine embryo". Thèse, [Montréal] : Université de Montréal, 2005. http://proquest.umi.com/pqdweb?index=0&did=1221731981&SrchMode=1&sid=1&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1191513626&clientId=48948.

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Thèse (Ph. D.)--Université de Montréal, 2006.
Titre de l'écran-titre (visionné le 4 oct. 2007). "Thèse présentée à la Faculté des études supérieures en vue de l'obtention du grade de Philosophiae Doctor (Ph.D.) en sciences vétérinaires option reproduction" Paraît aussi en version papier et en version microforme.

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Banet, Amanda Inez. "Evolutionary diversification of reproductive modes in livebearing fishes". Diss., [Riverside, Calif.] : University of California, Riverside, 2009. http://proquest.umi.com/pqdweb?index=0&did=1957301301&SrchMode=2&sid=4&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1268858219&clientId=48051.

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Thesis (Ph. D.)--University of California, Riverside, 2009.
Includes abstract. Available via ProQuest Digital Dissertations. Title from first page of PDF file (viewed March 17, 2010). Includes bibliographical references. Also issued in print.

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Lombardi, Lopes Flavia. "Regulation of vascular endothelial growth factor during the peri-implantation period in the American mink mustela vison /". Thèse, [Montréal] : Université de Montréal, 2005. http://proquest.umi.com/pqdweb?index=4&did=1155571621&SrchMode=1&sid=3&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1191512564&clientId=48948.

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Thèse (Ph.D.)--Université de Montréal, 2006.
Titre de l'écran-titre (visionné le 4 oct. 2007). "Thèse présentée à la Faculté des études supérieures en vue de l'obtention du grade de Philosophiae Doctor (Ph.D.) en sciences vétérinaires option reproduction" Paraît aussi en version papier et en version microforme.

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31

Possignolo, Luiz Fernando 1987. "Efeito da ingestão crônica de dieta hiperlipídica no metabolismo de ratas, e sobre a expressão de SR-BI e ABCA1 na placenta, intestino delgado, fígado e rins da prole destes animais = Effect of high fat diet chronic ingestion on the metabolism of female rats, and on the SR-BI and ABCA1 expression in the placenta, small intestine, liver and kidney of the offspring". [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309926.

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Orientador: José Antonio Rocha Gontijo
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-21T06:22:30Z (GMT). No. of bitstreams: 1 Possignolo_LuizFernando_M.pdf: 4767580 bytes, checksum: b843458e4c7049fc29741e4aca9f918d (MD5) Previous issue date: 2012
Resumo: Devido ao maior consumo de alimentos ricos em gordura e um estilo de vida mais sedentário, houve um aumento na incidência de desordens metabólicas relacionadas ao metabolismo lipídico como a resistência à insulina, dislipidemias, e sua associação com doenças cardiovasculares. A alimentação materna desequilibrada, durante a gestação e lactação, pode predispor a prole à doenças durante a vida adulta. Alguns transportadores como o Scavenger Receptor class B type I (SR-BI) e ATP-binding cassette transporter A1 (ABCA1) são descritos como responsáveis pela captação de colesterol e transporte deste a partir de lipoproteínas, principalmente no transporte reverso de colesterol, sendo denominados receptores antiaterogênicos podendo modificar seu padrão de expressão frente a uma dieta hiperlipídica. Ratas Wistar receberam dieta hiperlipídica (DHL) ou dieta padrão (CTL) desde o desmame, até a lactação. Após o desmame a prole de machos recebeu a dieta padrão até a 16ª semana de vida. Nas mães quanto e na prole foram analisados os seguintes parâmetros: ingestão alimentar, ganho ponderal, perfil lipídico e glicídico. Na prole foi estudada a expressão e localização de ABCA1 e SR-BI na placenta, no rim, fígado, e intestino delgado em animais com 17 dias pré-natal (E17), 12 dias pós-natal (PN12d) com 8 e 16 semanas pós-natal (PN8s e PN16s). As mães DHL apresentaram: 1) maior ingestão calórica com menor ganho ponderal; 2) aumento glicêmico associado à menor produção de insulina nos três períodos estudados e, 3) aumento nos níveis séricos de triglicérides em M8s. A prole de mães DHL apresentaram menor massa corporal desde E17 até PN8s, sem que tenha havido diferenças ponderais e na ingestão de ração. PN8s e PN16S apresentaram menor captação tissular de glicose associada à hiperinsulinemia, e aumento nos níveis séricos de triglicérides com PN16S. Não houve alterações nos níveis de colesterol e HDLcolesterol. Não foi observada alteração na expressão de SR-BI e ABCA1 no intestino delgado, placenta enquanto no fígado houve uma queda tempo-dependente para ambos transportadores. No rim da prole DHL aos PN12d e PN16s observou-se maior expressão de ABCA1. Este estudo mostrou que o consumo materno crônico de uma dieta hiperlipídica causa alterações metabólicas nas mães e predispõe a prole, a modificações no metabolismo lipídico e glicídico, além de elevação da expressão de ABCA1 no rim
Abstract: Due to the abundance and accessibility to foods high in fat and a more sedentary lifestyle, there is an increased incidence of metabolic disorders related to lipid metabolism such as insulin resistance, dyslipidemia, and a high correlation with cardiovascular disease. The unbalanced maternal diet during pregnancy and lactation predisposes the offspring to diseases during adult life. Some carriers such as scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA1) are described as responsible for raising cholesterol and transporting it to and from lipoproteins, due the participation in the reverse cholesterol transport, these receptors are called antiatherogenic and are subject to change its pattern of expression when exposed to a high fat diet. Female Wistar rats were fed a diet (HFD) or a standard chow (CTL) from weaning, during pregnancy and lactation. After weaning the male offspring was exposed to a standard chow until the 16th week of life. Both the dams and the offsprings food intake were monitored, weight gain, lipid profile and glucose level. It was analyzed in the offspring the expression and localization of ABCA1 and SR-BI in the placenta, kidney, liver, and small intestine in animals at 17º prenatal day (E17), 12 days post-natal (PN12d), 8 and 16 postnatal weeks (PN8s PN16s respectively). DHL dams had a higher intake of calories in the diet, but the weight was smaller, they had higher blood glucose due to decreased production of insulin in the pre-pregnancy (m8s), during pregnancy (M17g) and lactation (M15l) and a higher triglyceride level in m8s. The offspring of dam fed a high fat diet had lower weight since E17 until PN8s, with no differences in weight gain and food intake. PN8s and PN16s had lower glucose uptake and hyperinsulinemia, and high triglycerides with PN16s, no changes were observed in cholesterol and HDL-cholesterol levels. There were no changes in the expression of SR-BI and ABCA1 in the small intestine, placenta and liver, however there was a decrease over the age for both receptors, and kidney of the offspring and DHL PN12d PN16s showed higher expression of ABCA1. The present study showed that chronic consumption of high fat diet causes metabolic changes in dams and predisposes offspring to changes in lipid and glucose metabolism of the offspring, increasing the expression of ABCA1 in the kidney
Mestrado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Mestre em Fisiopatologia Médica

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Hernández, Velasco Silvia Clara. "Genetics of litter size and prenatal survival in pigs". Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6467.

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Female reproductive performance is a critical component of sustainable pig production systems. There is abundant evidence of genetic variation in these traits among pig breeds. The aims of this study were to identify quantitative trait loci (QTL) affecting reproductive traits and to identify and characterise positional candidate gene(s) underlying the QTL. A Large White - Meishan F2 population was scanned for QTL with effects on reproductive traits. This analysis revealed 13 putative QTLs on seven different chromosomes with effects on five different traits: ovulation rate (OR), teat number (TN), prenatal survival (PS), total born alive (TBA) and litter size (LS). QTL for PS and LS on chromosome 8 were fine mapped and Secreted Phosphoprotein 1 (SPP1) confirmed as a candidate gene. A genome-wide association study was performed on a diverse population of different breeds and crosses lines, for reproductive traits including LS, TBA, number of stillborn piglets, and number of mummified piglets. Fourteen SNPs were found significantly associated with reproductive traits. The functional study of SPP1 examined the hypothesis that differences in foetal growth may be associated with the effectiveness of conceptus attachment, as measured by SPP1 expression. Patterns of SPP1 mRNA and protein expression in placental and uterine tissues supplying the smallest and a normal-sized foetus from the same uterus were examined in Large White-Landrace (LW-LR), Large White (LW) and Meishan (MS) females 40 and 45 of pregnancy. The smallest LW-LR foetuses tended to have a higher level of SPP1 mRNA in endometrium tissue compared to the normal-sized foetuses. However, placenta expression was higher in the normal-sized foetuses compared to the smallest ones. SPP1 protein levels in normal sized foetuses were significantly higher than in the smallest litter mates for all the tissues. Significantly higher levels of SPP1 mRNA and protein were found in MS compared to LW. In both breeds, significant differences between sizes were found in some tissues, with similar expression patterns in respect to size, for both mRNA and protein in endometrial tissues when compared to contemporary LW. In placenta, the direction of the expression differed between breeds, with a higher expression of mRNA and protein in the normal-sized MS foetuses and in the smallest sized LW foetuses. The comparison of SPP1 expression between different foetal sizes and different breeds revealed associations between breed, foetal size, and SPP1 protein, factors implicated in PS and LS. These results together with the genetic evidence indicate that the potential role of SPP1 in placental and foetal development merits further investigation.

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Buffat, Christophe. "Retard de croissance intra utérin et origine précoce des maladies de l'adulte : mécanismes physiopathologiques et moléculaires". Paris 7, 2008. http://www.theses.fr/2008PA077053.

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La restriction de croissance intra-uterine et une croissance postnatale trop rapide sont reconnues comme des facteurs de risques des maladies cardiovasculaires de l'adulte. Les mecanismes qui en sont responsable ne sont pas reellement connus. Au cours de ce travail de these, 2 approches ont ete suivies a l'aide d'un modele rat. La 1ere partie a pour but de caracteriser a l'aide de microarrays des alterations precoces de l'expression de genes du placenta et du rein de ratons hypotrophes. Une vue hierarchique des mecanismes regulant massivement des familles de genes modules ainsi qu'une regulation specifique des facteurs de transcription dans ces 2 organes. La 2eme partie a pour but d'evaluer les effets a tres long terme chez le rat d'une suralimentation postnatale. Une augmentation de la pression arterielle et du nombre de glomerules associee a des alterations de la structure renale ont ete observes chez les ratons hyperalimentes. La caracterisation d'alterations specifiques de l'expression de genes et de leurs regulations au niveau placentaire et renale vise a mieux comprendre les mecanismes impliques dans l'adaptation du fŒtus a des circonstances deleteres. Par ailleurs, la croissance postnatale via des effets renaux autre que le deficit nephronique, pourrait egalement intervenir dans le developpement a long terme des maladies cardiovasculaires. Ainsi la comprehension des mecanismes impliques dans l'origine precoce des maladies de l'adulte ouvre actuellement de nouvelles voies diagnostiques par l'identification de marqueurs precoces de ce risque et pourrait a plus long terme permettre de developper des voies therapeutiques, pharmacologiques ou nutritionnelles
Intra-uterin growth restriction (iugr) and postnatal overfeeding is an important cause of the metabolic syndrome and cardiovascular diseases in adulthood. However, the detailed mechanisms of such programming are still incompletely known. Two experimental approaches in the rat were used in this work of thesis: first, protein depletion during the gestation of rat females has been widely used as a model for human. A transcriptome analysis of control and protein-deprived rat placentas and kidneys was used to better understand the molecular basis of early origin of the diseases in adulthood. Our approach permitted the proposition of hypotheses on a hierarchy of gene inductions/repressions leading to massive transcriptional alterations in the iugr placenta and kidney. Moreover, postnatal growth via renal effects other than glomerular number reduction are likely to contribute to arterial hypertension induced by early postnatal overfeeding. Thus, the comprehension of the mechanisms imply in the early origin of cardiovascular and metabolic diseases in adulthood, currently opens news diagnostic ways by the identification of early markers of this risk and could later on ollow to develop therapeutic, pharmacological or nutritionalways

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Soto, Sônia de Fátima. "Alterações placentárias em resposta à exposição de ratas Wistar à poluição atmosférica". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-20052015-081635/.

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Introdução: A exposição à poluição atmosférica durante a gestação provoca alterações nas características da placenta e pode resultar em restrição de crescimento intrauterino. Sabe-se que o transforming growth factor beta 1 (TGFbeta1), o sistema renina-angiotensina uteroplacentário (SRA) e os fatores angiogênicos, tais como vascular endothelial growth factor A (VEGF-A) participam do processo de placentação e regulação do fluxo sanguíneo uteroplacentário. Assim, o objetivo do presente estudo foi investigar o efeito da exposição à poluição do ar sobre a morfologia, função e SRA placentários. Métodos: Ratas Wistar fêmeas foram expostas ao ar filtrado (F) ou ao material particulado 2.5um (P) durante 15 dias. Depois o cruzamento, as ratas foram divididas em 4 grupos e novamente expostas a F ou P (FF, FP, PF, PP). No 19º dia de gestação, as porções maternas e fetais das placentas foram coletadas. Estrutura da placenta, TGFbeta1, VEGF-A e seus receptores e os componentes do SRA foram avaliados. Resultados: A exposição ao material particulado diminuiu massa, tamanho e área de superfície placentária, um indicativo da interação materno-fetal. As concentrações placentárias de TGF beta1, VEGF-A e Flk-1 e os componentes do SRA foram alterados e isso pode indicar um prejuízo na invasão do trofoblasto, angiogênese placentária e troca de nutrientes e gases entre mãe e fetos. Discussão: Os resultados indicam que a exposição a partículas compromete a interação materno-fetal e pode refletir sobre a nutrição e crescimento fetal
Introduction: Exposure to air pollution during pregnancy causes alterations in placental characteristics and may result in intrauterine growth restriction. It was suggested that transforming growth factor beta 1 (TGFbeta1), the uteroplacental renin-angiotensin system (RAS) and angiogenic factors, such as vascular endothelial growth factor A (VEGF-A) participates of the placentation process and regulation of the uteroplacental blood flow. Thus, the aim of the present study was to investigate the effect of exposure to air pollution on the placental morphology, function and placental RAS. Methods: Female Wistar rats were exposed to filtrated air (F) or to concentrated particulate matter 2.5um (P) for 15 days. After mating, rats were divided in 4 groups and again exposed to F or P (FF, FP, PF, PP). At 19th day of pregnancy, maternal and fetal portions of placenta were collected. Placental structure, TGFbeta1, VEGF-A and its receptors and RAS components were evaluated. Results: Exposure to particulate matter decreased placental mass, size and surface area, an indicative of maternal-fetal interaction. Placental TGFbeta1, RAS components and VEGF-A and receptors Flk-1 concentrations were altered and this may indicate a prejudice in the trophoblast invasion, placental angiogenesis and maternal-fetal nutrients and gases exchange. Discussion: These findings indicate that exposure to particulate matter compromises the maternal-fetal interaction and may reflect on fetal nutrition and growth

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Haapsamo, M. (Mervi). "Low-dose aspirin therapy in IVF and ICSI patients". Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514296208.

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Abstract The first aim of this randomized, placebo-controlled and double-blind study was to investigate whether low-dose aspirin therapy, started prior to controlled ovarian hyperstimulation, improves ovarian stimulation response, uterine haemodynamics and clinical pregnancy rates in unselected patients who underwent in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI). The second aim was to examine if the maternal serum placental proteome is different in IVF/ICSI pregnancies compared with spontaneous pregnancies, and whether low-dose aspirin modifies maternal serum placental protein expression and uteroplacental haemodynamics during the first half of pregnancy. Finally, the effect of low-dose aspirin therapy on the incidence of hypertensive pregnancy complications among women who became pregnant after IVF/ICSI was investigated. Low-dose aspirin therapy did not increase the number of oocytes retrieved, the total number of embryos or number of top-quality embryos, endometrial thickness or uterine haemodynamics on the day of embryo transfer (ET) or clinical pregnancy rates compared with placebo-treated IVF/ICSI women. On the day of ET, low-dose aspirin did not affect UtA vascular impedance, but the incidence of non-optimal uterine artery haemodynamics (UtA PI≥3.0) was statistically significantly lower (p<0.05) in the aspirin group compared with the placebo group. In the placebo-treated IVF/ICSI patients, maternal serum proteome analysis showed altered protein expression compared with women with spontaneous pregnancies. Between aspirin- and placebo-treated IVF/ICSI patients, proteome analysis showed a unique and distinct pattern of differentially expressed proteins including extra-cellular matrix, complement and transport proteins. At 6 weeks’ gestation, arcuate artery PI and at 18 weeks’ gestation, UtA PI values were lower (p<0.05) in the aspirin group than in the placebo group. In conclusion, low-dose aspirin therapy, when started concomitantly with controlled ovarian hyperstimulation, did not improve ovarian responsiveness, uterine receptivity, pregnancy outcome in unselected IVF/ICSI women or affect UtA vascular impedance on the day of ET. Low-dose aspirin modified the early placentation process and reduced uteroplacental vascular impedance in mid-pregnancy, but did not decrease the incidence of hypertensive pregnancy complications
Tiivistelmä Keinoalkuisten hedelmöityshoitojen seurauksena keskimäärin reilu kolmannes naisista tulee raskaaksi hoitokertaa kohti. Näissä raskauksissa äidin seerumista määritettyjen istukkaperäisten merkkiaineiden pitoisuuksissa on eroavaisuuksia verrattuna spontaanisti raskaaksi tulleiden naisten seerumipitoisuuksiin ensimmäisen ja toisen raskauskolmanneksen aikana. Pre-eklampsian eli raskausmyrkytyksen riski on myös lisääntynyt. Syyksi arvellaan istukan verisuonipuuston poikkeavaa kehitystä. Pre-eklampsiaan liitetään intravaskulaarisen prostasykliinin ja tromboksaanin epätasapaino, joka johtaa verihiutaleiden aggregaation lisääntymiseen ja verisuonten supistumiseen. Matala-annoksinen asetyylisalisyylihappo (ASA) vähentää tromboksaanituotantoa ja korjaa tromboksaani- ja prostasykliinituotannon epätasapainoa, mutta sen ei ole todettu merkittävästi vähentävän näiden raskauskomplikaatioiden esiintyvyyttä edes riskiryhmillä, kun lääkitys on aloitettu toisen raskauskolmanneksen aikana. Tämän satunnaistetun ja plasebo-kontrolloidun kaksoissokkotutkimuksen tavoitteena oli tutkia keinoalkuisia hedelmöityshoitoja saavilla naisilla matala-annoksisen ASA-hoidon (100 mg/vrk) merkitystä munasarjojen stimulaatiovasteeseen, alkion kiinnittymiseen, istukan muodostumiseen ja kehittymiseen sekä lääkehoidon vaikutusta kohdun, istukan ja sikiön verenkiertoon, kun lääkitys aloitettiin munasarjojen stimulaatiohoidon alkaessa. Lisätavoitteena oli selvittää, onko lapsettomuushoitoja saavien naisten raskauksissa todettavissa spesifinen istukkaproteomiikkalöydös (istukan tuottamat valkuaisaineet) verrattuna spontaanisti raskaaksi tulleisiin naisiin ja voidaanko siihen vaikuttaa matala-annoksisella ASA-hoidolla. Toisena lisätavoitteena oli selvittää matala-annoksisen ASA-hoidon vaikutus pre-eklampsian esiintyvyyteen loppuraskaudessa. Matala-annoksinen asetyylisalisyylihappo (ASA) ei paranna keinoalkuisten hedelmöityshoitojen hoitotuloksia eikä vaikuta kohdun verenkiertoon tai kohdun limakalvon paksuuteen ultraäänellä arvioituna alkion siirtopäivänä. Matala-annoksista ASA-hoitoa käyttäneiden potilaiden ryhmässä todettiin kuitenkin merkitsevästi vähemmän naisia, joilla oli huonoa hoitotulosta keinoalkuisissa hedelmöityshoidoissa ennakoiva korkea molemminpuolinen kohtuvaltimoiden verenvirtausvastus alkion siirtopäivänä verrattuna plasebo-ryhmään. Raskaaksi tulleilla naisilla, jotka käyttivät matala-annoksista ASA-hoitoa, todettiin kohdun verenvirtausvastus matalammaksi alku- ja keskiraskaudessa verrattuna plasebo-ryhmän naisiin. Istukkaproteomiikkatutkimusten mukaan varhaisistukan proteiinituotanto on erilainen keinoalkuisissa raskauksissa verrattuna spontaanisti alkaneisiin raskauksiin ja siihen voidaan vaikuttaa matala-annoksisella ASA-hoidolla. Pre-eklampsian ja sikiön kasvunhidastuman esiintyvyydessä ei ryhmien välillä todettu eroa. Matala-annoksinen ASA-hoito aloitettuna ennen raskautta munasarjojen stimulaatiohoidon alkaessa ei paranna munasarjojen vastetta lapsettomuushoidoissa käytettäville hormonihoidoille, raskauslukuja eikä kohdun verenkiertoa alkion siirtopäivänä. Hoidon todettiin kuitenkin vaikuttavan varhaisistukan kehittymiseen sekä parantavan kohdun verenkierto alku- ja keskiraskaudessa viitaten istukan verisuonipuuston parempaan kehittymiseen. Matala-annoksinen ASA-hoito ei vähentänyt istukkaperäisten raskauskomplikaatioiden esiintymistä

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36

Alvarenga, Cláudia Maria Domingues. "Avaliação dos mecanismos de ação interceptiva e/ou embriotóxica do extrato aquoso de Plectranthus barbatus Andr.(bolbo-brasileiro) administrado a ratas prenhez no período de pré-implantação /". Botucatu : [s.n.], 2006. http://hdl.handle.net/11449/104597.

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Orientador: Ione Pellegatti Lemonica
Banca: João Lauro Viana de Camargo
Banca: Márcia Guimarães da Silva
Banca: Silvana Lima Górniak
Banca: Regiane Kawakami
Tese não possui um resumo geral, possue um resumo para cada capítulo
Resumo : O objetivo do presente estudo foi verificar, experimentalmente, o possível mecanismo pelo qual o extrato aquoso de Plectranthus barbatus (boldo-brasileiro), planta utilizada popularmente como abortiva, atua sobre o organismo materno ou sobre o desenvolvimento do concepto durante o período de pré-implantação, correlacionando sua ingestão com possíveis alterações no transporte e desenvolvimento embrionário ou com alterações hormonais maternas...(Resumo completo, clicar acesso eletrônico abaixo)
Abstract : The present study was conducted to determine the possible mechanism by which the aqueous extract of Plectranthus barbatus (brazilian-boldo), a plant used popularly as abortive agent, can lead to early loss of pregnancy, correlating this possible effect with morphological alterations in the embryo, oviductal motility dysfunctions or maternal hormonal level modifications...(Complete abstract, access undermentioned electronic address)
Doutor

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37

Alvarenga, Cláudia Maria Domingues [UNESP]. "Avaliação dos mecanismos de ação interceptiva e/ou embriotóxica do extrato aquoso de Plectranthus barbatus Andr.(bolbo-brasileiro) administrado a ratas prenhez no período de pré-implantação". Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/104597.

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Made available in DSpace on 2014-06-11T19:33:25Z (GMT). No. of bitstreams: 0 Previous issue date: 2006-08-24Bitstream added on 2014-06-13T18:45:06Z : No. of bitstreams: 1 alvarenga_cmd_dr_botfm_prot.pdf: 1786103 bytes, checksum: 14d9f0d294fb6c639b79eab0f8e823c6 (MD5)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O objetivo do presente estudo foi verificar, experimentalmente, o possível mecanismo pelo qual o extrato aquoso de Plectranthus barbatus (boldo-brasileiro), planta utilizada popularmente como abortiva, atua sobre o organismo materno ou sobre o desenvolvimento do concepto durante o período de pré-implantação, correlacionando sua ingestão com possíveis alterações no transporte e desenvolvimento embrionário ou com alterações hormonais maternas...
The present study was conducted to determine the possible mechanism by which the aqueous extract of Plectranthus barbatus (brazilian-boldo), a plant used popularly as abortive agent, can lead to early loss of pregnancy, correlating this possible effect with morphological alterations in the embryo, oviductal motility dysfunctions or maternal hormonal level modifications...(Complete abstract, access undermentioned electronic address)

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38

Bobé, Pierre. "La gestation : un modele d'etude de la regulation de la reponse immunitaire". Paris 7, 1987. http://www.theses.fr/1987PA077192.

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"Longitudinal multimodal imaging of in vivo placental function during the onset of preeclampsia and in response to therapeutic intervention in the reduced uterine perfusion pressure rat". Tulane University, 2021.

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archives@tulane.edu
Preeclampsia is a leading cause of maternal and fetal mortality, affecting up to 8% of pregnancies. Clinically, preeclampsia is diagnosed by the new onset of maternal hypertension and proteinuria presenting in the second half of gestation. The etiology of this disease, however, occurs during early development with abnormal vascular remodeling that results in reduced placental perfusion and hypoxia. This abnormal placental function increases the production of soluble antiangiogenic factors which are then released into maternal circulation, creating the systemic endothelial dysfunction associated with maternal symptoms. Despite being a critical indicator of disease progression and therapeutic response, placental function cannot be fully characterized by existing imaging modalities. The objective of this work was to develop multimodal imaging and image processing tools characterize placental function in the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. We demonstrate spectral photoacoustic (sPA) imaging and contrast-enhanced ultrasound (CEUS) imaging of the longitudinal changes in placental oxygenation, perfusion, and vascular growth in the development of preeclampsia and evaluate the placental response to therapeutic intervention.
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Dylan J Lawrence

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40

Ozturk, Arzu. "Identification of cis- elements and trans- acting factors that are involved in rat placental lactogen II (rPLII) gene expression in placenta". 2007. http://hdl.handle.net/1993/20578.

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Peden, Laura. "Nucleotide sequence determination of a novel prolactin-like cDNA clone from the developing rat placenta". 1986. http://hdl.handle.net/1993/15459.

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42

Shearman, Lauren Patricia. "Cocaine-sensitive monoamine transporters in rat placenta labeled with (iodine-125)RTI-55 and tritiated nisoxetine". 1996. https://scholarworks.umass.edu/dissertations/AAI9619437.

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Some of the adverse effects of prenatal cocaine exposure have been associated with uteroplacental vasculature, and (3H) cocaine binding sites were previously reported in human placental villus tissue (Ahmed et al., 1990). Specific uptake systems for serotonin (5-HT) and norepinephrine (NE) are present in human placental syncytiotrophoblastic cells and may be substrates for cocaine action (Cool et al.. 1990; Ramamoorthy et al., 1993b). To investigate whether monoamine transporters are present in rat placenta, I studied the characteristics of placental cocaine recognition sites, and the influence of maternal cocaine treatment on placental and fetal brain monoamine transporter binding. First, saturation analyses were performed with (125I) RTI-55, a potent cocaine congener, on membrane fractions from gestational day (GD) 20 rat placenta. Results yielded curvilinear Scatchard plots that were resolved by non-linear curve-fitting into high- and low-affinity components. Mean Kd values were 0.29 nM and 7.9 nM for high- and low-affinity binding sites respectively, and resembled those found in adult rat brain. Drug displacement studies with monoamine uptake inhibitors indicated that the majority of high-affinity (125I) RTI-55 binding was to the 5-HT transporter. The selective ligands (3H) GBR 12935 and (3H) nisoxetine were used to ascertain whether the rat placenta also possessed dopamine (DA) and/or NE transporters. No saturable binding was detected with (3H) GBR 12935. In contrast, the NE transporter-selective ligand (3H) nisoxetine labeled a single population of binding sites with a Kd of 1.0 nM and a Bmax of 1.2 pmol/mg protein. Drug competition studies confirmed that (3H) nisoxetine labeled NE transporters in rat placenta. Additionally, monoamine transporter binding was localized in GD 20 placenta using in vitro film and dry emulsion autoradiography. (3H) Nisoxetine-labeled NE transporters were visible throughout the placenta, with high densities in giant trophoblastic cells and moderate labeling in the labyrinth. Cocaine-like binding sites labeled with (125I) RTI-55 were mainly distributed in the labyrinth and decidua. To verify the presence of 5-HT transporters in rat placenta, 5-HT immunocytochemistry was carried out. The distribution of 5-HT-immunoreactive cells paralleled sites of (125I) RTI-55 binding in the rat placenta. In the final experiment, pregnant dams received cocaine continuously via s.c. Silastic implants from GD 17 to GD 20, and changes in fetal brain and placental (125I) RTI-55 and (3H) nisoxetine binding were assessed. Cocaine treatment did not alter (125I) RTI-55 binding in the placenta. No effect was found in fetal brain, whereas cocaine produced a marked upregulation of NE transporter density in the placenta at GD 20. These studies demonstrate that rat placenta, a noninnervated tissue, possesses cocaine-like binding sites and 5-HT and NE transporters. Placenta is thus a potential target for mediating some effects of cocaine on fetal development.

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Black, Amy Maxine. "Broccoli sprout supplementation during placental insufficiency confers structural and functional neuroprotection to the fetal rat". Master's thesis, 2010. http://hdl.handle.net/10048/913.

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Thesis (M.Sc.)--University of Alberta, 2010.
A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Master of Science, Centre for Neuroscience. Title from pdf file main screen (viewed on January 27, 2010). Includes bibliographical references.

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Bibeau, Karine. "Hypoxie placentaire et atteinte surrénalienne foetale dans un modèle de restriction de croissance intra-utérine chez le rat". Thèse, 2008. http://hdl.handle.net/1866/6511.

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Shah, Paresh C. "Isolation and characterization of the rat placental lactogen-II gene". 1987. http://hdl.handle.net/1993/24366.

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Kirk, Kathryn Lee. "Structural characterization of complementary DNA clones to rat placental lactogen II messenger RNA". 1986. http://hdl.handle.net/1993/15391.

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Sun, Yuxiang. "The effects of transforming growth factor [alpha] on the expression of rat placental lactogens". 1996. http://hdl.handle.net/1993/19345.

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FALCON, BANI JADIEL. "Abnormal inflammation in a rat model of spontaneous fetal loss leads to maternal coagulopathies associated with placental haemostatic alterations". Thesis, 2011. http://hdl.handle.net/1974/6634.

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Spontaneous foetal loss is the most common complication of pregnancy, affecting up to 20% of recognized pregnancies and recurring in 1-3% of cases. Abnormal maternal inflammation and systemic maternal coagulopathies are associated with foetal loss; however, the causal role of inflammation in the development of obstetric coagulopathies has not been determined. Further, questions remain as to whether maternal systemic coagulopathies are associated with placental haemostatic alterations and what role these local alterations play in foetal outcome. We hypothesized that abnormal maternal inflammation during pregnancy is causally linked to maternal coagulopathies and that these coagulopathies are associated with impaired utero-placental blood flow preceding foetal death. To induce inflammation-mediated fetal death, we administered lipopolysaccharide (LPS; 100-µg/kg) to Wistar rats on gestational day 14.5 and characterized the systemic maternal coagulation status 1hr post LPS administration using thromboelastograpy. Utero-placental haemostatic alterations were analyzed by periodic acid Schiff staining (PAS) and immunohistochemistry for fibrin/fibrinogen. Spiral arteriole peak flow velocity was determined by Doppler ultrasound. To determine causality between abnormal maternal inflammation, coagulopathies, and placental hemodynamics, the TNF -inhibitor etanercept (Enbrel®) was administered six hours prior to LPS administration. Systemic maternal coagulopathies were evident in 82% of LPS-treated dams and were associated with specific placental haemostatic alterations as well as reduced utero-placental blood flow. Etanercept administration prevented the development of systemic coagulopathies and placental haemostatic alterations. Furthermore, etanercept maintained normal spiral arteriole peak flow velocity. This study demonstrated that abnormal maternal inflammation is causally linked to systemic coagulopathies specific to pregnancy. Moreover, we showed that inflammation-induced systemic coagulopathies are associated with placental haemostatic alterations and reduced utero-placental blood flow preceding foetal death. Modulation of maternal inflammation may thus be useful in the prevention of coagulopathies associated with complications of pregnancy.
Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2011-08-01 14:29:12.489

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Ramesar, Shamal Vinesh. "The effect of sildenafil citrate and kraussianone-2 on pre-eclampsia-like manifestations in Sprague-Dawley rats". Thesis, 2011. http://hdl.handle.net/10413/10120.

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Pre-eclampsia, often described as toxaemia of pregnancy, historically represents one of the most widely investigated conditions relating to human reproduction. To date no firm cure has been found and a clear, well defined mechanism has not been ascribed to the pathogenesis of the disease. Researchers seem to focus on single pathways in isolation of others. The disease rather represents a multitude of possible underlying pathologies nvolving genetics, immune dysregulation, vascular maladaptation, and sociobiological factors thus complicating the approach to treatment. However, a central theme is the presence of reduced placental perfusion resulting in a hypoxic and/or ischaemic placenta and the subsequent secretion of various factors that initiate the maternal syndrome. It is within this context that we examine how an intervention such as increasing placental perfusion may represent a promising treatment strategy for this disease. We sought to manipulate the vasodilatory mechanisms of the uterine vasculature using sildenafil citrate and a flavonoid extracted from Eriosema kraussianum (Kr2), in Sprague-Dawley rats that exhibited preeclampsia-like manifestations. Both treatment regimens improved fetal outcomes and reduced blood pressure amplification and proteinuria. They also reduced the plasma concentrations of the two anti-angiogenic factors; sFlt1 and sEng. Only sildenafil citrate improved nitric oxide levels which was expected, suggesting that Kr2 causes vasodilation by some other mechanism. Nevertheless, both compounds improved both pup and placental weights, suggesting that they also improve utero-placental perfusion. These findings that selective uterine vascular dilation improves placental perfusion may be promising in averting possible death to mothers and their babies from pre-eclampsia especially in low resource environments.
Thesis (Ph.D.)-University of KwaZulu-Natal, Westville, 2011.

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Sperou, Arissa. "Heightened maternal inflammation is linked to placental oxidative and nitrosative stress associated with fetal growth restriction in the rat". Thesis, 2013. http://hdl.handle.net/1974/8105.

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Deficient trophoblast invasion and spiral artery remodeling are associated with pregnancy complications such as pre-eclampsia (PE) and fetal growth restriction (FGR). Using a model in which pregnant Wistar rats are given daily, low-dose, injections of bacterial lipopolysaccharide (LPS; 10 – 40 µg/kg) on gestational days (GD) 13.5 – 16.5, our group has shown that abnormal maternal inflammation is causally linked to shallow trophoblast invasion, deficient spiral artery remodeling, and altered utero-placental hemodynamics leading to FGR/PE; these alterations were shown to be mediated by TNF-a. The present research evaluated certain consequences of decreased placental perfusion; this was accomplished by examining placental alterations indicative of decreased placental perfusion. Additionally, the role of glyceryl trinitrate (GTN) was determined as a potential therapeutic to prevent the consequences of decreased placental perfusion. Results indicated that dams experiencing heightened maternal inflammation showed significantly greater expression of hypoxia-inducible factor-1a (HIF-1a) and nitrotyrosine, both of which are markers of decreased perfusion and oxidative/nitrosative stress. Contrary to expectations, inflammation did not appear to affect nitric oxide (NO) bioavailability, as revealed by a lack of change in placental or plasma levels of cyclic guanosine monophosphate (cGMP). However, continuous transdermal administration of GTN (25 µg/hr) on GD 12.5 – 16.5 prevented the accumulation of HIF-1a and nitrotyrosine in placentas from LPS-treated rats. These results support the concept that maternal inflammation contributes to placental hypoxia and oxidative/nitrosative stress. Additionally, they indicate that GTN has potential applications in the treatment and/or prevention of pregnancy complications associated with abnormal maternal inflammation.
Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2013-07-05 14:37:05.15

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