Academic literature on the topic 'Cellule Fetali'
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Journal articles on the topic "Cellule Fetali"
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Bozzato, Gianni. "Quando inizia ad esistere l’individuo umano?" Medicina e Morale 48, no. 1 (February 28, 1999): 77–93. http://dx.doi.org/10.4081/mem.1999.811.
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Nel saggio sono posti in rilievo i seguenti principali aspetti di ordine biologico che contrastano con le argomentazioni sostenute da N. M. Ford nel suo libro When did I begin?
1) Nel cosiddetto pre-embrione, le cellule non sono totipotenti. (Ossia, non sono in grado di esprimere la totipotenza residua nucleare e cioè produrre altrettanti pre-embrioni. Nel presente articolo l’analisi della questione riguardante la totipotenza del pre-embrione, delle sue cellule o del loro nucleo viene soltanto appena accennata). La possibilità che il pre-embrione (individuo originario) dia origine a più gemelli monozigoti c. d. “identici” non è la conseguenza della totipotenza delle cellule, ma del loro distacco fisico dal pre-embrione, oppure della loro semplice “separazione/isolamento” dal suo schema di organizzazione dell’espressione genica del DNA (schema di OEG-DNA). 2) Le cellule del pre-embrione, inoltre, sono “identiche e indiscernibili” soltanto dal punto di vista genetico (genotipico), ma non da quello biologico (fenotipico). Anche dal punto di vista biologico (v. schema di OEG-DNA) il pre-embrione non è un semplice aggregato di cellule individuali, ma è una unità integrata e cioè un sistema individuale di cellule che possiede già una sua identità biologica, dunque ontologica. 3) Durante lo sviluppo, le cosiddette fasi (o stadi) e le forme anatomiche dell’embrione sono sempre precedute e prodotte da forme temporali (schemi di processi biochimici). Pertanto, sempre dal punto di vista dell’identità biologica (e ontologica), lo zigote (o il pre-embrione), anche nel caso di successiva gemellazione, è già un individuo umano in sviluppo (in atto) molto tempo prima che “appaia” - all’osservatore - un indizio “visibile” della sua forma anatomica individuale; dunque, ancor prima della “comparsa” della stria primitiva. 4) Proprio per il fatto che l’identità biologica dell’individuo umano non corrisponde alla sua identità genetica (ovvero il genotipo non è il fenotipo), i gemelli c. d. “identici” non sono mai veramente identici tra loro; essi sono sempre diversi fin dall’inizio del loro sviluppo, il quale avviene per biforcazione (una rottura di simmetria) dello schema di OEG-DNA dell’individuo pre-embrione originario. Lo studio della conformazione delle loro membrane fetali ci consente, infatti, di dedurre e di affermare che essi sono già in formazione (in atto) molto tempo prima della comparsa della stria primitiva e, in quanto biologicamente diversi, che sono già distinti; dunque, potenzialmente discernibili.
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Jordan, Jeanne A., Dale Huff, and Julie A. DeLoia. "Placental Cellular Immune Response in Women Infected with Human Parvovirus B19 during Pregnancy." Clinical Diagnostic Laboratory Immunology 8, no. 2 (March 1, 2001): 288–92. http://dx.doi.org/10.1128/cdli.8.2.288-292.2001.
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ABSTRACT Human parvovirus B19 can cause congenital infection with variable morbidity and mortality in the fetus and neonate. Although much information exists on the B19-specific antibody response in pregnant women, little information is available describing the cell-mediated immune (CMI) response at the maternal-fetal interface. The focus of this study was to characterize the CMI response within placentas from women who seroconverted to B19 during their pregnancies and compare it to controls. Immunohistochemical techniques were used to identify the various immune cells and the inflammatory cytokine present within placental tissue sections. Group 1 consisted of placentas from 25 women whose pregnancies were complicated by B19 infection; 6 women with good outcome (near-term or term delivery), and 19 with poor outcome (spontaneous abortion, nonimmune hydrops fetalis, or fetal death). Group 2 consisted of placentas from 20 women whose pregnancies were complicated with nonimmune hydrops fetalis of known, noninfectious etiology. Group 3 consisted of placentas from eight women whose pregnancies ended in either term delivery or elective abortion. The results of the study revealed a statistically significant increase in the number of CD3-positive T cells present within placentas from group 1 compared to group 2 or 3 (13.3 versus 2 and 1, respectively) (P < 0.001). In addition, the inflammatory cytokine interleukin 2 was detected in every placenta within group 1 but was absent from all placentas evaluated from groups 2 and 3. Together, these findings demonstrate evidence for an inflammation-mediated cellular immune response within placentas from women whose pregnancies are complicated with B19 infection.
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Jeanty, Cerine, S. Christopher Derderian, and Tippi C. MacKenzie. "Maternal–fetal cellular trafficking." Current Opinion in Pediatrics 26, no. 3 (June 2014): 377–82. http://dx.doi.org/10.1097/mop.0000000000000087.
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Fjeldstad, Heidi ES, Guro M. Johnsen, and Anne Cathrine Staff. "Fetal microchimerism and implications for maternal health." Obstetric Medicine 13, no. 3 (December 6, 2019): 112–19. http://dx.doi.org/10.1177/1753495x19884484.
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This review paper outlines the definition, pathophysiology, and potential maternal health consequences of cellular fetal microchimerism, the maternal acquisition of intact cells of fetal origin during pregnancy. Increased rates and amounts of cellular fetal microchimerism are associated with several placental syndromes, including preeclampsia and fetal growth restriction. The discovery of cellular fetal microchimerism and methods of detection are briefly outlined, and we present the mechanisms hypothesized to govern pregnancy-related and long-term maternal health effects of cellular fetal microchimerism. Specifically, we discuss the potential implications of cellular fetal microchimerism in wound healing, autoimmunity, cancer, and possibly cardiovascular disease. Cellular fetal microchimerism represents a novel area of research on maternal and transgenerational health and disease, providing exciting opportunities for developing new disease biomarkers and precision medicine with targeted prophylaxis against long-term maternal disease.
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Gammill, Hilary S., Tessa M. Aydelotte, Katherine A. Guthrie, Evangelyn C. Nkwopara, and J. Lee Nelson. "Cellular Fetal Microchimerism in Preeclampsia." Hypertension 62, no. 6 (December 2013): 1062–67. http://dx.doi.org/10.1161/hypertensionaha.113.01486.
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Saadai, Payam, Tzong-Hae Lee, Geoanna Bautista, Kelly D. Gonzales, Amar Nijagal, Michael P. Busch, Chong Jai Kim, et al. "Alterations in maternal-fetal cellular trafficking after fetal surgery." Journal of Pediatric Surgery 47, no. 6 (June 2012): 1089–94. http://dx.doi.org/10.1016/j.jpedsurg.2012.03.012.
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Hart, Bethany, Elizabeth Morgan, and Emilyn U. Alejandro. "Nutrient sensor signaling pathways and cellular stress in fetal growth restriction." Journal of Molecular Endocrinology 62, no. 2 (February 2019): R155—R165. http://dx.doi.org/10.1530/jme-18-0059.
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Fetal growth restriction is one of the most common obstetrical complications resulting in significant perinatal morbidity and mortality. The most frequent etiology of human singleton fetal growth restriction is placental insufficiency, which occurs secondary to reduced utero-placental perfusion, abnormal placentation, impaired trophoblast invasion and spiral artery remodeling, resulting in altered nutrient and oxygen transport. Two nutrient-sensing proteins involved in placental development and glucose and amino acid transport are mechanistic target of rapamycin (mTOR) and O-linked N-acetylglucosamine transferase (OGT), which are both regulated by availability of oxygen. Impairment in either of these pathways is associated with fetal growth restriction and accompanied by cellular stress in the forms of hypoxia, oxidative and endoplasmic reticulum (ER) stress, metabolic dysfunction and nutrient starvation in the placenta. Recent evidence has emerged regarding the potential impact of nutrient sensors on fetal stress response, which occurs in a sexual dysmorphic manner, indicating a potential element of genetic gender susceptibility to fetal growth restriction. In this mini review, we focus on the known role of mTOR and OGT in placental development, nutrient regulation and response to cellular stress in human fetal growth restriction with supporting evidence from rodent models.
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Korchynska, N. S., О. М. Slobodian, and V. O. Kostyuk. "FETAL ANATOMY OF THE MAXILLARY CELLULAR PROCESS." Clinical anatomy and operative surgery 18, no. 1 (January 23, 2019): 62–66. http://dx.doi.org/10.24061/1727-0847.18.1.2019.10.
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Nijagal, Amar, and Tippi C. MacKenzie. "Clinical implications of maternal-fetal cellular trafficking." Seminars in Pediatric Surgery 22, no. 1 (February 2013): 62–65. http://dx.doi.org/10.1053/j.sempedsurg.2012.10.011.
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Olney, John. "Fetal alcohol syndrome at the cellular level." Addiction Biology 9, no. 2 (June 2004): 137–49. http://dx.doi.org/10.1080/13556210410001717006.
Full textDissertations / Theses on the topic "Cellule Fetali"
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Costa, Roberta <1983>. "Caratteristiche biologiche e potenziale applicativo delle cellule staminali derivate da membrane fetali." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5757/1/Costa_Roberta_tesi.pdf.
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La ricerca sulle cellule staminali apre nuove prospettive per approcci di terapia cellulare. Molta attenzione è concentrata sulle cellule staminali isolate da membrane fetali, per la facilità di recupero del materiale di partenza, le limitate implicazioni etiche e le caratteristiche delle popolazioni di cellule staminali residenti. In particolare a livello dell’epitelio amniotico si concentra una popolazione di cellule (hAECs) con interessanti caratteristiche di staminalità, pluripotenza e immunomodulazione. Restano però una serie di limiti prima di arrivare ad un’applicazione clinica: l’uso di siero di origine animale nei terreni di coltura e le limitate conoscenze legate alla reazione immunitaria in vivo. La prima parte di questo lavoro è focalizzata sulle caratteristiche delle hAECs coltivate in un terreno privo di siero, in confronto a un terreno di coltura classico. Lo studio è concentrato sull’analisi delle caratteristiche biologiche, immunomodulatorie e differenziative delle hAECs. L’interesse verso le caratteristiche immunomodulatorie è legato alla possibilità che l’uso di un terreno serum free riduca il rischio di rigetto dopo trapianto in vivo. La maggior parte degli studi in vivo con cellule isolate da membrane fetali sono stati realizzati con cellule di derivazione umana in trapianti xenogenici, ma poco si sa circa la sopravvivenza di queste cellule in trapianti allogenici, come nel caso di trapianti di cellule di derivazione murina in modelli di topo. La seconda parte dello studio è focalizzata sulla caratterizzazione delle cellule derivate da membrane fetali di topo (mFMSC). Le caratteristiche biologiche, differenziative e immunomodulatorie in vitro e in vivo delle mFMSC sono state confrontate con i fibroblasti embrionali di topo. In particolare è stata analizzata la risposta immunitaria a trapianti di mFMSC nel sistema nervoso centrale (CNS) in modelli murini immunocompetenti.The stem cell research opens new perspectives for cell therapy approaches. Much attention has been focused on stem cells isolated from fetal membranes, for the easy recovery of these tissues, the limited ethical implications and the characteristics of resident stem cells. In particular from the amniotic epithelium it is possible to isolate a population of cells (hAECs) with interesting characteristics of stemness, pluripotency and immunomodulation. However, before going to clinic there are some limitations to overcome: the use of culture media supplemented with animal serum and the limited knowledge related to immune reactions in vivo. The first part of this work is focused on the characterization of hAECs cultured in a serum-free medium, in comparison to a classical culture medium. The study is concerned with the biological, immunomodulatory and differentiation properties of hAECs. The interest towards immunomodulatory characteristics is related to the possibility that using a serum free medium could reduce the risk of grafts rejection after transplantation in vivo. The majority of in vivo studies with cells isolated from fetal membranes were carried out with human-derived cells in xenogeneic transplantation, but little is known about the survival of these cells in allogeneic settings, as for transplantation of murine cells in mouse models. The second part of this study is focused on the characterization of cells derived from murine fetal membranes (mFMSC). Biological characteristics, differentiation potential, in vitro and in vivo immunomodulatory properties of mFMSC has been compared with mouse embryonic fibroblasts. In particular we analyzed the immune response towards mFMSC grafted in the central nervous system (CNS) of immunocompetent mice.
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Costa, Roberta <1983>. "Caratteristiche biologiche e potenziale applicativo delle cellule staminali derivate da membrane fetali." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5757/.
Full textAbstract:
La ricerca sulle cellule staminali apre nuove prospettive per approcci di terapia cellulare. Molta attenzione è concentrata sulle cellule staminali isolate da membrane fetali, per la facilità di recupero del materiale di partenza, le limitate implicazioni etiche e le caratteristiche delle popolazioni di cellule staminali residenti. In particolare a livello dell’epitelio amniotico si concentra una popolazione di cellule (hAECs) con interessanti caratteristiche di staminalità, pluripotenza e immunomodulazione. Restano però una serie di limiti prima di arrivare ad un’applicazione clinica: l’uso di siero di origine animale nei terreni di coltura e le limitate conoscenze legate alla reazione immunitaria in vivo. La prima parte di questo lavoro è focalizzata sulle caratteristiche delle hAECs coltivate in un terreno privo di siero, in confronto a un terreno di coltura classico. Lo studio è concentrato sull’analisi delle caratteristiche biologiche, immunomodulatorie e differenziative delle hAECs. L’interesse verso le caratteristiche immunomodulatorie è legato alla possibilità che l’uso di un terreno serum free riduca il rischio di rigetto dopo trapianto in vivo. La maggior parte degli studi in vivo con cellule isolate da membrane fetali sono stati realizzati con cellule di derivazione umana in trapianti xenogenici, ma poco si sa circa la sopravvivenza di queste cellule in trapianti allogenici, come nel caso di trapianti di cellule di derivazione murina in modelli di topo. La seconda parte dello studio è focalizzata sulla caratterizzazione delle cellule derivate da membrane fetali di topo (mFMSC). Le caratteristiche biologiche, differenziative e immunomodulatorie in vitro e in vivo delle mFMSC sono state confrontate con i fibroblasti embrionali di topo. In particolare è stata analizzata la risposta immunitaria a trapianti di mFMSC nel sistema nervoso centrale (CNS) in modelli murini immunocompetenti.The stem cell research opens new perspectives for cell therapy approaches. Much attention has been focused on stem cells isolated from fetal membranes, for the easy recovery of these tissues, the limited ethical implications and the characteristics of resident stem cells. In particular from the amniotic epithelium it is possible to isolate a population of cells (hAECs) with interesting characteristics of stemness, pluripotency and immunomodulation. However, before going to clinic there are some limitations to overcome: the use of culture media supplemented with animal serum and the limited knowledge related to immune reactions in vivo. The first part of this work is focused on the characterization of hAECs cultured in a serum-free medium, in comparison to a classical culture medium. The study is concerned with the biological, immunomodulatory and differentiation properties of hAECs. The interest towards immunomodulatory characteristics is related to the possibility that using a serum free medium could reduce the risk of grafts rejection after transplantation in vivo. The majority of in vivo studies with cells isolated from fetal membranes were carried out with human-derived cells in xenogeneic transplantation, but little is known about the survival of these cells in allogeneic settings, as for transplantation of murine cells in mouse models. The second part of this study is focused on the characterization of cells derived from murine fetal membranes (mFMSC). Biological characteristics, differentiation potential, in vitro and in vivo immunomodulatory properties of mFMSC has been compared with mouse embryonic fibroblasts. In particular we analyzed the immune response towards mFMSC grafted in the central nervous system (CNS) of immunocompetent mice.
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Calzarossa, C. "Terapia cellulare : potenzialità e applicazioni terapeutiche di cellule staminali fetali e adulte in modelli animali di neurodegenerazione." Doctoral thesis, Università degli Studi di Milano, 2008. http://hdl.handle.net/2434/61187.
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Ditadi, Andrea. "Approccio di terapia cellulare mediante l'utilizzo di cellule fetali isolate dal liquido amniotico per malattie del sistema ematopoieico." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425090.
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Cell therapy is an attractive perspective for the treatment of life threatening disorders. In this context, foetal tissues are gaining interest as sources of cells for auto- and allo-transplantation, because of their pluripotency, proliferative capability and their low, if any, immunogenicity. Recently a pluripotent stem cell population has been isolated from Amniotic Fluid (AF). It is able to proliferate for more than 18 months, maintaining their differentiative ability as well as a normal karyotype. In term of differentiation potential, we succeeded in obtaining in vitro mesenchymal-, ectodermal- and endodermal-derived tissues from human Amniotic Fluid Stem (AFS) cells. Furthermore, murine AFS cells injected in blastocytes took part to the formation not only of several different foetal organs, but also of the placenta and the umbilical cord. In the present study we investigated the possibility of differentiating AFS cells towards the hematopoietic pathway.
AFS cells isolated from human amniotic fluid, collected during routine diagnostic procedures and obtained under informed consent, were firstly expanded in vitro and selected on the basis of their ckit expression. We achieved a reproducible erythroid differentiation by culturing hAFSCs as embryoid bodies (EBs) under serum free conditions with haematopoietic cytokines. Erythroid cells expressing CD235a constituted 70% of the total hAFSCs forming EBs showing also a co-expression of CD36 and CD71. Furthermore, human erythrocytes (human CD235a) were isolated from bone marrow and spleen of sublethally irradiated NOD/SCID mice at 3 months after the injection of hAFSCs.
To determine if the expansion procedure had led to a restriction of the hematopoietic potential towards the erythroid pathway, we compared expanded AFSCs and freshly isolated cKit+ Lin- (AFKL) cells. We also harvested cKit+ Lin- KL cells from the membrane surrounding the AF, the Amnion, in search for a possible origin. We compared the hematopoietic potential of mAFKL and mAmKL to Fetal Liver KL, the main source of fetal HSC. When cultivated immediatly after their sorting, freshly isolated murine AFKL and AmKL cells gave rise to all the different hematopoietic lineages both in vitro and in vivo. Actually, when cocultivated with OP9(d)1 cells, AFKL and AmKL undergo complete T cell differentiation within 2 weeks. They also generate myeloid and erythroid colonies when cultivated in methylcellulose for clonogenic assay. The erythroid restricted potential of human AFS cells was thus probably linked to the in vitro expansion procedure.
Moreover, cells belonging to all the three hematopoietic lineages (lymphoid, myeloid and erythroid) and arising from freshly isolated mAFKL and mAmKL are found in the peripheral blood of sublethally irradiated RAG1 deficient mice only 4 weeks after transplantation. Four month later, transplanted mice showed mAFKL-derived lymphoid, myeloid and erythroid cells, in all the hematopoietic organs. Successful econdary transplantation strongly suggest that mAFKL and mAmKL comprise HSC, with self-renewal ability. Those results were very similar to those obtained with mFLKL, confirming the strong hematopoietic potential of mAFKL and mAmKL. Experiments with freshly isolated hAFKL gave good results in the in vitro assays being able to give rise to erythroid, myeloid and lymphoid lineages, but failed to reconstitute the hematopoietic system in irradiated NOD/SCID mice, probably due to the poor amount of cells injected.
This is the first report demonstrating that AFKL and AmKL do have an haematopoietic potential, supporting the idea that AF and Am may be an excellent source for therapeutic application.
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Soncini, M. "Caratterizzazione fenotipica e potenzialità differenziative delle cellule isolate dalle membrane fetali di placenta umana a termine." Doctoral thesis, Università degli Studi di Milano, 2007. http://hdl.handle.net/2434/33611.
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The work here presented is a part of a bigger project at the Centro di Ricerca E. Menni (Fondazione Poliambulanza, Istituto Ospedaliero, Brescia), aimed to identify new adult stem cells sources. In these last years, in order to find a tissue easy to procure and that allows to obtain high cell yeld researchers have turned their attention to alternative sources of adult stem cells as adipose tissue, peripheral blood, cord blood and, more recently, placenta tissue. In this field, placenta is of particular interest either because of its immunological role in maintaining fetus-maternal tolerance either because of its early embryological origin which may entail an immature phenotype. In particular we are focusing our attention on fetal membranes, amnion and chorion, which form the outer limit of the sac that encloses the fetus. The amnion is an unique avascular tissue and is comprised of an epithelial monolayer on the top of a mesodermal layer. The amniotic mesoderm is loosely connected to the chorionic mesoderm, in contact to the trophoblastic layer which is in intimate contact with the maternal decidua. The aim of this study was to isolate different cell populations from the 4 layers which costitute the fetal membranes, evaluating all the features that contribute to hypothesize the presence of stem cells. In particular the phenotypic profile and the differentiation potential toward mesodermal lineages of the different cell populations were evaluated, in comparison with bone marrow stromal cells.
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DOFFINI, ANNA. "A cell-based NIPD (Non-invasive prenatal diagnosis) procedure to select fetal cells from pregnant women maternal blood." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/365173.
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Attualmente i metodi di diagnosi prenatale esistenti, consentono di ottenere cellule fetali solamente mediante metodiche invasive che comportano un rischio sia per la madre che per il feto. La scoperta nel 1979 della presenza di cellule fetali circolanti nel sangue materno, ha aperto la strada per lo sviluppo di metodi non invasivi per l’identificazione di anomalie fetali. Tutti i metodi sviluppati fino ad oggi tuttavia sono risultati inefficienti nel garantire un adeguato numero di cellule fetali, essendo estremamente laboriosi, richiedendo molto tempo ed essendo operatori-dipendenti.
Questo progetto ha lo scopo di sviluppare un metodo non invasivo per l’isolamento di singole cellule fetali dal sangue materno, per una analisi diretta dei cromosomi fetali. La prima parte è stata dedicata alla ricerca e test di diversi marcatori specifici per l’arricchimento e l’identificazione delle cellule fetali. Una volta messo a punto lo step di arricchimento, quest’ultimo è stato implementato e integrato in un worklow più ampio che prevedeva: prelievi di sangue da donne in gravidanza, arricchimento positivo magnetico, marcatura delle cellule fetali, isolamento come singole cellule e analisi genetica. Appena l’intero flusso è stato standardizzato abbiamo cominciato una valutazione clinica su donne in gravidanza. Al fine di determinare la percentuale di successo e il numero di cellule fetali per campione, un totale di 372 donne sono state reclutate e stratificate in base alla loro settimana gestazionale al momento del prelievo. Al meno una cellula fetale è stata isolata nel 90.7% dei casi prelevati tra la decima e undicesima settimana gestazionale, con un numero medio totale di 3.5 cellule fetali per paziente. Inoltre dati preliminari ottenuti da 131 donne che venivano sottoposte all’esame invasivo, hanno mostrato un alto livello di concordanza tra le cellule isolate singolarmente e analizzate con la nostra metodica e i risultati derivanti dall’esame diagnostico.
Complessivamente, i risultati derivanti da questo studio, supportano la fattibilità clinica di un isolamento automatico e riproducibile delle cellule fetali circolanti ottenute in maniera non invasiva, da utilizzare per le analisi genetiche. Per questo motivo uno studio clinico di valutazione delle performance comincerà a breve su 1500 pazienti, reclutate in cinque diversi ospedali italiani. Obiettivi primari di questo studio saranno la valutazione delle performance in termini di sensibilità’ e specificità del metodo sviluppato, per il rilevamento delle aneuploidie fetali nelle gravidanze ad alto rischio. I risultati saranno comparati con i dati derivanti dalla diagnosi prenatale invasiva ottenuti dalle stesse donne che eseguiranno l’amniocentesi e la villocentesi. L’analisi comparativa determinerà i falsi postivi, falsi negativi, veri postivi e veri negativi del metodo sviluppato.Current methods of prenatal diagnosis require fetal cells to be obtained through invasive procedures, risky for mother and fetus. The discovery of circulating fetal cells in 1979 and the possibility that these cells could be isolated from maternal blood during pregnancy was key to the development of alternative noninvasive approaches for identifying most fetal genetic abnormalities. All these methods result in a laborious, operator depending, time-consuming approach which until now it has not allowed to achieve a high and consistent purification of fetal cells. This project aims to develop a non-invasive method for the isolation of single fetal cells from maternal blood, for direct analysis of fetal chromosomes. The first part was dedicated to the research and testing of different specific markers for fetal cells enrichment and identification. Once optimized, the enrichment step was implemented to be automatic and integrated in a full workflow consisting of: pregnant women blood collection, positive magnetic enrichment, cell staining, single cell isolation and genetic analysis. As soon as the full workflow was standardized we started a clinical evaluation. To determine the success rate and number of trophoblast per sample, a total of 372 women were enrolled and stratified by gestational age at the time of blood collection. At least one fetal cell was isolated in 90.7% of the women sampled between 10-11 gestational weeks with an overall mean number of 3.5 recovered trophoblasts per patient. Furthermore, preliminary data from 131 women, showed a high concordance rate between isolated single trophoblastic cells and fetal karyotype for common trisomies and normal results deriving from gold standard invasive procedure. Overall, the results coming out from this study support the clinical feasibility of an automated and reproducible isolation of fetal cells for non-invasive prenatal genetic testing, well suited to the routine clinical practice. For this reason a clinical performance evaluation study will start soon, on 1500 patients, enrolled from five different Italian Hospital. Primary endpoints of the study will be the performance evaluation, in terms of sensitivity and specificity, of the developed workflow for fetal aneuploidies and segmental imbalances detection in a high-risk pregnancies population. Results will be compared with data resulting from invasive prenatal diagnosis for chromosomal abnormalities obtained on the same women presenting for hospital invasive procedure because classified from the physician as high risk pregnancy. The comparative analysis will determine the false positive, false negative, true positive, and true negative rates of the developed technology.
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TONDELLI, BARBARA. "TECNICHE AVANZATE NELLA MESSA A PUNTO DI TECNOLOGIE TRANSGENICHE E NON NELLA SPECIE MURINA." Doctoral thesis, Università Cattolica del Sacro Cuore, 2009. http://hdl.handle.net/10280/406.
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L’osteopetrosi autosomale recessiva (ARO) è un gruppo di malattie dovute a un difettoso funzionamento degli osteoclasti che preclude un rimodellamento osseo corretto. Nel 50% dei casi umani il difetto è dovuto ad una delezione nel gene Tcirg1. Il modello murino mutante oc/oc porta lo stesso difetto genetico e fenotipico umano. Nel lavoro di tesi si è dimostrato che gli epatociti fetali di 12.5 giorni di gestazione trapiantati in utero in feti mutati di 13.5 giorni di gestazione sono in grado di curare il fenotipo malato. Si è inoltre derivata una sottolinea di cellule staminali embrionali murine transgeniche per il costrutto plasmidico GOF18eGFP. Si vuole utilizzare la GFP sotto il controllo del promotore del gene Oct-4 come marcatore del livello di staminalità cellulare per microiniettare le ESC in blastocisti murine mutate oc/oc.Autosomal recessive osteopetrosis (ARO) is a group of genetic disorders due to defects that preclude normal function of osteoclasts. In half the cases, human ARO is due to mutations in the Tcirg1 gene. The oc/oc mutant mouse closely recapitulates human Tcirg1-dependent ARO. In ths work we demonstrate that in utero injection of allogenic fetal liver cells on 12.5 days into oc/oc fetuses at 13.5 day post coitum completely rescue the osteopetrotic phenotype. Moreover, an embryonic stem cells line transgenic for GOF18eGFP was produced. The goal is to use the GFP under the transcriptional control of the Oct-4 promoter as a marker of pluripotency of the ESC that are to microinject into oc/oc blastocysts.
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TONDELLI, BARBARA. "TECNICHE AVANZATE NELLA MESSA A PUNTO DI TECNOLOGIE TRANSGENICHE E NON NELLA SPECIE MURINA." Doctoral thesis, Università Cattolica del Sacro Cuore, 2009. http://hdl.handle.net/10280/406.
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L’osteopetrosi autosomale recessiva (ARO) è un gruppo di malattie dovute a un difettoso funzionamento degli osteoclasti che preclude un rimodellamento osseo corretto. Nel 50% dei casi umani il difetto è dovuto ad una delezione nel gene Tcirg1. Il modello murino mutante oc/oc porta lo stesso difetto genetico e fenotipico umano. Nel lavoro di tesi si è dimostrato che gli epatociti fetali di 12.5 giorni di gestazione trapiantati in utero in feti mutati di 13.5 giorni di gestazione sono in grado di curare il fenotipo malato. Si è inoltre derivata una sottolinea di cellule staminali embrionali murine transgeniche per il costrutto plasmidico GOF18eGFP. Si vuole utilizzare la GFP sotto il controllo del promotore del gene Oct-4 come marcatore del livello di staminalità cellulare per microiniettare le ESC in blastocisti murine mutate oc/oc.Autosomal recessive osteopetrosis (ARO) is a group of genetic disorders due to defects that preclude normal function of osteoclasts. In half the cases, human ARO is due to mutations in the Tcirg1 gene. The oc/oc mutant mouse closely recapitulates human Tcirg1-dependent ARO. In ths work we demonstrate that in utero injection of allogenic fetal liver cells on 12.5 days into oc/oc fetuses at 13.5 day post coitum completely rescue the osteopetrotic phenotype. Moreover, an embryonic stem cells line transgenic for GOF18eGFP was produced. The goal is to use the GFP under the transcriptional control of the Oct-4 promoter as a marker of pluripotency of the ESC that are to microinject into oc/oc blastocysts.
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LA, SALA GINA. "Effetti degli estrogeni e dei distruttori endocrini sulle cellule germinali embrionali di topo e sulle cellule somatiche della gonade." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/901.
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Negli ultimi anni si è assistito ad un crescente aumento nell’ambiente di sostanze che sono in grado di alterare il sistema endocrino poiché agiscono come l’ormone naturale estrogeno e per questo definite distruttori endocrini (EDs). Si ipotizza che l’esposizione agli EDs durante il periodo fetale e neo-natale sia la causa dell’insorgenza di numerosi disordini dell’apparato riproduttivo maschile come sterilità, cancro del testicolo, criptorchidismo e ipospadia che vengono definite con il termine unico di sindrome del testicolo disgenico (TDS). E’ importante studiare gli effetti degli estrogeni e degli xenoestrogeni, una classe di EDs, durante il periodo fetale ed in particolare durante lo sviluppo dell’apparto riproduttivo e conoscere i meccanismi, con cui tali sostanze esplicano i loro effetti.
OBIETTIVI. Verificare l'espressione dei recettori degli estrogeni (ERs) nei precursori dei gameti adulti, ovvero nelle cellule germinali di topo denominate PGCs e analizzare i pathways molecolari attivati in queste cellule dagli estrogeni e dallo xenoestrogeno lindano. Inoltre si vuole verificare la presenza di ERs funzionali nelle cellule somatiche testicolari embrionali utilizzando costrutti ERE-luc e AP1-Luc per valutare l'attività estrogenica di xenoestrogeni.
RISULTATI. Lo studio condotto in questa tesi mette in evidenza l'esistenza di pathways molecolari attivabili dall’estrogeno (E2) nelle gonadi embrionali di topo, in particolare, nel testicolo, sia nelle cellule germinali primordiali che nelle cellule somatiche. Abbiamo osservato che l’E2 è in grado di attivare, attraverso il recettore degli estrogeni ERα , importanti chinasi nelle PGCs (AKT, ERK1/2 e SRC) con effetti positivi sulla crescita e proliferazione di tali cellule. Si è osservato che il lindano, al contrario dell’E2, influenza negativamente la sopravvivenza di tali cellule attraverso una azione pro-apoptotica diretta, probabilmente derivante da effetti negativi sull’attività chinasica AKT. Inoltre abbiamo descritto per la prima volta l'esistenza di un recettore dell’estrogeno funzionale nelle cellule del Leydig testicolari durante lo stadio precoce dello sviluppo e messo a punto un test in vitro che può essere utilizzato per valutare l'attività estrogenica di xenoestrogeni direttamente sulle cellule del testicolo embrionale di mammiferi.
CONCLUSIONI: Questi risultati rafforzano l’ipotesi dell’origine fetale della TDS. Numerosi studi hanno messo in evidenza gli effetti diretti degli estrogeni sul sistema endocrino, sull'espressione genica e su funzioni specifiche delle cellule somatiche testicolari embrionali, in particolare sulle cellule del Leydig, tuttavia tali studi sono carenti nelle cellule germinali. E’ importante conoscere i meccanismi di azione degli xenoestrogeni sullePGCs visto che attraverso esse viene trasmesso il genoma alle generazioni successive.In the recent years the increased presence of human made compounds that mimic the action of estrogens termed endocrine disrupters (ED) in environment and in food and the exposure to these compounds during fetal and neonatal period has been hypotized to be the cause of the raise of disorders of male reproductive function, such a decrease of sperm count, increase in the incidence of testicular cancer and cryptorchidism and hypospadias termed Testicular Dysgenesis Syndrome (TDS). For these reason, it is important to know how the estrogens and xenoestrogens, a class of ED, act during the fetal development and to know the mechanism by which these compounds exert their effects. AIMS: To study the expression of estrogen receptors (ERs) in the embryonic precursors of the adult gametes termed PGCs and to analyze the existence in such cells of intracellular molecular pathways modulable by estrogens and xenoestrogen lindane. To verify the presence of functional ER-beta in embryonic testicular somatic cells using an ERE-luc and AP1-Luc assay and to evaluate estrogenic activity of putative EDs on mammalian embryonic testis. RESULTS: The data described in this thesis highlights the existence of functional estrogen-dependent pathways in embryonic mouse gonads in particular in testis, both in germ and somatic cells. We found that E2 is able to activate via ER-beta multiple intracellular signalling in PGCs and that the xenoestrogens, lindane affect the survival in such cells through a direct pro-apoptotic action likely resulting from its adverse effect on AKT activity. Othermore, we described for the first time the existence of a functional ERα pathway in putative Leydig cells from early stage of testis development and describe an in vitro assay that can be used to evaluate estrogenic activity of compounds on mammalian embryonic testis. CONCLUSIONS: These results support the notion of the TDS origin during early stages of testis development. While data are accumulating showing direct effect of estrogens and EDs on gene expression and specific functions of somatic cells of the embryonic testes, in particular Leydig cells, such results on germ cells are lacking and further studies are needed to investigate the effects of these compounds on embryonic germ cell function including epigenetic regulation.
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CONTINI, ANTONELLA. "Diagnosi prenatale non invasiva di malattie monogeniche attraverso la ricerca e l'isolamento di cellule e DNA fetale nel sangue materno." Doctoral thesis, Università degli Studi di Cagliari, 2012. http://hdl.handle.net/11584/266061.
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Prenatal genetic diagnosis of monogenic diseases and chromosomal abnormalities is usually performed collecting fetal samples through villocentesis or amniocentesis.
These invasive procedures are associated with 0.5-1% risk for the fetus. Due to it, in recent years, much effort has been made to develop non invasive prenatal diagnosis (NIPD). Two potential non invasive approaches involve the analysis of fetal cells and cell-free fetal DNA (cffDNA) found in the maternal circulation. The presence of fetal cells in the maternal circulation was first documented by 1893 when the fetal cells were found in pregnant women died for eclampsia. The Fetal erythroblasts (NRBC) from the maternal circulation have been considered the best potential target for NIPD because they can be detected early in pregnancy, are nucleated and have short life. The NRBC isolation from maternal circulation is still
difficult because the number of NRBC is small and a fetal specific antibody is not currently available. Cff-DNA detected in the maternal circulation during pregnancy, could potentially offer an excellent method for early NIPD of the genetic status of a fetus. In a recent study has been
shown that, during the pregnancy, the cffDNA is cleared from the maternal circulation, 16 min following delivery. Moreover, it has been demonstrated that cffDNA has a mean
fractional concentration of about 10%. The goal of our project was to develop and validate a protocol for NIPD of monogenic diseases by two experimental procedures: the isolation and the molecular characterization of fetal NRBC, and the analysis of cffDNA in maternal plasma. We recruited 95 pregnant women between 6th and 14th week of gestation. In our study we have developed a protocol for fetal NRBC isolation from maternal blood that unfortunately require further refinements the isolation procedure. In parallel we have developed a protocol for non invasive fetal sexing from cffDNA. This method appears to be highly accurate showing 100% sensitivity and 96% specificity. In the next future we are planning to analyze cffDNA both for monogenic diseases and for the most frequent aneuploidies using massively parallel sequencing.
Books on the topic "Cellule Fetali"
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G, Wegmann Thomas, Gill Thomas J, Nisbet-Brown Eric, and Banff Conference on Reproductive Immunology (3rd : 1989 : Banff, Alta.), eds. Molecular and cellular immunobiology of the maternal fetal interface. New York: Oxford University Press, 1991.
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E, Broxmeyer Hal, ed. Cellular characteristics of cord blood and cord blood transplantation. Bethesda, Md: AABB Press, 1998.
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National Institute of Child Health & Human Development Research Planning Workshop (1987 Bethesda, Md.). The onset of labor: Cellular and integrative mechanisms : a National Institute of Child Health & Human Development Research Planning Workshop, November 29-December 1, 1987. Ithaca, NY, U.S.A: Publisher and sole distributor, Perinatology Press, 1988.
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Raz, Yirmiya, and Taylor Anna N, eds. Alcohol, immunity, and cancer. Boca Raton: CRC Press, 1993.
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G, Payne Anthony, ed. Umbilical-cord stem-cell therapy: The gift of healing from healthy newborns. Laguna Beach, CA: Basic Health Publications, 2006.
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F, Mowbray James, Chaouat Gérard, and Institut national de la santé et de la recherche médicale (France), eds. Cellular and molecular biology of the materno-fetal relationship: Proceedings of the 2nd meeting on reproductive immunology held in Paris (France), December 17-20, 1990 = Biologie cellulaire et moléculaire de la relation materno-fœtale. Paris: J. Libbey Eurotext, 1991.
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1962-, Baker Philip, and Sibley Colin, eds. The placenta and neurodisability. London: Mac Keith Press, 2006.
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Ridsdale, Ross Allan. CTP:phosphocholine cytidylyltransferase alpha overexpression and cellular distribution in fetal lung. 2005.
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Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, and Michelle Fink. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.
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Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, and Michelle Fink. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.
Find full textBook chapters on the topic "Cellule Fetali"
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Sedlmayr, Peter. "Fetal Erythrocytes." In Cellular Diagnostics, 680–86. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209186.
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Hill, D. J., and V. K. M. Han. "Control of cellular multiplication and differentiation." In Fetal Growth, 83–98. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1707-0_8.
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Dame, Christof, Viola Lorenz, and Martha Sola-Visner. "Fetal and Neonatal Megakaryopoiesis and Platelet Biology." In Molecular and Cellular Biology of Platelet Formation, 267–91. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39562-3_12.
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Kratochwil, Klaus. "Epithelium — Mesenchyme Interaction in the Fetal Mammary Gland." In Cellular and Molecular Biology of Mammary Cancer, 67–80. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0943-7_5.
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Freemark, Michael. "The Roles of Growth Hormone, Prolactin, and Placental Lactogen in Human Fetal Development." In Molecular and Cellular Pediatric Endocrinology, 57–83. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-697-3_5.
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Halloran, Bernard P. "Cellular Growth and Differentiation during Embryogenesis and Fetal Development." In Advances in Experimental Medicine and Biology, 227–36. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-2575-6_20.
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Longo, Lawrence D. "Fetal Growth Restriction at High Altitude: Basic Cellular and Subcellular Physiologic Considerations." In The Rise of Fetal and Neonatal Physiology, 435–99. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7483-2_15.
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McCallion, R. L., and M. W. J. Ferguson. "Fetal Wound Healing and the Development of Antiscarring Therapies for Adult Wound Healing." In The Molecular and Cellular Biology of Wound Repair, 561–600. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-0185-9_18.
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Jacques, Danielle, Ghassan Bkaily, Gaétan Jasmin, Daniel Ménard, and Libuse Proschek. "Early fetal like slow Na+ current in heart cells of cardiomyopathic hamster." In The Cellular Basis of Cardiovascular Function in Health and Disease, 249–56. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5765-4_32.
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Buttar, Harpal S. "An overview of the influence of ACE inhibitors on fetal-placental circulation and perinatal development." In The Cellular Basis of Cardiovascular Function in Health and Disease, 61–71. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5765-4_9.
Full textConference papers on the topic "Cellule Fetali"
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Hassan, H. J., A. Leonardi, C. Chelucci, R. Guerriero, P. M. Mannucci, and C. Peschle. "EXPRESSION IN ONTOGENESIS OF HUMAN BLOOD COAGULATION FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644610.
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We have analyzed the expression of several blood coagulation factors (IX, VIII, X, fibrinogen chains) and inhibitors (antithrombin III, protein C) in human embryonic and fetal livers, obtained from legal abortions at 6-11 week post-conception. The age was established by morphologic staging and particularly crown-rump lenght measurement.Total cellular RNA was isolated from partially purified hepatocytes or total liver homogenate using the guanidine isothiocyanate method. Poly(A)+ RNA was selected by oligodT cellulose chromatography. The size and the number of the embryonic and fetal transcripts are equivalent to those observed in adult liver, as evaluated by Northern blot analysis of total or poly(A)+ RNA hybridized to human cDNA probes.The level of coagulation factor transcripts in embryonic and fetal liver was evaluated by dot hybridization of total RNA (0.5-10 ug), as compared to RNA extracted from normal adult liver biopsies. The expression of blood coagulation factors in embryos is generally reduced for all factors, but at a different degree. In 5-11 wk liver, the level of factor IX is 5-10% of that observed in adults, while fibrinogen, protein C, antithrombin III RNA level rises from 25 to 50% and factor X is expressed at a level comparable to that observed in adult liver.We conclude that during these stages of development blood coagulation factors are expressed according to three different time, curves, possibly due to the effect of different types of regulatory mechanisms.
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Najrana, Tanbir, Juan Sanchez-Esteban, and Rasha Abu Eid. "The Effect of Oligohydramnios on Tissue and Cellular Morphometry in the Developing Fetal Murine Lung." In 2017 21st International Conference on Control Systems and Computer Science (CSCS). IEEE, 2017. http://dx.doi.org/10.1109/cscs.2017.52.
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Moore, John J., Robert M. Moore, Deepak Kumar, Joseph M. Mansour, Brian M. Mercer, Elizabeth Yohannes, Jillian Novak, and Mark Chance. "Differential Expression of Fibulin Family Proteins in Mechanically Strong vs. Weak Fetal Membrane Fragments." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175332.
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Untimely rupture of the fetal membranes (FM), the amnion and choriodecidua, which normally surround and protect the fetus prior to delivery, is a major cause of preterm birth and results in significant infant mortality and morbidity. The physiological mechanism which normally leads the FM to weaken and fail prior to birth is not known. Conventional thinking that FM rupture is precipitated by the stress of uterine contractions during labor fails to explain the 10% of term deliveries and 40% of preterm deliveries in which FM rupture is the sentinel event, preceding any uterine contractions. Recent studies from several laboratories indicate that the FM undergo a genetically-programmed, biochemically-mediated, maturation process, near term, which is characterized by collagen remodeling and apoptosis. In human FM, in contrast to rat membranes, these changes are limited to the region of the FM overlying the cervix [1]. In a series of publications, our group has demonstrated that human FM have a zone of physical weakness (decreased force to rupture and work to rupture relative to the other areas of the same FM) overlying the cervical opening of the uterus. We further demonstrate that this same zone is characterized by specific markers of increased collagen remodeling and apoptosis [1–3]. These regional characteristics develop prior to the onset of contractions of labor and persist until delivery. Furthermore, the rupture tear line of the FM intersects this weak zone and thus the rupture process is hypothesized to initiate in this weak zone [3]. In order to investigate how differences in the biochemical composition of the extra-cellular matrix of the weak and the strong zones of FM reflect their different biomechanical properties, we utilized a proteomics approach to identify differences in the abundance of specific proteins in weak and strong FM fragments. Initial 2-DIGE screening resolved differences in Fibulin 5 protein expression. This prompted further analysis of additional members of the Fibulin protein family.
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Muszbek, L., and R. Adány. "CELLULAR DISTIBUTION OF FACTOR XIII IN HUMAN UTERUS AND PLACENTA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644648.
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As spontaneous abortion is a frequent finding in females with Factor XIII (FXIIl) deficiency it has been presumed that the plasmatic or cellular form of this clotting factor is essential to normal fetus development. In this context it is of special interestthat FXIII subunit a has been demonstrated in the homoge-nate of human uterus and placenta by activity measurements and immunobiochemical methods. However, no information on its cellular distribution has beenpublished, so far. In the present study first FXIII subunit a was detected in paraformaldehyde-fixed, paraffin-embedded sections by immunoperoxidase technique. FXIII containing cells were localized in the connective tissue of uterus and in the mesenchyme of placental chorionic villi. Though in a single report FXIII containing connective tissue cells were interpreted as fibroblasts (Fear et al., J.Clin.Pathoi.,37,560, 1984) the mononuclear, multipolar, stellate morphological appearance of these cells suggested that they rather belong to the monocyte/macrophage cell line. To characterize them the immuno-fluorescent detection of FXIII subunit a was combined by the visualization of different marker antigens for tissue macrophages (RFDT, Leu M3, HLA-DR) and fibroblasts (IIG10) on frozen sections. The coexpression of FXIII subunit a with RFD7 and Leu M3 macrophage markers, butnot with fibroblast membrane antigen IIG10 clearly proves that FXIII containing cells both in the uterusand in the placenta are tissue macrophages. HLA-DR was strongly expressed in cells positive for FXIII subunit a. in the uterus, but not or only very weakly in the placental mesenchyme, which might be due to the relative absence of extrinsic antigens during fetal development. The morphological findings on the presence of FXIII subunit a in placental macrophages were further strengthened by immunobiochemical experiments. FXIII subunit a, but not b content of isolated placental macrophages was also verified by immunoblotting, while fibroblasts were shown to be exemptof this factor. The results well agree with our previous findings demonstrating FXIII subunit a in humanmonocytes and peritoneal macrophages (Muszbek et al., Thrombos. Res. ,37, 401,1985; Adány et al. , Eur.J.Cell Biol.,38,171,1985).
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Briggs, Brandi N., and Virginia L. Ferguson. "Shear and Friction in the Delamination of Human Chorioamnion." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19681.
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The chorioamnion (CA), or placental, membrane is the sac that surrounds the fetus in utero. It is comprised of two layers; the inner fibrous amnion, composed of mainly collagen, and the thick, cellular chorion. The CA membrane exhibits incredible toughness under tension, while still allowing the two layers to easily slide over one another1,2. The interface between the chorion and amnion consists of gyri (folds) and sulci (furrows)3, which enable the two layers to tightly interlock and facilitate the intact membrane’s resistance to tension. This complex structure also allows the two layers to expand during gestation without losing mechanical integrity. The gyrus and sulcus from one section are believed to uncouple, slide laterally, and then lock into their new position while the remaining membrane is unaffected by the motion3. SEM imaging of freeze-fractured CA has revealed a multitude of fine fibers connecting the two layers as illustrated in Figure 1. These are suggested to serve as “guy ropes”, which restrict the amount that the two layers could slide over one another3. Also of importance at this interface is the presence of hyaluronan, a glycosaminoglycan. The hyaluronan has been suggested to reduce the resistance between the two layers so that they may glide over one another more easily throughout gestation and with vigorous fetal movements1. The combination of the elaborate topography of the interface and the lubricating glycosaminoglycans present throughout this layer play a role in the mechanics of the interface between chorion and amnion.
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BOUTHERIN-FALSON, O., and N. BLAES. "MODULATION of PROSTACYCLIN PRODUCTION BY HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS WITH ECGF/HEPARIN MEDIUM : ROLE OF CELLULAR DENSITY AT CONFLUENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643376.
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Prostacyclin (PGI2) is a major product of arachidonic acid metabolism in vascular endothelial cells. In addition to the role of exogenous agents, its production could be modulated by culture conditions : proliferative state, medium renewal, subcultivation... The use of endothelial cell growth factor (ECGF) associated with heparin has been shown to improve human endothelial cell proliferation. Here we report that human umbilical vein endothelial cells (HUVEC) grown in that medium produce less prostacyclin than without growth factor.HUVEC were cultured in RPMI-199 1:1 + 20% fetal calf serum, added or not with ECGF (Bovine hypothalamus extract BTI Cambridge, 24 ug/ml) and heparin (from porcine intestinal mucosa, Signa, 90 ug/ml). After 4 days in culture, medium was removed and replaced by Tyrode Hepes buffer and basal production was measured after 20 min. Cells were then submitted to 5 min thrombin to assess PGI2 production in stimulated conditions. PGI2 production was estimated by specific radioimmunoassay for 6 keto PGFjalpha. For each point, cell number in the culture was counted after Trypsin EDTA treatment. In the present study, cells grown in ECGF-heparin medium produce lower amount of PGI2, compared to heparin or control medium. This result was observed in both basal and stimulated conditions. For each medium (ECGF-heparin, heparin, control), correlations between PGI2 production per cell and log cell density were shown to be significantly negative.These observations suggest that ECGF effect on PGI2 production could be a consequence of its growth factor activity, notably by the fact that it leads to an endothelial monolayer made of more numerous cells. Since it is now suggested by a number of clinical observations that PGI2 is rather produced in pathological conditions, culture models showing a weak production of PGI2 appear in that connection doser to the physiological conditions.
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Setty, B. N. Y., and M. J. Stuart. "THE MITOGENIC EFFECT OF 15-HETE ON ENDOTHELIAL CELLS IS MEDIATED VIA DIGLYCERIDE KINASE INHIBITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643946.
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We have previously demonstrated that 15-HETE, a mitogen for fetal bovine aortic endothelial cells (FBAECs), caused an accumulation of diglyceride (DG). Stimulation of DNA synthesis by 0AG (a synthetic DG analog) suggested that this mitogenic effect was mediated via elevation of cellular DG levels. In the present study we have delineated the mechanism by which 15-HETE causes DG accumulation by evaluating the effects of 15-HETE on the phosphati-dylinositol (PI) cycle. In [3H]inositol labeled cells, 15-HETE caused a decrease in PI content under both basal conditions (27%) and following A23187 stimulation (23%). The accumulation of DG and the decrease in PI suggested activation of phosphilipase C. However, no effect of 15-HETE was found on endothelial cell phos-pholipase C. A modulatory effect of 15-HETE on PI resynthesis was next evaluated using [3H] inositol. In 5 experiments, 15-HETE (30μM) inhibited the synthesis of PI in both unstimulated (51+15%, 1SD, P<0.001) and A23187 stimulated cells (80±19%, P<0.001). DG accumulation and inhibition of PI synthesis suggested a 15-HETE effect on the conversion of DG to phosphatidic acid (PA) via DG kinase. Using endothelial cell membranes as a source of this enzyme, formation of PA was nonlinear with time, suggesting an interference by PA phosphatase on PA formation. Human red cell membranes were therefore used in lieu of FBAECs as a source of DG kinase. In this system, production of PA was inhibited by 15-HETE in a concentration-dependent manner (IC50 of 22μM). This is the first report of the presence of a DG kinase inhibitor of biological origin. Our studies also delineate the mechanism by which 15-HETE exerts its mitogenic effect on endothelial cells.
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Setty, B. N. Y., M. Berger, and M. J. Stuart. "13-HYDROXY-9,11-OCTADECADIENOIC ACID (13-HOD) INCREASES PROSTACYCLIN PRODUCTION IN ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643948.
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Recently, endothelial cells (ECs) have been shown to generate a potent vascular chemorepellant factor. This metabolite, 13-HOD is reported to be the major lipoxygenase product produced in microgram amounts in ECs (JBC 260:16056, 1985). We have studied the effect of 13-HOD on EC arachidonic acid (AA) metabolism, and report modulation of both AA release and conversion to prostacyclin. Using fetal bovine aortic ECs, 13-HOD stimulated prostacyclin production (RIA for 6KPGF1α ) by 40±13% (1SE), and 51±09% at 10 and 30μM (P<0.05; n=5). When the time-course of this effect was evaluated, 13-HOD (30μM) significantly enhanced the time-dependent release of 6KPGF1α by 31 to 51% between 5 and 120 min. (P<0.05 to 0.01; n=5). In [14C]AA labeled cells, this compound modulated both AA release and its subsequent conversion. In 5 paired experiments, 13-HOD (30μM) enhanced the release of AA from membrane phospholipids (9065±0553 cpm/well in controls vs 10738±1725 in 13-HOD treated cells; PC0.01). Analysis of cellular phospholipids revealed a significant decrease in [14C]phosphatidylethanolamine (62312±3963 cpm/well in controls vs 56959±4104 in 13-HOD treated cells; P<0.02). No significant changes were seen in the levels of phosphatidyl-choline, -serine, -inositol, or phosphatidic acid. Production of [14C]prostacyclin was stimulated by 56±16% (P<0.01 ), while total cyclooxygenase metabolites increased by 28±8% (P<0.01), suggesting effects on both cyclooxygenase and prostacyclin synthetase. 13-HOD, the major vascular product of linoleic acid enhances both AA release and metabolism, thus demonstrating an intimate hemostatic interaction between the metabolic products of these two polyunsaturated fatty acids in endothelial cells.
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Bukowski, Michael, Brij Singh, James Roemmich, and Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.
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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.