Relevant bibliographies by topics / Fetal cell

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Fetal cell'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Fetal cell"

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McCook, Alison. "Fetal Cell Setback." Scientific American 284, no. 5 (May 2001): 25. http://dx.doi.org/10.1038/scientificamerican0501-25c.

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Cassar-Malek, Isabelle, Brigitte Picard, Catherine Jurie, Anne Listrat, Michel Guillomot, Pascale Chavatte-Palmer, and Yvan Heyman. "Myogenesis Is Delayed in Bovine Fetal Clones." Cellular Reprogramming 12, no. 2 (April 2010): 191–201. http://dx.doi.org/10.1089/cell.2009.0065.

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Brodowski, L., B. Schröder-Heurich, C. A. Hubel, T. H. Vu, C. S. von Kaisenberg, and F. von Versen-Höynck. "Role of vitamin D in cell-cell interaction of fetal endothelial progenitor cells and umbilical cord endothelial cells in a preeclampsia-like model." American Journal of Physiology-Cell Physiology 317, no. 2 (August 1, 2019): C348—C357. http://dx.doi.org/10.1152/ajpcell.00109.2019.

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Maternal endothelial dysfunction is a cental feature of preeclampsia (PE), a hypertensive disorder of pregnancy. Factors in the maternal circulation are thought to contribute to this endothelial dysfunction. Although understudied, factors in the fetal circulation may influence fetal endothelial cell interactions with endothelial progenitor cells as critical steps in placental angiogenesis. We hypothesize that cell-cell interactions that are important for pregnancy health are impaired by fetal serum from PE pregnancies and that 1,25(OH)2-vitamin D3 attenuates the negative effects of this serum on cell function. We tested the ability of fetal cord blood-derived endothelial progenitor cells [endothelial colony-forming cells (ECFCs)] to invade into established monolayers and capillary tubule-like structures of human fetal umbilical venous endothelial cells (HUVECs), while in the presence/absence of fetal cord serum from uncomplicated or PE pregnancies, and tested the ability of 1,25(OH)2-vitamin D3 to modulate the serum-mediated effects. PE cord serum reduced the invasion of fetal ECFCs into HUVEC monolayers or tubule networks. Vitamin D attenuated these effects of PE fetal serum on endothelial functional properties. Immunocytochemical studies revealed involvement of VE-cadherin contacts in interactions between ECFCs and mature fetal endothelial cells. PE cord serum reduces the ability of fetal endothelial progenitor cells to incorporate into fetal endothelial cell networks. Physiologic concentrations of vitamin D reverse these PE serum-mediated effects. These data appear consistent with lines of evidence that vitamin D has antipreeclampsia effects.
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KATLAN, Doruk Cevdi, and Feride SÖYLEMEZ. "Cell-Free Fetal DNA in Prenatal Screening." Turkiye Klinikleri Journal of Health Sciences 2, no. 3 (2017): 165–73. http://dx.doi.org/10.5336/healthsci.2016-51564.

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Kearney, J., F. Martin, C. Benedict, and A. Oliver. "Fetal B cell development." Immunology Letters 56 (May 1997): 98. http://dx.doi.org/10.1016/s0165-2478(97)85389-8.

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Kearney, J. "Fetal B cell development." Immunology Letters 56, no. 1-3 (May 1997): 98. http://dx.doi.org/10.1016/s0165-2478(97)87227-6.

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Tiblad, Eleonor, and Magnus Westgren. "Fetal stem-cell transplantation." Best Practice & Research Clinical Obstetrics & Gynaecology 22, no. 1 (February 2008): 189–201. http://dx.doi.org/10.1016/j.bpobgyn.2007.07.007.

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Frost, Mackenzie S., Aqib H. Zehri, Sean W. Limesand, William W. Hay, and Paul J. Rozance. "Differential Effects of Chronic Pulsatile versus Chronic Constant Maternal Hyperglycemia on Fetal Pancreaticβ-Cells." Journal of Pregnancy 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/812094.

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Constant maternal hyperglycemia limits, while pulsatile maternal hyperglycemia may enhance, fetal glucose-stimulated insulin secretion (GSIS) in sheep. However, the impact of such different patterns of hyperglycemia on the development of the fetalβ-cell is unknown. We measured the impact of one week of chronic constant hyperglycemia (CHG,n=6) versus pulsatile hyperglycemia (PHG,n=5) versus controls (n=7) on the percentage of the fetal pancreas staining for insulin (β-cell area), mitotic and apoptotic indices and size of fetalβ-cells, and fetal insulin secretion in sheep. Baseline insulin concentrations were higher in CHG fetuses (P<0.05) compared to controls and PHG. GSIS was lower in the CHG group (P<0.005) compared to controls and PHG. PHGβ-cell area was increased 50% (P<0.05) compared to controls and CHG. CHGβ-cell apoptosis was increased over 400% (P<0.05) compared to controls and PHG. These results indicate that late gestation constant maternal hyperglycemia leads to significantβ-cell toxicity (increased apoptosis and decreased GSIS). Furthermore, pulsatile maternal hyperglycemia increases pancreaticβ-cell area but did not increase GSIS, indicating decreasedβ-cell responsiveness. These findings demonstrate differential effects that the pattern of maternal hyperglycemia has on fetal pancreaticβ-cell development, which might contribute to later life limitation in insulin secretion.
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Zhao, Xiao Xi, Nobuhiro Suzumori, Yasuhiko Ozaki, Takeshi Sato, and Kaoru Suzumori. "Examination of Fetal Cells and Cell-Free Fetal DNA in Maternal Blood for Fetal Gender Determination." Gynecologic and Obstetric Investigation 58, no. 1 (2004): 57–60. http://dx.doi.org/10.1159/000078577.

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Ng, Melissa, Theodore Roth, Ventura Mendoza, Alexander Marson, and Trevor Burt. "Helios predisposes human fetal CD4+ naive T cells towards regulatory T cell differentiation." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 124.9. http://dx.doi.org/10.4049/jimmunol.202.supp.124.9.

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Abstract Activation of naïve CD4+ T cells by T cell receptor (TCR) stimulation and cytokine cues lead to differentiation into effector T cell populations with distinct pro-inflammatory or regulatory functions. Unlike adult naïve T cells, human fetal naïve CD4+ T cells uniquely differentiate into FOXP3+ regulatory T (Treg) cells upon TCR activation independent of exogenous cytokine signalling. This facility for Treg differentiation is crucial for generating tolerance in utero; however, the mechanisms underlying this ability in fetal naïve cells are largely unknown. Here, we reveal FOXP3-independent transcriptional and epigenetic programs shared between fetal naive T cells and committed adult Treg cells that are inactive in adult naive T cells. We show that a subset of adult Treg-specific super-enhancers is active within fetal naive T cells, including two super-enhancers at Helios, a thymic Treg gene. Helios is expressed in fetal naive T cells, but not in adult naïve T cells, and only fetal-derived induced Treg (iTreg) cells continue to express Helios. Fetal, but not adult iTreg cells, have suppressed IL-2 production, which is regulated by Helios in committed Treg cells. CRISPR-Cas9 ablation of Helios in fetal naive T cells then resulted in increased IL-2 production in fetal iTreg cells. Crucially, the loss of Helios expression in fetal naïve T cells impaired their differentiation into Treg cells upon TCR stimulation, indicating Helios as a critical contributor to the cell-intrinsic predisposition of fetal naive T cells for Treg cell differentiation. Treg-biased transcriptional and epigenetic programs within fetal naive T cells identified here could be utilized to engineer enhanced adult iTreg populations for adoptive cellular therapies.
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Dissertations / Theses on the topic "Fetal cell"

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Götherström, Cecilia. "Characterisation of human fetal mesenchymal stem cells /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-139-3/.

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Weinhaus, Anthony James. "Physiology of the fetal B-cell." Thesis, The University of Sydney, 1994. https://hdl.handle.net/2123/26826.

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The use of islets isolated from the human fetal pancreas may provide a source of transplantable tissue with the potential to reverse diabetes. Further research is required before there is enough knowledge of the function of these islets to enable their successful transplantation to humans. Chapter 1 Experiments on fetal pancreas are limited by the paucity and irregularity of the supply of donor tissue. Therefore, a human fetal pancreatic B—cell line would be of considerable use in the better understanding of this potential source of transplantable tissue. In chapter 1 of this thesis, success in isolating an immortalised fetal lung fibroblast cell line by SV—40 viral infection is described. Satisfied with this procedure, attempts were then made to isolate a human fetal pancreatic .cell line by infection with SV—4O virus and transfection with plasmid vectors containing SV—4O genes. Although unsuccessful in isolating an immortalised cell line, a protocol was established for the transfection of human fetal endocrine cells in the future. Chapter 2 It has been well established that the fetal rat and human pancreatic islet B—cell secretes insulin poorly in response to glucose compared to that from adult B—cells. However, the cellular mechanism for this is unknown. In chapter 2, microfluorometric studies are described using the intracellular fluorescent dye fura—Z to measure changes in the cytoplasmic free Ca2+ concentration in fetal, neonatal and adult rat B—cells to determine the ability of glucose and other insulin secretagogues to cause an increase in [Ca2+]i believed to be the trigger for insulin secretion. The fetal B-cell responded to various insulin secretagogues, but not glucose, with an increase in [Ca2+].l and insulin release. The immature insulin secretory response to glucose by the fetal B—cell is, therefore, due to its inability to translate glucose stimulation into an increase in [Ca2+]i required for exocytosis of insulin. Chapter 3 The protocols used in experiments conducted on rat fetal B-cells were used for experiments on human fetal B—cells described in chapter 3 to determine the ability of glucose and other insulin secretogogues to cause an increase in [Ca“1i. In this study, mid-gestation fetal human and late—gestation fetal porcine islet—like cell clusters, as well as adult human islets and the only available human B—cell line, the adult insulinoma cell line HP—62, were studied using microfluorometric methods. Both the mid—gestation human fetal B-cell and the late—gestation porcine fetal B—cell possesses the complete mechanism required to translate stimulation by secretagogues other than glucose into an increase in [Ca2+]i required for secretion of insulin. The end-stage of the signal transduction pathway in these fetal B—cell is, therefore, mature. The immature secretory response to glucose must, therefore, be located at some other step of glucose-induced stimulation such as glucose transport, glucose metabolism or in the linkage between glycolysis and mitochondrial metabolism. Chapter 4 The amino acid arginine is known to cause insulin release from glucose—insensitive human and rat fetal B—cells, as well as from rat adult perfused pancreas, pancreatic explants and perifused islets. Exposure of rat and human fetal B—cells to arginine was found in the studies described in chapter 2 and 3 to cause an increase in [Ca“]r The cellular mechanisms involved in the B—cell response to arginine are not well described. Experiments described in chapter 4 were conducted to identify the mechanisms involved in arginine-induced stimulation of the B—cell using an insulinoma cell line (NIT—l). As in the studies described. in Chapters 2 and 3, the ratiometric fluorescent probe of Ca”) fura—Z, was used to directly monitor changes in [Ca”1i. The effects of L—arginine, and its analogues which do not produce nitric oxide were investigated to characterise the mechanisms of arginine—induced B—cell stimulation and determine if nitric oxide production plays a role in this stimulation. The data demonstrate that L—arginine, and its analogues, caused similar increases in [Ca2+]i and insulin release. This suggests that nitric oxide production has no role in the arginine—induced increase in [Ca2+]i in the NIT—l cell. The increase in [Ca2+]i is due to a combination of the direct depolarisation of the membrane due to the electrogenic effect of arginine plus an effect due to the metabolism of the amino acid.
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Cowan, Gillian. "Fetal germ cell differentiation and the impact of the somatic cells." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4164.

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Specification of a germ cell lineage and appropriate maturation are essential for the transfer of genetic information from one generation to the next. Germ cells form from pluripotent precursor cells that migrate into the gonadal ridge and undergo commitment to either the female or male lineage. In the fetal ovary, germ cells enter meiotic prophase I, then arrest at the diplotene stage; in the testis germ cells do not begin meiosis until puberty. Abnormal differentiation of germ cells can result in malignant transformation. Somatic cells play a key role in modulating the developmental fate of the germ cells. Research into germ cell development during fetal life has almost exclusively focused on studies in rodents, but we, and others, have reported several fundamental differences in the expression of germ cell specific markers in the human compared with the mouse. The studies described in this thesis have investigated germ cell-specific gene expression and the possible impact of the somatic cells during development. This was achieved by studying human fetal gonads obtained during the 1st and 2nd trimesters of pregnancy and through the use of both wild-type and mutant mouse ES cell lines. Studies on germ cells in the human fetal testis have extended the findings of others, and confirmed that germ cell populations at different stages of maturation co-exist in the human fetal testis, a situation that is in contrast to that in rodents. For example expression of M2A and AP2γ was restricted to the OCT4-positive gonocyte population, while VASA and NANOS1 were localised exclusively to the to the OCT4-negative prespermatogonia. DAZL was expressed in both populations. Analysis also revealed that both the gonocyte and prespermatogonial populations proliferate throughout the 2nd trimester. Recent studies have implicated retinoic acid (RA) in the control of meiotic entry in germ cells of the fetal mouse ovary. In this study we demonstrated for the first time that two genes implicated in the action of RA in mouse gonad, STRA8 and NANOS2, are also expressed in a similar sexspecific- manner in the human fetal gonads, and that the RA receptors are present in both somatic and germ cells suggesting that RA may regulate germ cell function in the human as well as the mouse. However, whilst the mesonephros appears to be the primary site of RA synthesis in the mouse our initial studies indicate that in the human the gonad itself may be a more likely site of RA biosynthesis. In the fetal mouse testis, RA is degraded by the enzyme Cyp26b1 present in the somatic cells and germ cells do not enter meiosis, our novel findings suggest that CYP26B1 is more abundant in the human fetal ovary than the testis, suggesting that meiotic entry may be controlled by an alternative signalling pathway in the human. One of the methods that can aid our understanding of somatic cell gene expression in the gonad is in vitro culture. To date, there have been no published reports of the successful in vitro culture of somatic cells from the human fetal testis. In the current study, populations of human somatic cells were dissociated and maintained in vitro and characterised. Analysis demonstrated that cells expressing mRNAs characteristic of Sertoli cells, Leydig cells and peritubular myoid (PTM) cells were present initially, but long-term culture resulted in downregulation in expression of mRNAs specific for Sertoli cells and Leydig cells, suggesting that these cells either failed to survive or underwent alterations to their phenotype. In contrast PTM/fibroblast cells proliferated in vitro and initially maintained androgen receptor expression. These cultures therefore hold promise for studies into the signalling or cell-cell interactions in testicular somatic cells especially those relevant to the PTM population. Several studies have claimed differentiation of putative germ cells from ES cells. In the current study, analysis of mouse ES cell lines has expanded on results showing that ES cells and early germ cells express a number of genes in common. Kit signalling was shown to be important for ES cell survival as they differentiate although expression of Kit was heterogeneous. We also demonstrated that ES cells that did not express Kit displayed a decreased expression of the early germ cell genes Blimp1, Fragilis and Stella, implicating Kit signalling in the control of germ cell-associated gene expression in ES cells. This may be important to future studies optimising germ cell derivation from ES cells. In conclusion, this study has demonstrated important differences in protein expression patterns in germ cells of the human fetal testis compared to the mouse, and has raised questions about whether the proposed mechanism controlling meiotic entry of germ cells in the mouse can be applied to the human. The establishment of a system for culturing human fetal gonadal somatic cells may lead to further understanding of gene expression and development in the human fetal testis, and data suggest that the Kit/Kitl signalling system may influence germ cell gene expression in mouse ES cells.
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Li, Qinggang. "In vitro regulation of fetal bovine erythropoiesis." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42078.

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Fetal bovine serum (FBS) is one of the most important supplements for cell culture, and is a rich source of both defined and unknown factors required for proper cell growth. A serum-free bioassay system was developed to facilitate the purification and characterization of the heparin-binding growth factors in FBS. Three factors with different effects on erythropoiesis were isolated and identified with the combination of several chromatographic techniques. An 8 kd heparin-binding peptide which stimulated thymidine incorporation into fetal erythroid cells had an N-terminal sequence identical to insulin-like growth factor (IGF II). The growth promoting effect of this peptide was potentiated by heparin in culture. It was also found that the relative affinity of IGFs was in the order of IGF II $>$ IGF I $>$ insulin. The second heparin-binding erythroid regulating factor isolated was a 46 kd protein. The N-terminal sequence of this protein was identical to that of apolipoprotein H (Apo H). It inhibited thymidine incorporation into fetal erythroid cells with an ED$ sb{50}$ of 36 nM. A 100% inhibition of thymidine incorporation and a 40% decrease in cell numbers in culture were observed at 840 nM. The third factor identified was an 11 kd peptide with an N-terminal sequence similar to C4a, a fragment of complement C4. This peptide was a potent cytotoxic agent and was not species-specific, lysing not only bovine fetal erythroid cells, but also human adult red blood cells at very low concentrations.
A clonal assay system for bovine fetal liver cells was developed to further characterize the erythropoietic effects of IGF II, the most important of the isolated factors. It was found that bovine fetal erythroid colonies could not be developed at low concentrations of FBS, unless they were grown over stromal cells. Bovine fetal liver stromal cell lines could support erythroid growth through secreting soluble factor(s) and by direct contact to erythroid cells. It was clear that IGFs stimulated erythropoiesis in this system.
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Saleh, A. W. "Modulation of fetal hemoglobin in sickle cell anemia." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8498.

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Maciaczyk, Jaroslaw. "Human fetal neural precursor cells: a putative cell source for neurorestorative strategies." [S.l. : s.n.], 2005. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-57885.

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Ditadi, Andrea. "Cell therapy approach for hematopoietic diseases using fetal cells issued from amniotic fluid." Paris 5, 2008. http://www.theses.fr/2008PA05T036.

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Dans la présente étude, nous avons étudié la possibilité de différencier les cellules souches du liquide amniotique humain (hAFSC) et murin (mAFSC) vers la voie hématopoïétique à la fois in vitro et in vivo. Nous avons de manière reproductible réalisé une différenciation érythroïde par culture des hAFSCs en corps embryoïdes (EB). Plus de 70% des cellules constituant les EB coexprimaient des marqueurs erythroïdes. De plus, 3 mois après l'injection de hAFSC à des souris NOD/SCID irradiées, nous avons pu détecter dans la rate et la moelle osseuse des receveurs des érythrocytes humains. Nous avons ainsi comparé le potentiel hématopoïétique des mAFKL, des mAmKL aux KL issues du foie foetal (mFLKL), qui constituent la source principale de cellules souches hématopoïétiques à ce stade de développement. In vivo, nous avons retrouvé dans le sang de souris déficientes pour RAG1, des cellules appartenant aux trois lignées hématopoïétiques (lymphoïde, erythroïdes et myéloïdes) 4 semaines seulement après la greffe de mAFKL et mAmKL. Analysées quatre mois plus tard, les souris greffées présentent des lymphocytes, des érythrocytes et des cellules myéloïdes provenant des mAFKL et mAmKL dans tous les organes hématopoïétiques. Le succès de transplantations secondaires a confirmé que les mAFKL et mAmKL comprennent des progéniteurs hématopoïétiques capables d'auto-renouvellement, ce qui correspond à la définition d'une cellule souche hématopoïétique
In the present study we investigated the possibility of differentiating AFS cells towards the hematopoietic pathway. We achieved a reproducible erythroid differentiation by culturing hAFSCs as embryoid bodies (EBs) under serum free conditions with haematopoietic cytokines. 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. 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. 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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Huygens, Ariane. "Fetal T cell response to human congenital cytomegalovirus infection." Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209450.

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Les nouveau-nés et les jeunes enfants ont une susceptibilité plus élevée aux infections par rapport aux enfants plus âgés et aux adultes. Cette caractéristique est en partie attribuée à l’immaturité de leur système immunitaire qui est associée à une capacité limitée à développer des réponses immunitaires à médiation cellulaire. L’infection par le cytomégalovirus (HCMV) est la cause la plus fréquente d’infection congénitale chez l’Homme et une cause majeure de surdité et de retard mental. En Belgique, le dépistage anténatal de l’infection primaire par le HCMV chez les femmes enceintes offre l’opportunité d’étudier les réponses immunitaires du foetus à ce virus et de les comparer à celles de leur maman.

Les lymphocytes T CD4+ Th1 et les lymphocytes T CD8+ cytotoxiques jouent un rôle crucial dans le contrôle des pathogènes intracellulaires dont le HCMV fait partie. La littérature montre une capacité limitée des enfants congénitalement infectés par le HCMV à développer des réponses T CD4+ spécifiques du HCMV. En contraste, des réponses de lymphocytes T CD8+ spécifiques du HCMV ont été rapportées chez des enfants infectés in utero, mais ces réponses n’ont pas été comparées en détails à celles de l’adulte. De plus, notre connaissance des réponses T spécifiques du HCMV durant l’infection primaire par ce virus est limitée. Des études antérieures ont rapporté un défaut de prolifération et de production d’IL-2 des lymphocytes T spécifiques du HCMV chez des adultes avec durant la phase primaire de l’infection, mais les mécanismes restent non-élucidés.

Nous avons caractérisé les réponses de lymphocytes T CD4+ et CD8+ spécifiques du HCMV provenant du sang de cordon de nouveau-nés congénitalement infectés par le HCMV, et nous avons comparé ces réponses à celles de leurs mamans diagnostiquées avec une infection primaire par le HCMV durant la grossesse. En plus, nous avons comparé les réponses T CD4+ et CD8+ de ces mamans à celles d’adultes infectés chroniquement par le virus. Chez les nouveau-nés, nous avons démontré que des lymphocytes T CD4+ de sang de cordon exprimant un phénotype de différentiation spécifique du HCMV (CD27-CD28-) ainsi qu’un phénotype Th1 similaire à celui des cellules maternelles étaient induits in utero lors de l’infection congénitale par le HCMV. De plus, la détection d’expansions oligoclonales suggérait fortement une expansion antigène-spécifique de ces cellules. Cependant, les T CD4+ de nouveau-nés présentaient une capacité fortement réduite à produire des cytokines anti-virales (IFN-γ, TNF-α et MIP-1β) en réponse à une stimulation ex vivo avec les antigènes du HCMV, par rapport aux cellules maternelles. Les lymphocytes T (CD27-CD28-) CD4+ de nouveau-nés produisaient également des niveaux plus bas de cytokines antivirales en réponse à des stimulations polyclonales avec l’anti-CD3 et la PMA/ionomycine, suggérant des altérations en amont et en aval de la voie de signalisation du TCR. Nos résultats suggèrent que ces altérations pourraient impliquer la diminution de l’expression de molécules impliquées dans cette voie de signalisation. De la même manière, nous

avons montré que chez le nouveau-né, la fonction des T CD8+ spécifiques du HCMV était altérée par rapport à celle de l’adulte. Nous avons observé des proportions similaires de T CD8+ (CD27-CD28-) chez les nouveau-nés et les adultes. De plus, l’analyse du répertoire du TCR Vβ de ces cellules par séquençage haut-débit a révélé une capacité similaire à générer un répertoire T diversifié dans les deux groupes. Comme rapporté précédemment, nous avons détecté des fréquences similaires de lymphocytes T CD8+ spécifiques pour l’antigène immunodominant pp65. Cependant, lorsque les stimulations ont été étendues à d’autres antigènes du HCMV, nous avons observé que le répertoire antigénique reconnu par ces cellules était significativement réduit chez les nouveau-nés, en association avec une diminution de la polyfonctionalité et de la production de cytokines par cellule.

Nous avons également montré que, dans une moindre mesure, la fonction des lymphocytes T spécifiques du HCMV était diminuée durant l’infection primaire chez l’adulte. Comme reporté précédemment, les T CD4+ spécifiques du HCMV proliféraient moins et produisaient moins d’IL-2 par rapport à des individus dans la phase chronique de l’infection. Ce défaut de production d’IL-2 affectait à la fois les populations de cellules CD28+ et CD28-, montrant que l’accumulation de lymphocytes T CD4+ ayant perdu l’expression de la molécule CD28 (un signal de co-stimulation important pour la production d’IL-2) est seulement un des facteurs contribuant à la diminution de la production d’IL-2 par les cellules spécifiques du HCMV. En accord avec cette observation, nous avons montré une diminution de la production par cellule d’IFN-γ et de TNF-α touchant également à la fois les populations de T CD4+ CD28+ et CD28- durant la phase primaire de l’infection, un défaut associé avec une avidité fonctionnelle diminuée de ces cellules. De la même manière, la polyfonctionalité et la production de cytokines par cellule des lymphocytes T CD8+ spécifiques du HCMV étaient également diminuées chez les adultes durant la phase d’infection primaire.

En résumé, nos résultats montrent que la fonction des lymphocytes T spécifiques du HCMV de nouveau-nés et d’adultes est altérée durant l’infection primaire par rapport à des individus infectés chroniquement par le virus. Nous montrons que cette régulation fonctionnelle ressemble à l’exhaustion fonctionnelle des lymphocytes T observée durant les infections virales chroniques associées à des charges virales élevées. L’infection primaire par le HCMV est caractérisée par une réplication virale intense qui dure pendant plusieurs mois suivant l’infection. Nous émettons l’hypothèse que les hauts taux de réplication virale observés durant l’infection congénitale et chez l’adulte durant l’infection primaire par le HCMV pourraient interférer avec certaines fonctions des lymphocytes T./Neonates and young infants have a higher susceptibility to infections compared to older infants or adults. This feature is in part attributed to the immaturity of their immune system associated with a limited capacity to mount cellular-mediated immune responses. Congenital human cytomegalovirus (HCMV) infection is the most common cause of congenital infection worldwide and a major cause of hearing loss and mental retardation. In Belgium, antenatal screening of pregnant women for primary HCMV infection offers an opportunity to study neonatal immune responses to the virus and to compare them to those of their mother.

T lymphocytes are major players of the immune system. In particular, Th1 CD4+ T cells and CD8+ cytotoxic T cells play a crucial role in the control of intracellular pathogens, including HCMV infection. Previous literature has reported a limited capacity of infants born with congenital HCMV infection to mount HCMV-specific CD4+ T cell responses. In contrast, fetal antigen-specific CD8+ T cell responses have been reported following in utero HCMV infection, but these responses have not been compared in detail to those of adults with primary infection. In addition, our knowledge regarding adult HCMV-specific T cell responses during primary HCMV infection is limited. Previous studies have reported defective T cell proliferation and IL-2 production in adults with primary HCMV infection, showing that some of the T cell functions are altered during primary infection.

In this study, we have characterized neonatal HCMV-specific CD4+ and CD8+ T cell responses from the cord blood of newborns with congenital HCMV infection, and we have compared these responses to that of their mothers diagnosed with primary HCMV infection during pregnancy. Also, we compared CD4+ and CD8+ T cell responses of adults with primary HCMV infection to that of adults with chronic infection.

In newborns, it was not known if the defective CD4+ T cell responses could be attributed to the absence of HCMV-specific cells or to the induction of dysfunctional cells. We demonstrate that neonatal CD4+ T cells with a differentiation phenotype typical of HCMV infection (CD27-CD28-) and expressing a Th1 phenotype similar to that of maternal cells can differentiate in utero following HCMV infection. In addition, the detection of oligoclonal expansions by spectratyping and flow cytometry analyses strongly suggests antigen-specific responses. However, neonatal CD4+ T cells were markedly less able to produce antiviral cytokines (IFN-γ, TNF-α and MIP-1β) following ex vivo stimulation with HCMV antigens, compared to maternal cells. Also, neonatal CD27-CD28- CD4+ T cells produce lower levels of antiviral cytokines in response to polyclonal stimulations with anti-CD3 and PMA/ionomycin, suggesting alterations up-stream and down-stream of the TCR signaling pathway. Our results suggest that these alterations could involve the down-regulation of the expression of molecules that are part of the TCR signaling pathway. Similarly, we show that the function of

neonatal HCMV-specific CD8+ T cells is impaired compared to adults. Similar proportions of (CD27-CD28-) CD8+ T cells, typical of HCMV infection, were detected in newborns and adults. Analysis of the TCR Vβ repertoire of neonatal and maternal (CD27-CD28-) CD8+ T cells by high-throughput sequencing revealed a similar capacity to generate a diverse clonal repertoire. As previously reported, we detected similar frequencies of HCMV-specific CD8+ T cells specific for the immunodominant viral antigen pp65. However, when extending ex vivo stimulations to other HCMV antigens, we observed that the antigenic repertoire recognized by these cells was significantly reduced in newborns. In addition, neonatal CD8+ T cells had a reduced polyfunctionality and per cell cytokine production.

To a lower extent, the function of adult HCMV-specific T cells was also impaired during primary infection. As previously reported, maternal HCMV-specific CD4+ T cells were markedly less able to produce IL-2 and to proliferate compared to individuals in the chronic stage of the disease. Both CD28+ and CD28- T cell subsets produced decreased levels of IL-2. This observation shows that the accumulation of HCMV-specific CD4+ T cells having lost the expression of the CD28 molecule (an important co-stimulatory signal for IL-2 production) during primary infection is only one of the factors contributing to the decreased IL-2 production. Accordingly, both CD28+ and CD28- CD4+ T cell subsets had a decreased per cell production of IFN-γ and TNF-α during primary HCMV infection. This defect was associated with a lower functional avidity of these cells. Similarly, the polyfunctionality and per cell cytokine production of adult HCMV-specific CD8+ T cells was also impaired compared to adults with chronic infection.

Altogether, our results show that adult and neonatal HCMV-specific T cell responses are impaired during primary infection, compared to individuals with chronic infection. We show that this functional regulation resembles that of functional T cell exhaustion observed during chronic viral infections that are associated with high levels of viral replication. Primary HCMV infection is characterized by an intense viral replication lasting for several months post-infection. We hypothesize that the high levels of viral replication observed during congenital and adult primary HCMV infection could interfere with some of the T cell functions.
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Schneidereith, Tonya A. "The pharmacogenetics of fetal hemoglobin and f-cell variation." Available to US Hopkins community, 2003. http://wwwlib.umi.com/dissertations/dlnow/308076.

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Ferreira, Leonardo. "Transcriptional Control of Maternal-Fetal Immune Tolerance." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493333.

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Human leukocyte antigens (HLA) are important determinants of self-nonself immune recognition. HLA-G, uniquely expressed in the placenta, is believed to be key to fetus-induced immune tolerance during pregnancy. The tissue-specific expression of HLA-G, however, remains poorly understood. Using a Massively Parallel Reporter Assay (MPRA), we discovered a 121 bp sequence 12 kb upstream of HLA-G with enhancer activity, Enhancer L. Strikingly, deletion of Enhancer L using a CRISPR/Cas9 dual guide approach resulted in complete ablation of HLA-G expression in a trophoblast cell line. This finding was confirmed in primary extravillous trophoblasts isolated from human placenta. RNA-seq analysis demonstrated that Enhancer L regulates HLA-G expression specifically. Moreover, DNase-seq and Chromatin Conformation Capture (3C) defined Enhancer L as a cell type-specific enhancer that loops into the HLA-G promoter. GATA2, GATA3, and CEBPB, factors essential for placentation, associate with Enhancer L and regulate HLA-G expression levels. These results establish long-range chromatin looping as a novel mechanism controlling trophoblast-specific HLA-G expression at the maternal-fetal interface.
Biology, Molecular and Cellular
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Books on the topic "Fetal cell"

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Fetal Cell Workshop (11th 2000 Basel, Switzerland). Fetal cells and fetal DNA in maternal blood: New developments for a new millennium : 11th Fetal Cell Workshop, Basel, April 15, 2000. Edited by Hahn Sinuhe and Holzgreve Wolfgang. Basel: Karger, 2001.

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A, Cohen Shara B., ed. Cord blood characteristics: Role in stem cell transplantation. London: Dunitz, 2000.

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Arthur, Ann V. Analysis of fetal globin gene expression in Kuwaitis with sickle cell disease. [New Haven: s.n.], 1990.

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1943-, Simpson Joe Leigh, Elias Sherman, and New York Academy of Sciences., eds. Fetal cells in maternal blood: Prospects for noninvasive prenatal diagnosis. New York: New York Academy of Sciences, 1994.

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Magin, Angela Susanne. Humane Primärzellen als Feederzellen für die Kokultur mit hämatopoetischen Stammzellen aus Nabelschnurblut. Jülich: Forschungszentrum Jülich, Zentralbibliothek, 2006.

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Vinnedge, Debra L. Aborted fetal cell line vaccines and the Catholic family: A moral perspective. Largo, Fla: Children of God for life, 2003.

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Wolfgang, Holzgreve, and Lessl M. 1966-, eds. Stem cells from cord blood, in utero stem cell development, and transportation-inclusive gene therapy /cW. Holzgreve, M. Lessl, editors. New York: Springer, 2001.

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Frontiers in cord blood science. London: Springer, 2009.

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1955-, Freeman Thomas B., and Widner Hakan, eds. Cell transplantation for neurological disorders: Toward reconstruction of the human central nervous system. Totowa, N.J: Humana Press, 1998.

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United, States Congress Senate Committee on Health Education Labor and Pensions. Stem Cell Therapeutic and Research Act of 2005: Report (to accompany S. 1317). [Washington, D.C: U.S. G.P.O., 2005.

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Book chapters on the topic "Fetal cell"

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Sumitran-Holgersson, Suchitra, Meghnad Joshi, and Michael Olausson. "Fetal Liver Cell Transplantation." In Human Fetal Tissue Transplantation, 219–35. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4171-6_17.

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Albanna, Mohammad Z., and Erik J. Woods. "Fetal Stem Cell Banking." In Fetal Stem Cells in Regenerative Medicine, 295–316. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3483-6_16.

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Parrish, Marc R., and John C. Morrison. "Sickle cell disease." In Clinical Maternal-Fetal Medicine Online, 19.1–19.7. 2nd ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003222590-17.

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Gao, Zimeng. "Sickle Cell Disease." In Maternal-Fetal Evidence Based Guidelines, 153–60. 4th ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003099062-15.

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Kondo, Yasushi, Tsuyoshi Okuno, Sayaka Asari, and Shin-ichi Muramatsu. "Cell Therapy for Parkinson’s Disease." In Human Fetal Tissue Transplantation, 193–203. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4171-6_15.

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Darbinian, Nune, Armine Darbinyan, Kamel Khalili, and Shohreh Amini. "Fetal Brain Injury Models of Fetal Alcohol : Examination of Neuronal Morphologic Condition Using Sholl Assay." In Neuronal Cell Culture, 195–201. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1437-2_16.

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Mandel, Thomas E. "Fetal tissue transplantation." In Yearbook of Cell and Tissue Transplantation 1996–1997, 107–16. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0165-0_10.

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Lim, Jeong Mook, and Ji Yeon Ahn. "Fetal Cell Reprogramming and Transformation." In Fetal Stem Cells in Regenerative Medicine, 101–30. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3483-6_6.

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Flomerfelt, Francis A., and Ronald E. Gress. "Bone Marrow and Fetal Liver Radiation Chimeras." In T-Cell Development, 109–15. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_9.

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Teixeiro, Emma, and Mark A. Daniels. "Fetal Thymic Organ Culture and Negative Selection." In T-Cell Development, 293–302. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2740-2_18.

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Conference papers on the topic "Fetal cell"

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Turzhitsky, Vladimir, Lei Zhang, Lianyu Guo, Edward Vitkin, Le Qiu, Irving Itzkan, Kee-Hak Lim, and Lev T. Perelman. "Single Cell Spectroscopy for Isolating Fetal Cells from Maternal Blood." In Biomedical Optics. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/biomed.2014.bm2b.2.

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Vogelgesang, Anja, Caroline Barone, Frauke G. Gerdts, Anna Blumental-Perry, and Christiane Dammann. "Will Maternal Smoking During Pregnancy Influence Fetal-Maternal Cell Trafficking?" In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4197.

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El-Maarri, Osman, Muhammad Ahmer Jamil, Heike Singer, Rawya Al-Rifai, and Johannes Oldenburg. "Molecular Profiling of Fetal and Adult Liver Sinusoidal Endothelial Cells: A F8 Secreting Cell." In Hamburger Hämophilie Symposion Hamburg, Germany. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1721572.

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Marawan, Radwa. "137 Circulating maternal total cell-free DNA, cell-free fetal dna and soluble endoglin levels in preeclampsia: predictors of adverse fetal outcome? a cohort study." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.134.

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Kieffer, N., L. Edelman, P. Edelman, C. Legrand, J. Breton-Gori us, and W. Vainchenker. "A MONOCLONAL ANTIBODY AGAINST AN ERYTHROID ONTOGENIC ANTIGEN IDENTIFIES GP IV ON HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643532.

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A murine monoclonal antibody (FA6-152), obtained by immunizing mice with fetal human erythrocytes agglutinated fetal but not adult erythrocytes and bound to both adultand fetal monocytes, platelets andreticulocytes. The antibody did not react with lymphocytes or granulocytes (P. Edelman et al., Blood, 1986, 67, 56). Fluorescent labeling of marrow cells and of in vitro BFU-E, CFU-GM and CFU-MK derivedcolonies revealed that the antigen defined by FA6 was absent from the granulocytic precursors and was detected on the megakaryo-cytic lineage at a later stage of differentiation than major platelet membraneglycoprotein markers. In contrast,the antigen appeared as a very early marker of erythroid differentiation.In the present report, we performed immunoprecipitation experiments on surface labeled platelets toidentify the platelet FA6 antigen.A band of apparent Mr - 85,000 wasimmunoprecipitated from iodinated platelets. This band was also revealed after periodate/Na[3H]BH4 orneuraminidase galactose oxidase/Na[3H]BH4 surface labeling of the platelets, providing evidence that the FA6 antigen corresponds to platelet GP IV. Preliminary studies revealed that FA6-IgG inhibited platelet aggregation induced by low doses of thrombin without affecting the platelet release reaction. Our results therefore suggest that GP IV, which isa multi-lineage hematopoietic differentiation marker, could play a role in cell-cell or cell-substrateinteractions common to different hematopoietic cell types.
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Pham, Lucia D., Sana Mujahid, Sandy L. Murray, MaryAnn V. Volpe, and Heber C. Nielsen. "Androgen Inhibits TACE-Mediated Components Of Fetal Type II Cell Surfactant Synthesis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3761.

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DeCoux, Ashley, Jennifer Chaplin, Glen Wilson, John Benjamin, and Sarah A. Gebb. "Hyperoxia-Induced Toll-Like Receptor-2 Signaling Causes Fetal Lung Mesenchymal Cell Dysfunction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1227.

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Brockmeyer, T., R. Williams, AB Knoll, S. Murray, HC Nielsen, and CE Dammann. "Effects of Fetal Rat Lung Type II Cells and Fibroblasts on Bone Marrow Mesenchymal Stem Cell Behavior." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3275.

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Mitra, Siddhartha S., Sharareh Gholamin, Abdullah Feroze, Samuel H. Cheshier, and Irving L. Weissman. "Abstract 5007: Delineating human fetal CNS stem cell hierarchy reveals a progenitor cell of origin for human Gliobastoma Multiforme." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5007.

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Suparto, Irma H., Chandra Nur Khalam, Willy Praira, and Dondin Sajuthi. "Silkworm (Bombyx mori) hemolymph unable to substitute fetal bovine serum in insect cell culture." In 4TH INTERNATIONAL CONFERENCE ON MATHEMATICS AND NATURAL SCIENCES (ICMNS 2012): Science for Health, Food and Sustainable Energy. AIP Publishing LLC, 2014. http://dx.doi.org/10.1063/1.4868803.

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Reports on the topic "Fetal cell"

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Henderson, R. F., J. J. Waide, and J. F. Lechner. Characterization of cloned cells from an immortalized fetal pulmonary type II cell line. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381391.

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Paul, Satashree. Turning Back the Sickle Cell Disease: A New Drug into Play. Science Repository OÜ, May 2021. http://dx.doi.org/10.31487/sr.blog.38.

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Researchers at the Fulcrum Therapeutics developed a bioavailable drug candidate called FTX 6058 – (a novel small molecular fetal haemoglobin inducer for sickle cell disease) that can restore the body’s ability to produce fetal haemoglobin
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Durgud, Meriem R., Vili K. Stoyanova, Nikolay T. Popov, Danail S. Minchev, Hristo Y. Ivanov, Ivan N. Minkov, and Tihomir I. Vachev. Non-invasive Prenatal Sex Identification Using Cell-free Fetal DNA in Maternal Circulation. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, December 2018. http://dx.doi.org/10.7546/crabs.2018.12.14.

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Chepko, Gloria, and Leena Hilakivi-Clarke. Role of the Stem Cell Niche in Hormone-induced Tumorigenesis in Fetal Mouse Mammary Epithelium. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada471087.

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Pailino, Lia, Lihua Lou, Alberto Sesena Rubfiaro, Jin He, and Arvind Agarwal. Nanomechanical Properties of Engineered Cardiomyocytes Under Electrical Stimulation. Florida International University, October 2021. http://dx.doi.org/10.25148/mmeurs.009775.

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Engineered cardiomyocytes made of human-induced pluripotent stem cells (iPSC) present phenotypical characteristics similar to human fetal cardiomyocytes. There are different factors that are essential for engineered cardiomyocytes to be functional, one of them being that their mechanical properties must mimic those of adult cardiomyocytes. Techniques, such as electrical stimulation, have been used to improve the extracellular matrix's alignment and organization and improve the intracellular environment. Therefore, electrical stimulation could potentially be used to enhance the mechanical properties of engineered cardiac tissue. The goal of this study is to establish the effects of electrical stimulation on the elastic modulus of engineered cardiac tissue. Nanoindentation tests were performed on engineered cardiomyocyte constructs under seven days of electrical stimulation and engineered cardiomyocyte constructs without electrical stimulation. The tests were conducted using BioSoft™ In-Situ Indenter through displacement control mode with a 50 µm conospherical diamond fluid cell probe. The Hertzian fit model was used to analyze the data and obtain the elastic modulus for each construct. This study demonstrated that electrically stimulated cardiomyocytes (6.98 ± 0.04 kPa) present higher elastic modulus than cardiomyocytes without electrical stimulation (4.96 ± 0.29 kPa) at day 7 of maturation. These results confirm that electrical stimulation improves the maturation of cardiomyocytes. Through this study, an efficient nanoindentation method is demonstrated for engineered cardiomyocyte tissues, capable of capturing the nanomechanical differences between electrically stimulated and non-electrically stimulated cardiomyocytes.
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Halevy, Orna, Zipora Yablonka-Reuveni, and Israel Rozenboim. Enhancement of meat production by monochromatic light stimuli during embryogenesis: effect on muscle development and post-hatch growth. United States Department of Agriculture, June 2004. http://dx.doi.org/10.32747/2004.7586471.bard.

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The original objectives were: A. To determine the critical embryonic age for monochromatic green light stimulation. B. To follow the ontogeny of embryos exposed to monochromatic green light vs. darkness. C. To investigate the effects of monochromatic green light illumination on myoblast and fiber development in the embryo. D. To investigate the stimulatory effect of light combinations during embryo and post-hatch periods on growth and meat production. E. To evaluate the direct effect of monochromatic green light on cultured embryonic and adult myoblasts. The overall purpose of this study was to investigate the effect of monochromatic light stimuli during incubation period of broilers on muscle development and satellite cell myogenesis. Based on previous studies (Halevy et al., 1998; Rozenboim et al., 1999) that demonstrated the positive effects of green-light illumination on body and muscle growth, we hypothesized that monochromatic light illumination accelerates embryo and muscle development and subsequently enhances muscle growth and meat production. Thus, further decreases management costs. Under the cooperation of the laboratories at the Hebrew University of Jerusalem and University of Washington we have conducted the following: 1. We have established the critical stage for exposure to green monochromatic light which has the maximal effect on body and muscle growth (Objective A). We report that embryonic day 5 is optimal for starting illumination. The optimal regime of lighting that will eliminate possible heat effects was evaluated by monitoring egg core temperature at various illumination periods. We found that intermitted lighting (15 min. on; 15 min. off) is optimal to avoid heat effects. 2. We have evaluated in detail gross changes in embryo development profile associated to green light stimuli vs. darkness. In addition, we have investigated the stimulatory effect of light combinations during embryo and post-hatch periods on body and muscle growth (Objective B,D). 3. We have studied the expression profile of muscle regulatory proteins during chicken muscle cell differentiation in cultures using newly developed antibodies. This study paved the way for analyzing the expression of these proteins in our photo stimulation experiments (Objective C). 4. We have studied the pattern ofPax7 expression during myogenesis in the posthatch chicken. Experimental chick pectoralis muscles as well adult myoblast cultures were used in this study and the results led us to propose a novel model for satellite cell differentiation and renewal. 5. The effects of monochromatic green light illumination during embryogenesis have been studied. These studies focused on fetal myoblast and satellite cell proliferation and differentiation at pre- and posthatch periods and on the effects on the expression of muscle regulatory proteins which are involved in these processes. In addition, we have analyzed the effect of photo stimulation in the embryo on myofiber development at early posthatch (Objective C). 6. In follow the reviewers' comments we have not conducted Objective E. The information gathered from these studies is of utmost importance both, for understanding the molecular basis of muscle development in the posthatch chicks and for applied approach for future broiler management. Therefore, the information could be beneficial to agriculture in the short term on the one hand and to future studies on chick muscle development in the embryo and posthatch on the other hand.
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Fields, Michael J., Mordechai Shemesh, and Anna-Riitta Fuchs. Significance of Oxytocin and Oxytocin Receptors in Bovine Pregnancy. United States Department of Agriculture, August 1994. http://dx.doi.org/10.32747/1994.7568790.bard.

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Oxytocin has multiple actions in bovine reproductive tract and it was our purpose to determine the nature of these actions and their significance for the physiology of bovine reproduction. The bovine oxytocin receptors (OTR) gene was cloned and its expression studied during the cycle and pregnancy. OTR mRNA changed in parallel with OTR with control occurring mainly at the transcriptional level. However, the endocrine regulation of OTR were found in endometrium and cervical mucosa at estrus and at parturition. In both tissues OTR were suppressed in the luteal phase and early pregnancy. Whereas cervical OTR remained suppressed throughout pregnancy, endometrial OTR began to increase soon after implantation and reached higher concentrations in midpregnancy than at estrus. OTR in caruncles did not increase until third trimester, and OTR in cervical mucosa, cotyledons and fetal membranes increased only at term. Myometrial OTR showed less variation and OTR were present throughout the cycle and pregnancy but increased significantly during mid- and late pregnancy. OTR were localized in endometrial epithelial cells and lumina epithelial cells of cervical mucosa as determined by immunohistochemistry. Endometrial OTR were functional throughout pregnancy and mediated PGF release from day 50 onwards in a receptor density related manner. OTR in cervical mucosa mediated PGE release both in vivo and in vitro, as shown in cyclic cows. The ontogeny of uterine OTR was studied from third trimester fetal stage until puberty. OTR were present in endometrium and cervical mucosa in high concentrations throughout this period; myometrial OTR began to increase somewhat later but also reached adult values by 6-mo of age. In the prepuberal heifers OT injections failed to initiate PGF2a, release. The influence of steroids on the effect of OT was examined. Ovariectomy and E2 were without effect, but P4 with or without E2 induced a massive PGF2a release in response to OT in spite of reduced OTR. Bovine cyclooxygenases (COX-1 and COX-2) were cloned and their expression studied in the endometrium of prepuberal heifers and pregnant cows. Untreated and E2 treated prepuberal heifers did not express COX-2 but P4 treated heifers did express the mRNA for COX-2, albeit weakly. During the second half of pregnancy COX-2 mRNA was strongly expressed in cotyledons and somewhat less in caruncles, whereas endometrium, myometrium and cervical mucosa showed only weak, if any, COX-2 mRNA under basal conditions. However, 2 h after OT injection significant increases in COX-2 mRNA were found in endometrial RNA. Thus OT is capable of inducing the expression of the inducible COX-2 gene, and hence the conversion of arachidonic acid to prostanoids. The results indicate that the functions of OT are numerous and probably essential for successful pregnancy and parturition.
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Gillor, Osnat, Stefan Wuertz, Karen Shapiro, Nirit Bernstein, Woutrina Miller, Patricia Conrad, and Moshe Herzberg. Science-Based Monitoring for Produce Safety: Comparing Indicators and Pathogens in Water, Soil, and Crops. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7613884.bard.

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Using treated wastewater (TWW) for crop irrigation represents an important opportunity for ensuring adequate food production in light of growing freshwater scarcity worldwide. However, the environmentally sustainable approach of using TWW for irrigation can lead to contamination of produce with fecal pathogens that may remain in treated water. The overall goal of this research was to evaluate the correlation between the presence of fecal indicator bacteria (FIB) and that of a suite of human pathogens in TWW, the irrigated soil, and crops. Field experiments were conducted to compare secondary and tertiary TWW with dechlorinated tap water for irrigation of tomatoes, a typical commercial crop, in Israel, a semi-arid country. Human pathogens including bacteria (Salmonella), protozoa (Cryptosporidiumand Giardia), and viruses (Adenovirus [AV Types A, B, C & 40/41] and Enterovirus [EV71 subtypes]) were monitored in two field trials using a combination of microscopic, cultivation-based, and molecular (qPCR) techniques. Results from the field trials indicate that microbial contamination on the surface of tomatoes did not appear to be associated with the source of irrigated waters; FIB contamination was not statistically different on tomatoes irrigated with TWW as compared to tomatoes irrigated with potable water. In fact, Indicator bacteria testing did not predict the presence of pathogens in any of the matrices tested. High concentrations of FIB were detected in water and on tomato surfaces from all irrigation treatment schemes, while pathogen contamination on tomato surfaces (Cryptosporidiumand Salmonella) was only detected on crops irrigated with TWW. These results suggest that regular monitoring for pathogens should take place to accurately detect presence of harmful microorganisms that could threaten consumer safety. A notable result from our study is that the large numbers of FIB in the water did not appear to lead to FIB accumulation in the soil. With the exception of two samples, E. coli that was present at 10³ to 10⁴ cells/100 mL in the water, was not detected in the soil. Other bacterial targets associated with the enteric environment (e. g., Proteusspp.) as well as protozoal pathogens were detected in the TWW, but not in the soil. These findings suggest that significant microbial transfer to the soil from TWW did not occur in this study. The pattern of FIB contamination on the surfaces of tomatoes was the same for all treatment types, and showed a temporal effect with more contamination detected as the duration of the field trial increased. An important observation revealed that water quality dramatically deteriorated between the time of its release from the wastewater treatment plant and the time it was utilized for irrigation, highlighting the importance of performing water quality testing throughout the growing season at the cultivation site.
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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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