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Journal articles on the topic 'Fetal cell'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

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

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Frost, Mackenzie S., Aqib H. Zehri, Sean W. Limesand, William W. Hay та 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 conce

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3

Cassar-Malek, Isabelle, Brigitte Picard, Catherine Jurie, et al. "Myogenesis Is Delayed in Bovine Fetal Clones." Cellular Reprogramming 12, no. 2 (2010): 191–201. http://dx.doi.org/10.1089/cell.2009.0065.

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4

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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5

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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6

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

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7

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

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8

McDougall, Annie R. A., Stuart B. Hooper, Valerie A. Zahra, et al. "The oncogeneTrop2regulates fetal lung cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 4 (2011): L478—L489. http://dx.doi.org/10.1152/ajplung.00063.2011.

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The factors regulating growth of the developing lung are poorly understood, although the degree of fetal lung expansion is critical. The oncogene Trop2 (trophoblast antigen 2) is upregulated during accelerated fetal lung growth, and we hypothesized that it may regulate normal fetal lung growth. We investigated Trop2 expression in the fetal and neonatal sheep lung during accelerated and delayed lung growth induced by alterations in fetal lung expansion, as well as in response to glucocorticoids. Trop2 expression was measured using real-time PCR and localized spatially using in situ hybridizatio

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9

Wen, Qing, Yuqian Wang, Jixin Tang, C. Yan Cheng, and Yi-Xun Liu. "Sertoli Cell Wt1 Regulates Peritubular Myoid Cell and Fetal Leydig Cell Differentiation during Fetal Testis Development." PLOS ONE 11, no. 12 (2016): e0167920. http://dx.doi.org/10.1371/journal.pone.0167920.

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10

Thomson, Alison J., Hadrien Pierart, Stephen Meek, et al. "Reprogramming Pig Fetal Fibroblasts Reveals a Functional LIF Signaling Pathway." Cellular Reprogramming 14, no. 2 (2012): 112–22. http://dx.doi.org/10.1089/cell.2011.0078.

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11

Weiss, R. "Human Fetal-Cell Transplants Planned." Science News 132, no. 2 (1987): 22. http://dx.doi.org/10.2307/3971772.

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12

Shaaban, Aimen F., and Alan W. Flake. "Fetal hematopoietic stem cell transplantation." Seminars in Perinatology 23, no. 6 (1999): 515–23. http://dx.doi.org/10.1016/s0146-0005(99)80030-5.

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13

Coles, Peter. "French fetal cell transplant operations." Nature 348, no. 6303 (1990): 667. http://dx.doi.org/10.1038/348667b0.

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14

Abbott, Alison. "Fetal-cell revival for Parkinson’s." Nature 510, no. 7504 (2014): 195–96. http://dx.doi.org/10.1038/510195a.

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15

Tu, Jian, and Bernard E. Tuch. "Expression of Glucokinase in Glucose-Unresponsive Human Fetal Pancreatic Islet-Like Cell Clusters1." Journal of Clinical Endocrinology & Metabolism 82, no. 3 (1997): 943–48. http://dx.doi.org/10.1210/jcem.82.3.3837.

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Abstract Glucokinase (GK) is the glucose sensor in the adult β-cell, resulting in fuel for insulin synthesis and secretion. Defects in this enzyme in the β-cell are responsible for the genetic disorder maturity-onset diabetes of the young, with the β-cell being unable to secrete insulin appropriately when challenged with glucose. The human fetalβ -cell is also unable to secrete insulin when exposed to glucose, but whether GK is present and functional in this developing cell is unknown. To determine the expression of GK in human fetal pancreatic tissue, cytosolic protein was extracted from huma

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16

Everett, T. R., and L. S. Chitty. "Cell-free fetal DNA: the new tool in fetal medicine." Ultrasound in Obstetrics & Gynecology 45, no. 5 (2015): 499–507. http://dx.doi.org/10.1002/uog.14746.

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17

Jotereau, F., F. Heuze, V. Salomon-Vie, and H. Gascan. "Cell kinetics in the fetal mouse thymus: precursor cell input, proliferation, and emigration." Journal of Immunology 138, no. 4 (1987): 1026–30. http://dx.doi.org/10.4049/jimmunol.138.4.1026.

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Abstract The entry and differentiation of lymphoid precursor cells (LPC) in grafted mouse fetal thymuses and the emigration of explants thymocytes has been followed in a system in which donor and host lymphocytes could be distinguished on the basis of Thy-1 expression. It appears that LPC that invade the fetal mouse thymus between 10 and 13 days rapidly differentiate into Thy-1 positive thymocytes, giving rise to all of the lymphoid populations of both cortical and medullary locations until approximately the end of the first week after birth. Lymphoid precursor cells that enter the fetal thymu

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18

Haynes, B. F., M. E. Martin, H. H. Kay, and J. Kurtzberg. "Early events in human T cell ontogeny. Phenotypic characterization and immunohistologic localization of T cell precursors in early human fetal tissues." Journal of Experimental Medicine 168, no. 3 (1988): 1061–80. http://dx.doi.org/10.1084/jem.168.3.1061.

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During early fetal development, T cell precursors home from fetal yolk sac and liver to the epithelial thymic rudiment. From cells that initially colonize the thymus arise mature T cells that populate T cell zones of the peripheral lymphoid system. Whereas colonization of the thymus occurs late in the final third of gestation in the mouse, in birds and humans the thymus is colonized by hematopoietic stem cell precursors during the first third of gestation. Using a large series of early human fetal tissues and a panel of monoclonal antibodies that includes markers of early T cells (CD7, CD45),

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19

Wucherpfennig, K. W., Y. J. Liao, M. Prendergast, J. Prendergast, D. A. Hafler, and J. L. Strominger. "Human fetal liver gamma/delta T cells predominantly use unusual rearrangements of the T cell receptor delta and gamma loci expressed on both CD4+CD8- and CD4-CD8- gamma/delta T cells." Journal of Experimental Medicine 177, no. 2 (1993): 425–32. http://dx.doi.org/10.1084/jem.177.2.425.

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Substantial numbers of both alpha/beta and gamma/delta T cells are present in human fetal liver, which suggests a role of the fetal liver in T cell development. The diversity of fetal liver T cell receptor (TCR) gamma and delta chain rearrangements was examined among both CD4+CD8- and CD4-CD8- gamma/delta T cell clones. In addition, TCR delta chain transcripts from three fetal livers were sequenced after polymerase chain reaction amplification of TCR delta chains with V delta 1 or V delta 2 rearrangements. Five of six fetal liver gamma/delta T cell clones had a V delta 2-D delta 3-J delta 3 ge

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20

Tang, Yanjuan, Claudia Peitzsch, Hojjatollah Nozad Charoudeh, et al. "Emergence of NK-cell progenitors and functionally competent NK-cell lineage subsets in the early mouse embryo." Blood 120, no. 1 (2012): 63–75. http://dx.doi.org/10.1182/blood-2011-02-337980.

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Abstract The earliest stages of natural killer (NK)–cell development are not well characterized. In this study, we investigated in different fetal hematopoietic tissues how NK-cell progenitors and their mature NK-cell progeny emerge and expand during fetal development. Here we demonstrate, for the first time, that the counterpart of adult BM Lin−CD122+NK1.1−DX5− NK-cell progenitor (NKP) emerges in the fetal liver at E13.5. After NKP expansion, immature NK cells emerge at E14.5 in the liver and E15.5 in the spleen. Thymic NK cells arise at E15.5, whereas functionally competent cytotoxic NK cell

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21

Adkins, B. "Developmental regulation of the intrathymic T cell precursor population." Journal of Immunology 146, no. 5 (1991): 1387–93. http://dx.doi.org/10.4049/jimmunol.146.5.1387.

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Abstract The maturation potential of CD4-8- thymocytes purified from mice of different developmental ages was examined in vivo after intrathymic injection. As previously reported, 14-day fetal CD4-8- thymocytes produced fewer CD4+ than CD8+ progeny in peripheral lymphoid tissues, resulting in a CD4+:CD8+ ratio of less than or equal to 1.0. In contrast, adult CD4-8- thymocytes generated CD4+ or CD8+ peripheral progeny in the proportions found in the normal adult animal (CD4+:CD8+ = 2 to 3). Here we have shown that CD4-8- precursor cells from the 17-day fetal thymus also produced peripheral lymp

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22

Yang, Hsin-Yu, Che-Hsien Lin, Yi-Wen Hu, et al. "Automatic Single-Cell Harvesting for Fetal Nucleated Red Blood Cell Isolation on a Self-Assemble Cell Array (SACA) Chip." Micromachines 15, no. 12 (2024): 1515. https://doi.org/10.3390/mi15121515.

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(1) Background: Fetal chromosomal examination is a critical component of modern prenatal testing. Traditionally, maternal serum biomarkers such as free β-human chorionic gonadotropin (Free β-HCG) and pregnancy-associated plasma protein A (PAPPA) have been employed for screening, achieving a detection rate of approximately 90% for fetuses with Down syndrome, albeit with a false positive rate of 5%. While amniocentesis remains the gold standard for the prenatal diagnosis of chromosomal abnormalities, including Down syndrome and Edwards syndrome, its invasive nature carries a significant risk of

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23

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 (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

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24

Blondeau, B., J. Lesage, P. Czernichow, J. P. Dupouy та B. Bréant. "Glucocorticoids impair fetal β-cell development in rats". American Journal of Physiology-Endocrinology and Metabolism 281, № 3 (2001): E592—E599. http://dx.doi.org/10.1152/ajpendo.2001.281.3.e592.

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In rats, poor fetal growth due to maternal food restriction during pregnancy is associated with decreased β-cell mass at birth and glucose intolerance in adulthood. Overexposure to glucocorticoids in utero can induce intrauterine growth retardation in humans and animals and subsequent glucose intolerance in rodents. The aims of this study were to investigate whether glucocorticoid overexposure mediates the effect of undernutrition on β-cell mass and to study their potential role in normally nourished rats. Undernutrition significantly increased maternal and fetal corticosterone levels. Twenty-

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25

Khalaf, Ahmed Saadi. "Isolation and detection of rotavirus by Enzyme linked Immune assay in fecal specimens of buffalo calves." Iraqi Journal of Veterinary Medicine 42, no. 2 (2019): 1–6. http://dx.doi.org/10.30539/iraqijvm.v42i2.280.

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A total of 50 fecal samples were collected from buffalo calves ages between 3 days to 4 months, in middle area of Iraq (Baghdad, Salahaldden, Babylon, Diyala, and Wasit) between July 2016 to June 2017. All samples were examined by Immuno-chromatographic rapid tests for detection of buffalo rotavirus, twenty samples were positive. Enzyme-Linked Immunosorbent Assay. test was also used and revealed only 8 positive samples, the later samples were used for viral isolation on fetal bovine kidney cell culture for detection the cytopathogenic effects of the virus. The cytopathogenic effects of virus w

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26

Park, Hee Jin, Hee Young Cho, and Dong Hyun Cha. "The Amniotic Fluid Cell-Free Transcriptome Provides Novel Information about Fetal Development and Placental Cellular Dynamics." International Journal of Molecular Sciences 22, no. 5 (2021): 2612. http://dx.doi.org/10.3390/ijms22052612.

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The amniotic fluid (AF) is a complex biofluid that reflects fetal well-being during development. AF con be divided into two fractions, the supernatant and amniocytes. The supernatant contains cell-free components, including placenta-derived microparticles, protein, cell-free fetal DNA, and cell-free fetal RNA from the fetus. Cell-free mRNA (cfRNA) analysis holds a special position among high-throughput analyses, such as transcriptomics, proteomics, and metabolomics, owing to its ease of profiling. The AF cell-free transcriptome differs from the amniocyte transcriptome and alters with the progr

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27

Stonestreet, B. S., M. Goldstein, W. Oh, and J. A. Widness. "Effects of prolonged hyperinsulinemia on erythropoiesis in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (1989): R1199—R1204. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1199.

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Offspring of diabetic mothers have an increased incidence of neonatal polycythemia, decreased oxygen tension in cord blood at delivery, and elevated plasma erythropoietin levels at birth. Experimental fetal hyperinsulinemia has been associated with reduced fetal oxygen content and increased erythropoietin concentration. To test the hypothesis that prolonged fetal hyperinsulinemia results in increased fetal erythropoiesis and red cell volume during gestation, we infused insulin or placebo for 11 +/- 0.2 (+/- SE) days into chronically catheterized fetal sheep, beginning at 124 days of gestation.

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28

Wasserman, R., Y. S. Li, S. A. Shinton, et al. "A Novel Mechanism for B Cell Repertoire Maturation Based on Response by B Cell Precursors to Pre–B Receptor Assembly." Journal of Experimental Medicine 187, no. 2 (1998): 259–64. http://dx.doi.org/10.1084/jem.187.2.259.

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The expression of different sets of immunoglobulin specificities by fetal and adult B lymphocytes is a long-standing puzzle in immunology. Recently it has become clear that production of immunoglobulin μ heavy chain and subsequent assembly with a surrogate light chain to form the pre-B cell receptor complex is critical for development of B cells. Here we show that instead of promoting pre–B cell progression as in adult bone marrow, this complex inhibits pre–B cell growth in fetal liver. Curiously, we identify a fetal-associated VH11 μ heavy chain that allows continued pre-B proliferation in fe

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29

Pei, Yixuan Amy, and Ming Pei. "Hypoxia Modulates Regenerative Potential of Fetal Stem Cells." Applied Sciences 12, no. 1 (2021): 363. http://dx.doi.org/10.3390/app12010363.

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Adult mesenchymal stem cells (MSCs) are prone to senescence, which limits the scope of their use in tissue engineering and regeneration and increases the likelihood of post-implantation failure. As a robust alternative cell source, fetal stem cells can prevent an immune reaction and senescence. However, few studies use this cell type. In this study, we sought to characterize fetal cells’ regenerative potential in hypoxic conditions. Specifically, we examined whether hypoxic exposure during the expansion and differentiation phases would affect human fetal nucleus pulposus cell (NPC) and fetal s

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30

Shafritz, David A., Mo R. Ebrahimkhani, and Michael Oertel. "Therapeutic Cell Repopulation of the Liver: From Fetal Rat Cells to Synthetic Human Tissues." Cells 12, no. 4 (2023): 529. http://dx.doi.org/10.3390/cells12040529.

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Progenitor cells isolated from the fetal liver can provide a unique cell source to generate new healthy tissue mass. Almost 20 years ago, it was demonstrated that rat fetal liver cells repopulate the normal host liver environment via a mechanism akin to cell competition. Activin A, which is produced by hepatocytes, was identified as an important player during cell competition. Because of reduced activin receptor expression, highly proliferative fetal liver stem/progenitor cells are resistant to activin A and therefore exhibit a growth advantage compared to hepatocytes. As a result, transplante

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31

Miller, BA, M. Salameh, M. Ahmed, et al. "High fetal hemoglobin production in sickle cell anemia in the eastern province of Saudi Arabia is genetically determined." Blood 67, no. 5 (1986): 1404–10. http://dx.doi.org/10.1182/blood.v67.5.1404.1404.

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Abstract Homozygous sickle cell disease in the eastern province of Saudi Arabia is clinically mild. Circulating fetal hemoglobin levels of 16.0 +/- 7.4% were found in these anemic patients, but only 1.09 +/- 0.97% in their sickle trait parents. To determine whether these sickle cell anemia patients inherit an increased capacity to synthesize fetal hemoglobin, a radioimmunoassay of fetal and adult hemoglobin was performed on erythroid progenitor (BFU-E)-derived erythroblasts from Saudi Arabian sickle cell patients and their parents. Mean fetal hemoglobin content per BFU-E-derived erythroblast f

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32

Miller, BA, M. Salameh, M. Ahmed, et al. "High fetal hemoglobin production in sickle cell anemia in the eastern province of Saudi Arabia is genetically determined." Blood 67, no. 5 (1986): 1404–10. http://dx.doi.org/10.1182/blood.v67.5.1404.bloodjournal6751404.

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Homozygous sickle cell disease in the eastern province of Saudi Arabia is clinically mild. Circulating fetal hemoglobin levels of 16.0 +/- 7.4% were found in these anemic patients, but only 1.09 +/- 0.97% in their sickle trait parents. To determine whether these sickle cell anemia patients inherit an increased capacity to synthesize fetal hemoglobin, a radioimmunoassay of fetal and adult hemoglobin was performed on erythroid progenitor (BFU-E)-derived erythroblasts from Saudi Arabian sickle cell patients and their parents. Mean fetal hemoglobin content per BFU-E-derived erythroblast from Saudi

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33

Carlyle, James R., Alison M. Michie, Sarah K. Cho та Juan Carlos Zúñiga-Pflücker. "Natural Killer Cell Development and Function Precede αβ T Cell Differentiation in Mouse Fetal Thymic Ontogeny". Journal of Immunology 160, № 2 (1998): 744–53. http://dx.doi.org/10.4049/jimmunol.160.2.744.

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Abstract Natural killer (NK) cells mediate MHC-unrestricted cytolysis of virus-infected cells and tumor cells. In the adult mouse, NK cells are bone marrow-derived lymphocytes that mature predominantly in extrathymic locations but have also been suggested to share a common intrathymic progenitor with T lymphocytes. However, mature NK cells are thought to be absent in mouse fetal ontogeny. We report the existence of thymocytes with a mature NK cell phenotype (NK1.1+/CD117−) as early as day 13 of gestation, approximately 3 days before the appearance of CD4+/CD8+ cells in T lymphocyte development

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34

Gerovassili, Ageliki, Kypros H. Nicolaides, Swee Lay Thein, and David Rees. "Cell Free Fetal and Total DNA Levels in Pregnancies at Risk of Sickle Cell Disease and Significant Ethnic Variation." Blood 108, no. 11 (2006): 3791. http://dx.doi.org/10.1182/blood.v108.11.3791.3791.

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Abstract Cell free (cf) DNA in maternal circulation is increasingly investigated in pregnancy. We aimed to determine if sickle cell trait women had quantitative differences of cfDNA with controls and if there was an ethnic difference between the cfDNA levels of Northern European and African/African-Caribbean populations. Non-invasive prenatal diagnosis through quantification of fetal and total cfDNA was tested in 33 pregnant women at risk of carrying a fetus affected with sickle cell disease and 124 control pregnancies. Fetal cfDNA assays were based on two Y chromosome specific markers (SRY an

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35

de Leon, Priscila Marques Moura, Vinicius Farias Campos, Odir Antônio Dellagostin, João Carlos Deschamps, Fabiana Kömmling Seixas, and Tiago Collares. "Equine fetal sex determination using circulating cell-free fetal DNA (ccffDNA)." Theriogenology 77, no. 3 (2012): 694–98. http://dx.doi.org/10.1016/j.theriogenology.2011.09.005.

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36

Whitby, D. J., M. T. Longaker, M. R. Harrison, N. S. Adzick, and M. W. Ferguson. "Rapid epithelialisation of fetal wounds is associated with the early deposition of tenascin." Journal of Cell Science 99, no. 3 (1991): 583–86. http://dx.doi.org/10.1242/jcs.99.3.583.

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Wound healing is a complex process involving the interaction of many cell types with the extracellular matrix (ECM). Fetal skin wound healing differs from that in the adult in that it occurs rapidly and without scar formation. The mechanisms underlying these differing processes may be related to the fetal environment, the stage of differentiation of the fetal cells or the ECM deposited in the wound. The spatial and temporal distribution of two components of the ECM, fibronectin and tenascin, were studied by immunostaining of cryosections from trunk wounds of fetal and adult sheep. Epithelialis

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37

Wang, Yang, Chaoqun Huang, Narendranath Reddy Chintagari, Dong Xi, Tingting Weng, and Lin Liu. "miR-124 regulates fetal pulmonary epithelial cell maturation." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 4 (2015): L400—L413. http://dx.doi.org/10.1152/ajplung.00356.2014.

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MicroRNAs are a family of small noncoding RNAs that regulate the expression of their target proteins at the posttranscriptional level. Their functions cover almost every aspect of cell physiology. However, the roles of microRNAs in fetal lung development are not completely understood. The objective of this study is to investigate the regulation and molecular mechanisms of alveolar epithelial cell maturation during fetal lung development by miR-124. We discovered that miR-124 was downregulated during rat fetal lung development and predominantly expressed in the epithelial cells at late stage of

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38

Xu, Jing, Mingyao Liu, A. Keith Tanswell, and Martin Post. "Mesenchymal determination of mechanical strain-induced fetal lung cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 3 (1998): L545—L550. http://dx.doi.org/10.1152/ajplung.1998.275.3.l545.

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Fetal breathing movements play an important role in normal fetal lung growth. We have previously shown that an intermittent mechanical strain regimen (60 cycles/min, 15 min/h), simulating normal fetal breathing movements, stimulated growth of mixed fetal rat lung cells in organotypic culture. In the present study, we examined the individual responses of the two major fetal lung cell types, fibroblasts and epithelial cells, to mechanical strain. Also, we investigated the effect of mesenchymal-epithelial interactions on strain-induced cell proliferation during fetal lung development. Fibroblasts

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39

Salehi, Faraz, Vanessa Redecke, and Hans Häcker. "Conditionally immortalized cell lines with mast cell potential." Journal of Immunology 212, no. 1_Supplement (2024): 1050_5261. http://dx.doi.org/10.4049/jimmunol.212.supp.1050.5261.

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Abstract Prior to the establishment of definitive hematopoiesis, mast cells (MCs) derived from the yolk sac and fetal liver colonize diverse tissues, maintaining a presence throughout life. Following the establishment of definitive hematopoiesis, hematopoietic stem cells from the bone marrow (BM) also contribute to the MC pool. The diverse origins and tissue-resident nature of MCs complicate their study. Therefore, a system facilitating the expansion of MC progenitors and their controlled differentiation becomes crucial. This report outlines the development of conditionally immortalized MC pro

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40

Mulla-Ali, Dalal H., Kevin H. M. Kuo, Mathew Sermer, and Anne Mcleod. "The Relationship Between Pre-Pregnancy Sickle Cell Disease-Specific Complications and Maternal and Fetal Outcomes in Sickle Cell Disease Pregnancies." Blood 118, no. 21 (2011): 4848. http://dx.doi.org/10.1182/blood.v118.21.4848.4848.

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Abstract Abstract 4848 Introduction: Patients with sickle cell disease (SCD) have worse maternal and fetal outcomes compared to the general population, and experience antepartum complications unique to SCD patients, including painful vasoocclusive crises (VOC), acute chest syndrome (ACS), stroke and symptomatic anemia. The relationship between pre-pregnancy SCD-specific complications and maternal/fetal outcomes and antepartum complications has not been explored. We hypothesize that increased rates of SCD-specific complications are associated with increased rates of antepartum SCD-specific comp

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41

Ghorbian, Saeid. "Applications of Cell-Free Fetal DNA in Maternal Serum." International Journal of Infertility & Fetal Medicine 3, no. 2 (2012): 33–39. http://dx.doi.org/10.5005/jp-journals-10016-1038.

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ABSTRACT Cell-free fetal DNA (cffDNA) is available in the maternal circulation throughout pregnancy and can be used for noninvasive prenatal diagnosis including, determination of fetal sex, identification of specific single gene disorders, typing of fetal blood groups (RhD), paternity determination and potentially routine use for Down's syndrome (DS) testing of all pregnancies. I searched published literature on the PubMed and databases on Scopus interface systematically using keyword's cffDNA, noninvasive diagnosis, fetal DNA in the maternal serum. Reference lists from the papers were also se

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42

Rivera, Alicia. "Sickle cell disease and fetal hemoglobin." Saudi Journal of Medicine and Medical Sciences 6, no. 3 (2018): 131. http://dx.doi.org/10.4103/sjmms.sjmms_128_18.

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43

Weiss, R. "Fetal-Cell Transplants Put on Hold." Science News 133, no. 17 (1988): 260. http://dx.doi.org/10.2307/3972443.

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Weiss, R. "Fetal-Cell Transplants Show Few Benefits." Science News 134, no. 21 (1988): 324. http://dx.doi.org/10.2307/3972903.

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45

Weiss, Rick. "Forbidding Fruits of Fetal-Cell Research." Science News 134, no. 19 (1988): 296. http://dx.doi.org/10.2307/3973073.

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Samuelsen, Grethe Badsberg, Nenad Bogdanović, Henning Laursen, Niels Graem, Jørgen Falck Larsen, and Bente Pakkenberg. "TOTAL CELL NUMBER IN FETAL BRAIN." Image Analysis & Stereology 19, no. 1 (2011): 35. http://dx.doi.org/10.5566/ias.v19.p35-38.

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In this study the material comprises brains from three aborted fetuses and two fullterm infants who died at birth.The gestational ages ranged from the 22nd week to term. All cases were without malformations, known chromosomal abnormality, hydrops, and systemic infections, and all had normal birth weights with fetal growth indices (observed birth weight/expected mean birth weight) between 0.9 - 1.05. The preliminary results show a five fold increase in the total cell population in the marginal zone/cortical plate, MZ/CP (future neocortex), from week 22 until term. In the transient subplate zone

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Pilones, Karsten, Zhi-Wei Lai, and Jerrie Gavalchin. "Prenatal HgCl2Exposure Alters Fetal Cell Phenotypes." Journal of Immunotoxicology 4, no. 4 (2007): 295–301. http://dx.doi.org/10.1080/15476910701680178.

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Merchant, F. A. "Strategies for automated fetal cell screening." Human Reproduction Update 8, no. 6 (2002): 509–21. http://dx.doi.org/10.1093/humupd/8.6.509.

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Steinberg, Martin H. "Fetal hemoglobin in sickle cell anemia." Blood 136, no. 21 (2020): 2392–400. http://dx.doi.org/10.1182/blood.2020007645.

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Abstract Fetal hemoglobin (HbF) can blunt the pathophysiology, temper the clinical course, and offer prospects for curative therapy of sickle cell disease. This review focuses on (1) HbF quantitative trait loci and the geography of β-globin gene haplotypes, especially those found in the Middle East; (2) how HbF might differentially impact the pathophysiology and many subphenotypes of sickle cell disease; (3) clinical implications of person-to-person variation in the distribution of HbF among HbF-containing erythrocytes; and (4) reactivation of HbF gene expression using both pharmacologic and c

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Akinsheye, Idowu, Abdulrahman Alsultan, Nadia Solovieff, et al. "Fetal hemoglobin in sickle cell anemia." Blood 118, no. 1 (2011): 19–27. http://dx.doi.org/10.1182/blood-2011-03-325258.

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Abstract Fetal hemoglobin (HbF) is the major genetic modulator of the hematologic and clinical features of sickle cell disease, an effect mediated by its exclusion from the sickle hemoglobin polymer. Fetal hemoglobin genes are genetically regulated, and the level of HbF and its distribution among sickle erythrocytes is highly variable. Some patients with sickle cell disease have exceptionally high levels of HbF that are associated with the Senegal and Saudi-Indian haplotype of the HBB-like gene cluster; some patients with different haplotypes can have similarly high HbF. In these patients, hig

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