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Books on the topic 'Cellule Fetali'

Author: Grafiati

Published: 9 March 2023

Last updated: 11 March 2023

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1

G, Wegmann Thomas, Gill Thomas J, Nisbet-Brown Eric, and Banff Conference on Reproductive Immunology (3rd : 1989 : Banff, Alta.), eds. Molecular and cellular immunobiology of the maternal fetal interface. New York: Oxford University Press, 1991.

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2

E, Broxmeyer Hal, ed. Cellular characteristics of cord blood and cord blood transplantation. Bethesda, Md: AABB Press, 1998.

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3

National Institute of Child Health & Human Development Research Planning Workshop (1987 Bethesda, Md.). The onset of labor: Cellular and integrative mechanisms : a National Institute of Child Health & Human Development Research Planning Workshop, November 29-December 1, 1987. Ithaca, NY, U.S.A: Publisher and sole distributor, Perinatology Press, 1988.

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4

Raz, Yirmiya, and Taylor Anna N, eds. Alcohol, immunity, and cancer. Boca Raton: CRC Press, 1993.

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5

G, Payne Anthony, ed. Umbilical-cord stem-cell therapy: The gift of healing from healthy newborns. Laguna Beach, CA: Basic Health Publications, 2006.

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6

F, Mowbray James, Chaouat Gérard, and Institut national de la santé et de la recherche médicale (France), eds. Cellular and molecular biology of the materno-fetal relationship: Proceedings of the 2nd meeting on reproductive immunology held in Paris (France), December 17-20, 1990 = Biologie cellulaire et moléculaire de la relation materno-fœtale. Paris: J. Libbey Eurotext, 1991.

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7

1962-, Baker Philip, and Sibley Colin, eds. The placenta and neurodisability. London: Mac Keith Press, 2006.

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8

Ridsdale, Ross Allan. CTP:phosphocholine cytidylyltransferase alpha overexpression and cellular distribution in fetal lung. 2005.

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9

Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, and Michelle Fink. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.

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10

Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, and Michelle Fink. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.

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11

Hall, Christine M., Amaka C. Offiah, Mario Lituania, Michelle Fink, and Deborah Krakow. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.

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12

Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, and Michelle Fink. Fetal and Perinatal Skeletal Dysplasias: An Atlas of Multimodality Imaging. Taylor & Francis Group, 2012.

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13

Lopez-Arvizu, Carmen, Carmel Bogle, and Harolyn M. E. Belcher. Neurobiology of Fetal Alcohol Spectrum Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0179.

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Prenatal exposure to ethanol can result in a wide range of clinical presentations that are grouped under the term “Fetal Alcohol Spectrum Disorders” (FASD). The direct cellular teratogenic effects of ethanol on fetal neurodevelopment include damage to cell survival, proliferation, and migration mechanisms. Dysregulation of neurotransmission and alteration of genetic transcription have also been implicated in the neurotoxic effects of prenatal ethanol exposure. These deleterious events lead to brain volume reduction, corpus callosum dysgenesis, cerebellar, and other neuroanatomical anomalies that have been observed in individuals with FASD. Beyond direct ethanol-induced insults, the impact that ethanol has on maternal nutrition, metabolism, hormonal regulation, and placental physiology also adversely effects fetal development. The complex interactions between numerous neurobiological and psychosocial mechanisms that hinder optimal fetal neurodevelopment are reflected by the heterogeneous clinical presentation of FASD, including impaired growth, dysmorphic facial features, and cognitive and behavioral disorders.

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14

Cellular and molecular biology of the materno-fetal relationship: Proceedings of the 2nd meeting on reproductive immunology held in Paris (France), December ... la relation materno-fetale (Colloque INSERM). Editions INSERM, 1991.

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15

Fetal And Perinatal Skeletal Dysplasias An Atlas Of Multimodality Imaging. Radcliffe Publishing Ltd, 2012.

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16

Umbilical Cord Blood: A Future for Regenerative Medicine. World Scientific Publishing Co Pte Ltd, 2010.

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17

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Manganese in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0026.

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Manganese is both an essential element and a potent neurotoxin. It is involved in cellular metabolic processes and is a component of antioxidant enzymes. Uptake and efflux of manganese is tightly regulated, as both deficiency and excess can result in disease states. Manganese has essential functions in maternal health and fetal development, and in healthy women adequate amounts can be obtained from a mixed diet of grains, cereals, and fruits. Supplements containing manganese should be used with caution, as excess intake can have neurotoxic effects on the developing brain. Maternal intake in pregnancy and lactation is not likely to be a worry in most cases, as transfer of manganese to the fetus and into breast milk is limited.

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18

Maegawa, Gustavo H. B. Lysosomal Storage Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0068.

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The lysosomal storage disorders (LSDs) are a group of inborn organelle disorders, clinically heterogeneous, and biochemically characterized by accumulation of nondegraded macromolecules primarily in the lysosomal and other cellular compartments. Given the common and essential cellular function of the lysosomal system in different organs and systems, patients afflicted with these disorders present a broad range of clinical problems, including neurological problems, visceromegaly, and skeletal deformities. Onset of symptoms may range from fetal period to adulthood. The neurological problems include developmental delay, seizures, acroparesthesia, motor weakness, muscle wasting, behavioral/psychiatric disturbances, cerebrovascular ischemic events, and extrapyramidal signs. Patients may present with symptoms later that include psychiatric manifestations, are slowly progressive, and may precede other neurologic or systemic features. Most of LSDs are autosomal recessive; however, a few are X-linked with symptpmatic female carriers (e.g., Fabry disease). In most of them, the diagnosis is established by biochemical and/or molecular assays. In terms of management, disease-modifying therapies include enzyme replacement, hematopoietic stem cell transplantation, and substrate reduction therapy. Patients and their families require genetic counseling regarding reproductive risks, disease prognosis, and therapeutic options. Investigations of disease molecular mechanisms provide insights into potential targets for the development of therapeutic strategies. Supportive care has been the key and essential for most LSDs, resulting in substantial improvement in quality of life of patients and families.

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19

Steenblock, David A., and G. Ph D. Payne Anthony. Umbilical Cord Stem Cell Therapy: The Gift of Healing from Healthy Newborns. Basic Health Publications, 2006.

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20

Umbilical Cord Stem Cell Therapy: The Gift of Healing from Healthy Newborns. ReadHowYouWant.com, Limited, 2011.

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21

Sibley, Colin, and Phillip Baker. The Placenta and Neurodisability (Clinics in Developmental Medicine (Mac Keith Press)). MacKeith Press, 2006.

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