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  1. Book ; Online ; E-Book: Mouse models of development and disease

    Gridley, Thomas / Oxburgh, Leif

    (Issn)

    2022  

    Author's details edited by Thomas Gridley, Leif Oxburgh
    Series title Issn
    Keywords Animal models in research
    Subject code 616.027
    Language English
    Size 1 online resource (284 pages)
    Publisher Academic Press
    Publishing place Cambridge, Massachusetts
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 0-12-817132-4 ; 9780128171318 ; 978-0-12-817132-5 ; 0128171316
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Mouse models of development and disease: Preface.

    Gridley, Thomas / Oxburgh, Leif

    Current topics in developmental biology

    2022  Volume 148, Page(s) xi–xvii

    MeSH term(s) Animals ; Disease Models, Animal ; Mice
    Language English
    Publishing date 2022-03-31
    Publishing country United States
    Document type Editorial
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/S0070-2153(22)00059-X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mouse mutagenesis and phenotyping to generate models of development and disease.

    Gridley, Thomas / Murray, Stephen A

    Current topics in developmental biology

    2022  Volume 148, Page(s) 1–12

    Abstract: For many years, the laboratory mouse has been the favored model organism to study mammalian development, biology and disease. Among its advantages for these studies are its close concordance with human biology, the syntenic relationship between the mouse ...

    Abstract For many years, the laboratory mouse has been the favored model organism to study mammalian development, biology and disease. Among its advantages for these studies are its close concordance with human biology, the syntenic relationship between the mouse and other mammalian genomes, the existence of many inbred strains, its short gestation period, its relatively low cost for housing and husbandry, and the wide array of tools for genome modification, mutagenesis, and for cryopreserving embryos, sperm and eggs. The advent of CRISPR genome modification techniques has considerably broadened the landscape of model organisms available for study, including other mammalian species. However, the mouse remains the most popular and utilized system to model human development, biology, and disease processes. In this review, we will briefly summarize the long history of mice as a preferred mammalian genetic and model system, and review current large-scale mutagenesis efforts using genome modification to produce improved models for mammalian development and disease.
    MeSH term(s) Animals ; Genome ; Male ; Mammals/genetics ; Mice ; Mutagenesis/genetics ; Spermatozoa
    Language English
    Publishing date 2022-03-24
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/bs.ctdb.2022.02.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Twenty Years in Maine: Integrating Insights from Developmental Biology into Translational Medicine in a Small State.

    Gridley, Thomas

    Current topics in developmental biology

    2016  Volume 116, Page(s) 435–443

    Abstract: In this chapter, I give my personal reflections on more than 30 years of studying developmental biology in the mouse model, spending 20 of those years doing research in Maine, a small rural state. I also give my thoughts on my recent experience ... ...

    Abstract In this chapter, I give my personal reflections on more than 30 years of studying developmental biology in the mouse model, spending 20 of those years doing research in Maine, a small rural state. I also give my thoughts on my recent experience transitioning to a large medical center in Maine, and the issues involved with integrating insights from developmental biology and regenerative medicine into the fabric of translational and clinical patient care in such an environment.
    MeSH term(s) Animals ; Developmental Biology ; Humans ; Maine ; Mice ; Patient-Centered Care ; Precision Medicine ; Time Factors ; Translational Medical Research
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/bs.ctdb.2015.10.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: DIO3 protects against thyrotoxicosis-derived cranio-encephalic and cardiac congenital abnormalities.

    Martinez, M Elena / Pinz, Ilka / Preda, Marilena / Norton, Christine R / Gridley, Thomas / Hernandez, Arturo

    JCI insight

    2022  Volume 7, Issue 21

    Abstract: Maternal hyperthyroidism is associated with an increased incidence of congenital abnormalities at birth, but it is not clear which of these defects arise from a transient developmental excess of thyroid hormone and which depend on pregnancy stage, ... ...

    Abstract Maternal hyperthyroidism is associated with an increased incidence of congenital abnormalities at birth, but it is not clear which of these defects arise from a transient developmental excess of thyroid hormone and which depend on pregnancy stage, antithyroid drug choice, or unwanted subsequent fetal hypothyroidism. To address this issue, we studied a mouse model of comprehensive developmental thyrotoxicosis secondary to a lack of type 3 deiodinase (DIO3). Dio3-/- mice exhibited reduced neonatal viability on most genetic backgrounds and perinatal lethality on a C57BL/6 background. Dio3-/- mice exhibited severe growth retardation during the neonatal period and cartilage loss. Mice surviving after birth manifested brain and cranial dysmorphisms, severe hydrocephalus, choanal atresia, and cleft palate. These abnormalities were noticeable in C57BL/6J Dio3-/- mice at fetal stages, in addition to a thyrotoxic heart with septal defects and thin ventricular walls. Our findings stress the protecting role of DIO3 during development and support the hypothesis that human congenital abnormalities associated with hyperthyroidism during pregnancy are caused by transient thyrotoxicosis before clinical intervention. Our results also suggest thyroid hormone involvement in the etiology of idiopathic pathologies including cleft palate, choanal atresia, Chiari malformations, Kaschin-Beck disease, and Temple and other cranio-encephalic and heart syndromes.
    MeSH term(s) Humans ; Pregnancy ; Female ; Animals ; Mice ; Iodide Peroxidase/genetics ; Iodide Peroxidase/metabolism ; Mice, Inbred C57BL ; Choanal Atresia ; Cleft Palate ; Thyrotoxicosis/complications ; Thyroid Hormones ; Brain/metabolism ; Hyperthyroidism ; Heart Defects, Congenital
    Chemical Substances Iodide Peroxidase (EC 1.11.1.8) ; Thyroid Hormones
    Language English
    Publishing date 2022-11-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.161214
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Notch signaling in the vasculature.

    Gridley, Thomas

    Current topics in developmental biology

    2010  Volume 92, Page(s) 277–309

    Abstract: Notch signaling is an evolutionarily conserved, intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include the regulation of arteriovenous specification and differentiation in ... ...

    Abstract Notch signaling is an evolutionarily conserved, intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include the regulation of arteriovenous specification and differentiation in both endothelial cells and vascular smooth muscle cells, regulation of blood vessel sprouting and branching during normal and pathological angiogenesis, and the physiological responses of vascular smooth muscle cells. Defects in Notch signaling also cause inherited vascular diseases, such as the degenerative vascular disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. This review summarizes recent studies that highlight the multiple roles the Notch signaling pathway plays during vascular development and physiology.
    MeSH term(s) Animals ; Blood Vessels/physiology ; Humans ; Neovascularization, Pathologic/metabolism ; Receptors, Notch/physiology ; Signal Transduction ; Vascular Diseases/metabolism
    Chemical Substances Receptors, Notch
    Language English
    Publishing date 2010-04-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 1557-8933 ; 0070-2153
    ISSN (online) 1557-8933
    ISSN 0070-2153
    DOI 10.1016/S0070-2153(10)92009-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DIO3 protects against thyrotoxicosis-derived cranio-encephalic and cardiac congenital abnormalities

    M. Elena Martinez / Ilka Pinz / Marilena Preda / Christine R. Norton / Thomas Gridley / Arturo Hernandez

    JCI Insight, Vol 7, Iss

    2022  Volume 21

    Abstract: Maternal hyperthyroidism is associated with an increased incidence of congenital abnormalities at birth, but it is not clear which of these defects arise from a transient developmental excess of thyroid hormone and which depend on pregnancy stage, ... ...

    Abstract Maternal hyperthyroidism is associated with an increased incidence of congenital abnormalities at birth, but it is not clear which of these defects arise from a transient developmental excess of thyroid hormone and which depend on pregnancy stage, antithyroid drug choice, or unwanted subsequent fetal hypothyroidism. To address this issue, we studied a mouse model of comprehensive developmental thyrotoxicosis secondary to a lack of type 3 deiodinase (DIO3). Dio3–/– mice exhibited reduced neonatal viability on most genetic backgrounds and perinatal lethality on a C57BL/6 background. Dio3–/– mice exhibited severe growth retardation during the neonatal period and cartilage loss. Mice surviving after birth manifested brain and cranial dysmorphisms, severe hydrocephalus, choanal atresia, and cleft palate. These abnormalities were noticeable in C57BL/6J Dio3–/– mice at fetal stages, in addition to a thyrotoxic heart with septal defects and thin ventricular walls. Our findings stress the protecting role of DIO3 during development and support the hypothesis that human congenital abnormalities associated with hyperthyroidism during pregnancy are caused by transient thyrotoxicosis before clinical intervention. Our results also suggest thyroid hormone involvement in the etiology of idiopathic pathologies including cleft palate, choanal atresia, Chiari malformations, Kaschin-Beck disease, and Temple and other cranio-encephalic and heart syndromes.
    Keywords Development ; Endocrinology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2022-11-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Vascular biology: vessel guidance.

    Gridley, Thomas

    Nature

    2007  Volume 445, Issue 7129, Page(s) 722–723

    MeSH term(s) Animals ; Arteries/cytology ; Arteries/embryology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/metabolism ; Mice ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neovascularization, Pathologic ; Neovascularization, Physiologic/physiology ; Receptors, Notch/metabolism ; Signal Transduction/drug effects ; Vascular Endothelial Growth Factor A/metabolism ; Zebrafish/embryology
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Receptors, Notch ; Vascular Endothelial Growth Factor A ; delta protein
    Language English
    Publishing date 2007-02-15
    Publishing country England
    Document type Comment ; News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/445722a
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  9. Article: Notch signaling in vascular development and physiology.

    Gridley, Thomas

    Development (Cambridge, England)

    2007  Volume 134, Issue 15, Page(s) 2709–2718

    Abstract: Notch signaling is an ancient intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include regulation of artery/vein differentiation in endothelial and vascular smooth muscle ... ...

    Abstract Notch signaling is an ancient intercellular signaling mechanism that plays myriad roles during vascular development and physiology in vertebrates. These roles include regulation of artery/vein differentiation in endothelial and vascular smooth muscle cells, regulation of blood vessel sprouting and branching during both normal development and tumor angiogenesis, and the differentiation and physiological responses of vascular smooth muscle cells. Defects in Notch signaling also cause inherited vascular and cardiovascular diseases. In this review, I summarize recent findings and discuss the growing relevance of Notch pathway modulation for therapeutic applications in disease.
    MeSH term(s) Animals ; Arteries/cytology ; Arteries/embryology ; Blood Vessels/embryology ; Blood Vessels/physiology ; CADASIL/etiology ; CADASIL/genetics ; CADASIL/physiopathology ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/genetics ; Cell Differentiation ; Endothelial Cells/cytology ; Humans ; Models, Biological ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/physiology ; Neoplasms, Vascular Tissue/etiology ; Neovascularization, Pathologic/etiology ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Receptors, Notch/physiology ; Signal Transduction ; Veins/cytology ; Veins/embryology
    Chemical Substances Receptors, Notch
    Language English
    Publishing date 2007-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.004184
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: The long and short of it: somite formation in mice.

    Gridley, Thomas

    Developmental dynamics : an official publication of the American Association of Anatomists

    2006  Volume 235, Issue 9, Page(s) 2330–2336

    Abstract: A fundamental characteristic of the vertebrate body plan is its segmentation along the anterior-posterior axis. This segmental pattern is established during embryogenesis by the formation of somites, the transient epithelial blocks of cells that derive ... ...

    Abstract A fundamental characteristic of the vertebrate body plan is its segmentation along the anterior-posterior axis. This segmental pattern is established during embryogenesis by the formation of somites, the transient epithelial blocks of cells that derive from the unsegmented presomitic mesoderm. Somite formation involves a molecular oscillator, termed the segmentation clock, in combination with gradients of signaling molecules such as fibroblast growth factor 8, WNT3A, and retinoic acid. Disruption of somitogenesis in humans can result in disorders such as spondylocostal dysostosis, which is characterized by vertebral malformations. This review summarizes recent findings concerning the role of Notch signaling in the segmentation clock, the complex regulatory network that governs somitogenesis, the genes that cause inherited spondylocostal dysostosis, and the mechanisms that regulate bilaterally symmetric somite formation.
    MeSH term(s) Animals ; Biological Clocks ; Body Patterning ; Female ; Gene Expression Regulation, Developmental ; Genes, Homeobox ; Humans ; Mesoderm/cytology ; Mesoderm/metabolism ; Mice ; Mutation ; Pregnancy ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction ; Somites/cytology ; Somites/metabolism ; Spine/abnormalities ; Spine/embryology
    Chemical Substances Receptors, Notch
    Language English
    Publishing date 2006-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1102541-4
    ISSN 1097-0177 ; 1058-8388
    ISSN (online) 1097-0177
    ISSN 1058-8388
    DOI 10.1002/dvdy.20850
    Database MEDical Literature Analysis and Retrieval System OnLINE

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