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  1. Article ; Online: Midkine

    Tsai, Stephanie L / Baselga-Garriga, Clara / Melton, Douglas A

    eLife

    2020  Volume 9

    Abstract: Formation of a specialized wound epidermis is required to initiate salamander limb regeneration. Yet little is known about the roles of the early wound epidermis during the initiation of regeneration and the mechanisms governing its development into the ... ...

    Abstract Formation of a specialized wound epidermis is required to initiate salamander limb regeneration. Yet little is known about the roles of the early wound epidermis during the initiation of regeneration and the mechanisms governing its development into the apical epithelial cap (AEC), a signaling structure necessary for outgrowth and patterning of the regenerate. Here, we elucidate the functions of the early wound epidermis, and further reveal
    MeSH term(s) Ambystoma mexicanum/physiology ; Animals ; Cell Proliferation ; Epidermis/metabolism ; Extracellular Matrix/metabolism ; Extremities/physiology ; In Situ Hybridization ; Inflammation/metabolism ; Midkine/metabolism ; Regeneration ; Signal Transduction ; Transcription, Genetic ; Wound Healing
    Chemical Substances Midkine (137497-38-2)
    Language English
    Publishing date 2020-01-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.50765
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Prevalence of neurocognitive disorder in Huntington's disease using the Enroll-HD dataset.

    Sierra, Luis A / Ullman, Clementina J / Baselga-Garriga, Clara / Pandeya, Sarbesh R / Frank, Samuel A / Laganiere, Simon

    Frontiers in neurology

    2023  Volume 14, Page(s) 1198145

    Abstract: Background: Cognitive decline in Huntington's disease (HD) begins early in the disease course, however the reported prevalence and severity of cognitive impairment varies based on diagnostic approach. A Movement Disorders Society Task Force recently ... ...

    Abstract Background: Cognitive decline in Huntington's disease (HD) begins early in the disease course, however the reported prevalence and severity of cognitive impairment varies based on diagnostic approach. A Movement Disorders Society Task Force recently endorsed the use of standardized DSM-5-based criteria to diagnose neurocognitive disorder (NCD) in Huntington's disease.
    Objectives: To determine the prevalence and severity of cognitive impairment across different stages of HD by applying NCD criteria (mild and major) to participant data from the Enroll-HD database.
    Methods: Enroll-HD participants were triaged into either premanifest (preHD), manifest or control groups. PreHD was further dichotomized into preHD near or preHD far based on predicted time to diagnosis using the scaled CAG-age product score (CAPs). Embedded cognitive performance and functional independence measures were used to determine prevalence of NCD (mild and major) for all groups.
    Results: Prevalence of NCD-mild was 25.2%-38.4% for manifest HD, 22.8%-47.3% for preHD near, 11.5%-25.1% for preHD far, and 8.8%-19.1% for controls. Prevalence of NCD-major was 21.1%-57.7% for manifest HD, 0.5%-16.3% for preHD near, 0.0%-4.5% for preHD far, and 0.0%-3.0% for controls.
    Conclusion: The prevalence of NCD in HD is elevated in preHD and demonstrates a sharp rise prior to diagnosis. In manifest HD, the vast majority of participants meet criteria for NCD. These findings are important for optimizing clinical care and/or anticipating the need for supportive services.
    Language English
    Publishing date 2023-07-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2023.1198145
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Blastemal progenitors modulate immune signaling during early limb regeneration.

    Tsai, Stephanie L / Baselga-Garriga, Clara / Melton, Douglas A

    Development (Cambridge, England)

    2019  Volume 146, Issue 1

    Abstract: Blastema formation, a hallmark of limb regeneration, requires proliferation and migration of progenitors to the amputation plane. Although blastema formation has been well described, the transcriptional programs that drive blastemal progenitors remain ... ...

    Abstract Blastema formation, a hallmark of limb regeneration, requires proliferation and migration of progenitors to the amputation plane. Although blastema formation has been well described, the transcriptional programs that drive blastemal progenitors remain unknown. We transcriptionally profiled dividing and non-dividing cells in regenerating stump tissues, as well as the wound epidermis, during early axolotl limb regeneration. Our analysis revealed unique transcriptional signatures of early dividing cells and, unexpectedly, repression of several core developmental signaling pathways in early regenerating stump tissues. We further identify an immunomodulatory role for blastemal progenitors through interleukin 8 (IL-8), a highly expressed cytokine in subpopulations of early blastemal progenitors. Ectopic
    MeSH term(s) Ambystoma mexicanum ; Amphibian Proteins/immunology ; Animals ; Blastoderm/cytology ; Blastoderm/immunology ; Cell Differentiation/immunology ; Hindlimb/physiology ; Interleukin-8/immunology ; Receptors, Interleukin-8A/immunology ; Receptors, Interleukin-8B/immunology ; Signal Transduction/immunology ; Stem Cells/cytology ; Stem Cells/immunology
    Chemical Substances Amphibian Proteins ; Interleukin-8 ; Receptors, Interleukin-8A ; Receptors, Interleukin-8B
    Language English
    Publishing date 2019-01-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.169128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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