Results 161 to 170 of about 13,916 (214)

Deregulated miR-145 and miR-27b in Hutchinson-Gilford progeria syndrome: implications for adipogenesis. [PDF]

Aging (Albany NY)
Fenzl FQ, Lederer EM, Brumma L, Krüger P, Schroll M, Wilming F, Djabali K.   +6 more
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Baricitinib and Lonafarnib Synergistically Target Progerin and Inflammation, Improving Lifespan and Health in Progeria Mice. [PDF]

Int J Mol Sci
Krüger P, Schroll M, Fenzl FQ, Hartinger R, Lederer EM, Görlach A, Gordon LB, Cavalcante P, Iacomino N, Rathkolb B, Pimentel JAA, Östereicher M, Spielmann N, Wolf CM, de Angelis MH, Djabali K.   +15 more
europepmc   +1 more source

Radiation symptoms resemble laminopathies and the physical underlying cause may sit at the lamin A C-terminus. [PDF]

Mol Med
Waldherr A, Fogtman A.
europepmc   +1 more source

Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson-Gilford Progeria Syndrome. [PDF]

Int J Mol Sci
Vakili S, Cao K.
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Progeroid features in a patient with Malouf syndrome due to a rare LMNA variant: a case report and review of the literature. [PDF]

Arch Endocrinol Metab
Pekmezci A, Gumus AA, Korkmaz OP.
europepmc   +1 more source

Endothelial senescence drives intrinsic skin aging via the neuroimmune CGRP-mast cell axis in mice. [PDF]

Commun Biol
Wicaksono SA, Ryanto GRT, Suzuki Y, Hara T, Ikeda K, Fukumoto T, Hirata KI, Otake H, Emoto N.   +8 more
europepmc   +1 more source

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PROGERIA

Pediatrics, 1956
A typical case of progeria (Hutchinson-Gilford syndrome) is reported including the findings of the necropsy. Death occurred at the age of 11 years as the result of an accident. Analysis of cephalometric roentgenograms of this patient revealed that the characteristic facies of progeria results from marked retardation of facial growth in the presence of ...
Ira M. Rosenthal, I. Pat Bronstein, Frederick D. Dallenbach, Samuel Pruzansky, Alan K. Rosenwald   +4 more
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Progeria

Archives of Dermatology, 1989
Progeria, also known as the Hutchinson-Gilford syndrome, is an extremely rare condition that was initially reported by Johnathan Hutchinson in 1886 and further described by Hastings Gilford in 1904. Transmission is most likely from a sporadic autosomal dominant mutation.
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