Results 41 to 50 of about 17,639 (297)

Farnesyltransferase inhibitor treatment restores chromosome territory positions and active chromosome dynamics in Hutchinson-Gilford progeria syndrome cells [PDF]

open access: yes, 2011
Copyright @ 2011 Mehta et al.; licensee BioMed Central Ltd. This article has been made available through the Brunel Open Access Publishing Fund. This is an open access article distributed under the terms of the Creative Commons Attribution License ...
Arican, HD   +4 more
core   +2 more sources

Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies

open access: yesAging, 2018
DNA methylation (DNAm)-based biomarkers of aging have been developed for many tissues and organs. However, these biomarkers have sub-optimal accuracy in fibroblasts and other cell types used in ex vivo studies.
S. Horvath   +22 more
semanticscholar   +1 more source

Aging of Hutchinson-Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis [PDF]

open access: yes, 2004
Hutchinson-Gilford progeria syndrome is a rare genetic disorder that mimics certain aspects of aging prematurely. Recent work has revealed that mutations in the lamin A gene are a cause of the disease.
Bridger, JM, Kill, IR
core   +1 more source

Mammalian telomeres and their partnership with lamins [PDF]

open access: yes, 2016
Chromosome ends are complex structures, which require a panel of factors for their elongation, replication, and protection. We describe here the mechanics of mammalian telomeres, dynamics and maintainance in relation to lamins.
BURLA, ROMINA   +2 more
core   +1 more source

Schizophrenia as segmental progeria [PDF]

open access: yesJournal of the Royal Society of Medicine, 2011
Schizophrenia is associated with a variety of physical manifestations (i.e. metabolic, neurological) and despite psychotropic medication being blamed for some of these (in particular obesity and diabetes), there is evidence that schizophrenia itself confers an increased risk of physical disease and early death.
Papanastasiou, Evan   +2 more
openaire   +4 more sources

Altered modulation of lamin A/C-HDAC2 interaction and p21 expression during oxidative stress response in HGPS [PDF]

open access: yes, 2018
Defects in stress response are main determinants of cellular senescence and organism aging. In fibroblasts from patients affected by Hutchinson-Gilford progeria, a severe LMNA-linked syndrome associated with bone resorption, cardiovascular disorders, and
Andrenacci, Davide   +13 more
core   +2 more sources

PROGRESSIVE OSTEOLYSIS IN PROGERIA [PDF]

open access: yesAmerican Journal of Roentgenology, 1967
Complete resorption of the clavicles over a 4 year period was seen in a 7 year old girl with progeria. During this time there was continued resorption of the upper ribs and repeated humeral fractures. Progressive bone resorption has been described only twice previously in progeria.The similarity of the findings in this disease are discussed in relation
M. B. Ozonoff, A. R. Clemett
openaire   +3 more sources

Cerenkov luminescence imaging and metabolic activity of brown adipose tissue in a mouse model of progeria

open access: yesDi-san junyi daxue xuebao, 2019
Objective To study the changes in the metabolic activity of brown adipose tissues in a mouse model of progeria using Cerenkov luminescence imaging. Methods 18F-FDG PET/CT imaging and Cerenkov luminescence imaging were used to dynamically monitor the ...
WANG Zhengjie   +4 more
doaj   +1 more source

Genomic instability and DNA replication defects in progeroid syndromes [PDF]

open access: yes, 2018
Progeroid syndromes induced by mutations in lamin A or in its interactors – named progeroid laminopathies – are model systems for the dissection of the molecular pathways causing physio- logical and premature aging.
Chiara Merigliano   +4 more
core   +1 more source

Progeria in siblings: A rare case report

open access: yesIndian Journal of Dermatology, 2011
Progeria, also known as Hutchinson-Gilford syndrome, is an extremely rare, severe genetic condition wherein symptoms resembling aspects of aging are manifested at an early age. It is an autosomal dominant disorder.
R Sowmiya, D Prabhavathy, S Jayakumar
doaj   +1 more source

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