Results 11 to 20 of about 13,916 (214)

Hereditary syndromes with signs of premature aging [PDF]

open access: yesОстеопороз и остеопатии, 2020
Aging is a multi-factor biological process that inevitably affects everyone. Degenerative processes, starting at the cellular and molecular levels, gradually influence the change in the functional capabilities of all organs and systems.
Olga O. Golounina   +2 more
doaj   +1 more source

Progeria and Aging—Omics Based Comparative Analysis

open access: yesBiomedicines, 2022
Since ancient times aging has also been regarded as a disease, and humankind has always strived to extend the natural lifespan. Analyzing the genes involved in aging and disease allows for finding important indicators and biological markers for ...
Aylin Caliskan   +4 more
doaj   +1 more source

Inguinal herniotomy in a patient with progeria

open access: yesJournal of Pediatric Surgery Case Reports, 2020
Hutchinson–Gilford progeria syndrome or progeria is a rare finding, Herein, we report a 4-year- old boy with progeria who underwent herniotomy and herniorrhaphy for left indirect inguinal hernia.
Tanvir K. Chowdhury   +3 more
doaj   +1 more source

The intrinsic stiffness of human trabecular meshwork cells increases with senescence. [PDF]

open access: yes, 2015
Dysfunction of the human trabecular meshwork (HTM) plays a central role in the age-associated disease glaucoma, a leading cause of irreversible blindness.
Chang, Yow-Ren   +4 more
core   +7 more sources

DNA Methylation Signatures of Cellular Senescence Are Not Reversed by Senolytic Treatment. [PDF]

open access: yesAging Cell
We found very little overlap between CpGs that were correlated with in vitro senescence, chronological age, and mortality. While we were able to train epigenetic clocks with CpGs that accelerated with cellular senescence, these clocks did not decelerate with Senolytic treatment. ABSTRACT Epigenetic clocks are commonly used aging biomarkers based on DNA
Kasamoto J   +7 more
europepmc   +2 more sources

Premature aging of the body - the role of laminopathy [PDF]

open access: yesFarmacja Polska, 2021
Aging is a process, that went off inevitable and it is associated with the accumulation of macromolecular damage, genomic instability, and loss of heterochromatin. All these changes conduct to deterioration function of stem cells and reducing the ability
Julia Wiśniewska   +7 more
doaj   +1 more source

Nuclear Pore Complexes Cluster in Dysmorphic Nuclei of Normal and Progeria Cells during Replicative Senescence

open access: yesCells, 2021
Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disease caused by a mutation in LMNA. A G608G mutation in exon 11 of LMNA is responsible for most HGPS cases, generating a truncated protein called “progerin”.
Jennifer M. Röhrl   +2 more
doaj   +1 more source

Doubled lifespan and patient‐like pathologies in progeria mice fed high‐fat diet [PDF]

open access: yes, 2019
Hutchinson-Gilford Progeria Syndrome (HGPS) is a devastating premature aging disease. Mouse models have been instrumental for understanding HGPS mechanisms and for testing therapies, which to date have had only marginal benefits in mice and patients ...
Albert, Carolyn J   +10 more
core   +2 more sources

iPSC-Derived Endothelial Cells Affect Vascular Function in a Tissue-Engineered Blood Vessel Model of Hutchinson-Gilford Progeria Syndrome

open access: yesStem Cell Reports, 2020
Summary: Hutchinson-Gilford progeria syndrome (HGPS) is a rare disorder caused by a point mutation in the Lamin A gene that produces the protein progerin. Progerin toxicity leads to accelerated aging and death from cardiovascular disease.
Leigh Atchison   +7 more
doaj   +1 more source

Case of mandibuloacral dysplasia with type B lipodystrophy

open access: yesIndian Journal of Paediatric Dermatology, 2021
Introduction: Mandibuloacral dysplasia with type B lipodystrophy (MADB) caused by compound heterozygous mutation in the ZMPSTE24 gene is characterized by generalized lipodystrophy and short stature.
Sanober Burzin Daruwalla   +3 more
doaj   +1 more source

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