Results 111 to 120 of about 7,722 (240)

The Evolving Landscape of Clinical Aging Clocks: From Epigenetic to Multi‐Omics Integration

open access: yesAging Cell, Volume 25, Issue 6, June 2026.
Multi‐omics aging clocks capture biological heterogeneity beyond single‐omics models, improving risk stratification. Key challenges include unknown biological meaning, timescale mismatches, and validation gaps. Future clocks must distinguish pathological damage from adaptive remodeling—damage accumulation is the most actionable target for anti‐aging ...
Liying Liu   +13 more
wiley   +1 more source

Temsirolimus does not impact the levels of reactive oxygen species and superoxide in HGPS cells. [PDF]

open access: yes, 2016
(A) Immunochemistry was performed on control (GMO3349C) and HGPS (HGADFN003) fibroblasts mock-treated or temsirolimus-treated for the indicated periods. Live cells were stained with an oxidative stress detection reagent for ROS and a superoxide detection
Diana Gabriel (3608093)   +2 more
core   +1 more source

Vascular cells derived from Hutchinson-Gilford progeria syndrome (HGPS) inducible pluripotent stem cells [PDF]

open access: yes, 2014
To study the vulnerability of smooth muscle cells (SMCs) in Hutchinson-Gilford Progeria Syndrome (HGPS)
Rocha, I.   +4 more
core  

In situ localization of progerin on human skin sections derived from a subject with HGPS and from unaffected individuals. [PDF]

open access: yes, 2013
A, HGPS skin sections immunostained with anti-progerin (prog), anti-lamin A (LMNA) antibody, or anti-α smooth muscle actin antibody (αSMA) and counterstained with a DNA stain (dapi).
Desiree Ratner (82177)   +6 more
core   +1 more source

Proposed model to explain the down-regulation of PRPS1 in HGPS. [PDF]

open access: yes, 2018
Enzymes in blue are detected as down-regulated and those in red as up-regulated in the present study. High glycolitic rate in HGPS drives to a decrease in the levels of D-Ribose-5-phosphate available for de novo purine synthesis.
Juan Fafián-Labora (5917748)   +8 more
core   +1 more source

Are There Common Mechanisms Between the Hutchinson–Gilford Progeria Syndrome and Natural Aging?

open access: yesFrontiers in Genetics, 2019
The Hutchinson–Gilford progeria syndrome (HGPS) is a premature aging disease caused by mutations of the LMNA gene leading to increased production of a partially processed form of the nuclear fibrillar protein lamin A – progerin.
Vasily V. Ashapkin   +3 more
doaj   +1 more source

Effect of hypotonicity and ATP on [Ca2+]i in IMR90-iPSC-ECs and HGPS-iPSC-ECs. [PDF]

open access: yes, 2014
(A and B), Representative traces (A) and data summary (B) showing the effect of hypotonicity (210 mOsm) on [Ca2+]i (fluorescence ratio F1/F0) in IMR90-iPSC-ECs and HGPS-iPSC-ECs bathed in isotonic solution. n  =  6-7 experiments.
Nelson L. Tang (515416)   +8 more
core   +1 more source

Tissue Engineered Blood Vessels to Study Endothelial Dysfunction in Hutchinson-Gilford Progeria Syndrome [PDF]

open access: yes, 2022
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, fatal genetic disease that causes progressive atherosclerosis and accelerated aging in children resulting in fatality at an average of 14.6 years of age.
Abutaleb, Nadia Osama
core  

Inhibition of JAK-STAT Signaling with Baricitinib Reduces Inflammation and Improves Cellular Homeostasis in Progeria Cells

open access: yesCells, 2019
Hutchinson-Gilford progeria syndrome (HGPS), a rare premature aging disorder that leads to death at an average age of 14.7 years due to myocardial infarction or stroke, is caused by mutations in the LMNA gene.
Chang Liu   +3 more
doaj   +1 more source

Fact sheet for the Hawaii Geothermal Project (HGP) [PDF]

open access: yes, 1976
This fact sheet for distribution at the flash and flow test of HGP-A, July 22, 1976 contains a temperature-depth plot, a brief chronology, and a budget summary. (MHR)
openaire   +2 more sources

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