This study was another case of a detailed genetic analysis of an unusual recombination region in the maize genome.”
“PURPOSE. To determine the protection factor (PF) for glutaredoxin-1 (Grx1) with regard to UVR-induced cataract by comparison
of in vivo ultraviolet radiation (UVR) lens toxicity between double knockout Grx1(-/-) and Grx1(-/-) mice.\n\nMETHODS. Twenty Grx1(-/-) mice and 20 Grx1(-/-) mice were unilaterally exposed in vivo to UVR for 15 minutes. Groups of four animals each received 0.0, 2.1, 2.9, 3.6, and 4.1 kJ/m(2) UVR-300 nm. At 48 hours after UVR exposure, light-scattering in the exposed and contralateral this website nonexposed lenses was measured quantitatively. Macroscopic lens changes were documented with dark-field illumination photography.\n\nRESULTS. UVR-300 nm induced subcapsular and cortical cataract in Grx1(-/-) and Grx1(-/-) mice. In both Grx1(-/-) and Grx1(-/-), the light-scattering intensified with increased in vivo exposure doses of UVR-300 nm. The intensity of forward light-scattering was higher in the lenses of Grx1(-/-) mice than in the lenses of Grx1(-/-) mice. The threshold dose for in vivo UVR-300 nm-induced cataract, expressed as MTD2.3:16, was 3.8 in
the Grx1(-/-) group and 3.0 in the Grx1(-/-) group, resulting in a PF of 1.3.\n\nCONCLUSIONS. The PF is an objective relative measure of protective properties. The Selleck Elafibranor Grx1 gene is associated with an in vivo PF of 1.3. This result signifies that the presence of the gene allows a 1.3 times longer in vivo exposure to UVR, at equivalent irradiance, than the check details absence of the gene before early-onset, UVR-induced cataract occurs. This finding indicates the important role of the Grx1 gene in the oxidation defense system of the lens. (Invest Ophthalmol Vis Sci. 2012;53:248-252) DOI: 10.1167/iovs.11-8504″
“The ability to measure human aging from molecular profiles has practical implications in many fields, including disease prevention and treatment, forensics, and extension of
life. Although chronological age has been linked to changes in DNA methylation, the methylome has not yet been used to measure and compare human aging rates. Here, we build a quantitative model of aging using measurements at more than 450,000 CpG markers from the whole blood of 656 human individuals, aged 19 to 101. This model measures the rate at which an individual’s methylome ages, which we show is impacted by gender and genetic variants. We also show that differences in aging rates help explain epigenetic drift and are reflected in the transcriptome. Moreover, we show how our aging model is upheld in other human tissues and reveals an advanced aging rate in tumor tissue. Our model highlights specific components of the aging process and provides a quantitative readout for studying the role of methylation in age-related disease.