Telomere shortening is a hallmark of aging. Telomere length (TL) in blood cells has been studied extensively as a biomarker of human aging and disease; however, little is known regarding variability in TL in nonblood, disease-relevant tissue types. Here, we characterize variability in TLs from 6391 tissue samples, representing >20 tissue types and 952 individuals from the Genotype-Tissue Expression (GTEx) project. We describe differences across tissue types, positive correlation among tissue types, and associations with age and ancestry. We show that genetic variation affects TL in multiple tissue types and that TL may mediate the effect of age on gene expression. Our results provide the foundational knowledge regarding TL in healthy tissues that is needed to interpret epidemiological studies of TL and human health.

Telomere shortening is a hallmark of aging. Telomere length (TL) in blood cells has been studied extensively as a biomarker of human aging and disease; however, little is known regarding variability in TL in non-blood, disease-relevant tissue types. Here we characterize variability in TL measurements for 6,391 tissue samples, representing >20 tissue types and 952 individuals from the Genotype-Tissue Expression (GTEx) Project. We describe differences across tissue types, positive correlation among tissue types, and associations with age and ancestry. We show that genetic variation impacts TL in multiple tissue types, and that TL can mediate the effect of age on gene expression. Our results provide the foundational knowledge regarding TL in healthy tissues that is needed to interpret epidemiological studies of TL and human health. ONE SENTENCE SUMMARYTelomere length varies by tissue type but is generally correlated among tissue types (positively) and with age (negatively). MAIN TEXTTelomeres are DNA-protein complexes located at the end of chromosomes that protect chromosome ends from degradation and fusion (1). The length of the DNA component of telomeres shortens as cells divide (2) with short telomeres eventually triggering cellular senescence (3,4). In most human tissues, TL gradually shortens over the life course, and TL shortening is considered a hallmark (and a potential underlying cause) of human aging (5). In human studies, short TL measured in leukocytes is associated with increased risk of aging-related diseases including cardiovascular disease (6) and type II diabetes (7) as well as all-cause mortality (8). However, long TL may increase risk for some types of cancer (9-11). Leukocyte TL is influenced by inherited genetic variation (single nucleotide polymorphisms [SNPs]), some of which reside near genes with roles in telomere maintenance (12)(13)(14)(15). Leukocyte TL is also associated with lifestyle factors (e.g., obesity) and exposures (e.g., cigarette smoking) (16,17).Epidemiologic studies of TL predominantly use blood (occasionally saliva) as a DNA source. Thus, our understanding of variation in TL, its determinants (e.g., demographic, lifestyle, and genetic factors), and its associations with disease phenotypes is based almost entirely on TL measured in leukocytes from whole blood. Few prior studies have compared TL in leukocytes to TL in other human tissue types; these prior studies are relatively small (<100 participants; <5 tissue types) but provide evidence that TL differs across tissue types and that TL measurements from different tissue types are correlated (18,19). However, larger studies of many additional tissue types are needed to gain a comprehensive understanding of variation in TL and its determinants within and across a wide range of human tissues and cell types. In order to address these gaps in our understanding of TL and its role as a biomarker of aging and disease risk, we measured TL in > 6,000 unique tissue samples, representing >20 distinct tissue types and > 950 individual don...

Drosophila flies placed in a habitat with two lateral boxes demonstrated sensitivity to magnetic fields: Oviposition decreased by exposure to pulsated (extremely low frequency (ELF) (100 Hz, 1.76 miliTesla (mT) ) and sinusosidal fields (50 Hz, 1 mT), while there was no initial effect of exposure to a static magnetic field (4.5 mT). Drosophila eggs treated for 48 h with the above described fields showed that 1) mortality of eggs was lower in controls than in eggs exposed to all tested magnetic fields; 2) mortality of larvae increased when a permanent magnet was used; 3) mortality of pupae was highest when a permanent magnet was used; and 4) general adult viability was highest in controls (67%) and diminished progressively when eggs were exposed to pulsated (55%), sinusoidal (45%), and static (35%) magnetic fields.