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Browsing Recipients of OA Publishing Fund by Subject "Aging"
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Item Age-Independent Rise of Inflammatory Scores May Contribute to Accelerated Aging in Multi-Morbidity(Impact Journals, LLC, 2015-02-10) Stepanova, Maria; Rodriguez, Edgar; Birerdinc, Aybike; Baranova, AnchaAging is associated with an increase in a chronic, low-grade inflammation. This phenomenon, termed “inflammaging” is also a risk factor for both morbidity and mortality in the elderly. Frequent co-occurrence of chronic diseases, known as multi-morbidity, may be explained by interconnected pathophysiology of these conditions, most of which depend on its inflammatory component. Here we present an analysis of the U.S. National Health and Nutrition Examination Survey data collected between 1999 and 2008, for the presence, and the number, of chronic diseases along with HDL-cholesterol, C-reactive protein, white blood cell count, lymphocyte percent, monocyte percent, segmented neutrophils percent, eosinophils percent, basophils percent, and glycohemoglobin levels. Importantly, even after adjustment for age and BMI, many inflammatory markers continued to be associated to multi-morbidity. C-reactive protein (CRP) levels and Glasgow Prognostic Score (GPS) were most dramatically increased in parallel with an accumulation of chronic diseases, and may be utilized as multi-morbidity predictors. These observations point at background inflammation as direct, age-independent contributor to an accumulation of the disease burden. Our findings also suggest a possibility that systemic inflammation associated with chronic diseases may explain accelerated aging phenomenon previously observed among the patients with heavy disease burden.Item Older adults report moderately more detailed autobiographical memories(Frontiers Media, 2015-05-19) Gardner, Robert, S; Mainetti, Matteo; Ascoli, Giorgio, AAutobiographical memory (AM) is an essential component of the human mind. Although the amount and types of subjective detail (content) that compose AMs constitute important dimensions of recall, age-related changes in memory content are not well characterized. Previously, we introduced the Cue-Recalled Autobiographical Memory test (CRAM; see http://cramtest.info), an instrument that collects subjective reports of AM content, and applied it to college-aged subjects. CRAM elicits AMs using naturalistic word-cues. Subsequently, subjects date each cued AM to a life period and count the number of remembered details from specified categories (features), e.g., temporal detail, spatial detail, persons, objects, and emotions. The current work applies CRAM to a broad range of individuals (18–78 years old) to quantify the effects of age on AM content. Subject age showed a moderately positive effect on AM content: older compared with younger adults reported ∼16% more details (∼25 vs. ∼21 in typical AMs). This age-related increase in memory content was similarly observed for remote and recent AMs, although content declined with the age of the event among all subjects. In general, the distribution of details across features was largely consistent among younger and older adults. However, certain types of details, i.e., those related to objects and sequences of events, contributed more to the age effect on content. Altogether, this work identifies a moderate age-related feature-specific alteration in the way life events are subjectively recalled, among an otherwise stable retrieval profile.Item Pathways of aging: comparative analysis of gene signatures in replicative senescence and stress induced premature senescence(BMC Genomics, 2016-12-28) Kural, Kamil Can; Tandon, Neetu; Skoblov, Mikhail; Kel-Margoulis, Olga V.; Baranova, AnchaBackground In culturing normal diploid cells, senescence may either happen naturally, in the form of replicative senescence, or it may be a consequence of external challenges such as oxidative stress. Here we present a comparative analysis aimed at reconstruction of molecular cascades specific for replicative (RS) and stressinduced senescence (SIPS) in human fibroblasts. Results An involvement of caspase-3/keratin-18 pathway and serine/threonine kinase Aurora A/ MDM2 pathway was shared between RS and SIPS. Moreover, stromelysin/MMP3 and N-acetylglucosaminyltransferase enzyme MGAT1, which initiates the synthesis of hybrid and complex Nglycans, were identified as key orchestrating components in RS and SIPS, respectively. In RS only, Aurora-B driven cell cycle signaling was deregulated in concert with the suppression of anabolic branches of the fatty acids and estrogen metabolism. In SIPS, Aurora-B signaling is deprioritized, and the synthetic branches of cholesterol metabolism are upregulated, rather than downregulated. Moreover, in SIPS, proteasome/ubiquitin ligase pathways of protein degradation dominate the regulatory landscape. This picture indicates that SIPS proceeds in cells that are actively fighting stress which facilitates premature senescence while failing to completely activate the orderly program of RS. The promoters of genes differentially expressed in either RS or SIPS are unusually enriched by the binding sites for homeobox family proteins, with particular emphasis on HMX1, IRX2, HDX and HOXC13. Additionally, we identified Iroquois Homeobox 2 (IRX2) as a master regulator for the secretion of SPP1-encoded osteopontin, a stromal driver for tumor growth that is overexpressed by both RS and SIPS fibroblasts. The latter supports the hypothesis that senescence-specific de-repression of SPP1 aids in SIPS-dependent stromal activation. Conclusions Reanalysis of previously published experimental data is cost-effective approach for extraction of additional insignts into the functioning of biological systems.