Volume 8, Issue 7

Hall BM, Balan V, Gleiberman AS, Strom E, Krasnov P, Virtuoso LP, Rydkina E, Vujcic S, Balan K, Gitlin I, Leonova K, Polinsky A, Chernova OB, et al, . Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells. . 8:1294-1315. https://doi.org/10.18632/aging.100991

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                TY  - JOUR
                AU  - Hall, Brandon M. 
                AU  - Balan, Vitaly 
                AU  - Gleiberman, Anatoli S. 
                AU  - Strom, Evguenia 
                AU  - Krasnov, Peter 
                AU  - Virtuoso, Lauren P. 
                AU  - Rydkina, Elena 
                AU  - Vujcic, Slavoljub 
                AU  - Balan, Karina 
                AU  - Gitlin, Ilya 
                AU  - Leonova, Katerina 
                AU  - Polinsky, Alexander 
                AU  - Chernova, Olga B. 
                AU  - Gudkov, Andrei V. 
                TI  - Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100991
                DO  - 10.18632/aging.100991
                SP  - 1294
                EP  - 1315
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Hall, Brandon M. 
                AU  - Balan, Vitaly 
                AU  - Gleiberman, Anatoli S. 
                AU  - Strom, Evguenia 
                AU  - Krasnov, Peter 
                AU  - Virtuoso, Lauren P. 
                AU  - Rydkina, Elena 
                AU  - Vujcic, Slavoljub 
                AU  - Balan, Karina 
                AU  - Gitlin, Ilya 
                AU  - Leonova, Katerina 
                AU  - Polinsky, Alexander 
                AU  - Chernova, Olga B. 
                AU  - Gudkov, Andrei V. 
                TI  - Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100991
                DO  - 10.18632/aging.100991
                SP  - 1294
                EP  - 1315
                PY  - 
                AB  - Senescent cells (SCs) have been considered a source of age-related chronic sterile systemic inflammation and a target for anti-aging therapies. To understand mechanisms controlling the amount of SCs, we analyzed the phenomenon of rapid clearance of human senescent fibroblasts implanted into SCID mice, which can be overcome when SCs were embedded into alginate beads preventing them from immunocyte attack. To identify putative SC killers, we analyzed the content of cell populations in lavage and capsules formed around the SC-containing beads. One of the major cell types attracted by secretory factors of SCs was a subpopulation of macrophages characterized by p16(Ink4a) gene expression and β-galactosidase activity at pH6.0 (β-galpH6), thus resembling SCs. Consistently, mice with p16(Ink4a) promoter-driven luciferase, developed bright luminescence of their peritoneal cavity within two weeks following implantation of SCs embedded in alginate beads. p16(Ink4a)/β-galpH6-expressing cells had surface biomarkers of macrophages F4/80 and were sensitive to liposomal clodronate used for the selective killing of cells capable of phagocytosis. At the same time, clodronate failed to kill bona fide SCs generated in vitro by genotoxic stress. Old mice with elevated proportion of p16(Ink4a)/β-galpH6-positive cells in their tissues demonstrated reduction of both following systemic clodronate treatment, indicating that a significant proportion of cells previously considered to be SCs are actually a subclass of macrophages. These observations point at a significant role of p16(Ink4a)/β-galpH6-positive macrophages in aging, which previously was attributed solely to SCs. They require re-interpretation of the mechanisms underlying rejuvenating effects following eradication of p16(Ink4a)/β-galpH6-positive cells and reconsideration of potential cellular target for anti-aging treatment.
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Unbiased analysis of senescence associated secretory phenotype (SASP) to identify common components following different genotoxic stresses

Servet Özcan, Nicola Alessio, Mustafa B. Acar, Eda Mert, Fatih Omerli, Gianfranco Peluso, Umberto Galderisi,

https://doi.org/10.18632/aging.100971 pp 1316—1329

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Özcan S, Alessio N, Acar MB, Mert E, Omerli F, Peluso G, Galderisi U, . Unbiased analysis of senescence associated secretory phenotype (SASP) to identify common components following different genotoxic stresses. . 8:1316-1329. https://doi.org/10.18632/aging.100971

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                TY  - JOUR
                AU  - Özcan, Servet 
                AU  - Alessio, Nicola 
                AU  - Acar, Mustafa B.
                AU  - Mert, Eda 
                AU  - Omerli, Fatih 
                AU  - Peluso, Gianfranco 
                AU  - Galderisi, Umberto 
                TI  - Unbiased analysis of senescence associated secretory phenotype (SASP) to identify common components following different genotoxic stresses
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100971
                DO  - 10.18632/aging.100971
                SP  - 1316
                EP  - 1329
                PY  - 
                AB  - Senescent cells secrete senescence-associated secretory phenotype (SASP) proteins to carry out several functions, such as sensitizing surrounding cells to senesce; immunomodulation; impairing or fostering cancer growth; and promoting tissue development. Identifying secreted factors that achieve such tasks is a challenging issue since the profile of secreted proteins depends on genotoxic stress and cell type. Currently, researchers are trying to identify common markers for SASP. The present investigation compared the secretome composition of five different senescent phenotypes in two different cell types: bone marrow and adipose mesenchymal stromal cells (MSC). We induced MSC senescence by oxidative stress, doxorubicin treatment, X-ray irradiation, and replicative exhaustion. We took advantage of LC-MS/MS proteome identification and subsequent gene ontology (GO) evaluation to perform an unbiased analysis (hypothesis free manner) of senescent secretomes. GO analysis allowed us to distribute SASP components into four classes: extracellular matrix/cytoskeleton/cell junctions; metabolic processes; ox-redox factors; and regulators of gene expression. We used Ingenuity Pathway Analysis (IPA) to determine common pathways among the different senescent phenotypes. This investigation, along with identification of eleven proteins that were exclusively expressed in all the analyzed senescent phenotypes, permitted the identification of three key signaling paths: MMP2 - TIMP2; IGFBP3 - PAI-1; and Peroxiredoxin 6 - ERP46 - PARK7 - Cathepsin D - Major vault protein. We suggest that these paths could be involved in the paracrine circuit that induces senescence in neighboring cells and may confer apoptosis resistance to senescent cells.
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Mitophagy-driven mitochondrial rejuvenation regulates stem cell fate

Alejandro Vazquez-Martin, Chris Van den Haute, Sílvia Cufí, Bruna Corominas Faja, Elisabet Cuyàs, Eugeni Lopez-Bonet, Esther Rodriguez-Gallego, Salvador Fernández-Arroyo, Jorge Joven, Veerle Baekelandt, Javier A. Menendez,

https://doi.org/10.18632/aging.100976 pp 1330—1352

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Vazquez-Martin A, den Haute CV, Cufí S, Faja BC, Cuyàs E, Lopez-Bonet E, Rodriguez-Gallego E, Fernández-Arroyo S, Joven J, Baekelandt V, Menendez JA, . Mitophagy-driven mitochondrial rejuvenation regulates stem cell fate. . 8:1330-1352. https://doi.org/10.18632/aging.100976

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                TY  - JOUR
                AU  - Vazquez-Martin, Alejandro 
                AU  - den Haute, Chris Van
                AU  - Cufí, Sílvia 
                AU  - Faja, Bruna Corominas
                AU  - Cuyàs, Elisabet 
                AU  - Lopez-Bonet, Eugeni 
                AU  - Rodriguez-Gallego, Esther 
                AU  - Fernández-Arroyo, Salvador 
                AU  - Joven, Jorge 
                AU  - Baekelandt, Veerle 
                AU  - Menendez, Javier A.
                TI  - Mitophagy-driven mitochondrial rejuvenation regulates stem cell fate
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100976
                DO  - 10.18632/aging.100976
                SP  - 1330
                EP  - 1352
                PY  - 
                AB  - Our understanding on how selective mitochondrial autophagy, or mitophagy, can sustain the archetypal properties of stem cells is incomplete. PTEN-induced putative kinase 1 (PINK1) plays a key role in the maintenance of mitochondrial morphology and function and in the selective degradation of damaged mitochondria by mitophagy. Here, using embryonic fibroblasts fromPINK1 gene-knockout (KO) mice, we evaluated whether mitophagy is a causal mechanism for the control of cell-fate plasticity and maintenance of pluripotency. Loss of PINK1-dependent mitophagy was sufficient to dramatically decrease the speed and efficiency of induced pluripotent stem cell (iPSC) reprogramming. Mitophagy-deficient iPSC colonies, which were characterized by a mixture of mature and immature mitochondria, seemed unstable, with a strong tendency to spontaneously differentiate and form heterogeneous populations of cells. Although mitophagy-deficient iPSC colonies normally expressed pluripotent markers, functional monitoring of cellular bioenergetics revealed an attenuated glycolysis in mitophagy-deficient iPSC cells. Targeted metabolomics showed a notable alteration in numerous glycolysis- and TCA-related metabolites in mitophagy-deficient iPSC cells, including a significant decrease in the intracellular levels of α-ketoglutarate -a key suppressor of the differentiation path in stem cells. Mitophagy-deficient iPSC colonies exhibited a notably reduced teratoma-initiating capacity, but fully retained their pluripotency and multi-germ layer differentiation capacity in vivo. PINK1-dependent mitophagy pathway is an important mitochondrial switch that determines the efficiency and quality of somatic reprogramming. Mitophagy-driven mitochondrial rejuvenation might contribute to the ability of iPSCs to suppress differentiation by directing bioenergetic transition and metabolome remodeling traits. These findings provide new insights into how mitophagy might influence the stem cell decisions to retain pluripotency or differentiate in tissue regeneration and aging, tumor growth, and regenerative medicine.
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Telomerase and estrogen-sensing activities are essential for continued mammary growth in vivo but dispensable for "reprogramming" neural stem cells

Andrea L. George, Corinne A. Boulanger, Gilbert H. Smith,

https://doi.org/10.18632/aging.100985 pp 1353—1363

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George AL, Boulanger CA, Smith GH, . Telomerase and estrogen-sensing activities are essential for continued mammary growth in vivo but dispensable for "reprogramming" neural stem cells. . 8:1353-1363. https://doi.org/10.18632/aging.100985

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                TY  - JOUR
                AU  - George, Andrea L.
                AU  - Boulanger, Corinne A.
                AU  - Smith, Gilbert H.
                TI  - Telomerase and estrogen-sensing activities are essential for continued mammary growth in vivo but dispensable for "reprogramming" neural stem cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100985
                DO  - 10.18632/aging.100985
                SP  - 1353
                EP  - 1363
                PY  - 
                AB  - It has been proposed that the erosion of telomere length is a limiting factor in replicative capacity and important in cell senescence. To determine if this activity was essential in the mouse mammary glandin vivo, we serially transplanted mammary fragments from wild type (TER+/+), heterozygous (TER+/-), and homozygous (TER-/-) mammary tissues into the cleared mammary fat pads of immune-compromised nude mice. Individual implants from both homozygous and heterozygous TER null outgrowths showed growth senescence beginning at transplant generation two, earlier than implants from TER+/+ mammary glands which continued to show growth. This result suggests that either mammary epithelial stem cells maintain their telomere length in order to self renew, or that the absence or reduction of telomerase template results in more frequent death/extinction of stem cells during symmetric divisions. A third possibility is the inability of signaling cells in the niche to replicate resulting in reduction of the maintenance signals necessary for stem cell renewal. Consistent with this, examination of senescent outgrowths revealed the absence of estrogen receptor alpha (ERα+) epithelium although progesterone receptor (PR+) cells were abundant. Despite their inability to establish mammary growth in vivo, TER+/- cells were able to direct neural stem cells to mammary cell fates.
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Genetic variants determining survival and fertility in an adverse African environment: a population-based large-scale candidate gene association study

Jacob J.E. Koopman, Jeroen Pijpe, Stefan Böhringer, David van Bodegom, Ulrika K. Eriksson, Hernando Sanchez-Faddeev, Juventus B. Ziem, Bas Zwaan, P. Eline Slagboom, Peter de Knijff, Rudi G.J. Westendorp,

https://doi.org/10.18632/aging.100986 pp 1364—1383

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Koopman JJ, Pijpe J, Böhringer S, Bodegom Dv, Eriksson UK, Sanchez-Faddeev H, Ziem JB, Zwaan B, Slagboom PE, Knijff Pd, Westendorp RG, . Genetic variants determining survival and fertility in an adverse African environment: a population-based large-scale candidate gene association study. . 8:1364-1383. https://doi.org/10.18632/aging.100986

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                TY  - JOUR
                AU  - Koopman, Jacob J.E.
                AU  - Pijpe, Jeroen 
                AU  - Böhringer, Stefan 
                AU  - Bodegom, David van
                AU  - Eriksson, Ulrika K.
                AU  - Sanchez-Faddeev, Hernando 
                AU  - Ziem, Juventus B.
                AU  - Zwaan, Bas 
                AU  - Slagboom, P. Eline
                AU  - Knijff, Peter de
                AU  - Westendorp, Rudi G.J.
                TI  - Genetic variants determining survival and fertility in an adverse African environment: a population-based large-scale candidate gene association study
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100986
                DO  - 10.18632/aging.100986
                SP  - 1364
                EP  - 1383
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Koopman, Jacob J.E.
                AU  - Pijpe, Jeroen 
                AU  - Böhringer, Stefan 
                AU  - Bodegom, David van
                AU  - Eriksson, Ulrika K.
                AU  - Sanchez-Faddeev, Hernando 
                AU  - Ziem, Juventus B.
                AU  - Zwaan, Bas 
                AU  - Slagboom, P. Eline
                AU  - Knijff, Peter de
                AU  - Westendorp, Rudi G.J.
                TI  - Genetic variants determining survival and fertility in an adverse African environment: a population-based large-scale candidate gene association study
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100986
                DO  - 10.18632/aging.100986
                SP  - 1364
                EP  - 1383
                PY  - 
                AB  - Human survival probability and fertility decline strongly with age. These life history traits have been shaped by evolution. However, research has failed to uncover a consistent genetic determination of variation in survival and fertility. As an explanation, such genetic determinants have been selected in adverse environments, in which humans have lived during most of their history, but are almost exclusively studied in populations in modern affluent environments. Here, we present a large-scale candidate gene association study in a rural African population living in an adverse environment. In 4387 individuals, we studied 4052 SNPs in 148 genes that have previously been identified as possible determinants of survival or fertility in animals or humans. We studied their associations with survival comparing newborns, middle-age adults, and old individuals. In women, we assessed their associations with reported and observed numbers of children. We found no statistically significant associations of these SNPs with survival between the three age groups nor with women's reported and observed fertility. Population stratification was unlikely to explain these results. Apart from a lack of power, we hypothesise that genetic heterogeneity of complex phenotypes and gene-environment interactions prevent the identification of genetic variants explaining variation in survival and fertility in humans.
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FOXM1 regulates proliferation, senescence and oxidative stress in keratinocytes and cancer cells

Artem Smirnov, Emanuele Panatta, AnnaMaria Lena, Daniele Castiglia, Nicola Di Daniele, Gerry Melino, Eleonora Candi,

https://doi.org/10.18632/aging.100988 pp 1384—1397

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Smirnov A, Panatta E, Lena A, Castiglia D, Di Daniele N, Melino G, Candi E, . FOXM1 regulates proliferation, senescence and oxidative stress in keratinocytes and cancer cells. . 8:1384-1397. https://doi.org/10.18632/aging.100988

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                TY  - JOUR
                AU  - Smirnov, Artem 
                AU  - Panatta, Emanuele 
                AU  - Lena, AnnaMaria 
                AU  - Castiglia, Daniele 
                AU  - Di Daniele, Nicola 
                AU  - Melino, Gerry 
                AU  - Candi, Eleonora 
                TI  - FOXM1 regulates proliferation, senescence and oxidative stress in keratinocytes and cancer cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100988
                DO  - 10.18632/aging.100988
                SP  - 1384
                EP  - 1397
                PY  - 
                AB  - Several transcription factors, including the master regulator of the epidermis, p63, are involved in controlling human keratinocyte proliferation and differentiation. Here, we report that in normal keratinocytes, the expression of FOXM1, a member of the Forkhead superfamily of transcription factors, is controlled by p63. We observe that, together with p63, FOXM1 strongly contributes to the maintenance of high proliferative potential in keratinocytes, whereas its expression decreases during differentiation, as well as during replicative-induced senescence. Depletion of FOXM1 is sufficient to induce keratinocyte senescence, paralleled by an increased ROS production and an inhibition of ROS-scavenger genes (SOD2, CAT, GPX2, PRDX). Interestingly, FOXM1 expression is strongly reduced in keratinocytes isolated from old human subjects compared with young subjects. FOXM1 depletion sensitizes both normal keratinocytes and squamous carcinoma cells to apoptosis and ROS-induced apoptosis. Together, these data identify FOXM1 as a key regulator of ROS in normal dividing epithelial cells and suggest that squamous carcinoma cells may also use FOXM1 to control oxidative stress to escape premature senescence and apoptosis.
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Longitudinal decline of leukocyte telomere length in old age and the association with sex and genetic risk

Kari Berglund, Chandra A. Reynolds, Alexander Ploner, Lotte Gerritsen, Iiris Hovatta, Nancy L. Pedersen, Sara Hägg,

https://doi.org/10.18632/aging.100995 pp 1398—1415

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Berglund K, Reynolds CA, Ploner A, Gerritsen L, Hovatta I, Pedersen NL, Hägg S, . Longitudinal decline of leukocyte telomere length in old age and the association with sex and genetic risk. . 8:1398-1415. https://doi.org/10.18632/aging.100995

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                TY  - JOUR
                AU  - Berglund, Kari 
                AU  - Reynolds, Chandra A. 
                AU  - Ploner, Alexander 
                AU  - Gerritsen, Lotte 
                AU  - Hovatta, Iiris 
                AU  - Pedersen, Nancy L. 
                AU  - Hägg, Sara 
                TI  - Longitudinal decline of leukocyte telomere length in old age and the association with sex and genetic risk
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100995
                DO  - 10.18632/aging.100995
                SP  - 1398
                EP  - 1415
                PY  - 
                AB  - Telomeres are DNA-protein structures at the ends of chromosomes. Leukocyte telomere length (LTL) shortening has been associated with advanced age. However, most studies use cross-sectional data, hence, the aim of our study was to model longitudinal trajectories of LTL attrition across 20 years at old age. Assessments of LTL were done by qPCR in SATSA (Swedish Adoption/Twin Study of Aging; N=636 individuals). Cross-sectional and longitudinal associations with age were estimated, the latter using latent growth curve analysis. A genetic risk score (GRS) for LTL was further assessed and included in the models. We confirmed an inverse cross-sectional association of LTL with age (B=−0.0022 T/S-ratio; 95% CI: −0.0035, −0.0009, p-value=0.0008). Longitudinal LTL analyses adjusted for sex (1598 samples; ≤5 measurements) suggested modest average decline until 69 years of age but accelerating decline after 69 years, with significant inter-individual variation. Women had on average ∼6% T/S-ratio units longer LTL at baseline, and inclusion of the GRS improved the model where four risk alleles was equivalent to the effect size difference between the sexes. In this cohort of old individuals, baseline LTL varied with age, sex and genetic background. The rate of change of LTL accelerated with age and varied considerably between individuals.
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Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans

Simin N. Meydani, Sai K. Das, Carl F. Pieper, Michael R. Lewis, Sam Klein, Vishwa D. Dixit, Alok K. Gupta, Dennis T. Villareal, Manjushri Bhapkar, Megan Huang, Paul J. Fuss, Susan B. Roberts, John O. Holloszy, Luigi Fontana,

https://doi.org/10.18632/aging.100994 pp 1416—1431

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Meydani SN, Das SK, Pieper CF, Lewis MR, Klein S, Dixit VD, Gupta AK, Villareal DT, Bhapkar M, Huang M, Fuss PJ, Roberts SB, Holloszy JO, et al, . Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans. . 8:1416-1431. https://doi.org/10.18632/aging.100994

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                TY  - JOUR
                AU  - Meydani, Simin N. 
                AU  - Das, Sai K. 
                AU  - Pieper, Carl F. 
                AU  - Lewis, Michael R. 
                AU  - Klein, Sam 
                AU  - Dixit, Vishwa D. 
                AU  - Gupta, Alok K. 
                AU  - Villareal, Dennis T. 
                AU  - Bhapkar, Manjushri 
                AU  - Huang, Megan 
                AU  - Fuss, Paul J. 
                AU  - Roberts, Susan B. 
                AU  - Holloszy, John O. 
                AU  - Fontana, Luigi 
                TI  - Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100994
                DO  - 10.18632/aging.100994
                SP  - 1416
                EP  - 1431
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Meydani, Simin N. 
                AU  - Das, Sai K. 
                AU  - Pieper, Carl F. 
                AU  - Lewis, Michael R. 
                AU  - Klein, Sam 
                AU  - Dixit, Vishwa D. 
                AU  - Gupta, Alok K. 
                AU  - Villareal, Dennis T. 
                AU  - Bhapkar, Manjushri 
                AU  - Huang, Megan 
                AU  - Fuss, Paul J. 
                AU  - Roberts, Susan B. 
                AU  - Holloszy, John O. 
                AU  - Fontana, Luigi 
                TI  - Long-term moderate calorie restriction inhibits inflammation without impairing cell-mediated immunity: a randomized controlled trial in non-obese humans
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100994
                DO  - 10.18632/aging.100994
                SP  - 1416
                EP  - 1431
                PY  - 
                AB  - Calorie restriction (CR) inhibits inflammation and slows aging in many animal species, but in rodents housed in pathogen-free facilities, CR impairs immunity against certain pathogens. However, little is known about the effects of long-term moderate CR on immune function in humans. In this multi-center, randomized clinical trial to determine CR's effect on inflammation and cell-mediated immunity, 218 healthy non-obese adults (20-50 y), were assigned 25% CR (n=143) or an ad-libitum (AL) diet (n=75), and outcomes tested at baseline, 12, and 24 months of CR. CR induced a 10.4% weight loss over the 2-y period. Relative to AL group, CR reduced circulating inflammatory markers, including total WBC and lymphocyte counts, ICAM-1 and leptin. Serum CRP and TNF-α concentrations were about 40% and 50% lower in CR group, respectively. CR had no effect on the delayed-type hypersensitivity skin response or antibody response to vaccines, nor did it cause difference in clinically significant infections. In conclusion, long-term moderate CR without malnutrition induces a significant and persistent inhibition of inflammation without impairing key in vivo indicators of cell-mediated immunity. Given the established role of these pro-inflammatory molecules in the pathogenesis of multiple chronic diseases, these CR-induced adaptations suggest a shift toward a healthy phenotype.
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Stroke sensitivity in the aged: sex chromosome complement vs. gonadal hormones

Louise D. McCullough, Mehwish A. Mirza, Yan Xu, Kathryn Bentivegna, Eleanor B. Steffens, Rodney Ritzel, Fudong Liu,

https://doi.org/10.18632/aging.100997 pp 1432—1441

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McCullough LD, Mirza MA, Xu Y, Bentivegna K, Steffens EB, Ritzel R, Liu F, . Stroke sensitivity in the aged: sex chromosome complement vs. gonadal hormones. . 8:1432-1441. https://doi.org/10.18632/aging.100997

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                TY  - JOUR
                AU  - McCullough, Louise D. 
                AU  - Mirza, Mehwish A. 
                AU  - Xu, Yan 
                AU  - Bentivegna, Kathryn 
                AU  - Steffens, Eleanor B. 
                AU  - Ritzel, Rodney 
                AU  - Liu, Fudong 
                TI  - Stroke sensitivity in the aged: sex chromosome complement vs. gonadal hormones
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100997
                DO  - 10.18632/aging.100997
                SP  - 1432
                EP  - 1441
                PY  - 
                AB  - Stroke is a sexually dimorphic disease. Elderly women not only have higher stroke incidence than age-matched men, but also have poorer recovery and higher morbidity and mortality after stroke. In older, post-menopausal women, gonadal hormone levels are similar to that of men. This suggests that tissue damage and functional outcomes are influenced by biologic sex (XX vs. XY) rather than the hormonal milieu at older ages. We employed the Four Core Genotype (FCG) mouse model to study the contribution of sex chromosome complement and gonadal hormones to stroke sensitivity in aged mice in which the testis determining gene (Sry) is removed from the Y chromosome, allowing for the generation of XX males and XY females. XXF, XXM, XYF, XYM and XYwt aged mice were subjected to middle cerebral artery occlusion (MCAO). XXF and XXM mice had significantly larger infarct volumes than XYF and XYM cohorts respectively. There was no significant difference in hormone levels among aged FCG mice. XXF/XXM mice also had more robust microglial activation and higher serum levels of pro-inflammatory cytokines than XYF/XYM cohort respectively. We concluded that the sex chromosome complement contributes to ischemic sensitivity in aged animals and leads to sex differences in innate immune responses.
                ER  -

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miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells

Mingyang He, Yi Lin, Yunlan Tang, Yi Liu, Weiwei Zhou, Chuang Li, Guihong Sun, Mingxiong Guo,

https://doi.org/10.18632/aging.100998 pp 1442—1456

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He M, Lin Y, Tang Y, Liu Y, Zhou W, Li C, Sun G, Guo M, . miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells. . 8:1442-1456. https://doi.org/10.18632/aging.100998

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                TY  - JOUR
                AU  - He, Mingyang 
                AU  - Lin, Yi 
                AU  - Tang, Yunlan 
                AU  - Liu, Yi 
                AU  - Zhou, Weiwei 
                AU  - Li, Chuang 
                AU  - Sun, Guihong 
                AU  - Guo, Mingxiong 
                TI  - miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100998
                DO  - 10.18632/aging.100998
                SP  - 1442
                EP  - 1456
                PY  - 
                AB  - The reduction of DNA damage repair capacity in terminally differentiated cells may be involved in sensitivity to cancer chemotherapy drugs; however, the underlying molecular mechanism is still not fully understood. Herein, we evaluated the role of miR-638 in the regulation of DNA damage repair in terminally differentiated cells. Our results show that miR-638 expression was up-regulated during cellular terminal differentiation and involved in mediating DNA damage repair processes. Results from a luciferase reporting experiment show that structural maintenance of chromosomes (SMC)1A was a potential target of miR-638; this was verified by western blot assays during cell differentiation and DNA damage induction. Overexpression of miR-638 enhanced the sensitivity of cancer cells to cisplatin, thus reducing cell viability in response to chemotherapy drug treatment. Furthermore, miR-638 overexpression affected DNA damage repair processes by interfering with the recruitment of the DNA damage repair-related protein, γH2AX, to DNA break sites. These findings indicate that miR-638 might act as a sensitizer in cancer chemotherapy and accompany chemotherapy drugs to enhance chemotherapeutic efficacy and to improve the chance of recovery from cancer.
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Skin aging: are adipocytes the next target?

Ilja L. Kruglikov, Philipp E. Scherer,

https://doi.org/10.18632/aging.100999 pp 1457—1469

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Kruglikov IL, Scherer PE, . Skin aging: are adipocytes the next target?. . 8:1457-1469. https://doi.org/10.18632/aging.100999

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                TY  - JOUR
                AU  - Kruglikov, Ilja L. 
                AU  - Scherer, Philipp E. 
                TI  - Skin aging: are adipocytes the next target?
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100999
                DO  - 10.18632/aging.100999
                SP  - 1457
                EP  - 1469
                PY  - 
                AB  - Dermal white adipose tissue (dWAT) is increasingly appreciated as a special fat depot. The adipocytes in this depot exert a variety of unique effects on their surrounding cells and can undergo massive phenotypic changes. Significant modulation of dWAT content can be observed both in intrinsically and extrinsically aged skin. Specifically, skin that has been chronically photo-damaged displays a reduction of the dWAT volume, caused by the replacement of adipocytes by fibrotic structures. This is likely to be caused by the recently uncovered process described as “adipocyte-myofibroblast transition” (AMT). In addition, contributions of dermal adipocytes to the skin aging processes are also indirectly supported by spatial correlations between the prevalence of hypertrophic scarring and the appearance of signs of skin aging in different ethnic groups. These observations could elevate dermal adipocytes to prime targets in strategies aimed at counteracting skin aging.
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Caloric restriction stimulates autophagy in rat cortical neurons through neuropeptide Y and ghrelin receptors activation

Marisa Ferreira-Marques, Célia A. Aveleira, Sara Carmo-Silva, Mariana Botelho, Luís Pereira de Almeida, Cláudia Cavadas,

https://doi.org/10.18632/aging.100996 pp 1470—1484

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Ferreira-Marques M, Aveleira CA, Carmo-Silva S, Botelho M, Pereira de Almeida L, Cavadas C, . Caloric restriction stimulates autophagy in rat cortical neurons through neuropeptide Y and ghrelin receptors activation. . 8:1470-1484. https://doi.org/10.18632/aging.100996

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                TY  - JOUR
                AU  - Ferreira-Marques, Marisa 
                AU  - Aveleira, Célia A. 
                AU  - Carmo-Silva, Sara 
                AU  - Botelho, Mariana 
                AU  - Pereira de Almeida, Luís 
                AU  - Cavadas, Cláudia 
                TI  - Caloric restriction stimulates autophagy in rat cortical neurons through neuropeptide Y and ghrelin receptors activation
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100996
                DO  - 10.18632/aging.100996
                SP  - 1470
                EP  - 1484
                PY  - 
                AB  - Caloric restriction is an anti-aging intervention known to extend lifespan in several experimental models, at least in part, by stimulating autophagy. Caloric restriction increases neuropeptide Y (NPY) in the hypothalamus and plasma ghrelin, a peripheral gut hormone that acts in hypothalamus to modulate energy homeostasis. NPY and ghrelin have been shown to be neuroprotective in different brain areas and to induce several physiological modifications similar to those induced by caloric restriction. However, the effect of NPY and ghrelin in autophagy in cortical neurons is currently not known. Using a cell culture of rat cortical neurons we investigate the involvement of NPY and ghrelin in caloric restriction-induced autophagy. We observed that a caloric restriction mimetic cell culture medium stimulates autophagy in rat cortical neurons and NPY or ghrelin receptor antagonists blocked this effect. On the other hand, exogenous NPY or ghrelin stimulate autophagy in rat cortical neurons. Moreover, NPY mediates the stimulatory effect of ghrelin on autophagy in rat cortical neurons. Since autophagy impairment occurs in aging and age-related neurodegenerative diseases, NPY and ghrelin synergistic effect on autophagy stimulation may suggest a new strategy to delay aging process.
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Huntington's disease accelerates epigenetic aging of human brain and disrupts DNA methylation levels

Steve Horvath, Peter Langfelder, Seung Kwak, Jeff Aaronson, Jim Rosinski, Thomas F. Vogt, Marika Eszes, Richard L.M. Faull, Maurice A. Curtis, Henry J. Waldvogel, Oi-Wa Choi, Spencer Tung, Harry V. Vinters, Giovanni Coppola, X. William Yang,

https://doi.org/10.18632/aging.101005 pp 1485—1512

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Horvath S, Langfelder P, Kwak S, Aaronson J, Rosinski J, Vogt TF, Eszes M, Faull RL, Curtis MA, Waldvogel HJ, Choi O, Tung S, Vinters HV, et al, . Huntington's disease accelerates epigenetic aging of human brain and disrupts DNA methylation levels. . 8:1485-1512. https://doi.org/10.18632/aging.101005

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                TY  - JOUR
                AU  - Horvath, Steve 
                AU  - Langfelder, Peter 
                AU  - Kwak, Seung 
                AU  - Aaronson, Jeff 
                AU  - Rosinski, Jim 
                AU  - Vogt, Thomas F. 
                AU  - Eszes, Marika 
                AU  - Faull, Richard L.M. 
                AU  - Curtis, Maurice A. 
                AU  - Waldvogel, Henry J. 
                AU  - Choi, Oi-Wa 
                AU  - Tung, Spencer 
                AU  - Vinters, Harry V. 
                AU  - Coppola, Giovanni 
                AU  - Yang, X. William 
                TI  - Huntington's disease accelerates epigenetic aging of human brain and disrupts DNA methylation levels
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101005
                DO  - 10.18632/aging.101005
                SP  - 1485
                EP  - 1512
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Horvath, Steve 
                AU  - Langfelder, Peter 
                AU  - Kwak, Seung 
                AU  - Aaronson, Jeff 
                AU  - Rosinski, Jim 
                AU  - Vogt, Thomas F. 
                AU  - Eszes, Marika 
                AU  - Faull, Richard L.M. 
                AU  - Curtis, Maurice A. 
                AU  - Waldvogel, Henry J. 
                AU  - Choi, Oi-Wa 
                AU  - Tung, Spencer 
                AU  - Vinters, Harry V. 
                AU  - Coppola, Giovanni 
                AU  - Yang, X. William 
                TI  - Huntington's disease accelerates epigenetic aging of human brain and disrupts DNA methylation levels
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101005
                DO  - 10.18632/aging.101005
                SP  - 1485
                EP  - 1512
                PY  - 
                AB  - Age of Huntington's disease (HD) motoric onset is strongly related to the number of CAG trinucleotide repeats in the huntingtin gene, suggesting that biological tissue age plays an important role in disease etiology. Recently, a DNA methylation based biomarker of tissue age has been advanced as an epigenetic aging clock. We sought to inquire if HD is associated with an accelerated epigenetic age. DNA methylation data was generated for 475 brain samples from various brain regions of 26 HD cases and 39 controls. Overall, brain regions from HD cases exhibit a significant epigenetic age acceleration effect (p=0.0012). A multivariate model analysis suggests that HD status increases biological age by 3.2 years. Accelerated epigenetic age can be observed in specific brain regions (frontal lobe, parietal lobe, and cingulate gyrus). After excluding controls, we observe a negative correlation (r=−0.41, p=5.5×10−8) between HD gene CAG repeat length and the epigenetic age of HD brain samples. Using correlation network analysis, we identify 11 co-methylation modules with a significant association with HD status across 3 broad cortical regions. In conclusion, HD is associated with an accelerated epigenetic age of specific brain regions and more broadly with substantial changes in brain methylation levels.
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Dietary and microbiome factors determine longevity in Caenorhabditis elegans

Adolfo Sánchez-Blanco, Alberto Rodríguez-Matellán, Ana González-Paramás, Susana González-Manzano, Stuart K. Kim, Faustino Mollinedo,

https://doi.org/10.18632/aging.101008 pp 1513—1539

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Sánchez-Blanco A, Rodríguez-Matellán A, González-Paramás A, González-Manzano S, Kim SK, Mollinedo F, . Dietary and microbiome factors determine longevity in Caenorhabditis elegans. . 8:1513-1539. https://doi.org/10.18632/aging.101008

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                TY  - JOUR
                AU  - Sánchez-Blanco, Adolfo 
                AU  - Rodríguez-Matellán, Alberto 
                AU  - González-Paramás, Ana 
                AU  - González-Manzano, Susana 
                AU  - Kim, Stuart K. 
                AU  - Mollinedo, Faustino 
                TI  - Dietary and microbiome factors determine longevity in <i>Caenorhabditis elegans</i>
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101008
                DO  - 10.18632/aging.101008
                SP  - 1513
                EP  - 1539
                PY  - 
                AB  - Diet composition affects organismal health. Nutrient uptake depends on the microbiome. Caenorhabditis elegans fed a Bacillus subtilis diet live longer than those fed the standard Escherichia coli diet. Here we report that this longevity difference is primarily caused by dietary coQ, an antioxidant synthesized by E. coli but not by B. subtilis. CoQ-supplemented E. coli fed worms have a lower oxidation state yet live shorter than coQ-less B. subtilis fed worms. We showed that mutations affecting longevity for E. coli fed worms do not always lead to similar effects when worms are fed B. subtilis. We propose that coQ supplementation by the E. coli diet alters the worm cellular REDOX homeostasis, thus decreasing longevity. Our results highlight the importance of microbiome factors in longevity, argue that antioxidant supplementation can be detrimental, and suggest that the C. elegans standard E. coli diet can alter the effect of signaling pathways on longevity.
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Cyclin A2 promotes DNA repair in the brain during both development and aging

Patrick E. Gygli, Joshua C. Chang, Hamza N. Gokozan, Fay P. Catacutan, Theresa A. Schmidt, Behiye Kaya, Mustafa Goksel, Faisal S. Baig, Shannon Chen, Amelie Griveau, Wojciech Michowski, Michael Wong, Kamalakannan Palanichamy, Piotr Sicinski, Randy J. Nelson, Catherine Czeisler, José J. Otero,

https://doi.org/10.18632/aging.100990 pp 1540—1570

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Gygli PE, Chang JC, Gokozan HN, Catacutan FP, Schmidt TA, Kaya B, Goksel M, Baig FS, Chen S, Griveau A, Michowski W, Wong M, Palanichamy K, et al, . Cyclin A2 promotes DNA repair in the brain during both development and aging. . 8:1540-1570. https://doi.org/10.18632/aging.100990

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                TY  - JOUR
                AU  - Gygli, Patrick E. 
                AU  - Chang, Joshua C. 
                AU  - Gokozan, Hamza N. 
                AU  - Catacutan, Fay P. 
                AU  - Schmidt, Theresa A. 
                AU  - Kaya, Behiye 
                AU  - Goksel, Mustafa 
                AU  - Baig, Faisal S. 
                AU  - Chen, Shannon 
                AU  - Griveau, Amelie 
                AU  - Michowski, Wojciech 
                AU  - Wong, Michael 
                AU  - Palanichamy, Kamalakannan 
                AU  - Sicinski, Piotr 
                AU  - Nelson, Randy J. 
                AU  - Czeisler, Catherine 
                AU  - Otero, José J. 
                TI  - Cyclin A2 promotes DNA repair in the brain during both development and aging
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100990
                DO  - 10.18632/aging.100990
                SP  - 1540
                EP  - 1570
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Gygli, Patrick E. 
                AU  - Chang, Joshua C. 
                AU  - Gokozan, Hamza N. 
                AU  - Catacutan, Fay P. 
                AU  - Schmidt, Theresa A. 
                AU  - Kaya, Behiye 
                AU  - Goksel, Mustafa 
                AU  - Baig, Faisal S. 
                AU  - Chen, Shannon 
                AU  - Griveau, Amelie 
                AU  - Michowski, Wojciech 
                AU  - Wong, Michael 
                AU  - Palanichamy, Kamalakannan 
                AU  - Sicinski, Piotr 
                AU  - Nelson, Randy J. 
                AU  - Czeisler, Catherine 
                AU  - Otero, José J. 
                TI  - Cyclin A2 promotes DNA repair in the brain during both development and aging
                JO  - 
                JA  - 
                VL  - 8
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100990
                DO  - 10.18632/aging.100990
                SP  - 1540
                EP  - 1570
                PY  - 
                AB  - Various stem cell niches of the brain have differential requirements for Cyclin A2. Cyclin A2 loss results in marked cerebellar dysmorphia, whereas forebrain growth is retarded during early embryonic development yet achieves normal size at birth. To understand the differential requirements of distinct brain regions for Cyclin A2, we utilized neuroanatomical, transgenic mouse, and mathematical modeling techniques to generate testable hypotheses that provide insight into how Cyclin A2 loss results in compensatory forebrain growth during late embryonic development. Using unbiased measurements of the forebrain stem cell niche, we parameterized a mathematical model whereby logistic growth instructs progenitor cells as to the cell-types of their progeny. Our data was consistent with prior findings that progenitors proliferate along an auto-inhibitory growth curve. The growth retardation in CCNA2-null brains corresponded to cell cycle lengthening, imposing a developmental delay. We hypothesized that Cyclin A2 regulates DNA repair and that CCNA2-null progenitors thus experienced lengthened cell cycle. We demonstrate that CCNA2-null progenitors suffer abnormal DNA repair, and implicate Cyclin A2 in double-strand break repair. Cyclin A2’s DNA repair functions are conserved among cell lines, neural progenitors, and hippocampal neurons. We further demonstrate that neuronal CCNA2 ablation results in learning and memory deficits in aged mice.
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Erratum: Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell

Daniele Lettieri Barbato, Giuseppe Tatulli, Katia Aquilano, Maria R. Ciriolo,

https://doi.org/10.18632/aging.101003 pp 1571

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Barbato DL, Tatulli G, Aquilano K, Ciriolo MR, . Erratum: Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell. . 8:1571-1571. https://doi.org/10.18632/aging.101003

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Volume 8, Issue 7

About the Cover

Editorials

Zdena Palková, Libuše Váchová,

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Laurence Booth, Mark Malkin, Paul Dent,

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Schammim Ray Amith, Larry Fliegel,

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Kacie A. Gardella, Richa Tiwary, Casey W. Wright,

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Research Papers

Brandon M. Hall, Vitaly Balan, Anatoli S. Gleiberman, Evguenia Strom, Peter Krasnov, Lauren P. Virtuoso, Elena Rydkina, Slavoljub Vujcic, Karina Balan, Ilya Gitlin, Katerina Leonova, Alexander Polinsky, Olga B. Chernova, Andrei V. Gudkov,

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Servet Özcan, Nicola Alessio, Mustafa B. Acar, Eda Mert, Fatih Omerli, Gianfranco Peluso, Umberto Galderisi,

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Alejandro Vazquez-Martin, Chris Van den Haute, Sílvia Cufí, Bruna Corominas Faja, Elisabet Cuyàs, Eugeni Lopez-Bonet, Esther Rodriguez-Gallego, Salvador Fernández-Arroyo, Jorge Joven, Veerle Baekelandt, Javier A. Menendez,

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Andrea L. George, Corinne A. Boulanger, Gilbert H. Smith,

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Jacob J.E. Koopman, Jeroen Pijpe, Stefan Böhringer, David van Bodegom, Ulrika K. Eriksson, Hernando Sanchez-Faddeev, Juventus B. Ziem, Bas Zwaan, P. Eline Slagboom, Peter de Knijff, Rudi G.J. Westendorp,

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Artem Smirnov, Emanuele Panatta, AnnaMaria Lena, Daniele Castiglia, Nicola Di Daniele, Gerry Melino, Eleonora Candi,

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Kari Berglund, Chandra A. Reynolds, Alexander Ploner, Lotte Gerritsen, Iiris Hovatta, Nancy L. Pedersen, Sara Hägg,

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Simin N. Meydani, Sai K. Das, Carl F. Pieper, Michael R. Lewis, Sam Klein, Vishwa D. Dixit, Alok K. Gupta, Dennis T. Villareal, Manjushri Bhapkar, Megan Huang, Paul J. Fuss, Susan B. Roberts, John O. Holloszy, Luigi Fontana,

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Louise D. McCullough, Mehwish A. Mirza, Yan Xu, Kathryn Bentivegna, Eleanor B. Steffens, Rodney Ritzel, Fudong Liu,

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Mingyang He, Yi Lin, Yunlan Tang, Yi Liu, Weiwei Zhou, Chuang Li, Guihong Sun, Mingxiong Guo,

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Ilja L. Kruglikov, Philipp E. Scherer,

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Marisa Ferreira-Marques, Célia A. Aveleira, Sara Carmo-Silva, Mariana Botelho, Luís Pereira de Almeida, Cláudia Cavadas,

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Steve Horvath, Peter Langfelder, Seung Kwak, Jeff Aaronson, Jim Rosinski, Thomas F. Vogt, Marika Eszes, Richard L.M. Faull, Maurice A. Curtis, Henry J. Waldvogel, Oi-Wa Choi, Spencer Tung, Harry V. Vinters, Giovanni Coppola, X. William Yang,

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Adolfo Sánchez-Blanco, Alberto Rodríguez-Matellán, Ana González-Paramás, Susana González-Manzano, Stuart K. Kim, Faustino Mollinedo,

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Patrick E. Gygli, Joshua C. Chang, Hamza N. Gokozan, Fay P. Catacutan, Theresa A. Schmidt, Behiye Kaya, Mustafa Goksel, Faisal S. Baig, Shannon Chen, Amelie Griveau, Wojciech Michowski, Michael Wong, Kamalakannan Palanichamy, Piotr Sicinski, Randy J. Nelson, Catherine Czeisler, José J. Otero,

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