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The art and science of personality development
\"Integrating state-of-the-art personality and developmental research, this book presents a new and broadly integrative theory of how people come to be who they are over the life course. Preeminent researcher Dan P. McAdams traces the development of three distinct layers of personality--the social actor who expresses emotional and behavioral traits, the motivated agent who pursues goals and values, and the autobiographical author who constructs a personal story for life. Highly readable and accessible to scholars and students at all levels, the book uses rich portraits of the lives of famous people to illustrate theoretical concepts and empirical findings\"-- Provided by publisher.
Book
Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances
We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1, ATXN2/BRAP, FURIN/FES, ZW10, PSORS1C3, and 13q21.31, and identify and replicate novel findings near ABO, ZC3HC1, and IGF2R. We also validate previous findings near 5q33.3/EBF1 and FOXO3, whilst finding contradictory evidence at other loci. Gene set and cell-specific analyses show that expression in foetal brain cells and adult dorsolateral prefrontal cortex is enriched for lifespan variation, as are gene pathways involving lipid proteins and homeostasis, vesicle-mediated transport, and synaptic function. Individual genetic variants that increase dementia, cardiovascular disease, and lung cancer – but not other cancers – explain the most variance. Resulting polygenic scores show a mean lifespan difference of around five years of life across the deciles. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter ). Ageing happens to us all, and as the cabaret singer Maurice Chevalier pointed out, \"old age is not that bad when you consider the alternative\". Yet, the growing ageing population of most developed countries presents challenges to healthcare systems and government finances. For many older people, long periods of ill health are part of the end of life, and so a better understanding of ageing could offer the opportunity to prolong healthy living into old age. Ageing is complex and takes a long time to study – a lifetime in fact. This makes it difficult to discern its causes, among the countless possibilities based on an individual’s genes, behaviour or environment. While thousands of regions in an individual’s genetic makeup are known to influence their risk of different diseases, those that affect how long they will live have proved harder to disentangle. Timmers et al. sought to pinpoint such regions, and then use this information to predict, based on their DNA, whether someone had a better or worse chance of living longer than average. The DNA of over 500,000 people was read to reveal the specific ‘genetic fingerprints’ of each participant. Then, after asking each of the participants how long both of their parents had lived, Timmers et al. pinpointed 12 DNA regions that affect lifespan. Five of these regions were new and had not been linked to lifespan before. Across the twelve as a whole several were known to be involved in Alzheimer’s disease, smoking-related cancer or heart disease. Looking at the entire genome, Timmers et al. could then predict a lifespan score for each individual, and when they sorted participants into ten groups based on these scores they found that top group lived five years longer than the bottom, on average. Many factors beside genetics influence how long a person will live and our lifespan cannot be read from our DNA alone. Nevertheless, Timmers et al. had hoped to narrow down their search and discover specific genes that directly influence how quickly people age, beyond diseases. If such genes exist, their effects were too small to be detected in this study. The next step will be to expand the study to include more participants, which will hopefully pinpoint further genomic regions and help disentangle the biology of ageing and disease.
Journal Article
Me, myself, and us : the science of personality and the art of well-being
\"In the past few decades, personality psychology has made considerable progress in raising new questions about human nature-and providing some provocative answers. New scientific research has transformed old ideas about personality based on the theories of Freud, Jung, and the humanistic psychologies of the nineteen sixties, which gave rise to the simplistic categorizations of the Meyer-Briggs Inventory and the 'enneagream'. But the general public still knows little about the new science and what it reveals about who we are. In Me, Myself, and Us, Brian Little, one of the psychologists who helped re-shape the field, provides the first in-depth exploration of the new personality science and its provocative findings for general readers. The book explores questions that are rooted in the origins of human consciousness but are as commonplace as yesterday's breakfast conversation. Are our first impressions of other people's personalities usually fallacious? Are creative individuals essentially maladjusted? Are our personality traits, as William James put it \"set like plaster\" by the age of thirty? Is a belief that we are in control of our lives an unmitigated good? Do our singular personalities comprise one unified self or a confederacy of selves, and if the latter, which of our mini-me-s do we offer up in marriage or mergers? Are some individuals genetically hard-wired for happiness? Which is the more viable path toward human flourishing, the pursuit of happiness or the happiness of pursuit? Little provides a resource for answering such questions, and a framework through which readers can explore the personal implications of the new science of personality. Questionnaires and interactive assessments throughout the book facilitate self-exploration, and clarify some of the stranger aspects of our own conduct and that of others. Brian Little helps us see ourselves, and other selves, as somewhat less perplexing and definitely more intriguing. This is not a self-help book, but students at Harvard who took the lecture course on which it is based claim that it changed their lives. \"-- Provided by publisher.
Book
Genetic differences and longevity‐related phenotypes influence lifespan and lifespan variation in a sex‐specific manner in mice
Epidemiological studies of human longevity found two interesting features, robust advantage of female lifespan and consistent reduction of lifespan variation. To help understand the genetic aspects of these phenomena, the current study examined sex differences and variation of longevity using previously published mouse data sets including data on lifespan, age of puberty, and circulating insulin‐like growth factor 1 (IGF1) levels in 31 inbred strains, data from colonies of nuclear‐receptor‐interacting protein 1 (Nrip1) knockout mice, and a congenic strain, B6.C3H‐Igf1. Looking at the overall data for all inbred strains, the results show no significant difference in lifespan and lifespan variation between sexes; however, considerable differences were found among and within strains. Across strains, lifespan variations of female and male mice are significantly correlated. Strikingly, between sexes, IGF1 levels correlate with the lifespan variation and maximum lifespan in different directions. Female mice with low IGF1 levels have higher variation and extended maximum lifespan. The opposite is detected in males. Compared to domesticated inbred strains, wild‐derived inbred strains have elevated lifespan variation due to increased early deaths in both sexes and extended maximum lifespan in female mice. Intriguingly, the sex differences in survival curves of inbred strains negatively associated with age of female puberty, which is significantly accelerated in domesticated inbred strains compared to wild‐derived strains. In conclusion, this study suggests that genetic factors are involved in the regulation of sexual disparities in lifespan and lifespan variation, and dissecting the mouse genome may provide novel insight into the underlying genetic mechanisms. Among inbred strains, the lifespan variations of female and male mice are significantly correlated, suggesting the genetic co‐regulation of lifespan variation between sexes. IGF1 levels associate with lifespan variation and maximum lifespan in a sex‐specific manner. Importantly, female mice with lower IGF1 have longer maximum lifespan, while the male mice with higher IGF1 have longer maximum lifespan.
Journal Article
Repetitive seasonal drought causes substantial species-specific shifts in fine-root longevity and spatio-temporal production patterns in mature temperate forest trees
• Temperate forest ecosystems are exposed to a higher frequency, duration and severity of drought. To promote forest longevity in a changing climate, we require a better understanding of the long-term impacts of repetitive drought events on fine-root dynamics in mature forests.
• Using minirhizotron methods, we investigated the effect of seasonal drought on fine-root dynamics in single-species and mixed-species arrangements of Fagus sylvatica (European beech) and Picea abies (Norway spruce) by means of a 4-yr-long throughfall-exclusion experiment.
• Fine-root production of both species decreased under drought. However, this reduction was not evident for P. abies when grown intermixed with F. sylvatica. Throughfall-exclusion prolonged the lifespan of P. abies roots but did not change the lifespan of F. sylvatica roots, except in 2016. Fagus sylvatica responded to drought by reducing fine-root production at specific depths and during roof closure.
• This is the first study to examine long-term trends in mature forest fine-root dynamics under repetitive drought events. Species-specific fine-root responses to drought have implications for the rate and depth of root-derived organic matter supply to soil. From a root dynamics perspective, intermixing tree species is not beneficial to all species but dampens drought impacts on the belowground productivity of P. abies.
Journal Article
Spontaneous cortical dynamics from the first years to the golden years
In the largest and most expansive lifespan magnetoencephalography (MEG) study to date (n = 434, 6 to 84 y), we provide critical data on the normative trajectory of resting- state spontaneous activity and its temporal dynamics. We perform cutting-edge analyses to examine age and sex effects on whole-brain, spatially-resolved relative and absolute power maps, and find significant age effects in all spectral bands in both types of maps. Specifically, lower frequencies showed a negative correlation with age, while higher frequencies positively correlated with age. These correlations were further probed with hierarchical regressions, which revealed significant nonlinear trajectories in key brain regions. Sex effects were found in absolute but not relative power maps, highlighting key differences between outcome indices that are generally used interchangeably. Our rigorous and innovative approach provides multispectral maps indicating the unique trajectory of spontaneous neural activity across the lifespan, and illuminates key methodological considerations with the widely used relative/absolute power maps of spontaneous cortical dynamics.
Journal Article
Methionine metabolism and methyltransferases in the regulation of aging and lifespan extension across species
Methionine restriction (MetR) extends lifespan across different species and exerts beneficial effects on metabolic health and inflammatory responses. In contrast, certain cancer cells exhibit methionine auxotrophy that can be exploited for therapeutic treatment, as decreasing dietary methionine selectively suppresses tumor growth. Thus, MetR represents an intervention that can extend lifespan with a complementary effect of delaying tumor growth. Beyond its function in protein synthesis, methionine feeds into complex metabolic pathways including the methionine cycle, the transsulfuration pathway, and polyamine biosynthesis. Manipulation of each of these branches extends lifespan; however, the interplay between MetR and these branches during regulation of lifespan is not well understood. In addition, a potential mechanism linking the activity of methionine metabolism and lifespan is regulation of production of the methyl donor S‐adenosylmethionine, which, after transferring its methyl group, is converted to S‐adenosylhomocysteine. Methylation regulates a wide range of processes, including those thought to be responsible for lifespan extension by MetR. Although the exact mechanisms of lifespan extension by MetR or methionine metabolism reprogramming are unknown, it may act via reducing the rate of translation, modifying gene expression, inducing a hormetic response, modulating autophagy, or inducing mitochondrial function, antioxidant defense, or other metabolic processes. Here, we review the mechanisms of lifespan extension by MetR and different branches of methionine metabolism in different species and the potential for exploiting the regulation of methyltransferases to delay aging. A potential mechanism linking the activity of methionine metabolism and lifespan is regulation of production of the methyl donor S‐adenosylmethionine (SAM), which, after transferring its methyl group, is converted to S‐adenosylhomocysteine (SAH). Methionine metabolism determines the ratio of SAM/SAH metabolites and affects most of the methylation reactions in the cell, which in turn regulate a wide range of processes including ones that were attributed to be responsible for the lifespan extension by MetR.
Journal Article
The UNC/UMN Baby Connectome Project (BCP): An overview of the study design and protocol development
The human brain undergoes extensive and dynamic growth during the first years of life. The UNC/UMN Baby Connectome Project (BCP), one of the Lifespan Connectome Projects funded by NIH, is an ongoing study jointly conducted by investigators at the University of North Carolina at Chapel Hill and the University of Minnesota. The primary objective of the BCP is to characterize brain and behavioral development in typically developing infants across the first 5 years of life. The ultimate goals are to chart emerging patterns of structural and functional connectivity during this period, map brain-behavior associations, and establish a foundation from which to further explore trajectories of health and disease. To accomplish these goals, we are combining state of the art MRI acquisition and analysis techniques, including high-resolution structural MRI (T1-and T2-weighted images), diffusion imaging (dMRI), and resting state functional connectivity MRI (rfMRI). While the overall design of the BCP largely is built on the protocol developed by the Lifespan Human Connectome Project (HCP), given the unique age range of the BCP cohort, additional optimization of imaging parameters and consideration of an age appropriate battery of behavioral assessments were needed. Here we provide the overall study protocol, including approaches for subject recruitment, strategies for imaging typically developing children 0–5 years of age without sedation, imaging protocol and optimization, a description of the battery of behavioral assessments, and QA/QC procedures. Combining HCP inspired neuroimaging data with well-established behavioral assessments during this time period will yield an invaluable resource for the scientific community.
•Complete description of the UNC/UMN Baby Connectome Project (BCP) protocol.•The importanc'e of dense longitudinal sampling.•Protocol optimization and preliminary results of optimized imaging protocol.•BCP study data as a unique resource for the scientific community.
Journal Article
Sex‐specific aging in animals: Perspective and future directions
Sex differences in aging occur in many animal species, and they include sex differences in lifespan, in the onset and progression of age‐associated decline, and in physiological and molecular markers of aging. Sex differences in aging vary greatly across the animal kingdom. For example, there are species with longer‐lived females, species where males live longer, and species lacking sex differences in lifespan. The underlying causes of sex differences in aging remain mostly unknown. Currently, we do not understand the molecular drivers of sex differences in aging, or whether they are related to the accepted hallmarks or pillars of aging or linked to other well‐characterized processes. In particular, understanding the role of sex‐determination mechanisms and sex differences in aging is relatively understudied. Here, we take a comparative, interdisciplinary approach to explore various hypotheses about how sex differences in aging arise. We discuss genomic, morphological, and environmental differences between the sexes and how these relate to sex differences in aging. Finally, we present some suggestions for future research in this area and provide recommendations for promising experimental designs. Sex difference in aging occurs across the animal kingdom, but there is considerable variation and they are not universal. The processes leading to sex‐specific aging are poorly understood and might originate in sex‐specific genome architecture, organismal biology, or environmental interactions. Here, we take a comparative approach to review the various hypotheses and suggest promising areas of research for further study.
Journal Article