bluuebunny/crossref_metadata_2025_split huggingface dataset:
Life-history theory in psychology and evolutionary biology: one research programme or two?
Authors: Nettle Daniel , Frankenhuis Willem E. 
Published: May 2020

The term ‘life-history theory’ (LHT) is increasingly often invoked in psychology, as a framework for integrating understanding of psychological traits into a broader evolutionary context. Although LHT as presented in psychology papers (LHT-P) is typically described as a straightforward extension of the theoretical principles from evolutionary biology that bear the same name (LHT-E), the two bodies of work are not well integrated. Here, through a close reading of recent papers, we argue that LHT-E and LHT-P are different research programmes in the Lakatosian sense. The core of LHT-E is built around ultimate evolutionary explanation, via explicit mathematical modelling, of how selection can drive divergent evolution of populations or species living under different demographies or ecologies. The core of LHT-P concerns measurement of covariation, across individuals, of multiple psychological traits; the proximate goals these serve; and their relation to childhood experience. Some of the links between LHT-E and LHT-P are false friends. For example, elements that are marginal in LHT-E are core commitments of LHT-P, and where explanatory principles are transferred from one to the other, nuance can be lost in transmission. The methodological rules for what grounds a prediction in theory are different in the two cases. Though there are major differences between LHT-E and LHT-P at present, there is much potential for greater integration in the future, through both theoretical modelling and further empirical research.
This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
The developmental support hypothesis: adaptive plasticity in neural development in response to cues of social support
Authors: Snell-Rood Emilie , Snell-Rood Claire 
Published: May 2020

Across mammals, cues of developmental support, such as touching, licking or attentiveness, stimulate neural development, behavioural exploration and even overall body growth. Why should such fitness-related traits be so sensitive to developmental conditions? Here, we review what we term the ‘developmental support hypothesis’, a potential adaptive explanation of this plasticity. Neural development can be a costly process, in terms of time, energy and exposure. However, environmental variability may sometimes compromise parental care during this costly developmental period. We propose this environmental variation has led to the evolution of adaptive plasticity of neural and behavioural development in response to cues of developmental support, where neural development is stimulated in conditions that support associated costs. When parental care is compromised, offspring grow less and adopt a more resilient and stress-responsive strategy, improving their chances of survival in difficult conditions, similar to existing ideas on the adaptive value of early-life programming of stress. The developmental support hypothesis suggests new research directions, such as testing the adaptive value of reduced neural growth and metabolism in stressful conditions, and expanding the range of potential cues animals may attend to as indicators of developmental support. Considering evolutionary and ecologically appropriate cues of social support also has implications for promoting healthy neural development in humans.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
The adaptive origins of uniquely human sociality
Authors: Tomasello Michael 
Published: May 2020

Humans possess some unique social-cognitive skills and motivations, involving such things as joint attention, cooperative communication, dual-level collaboration and cultural learning. These are almost certainly adaptations for humans' especially complex sociocultural lives. The common assumption has been that these unique skills and motivations emerge in human infancy and early childhood as preparations for the challenges of adult life, for example, in collaborative foraging. In the current paper, I propose that the curiously early emergence of these skills in infancy––well before they are needed in adulthood––along with other pieces of evidence (such as almost exclusive use with adults not peers) suggests that aspects of the evolution of these skills represent ontogenetic adaptations to the unique socio-ecological challenges human infants face in the context of a regime of cooperative breeding and childcare.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
Innovation, life history and social networks in human evolution
Authors: Sterelny Kim 
Published: May 2020

There is a famous puzzle about the first 3 million years of archaeologically visible human technological history. The pace of change, of innovation and its uptake, is extraordinarily slow. In particular, the famous handaxes of the Acheulian technological tradition first appeared about 1.7 Ma, and persisted with little change until about 800 ka, perhaps even longer. In this paper, I will offer an explanation of that stasis based in the life history and network characteristics that we infer (on phylogenetic grounds) to have characterized earlier human species. The core ideas are that (i) especially in earlier periods of hominin evolution, we are likely to find archaeological traces only of widespread and persisting technologies and practices; (ii) the record is not a record of the rate of innovation, but the rate of innovations establishing in a landscape; (iii) innovations are extremely vulnerable to stochastic loss while confined to the communities in which they are made and established; (iv) the export of innovation from the local group is sharply constrained if there is a general pattern of hostility and suspicion between groups, or even if there is just little contact between adults of adjoining groups. That pattern is typical of great apes and likely, therefore, to have characterized at least early hominin social lives. Innovations are unlikely to spread by adult-to-adult interactions across community boundaries. (v) Chimpanzees and bonobos are characterized by male philopatry and subadult female dispersal; that is, therefore, the most likely early hominin pattern. If so, the only innovations at all likely to expand beyond the point of origin are those acquired by subadult females, and ones that can be expressed by those females, at high enough frequency and salience for them to spread, in the bands that the females join. These are very serious filters on the spread of innovation.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
The human life history is adapted to exploit the adaptive advantages of culture
Authors: Richerson Peter J. , Boyd Robert 
Published: May 2020

Humans evolved from an ape ancestor that was highly intelligent, moderately social and moderately dependent on cultural adaptations for subsistence technology (tools). By the late Pleistocene, humans had become highly dependent on culture for subsistence and for rules to organize a complex social life. Adaptation by cultural traditions transformed our life history, leading to an extended juvenile period to learn subsistence and social skills, post-reproductive survival to help conserve and transmit skills, a dependence on social support for mothers of large-brained, very dependent and nutrient-demanding offspring, males devoting substantial effort to provisioning rather than mating, and the cultivation of large social networks to tap pools in information unavailable to less social species. One measure of the success of the exploitation of culture is that the minimum inter-birth interval of humans is nearly half that of our ape relatives. Another measure is the wide geographical distribution of humans compared with other apes, based on subsistence systems adapted to fine-scale spatial environmental variation. An important macro-evolutionary question is why our big-brained, culture-intensive life-history strategy evolved so recently and in only our lineage. We suggest that increasing spatial and temporal variation in the Pleistocene favoured cultural adaptations.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals'.
The optimal timing of teaching and learning across the life course
Authors: Gurven Michael D. , Davison Raziel J. , Kraft Thomas S. 
Published: May 2020

The evolutionary biologist W. D. Hamilton (Hamilton 1966J. Theor. Biol.12, 12–45. (doi:10.1016/0022-5193(66)90184-6)) famously showed that the force of natural selection declines with age, and reaches zero by the age of reproductive cessation. However, in social species, the transfer of fitness-enhancing resources by postreproductive adults increases the value of survival to late ages. While most research has focused on intergenerational food transfers in social animals, here we consider the potential fitness benefits of information transfer, and investigate the ecological contexts where pedagogy is likely to occur. Although the evolution of teaching is an important topic in behavioural biology and in studies of human cultural evolution, few formal models of teaching exist. Here, we present a modelling framework for predicting the timing of both information transfer and learning across the life course, and find that under a broad range of conditions, optimal patterns of information transfer in a skills-intensive ecology often involve postreproductive aged teachers. We explore several implications among human subsistence populations, evaluating the cost of hunting pedagogy and the relationship between activity skill complexity and the timing of pedagogy for several subsistence activities. Long lifespan and extended juvenility that characterize the human life history likely evolved in the context of a skills-intensive ecological niche with multi-stage pedagogy and multigenerational cooperation.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
Cognitive consequences of our grandmothering life history: cultural learning begins in infancy
Authors: Hawkes Kristen 
Published: May 2020

Postmenopausal longevity distinguishes humans from our closest living evolutionary cousins, the great apes, and may have evolved in our lineage when the economic productivity of grandmothers allowed mothers to wean earlier and overlap dependents. Since increased longevity retards development and expands brain size across the mammals, this hypothesis links our slower developing, bigger brains to ancestral grandmothering. If foraging interdependence favoured postmenopausal longevity because grandmothers' subsidies reduced weaning ages, then ancestral infants lost full maternal engagement while their slower developing brains were notably immature. With survival dependent on social relationships, sensitivity to reputations is wired very early in neural ontogeny, beginning our lifelong preoccupation with shared intentionality.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
Childhood as a solution to explore–exploit tensions
Authors: Gopnik Alison 
Published: May 2020

I argue that the evolution of our life history, with its distinctively long, protected human childhood, allows an early period of broad hypothesis search and exploration, before the demands of goal-directed exploitation set in. This cognitive profile is also found in other animals and is associated with early behaviours such as neophilia and play. I relate this developmental pattern to computational ideas about explore–exploit trade-offs, search and sampling, and to neuroscience findings. I also present several lines of empirical evidence suggesting that young human learners are highly exploratory, both in terms of their search for external information and their search through hypothesis spaces. In fact, they are sometimes more exploratory than older learners and adults.This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.
A Simple Method of Finding an Approximate Pattern of the COVID-19 Spread
Authors: Baruah Hemanta Kumar 
Published: May 2020

ABSTRACTWe are going to show that the pattern of spread of COVID-19 outside China is not monotonic. We have considered the data outside China because we are going to study the data starting from March 21, and by that time the spread had almost come to a stop in China. We have used for our analysis data on total cases outside China till April 25, 2020, and data from April 26 to April 30 for comparison of forecasts and observed values. Right from the beginning the spread pattern was nonlinear, and by the end of the third week of March the nonlinearity became nearly exponential. The exponential pattern thereafter has changed by around March 28, April 5, April 11 and April 18. Since March 21, the spread is following a nearly exponential pattern of growth changing observably at almost regular intervals of seven days. It is but natural that at some point of time the countries that had been contributing in observably large numbers to the total cases would start to show diminishing growth patterns. Therefore long term forecasts using our method would give us slightly overestimated results. However, for short term forecasting our simple method does work very well when we consider the total number of cases in the world and not in any particular country.
Local chromatin context dictates the genetic determinants of the heterochromatin spreading reaction
Authors: Greenstein R.A. , Ng Henry , Barrales Ramon R. , Tan Catherine , Braun Sigurd , Al-Sady Bassem 
Published: May 2020

ABSTRACTHeterochromatin spreading, the expansion of gene-silencing structures from DNA-encoded nucleation sites, occurs in distinct settings. Spreading re-establishes gene-poor constitutive heterochromatin every cell cycle, but also invades gene-rich euchromatin de novo to steer cell fate decisions. How chromatin context, i.e. euchromatic, heterochromatic, or different nucleator types, influences the determinants of this process remains poorly understood. By screening a nuclear function gene deletion library in fission yeast using a previously established heterochromatin spreading sensor system, we identified regulators that positively or negatively alter the propensity of a nucleation site to spread heterochromatin. We find that different chromatin contexts are dependent on unique sets of genes for the regulation of heterochromatin spreading. Further, we find that spreading in constitutive heterochromatin requires Clr6 histone deacetylase complexes containing the Fkh2 transcription factor, while the Clr3 deacetylase is globally required for silencing. Fkh2 acts by recruiting Clr6 to nucleation-distal chromatin sites. Our results segregate the pathways that control lateral heterochromatin spreading from those that instruct DNA-directed assembly in nucleation.
Decoding the role of CBLB for innate immune responses regulating systemic dissemination during Non-Tuberculous Mycobacteria infection
Authors: Mudalagiriyappa Srinivasu , Sharma Jaishree , Abdelaal Hazem F. M. , Kelly Thomas C. , Choi Woosuk , Vieson Miranda D. , Talaat Adel M. , Nanjappa Som G. 
Published: May 2020

AbstractNon-Tuberculous Mycobacteria (NTM) are ubiquitous in nature, present in soil and water, and cause primary leading to disseminated infections in immunocompromised individuals. NTM infections are surging in recent years due to an increase in an immune-suppressed population, medical interventions, and patients with underlying lung diseases. Host regulators of innate immune responses, frontiers for controlling infections and dissemination, are poorly defined during NTM infections. Here, we describe the role of CBLB, an E3-ubiquitin ligase, for innate immune responses and disease progression in a mouse model of NTM infection under compromised T-cell immunity. We found that CBLB thwarted NTM growth and dissemination in a time- and infection route- dependent manner. Mechanistically, we uncovered defects in many innate immune cells in the absence ofCblb, including poor responses of NK cells, inflammatory monocytes, and conventional dendritic cells. Strikingly, Cblb-deficient macrophages were competent to control NTM growthin vitro. Histopathology suggested the lack of early formation of granulomatous inflammation in the absence of CBLB. Collectively, CBLB is essential to mount productive innate immune responses and help prevent the dissemination during an NTM infection under T-cell deficiency.
Pervasive additive and non-additive effects within the HLA region contribute to disease risk in the UK Biobank
Authors: Venkataraman Guhan Ram , Olivieri Julia Eve , DeBoever Christopher , Tanigawa Yosuke , Justesen Johanne Marie , Dilthey Alexander , Rivas Manuel A. 
Published: May 2020

AbstractThe human leukocyte antigen (HLA) region is one of the most disease-associated regions of the human genome, yet even well-studied alleles in the HLA region have unknown impact on disease. Here, we study the effect of 156 HLA alleles on 677 binary phenotypes for 337,138 individuals in the UK Biobank. We assess HLA allele associations and subsequently use Bayesian Model Averaging for conditional analysis, a) replicating 88 known associations between HLA alleles and binary disease phenotypes such as cancer, and b) discovering 90 novel associations to phenotypes such as skin and reproductive tract cancers and to other phenotypes not previously associated with the HLA region (e.g. anemias and acne). We find several non-additive effects, suggesting a more complex landscape of disease-modifying effects throughout the region. Finally, we discover associations between homozygous HLA allele burden and several cancer and other phenotypes, suggesting that peptide presentation spectra as coded for by the HLA region are important in determining disease risk. Our results demonstrate the HLA region’s complexity and richness while underscoring its clinical relevance.
CREBBPandSTAT6co-mutation and 16p13 and 1p36 loss define the t(14;18)-negative diffuse variant of follicular lymphoma
Authors: Xian Rena R. , Xie Yi , Haley Lisa M. , Yonescu Raluca , Pallavajjala Aparna , Pittaluga Stefania , Jaffe Elaine S. , Duffield Amy S. , McCall Chad M. , Gheith Shereen M. F. , Gocke Christopher D. 
Published: May 2020

AbstractThe diffuse variant of follicular lymphoma (dFL) is a rare variant of FL lacking t(14;18) that was first described in 2009. In this study, we use a comprehensive approach to define unifying pathologic and genetic features through gold-standard pathologic review, FISH, SNP-microarray and next-generation sequencing of 16 cases of dFL. We found unique morphologic features, including interstitial sclerosis, microfollicle formation, and rounded nuclear cytology, confirmed absence of t(14;18) and recurrent deletion of 1p36, and showed a novel association with deletion/CN-LOH of 16p13 (inclusive ofCREBBP, CIITAandSOCS1). Mutational profiling demonstrated near-uniform mutations inCREBBPandSTAT6, with clonal dominance ofCREBBP, among other mutations typical of germinal-center B-cell lymphomas. FrequentCREBBPandCIITAco-deletion/mutation suggested a mechanism for immune evasion, while subclonalSTAT6activating mutations with concurrentSOCS1loss suggested a mechanism of BCL-xL/BCL2L1 upregulation in the absence ofBCL2rearrangements. A review of the literature showed significant enrichment for 16p13 and 1p36 loss/CN-LOH,STAT6mutation, andCREBBPandSTAT6co-mutation in dFL, as compared to conventional FL. With this comprehensive approach, our study demonstrates confirmatory and novel genetic associations that can aid in the diagnosis and subclassification of this rare type of lymphoma.
Correction for both common and rare cell types in blood is important to identify genes that correlate with age
Authors: Pellegrino Coppola Damiano , Claringbould Annique , Stutvoet Maartje ,   BIOS Consortium, Boomsma Dorret I. , Ikram M. Arfan , Slagboom Eline , Westra Harm-Jan , Franke Lude 
Published: May 2020

AbstractBackgroundAging is a multifactorial process that affects multiple tissues and is characterized by changes in homeostasis over time, leading to increased morbidity. Whole blood gene expression signatures have been associated with aging and have been used to gain information on its biological mechanisms, which are still not fully understood. However, blood is composed of many cell types whose proportions in blood vary with age. As a result, previously observed associations between gene expression levels and aging might be driven by cell type composition rather than intracellular aging mechanisms. To overcome this, previous aging studies already accounted for major cell types, but the possibility that the reported associations are false positives driven by less prevalent cell subtypes remains.ResultsHere, we compared the regression model from our previous work to an extended model that corrects for 33 additional white blood cell subtypes. Both models were applied to whole blood gene expression data from 3165 individuals belonging to the general population (age range of 18-81 years). We evaluated that the new model is a better fit for the data and it identified fewer genes associated with aging (625, compared to the 2808 of the initial model; P ≤ 2.5 × 10−6). Moreover, 511 genes (∼18% of the 2,808 genes identified by the initial model) were found using both models, indicating that the other previously reported genes could be proxies for less abundant cell types. In particular, functional enrichment of the genes identified by the new model highlighted pathways and GO terms specifically associated with platelet activity.ConclusionsWe conclude that gene expression analyses in blood strongly benefit from correction for both common and rare blood cell types, and recommend using blood-cell count estimates as standard covariates when studying whole blood gene expression.
Computational hypothesis: How Intra-hepatic functional heterogeneity may influence the cascading progression of free fatty acid-induced non-alcoholic fatty liver disease (NAFLD)
Authors: Holzhütter Hermann-Georg , Berndt Nikolaus 
Published: May 2020

AbstractNon-Alcoholic Fatty Liver Disease (NAFLD) is the most common type of chronic liver disease in developed nations, affecting around 25% of the population. Elucidating the factors causing NAFLD in individual patients to progress in different rates and to different degrees of severity, is a matter of active medical research. Here, we aim to provide evidence that the intra-hepatic heterogeneity of rheological, metabolic and tissue-regenerating capacities plays a central role in disease progression. We developed a generic mathematical model that constitutes the liver as ensemble of small liver units differing in their capacities to metabolize potentially cytotoxic free fatty acids (FFAs) and to repair FFA-induced cell damage. Transition from simple steatosis to more severe forms of NAFLD is described as self-amplifying process of cascading liver failure, which to stop depends essentially on the distribution of functional capacities across the liver. Model simulations provided the following insights: (1) A persistently high plasma level of FFAs is sufficient to drive the liver through different stages of NAFLD; (2) Presence of NAFLD amplifies the deleterious impact of additional tissue-damaging hits; and (3) Coexistence of non-steatotic and highly steatotic regions is indicative for the later occurrence of severe NAFLD stages.