The animal nature of spontaneous human laughter

a b s t r a c t a r t i c l e i n f o Laughter is a universally produced vocal signal that plays an important role in human social interaction. Researchers have distinguished between spontaneous and volitional laughter, but no empirical work has explored possible acoustic and perceptual differences. If spontaneous laughter is an honest signal of cooperative intent (e.g., derived from play breathing patterns), then the ability to mimic these sounds volitionally could have shaped perceptual systems to be attuned to aspects of spontaneous laughs that are harder to fake-features associated with phylogenetically older vocal control mechanisms. We extracted spontaneous laughs from conversations between friends and volitional laughs elicited by instruction without other provocation. In three perception experiments we found that, 1) participants could distinguish between spontaneous and volitional laughter, 2) when laugh speed was increased (duration decreased 33% and pitch held constant), all laughs were judged as more "real," with judgment accuracy increasing for spontaneous laughter and decreasing for volitional laughter, and 3) when the laughs were slowed down (duration increased 260% and pitch altered proportionally), participants could not distinguish spontaneous laughs from nonhuman vocalizations but could identify volitional laughs as human-made. These findings and acoustic data suggest that spontaneous and volitional laughs are produced by different vocal systems, and that spontaneous laughter might share features with nonhuman animal vocalizations that volitional laughter does not

The future of evolutionary medicine: sparking innovation in biomedicine and public health

Evolutionary medicine - i.e. the application of insights from evolution and ecology to biomedicine - has tremendous untapped potential to spark transformational innovation in biomedical research, clinical care and public health. Fundamentally, a systematic mapping across the full diversity of life is required to identify animal model systems for disease vulnerability, resistance, and counter-resistance that could lead to novel clinical treatments. Evolutionary dynamics should guide novel therapeutic approaches that target the development of treatment resistance in cancers (e.g., via adaptive or extinction therapy) and antimicrobial resistance (e.g., via innovations in chemistry, antimicrobial usage, and phage therapy). With respect to public health, the insight that many modern human pathologies (e.g., obesity) result from mismatches between the ecologies in which we evolved and our modern environments has important implications for disease prevention. Life-history evolution can also shed important light on patterns of disease burden, for example in reproductive health. Experience during the COVID-19 (SARS-CoV-2) pandemic has underlined the critical role of evolutionary dynamics (e.g., with respect to virulence and transmissibility) in predicting and managing this and future pandemics, and in using evolutionary principles to understand and address aspects of human behavior that impede biomedical innovation and public health (e.g., unhealthy behaviors and vaccine hesitancy). In conclusion, greater interdisciplinary collaboration is vital to systematically leverage the insight-generating power of evolutionary medicine to better understand, prevent, and treat existing and emerging threats to human, animal, and planetary health

Descriptive Norms Caused Increases in Mask Wearing During the COVID-19 Pandemic

Human sociality is governed by two types of social norms: injunctive norms, which prescribe what people ought to do, and descriptive norms, which reflect what people actually do. The process by which these norms emerge and their causal influences on cooperative behavior over time are not well understood. Here, we study these questions through social norms influencing mask wearing during the COVID-19 pandemic. Leveraging 2 years of data from the United States (18 time points; n = 915), we tracked mask wearing and perceived injunctive and descriptive mask wearing norms as the pandemic unfolded. Longitudinal trends suggested that norms and behavior were tightly coupled, changing quickly in response to public health recommendations. In addition, longitudinal modeling revealed that descriptive norms caused future increases in mask wearing across multiple waves of data collection. These cross-lagged causal effects of descriptive norms were large, even after controlling for non-social beliefs and demographic variables. Injunctive norms, by contrast, had less frequent and generally weaker causal effects on future mask wearing. During uncertain times, cooperative behavior is more strongly driven by what others are actually doing, rather than what others think ought to be done

Understanding cooperation through fitness interdependence

Some acts of human cooperation are not easily explained by traditional models of kinship or reciprocity. Fitness interdependence may provide a unifying conceptual framework, in which cooperation arises from the mutual dependence for survival or reproduction, as occurs among mates, risk-pooling partnerships and brothers-in-arms

Ionizing radiation, higher plants, and radioprotection: From acute high doses to chronic low doses

© 2018 Caplin and Willey. Understanding the effects of ionizing radiation (IR) on plants is important for environmental protection, for agriculture and horticulture, and for space science but plants have significant biological differences to the animals from which much relevant knowledge is derived. The effects of IR on plants are understood best at acute high doses because there have been; (a) controlled experiments in the field using point sources, (b) field studies in the immediate aftermath of nuclear accidents, and (c) controlled laboratory experiments. A compilation of studies of the effects of IR on plants reveals that although there are numerous field studies of the effects of chronic low doses on plants, there are few controlled experiments that used chronic low doses. Using the Bradford-Hill criteria widely used in epidemiological studies we suggest that a new phase of chronic low-level radiation research on plants is desirable if its effects are to be properly elucidated. We emphasize the plant biological contexts that should direct such research. We review previously reported effects from the molecular to community level and, using a plant stress biology context, discuss a variety of acute high-and chronic low-dose data against Derived Consideration Reference Levels (DCRLs) used for environmental protection. We suggest that chronic low-level IR can sometimes have effects at the molecular and cytogenetic level at DCRL dose rates (and perhaps below) but that there are unlikely to be environmentally significant effects at higher levels of biological organization. We conclude that, although current data meets only some of the Bradford-Hill criteria, current DCRLs for plants are very likely to be appropriate at biological scales relevant to environmental protection (and for which they were intended) but that research designed with an appropriate biological context and with more of the Bradford-Hill criteria in mind would strengthen this assertion. We note that the effects of IR have been investigated on only a small proportion of plant species and that research with a wider range of species might improve not only the understanding of the biological effects of radiation but also that of the response of plants to environmental stress

Classifying the evolutionary and ecological features of neoplasms

The consensus conference was supported by Wellcome Genome Campus Advanced Courses and Scientific Conferences. C.C.M. is supported in part by US NIH grants P01 CA91955, R01 CA149566, R01 CA170595, R01 CA185138 and R01 CA140657 as well as CDMRP Breast Cancer Research Program Award BC132057. M.J. is supported by NIH grant K99CA201606. K.S.A. is supported by NCI 5R21 CA196460. K. Polyak is supported by R35 CA197623, U01 CA195469, U54 CA193461, and the Breast Cancer Research Foundation. K.J.P. is supported by NIH grants CA143803, CA163124, CA093900 and CA143055. D.P. is supported by the European Research Council (ERC-617457- PHYLOCANCER), the Spanish Ministry of Economy and Competitiveness (BFU2015-63774-P) and the Education, Culture and University Development Department of the Galician Government. K.S.A. is supported in part by the Breast Cancer Research Foundation and NCI R21CA196460. C.S. is supported by the Royal Society, Cancer Research UK (FC001169), the UK Medical Research Council (FC001169), and the Wellcome Trust (FC001169), NovoNordisk Foundation (ID 16584), the Breast Cancer Research Foundation (BCRF), the European Research Council (THESEUS) and Marie Curie Network PloidyNet. T.A.G. is a Cancer Research UK fellow and a Wellcome Trust funded Investigator. E.S.H. is supported by R01 CA185138-01 and W81XWH-14-1-0473. M.Gerlinger is supported by Cancer Research UK and The Royal Marsden/ICR National Institute of Health Research Biomedical Research Centre. M.Ge., M.Gr., Y.Y., and A.So. were also supported in part by the Wellcome Trust [105104/Z/14/Z]. J.D.S. holds the Edward B. Clark, MD Chair in Pediatric Research, and is supported by the Primary Children's Hospital (PCH) Pediatric Cancer Research Program, funded by the Intermountain Healthcare Foundation and the PCH Foundation. A.S. is supported by the Chris Rokos Fellowship in Evolution and Cancer. Y.Y. is a Cancer Research UK fellow and supported by The Royal Marsden/ICR National Institute of Health Research Biomedical Research Centre. E.S.H. was supported in part by PCORI grants 1505–30497 and 1503–29572, NIH grants R01 CA185138, T32 CA093245, and U10 CA180857, CDMRP Breast Cancer Research Program Award BC132057, a CRUK Grand Challenge grant, and the Breast Cancer Research Foundation. A.R.A.A. was funded in part by NIH grant U01CA151924. A.R.A.A., R.G. and J.S.B. were funded in part by NIH grant U54CA193489

Evolutionary foundations for cancer biology

New applications of evolutionary biology are transforming our understanding of cancer. The articles in this special issue provide many specific examples, such as microorganisms inducing cancers, the significance of within‐tumor heterogeneity, and the possibility that lower dose chemotherapy may sometimes promote longer survival. Underlying these specific advances is a large‐scale transformation, as cancer research incorporates evolutionary methods into its toolkit, and asks new evolutionary questions about why we are vulnerable to cancer. Evolution explains why cancer exists at all, how neoplasms grow, why cancer is remarkably rare, and why it occurs despite powerful cancer suppression mechanisms. Cancer exists because of somatic selection; mutations in somatic cells result in some dividing faster than others, in some cases generating neoplasms. Neoplasms grow, or do not, in complex cellular ecosystems. Cancer is relatively rare because of natural selection; our genomes were derived disproportionally from individuals with effective mechanisms for suppressing cancer. Cancer occurs nonetheless for the same six evolutionary reasons that explain why we remain vulnerable to other diseases. These four principles—cancers evolve by somatic selection, neoplasms grow in complex ecosystems, natural selection has shaped powerful cancer defenses, and the limitations of those defenses have evolutionary explanations—provide a foundation for understanding, preventing, and treating cancer.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/96232/1/eva12034.pd

When to walk away and when to stay: Cooperation evolves when agents can leave uncooperative partners and groups

Cooperation among group members, coworkers and community members can provide benefits for all involved parties. However, groups of all kinds are plagued by free riders, or individuals who take advantage of cooperative group members by benefiting from being a part of the group without contributing, resulting in a social dilemma or \u27tragedy of the commons.\u27 This phenomenon is not unique to humans; free riders can be identified in organisms as simple as bacteria. This has lead to the puzzling question of how cooperation is maintained in social groups of humans and other animals, given higher payoffs for free riding than for cooperation. In order to address this question, I simulate individuals who use a simple Walk Away rule to leave uncooperative partners or groups, and show that cooperation is favored under a variety of parameter values when agents can use this rule. When agents use the Walk Away rule, more cooperative partnerships and groups are more stable than less cooperative ones. This promotes assortment, or the preferential interaction of cooperators with one another, which favors the evolution of cooperation. It is shown that in dyadic partnerships Walk Away can outperform the well-known Tit-for-Tat strategy. In group-wise interactions, the Walk Away rule generates large number of relatively small groups and differential group stability based on average cooperativeness. These features maintain selection for cooperation by generating population structures that promote group selection. The simple Walk Away rule does not require complex individual level abilities such as long-term memory, recognition of group members or punishment, suggesting that complex cognitive abilities are not necessary for cooperation to be promoted