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Intra-group relatedness affects parental and helper investment rules in offspring care
In any system where multiple individuals jointly contribute to rearing offspring, conflict is expected to arise
over the relative contributions of each carer. Existing theoretical work on the conflict over care has: (a)
rarely considered the influence of tactical investment during offspring production on later contributions to
offspring rearing; (b) concentrated mainly on biparental care, rather than cooperatively caring groups
comprising both parents and helpers; and (c) typically ignored relatedness between carers as a potential
influence on investment behavior. We use a game-theoretical approach to explore the effects of female
production tactics and differing group relatedness structures on the expected rearing investment contributed
by breeding females, breeding males, and helpers in cooperative groups. Our results suggest that the
breeding female should pay higher costs overall when helpful helpers are present, as she produces additional
offspring to take advantage of the available care. We find that helpers related to offspring through the
breeding female rather than the breeding male should contribute less to care, and decrease their contribution
as group size increases, because the female refrains from producing additional offspring to exploit them.
Finally, within-group variation in helper relatedness also affects individual helper investment rules by
inflating the differences between the contributions to care of dissimilar helpers. Our findings underline the
importance of considering maternal investment decisions during offspring production to understand
investment across the entire breeding attempt, and provide empirically testable predictions concerning the
interplay between maternal, paternal and helper investment and how these are modified by different
relatedness structures.This work was supported by a Natural Environment Research Council Studentship to the University of Cambridge
(J.L.S.) and by a Royal Society University Research Fellowship (A.F.R.)This is the author accepted manuscript. The final version can be found on the publisher's website at: http://link.springer.com/article/10.1007%2Fs00265-013-1595-5# © Springer-Verlag Berlin Heidelberg 201
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Maternal costs in offspring production affect investment rules in joint rearing
When multiple individuals contribute to rearing the same offspring, conflict is expected to occur over the
relative amounts invested by each carer. Existing models of biparental care suggest that this conflict should
be resolved by partially compensating for changes by co-investors, but this has yet to be explicitly modeled
in cooperative breeders over a range of carer numbers. In addition, existing models of biparental and
cooperative care ignore potential variation in both the relative costs of offspring production to mothers and in
maternal allocation decisions. If mothers experience particularly high costs during offspring production, this
might be expected to affect their investment strategies during later offspring care. Here we show using a
game-theoretical model that a range of investment tactics can result depending on the number of carers and
the relative costs to the mother of the different stages within the breeding attempt. Additional carers result in
no change in investment by individuals when production costs are low, as mothers can take advantage of the
greater potential investment by increasing offspring number; however this tactic ultimately results in a
decrease in care delivered to each offspring. Conversely, when production costs prevent the mother from
increasing offspring number, our model predicts that other individuals should partially compensate for
additional carers and hence offspring should each receive a greater amount of care. Our results reinforce the
importance of considering investment across all stages in a breeding attempt, and provide some explanatory
power for the variation in investment rules observed across cooperative species.This work was supported by a Natural Environment Research Council studentship to
JLS, and by a Royal Society University Research Fellowship to AFR.This is the author accepted manuscript. The final version can be found on the publisher's website at: http://beheco.oxfordjournals.org/content/early/2012/11/20/beheco.ars203 © The Author 2012. Published by Oxford University Press on behalf of the International Society for Behavioral Ecology. All rights reserved
A consistent picture for large penguins in D -> pi+ pi-, K+ K-
A long-standing puzzle in charm physics is the large difference between the
D0 -> K+ K- and D0 -> pi+ pi- decay rates. Recently, the LHCb and CDF
collaborations reported a surprisingly large difference between the direct CP
asymmetries, Delta A_CP, in these two modes. We show that the two puzzles are
naturally related in the Standard Model via s- and d-quark "penguin
contractions". Their sum gives rise to Delta A_CP, while their difference
contributes to the two branching ratios with opposite sign. Assuming nominal
SU(3) breaking, a U-spin fit to the D0 -> K+ pi-, pi+ K-, pi+ pi-, K+ K- decay
rates yields large penguin contractions that naturally explain Delta A_CP.
Expectations for the individual CP asymmetries are also discussed.Comment: 24 pages, 8 figure
Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis
: Higher circulating levels of the branched-chain amino acids (BCAAs; i.e., isoleucine, leucine, and valine) are strongly associated with higher type 2 diabetes risk, but it is not known whether this association is causal. We undertook large-scale human genetic analyses to address this question.
: Genome-wide studies of BCAA levels in 16,596 individuals revealed five genomic regions associated at genome-wide levels of significance (p < 5 × 10-8). The strongest signal was 21 kb upstream of the PPM1K gene (beta in standard deviations [SDs] of leucine per allele = 0.08, p = 3.9 × 10-25), encoding an activator of the mitochondrial branched-chain alpha-ketoacid dehydrogenase (BCKD) responsible for the rate-limiting step in BCAA catabolism. In another analysis, in up to 47,877 cases of type 2 diabetes and 267,694 controls, a genetically predicted difference of 1 SD in amino acid level was associated with an odds ratio for type 2 diabetes of 1.44 (95% CI 1.26-1.65, p = 9.5 × 10-8) for isoleucine, 1.85 (95% CI 1.41-2.42, p = 7.3 × 10-6) for leucine, and 1.54 (95% CI 1.28-1.84, p = 4.2 × 10-6) for valine. Estimates were highly consistent with those from prospective observational studies of the association between BCAA levels and incident type 2 diabetes in a meta-analysis of 1,992 cases and 4,319 non-cases. Metabolome-wide association analyses of BCAA-raising alleles revealed high specificity to the BCAA pathway and an accumulation of metabolites upstream of branched-chain alpha-ketoacid oxidation, consistent with reduced BCKD activity. Limitations of this study are that, while the association of genetic variants appeared highly specific, the possibility of pleiotropic associations cannot be entirely excluded. Similar to other complex phenotypes, genetic scores used in the study captured a limited proportion of the heritability in BCAA levels. Therefore, it is possible that only some of the mechanisms that increase BCAA levels or affect BCAA metabolism are implicated in type 2 diabetes.
: Evidence from this large-scale human genetic and metabolomic study is consistent with a causal role of BCAA metabolism in the aetiology of type 2 diabetes.MRC Epidemiology Unit, Fenland study, EPIC-InterAct study, EPIC-Norfolk case-cohort study funding: this study was funded by the United Kingdom’s Medical Research Council through grants MC_UU_12015/1, MC_UU_12015/5, MC_PC_13046, MC_PC_13048 and MR/L00002/1. We acknowledge support from the National Institute for Health Research Biomedical Research Centre. The research leading to these results has received support from the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement number 115372, resources of which are composed of financial contribution from the European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA companies’ in kind contribution. EPIC-InterAct Study funding: funding for the InterAct project was provided by the EU FP6 programme (grant number LSHM_CT_2006_037197). MRC Human Nutrition Research funding: This research was supported by the Medical Research Council (MC_UP_A090_1006) and Cambridge Lipidomics Biomarker Research Initiative (G0800783). The SABRE study was funded at baseline by the UK Medical Research Council, Diabetes UK and the British Heart Foundation and at follow-up by a programme grant from the Wellcome Trust (WT082464) and British Heart Foundation (SP/07/001/23603); Diabetes UK funded the metabolomics analyses (13/0004774). RJOS, EN, JRZ and AK received funding from the Swedish Research Council, Stockholm County Council, Novo Nordisk Foundation and Diabetes Wellness. DBS is supported by the Wellcome Trust grant number 107064. MIM is a Wellcome Trust Senior Investigator and is supported by the following grants from the Wellcome Trust: 090532 and 098381. IB is supported by the Wellcome Trust grant WT098051
Building Babies - Chapter 16
In contrast to birds, male mammals rarely help to raise the offspring. Of all mammals, only among rodents, carnivores, and primates, males are sometimes intensively engaged in providing infant care (Kleiman and Malcolm 1981). Male caretaking of infants has long been recognized in nonhuman primates (Itani 1959). Given that infant care behavior can have a positive effect on the infant’s development, growth, well-being, or survival, why are male mammals not more frequently involved in “building babies”? We begin the chapter defining a few relevant terms and introducing the theory and hypotheses that have historically addressed the evolution of paternal care. We then review empirical findings on male care among primate taxa, before focusing, in the final section, on our own work on paternal care in South American owl monkeys (Aotus spp.). We conclude the chapter with some suggestions for future studies.Deutsche Forschungsgemeinschaft (HU 1746/2-1)
Wenner-Gren Foundation, the L.S.B. Leakey Foundation, the National Geographic Society, the National Science Foundation (BCS-0621020), the University of Pennsylvania Research Foundation, the Zoological Society of San Dieg
Genetic predisposition to an impaired metabolism of the branched-chain amino acids and risk of type 2 diabetes: a mendelian randomisation analysis
BACKGROUND: Higher circulating levels of the branched-chain amino acids (BCAAs; i.e., isoleucine, leucine, and valine) are strongly associated with higher type 2 diabetes risk, but it is not known whether this association is causal. We undertook large-scale human genetic analyses to address this question. METHODS AND FINDINGS: Genome-wide studies of BCAA levels in 16,596 individuals revealed five genomic regions associated at genome-wide levels of significance (p < 5 × 10-8). The strongest signal was 21 kb upstream of the PPM1K gene (beta in standard deviations [SDs] of leucine per allele = 0.08, p = 3.9 × 10-25), encoding an activator of the mitochondrial branched-chain alpha-ketoacid dehydrogenase (BCKD) responsible for the rate-limiting step in BCAA catabolism. In another analysis, in up to 47,877 cases of type 2 diabetes and 267,694 controls, a genetically predicted difference of 1 SD in amino acid level was associated with an odds ratio for type 2 diabetes of 1.44 (95% CI 1.26-1.65, p = 9.5 × 10-8) for isoleucine, 1.85 (95% CI 1.41-2.42, p = 7.3 × 10-6) for leucine, and 1.54 (95% CI 1.28-1.84, p = 4.2 × 10-6) for valine. Estimates were highly consistent with those from prospective observational studies of the association between BCAA levels and incident type 2 diabetes in a meta-analysis of 1,992 cases and 4,319 non-cases. Metabolome-wide association analyses of BCAA-raising alleles revealed high specificity to the BCAA pathway and an accumulation of metabolites upstream of branched-chain alpha-ketoacid oxidation, consistent with reduced BCKD activity. Limitations of this study are that, while the association of genetic variants appeared highly specific, the possibility of pleiotropic associations cannot be entirely excluded. Similar to other complex phenotypes, genetic scores used in the study captured a limited proportion of the heritability in BCAA levels. Therefore, it is possible that only some of the mechanisms that increase BCAA levels or affect BCAA metabolism are implicated in type 2 diabetes. CONCLUSIONS: Evidence from this large-scale human genetic and metabolomic study is consistent with a causal role of BCAA metabolism in the aetiology of type 2 diabetes
Capturing Community Context of Human Response to Forest Disturbance by Insects: A Multi-Method Assessment
The socioeconomic and environmental features of local places (community context) influence the relationship between humans and their physical environment. In times of environmental disturbance, this community context is expected to influence human perceptual and behavioral responses. Residents from nine Colorado communities experiencing a large outbreak of mountain pine beetles (Dendroctonus ponderosae) were surveyed in 2007. Multiple analytic methods including ordinary least squares regression and multilevel modeling techniques were used to evaluate a community-context conceptual model of factors influencing individual actions in response to forest disturbance by beetles. Results indicated that community biophysical and socioeconomic characteristics had important impacts on participation in beetle-related actions and influenced the relationships of individual-level variables in the conceptual model with beetle-related activities. Our findings have implications for natural resource management and policy related to forest disturbances, and for developing a methodology appropriate to measure the general community context of human-environment interactions
Chimpanzees modify intentional gestures to coordinate a search for hidden food
Humans routinely communicate to coordinate their activities, persisting and elaborating signals to pursue goals that cannot be accomplished individually. Communicative persistence is associated with complex cognitive skills such as intentionality, because interactants modify their communication in response to another's understanding of their meaning. Here we show that two language-trained chimpanzees effectively use intentional gestures to coordinate with an experimentally naive human to retrieve hidden food, providing some of the most compelling evidence to date for the role of communicative flexibility in successful coordination in nonhumans. Both chimpanzees (named Panzee and Sherman) increase the rate of nonindicative gestures when the experimenter approaches the location of the hidden food. Panzee also elaborates her gestures in relation to the experimenter's pointing, which enables her to find food more effectively than Sherman. Communicative persistence facilitates effective communication during behavioural coordination and is likely to have been important in shaping language evolution
Caveolin-1 expression in benign and malignant lesions of the breast
This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens
Surviving pediatric intensive care: physical outcome after 3 months
Objective: This study investigated the prevalence and nature of physical and neurocognitive sequelae in pediatric intensive care unit ( PICU) survivors. Design and setting: Prospective follow-up study 3 months after discharge from a 14-bed tertiary PICU in The Netherlands. Patients and participants: The families of 250 previously healthy children unexpectedly admitted to the PICU were invited to visit the outpatient follow-up clinic for structured medical examination of the child 3 months after discharge; 186 patients were evaluated. Measurements and results: Pediatric Cerebral Performance Category ( PCPC) and Pediatric Overall Performance Category ( POPC) values were determined at PICU discharge, at the outpatient follow-up clinic, and retrospectively before admission to the PICU. We found that 69% of children had physical sequelae. In 30% of cases these were caused by a previously unknown illness and in 39% by acquired morbidity. In 8% of the children the acquired morbidity was related to complications from PICU procedures. Three months after discharge 77% of the children had normal PCPC scores and 31% had normal POPC scores. Conclusions: Our results indicate that PICU survival may be associated with substantial physical sequelae. Structured follow-up research, preferably by multicenter studies, is warranted in PICU survivor
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