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      Fetal microchimerism and maternal health: A review and evolutionary analysis of cooperation and conflict beyond the womb

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          Abstract

          The presence of fetal cells has been associated with both positive and negative effects on maternal health. These paradoxical effects may be due to the fact that maternal and offspring fitness interests are aligned in certain domains and conflicting in others, which may have led to the evolution of fetal microchimeric phenotypes that can manipulate maternal tissues. We use cooperation and conflict theory to generate testable predictions about domains in which fetal microchimerism may enhance maternal health and those in which it may be detrimental. This framework suggests that fetal cells may function both to contribute to maternal somatic maintenance (e.g. wound healing) and to manipulate maternal physiology to enhance resource transmission to offspring (e.g. enhancing milk production). In this review, we use an evolutionary framework to make testable predictions about the role of fetal microchimerism in lactation, thyroid function, autoimmune disease, cancer and maternal emotional, and psychological health.

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          The delayed rise of present-day mammals.

          Did the end-Cretaceous mass extinction event, by eliminating non-avian dinosaurs and most of the existing fauna, trigger the evolutionary radiation of present-day mammals? Here we construct, date and analyse a species-level phylogeny of nearly all extant Mammalia to bring a new perspective to this question. Our analyses of how extant lineages accumulated through time show that net per-lineage diversification rates barely changed across the Cretaceous/Tertiary boundary. Instead, these rates spiked significantly with the origins of the currently recognized placental superorders and orders approximately 93 million years ago, before falling and remaining low until accelerating again throughout the Eocene and Oligocene epochs. Our results show that the phylogenetic 'fuses' leading to the explosion of extant placental orders are not only very much longer than suspected previously, but also challenge the hypothesis that the end-Cretaceous mass extinction event had a major, direct influence on the diversification of today's mammals.
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            How stem cells age and why this makes us grow old.

            Recent data suggest that we age, in part, because our self-renewing stem cells grow old as a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such as changes in their supporting niches. Mechanisms that suppress the development of cancer, such as senescence and apoptosis, which rely on telomere shortening and the activities of p53 and p16(INK4a), may also induce an unwanted consequence: a decline in the replicative function of certain stem-cell types with advancing age. This decreased regenerative capacity appears to contribute to some aspects of mammalian ageing, with new findings pointing to a 'stem-cell hypothesis' for human age-associated conditions such as frailty, atherosclerosis and type 2 diabetes.
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              Oxytocin pathways and the evolution of human behavior.

              C Carter (2014)
              This review examines the hypothesis that oxytocin pathways--which include the neuropeptide oxytocin, the related peptide vasopressin, and their receptors--are at the center of physiological and genetic systems that permitted the evolution of the human nervous system and allowed the expression of contemporary human sociality. Unique actions of oxytocin, including the facilitation of birth, lactation, maternal behavior, genetic regulation of the growth of the neocortex, and the maintenance of the blood supply to the cortex, may have been necessary for encephalization. Peptide-facilitated attachment also allows the extended periods of nurture necessary for the emergence of human intellectual development. In general, oxytocin acts to allow the high levels of social sensitivity and attunement necessary for human sociality and for rearing a human child. Under optimal conditions oxytocin may create an emotional sense of safety. Oxytocin dynamically moderates the autonomic nervous system, and effects of oxytocin on vagal pathways, as well as the antioxidant and anti-inflammatory effects of this peptide, help to explain the pervasive adaptive consequences of social behavior for emotional and physical health.
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                Author and article information

                Journal
                Bioessays
                Bioessays
                10.1002/(ISSN)1521-1878
                BIES
                Bioessays
                John Wiley and Sons Inc. (Hoboken )
                0265-9247
                1521-1878
                28 August 2015
                October 2015
                : 37
                : 10 ( doiID: 10.1002/bies.v37.10 )
                : 1106-1118
                Affiliations
                [ 1 ] Department of PsychologyArizona State University Tempe AZUSA
                [ 2 ] Center for Evolution and CancerUniversity of California San Francisco San Francisco CAUSA
                [ 3 ] Center for Evolution and Medicine The Biodesign InstituteArizona State University Tempe AZUSA
                [ 4 ] School of Life SciencesArizona State University Tempe AZUSA
                Author notes
                [*] [* ] Corresponding author:

                Amy M. Boddy

                E‐mail: amyboddy@ 123456gmail.com

                [†]

                Co‐senior authors.

                Article
                BIES201500059
                10.1002/bies.201500059
                4712643
                26316378
                83a9578c-fa19-42f3-9896-22b537d63f8b
                © 2015 The Authors. BioEssays Published by WILEY Periodicals, Inc.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Page count
                Pages: 13
                Funding
                Funded by: National Institutes of Health
                Award ID: R01 CA170595
                Award ID: R01 CA185138
                Award ID: NIH/NCI R01 PQC3
                Funded by: Genomic and Microenvironmental Diversity as Drivers of Progression
                Funded by: Biodesign Institute
                Categories
                Prospects & Overviews
                Prospects & Overviews
                Review Essays
                Custom metadata
                2.0
                bies201500059
                October 2015
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:06.10.2016

                Cell biology
                attachment,autoimmune disease,cancer,inflammation,lactation,maternal‐fetal conflict,parent‐offspring conflict

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