{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T01:09:52Z","timestamp":1773450592543,"version":"3.50.1"},"reference-count":54,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2018,1,1]],"date-time":"2018-01-01T00:00:00Z","timestamp":1514764800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,12,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Extracellular histones support rodent and human embryo development in at least two ways. First, these molecules in uterine secretions protect embryos from inflammation caused by pathogens that gain access to the reproductive tract. Also, histones in uterine secretions likely support penetration of the uterine epithelium by blastocysts during embryo implantation. Extracellular histones seem to preserve amino acid transport system B\n                    <jats:sup>0,+<\/jats:sup>\n                    in blastocysts by inhibiting its activity. Preservation of system B\n                    <jats:sup>0,+<\/jats:sup>\n                    is needed because, at the time of invasion of the uterine epithelium by motile trophoblasts, system B\n                    <jats:sup>0,+<\/jats:sup>\n                    is likely reactivated to help remove tryptophan from the implantation chamber. If tryptophan is not removed, T-cells proliferate and reject the implanting blastocyst. Epigenetic modification of histones could alter their promotion of normal implantation through, say, incomplete tryptophan removal and, thus, allow partial T-cell rejection of the conceptus. Such partial rejection could impair placental development, embryonal\/fetal nutrition, and weight gain prior to birth. Small-for-gestational-age offspring are predisposed to developing metabolic syndrome, obesity, and associated complications as adults. Shifting expression of these phenotypes might contribute to transgenerational variation and evolution. The spectrum of possible extracellular histone targets in early development warrant new research, especially since the effects of epigenetic histone modifications might be transgenerational.\n                  <\/jats:p>","DOI":"10.1515\/bmc-2018-0017","type":"journal-article","created":{"date-parts":[[2019,1,8]],"date-time":"2019-01-08T04:04:00Z","timestamp":1546920240000},"page":"176-183","source":"Crossref","is-referenced-by-count":8,"title":["Can uterine secretion of modified histones alter blastocyst implantation, embryo nutrition, and transgenerational phenotype?"],"prefix":"10.1515","volume":"9","author":[{"given":"Lon J.","family":"Van Winkle","sequence":"first","affiliation":[{"name":"Emeritus Professor, Department of Biochemistry , Midwestern University , chicago , USA"},{"name":"Professor, Department of Medical Humanities , Rocky Vista University (RVU) , Parker , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebecca","family":"Ryznar","sequence":"additional","affiliation":[{"name":"Assistant Professor of Molecular Biology , Department of Biomedical Sciences, RVU , 8401 S. 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