1,721,054 research outputs found
Morgue records, volume 11, certificate 216 : Fleming, Tom, 1910-11-18
No full textSuicide by drinking Carbolic Aci
Specific mRNA detection in single lineage-marked blastomeres from preimplantation embryos
No full textDevelopmental programming and epigenetics: DNA methylation makes its mark
No full textProgramming of adult disease risk has been widely reported as a consequence of altered nutrition during embryonic and fetal development; however the mechanisms underlying the physiological outcomes are poorly understood. Transmission of developmentally programmed phenotypes across several generations has highlighted the need to identify how the phenotype is initially established, and how it may then be passed on to future offspring, without exposure to an additional adverse developmental environment. Epigenetic modifications are emerging as a likely element involved in this programming activity. Modifications to the DNA and chromatin organisation which do not alter the DNA sequence can control gene expression patterns through changing the accessibility of specific genes to the transcriptional machinery. One such modification is DNA methylation, which is frequently associated with gene repression. Altered nutrient availability has been shown to influence the establishment of DNA methylation in the developing embryo and fetus, leading to inappropriate gene expression, and associated changes in physiological parameters. Changes in DNA methylation dynamics are also being identified as a likely mechanism for transmitting the programmed phenotype to future generations
Maternal protein restriction around conception increases foetal neuronal differentiation and is associated with adult memory deficits
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Tight junction biogenesis during early development
No full textThe tight junction (TJ) is an essential component of the differentiated epithelial cell required for polarised transport and intercellular integrity and signalling. Whilst much can be learnt about how the TJ is constructed and maintained and how it functions using a wide range of cellular systems, the mechanisms of TJ biogenesis within developmental models must be studied to gain insight into this process as an integral part of epithelial differentiation. Here, we review TJ biogenesis in the early mammalian embryo, mainly considering the mouse but also including the human and other species, and, briefly, within the amphibian embryo. We relate TJ biogenesis to inherent mechanisms of cell differentiation and biosynthesis occurring during cleavage of the egg and the formation of the first epithelium. We also evaluate a wide range of exogenous cues, including cell–cell interactions, protein kinase C signalling, gap junctional communication, Na+/K+-ATPase and cellular energy status, that may contribute to TJ biogenesis in the embryo and how these may shape the pattern of early morphogenesi
Blastocyst environment and its influence on offspring cardiovascular health: the heart of the matter
No full textThe development of adult-onset diseases such as type II diabetes, obesity and cardiovascular disease is traditionally attributed to adult lifestyle characteristics such as a lack of physical exercise, poor diet and smoking. However, evidence from both human and animal model studies has demonstrated that environmental factors such as an imbalance or reduction in maternal nutrition during gestation can have adverse effects on offspring metabolism and cardiovascular health. The severity and nature of the phenotypic changes induced in offspring is influenced by the period of gestation manipulated. In particular, the mammalian preimplantation embryo in different animal models displays particular sensitivity to environmental factors, either in vivo (maternal diet) or in vitro (embryo culture) that is associated with the onset of cardiovascular dysfunction in adult life. The detailed mechanisms by which environmental conditions can alter postnatal cardiovascular physiology are poorly understood. However, various factors including endothelial function, vascular responsiveness, the renin-angiotensin system, kidney structure and early postnatal growth dynamics have all been recognize as potential contributors. Here, we review the relationship between preimplantation embryo environment and postnatal cardiovascular disease risk, and consider biochemical, molecular, genetic and physiological pathways implicated in this association
The preimplantation embryo: handle with care
Full text linkThe past decade has seen considerable advances in our understanding of intrinsic developmental mechanisms associated with gametogenesis and embryogenesis and accompanying applications in the fields of reproductive medicine, embryonic stem cell biology, and nuclear reprogramming. However, a new focus has recently emerged concerning the homeostatic regulation of embryonic cells, how this is set, and how it may influence the longitudinal progression and optimization of the developmental program and indeed the phenotype of the offspring. Attention has been drawn to the preimplantation stage of development as a sensitive "window" when in vitro and in vivo manipulations, such as culture conditions or maternal diet, may have critical consequences. In this article, we review how changes in environmental conditions, mediated via a range of epigenetic, cellular, and metabolic mechanisms in the preimplantation embryo, may alter the pattern of cell division, gene expression, morphology, and potential. We consider how fetal and postnatal phenotype may become susceptible to the plasticity of the preimplantation embryo and the risks for adult health and physiology
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