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  • Book
    He-Feng Huang, Jian-Zhong Sheng, editors.
    Summary: The book Gamete and Embryo-fetal Origins of Adult Diseases introduces various diseases resulting from the abnormal gametogenesis and embryo development, which manifests as growth retardation, birth defects, or increased susceptibility to chronic metabolic diseases such as diabetes, cardiovascular disease and cancer in childhood and adult life, even fertility disorders and the risk of transgenerational transmission. Six common kinds of these diseases are discussed in separate chapters. The authors explore the connections between these diseases and epigenetic reprogramming, rapid cell differentiation and organ formation and environmental influences, including assisted reproductive technology and adverse intrauterine environments. With a summary of findings on the causes and progression of adult diseases at the phase of gametogenesis and embryo development, this book provides insights into the pathogenesis of disease and aids in the treatment and prevention of disease, meeting the requirement for improving the quality of the newborn population, and effectively preventing and curing major diseases at an early stage. This book offers new perspectives and will be an enlightening resource for obstetricians, paediatricians, epidemiologists, endocrinologists and sanitarians.

    Contents:
    Physiology of gametogenesis
    Physiology of embryo development
    Diabetes originated from embryo-fetal development
    Cardiovascular disease originated from embryo-fetal development
    Tumor originated from embryo-fetal development
    Obesity originated from embryo-fetal development
    Infertility originated from embryo-fetal development
    Mental health originated from embryo-fetal development
    Assisted reproductive technology (ART) and embryo-fetal origin of diseases
    Adverse intrauterine environment and embryo-fetal origin of diseases.
    Digital Access Springer 2014
  • Article
    Fernandez C, Möller G.
    Scand J Immunol. 1978;7(2):137-44.
    Mice were tolerized to the alpha1-6 epitope of native dextran. When their spleen cells were removed and activated by LPS, they did not synthesize antibodies against the tolerogen. However, when cells from tolerant mice were treated with dextranase or left untreated in culture for 24 h they were activated by LPS to the synthesis of antibodies against the tolerogen. When 24 h tolerized lymphocytes were treated with dextranase and transferred with immunogenic doses of dextran to irradiated mice they failed to produce antibodies against the tolerogen. In contrast, cells incubated with dextran for 2 h and thereafter dextranase treated were readily immunized by dextran in the same system. It is concluded that only the B cell clones having both Ig receptors and PBA receptors for the tolerogen become irreversibly tolerized, whereas B cells having Ig receptors for a different PBA are not tolerized, but remain in a resting state, even though their Ig receptors have bound the tolerogen.
    Digital Access Access Options