175 research outputs found

    The literature of low g propellant behavior

    Get PDF
    Annotated bibliography on low-g liquid propellant behavio

    The biological basis and clinical significance of hormonal imprinting, an epigenetic process

    Get PDF
    The biological phenomenon, hormonal imprinting, was named and defined by us (Biol Rev, 1980, 55, 47-63) 30 years ago, after many experimental works and observations. Later, similar phenomena were also named to epigenetic imprinting or metabolic imprinting. In the case of hormonal imprinting, the first encounter between a hormone and its developing target cell receptor—usually at the perinatal period—determines the normal receptor-hormone connection for life. However, in this period, molecules similar to the target hormone (members of the same hormone family, synthetic drugs, environmental pollutants, etc), which are also able to bind to the receptor, provoke faulty imprinting also with lifelong—receptorial, behavioral, etc.,—consequences. Faulty hormonal imprinting could also be provoked later in life in continuously dividing cells and in the brain. Faulty hormonal imprinting is a disturbance of gene methylation pattern, which is epigenenetically inherited to the further generations (transgenerational imprinting). The absence of the normal or the presence of false hormonal imprinting predispose to or manifested in different diseases (e.g., malignant tumors, metabolic syndrome) long after the time of imprinting or in the progenies

    Immune neuroendocrine phenotypes in Coturnix coturnix: Do avian species show LEWIS/FISCHER-like profiles?

    Get PDF
    Immunoneuroendocrinology studies have identified conserved communicational paths in birds and mammals, e.g. the Hypothalamus-Pituitary-Adrenal axis with anti-inflammatory activity mediated by glucocorticoids. Immune neuroendocrine phenotypes (INPs) have been proposed for mammals implying the categorization of a population in subgroups underlying divergent immune-neuroendocrine interactions. These phenotypes were studied in the context of the LEWIS/FISCHER paradigm (rats expressing high or low pro-inflammatory profiles, respectively). Although avian species have some common immunological mechanisms with mammals, they have also evolved some distinct strategies and, until now, it has not been studied whether birds may also share with mammals similar INPs. Based on corticosterone levels we determined the existence of two divergent groups in Coturnix coturnix that also differed in other immune-neuroendocrine responses. Quail with lowest corticosterone showed higher lymphoproliferative and antibody responses, interferon-γ and interleukin-1β mRNA expression levels and lower frequencies of leukocyte subpopulations distribution and interleukin-13 levels, than their higher corticosterone counterparts. Results suggest the existence of INPs in birds, comparable to mammalian LEWIS/FISCHER profiles, where basal corticosterone also underlies responses of comparable variables associated to the phenotypes. Concluding, INP may not be a mammalian distinct feature, leading to discuss whether these profiles represent a parallel phenomenon evolved in birds and mammals, or a common feature inherited from a reptilian ancestor millions of years ago

    Conserved Genes Act as Modifiers of Invertebrate SMN Loss of Function Defects

    Get PDF
    Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular defects. To find genes that modulate SMN function defects across species, two approaches were used. First, a genome-wide RNAi screen for C. elegans SMN modifier genes was undertaken, yielding four genes. Second, we tested the conservation of modifier gene function across species; genes identified in one invertebrate model were tested for function in the other invertebrate model. Drosophila orthologs of two genes, which were identified originally in C. elegans, modified Drosophila SMN loss of function defects. C. elegans orthologs of twelve genes, which were originally identified in a previous Drosophila screen, modified C. elegans SMN loss of function defects. Bioinformatic analysis of the conserved, cross-species, modifier genes suggests that conserved cellular pathways, specifically endocytosis and mRNA regulation, act as critical genetic modifiers of SMN loss of function defects across species

    Like mother, like child : investigating perinatal and maternal health stress in post-medieval London.

    Get PDF
    Post-Medieval London (sixteenth-nineteenth centuries) was a stressful environment for the poor. Overcrowded and squalid housing, physically demanding and risky working conditions, air and water pollution, inadequate diet and exposure to infectious diseases created high levels of morbidity and low life expectancy. All of these factors pressed with particular severity on the lowest members of the social strata, with burgeoning disparities in health between the richest and poorest. Foetal, perinatal and infant skeletal remains provide the most sensitive source of bioarchaeological information regarding past population health and in particular maternal well-being. This chapter examined the evidence for chronic growth and health disruption in 136 foetal, perinatal and infant skeletons from four low-status cemetery samples in post-medieval London. The aim of this study was to consider the impact of poverty on the maternal-infant nexus, through an analysis of evidence of growth disruption and pathological lesions. The results highlight the dire consequences of poverty in London during this period from the very earliest moments of life

    Cloacal gland and testes development in male Japanese quail selected for divergent adrenocortical responsiveness

    Get PDF
    The time course of sexual development in male quail from lines selected for either a reduced (low stress, LS) or an exaggerated (high stress, HS) plasma corticosterone response to brief restraint was determined. Sexual development was assessed by examination of cloacal gland area (CAREA) and volume (CVOL), proportion of individuals that produced cloacal gland foam, and the intensity of cloacal gland foam production (CFP) at 4, 5, 6, 8, 10, 14, and 16 wk of age. These intervals encompass ages during which growing, photostimulated quail would be expected to evolve from being totally prepubescent to well into adulthood. Testes weight (TW) and the proportion of individuals that had achieved a combined TW of 500 mg (PI500) were also measured at 6 and 16 wk of age. Mean CAREA and CVOL were similar in LS and HS quail at 4 wk of age. Beginning at 5 wk of age and thereafter, CAREA was greater (P < 0.05) in LS than in HS quail. Similarly, beginning at 6 wk of age and thereafter, CVOL was greater (P < 0.05) in LS than in HS quail. More LS than HS birds also expressed foam at 4 (P < 0.05), 5 (P = 0.15), and 6 wk (P < 0.05) of age. From 8 wk on, all birds were in foam production. CFP results mimicked those found for CAREA and CVOL in that LS quail tended toward higher CFP values than HS quail at all intervals of measurement. TW were higher (P < 0.02) in LS than HS quail when data from the 2 ages at which testes were harvested were combined. At 6 wk of age, the LS and HS birds showed a PI500 line difference (P < 0.08) of 1.0 and 0.91, respectively; by 16 wk, all birds exhibited a maximum PI500. The results suggest that 1) selection for reduced adrenocortical responsiveness in Coturnix is accompanied by an accelerated onset of puberty in males, and 2) enhanced reproductive development in LS males remains extant throughout early to middle-age adulthood.Fil: Marin, Raul Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; ArgentinaFil: Satterlee, D. G.. State University of Louisiana; Estados Unido
    corecore