44 research outputs found

    Julian Hart Lewis - Bibliography from JULIAN HART LEWIS. 12 August 1946 — 30 April 2014

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    Julian Hart Lewis was an outstanding embryologist and mathematical biologist whose breadth of interests and skills helped re-establish the importance of quantitative thinking to modern molecular developmental biology. He was most interested in the fundamental question of how the single-celled fertilized egg generates many different types of cells (e.g. nerves, skin, muscle) at the correct time and arranged in the right place. This remarkable generation of complexity is fundamental to an understanding of how animals develop and how this is orchestrated by their genes. Julian was exceptional in combining a ‘feel’ for biological questions and the ability to utilize rigorous and revealing mathematical models. He was also an outstanding mentor, writer and polymath, who was ahead of his time in breaching historical barriers between different scientific disciplines

    The Drugs Don't Work: Expectations and the Shaping of Pharmacogenetics

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    This article examines one particular set of technologies arising from developments in human genetics, those aimed at improving the targeting, design and use of conventional small molecule drugs - pharmacogenetics. Much of the debate about the applications and consequences of pharmacogenetics has been highly speculative, since little or no working technology is yet on the market. This article provides a novel analysis of the development of pharmacogenetics, and the social and ethical issues it raises, based on the sociology of technological expectations. In particular, it outlines how two alternative visions for the development of the technology are being articulated and embedded in a range of heterogeneous discourses, artefacts, actor strategies and practices, including: competing scientific research agendas, experimental technologies, emerging industrial structures and new ethical discourses. Expectations of how pharmacogenetics might emerge in each of these arenas are actively shaping the trajectory of this nascent technology and its potential socio-economic consequences

    Rohwer et al_data_21 July

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    Excel file with all data used in analyses presented in the paper

    Rohwer etal_nest transplant data

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    Data for nest fate, number of young fledged, nest temperature and humidity, parental behaviour, incubation duration, ectoparasites, adult female and nestling corticosterone, and nestling growth rates for nests used in transplant experiments between a subarctic and temperate site

    Imperfect wound healing sets the stage for chronic diseases.

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    Although the age of the genome gave us much insight about how our organs fail with disease, it also suggested that diseases do not arise from mutations alone; rather, they develop as we age. In this Review, we examine how wound healing might act to ignite disease. Wound healing works well when we are younger, repairing damage from accidents, environmental assaults, and battles with pathogens. Yet, with age and accumulation of mutations and tissue damage, the repair process can devolve, leading to inflammation, fibrosis, and neoplastic signaling. We discuss healthy wound responses and how our bodies might misappropriate these pathways in disease. Although we focus predominantly on epithelial-based (lung and skin) diseases, similar pathways might operate in cardiac, muscle, and neuronal diseases

    Image_2_Nutrient Deficiency Tolerance in Citrus Is Dependent on Genotype or Ploidy Level.pdf

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    Plants require essential minerals for their growth and development that are mainly acquired from soil by their roots. Nutrient deficiency is an environmental stress that can seriously affect fruit production and quality. In citrus crops, rootstock/scion combinations are frequently employed to enhance tolerance to various abiotic stresses. These tolerances can be improved in doubled diploid genotypes. The aim of this work was to compare the impact of nutrient deficiency on the physiological and biochemical response of diploid (2x) and doubled diploid (4x) citrus seedlings: Volkamer lemon, Trifoliate orange × Cleopatra mandarin hybrid, Carrizo citrange, Citrumelo 4475. Flhorag1 (Poncirus trifoliata + and willow leaf mandarin), an allotetraploid somatic hybrid, was also included in this study. Our results showed that depending on the genotype, macronutrient and micronutrient deficiency affected certain physiological traits and oxidative metabolism differently. Tetraploid genotypes, mainly Flhorag1 and Citrumelo 4475, appeared resistant compared to the other genotypes as indicated by the lesser decrease in photosynthetic parameters (Pnet, Fv/Fm, and Gs) and the lower accumulation of oxidative markers (MDA and H2O2) in roots and leaves, especially after long-term nutrient deficiency. Their higher tolerance to nutrient deficiency could be explained by better activation of their antioxidant system. For the other genotypes, tetraploidization did not induce greater tolerance to nutrient deficiency.</p

    Image_3_Nutrient Deficiency Tolerance in Citrus Is Dependent on Genotype or Ploidy Level.pdf

    No full text
    Plants require essential minerals for their growth and development that are mainly acquired from soil by their roots. Nutrient deficiency is an environmental stress that can seriously affect fruit production and quality. In citrus crops, rootstock/scion combinations are frequently employed to enhance tolerance to various abiotic stresses. These tolerances can be improved in doubled diploid genotypes. The aim of this work was to compare the impact of nutrient deficiency on the physiological and biochemical response of diploid (2x) and doubled diploid (4x) citrus seedlings: Volkamer lemon, Trifoliate orange × Cleopatra mandarin hybrid, Carrizo citrange, Citrumelo 4475. Flhorag1 (Poncirus trifoliata + and willow leaf mandarin), an allotetraploid somatic hybrid, was also included in this study. Our results showed that depending on the genotype, macronutrient and micronutrient deficiency affected certain physiological traits and oxidative metabolism differently. Tetraploid genotypes, mainly Flhorag1 and Citrumelo 4475, appeared resistant compared to the other genotypes as indicated by the lesser decrease in photosynthetic parameters (Pnet, Fv/Fm, and Gs) and the lower accumulation of oxidative markers (MDA and H2O2) in roots and leaves, especially after long-term nutrient deficiency. Their higher tolerance to nutrient deficiency could be explained by better activation of their antioxidant system. For the other genotypes, tetraploidization did not induce greater tolerance to nutrient deficiency.</p
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