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  • 2000-2004  (4)
  • 2002  (2)
  • 2000  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 143 (2000), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background  Atopic eczema is a chronic inflammatory skin disease, which in most children can be adequately controlled using topical therapy. However, in a small number of children it is necessary to use systemic treatments to gain an acceptable level of disease control. Objectives To evaluate azathioprine as a treatment for severe atopic eczema in children, and the value of pretreatment thiopurine methyltransferase (TPMT) levels in the identification of patients at high risk of myelosuppression. Methods Between January 1997 and May 2000, 91 children had erythrocyte TPMT assays with the intention of treating their atopic eczema with azathioprine. This study is based on retrospective examination of data taken from the hospital notes of these children, who had attended Great Ormond Street Hospital for Children and St John's Institute of Dermatology, London. Results The distribution of TPMT values corresponded closely to that previously described in adults. Forty-eight children were commenced on treatment with azathioprine. Twenty-eight had an excellent response to treatment, 13 had a good response and seven had a poor response. No patient developed neutropenia. Conclusions Azathioprine may prove a very valuable treatment for severe atopic eczema in children. We consider its short-term adverse effect profile in children with normal TPMT activity to have been entirely acceptable with our treatment protocol. As result, we now feel confident to initiate therapy at dose levels of 2·5–3·5 mg kg−1 in those with a normal TPMT level, and to reduce the frequency with which we undertake tests of bone marrow and liver function.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Streptomyces coelicolor is a representative of the group of soil-dwelling, filamentous bacteria responsible for producing most natural antibiotics used in human and veterinary medicine. Here we report the 8,667,507 base pair linear chromosome of this organism, containing the largest number of genes ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 14 (2000), S. 567-571 
    ISSN: 1432-198X
    Keywords: Key words Hyperglycemia ; Glucose intolerance ; Diabetes ; Metabolic effects ; Insulin-like growth factors ; Growth
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Overexpression of insulin-like growth factor-1 binding protein (IGFBP-1) in transgenic mice has provided insight into the physiological role of this binding protein in modulating the metabolic and growth-promoting effects of the IGFs. IGFBP-1 transgenic mice demonstrate both intrauterine and postnatal growth retardation. Organ weight was proportionately reduced relative to body weight in most organs, with the exception of the brain, which was disproportionately small in transgenic mice. There were no gross neurological manifestations of the reduction in brain size. Transgenic mice also demonstrated fasting hyperglycemia, impaired glucose tolerance, and modest insulin resistance in skeletal muscle and hepatic tissue. From these data, we can conclude that overexpression of IGFBP-1 results in inhibition of IGF action and in profound impairment of brain development, modest inhibition of fetal and postnatal growth, and inhibition of the metabolic effects of the IGFs. Increased expression of IGFBP-1 has been documented in a variety of situations, such as fetal nutritional deprivation and hypoxia, and has been considered to be a marker of metabolic disturbances that cause fetal growth retardation. The observations in IGFBP-1 transgenic mice suggest expression of IGFBP-1 may itself contribute to the growth retardation and impaired fetal brain development.
    Type of Medium: Electronic Resource
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