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  • 1
    Electronic Resource
    Electronic Resource
    Attenuation of Live E. coli–induced Acute Lung Injury by X-ray Irradiation in Guinea Pigs (2000)
    Springer
    Lung 178 (2000), S. 331-340 
    Details
    ISSN: 1432-1750
    Keywords: Key words: X-ray irradiation—E. coli bacterium—Inflammatory lung injury—Neutrophil function—Macrophage function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Irradiation is suspected to injure inflammatory cells, such as neutrophils and mononuclear phagocytes, cells known to contribute to the development of acute lung injury (ALI). This study examined whether preexposure to x-ray irradiation modifies ALI induced by E. coli injected intravenously in guinea pig. Thirty animals were divided into two control and two irradiated subgroups: the first control group received saline only (n= 8), and the second control group received E. coli, 2 × 109/kg body weight, suspended in saline (n= 6), IV. The first irradiated group received a single 12-Gy dose + saline (n= 6), and the second irradiated group received a single 12-Gy dose +E. coli (n= 10). The lung wet-to-dry-weight ratio (W/D) and 125I-albumin lung tissue/plasma ratio (T/P) were measured as markers of lung injury. W/D was significantly higher in the control E. coli group than in the other groups. T/P in the control E. coli group was also increased compared with T/P measured in the other groups. In the control E. coli group, a marked increase in bronchoalveolar lavage (BAL) neutrophils was observed compared with the control saline group. However, no significant difference in BAL neutrophil counts was observed between the control and irradiated E. coli groups. In contrast, BAL macrophages were significantly reduced in the irradiated E. coli groups compared with the control E. coli group. These findings suggest that x-ray irradiation attenuates E. coli–induced ALI in guinea pigs, an effect explained, at least in part, by a reduction in the number of alveolar macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004080000036
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Novel mutation of L718X in the ATP7A gene in a Japanese patient with classical Menkes disease, and four novel polymorphisms in the Japanese population (2000)
    Springer
    Journal of human genetics 45 (2000), S. 315-317 
    Details
    ISSN: 1435-232X
    Keywords: Key words Menkes disease ; ATP7A gene ; MNK gene ; Mutation ; Polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Menkes disease is an X-linked recessive disorder of the copper membrane transport system caused by mutations in the ATP7A gene. While various mutations in the ATP7A gene have been reported, a genotype-phenotype correlation has not been clearly defined. A novel mutation in the ATP7A gene in a Japanese patient with classical Menkes disease was identified via analysis of reverse-transcriptase polymerase chain reaction products and genomic DNA of the ATP7A gene. The nonsense mutation, L718X, was found to result in premature termination and immature ATP7A protein, unlikely to have normal functioning. Therefore, this nonsense mutation of the ATP7A gene is proposed to play a causative role in presenting the classical Menkes phenotype. Furthermore, four novel polymorphisms, C1535T (L464L), C2151T (T669I), G2253A (R703H), and C3677T (H1178Y) were also identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380070024
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Identification of two novel mutations of the carnitine/acylcarnitine translocase (CACT) gene in a patient with CACT deficiency (2000)
    Springer
    Journal of human genetics 45 (2000), S. 52-55 
    Details
    ISSN: 1435-232X
    Keywords: Key words Carnitine/acylcarnitine translocase ; CACT gene ; Lariat ; Branchpoint ; Deletion ; Exon skipping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Carnitine/acylcarnitine translocase (CACT) transports acylcarnitines into mitochondria in exchange for free carnitine, and is therefore an essential component within the fatty acid beta-oxidation pathway. CACT deficiency is an autosomal recessive disease caused by a mutation of the CACT gene. We have identified two novel mutations of the CACT gene in a patient with CACT deficiency. The first, a deletion mutation (146 del T), leads to premature termination and results in a very immature CACT protein. The second, a splicing mutation (261-10T〉G), results in either skipping of exons 3 and 4, or of exon 3 alone, and leads to truncation of the protein. Each of these mutations is hypothesized to destroy the function of the CACT protein. We propose that each of these mutations of the CACT gene play a causative role in the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380050010
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    Paper (German National Licenses)
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