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  • 1
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Selective IgM deficiency is commonly found in Bloom's syndrome (BS). We reported that membrane-bound μ (μ m) mRNA was well transcribed but secreted μ (μ s) mRNA was not, although there was no mutation or deletion in the sequence including the (is C-terminal coding sequence in the patients with BS. Furthermore, we have shown previously, preferential damage to IgM production by ultraviolet (UV) irradiation of the cells of the patient. In the study described here, mutation in the sequence which is upstream of the 5’ end of the μ s C-terminal coding sequence was induced by UV irradiation in the lymphoblastoid cell line (LCL) of BS patient. These results suggest that abnormal repair of DNA damage is present in this LCL, and that preferential damage to IgM production by UV irradiation in this LCL may be due to the abnormal repair of DNA damage.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 66 (1995), S. 908-910 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Polarization of 8×8 vertical cavity surface emitting laser (VCSEL) arrays is completely controlled. These index-guided VCSELs have a 6×5 μm rectangular poststructure consisting of DBR mirrors. All 64 VCSELs emit fundamental single-mode and linearly polarized light with a polarization angle deviation of only 2.9°. Their light output characteristics are almost the same as those of conventional 6×6 μm polarization-uncontrolled VCSELs. © 1995 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 45 (1997), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The specific defect that causes IgG2 deficiency, which is one of the primary immunodeficiencies, is unknown. Recently, it was shown that interferon-γ (IFN-γ) induces synthesis of human germline Cγ2 transcripts. In the authors’ previous study and the present one, peripheral blood lymphocytes (PBLs) of all five tested patients with IgG2 deficiency failed to produce enough IFN-γ when stimulated with phytohaemagglutinin or concanavalin A although they produced a sufficient amount of interleukin-2 (IL-2). The low level of IgG2 production in pokeweed mitogen-stimulated PBLs of four tested patients was improved by the addition of recombinant IFN-γ. In this study, the amount of IFN-γ messenger RNA showed various degrees of reduction in all five tested patients. Sequence analysis of the IFN-γ coding regions and flanking regions revealed neither a point mutation nor a deletion for any of the patients. Thus the results suggest that the reduced expression of IFN-γ messenger RNA may play an important role in the IgG2 deficiency of these patients.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 122 (1996), S. 437-442 
    ISSN: 1432-1335
    Keywords: Pharmacodynamics ; Carboplatin ; Thrombocytopenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Thrombocytopenia induced by carboplatin combined with etoposide for elderly lung cancer patients was analyzed in relation to the predicted thrombocytopenia by the equations advocated by Egorin et al. and Taguchi et al. The thrombocytopenia actually observed was strongly correlated with and significantly more severe than that predicted if carboplatin had been administered as a single agent. The AUC (area under the curve) of carboplatin predicted by Calvert's equation significantly affected the degree of thrombocytopenia. These data suggested that dosing of carboplatin should be determined individually on the basis of renal function, as recommended earlier. The reason for the enhancement of thrombocytopenia is yet to be determined in future trials.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2242
    Keywords: Key words Allelic interaction ; Dihydroflavonol 4-reductase gene ; Mobile element-like sequences ; Morning glory ; Mutable allele
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  The a-3 flecked [J] variegated line of Japanese morning glory bearing white flowers with normal-colored flecks and sectors has been shown to carry a 6.4-kb transposable element, Tpn1, inserted within the DFR-B gene, one of the anthocyanin biosynthesis genes encoding dihydroflavonol 4-reductase (DFR). The a flaked [M] variegated line of morning glory also bears white flowers with normal-colored flakes and sectors, and it was shown to carry multiple DNA rearrangements, including insertions of mobile element-like sequences, MELSIP1 and MELSIP2, in its DFR gene region. Unlike the a-3 flecked [J] mutation, the mutable a flaked [M] allele exhibited incomplete dominance. Interestingly, not only intensely colored flakes but also white spots and sectors were often observed in lightly colored flowers of morning glory in the heterozygous state A[M]/a flaked [M]. The interspecific F1 hybrids between Japanese morning glory and morning glory carrying both a-3 flecked [J]/A-3[M] and A[J]/ a flaked [M] in the heterozygous condition bear lightly colored flowers with intensely colored sectors as well as white flakes. The results clearly demonstrated that the DFR gene in the a flaked [M] line of morning glory is active and complements the DFR-B gene carrying Tpn1 in the a-3 flecked [J] line of Japanese morning glory. Interspecific allelic interactions between the mutable a flaked [M] gene of morning glory and the corresponding wild-type A[J] gene of Japanese morning glory resulted in incomplete dominance and the formation of white flakes and sectors. The appearance of the white flakes may be due to a somatic mutation of the A[J] gene.
    Type of Medium: Electronic Resource
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