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  • 1
    Electronic Resource
    Electronic Resource
    Coevolution of the Rust Fungi on Gramineae and Liliaceae and their Hosts (1979)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Phytopathology 17 (1979), S. 367-403 
    Details
    ISSN: 0066-4286
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.py.17.090179.002055
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of a partial pseudogene homologous to the Hermansky-Pudlak syndrome gene HPS-1; relevance for mutation detection (2000)
    Springer
    Human genetics 〈Berlin〉 106 (2000), S. 370-373 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The HPS-1 gene is the first gene found to be responsible for the autosomal recessive disorder Hermansky-Pudlak syndrome (HPS). HPS is characterized by oculocutaneous albinism, a platelet storage pool deficiency, and ceroid lipofuscinosis. The HPS-1 gene has been mapped to chromosome 10q23.1–23.3 and encodes a 79-kDa protein of unknown function with no homology to any known protein. A sequence database search has revealed that a portion of clone HS1119A7 shows high sequence similarity to HPS-1 cDNA. By performing sequence alignments and PCR amplification of cDNA from several human tissues, we have shown that part of this clone consists of an unprocessed partial HPS-1 pseudogene located on chromosome 22q12.2–12.3. The pseudogene contains several intact HPS-1 exons and shows 95% sequence homology to the HPS-1 cDNA. Exon 6 of the pseudogene has 100% sequence homology to exon 6 of HPS-1 itself. In the pseudogene, this exon is surrounded by portions of both its normal flanking introns. These data provide the first characterization of an HPS-1 pseudogene, called HPS1- ψ 1. During amplification of exon 6 of the HPS-1 gDNA for mutation identification, the pseudogene might also be amplified, leading to a false positive for mutation. In addition, amplification of specific parts of the HPS-1 cDNA (e.g., exons 2–5) for mutation detection might lead to false positives for mutations, if the cDNA is contaminated with gDNA. This calls for caution when employing these screening approaches.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390000255
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    A new virulent strain of Puccinia hordei (1978)
    Springer
    Euphytica 27 (1978), S. 185-189 
    Details
    ISSN: 1573-5060
    Keywords: Puccinia hordei ; brown barley leaf rust ; Ornithogalum sp. ; alternate host ; Hordeum vulgare ; barley
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: Summary Four cultures of Puccinia hordei isolated from the alternate Ornithogalum hosts in Israel were virulent on seedlings of barley cultivars carrying resistance genes Pa, Pa2, Pa2 + Pa5, Pa2 + Pa6, Pa3, Pa4, and Pa7. Cultures with such a spectrum of virulence have never been reported. The cultures remained stable through 20 successive inoculation and isolation cycles. One of the cultures, T-40SS, retained its specific virulence after selfing on the alternate host. The evolution of virulent races of obligate parasites in the centers of origin of their hosts is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00039134
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  • 4
    Electronic Resource
    Electronic Resource
    Prenatal detection of Canavan disease (aspartoacylase deficiency) by DNA analysis (1994)
    Springer
    Journal of inherited metabolic disease 17 (1994), S. 664-666 
    Details
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Amniocentesis was performed in four pregnancies at risk for Canavan disease (CD). In all families both parents were of Ashkenazi-Jewish origin and harboured the C854 mutation in the cDNA of the aspartoacylase gene. Using DNA analysis of the amniotic cells, three fetuses were predicted to be non-affected and one fetus was predicted to be affected. The concentration ofN-acetylaspartic acid (NAA) in the amniotic fluid was in agreement with these results. In urine samples of the three newborns predicted to be non-affected, the concentration of NAA was normal. Tissues of the aborted fetus were not available. We conclude that DNA analysis is probably a reliable method for prenatal diagnosis of CD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00712008
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    Paper (German National Licenses)
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