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  • 2000-2004  (5)
  • 2003  (5)
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  • 2000-2004  (5)
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  • 1
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    Unknown
    German Medical Science; Düsseldorf, Köln
    In:  67. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 89. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie und 44. Tagung des Berufsverbandes der Fachärzte für Orthopädie; 20031111-20031116; Berlin; DOC03dguF3-7 /20031111/
    Publication Date: 2003-11-11
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: SpoIVB is the critical determinant for intercompartmental signalling of pro-σK processing during sporulation in Bacillus subtilis. We show here that the SpoIVB serine peptidase can cleave the SpoIVFA protein, which is one component of the pro-σK processing complex. SpoIVFA has been shown elsewhere (Rudner, D.Z., and Losick, R., 2002, Genes Dev 16: 1007–1018) to tether BofA and SpoIVFB in a membrane-embedded heteroligomeric complex in which BofA directly inhibits the activity of SpoIVFB. Cleavage of SpoIVFA would provide the necessary signal to dissolve this complex and release BofA-mediated inhibition on the zinc metalloprotease, SpoIVFB, that is responsible for cleaving pro-σK to its mature form. We also show that the SpoIVB PDZ domain is required for self-recognition and trans cleavage of SpoIVB and is probably also used to target an internal motif within the C-terminal region of SpoIVFA exposed in the space between the inner and outer forespore membranes. This work reveals the mechanism of intercompartmental signalling and provides a unified model as to how σK-directed gene expression in the mother cell is co-ordinated with events in the forespore chamber.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2486
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Energy, Environment Protection, Nuclear Power Engineering , Geography
    Notes: Large-scale ecological surveillance data were analysed to determine the locations of apparent eutrophication effects across common British vegetation types between 1990 and 1998. Plant species composition was recorded from a total of 9514 fixed plots located in a stratified, random sample of 501 1 km squares across Britain. Changes in plant species composition along a gradient of substrate fertility were inferred from statistical tests of change in mean Ellenberg fertility value calculated for each fixed plot. Plots were grouped by eight vegetation types, five landscape features (hedges, road verges, watercourse banks, small biotopes, larger units in fields and unenclosed land) and six environmental zones. Tests of change in mean Ellenberg value were carried out on all combinations of these strata. Decision tree modelling was used to identify groups of test outcomes sharing the same direction of change and where each group was defined by a minimum number of strata. Post hoc power analysis was used to select statistically non-significant test outcomes that could be used to infer stability in the sampled sub-population.Out of a total of 142 tests of change in fertility value, 67% were increases, 8% were reductions and 25% indicated stability. The best overall predictor of increases in fertility value, and therefore of shifts in favour of plants suited to higher substrate fertility, was vegetation type. Irrespective of landscape feature and environmental zone, increased means were associated with infertile grasslands, moorland, upland woodlands and heath/bog. Already highly fertile grasslands and woodland assemblages in lowland Britain remained largely stable. The small number of decreasing test outcomes were associated with arable land in Scotland, Wales and western England. These patterns of change are hypothesized to reflect pervasive land-use drivers combined with the inherent responsiveness of the vegetation.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Kainate receptors (KARs) modulate synaptic transmission at both pre-synaptic and post-synaptic sites. The overlap in the distribution of KA-2 and GluR6/7 subunits in several brain regions suggests the co-assembly of these subunits in native KARs. The molecular mechanisms that control the assembly and surface expression of KARs are unknown. Unlike GluR5–7, the KA-2 subunit is unable to form functional homomeric KAR channels. We expressed the KA-2 subunit alone or in combination with other KAR subunits in HEK-293 cells. The cell surface expression of the KAR subunit homo- and heteromers were analysed using biotinylation and agonist-stimulated cobalt uptake. While GluR6 or GluR7 homomers were expressed on the cell surface, KA-2 alone was retained within the endoplasmic reticulum. We found that the cell surface expression of KA-2 was dramatically increased by co-expression with either of the low-affinity KAR subunits GluR5–7. However, co-expression with other related ionotropic glutamate receptor subunits (GluR1 and NR1) does not facilitate the cell surface expression of KA-2. The analysis of subcellular fractions of neocortex revealed that synaptic KARs have a relatively high KA-2 content compared to microsomal ones. Thus, KA-2 is likely to contain an endoplasmic reticulum retention signal that is shielded on assembly with other KAR subunits.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Alzheimer's disease (AD) is the most commonly diagnosed form of dementia in the elderly. Predominantly this disease is sporadic in nature with only a small percentage of patients exhibiting a familial trait. Early-onset AD may be explained by single gene defects; however, most AD cases are late onset (〉 65 years) and, although there is no known definite cause for this form of the disease, there are several known risk factors. Of these, the ε4 allele of the apolipoprotein E (apoE) gene (APOE) is a major risk factor. The ε4 allele of APOE is one of three (ɛ2 ɛ3 and ɛ4) common alleles generated by cysteine/arginine substitutions at two polymorphic sites. The possession of the ɛ4 allele is recognized as the most common identifiable genetic risk factor for late-onset AD across most populations. Unlike the pathogenic mutations in the amyloid precursor or those in the presenilins, APOEɛ4 alleles increase the risk for AD but do not guarantee disease, even when present in homozygosity. In addition to the cysteine/arginine polymorphisms at the ɛ2/ɛ3/ɛ4 locus, polymorphisms within the proximal promoter of the APOE gene may lead to increased apoE levels by altering transcription of the APOE gene. Here we review the genetic and biochemical evidence supporting the hypothesis that regulation of apoE protein levels may contribute to the risk of AD, distinct from the well known polymorphisms at the ɛ2/ɛ3/ɛ4 locus.
    Type of Medium: Electronic Resource
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