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  • 1
    Electronic Resource
    Electronic Resource
    Protection Against β-Amyloid Toxicity in Primary Neurons by Paclitaxel (Taxol) (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Neurofibrillary tangles in Alzheimer's disease contain aggregates of abnormally phosphorylated microtubule-associated protein τ, indicating that microtubule breakdown is a primary event in the neurodegenerative cascade. Recent studies have shown that addition to neuronal cultures of amyloid peptides found in Alzheimer's leads to abnormal phosphorylation of τ and neurofibrillary pathology. We tested the possibility that the microtubule-stabilizing drug paclitaxel (Taxol) might protect primary neurons against amyloid-induced toxicity. Neurons exposed to aggregated amyloid peptides 25–35 and 1–42 became pyknotic with degenerating neurites within 24 h. Treatment of cultures with paclitaxel either 2 h before or 2 h after addition of the peptide prevented these morphological alterations. When numbers of viable cells were determined in cultures exposed to amyloid peptide with or without paclitaxel for 24 or 96 h, the percentage of surviving cells was significantly higher in paclitaxel-treated cultures, and activation of the apoptosis-associated protease CPP32 was significantly reduced. These observations indicate that microtubule-stabilizing drugs may help slow development of the neurofibrillary pathology that leads to the loss of neuronal integrity in Alzheimer's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70041623.x
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  • 2
    Electronic Resource
    Electronic Resource
    Immunohistochemical and molecular characterization of cultured keratinocytes after dispase-mediated detachment from the growth substratum (2000)
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Keratinocyte activation comprises changes in protein and gene expression pattern resulting in phenotypic and functional changes necessary for re-epithelialization such as the expression of urokinase-type plasminogen activator (uPA) and its cell surface receptor (uPA-R; CD87). As uPA and uPA-R are rapidly induced after dispase-mediated detachment of cultured normal human epidermal keratinocytes (NHEK) we hypothesized that dispase-mediated detachment may cause a similar “activation” of keratinocytes with uPA and uPA-R being only one aspect of a complex “activation reaction”. To test this hypothesis we have comparatively analysed adherent versus detached keratinocyte sheets for selected indicators of keratinocyte activation by immunohistochemistry. Furthermore we have identified genes via subtraction cloning which are up-regulated upon dispase-induced detachment. The analyses provided evidence for an increased transcriptional and translational activity in detached keratinocytes, as indicated by over-expression of several ribosomal components (L3 and S10 ribosomal protein) and transcription factors (initiation factor 4A, elongation factor 1α). Increased proliferative activity was indicated by increased expression of the proliferation markers Ki67, keratin 6 and keratin 17. Finally, several markers of keratinocyte activation such as the integrin chain αv, psoriasin, glutathion-S-transferase and heparin-binding epidermal growth factor-like growth factor were up-regulated. Furthermore mevalonate kinase, a molecule as yet unknown to be expressed in keratinocytes, was identified. The findings provide evidence that dispase-mediated detachment in cultured keratinocytes induces a reaction, which comprises the up-regulation of a complex array of proliferation- and migration-related molecules. The pattern of which resembles the activation reaction observed in the re-epithelializing keratinocytes in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-0625.2000.009001058.x
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  • 3
    Electronic Resource
    Electronic Resource
    Plasminogen activator inhibitor type-2 in the lesional epidermis of lupus erythematosus (1996)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Under certain pathophysiological conditions epidermal keratinocytes produce urokinase-type plasminogen activator (LIPA) or tissue-type PA (tPA). These PAs are subject to regulation by PA inhibitors (PAI). including PAl type-2 (PAI-2). In the normal epidermis. PAI-2 is present in the differentiating suprabasal layers, albeit in the apparent absence of PAs. It has, therefore, been suggested that PAI-2 plays a role in epidermal differentiation not linked to its ability lo inhibit PAs. In line with this hypothesis, we have studied, by immunohistochemistry. the distribution of PAI-2. uPA and tPA in the normal and in the lesional epidermis of patients with lupus erythematosus (LE). a disease in which epidermal differentiation is disturbed. The PAI-2 antigen was detectable in the normal epidermis and in the lesional epidermis of LE. In the normal epidermis, the PAI-2 antigen was most pronounced in the granular layer. In the hyperkeratotic epidermal lesions of LE. the PAI-2 antigen was increased. In normal and lesional skin. PAI-2 was distributed along the cell periphery. Indicating its association with the cornified envelope. Neither uPA nor tPA was detectable in normal or lesional epidermis. Our findings show that PAI-2 is a major type of PAI in normal epidermis and in the lesional epidermis of LE, and that increased epidermal PAI-2 is observed in a disease which is not associated with an increase in epidermal PAs. The data support the hypothesis that epidermal PAI-2 may have other functions than the regulation of PA activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.1996.24759.x
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  • 4
    Electronic Resource
    Electronic Resource
    Enhanced fracture energy and effects of temperature at spalling in ceramics: continuum damage modelling (2000)
    Springer
    Archive of applied mechanics 70 (2000), S. 145-157 
    Details
    ISSN: 1432-0681
    Keywords: Key words spall ; ceramics ; strength ; fracture energy ; size effect ; continuum damage ; inhomogeneity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Summary Enhanced fracture energy losses at spalling and the temperature dependence of the spalling strength of alumina ceramic bars are analysed on the basis of the experimental tests conducted both in room temperature and within the temperature range up to 1500°C at strain rates of some 500 s−1. The experimental method and the measurements are first shortly outlined. The mechanical response of ceramic bars is modelled then as a heterogeneous distribution of brittle-elastic mesoelements undergoing continuum damage at the known strain history, corresponding to that registered in the experiments. The mesoelements are characterised by the values of initial damage randomly fluctuating within a given band-width superposed on a deterministic distribution, which corresponds to the fabrication conditions of the ceramic bars. The model has been tested in the evaluation of room-temperature experiments, its parameters: the average value of the initial damage, Young's modulus of the undamaged material and the energy absorption capacity in continuum damage are taken from the calibration fitting the experimental data. The registered energy losses at spalling, which exceed the static values of fracture energy by almost an order of magnitude, can be explained thus by the enhancement of the dissipation due to bulk damage, which is computed on the basis of the above parameters. The temperature change of the Young's modulus of the matrix material is taken as corresponding to the measured change of the uniaxial wave velocity in the bar, and corrected by the temperature change of the mass density. The analysis of the model shows that the drop in the spalling strength of the specimens with the increase of the temperature is phenomenologically related to the falling energy absorption capacity within the continuum damage mechanism. An explanation of this phenomenon is attempted, based on the grain-size-related mechanisms of the microfracture from pre-existing intergranular flaws distributed over the bulk of ceramics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004199900054
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