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  • 1990-1994  (4)
  • 1
    Electronic Resource
    Electronic Resource
    S35b, a new phenylsulfonylfuroxan compound, inhibits thrombin-induced synthesis of platelet-activating factor and prostacyclin in human endothelial cells (1993)
    Springer
    Inflammation research 40 (1993), S. 157-165 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Endothelial cells (EC) produce platelet activating factor (PAF) and prostacyclin (PGI2) in response to inflammatory agents such as thrombin. Upon cell stimulation a calcium-dependent phospholipase A2 (PLA2) is activated which hydrolyzes a membrane phospholipid to yield 1-0-alkyl-2-lyso-sn-glycero-3-phospho-choline (lyso-PAF) and free arachidonic acid. Lyso-PAF is in turn converted into PAF by a specific acetyltransferase and arachidonic acid is metabolized via cyclic endoperoxides to PGI2. In the present study we report that S35b (4-methyl-3-phenylsulfonylfuroxan), an new phenyl-sulfonylfuroxan compound with potent antiaggregatory effect, inhibits thrombin-induced PAF synthesis and acetyltransferase activation as well as PGI2 production in human umbilical vein endothelial cells (HUVEC) in a concentration dependent way. Additionally, we show that S35b stimulates the production of cyclic GMP (cGMP) in HUVEC in a concentration- and time-dependent manner. At high concentration, S35b potentiates the cAMP increase induced by iloprost or forskolin without having a significant influence on cAMP level itself. Potentiation of cAMP increase during agonist-induced EC stimulation seems not to be important for the effect of S35b on cellular function as the compound is active in inhibiting PAF production when endothelial cells are pretreated with indomethacin to block PGI2 synthesis. The increase of cGMP evoked by S35b may account for the effect on endothelial cell function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01984055
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Elevated plasma histamine levels in trauma patients: Results of a well-designed cross-sectional study with polytrauma and two control groups (1992)
    Springer
    Inflammation research 36 (1992), S. C168 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Several components of trauma (initial stressors, responses and burdens and therapeutic interventions) are able to induce histamine release, but our knowledge is very limited about the role of histamine in this fundamental scenario in human life. Previous studies suffer from unreliable histamine assays from biases in sample preparation and from confounding biases in the clinical setting. Hence a well-designed (6) crosssectional study was performed with polytrauma patients at the site of accident as a test group and two control groups in the hospital. The patients of the control groups suffered from single, peripheral trauma (more stress than injury) or being in the recovery period from single trauma and operation at day 5 (reconvalescence from traumatization). Patients at the normal ward had plasma histamine levels comparable to those of healthy human volunteers (〈0.5 ng/ml) whereas 40% of the single trauma patients and 80% of the polytrauma patients showed elevated plasma levels (〉=0.5 ng/ml). This was the case both at the place of the accident and in a second blood sample in the hospital. Hence the initial stimulus of injury was not the only cause of histamine release. Furthermore, histamine was one of the very early mediators in trauma. Its function has to be assessed as a contributory determinant in a multi-mediator scenario. Elevated plasma histamine concentrations of more than 1 ng/ml had a very bad prognosis for survival in previous studies, but the mechanism for that is not investigated at all.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01997324
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Cystic lung disease in Down syndrome (1994)
    Springer
    Pediatric radiology 24 (1994), S. 137-138 
    Details
    ISSN: 1432-1998
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well known that Down syndrome (DS) affects multiple organ systems, including cardiovascular, gastrointestinal, hematological, and musculoskeletal. Involvement of the lungs by a characteristic form of subpleural cystic disease is well described in the pathology literature. The imaging characteristics of changes caused by this disease have not been previously described in detail in the radiology literature, possibly because they are not well appreciated on plain chest radiographs. We present a child with DS in whom extensive cystic lung disease was discovered incidentally at CT, and review the current literature regarding the pathogenesis of cystic pulmonary abnormalities in children with DS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02020173
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Tumor necrosis factor receptor genes,TNFR1 andTNFR2, on human chromosomes 12 and 1 (1991)
    Springer
    Somatic cell and molecular genetics 17 (1991), S. 519-523 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Tumor necrosis factor, TNF, is a 17-kDa protein secreted by macrophages and classified as a cytokine. TNF binds to high-affinity receptors on the cell surface and is involved in a wide variety of biological responses. There are at least two types of receptors, tumor necrosis factor receptors 1 and 2 (TNFR1 and TNFR2). The genes for TNFR1, a 55-kDa protein, and TNFR2, a 70-kDa protein, have been mapped to human chromosomes 1 12 (12pter-cen) and (1pter-p32), respectively, by Southern blot analysis of human × Chinese hamster somatic cell hybrid panels. Recently, the corresponding genes in the mouse have been mapped to chromosomes 4 and 6 in regions that are conserved on human chromosomes 1 and 12.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01233176
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    Paper (German National Licenses)
    Fulltext
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