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  • Articles: DFG German National Licenses  (3)
  • 1995-1999  (2)
  • 1990-1994  (1)
  • Liver  (2)
  • Anterior pituitary  (1)
Source
  • Articles: DFG German National Licenses  (3)
Material
Years
  • 1995-1999  (2)
  • 1990-1994  (1)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 74 (1996), S. 51-58 
    ISSN: 1432-1440
    Keywords: Tumor necrosis factor ; Hemorrhagic shock ; Leukocyte adhesion ; Intravital microscopy ; Liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relevance of tumor necrosis factor-α (TNF-α) inducing early inflammatory reactions in the liver after hemorrhagic shock, for example, leukocyte adhesion, has been well described. This study evaluated the anti-inflammatory effects of a monoclonal antibody against TNF-α (TN3.19.12) in terms of the time of application, namely, prior to shock induction, at the time of resuscitation, and after resuscitation. The hepatic micro-circulation was investigated by intravital fluorescence microscopy in female Sprague-Dawley rats undergoing severe hemorrhagic shock for 60 min and subsequent resuscitation. TN3.19.12 or placebo was given in a randomized and blinded manner either 60 min prior to shock induction, l min prior to resuscitation, or 15 min after the onset of resuscitation. The number of firmly adherent leukocytes in the livers of treated animals depended on the time of application of TN3.19.12. Leukocyte adhesion was significantly reduced when TN3.19.12 was given prior to shock induction or at the time of resuscitation and was less effective when administered after the onset of resuscitation. The results further confirm that TNF-α initiates very early pathological leukocyte adhesion in the liver 5 h following shock. Inhibition of leukocyte adhesion after shock, however, depends strongly on the time of TNF-α blocking. While TN3.19.12 prior to shock induction resulted in most effective attenuation, only very early treatment allowed limitation of posttraumatically increased leukocyte adhesion.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 74 (1996), S. 51-58 
    ISSN: 1432-1440
    Keywords: Key words Tumor necrosis factor ; Hemorrhagic shock ; Leukocyte adhesion ; Intravital microscopy ; Liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The relevance of tumor necrosis factor-α (TNF-α) inducing early inflammatory reactions in the liver after hemorrhagic shock, for example, leukocyte adhesion, has been well described. This study evaluated the anti-inflammatory effects of a monoclonal antibody against TNF-α (TN3.19.12) in terms of the time of application, namely, prior to shock induction, at the time of resuscitation, and after resuscitation. The hepatic microcirculation was investigated by intravital fluorescence microscopy in female Sprague-Dawley rats undergoing severe hemorrhagic shock for 60 min and subsequent resuscitation. TN3.19.12 or placebo was given in a randomized and blinded manner either 60 min prior to shock induction, 1 min prior to resuscitation, or 15 min after the onset of resuscitation. The number of firmly adherent leukocytes in the livers of treated animals depended on the time of application of TN3.19.12. Leukocyte adhesion was significantly reduced when TN3.19.12 was given prior to shock induction or at the time of resuscitation and was less effective when administered after the onset of resuscitation. The results further confirm that TNF-α initiates very early pathological leukocyte adhesion in the liver 5 h following shock. Inhibition of leukocyte adhesion after shock, however, depends strongly on the time of TNF-α blocking. While TN3.19.12 prior to shock induction resulted in most effective attenuation, only very early treatment allowed limitation of posttraumatically increased leukocyte adhesion.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1432-2013
    Keywords: Thyrotropin-releasing hormone ; Intracellular calcium ; Inward-rectifying K+ current ; G proteins ; Cholera toxin ; Pertussis toxin ; GH3/B6cells ; Anterior pituitary
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In rat anterior pituitary tumour cells (GH3/B6) thyrotropin-releasing hormone (TRH) elicits a biphasic response. First, a release of intracellularly stored Ca2+ induces a hyperpolarization of the cell. Second, a depolarization thought to be induced by a reduction of the inward-rectifying K+ current (KIR) causes an increase in action potential frequency and a plateau-like increase in [Ca2+]i. It has been proposed that the two phases are induced by the actions of inositol 1,4,5-trisphosphate (InsP 3) and protein kinase C (PKC), respectively, but we demonstrate here that PKC is not responsible for the second phase increase in [Ca2+]i and suggest that the pathways diverge at the level of receptor and G protein coupling. Both phases of the TRH response were insensitive to pertussis toxin, but cholera toxin (CTX) selectively affected the second phase. After CTX pretreatment cells had a high spontaneous spiking frequency and smaller KIR amplitude. In these cells TRH failed to increase the action potential frequency after the first phase hyperpolarization, elicited only a transient peak increase in [Ca2+]i with no plateau phase and could only slightly reduce KIR. These effects of CTX are not mediated by its ability to increase cAMP via activation of GS, as increased cAMP levels neither inhibit KIR nor prevent its reduction by TRH. In addition, inhibition of protein kinase A activation did not block the second phase increase in [Ca2+]i induced by TRH, suggesting that the CTX-sensitive G protein mediating the second phase of the TRH response is not GS.
    Type of Medium: Electronic Resource
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