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  • 5-(N-ethyl-N-isopropyl)amiloride (EIPA)  (1)
  • A1 receptor agonist  (1)
  • Cyst Rathke's cleft  (1)
  • DnaA protein
  • Heat shock response
Source
Material
Years
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Rathke's cleft cyst with pituitary apoplexy: case report (1999)
    Springer
    Neuroradiology 41 (1999), S. 832-834 
    Details
    ISSN: 1432-1920
    Keywords: Key words Pituitary tumor ; Cyst Rathke's cleft ; Pituitary apoplexy ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report a Rathke's cleft cyst which presented as pituitary apoplexy, a rare presentation. A 46-year-old woman suffered sudden headache and visual loss. T1-weighted MRI 3 weeks after this apoplectic episode demonstrated a cystic lesion between the anterior and posterior lobes of the pituitary, with some high-signal material layering in it. The mass showed spontaneous regression on an image 3 weeks later. Trans-sphenoidal surgery confirmed the diagnosis of a Rathke's cleft cyst with a haematoma within it.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002340050851
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Phenotypes ofdnaA mutants ofEscherichia coli sensitive to phenothiazine derivatives (1996)
    Springer
    Molecular genetics and genomics 252 (1996), S. 212-215 
    Details
    ISSN: 1617-4623
    Keywords: Escherichia coli ; Phenothiazine derivatives ; DnaA protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The activation of DnaA protein by cardiolipin is inhibited by fluphenazinein vitro. We therefore examined the sensitivity of temperature-sensitivednaA mutants ofEscherichia coli to fluphenazine and other phenothiazine derivatives. Among the eightdnaA mutants tested,dnaA5, dnaA46 dnaA602, anddnaA604, mutants with mutations in the putative ATP binding site of DnaA protein, showed higher sensitivities to phenothiazine derivatives than did the wild-type strain. ThednaA508 anddnaA167 mutants, which have mutations in the N-terminal region of DnaA protein, also showed higher sensitivities to phenothiazine derivatives. On the other hand, thednaA204 anddnaA205 mutants, with lesions in the C-terminal region of the DnaA protein, showed the same sensitivity to phenothiazine derivatives as the wild-type strain. Complementation analysis with a plasmid containing the wild-typednaA gene and phage P1-mediated transduction confirmed thatdnaA mutations are responsible for these sensitivity phenotypes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02173222
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Increase in synthesis and stability of σ 32 on treatment with inhibitors of DNA gyrase in Escherichia coli (1996)
    Springer
    Molecular genetics and genomics 253 (1996), S. 297-302 
    Details
    ISSN: 1617-4623
    Keywords: Key words Inhibitors of DNA gyrase ; Heat shock response ; σ32
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  We report here that in Escherichia coli, the anti-bacterial agent nalidixic acid induces transient stabilization and increased synthesis of σ32, accompanied by the induction of heat shock proteins (Dnak and GroEL proteins). The induction of heat shock proteins, increased synthesis of σ32, and stabilization of σ32 observed on treatment of wild-type cells with nalidixic acid were not observed in a nalA26 mutant, a strain that is resistant to nalidixic acid as the result of a mutation in the gyrA gene. Not only oxolinic acid, but also novobiocin, whose targets are the A and B subunits of DNA gyrase, respectively, also induced stabilization and increased synthesis of σ32. Thus, inhibition of the activity of DNA gyrase may cause stabilization and increased synthesis of σ32, resulting in turn in induction of heat shock proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00008596
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  • 4
    Electronic Resource
    Electronic Resource
    Adenosine A1 Agonist at Reperfusion Trial (AART): Results of a Three-Center, Blinded, Randomized, Controlled Experimental Infarct Study (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 607-614 
    Details
    ISSN: 1573-7241
    Keywords: adenosine ; A1 receptor agonist ; GR79236 ; infarct size ; ischemia-reperfusion ; reperfusion injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Adenosine A1 receptor agonists given prior to myocardial ischemia limit ischemic injury in several species. However, the ability of adenosine receptor agonists to limit infarct size when given at reperfusion has proved controversial. We designed a three-center experimental study using a blinded, randomized treatment protocol to test the hypothesis that adenosine A1 receptor activation during early reperfusion can attenuate lethal reperfusion injury, thereby reducing infarct size. Sixty anesthetized rabbits (20 in each laboratory) underwent 30 minutes coronary artery occlusion followed by 120 minutes reperfusion. The selective adenosine A1 receptor agonist GR79236 (10.5 μg/kg, a dose shown to limit infarction in this model when given before ischemia) or vehicle were administered IV 10 minutes before reperfusion. Infarct size was assessed by tetrazolium staining and, after the randomization code was revealed, data from the three laboratories were pooled for statistical analysis. Infarct size was not modified by administration of GR79236. In the vehicle-treated group, the infarct-to-risk ratio was 28.9 ± 2.7% (n = 24) compared with 31.9 ± 2.6% (n = 26) in the GR79236-treated group (not significant). Risk zone volume was similar in the two groups (1.06 ± 0.05 cm3 vs 1.00 ± 0.05 cm3, respectively). A modest reduction in rate-pressure product was noted following the administration of GR79236, but this effect was transient. The same dose of GR79236 was found to limit infarct size when given prior to coronary artery occlusion. We conclude that A1 receptor activation does not modify lethal reperfusion injury in myocardium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007850527878
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  • 5
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; Na+/H+ exchange ; 5-(N-ethyl-N-isopropyl)amiloride (EIPA) ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6±2.8% of the risk zone to infarct in untreated Krebs buffer-perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4±2.0% and 7.0±1.0%, respectively (p〈0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1±1.5% infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50μM polymyxin B, a PKC inhibitor, or 1μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischemia caused 51.0±2.9% infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4±3.1% (p〈0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8±2.1% (p〈0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction in infarction was seen (23.8±3.5% infarction). To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia-induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which is quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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    Paper (German National Licenses)
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