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  • 1
    Electronic Resource
    Electronic Resource
    Reversal effect of itraconazole on adriamycin and etoposide resistance in human leukemia cells (1996)
    Springer
    Annals of hematology 72 (1996), S. 17-21 
    Details
    ISSN: 1432-0584
    Keywords: Key words Multidrug resistance ; P-glycoprotein ; Itraconazole ; Adriamycin ; Etoposide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Itraconazole is a triazole antifungal agent that inhibits cell membrane serol biosynthesis. Currently, itraconazole is a potent candidate for in vivouse to revert multidrug resistance in acute leukemias, with the added benefit of its antifungal effect. As previously reported, itraconazole, as well as verapamil, reversed adriamycin-resistant K562 cells (K562/ADR) and HL60 cells (HL60/ADR) in dosages compatible to the plasma levels achieved by the therapeutic dosages used for the treatment of fungal infections. By RT-PCR analysis of mdr1, mdr3, and mrp mRNA, these adriamycin-resistant cells showed a higher expression of the transcript of these genes than those of the parent cells. By FACS analysis, both the adriamycin-resistant cells showed a higher expression of P-glycoprotein on their cell surfaces. These results suggested the involvement of itraconazole in the mdr gene and/or mrp gene product-associated resistance. Furthermore, itraconazole partially reversed etoposide resistance in both the K562 and K562/ADR cells. The present study suggests that itraconazole may reverse multidrug resistance, at least in part, via a classical MDR-associated mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00663011
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Reversal effect of itraconazole on adriamycin and etoposide resistance in human leukemia cells (1996)
    Springer
    Annals of hematology 72 (1996), S. 17-21 
    Details
    ISSN: 1432-0584
    Keywords: Multidrug resistance ; P-glycoprotein Itraconazole ; Adriamycin ; Etoposide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Itraconazole is a triazole antifungal agent that inhibits cell membrane serol biosynthesis. Currently, itraconazole is a potent candidate for in vivo use to revert multidrug resistance in acute leukemias, with the added benefit of its antifungal effect. As previously reported, itraconazole, as well as verapamil, reversed adriamycin-resistant K562 cells (K562/ADR) and HL60 cells (HL60/ADR) in dosages compatible to the plasma levels achieved by the therapeutic dosages used for the treatment of fungal infections. By RT-PCR analysis of mdrl, mdr3, and mrp mRNA, these adriamycin-resistant cells showed a higher expression of the transcript of these genes than those of the parent cells. By FACS analysis, both the adriamycin-resistant cells showed a higher expression of P-glycoprotein on their cell surfaces. These results suggested the involvement of itraconazole in the mdr gene and/or mrp gene product-associated resistance. Furthermore, itraconazole partially reversed etoposide resistance in both the K562 and K562/ADR cells. The present study suggests that itraconazole may reverse multidrug resistance, at least in part, via a classical MDR-associated mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00663011
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway (1994)
    Springer
    Lung 172 (1994), S. 159-167 
    Details
    ISSN: 1432-1750
    Keywords: VIP-VIP Antagonist ; Human bronchus ; Smooth muscle ; Vagus nerve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been reported that a low concentration of exogenously applied vasoactive intestinal peptide (VIP) suppresses the release of acetylcholine (ACh) from vagus nerve terminals in the ferret and feline trachea. There has been, however, no documentation of the prejunctional action of VIP in the human airway. We observed the effects of VIP and VIP antagonists on cholinergic excitatory neuro-effector transmission in the human bronchus to study the possible role of endogenous VIP on excitatory neurotransmission. In the human bronchus, VIP (10−10 to 10−7 M) showed no effect on either the contractions evoked by electrical field stimulation (EPS) or those evoked by ACh. To investigate the possible role of endogenous VIP on the human bronchus, we observed the effects of the VIP antagonists [4-Cl-D-Phe6,Leu17]-VIP and [Ac-Tyr1,D-Phe2-]-GRF(1–29)-NH2 on excitatory neuroeffector transmission. Both VIP antagonists (10−8 M) significantly enhances the contractions evoked by EFS without affecting the ACh sensitivity of smooth muscle cells. These results indicate that VIP antagonists have a prejunctional action that enhances excitatory neurotransmission. This study suggests that endogenous VIP may suppresses ACh release from the vagus nerve terminals in the human airway. It is also suggested that exogenously applied VIP may be inactivated by some mechanism in the human airway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175944
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Airway epithelial cells modulate cholinergic neurotransmission in dog trachea (1994)
    Springer
    Lung 172 (1994), S. 241-249 
    Details
    ISSN: 1432-1750
    Keywords: Airway epithelial cell ; Airway hyperresponsiveness ; Vagus nerve ; Smooth muscle ; Neurotransmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of epithelial cells on excitatory cholinergic neurotransmission in dog trachea, to shed more light on the role of airway epithelial cells in regulating airway responsiveness. Airway epithelial cells were prepared by an enzymatic dissociation of the tracheal mucosa using protease-free collagenase. Tracheal smooth muscle contractions evoked by electrical field stimulation (EFS) or acetylcholine (ACh) were measured before and after the application of epithelial cells. Isolated and dispersed epithelial cells (3 × 105 cells/ml) suppressed the amplitude of the twitch-like contractions evoked by EFS in the combined presence of guanethidine sulfate (10−6 m) and indomethacin (10−5 m). In contrast, epithelial cells did not affect the contraction evoked by exogenously applied ACh. Atropine (10−6 m) or tetrodotoxin (10−7 m) abolished the contraction evoked by electrical field stimulation. These findings indicate that airway epithelial cells inhibit the excitatory neurotransmission of the vagus nerve, presumably by suppressing the release of ACh. Airway epithelial cells may therefore play an important role in regulating the response of smooth muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00164441
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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