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1

Baker's yeast as a tool for the development of antifungal kinase inhibitors - targeting protein kinase C and the cell integrity pathway

100%
Heinisch J. J.
Cellular and Molecular Biology Letters
|
2005
|
tom 10
|
nr Suppl.2
2

Modified substrates of DNA polymerases and design of antivirals

84%
Krayevsky A. A., Alexandrova L., Dyatkina N. B., Kukhanova M. K., Shirokova E. A.
Acta Biochimica Polonica
|
1996
|
tom 43
|
nr 1
The results obtained in our laboratory on investigating of substrate properties of a large number of compounds towards different DNA polymerases have been summarized. On the basis of systematic analysis a directed synthesis of nucleotides with antiviral properties was performed.
3
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Susceptibility testing of Aspergillus niger strains isolated from poultry to antifungal drugs - a comparative study of the disk diffusion, broth microdilution (M 38-A) and Etest methods

67%
Tokarzewski S., Ziolkowska G., Nowakiewicz A.
Polish Journal of Veterinary Sciences
|
2012
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tom 15
|
nr 1
The aim of this study was to determine the sensitivity of Aspergillus niger strains isolated from birds to available antifungal drugs using different in vitro assays - classical disk diffusion, Etest® and broth microdilution NCCLS/CLSI M 38-A. The study material consisted of about 2.000 swabs and samples from different species of birds. A. niger (n=10) was accounted for 6.81% of the total pool of strains isolated. Determinations were made for 13 antifungal drugs using the disk diffusion method. The A. niger exhibited high susceptibility to enilconazole, terbinafine, voriconazole, tioconazole and ketoconazole, low susceptibility to clotrimazole, miconazole and nystatin, and resistance to amphotericin B, itraconazole, pimaricin, fluconazole and 5-fluorocytosine. Minimum inhibitory concentration (MIC) was determined for 9 antifungal drugs using the micromethod of duplicate serial dilutions in a liquid medium. A. niger strains were most susceptible to enilconazole and voriconazole. MIC ranged from 0.0625 to 0.5 μg/ml for enilconazole, with MIC90-0.5 μg/ml and MIC50-0.125 μg/ml. The corresponding values for voriconazole were 0.25-1 μg/ml, 1 μg/ml and 0.5 μg/ml. MIC for amphotericin B and terbinafine ranged from 0.5 to 4 μg/ml, while the values for the remaining drugs were highly varied. MIC was measured by the gradient diffusion method using Etest® for 5 antifungal drugs: amphotericin B, fluconazole, itraconazole, ketoconazole and voriconazole. By far the highest susceptibility was obtained in the case of voriconazole, with MIC ranging from 0.0625 to 1 μg/ml. MIC for amphotericin B ranged from 0.25 to 4 μg/ml, for itraconazole and ketoconazole ranging from 0.5 to 16 μg/ml. Methods available for this purpose are not always applicable in field conditions. The present results indicate that the Etest® technique, due to its high percentage of agreement with the M 38-A microdilution method, should find application in medical and veterinary practice.
4

Mechanisms of resistance to azole antifungals

67%
Marichal P., Bossche H. V.
Acta Biochimica Polonica
|
1995
|
tom 42
|
nr 4
Until the late eighties, clinical resistance to azole antifungals was a rare pheno­menon. Only a few cases of resistance to ketoconazole were found in patients with chronic mucocutaneous candidiasis (CMC). The spread of AIDS and the widespread prophylactic and therapeutic use of the hydrophilic azole compound fluconazole resulted both in the selection and induction of resistant strains and in a shift in the nature of the infecting organisms. Most azole antifungals such as itraconazole, ketoconazole and fluconazole are active against a variety of fungal diseases. However, the concentration needed to inhibit growth is dependent on the nature of the infecting species. Mucor spp., e.g., are almost insensitive to present available azole compounds and can be regarded as intrinsically resistant to azole treatment. Physicochemical features, such as the hydrophobicity and pKa, of a given azole, define whether or not it will be active or cross-resistant against a given species. Fluconazole is almost inactive against Candida krusei and Aspergillus fumigatus, whereas the lipophilic itraconazole is active against these species. A third type of resistance is acquired or induced resistance. This is the most contro­versial type because, even within a given species, organisms may differ in their response to the same azole. For these strains, convincing evidence can only be obtained when there is a genotypically related strain, which does not show resistance. In a limited number of biochemical or molecular biological studies the mechanisms of resistance have been investigated at the molecular level. These studies show that resistance can occur when there is an insufficient intracellular content of the azole. This can be due to impermeability problems, inactivated uptake systems or, and more likely, the presence of active multidrug resistance gene products of the P-glycoprotein type. Alteration or overexpression of the target for azole antifungals, the cytochrome P450-dependent 14 a-demethylase, also induces resistance. The nature and amount of the accumulating sterols also are of great importance for azole-induced growth inhi­bition. This may explain why mutations in other enzymes of the ergosterol bio­synthesis pathway, e.g. the A5-6 desaturase, can contribute to azole resistance.
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