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Saygun, N., Ozcan, A. T., Cobanlí, B., Zamani, A.: Drug resistance in hospitalized patients with pulmonary tuberculosis. Solunum Hastaliklari 4 , 287–293 (1993). [Turkish with an English abstract] Zamani A

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The main target of the thesis was to investigate the drug resistance reversal on prokaryotic and eukaryotic model organisms. Based on DNA and protein complex formation properties of the given compounds the plasmid elimination of bacteria and the modification of the drug transporter proteins various experimental systems have been studied in bacteria and tumor cells.It was found that E. coli cells isolated from clinical specimen were less sensitive for the plasmid elimination than the laboratory strain carrying F prime plasmid, however, there was a complex formation between the antiplasmid compounds and the plasmid DNA isolated from both the clinical and laboratory strains. In addition there was a difference between the curing effect of two phenothiazines – the PMZ and TFP – on some E. coli strains in this study. The mechanism of action of different antiplasmid compounds was investigated on model nucleic acids such as calf thymus DNA and plasmid DNA. The pyrido[3,2-g] quinoline and phenothiazine derivatives seemed to have a complex formation with the model nucleic acids. Some of the compounds modified the activity of membrane efflux proteins. Based on the effect of trifluoromethyl ketones earlier studied my attention was focused on the combination of the trifluoromethyl ketone proton pump inhibitor TF18 with well-known antiplasmid compounds such as promethazine, trifluoperazine and 9-aminoacridine. In checkerboard studies the interaction between proton pump inhibitor and tricyclic compounds has been examined and it turned out that the interaction of proton pump inhibitor and trifluoperazine exerted synergistic antibacterial and plasmid curing effect on E. coli doxycycline resistant clinical strain due to the alteration of activity of membrane transporters. The role of proton pump system of the bacterial membrane was studied on Helicobacter pylori strains. The trifluoroketone proton pump inhibitor was able to block the proton motive forces and the activity of flagellar motor of both clarithromycin sensitive and resistant isolates of Helicobacter pylori . Since swimming was more sensitive to the inhibition than tumbling, I can suppose that TF18 works as an un-coupler in biological motor. The sensitivity of MDR1 type of eukaryotic ABC-transporter to resistance modifiers was studied on cancer cells. The synthetic benzo[b]-1,8-naphthyridine, pyridoquinoline, aza-oxafluorene and pregnane derivatives exerted reversing action of P-glycoprotein. Furthermore natural compounds, like coumarin derivatives and some fractions of persimmon extracts have been found to be potent resistance reversal agents against tumour cells.

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Authors: Nagendra Mishra, Tulika Prasad, Neeraj Sharma, Anurag Payasi, Rajendra Prasad, Dwijendra Gupta and Randhir Singh

Pathogenic yeasts from the genus Candida can cause serious infection in humans particularly, in immunocompromised patients and are now recognized as major agents of hospital acquired (nosocomial) infections. In the recent years, there has been a marked increase in the incidence of treatment failures in candidiasis patients receiving long-term antifungal therapy, which has posed a serious problem in its successful use in chemotherapy. Candida cells acquire drug resistance (MDR) during the course of the treatment. The mechanisms of resistance to azole antifungal agents have been elucidated in Candida species and can be mainly categorized as (i) changes in the cell wall or plasma membrane, which lead to impaired drug (azole) uptake; (ii) alterations in the affinity of the drug target Erg11p (lanosterol 14∝-demethylase) especially to azoles or in the cellular content of Erg11p due to target site mutation or overexpression of the ERG11 gene; and (iii) the efflux of drugs mediated by membrane transport proteins belonging to the ATP-binding cassette (ABC) transporters, namely CDR1 and CDR2 or to the major facilitator superfamily (MFS) transporter, CaMDR1 . Many such manifestations are associated with the formation of Candida biofilms including those occurring on devices like indwelling intravascular catheters. Biofilm-associated Candida show uniform resistance to a wide spectrum of antifungal drugs. A combination of different resistance mechanisms is responsible for drug resistance in clinical isolates of Candida species.

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Clavel, F., Hance, A. J.: Medical progress: HIV drug resistance. N Engl J Med 350 , 1023–1035 (2004). Hance A. J. Medical progress: HIV drug resistance

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2472 2482 Althaus, C. L., Bonhoeffer, S.: Stochastic interplay between mutation and recombination during the acquisition of drug resistance mutations in human immunodeficiency

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Abstract  

Gatifloxacin (GTN) was derivatized to its dithiocarbamate derivative and its radiolabeling with technetium-99m (99mTc) using the [99mTc≡N]2+ core was investigated. The appropriateness of the 99mTcN–gatifloxacin dithiocarbamate (99mTcN–GTND) complex as a potential multi-drug-resistance Streptococcus pneumoniae (MRSP) infection radiotracer was evaluated in terms of stability in saline, serum, in vitro binding with MRSP and biodistribution in artificially MRSP infected Male Wistar Rats (MWR). In saline the 99mTcN–GTND complex showed more than 90% labeling yield up to 4 h with a maximum yield of 98.25 ± 0.20%, after reconstitution. In serum the 99mTcN–GTND complex showed stability up to 16 h of incubation with the appearance of insignificant 15.95% undesirable side products. The 99mTcN–GTND complex demonstrated saturated in vitro binding with MRSP with a maximum value of 75.50 ± 1.00% (at 90 min). In MWR model of group A, almost six times higher uptake of the labeled GTND was monitored in the muscle of MWR infected with live MRSP as compared to the inflamed and normal muscles. Based on the higher labeling yield in saline, in vitro stability in serum, saturated in vitro binding with live MRSP and promising biodistribution in MWR model we recommend 99mTcN–gatifloxacin dithiocarbamate complex as a potential MRSP infection radiotracer.

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Authors: Kouassi N’Guessan, Timothée Ouassa, Anna S. Dean, Riccardo Alagna, Guy Damien Adagra, Valeri Ibode, Daniela M. Cirillo and Jacquemin Kouakou

public health challenge of drug-resistant TB. As Côte d'Ivoire does not yet have the capacity to routinely test all TB patients for drug susceptibility, two national drug resistance surveys were conducted in 1995 and 2006. The proportions of new TB cases

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Authors: Farideh Rahmani, Abbas Fooladi, Seyed Marashi and Mohammad Nourani

Cholera is a serious epidemic and endemic disease caused by the Gram-negative bacterium Vibrio cholerae. SXT is an integrative conjugation element (ICE) that was isolated from a V. cholerae; it encodes resistance to the antibiotics chloramphenicol, streptomycin and sulfamethoxazole/trimethoprim. One hundred seven V. cholerae O1 strains were collected from cholera patients in Iran from 2005 to 2007 in order to study the presence of SXT constin and antibiotic resistance.The study examined 107 Vibrio cholerae strains isolated from cholera prevalent in some Iranian provinces. Bacterial isolation and identification were carried out according to standard bacteriological methods. Minimum Inhibitory Concentration (MIC) and Minimum Bactericidal Concentration (MBC) to four antibiotics (chloramphenicol, streptomycin, sulfamethoxazole, and trimethoprim) were determined by broth microdilution method. PCR was employed to evaluate the presence of established antibiotic resistance genes and SXT constin using specific primer sets.The resistance of the clinical isolates to sulfamethoxazole, trimethoprime, chloramphenicol, and streptomycin was 97%, 99%, 99%, and 90%, respectively. The data obtained by PCR assay showed that the genes sulII, dfrA1, floR, strB, and sxt element were present in 95.3%, 95.3%, 81.3%, 95.3%, and 95.3% of the V. cholerae isolates.The Vibrio strains showed the typical multidrug-resistance phenotype of an SXT constin. They were resistant to sulfamethoxazole, trimethoprime, chloramphenicol, and streptomycin. The detected antibiotic resistance genes included dfrA for trimethoprim and floR, strB, sulII and int, respectively, for chloramphenicol, streptomycin, sulfamethoxazole, as well as the SXT element.

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Authors: András Dávid Tóth, Gergely Varga, Nikolett Wohner, Péter Farkas, Laura Horváth, Gergely Szombath, Andrea Ceglédi, András Kozma, Péter Reményi, Tamás Masszi and Gábor Mikala

compendium of known drug resistance mechanisms with emerging tumor profiling technologies. Leukemia 2019; 33: 863–883. 8 Abraham J, Salama NN, Azab AK. The role of P-glycoprotein in

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