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1

Bacteriophage therapy of bacterial infections: an update of our institute's experience

100%

Weber-Dabrowska B., Mulczyk M., Gorski A.

Archivum Immunologiae et Therapiae Experimentalis

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2000

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tom 48

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nr 6 Spec.Iss.

547-551

2

Overcoming the challenge; In Vivo efficacy of miltefosine for chronic cutaneous leishmaniasis

86%

Tunali V., Harman M., Cavus I., Gunduz C., Ozbilgin A., Turgay N.

Acta Parasitologica

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2021

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tom 66

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nr 2

3

E-test determination of antifungal susceptibility of Candida species isolated from turkeys

86%

Sokol I., Tokarzewski S., Bobrek K., Gawel A.

Journal of Veterinary Research

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2020

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tom 64

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nr 4

4

Upregulation of miR-340-5p reverses cisplatin sensitivity by inhibiting the expression of CDK6 in HepG2 cells

86%

Tian S., Liu Z., Zhou Q., Wu R., Huang X., Liang Z., Zhang Z., Tian X.

Folia Biologica

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2021

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tom 69

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nr 2

5

Characterization of phosphate transporter(s) and understanding their role in Leishmania donovani parasite

86%

Sindhu K. J., Kureel A. K., Saini S., Kumari S., Verma P., Rai A. K.

Acta Parasitologica

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2018

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tom 63

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nr 1

6

Characterization of transplasma membrane electron transport chain in wild and drug-resistant Leishmania donovani promastigote and amastigote

86%

Debnath D., Hossain M. A., Das M., Kabir A., Ibrahim M., Amin M. N., Chowdhury A., Pervin R.

Acta Parasitologica

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2019

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tom 64

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nr 4

7

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Design, molecular docking, drug-likeness, and molecular dynamics studies of 1,2,4-trioxane derivatives as novel Plasmodium falciparum falcipain-2 (FP-2) inhibitors

86%

Ghosh S., Chetia D., Gogoi N., Rudrapal M.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2021

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tom 102

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nr 3

8

Resistance for anti-tuberculosis drugs in Central Black Sea Region of Turkey

86%

Bilgin S., Unsal M., Cebi H. H., Akgunes A.

Polish Journal of Microbiology

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2010

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tom 59

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nr 2

125-128

One of the primary aims in tuberculosis (TB) management is to detect new cases as early as possible, and instigate the most appropriate therapy, for which it is important to know the characteristics of TB drug resistance in society. The aim of our study was to determine the resistance status of tuberculosis in the Samsun region of Turkey. To achieve that, the medical records of 1,029 pulmonary tuberculosis patients admitted to Samsun Chest Diseases and Chest Surgery Hospital between 2004 and 2006 were analyzed for drug resistance characteristics. In order to define the problem, isolates were tested on Lowenstein-Jensen medium. For drug susceptibility testing, isoni-azid (1), streptomycin (S), ethambutol (E), rifampicin (R) and the radiometric Bactec 460 TB system were used. Eighty-six percent (86%) of the cases (623/721) were new patients, and 13.5% (98/721) were previously treated cases. One hundred and thirty-four (134) of the 721 patients (18.6%) had resistance to one or more drugs. Resistance to any drug was determined in 16.9% (105/623) cases of new patients. I resistance was 13.2%, any R resistance was 2.9%, and multi-drug resistance (MDR) was 1.9%. In previously treated cases, resistance to any drug was 29.6%, any I resistance was 26.5%, any R resistance was 15.3%, and MDR was 13.3%. It was concluded that resistance to anti-tuberculosis drugs is an important problem in Samsun.

9

A case of a drug resistance of nematodes Oesophagostomum dentatum

86%

Gundlach J. L., Sadzikowski A. B., Tomczuk K.

Wiadomości Parazytologiczne

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1998

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tom 44

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nr 3

10

DNA repair in drug resistance induced by fusion tyrosine kinases

86%

Blasiak J.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

11

Potential role of transforming growth factor beta 1 in drug resistance of tumor cells

86%

Stoika R., Yakymovych M., Souchelnytskyi S., Yakymovych I.

Acta Biochimica Polonica

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2003

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tom 50

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nr 2

Acquired drug resistance of tumor cells is frequently observed in cancer patients undergoing chemotherapy. We studied murine leukemia L1210 cells sensitive and resistant to the cytotoxic action of cisplatin and showed that cisplatin-resistant leukemia cells were also refractory to TGF /β1-dependent growth inhibition and apoptosis. Addressing the question about the mechanisms responsible for the cross-resistance to cisplatin and TGF /β1, we found that cisplatin- and TGF /β1-resistant L1210 cells possessed a decreased expression of type I TGF /β1 receptor, while the expression of type II TGFβ1 receptor was not affected. Western blot analysis of Smad proteins 2, 3, 4, 6, and 7, which participate in signal transduction pathway down-stream of the TGF /β1 receptors, revealed an increased expression of Smad 6, inhibiting TGF β1 action, only in cisplatin- and TGFβ1-resistant L1210 cells. TGFβ1 and especially the cytotoxic mistletoe agglutinin increased Smad 6 expression in TGF β1-sensitive but not in TGF /β1-resistant L1210 cells. TGF /β1-resistant L1210 cells also differed from TGF /β1-sensitive cells by the lack of expression of the pro-apoptotic p53 protein and higher level of expression of the anti-apoptotic Bcl-2 protein. Thus, the described co-expression of tumor cell refractoriness to an anti-cancer drug and to the inhibitory cytokine TGF β1 is accompanied by multiple changes in the TGF β1 signal transduction pathway and in other regulatory systems of the target cells. Besides, we found that various anti-tumor drugs and cytotoxic plant lectins increased the level of TGF β1 expression in both TGF β1-sensitive and -resistant L1210 cells. A hypothesis is proposed that TGF β1 can at least partly mediate the effect of cell-stressing agents and, thus, the development of TGF β1 resistance may be responsible for the appearance of tumor cell refractoriness to the action of some anti-cancer drugs.

12

Molecular mechanism of resistance to antifolates, a review

86%

Banerjee D., Ercikan-Abali E., Waltham M., Schnieders B., Hochhauser D., Li W. W., Fan J., Gorlick R., Goker E., Bertino J. R.

Acta Biochimica Polonica

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1995

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tom 42

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nr 4

Methotrexate (MTX) is a clinically important antifolate that has been used in combination with other chemotherapeutic agents in the treatment of malignancies including acute lymphocytic leukemia, osteosarcoma, carcinomas of the breast, head and neck, choriocarcinoma and non-Hodgkin's lymphoma. The primary target of MTX is the enzyme dihydrofolate reductase (DHFR) which catalyzes the reduction of folate and 7,8-dihydrofoIate to 5,6,7,8-tetrahydrofolate. Understanding of MTX action has revealed how cells acquire resistance to this drug. The four known mechanisms of MTX resistance are a decrease in the uptake of the drug, a decrease in the retention of the drug due to defective polyglutamylation or an increase in polyglutamate breakdown, an increase in the enzyme activity and a decrease in the binding of MTX to DHFR. The molecular basis for some of these mechanisms has been elucidated in MTX resistant cell lines; in particular the occurrence of gene amplification resulting in increased DHFR and point mutations resulting in altered DHFR with reduced affinity for MTX. Cloning of the human folylpolyglutamate synthase gene and the reduced folate transport gene have been reported recently and should facilitate the identification of the molecular basis of these resistant phenotypes. DHFR protein has been shown to regulate its synthesis by exerting an inhibitory influence on its own translation. Addition of MTX relieves this inhibition thus providing a possible molecular explanation for the rapid rise in DHFR activity noted in some cells after MTX administration. Alterations in genes involved in regulating the cell cycle such as cyclin D1 and the retinoblastoma (Rb) gene have also been shown to influence cellular response to MTX. Overexpression of cyclin D1 in HT1080, a human fibrosarcoma cell line, results in decreased MTX sensitivity. The molecular basis of this observation is under investigation. Abnormalities in the Rb gene may also have profound effects on MTX sensitivity. Rb interacts with the family of transcription factors called E2F reducing transcription of genes that contain E2F binding sites in the promoter regions e.g. DHFR. When Rb is deleted or rendered nonfunctional levels of "free" or unbound E2F are high resulting in enhanced transcription of genes such as DHFR. This results in increased DHFR protein and may lead to MTX resistance. As the knowledge regarding mechanisms of resistance increases newer approaches to circumvent such resistance or to target resistant cells can be undertaken.

13

The effect of new anthracycline derivatives on the induction of apoptotic processes in human neoplastic cells

86%

Gruber B. M., Anuszewska E. L., Priebe W.

Folia Histochemica et Cytobiologica

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2004

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tom 42

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nr 2

14

Mesenchymal stromal cell therapy in MDR/XDR tuberculosis: a concise review

72%

Joshi L., Chelluri L. K., Gaddam S.

Archivum Immunologiae et Therapiae Experimentalis

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2015

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tom 63

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nr 6

15

Leukemic stem cells: from metabolic pathways and signaling to a new concept of drug resistance targeting

72%

Styczynski J., Drewa T.

Acta Biochimica Polonica

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2007

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tom 54

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nr 4

717-726

Cancer stem cells are a small subset of cancer cells constituting a reservoir of self-sustaining cells with the exclusive ability to self-renew and maintain the tumor. These cells are identified by specific stem cell markers: antigens, molecules and signaling pathways. Transcription factors and molecules associated with oncogenesis, such as NF-κB, Bmi-1, Notch, WNT beta-catenin, Sonic hedgehog and their biochemical pathways, active only in a small minority of cancer cells might play key roles in determining the biology and the overall long-term behavior of a tumor. The molecules and pathways specific for cancer stem cells, which contribute to their drug resistance, are potential targets for new therapeutic strategies.

16

Microbiology and drug resistance of pathogens in patients hospitalized at the nephrology department in the south of Poland

72%

Michno M., Sydor A., Walaszek M., Sulowicz W.

Polish Journal of Microbiology

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2018

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tom 67

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nr 4

A retrospective study was conducted among 498 patients with urinary tract infections (UTI) referred to our department from January 2013 to December 2015. This study was performed to evaluate the etiology of UTI and the antibiotic susceptibility profile of Escherichia coli (E.coli) as the main etiological factor in different age groups. Urine samples were examined using standard microbiological methods. Three hundred sixty-three samples (72.9%) were identified as E.coli, of which 29 (8.0%) can produce extended-spectrum β-lactamases (ESBL). E.coli was highly sensitive to imipenem (100.0%), gentamicin (91.0%), nitrofurantoin (89.4%), amikacin (88.2%), piperacillin/tazobactam (87.0%) and cephalosporins (79.7–89.5%). Low sensitivity was found in relation to fluoroquinolones (60.3–70.4%). E.coli was least sensitive to ampicillin (30.2%) and amoxicillin/clavulanic acid (49.9%). We observed a significant fall in susceptibility level to piperacillin/tazobactam (68.4% vs. 88.8%; p=0.017), amikacin (61.1% vs. 90.7%; p=0.001), gentamicin (70.0% vs. 93.2%; p=0.002), cefalexin (41.2% vs. 83.3%; p<0.001), cefotaxime (63.6% vs. 89.4%; p=0.002), ceftazidime (61.9% vs. 85.6%; p=0.008), cefepime (73.7% vs. 91.1%; p=0.025), ciprofloxacin (54.1% vs. 72.2%; p=0.024) and norfloxacin (40.5% vs. 62.5%; p=0.011) among patients with catheter-associated UTI (CAUTI) compared to those with non-CAUTI. A similar susceptibility profile was observed between different age groups. In the longevity, E.coli showed a higher sensitivity to cephalosporins than in the young-old group. E.coli susceptibility to fluoroquinolones was low, which excludes them as a first-line drug in our department. Nitrofurantoin may be used as an alternative drug to carbapenems. Monitoring of susceptibility pattern is of great importance.

17

The assessment of water sanitary quality and the presence of drug-resistant Escherichia coli strains in waters used for recreation in lesser Poland

72%

Chmiel M. J., Wojtowicz P., Lojas E.

Folia Pomeranae Universitatis Technologiae Stetinensis. Agricultura, Alimentaria, Piscaria et Zootechnica

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2017

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tom 41

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nr 1(332)

18

Apoptosis monitoring in human acute leukaemia cells stimulated by Bcl-2 antisense oligonucleotide and BAY K 8644

72%

Kocki J., Kocki T., Lancut M., Bogucka-Kocka A., Cioch M., Dmoszynska A., Wojcierowski J.

Polish Journal of Environmental Studies

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2004

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tom 13

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nr Suppl.2, Part 1

In this study we investigated effects of bcl-2 antisense oligonucleotides (AS) and BAY K 8644 (B), calcium channel agonist, on human leukaemic cells from non-treatment patients with acute myeloblastic leukaemias. Apoptotic cells were observed in electron and fluorescent microscopes. When we examined the effects of AS + B on cells, level of bcl-2 mRNA decreased more as in cells stimulated by AS only. These observations indicate that AS with B in human leukaemic cells disturb cell viability by inducing apoptosis.

19

Reversal of drug resistance by silencing Survivin gene expression in acute myeloid leukemia cells

72%

Wu Y. H., You Y., Chen Z.-C., Zou P.

Acta Biochimica Polonica

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2008

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tom 55

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nr 4

673-680

The role of Survivin in the pathogenesis of leukemia was explored in order to discover the effective avenues for gene therapy. Most primary leukemia cells isolated from patients as well as three leukemia cell lines (HL-60, K562, and U937) all expressed Survivin gene. To investigate the relationship between Survivin and chemotherapeutic resistance, HL-60 cells were treated with daunorubicin (DNR), mitoxantrone (MIT) or arsenious oxide (As2O3), and it was found that after 24h the level of Survivin mRNA was decreased by 9.7%, 41.0% and 27.5%, respectively. At 72 h, the level of Survivin mRNA was increased by 21.2% and 65.2% in HL-60 cells treated with DNR or MIT, but decreased by 33.2% in those treated with As2O3 as compared with that in the cells treated for 24 h. These results showed that DNR and MIT could initally decrease the expression of Survivin and then increase it, but As2O3 could decrease the Survivin expression continually. Furthermore, shRNA plasmids targeting the Survivin gene (pEGFP-Survivin), which can silence the expression of Survivin with a high specificity, were constructed. pEGFP-Survivin and pEGFP-H1 were transfected into HL-60 cells via electroporation and selected by G418, and HL-60/Survivin and HL-60/EGFP cells were obtained. After treatment with DNR, the cell survival rate and IC50 of DNR in HL-60/Survivin cells were decreased substantially as compared with those of HL-60/EGFP and HL-60 cells (IC50of DNR:18.3±2.45 vs40.8±6.37 and 39.2±5.91 ng/ml, respectively), and the apoptosis rate was elevated ((84.3±19.7)% vs(45.8±13.8)% and (50.9±12.4)%, respectively). These results suggest that shRNA can down-regulate the expression of Survivin in HL-60 cells substantially and improve their sensitivity to DNR. They also further explain the pathogenesis of leukemia drug resistance and provide new theory in the design of clinical therapies.

20

CD133-positive cells from non-small cell lung cancer show distinct sensitivity to cisplatin and afatinib

72%

Alama A., Gangemi R., Ferrini S., Barisione G., Orengo A. M., Truini M., Bello M. G. D., Grossi F.

Archivum Immunologiae et Therapiae Experimentalis

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2015

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tom 63

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nr 3

Ograniczanie wyników

Bacteriophage therapy of bacterial infections: an update of our institute's experience