• Title/Summary/Keyword: Double bladder

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Transfer of Genes for Antimicrobial Resistance and Toxin of Hemolytic Escherichia coli Isolated from Feces of Pig Suffering Diarrhea to Human Isolates (설사 증상의 돼지 분변에서 분리된 용혈성 대장균의 항생제 내성과 독소의 인체로부터 분리된 균주로의 전이)

  • Lee Kyenam;Jung Byeong Yeal;Lee Yeonhee
    • Korean Journal of Microbiology
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    • v.40 no.4
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    • pp.286-294
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    • 2004
  • Between 1997 and 1998 in Korea, 56 isolates of Escherichia coli were obtained from pig suffering diarrhea. Among those, 38 isolates that showed the hemolytic activity, antimicrobial resistance, and toxin production were studied. Among 38 isolates, thirty-six isolates $(94.7\%)$ were resistant to tetracycline, 27 isolates $(71.0\%)$ were resistant to ampicillin, 26 isolates $(68.4\%)$ were resistant to chloramphenicol, and 21 isolates $(55.2\%)$ were resistant to trimethoprim, while none was resistant to aztreonam, amikacin, and norfloxacin. Among these iso­lates, 21 isolates $(55.3\%)$ were multiple drug resistant to at least four different class antimicrobial agents. Extended spectrum $\beta-lactamase$ producing isolates were not detected in the double disk synergy test. In these hemolytic Escherichia coli, heat-stable enterotoxin $(89.5\%)$ was the most prevalent toxin, followed by vero­toxins $(47.4\%),$ and then heat-labile enterotoxin $(31.6\%).$ Except 8 isolates $(21.0\%)$ which produced ST only, 12 isolates $(31.6\%)$ produced ST and LT, 13 isolates $(34.2\%)$ produced ST, VT, and VTe, and 5 isolates $(13.2\%)$ produced VT and VTe. However, none produced all 4 types of toxin, simultaneously. The predominant serotype could not be determined by the agglutination method. Sixteen isolates $(42.1\%)$ were strongly adhered to T-24 bladder cell and 17 isolates $(44.7\%)$ were to Caco-2 intestinal cell. Especially, 11 strains $(28.9\%)$ were evaluated as strongly adhesive to both T-24 cells and Caco-2 cells. Genes for toxin and the antimicrobial resistance were transferred to clinical isolates of Escherichia coli from human urine by the filter mating method. Results suggest the possibility that antimicrobial resistance and toxin can be transferred from animals to humans by direct con­tact of resistant bacteria as well as gene transfer, although there was no correlation between toxin production, adherent activity, and antimicrobial resistance among hemolytic E. coli isolated from pig suffering diarrhea.

Licochalcone C Induces Autophagy in Gefitinib-sensitive or-resistant Human Non-small Cell Lung Cancer Cells (Gefitinib-민감성 또는 내성 비소세포폐암 세포에서 Licochalcone C에 의한 자가포식 유도)

  • Oh, Ha-Na;Yoon, Goo;Chae, Jung-Il;Shim, Jung-Hyun
    • Journal of Life Science
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    • v.29 no.12
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    • pp.1305-1313
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    • 2019
  • Licochalcone (LC), isolated from the roots of Glycyrrhiza inflata has multiple pharmacological effects including anti-inflammatory and anti-tumor activities. To date, Licochalcone C (LCC) has induced apoptosis and inhibited cell proliferation in oral and bladder cancer cells, but lung cancer has not yet been studied. In addition, no study reported LCC-induced autophagy in cancer until now. The present study was designed to investigate the effect of LCC on gefitinib-sensitive and -resistant lung cancer cells and elucidate the mechanism of its action. The 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay data showed that LCC significantly inhibited cell viability in non-small cell lung cancer (NSCLC) HCC827 (gefitinib-sensitive) and HCC827GR (gefitinib-resistant) cell lines. Interestingly, Annexin V/7-aminoactinomycin D double staining and cell cycle analysis showed an apoptosis rate within about 20% at the highest concentration of LCC. LCC induced G2/M arrest by reducing the expression of the cell cycle G2/M related proteins cyclin B1 and cdc2 in NSCLC cell lines. Treatment of LCC also induced autophagy by increasing the expression of the autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3) and the protein autophagy-related gene 5 involved in the autophagy process. In addition, LCC increased the production of reactive oxygen species (ROS), and the cell viability was partially restored by treatment with the ROS inhibitor N-acetyl-L-cysteine. In western blotting analysis, the expression of cdc2 was increased and LC3 was decreased by the simultaneous treatment of NAC and LCC. These results indicate that LCC may contribute to anti-tumor effects by inducing ROS-dependent G2/M arrest and autophagy in NSCLC. In conclusion, LCC treatment may be useful as a potential therapeutic agent against NSCLC.