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Author (up) Aarestrup, F.M.; Bager, F.; Jensen, N.E.; Madsen, M.; Meyling, A.; Wegener, H.C. file  url
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  Title Surveillance of antimicrobial resistance in bacteria isolated from food animals to antimicrobial growth promoters and related therapeutic agents in Denmark Type Journal Article
  Year 1998 Publication APMIS : Acta Pathologica, Microbiologica, et Immunologica Scandinavica Abbreviated Journal Apmis  
  Volume 106 Issue 6 Pages 606-622  
  Keywords Animals; Anti-Bacterial Agents/*pharmacology; Bacteria/*drug effects/*isolation & purification; Bacterial Infections/drug therapy/veterinary; Cattle; Cattle Diseases/drug therapy/microbiology; Cecum/microbiology; Chickens/growth & development; Drug Resistance, Microbial; Feces/microbiology; Meat/*microbiology; Microbial Sensitivity Tests/veterinary; Poultry Diseases/drug therapy/microbiology; Swine/growth & development; Swine Diseases/drug therapy/microbiology  
  Abstract This study was conducted to describe the occurrence of acquired resistance to antimicrobials used for growth promotion among bacteria isolated from swine, cattle and poultry in Denmark. Resistance to structurally related therapeutic agents was also examined. Three categories of bacteria were tested: 1) indicator bacteria (Escherichia coli, Enterococcus faecalis, Enterococcus faecium), 2) zoonotic bacteria (Campylobacter, Salmonella, Yersinia enterocolitica), and 3) animal pathogens (E. coli, Staphylococcus aureus, coagulase-negative staphylococci (CNS), Staphylococcus hyicus, Actinobacillus pleuropneumoniae). All antimicrobials used as growth promoters in Denmark and some structurally related therapeutic agents (in brackets) were included: Avilamycin, avoparcin (vancomycin), bacitracin, carbadox, flavomycin, monensin, olaquindox, salinomycin, spiramycin (erythromycin, lincomycin), tylosin (erythromycin, lincomycin), and virginiamycin (pristinamycin). Bacterial species intrinsically resistant to an antimicrobial were not tested towards that antimicrobial. Breakpoints for growth promoters were established by population distribution of the bacteria tested. A total of 2,372 bacterial isolates collected during October 1995 to September 1996 were included in the study. Acquired resistance to all currently used growth promoting antimicrobials was found. A frequent occurrence of resistance were observed to avilamycin, avoparcin, bacitracin, flavomycin, spiramycin, tylosin and virginiamycin, whereas resistance to carbadox, monensin, olaquindox and salinomycin was less frequent. The occurrence of resistance varied by animal origin and bacterial species. The highest levels of resistance was observed among enterococci, whereas less resistance was observed among zoonotic bacteria and bacteria pathogenic to animals. The association between the occurrence of resistance and the consumption of the antimicrobial is discussed. The results show the present level of resistance to growth promoters in bacteria from food animals in Denmark. They will form the baseline for comparison with future prospective studies, thereby enabling the determination of trends over time.  
  Call Number Serial 1676  
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Author (up) Aertsen, A.; Michiels, C.W. file  url
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  Title SulA-dependent hypersensitivity to high pressure and hyperfilamentation after high-pressure treatment of Escherichia coli lon mutants Type Journal Article
  Year 2005 Publication Research in Microbiology Abbreviated Journal Res Microbiol  
  Volume 156 Issue 2 Pages 233-237  
  Keywords Colony Count, Microbial; Culture Media; Escherichia coli--genetics, growth & development; Escherichia coli Proteins--genetics, metabolism; Gene Expression Regulation, Bacterial; Hydrostatic Pressure; Mutation; Protease La--genetics; SOS Response (Genetics); Ultraviolet Rays  
  Abstract High-pressure treatment (>100 MPa) is known to induce several heat shock proteins as well as an SOS response in Escherichia coli. In the current work, we have investigated properties with respect to high-pressure treatment of mutants-deficient in Lon, a pressure-induced ATP-dependent protease that belongs to the heat shock regulon but that also has a link to the SOS regulon. We report that lon mutants show increased pressure sensitivity and exhibit hyperfilamentation during growth after high-pressure treatment. Both phenotypes could be entirely attributed to the action of the SOS protein SulA, a potent inhibitor of the cell division ring protein FtsZ and a specific target of the Lon protease, since they were suppressed by knock-out of SulA. Introduction of the lexA1 allele, which effectively blocks the entire SOS response, also suppressed the high pressure hypersensitivity of lon mutants, but not their UV hypersensitivity. These results indicate the existence of a SulA-dependent pathway of high-pressure-induced cell filamentation, and suggest involvement of the SOS response, and particularly of SulA, in high-pressure-mediated cell death in E. coli strains which are compromised in Lon function.  
  Call Number Serial 301  
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Author (up) Anderson, J.L.; Albergotti, L.; Proulx, S.; Peden, C.; Huey, R.B.; Phillips, P.C. file  url
openurl 
  Title Thermal preference of Caenorhabditis elegans: a null model and empirical tests Type Journal Article
  Year 2007 Publication The Journal of Experimental Biology Abbreviated Journal J Exp Biol  
  Volume 210 Issue Pt 17 Pages 3107-3116  
  Keywords Acclimatization; Animals; Behavior, Animal; Body Temperature Regulation; Caenorhabditis elegans--physiology; Escherichia coli--growth & development; Models, Biological; Temperature  
  Abstract The preferred body temperature of ectotherms is typically inferred from the observed distribution of body temperatures in a laboratory thermal gradient. For very small organisms, however, that observed distribution might misrepresent true thermal preferences. Tiny ectotherms have limited thermal inertia, and so their body temperature and speed of movement will vary with their position along the gradient. In order to separate the direct effects of body temperature on movement from actual preference behaviour on a thermal gradient, we generate a null model (i.e. of non-thermoregulating individuals) of the spatial distribution of ectotherms on a thermal gradient and test the model using parameter values estimated from the movement of nematodes (Caenorhabditis elegans) at fixed temperatures and on a thermal gradient. We show that the standard lab strain N2, which is widely used in thermal gradient studies, avoids high temperature but otherwise does not exhibit a clear thermal preference, whereas the Hawaiian natural isolate CB4856 shows a clear preference for cool temperatures ( approximately 17 degrees C). These differences are not influenced substantially by changes in the starting position of worms in the gradient, the natal temperature of individuals or the presence and physiological state of bacterial food. These results demonstrate the value of an explicit null model of thermal effects and highlight problems in the standard model of C. elegans thermotaxis, showing the value of using natural isolates for tests of complex natural behaviours.  
  Call Number Serial 260  
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Author (up) Baylis, H.A.; Furuichi, T.; Yoshikawa, F.; Mikoshiba, K.; Sattelle, D.B. file  url
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  Title Inositol 1,4,5-trisphosphate receptors are strongly expressed in the nervous system, pharynx, intestine, gonad and excretory cell of Caenorhabditis elegans and are encoded by a single gene (itr-1) Type Journal Article
  Year 1999 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
  Volume 294 Issue 2 Pages 467-476  
  Keywords Amino Acid Sequence; Animals; Animals, Genetically Modified; Binding Sites; Caenorhabditis elegans/*genetics; Calcium Channels/*genetics/*metabolism; Cell Membrane/genetics/metabolism; Conserved Sequence; Gene Expression Profiling; Gonads/metabolism; Helminth Proteins/*genetics/*metabolism; Inositol 1,4,5-Trisphosphate Receptors; Intestines/metabolism; Molecular Sequence Data; Nervous System/metabolism; Pharynx/metabolism; RNA, Messenger; Receptors, Cytoplasmic and Nuclear/*genetics/*metabolism; Rectum/cytology/metabolism  
  Abstract Inositol 1,4,5-trisphosphate (InsP3) activates receptors (InsP3Rs) that mediate intracellular Ca(2+ )release, thereby modulating intracellular calcium signals and regulating important aspects of cellular physiology and gene expression. To further our understanding of InsP3Rs we have characterised InsP3Rs and the InsP3R gene, itr-1, from the model organism Caenorhabditis elegans. cDNAs encoding InsP3Rs were cloned enabling us to: (a) identify three putative transcription start sites that result in alternative mRNA 5' ends: (b) detect alternative splicing at three sites and: (c) determine the full genomic organisation of the itr-1 gene. The InsP3R protein (ITR-1) is approximately 42 % identical with known InsP3Rs and possesses conserved structural features. When the putative InsP3 binding domain was expressed in Escherichia coli, specific binding of InsP3 was detected. Using antibodies against ITR-1 we detected a protein of 220 kDa in C. elegans membranes. These antibodies and itr-1::GFP (green fluorescent protein) reporter constructs were used to determine the expression pattern of itr-1 in C. elegans. Strong expression was observed in the intestine, pharynx, nerve ring, excretory cell and gonad. These results demonstrate the high degree of structural and functional conservation of InsP3Rs from nematodes to mammals and the utility of C. elegans as a system for studies on InsP3R mediated signalling.  
  Call Number Serial 309  
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Author (up) Bhattacharya, R.; Beck, D.J. file  url
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  Title Survival and SOS induction in cisplatin-treated Escherichia coli deficient in Pol II, RecBCD and RecFOR functions Type Journal Article
  Year 2002 Publication DNA Repair Abbreviated Journal DNA Repair (Amst)  
  Volume 1 Issue 11 Pages 955-966  
  Keywords Antineoplastic Agents/*pharmacology; Bacterial Proteins/physiology; Cell Division/drug effects/genetics/radiation effects; Cisplatin/*pharmacology; DNA Damage/drug effects/radiation effects; DNA Polymerase II/*physiology; DNA Polymerase III/physiology; DNA Repair/drug effects/radiation effects; DNA-Binding Proteins/physiology; Dose-Response Relationship, Drug; Drug Resistance, Bacterial/physiology; Escherichia coli/*drug effects/enzymology; Escherichia coli Proteins/pharmacology/*physiology; Exodeoxyribonuclease V; Exodeoxyribonucleases/*physiology; Lac Operon; SOS Response (Genetics)/*physiology; beta-Galactosidase/metabolism  
  Abstract Cisplatin is a potent anticancer agent forming intrastrand-crosslinks in DNA. The efficacy of cisplatin in chemotherapy can be limited by the development of tumor resistances such as elevated DNA repair or damage tolerance. In Escherichia coli, cisplatin treatment causes induction of the SOS regulon resulting in elevated levels of DNA Pol II, DNA Pol IV, DNA Pol V, the cell division inhibitor SfiA (SulA), homologous recombination (HR) and DNA repair. In this work, the roles of Pol II and HR in facilitating resistance of E. coli to cisplatin are studied. SOS induction levels were measured by beta-galactosidase assays in cisplatin-treated and untreated E. coli PQ30 that has the lacZ gene fused to the sfiA promoter. Comparative studies were carried out with derivatives of PQ30 constructed by P1 transduction that have transposon insertions in the polB gene, the recB gene blocking the RecBCD pathway of HR and genes of the RecFOR pathway of HR. Resistance of E. coli strains to cisplatin as determined by plating experiments decreased in the following order: parent PQ30 strain, polB > recO, recR, recF > recB. Both the RecBCD and RecFOR pathways of HR are important for survival when E. coli is exposed to cisplatin, because treatment of double mutants deficient in both pathways reduced colony forming ability to 37% in 6-9min in comparison to 39-120min for single mutants. Pol II and RecF appear to function in two distinct pathways to initiate replication blocked due to damage caused by cisplatin because function of Pol II was required for survival in mutants deficient in the RecFOR pathway after 2h of cisplatin treatment. In contrast, Pol II was not required for survival in recB mutants. SOS induction was delayed in RecFOR deficient mutants but occurred at high levels in the recB mutant soon after cisplatin treatment in a RecFOR-dependent way. An SfiA independent, DNA damage dependent pathway is apparently responsible for the filamentous cells observed after cisplatin or MMC treatments of these SfiA defective strains.  
  Call Number Serial 407  
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