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      • Biochemical and Molecular Analysis of Deltamethrin Resistance in the Common Bed Bug, Cimex lectularius Linnaeus (Hemiptera: Cimicidae)

        Kyong Sup Yoon,Deok Ho Kwon,Joseph P. Strycharz,Craig S. Hollingsworth,J. Marshall Clark,Si Hyeock Lee 한국응용곤충학회 2009 한국응용곤충학회 학술대회논문집 Vol.2009 No.05

        The present investigation establishes deltamethrin resistance in the common bed bug, Cimex lectularius, populationcollected from New York City (NY-BB). The mortality resistance ratio indicated that NY-BB population was 264-fold more resistant to 1% deltamethrin in contact bioassay compared to one insecticide- susceptible population collected in Florida (FL-BB). Specific enzyme activities (general esterase, glutathione S-transferase, and 7-ethoxycoumarin O-deethylase) of NY-BB were not statistically different from those of FL-BB, indicating that the metabolic factors are not associated with the deltamethrin resistance in NY-BB. Complementary DNA fragments that encoded the open reading frame of voltage-sensitive sodium channel α-subunit genes from the FL-BB and NY-BB were obtained by homology probing PCR and sequenced. Sequence alignment of the internal and 5’ and 3’ RACE fragments generated a 6500 bp cDNA sequence contig, which was composed of a 6084 bp open reading frame (ORF) encoding 2027 amino acid residues and 186 bp 5’ and 230 bp 3’ untranslated regions (5’ and 3’UTRs, respectively). Sequence comparisons of the complete open reading frames of the sodium channel genes identified two point mutations (V419L and L925I) that were presented only in the NY-BB population. L925I, located the intracellular loop between IIS4 and IIS5, has been previously found in the pyrethroid-resistant populations of whitefly (Bemisia tabaci) that was more than 100-fold resistant to fenpropathrin. V419L, located in the IS6 transmembrane segment, is a novel mutation. This evidence suggests that the two mutations are likely the major resistance-causing mutations in the deltamethrin-resistant NY-BB via a knockdown-type nerve insensitivity mechanism.

      • SCISCIESCOPUS

        Development of multifunctional metabolic synergists to suppress the evolution of resistance against pyrethroids in insects that blood feed on humans

        Hardstone, Melissa C,Strycharz, Joseph P,Kim, Junheon,Park, Il‐,Kwon,Yoon, Kyong Sup,Ahn, Young Joon,Harrington, Laura C,Lee, Si Hyeock,Clark, J Marshall John Wiley Sons, Ltd 2015 Pest Management Science Vol.71 No.6

        <P><B>Abstract</B></P><P><B>BACKGROUND</B></P><P>Pyrethroids are the insecticides of choice when exposure to humans is likely, such as occurs in vector and public‐health‐related control programs. Unfortunately, the pyrethroids share a common resistance mechanism with dichlorodiphenyltrichloroethane (DDT), knockdown resistance (<I>kdr</I>), and prior extensive use of DDT has predisposed the pyrethroids to cross‐resistance via <I>kdr</I>. Given the widespread occurrence of <I>kdr</I>, the use of synergists with pyrethroids is considered to be prudent to guard against the selection of multiply resistant insects.</P><P><B>RESULTS</B></P><P>3‐Phenoxybenzyl hexanoate (PBH) was synthesized as a multifunctional pyrethroid synergist that, besides being a surrogate substrate for sequestration/hydrolytic carboxylesterases, now also functions as a substrate for oxidative xenobiotic metabolism. The addition of PBH to permethrin‐treated females of the ISOP450 strain of <I>Culex pipiens quinquefasciatus</I> resulted in a threefold increase in synergism, as judged by the synergistic ratio. Similarly, PBH synergized the action of deltamethrin sixfold on females of the common bed bug, <I>Cimex lectularius</I>, and was 2.8‐fold more synergistic than piperonyl butoxide (PBO).</P><P><B>CONCLUSIONS</B></P><P>PBH synergized the action of both type I and type II pyrethroids in a mosquito vector (<I>Cx. p. quinquefasciatus</I>) and in a public‐health pest, <I>C. lectularius</I>, respectively, indicating a broad spectrum of action on blood‐feeding insects. PBH appears to have residual properties similar to permethrin and is itself non‐toxic, unlike PBO, and therefore should be compatible with existing pyrethroid formulations used for insecticide‐treated nets and home/residential sprays. © 2014 Society of Chemical Industry</P>

      • Biochemical and molecular analysis of deltamethrin resistance in the common bed bug (Hemiptera: Cimicidae).

        Yoon, Kyong Sup,Kwon, Deok Ho,Strycharz, Joseph P,Hollingsworth, Craig S,Lee, Si Hyeock,Clark, J Marshall Entomology Dept., B.P. Bishop Museum 2008 Journal of medical entomology Vol.45 No.6

        <P>This study establishes deltamethrin resistance in a common bed bug, Cimex lectularius L., population collected from New York City (NY-BB). The NY-BB population was 264-fold more resistant to 1% deltamethrin in contact bioassay compared with an insecticide-susceptible population collected in Florida (FL-BB). General esterase, glutathione S-transferase, and 7-ethoxycoumarin O-deethylase activities of NY-BB were not statistically different from those of FL-BB. cDNA fragments that encoded the open reading frame of voltage-sensitive sodium channel alpha-subunit genes from the FL-BB and NY-BB populations, respectively, were obtained by homology probing polymerase chain reaction (PCR) and sequenced. Sequence alignment of the internal and 5' and 3' rapid amplification of cDNA ends (RACE) fragments generated a 6500-bp cDNA sequence contig, which was composed of a 6084-bp open reading frame (ORF) encoding 2027 amino acid residues and 186-bp 5' and 230-bp 3' untranslated regions (5' and 3' UTRs, respectively). Sequence comparisons of the open reading frames of the alpha-subunit genes identified two point mutations (V419L and L925I) that were presented only in the NY-BB population. L925I, located the intracellular loop between IIS4 and IIS5, has been previously found in a highly pyrethroid-resistant populations of whitefly (Bemisia tabaci). V419L, located in the IS6 transmembrane segment, is a novel mutation. A Val to Met mutation at the corresponding position of the bed bug V419, however, has been identified in the tobacco budworm as a kdr-type mutation. This evidence suggests that the two mutations are likely the major resistance-causing mutations in the deltamethrin-resistant NY-BB through a knockdown-type nerve insensitivity mechanism.</P>

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