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  1. Dang K, Doggett SL, Lee CY
    J Econ Entomol, 2023 Feb 10;116(1):29-39.
    PMID: 35639556 DOI: 10.1093/jee/toac068
    The residual performance of two pyrethroid-neonicotinoid mixture formulations: Temprid SC (10.5% beta-cyfluthrin and 21% imidacloprid) and Tandem (3.5% lambda-cyhalothrin and 11.6% thiamethoxam) on two substrates (glass and filter paper) against eight pyrethroid-resistant strains (BM-MY, BP-MY, CH-MY, GL-MY, KL-MY, SAJ-MY, TT-MY, and QLD-AU) of the tropical bed bug, Cimex hemipterus (F.) (Hemiptera: Cimicidae) collected from Malaysia, and Australia were evaluated. The aging effect of treatment residues on glass was also investigated. A susceptible C. lectularius L. strain (Monheim) was used for comparison. Temprid SC showed varying levels of performance against all C. hemipterus strains: TT-MY (PR50 = 6.5-fold, high performance), BM-MY, GL-MY, SAJ-MY, and QLD-AU (12.8-21.6-fold, moderate performance), BP-MY, and KL-MY (48.2-49-fold, poor performance), CH-MY (128.2-fold, very poor performance). On the other hand, Tandem displayed high performance against all C. hemipterus strains (1.8-8.3-fold). Tandem caused faster mortality than Temprid SC for all strains. Temprid SC and Tandem residues killed C. hemipterus significantly faster on glass than filter paper. Compared with fresh residues, the efficacy of Temprid SC residues significantly declined after one week of aging, while the effectiveness of Tandem residues declined after two weeks of aging. Further investigations using the topical assay method with a diagnostic dose of imidacloprid found two strains (CH-MY and GL-MY) resistant to imidacloprid. The six other strains (BM-MY, BP-MY, KL-MY, SAJ-MY, TT-MY, and QLD-AU) were susceptible.
  2. Dang K, Doggett SL, Leong XY, Veera Singham G, Lee CY
    J Econ Entomol, 2021 12 06;114(6):2473-2484.
    PMID: 34693975 DOI: 10.1093/jee/toab205
    The modern resurgence of the common (Cimex lectularius L.) and tropical bed bugs (C. hemipterus [F.]) is thought to be primarily due to insecticide resistance. While there are many reports on insecticide resistance mechanisms in C. lectularius, such information in C. hemipterus is limited. We examined dichloro-diphenyl-trichloroethane (DDT), malathion, deltamethrin, permethrin, lambda-cyhalothrin resistance, and the underlying mechanisms in several C. hemipterus strains (Australia: Queensland [QLD-AU]; Malaysia: Kuala Lumpur [KL-MY], Tanjung Tokong [TT-MY], Christian [CH-MY], and Green Lane [GL-MY]). We used a surface contact method, synergism studies (utilizing piperonyl butoxide [PBO], S,S,S-tributyl phosphorotrithioate [DEF], and diethyl maleate [DEM]), and molecular detection of kdr mutations. Results demonstrated that all C. hemipterus strains possessed high resistance to DDT and the pyrethroids and moderate to high resistance to malathion. Synergism studies showed that deltamethrin resistance in all strains was significantly (P < 0.05) inhibited by PBO. In contrast, deltamethrin resistance was not affected in DEF or DEM. Similar findings were found with lambda-cyhalothrin resistance. Malathion resistance was significantly (P < 0.05) reduced by DEF in all strains. Resistance to DDT was not affected by DEM in all strains. Multiple kdr mutations (M918I, D953G, and L1014F) were detected by molecular analyses. TT-MY strain was found with individuals possessing three kdr mutation combinations; D953G + L1014F (homozygous susceptible: M918), M918I + D953G + L1014F (heterozygous resistant: I918), and M918I + D953G + L1014F (homozygous resistant: I918). Individuals with M918I + D953G + L1014F (homozygous resistant: I918) survived longer on deltamethrin (>12 h) than those (≤1 h) with other combinations. M918I + L1014F mutations most likely conferred super-kdr characteristic toward pyrethroids and DDT in C. hemipterus.
  3. Dang K, Doggett SL, Veera Singham G, Lee CY
    Parasit Vectors, 2017 Jun 29;10(1):318.
    PMID: 28662724 DOI: 10.1186/s13071-017-2232-3
    The worldwide resurgence of bed bugs [both Cimex lectularius L. and Cimex hemipterus (F.)] over the past two decades is believed in large part to be due to the development of insecticide resistance. The transcriptomic and genomic studies since 2010, as well as morphological, biochemical and behavioral studies, have helped insecticide resistance research on bed bugs. Multiple resistance mechanisms, including penetration resistance through thickening or remodelling of the cuticle, metabolic resistance by increased activities of detoxification enzymes (e.g. cytochrome P450 monooxygenases and esterases), and knockdown resistance by kdr mutations, have been experimentally identified as conferring insecticide resistance in bed bugs. Other candidate resistance mechanisms, including behavioral resistance, some types of physiological resistance (e.g. increasing activities of esterases by point mutations, glutathione S-transferase, target site insensitivity including altered AChEs, GABA receptor insensitivity and altered nAChRs), symbiont-mediated resistance and other potential, yet undiscovered mechanisms may exist. This article reviews recent studies of resistance mechanisms and the genes governing insecticide resistance, potential candidate resistance mechanisms, and methods of monitoring insecticide resistance in bed bugs. This article provides an insight into the knowledge essential for the development of both insecticide resistance management (IRM) and integrated pest management (IPM) strategies for successful bed bug management.
  4. Dang K, Singham GV, Doggett SL, Lilly DG, Lee CY
    J Econ Entomol, 2017 04 01;110(2):558-566.
    PMID: 28115498 DOI: 10.1093/jee/tow296
    The performance of five insecticides (bendiocarb, deltamethrin, DDT, malathion, and imidacloprid) using three application methods (oil-based insecticide films on filter paper, and acetone-based insecticide deposits on two substrates: filter paper and glass) was assessed against a susceptible strain of Cimex lectularius (L.) and two resistant strains of Cimex hemipterus (F.). Substrate type significantly affected (P 
  5. Leong XY, Kim DY, Dang K, Singham GV, Doggett SL, Lee CY
    J Econ Entomol, 2020 02 08;113(1):353-366.
    PMID: 31586445 DOI: 10.1093/jee/toz266
    This study examined the presence of insecticide resistance in different developmental stages (adults, first instars, and eggs) of the tropical bed bug, Cimex hemipterus (F.) using several insecticide formulations. Adults and first instars of five strains (Queensland, Kuala Lumpur, Bukit Mertajam, Saujana, and Krystal Point) were evaluated using the surface contact method and compared with a susceptible strain (Monheim) of the common bed bug Cimex lectularius L. The insecticide formulations were used at their label rates in this study: Tandem (thiamethoxam [11.6%], lambda-cyhalothrin [3.5%]) at 183.96 mg/m2; Temprid SC (imidacloprid [21%], beta-cyfluthrin [10.5%]) at 106.13 mg/m2; Sumithion 20CS (fenitrothion [20%]) at 250 mg/m2; Pesguard FG161 (d-tetramethrin [4.4%], cyphenothrin [13.2%]) at 110 mg/m2; and Sumithrin 10SEC (d-phenothrin [10%]) at 100 mg/m2. Results showed a very high level of resistance to Pesguard FG161 (388.3 to >605.0 times) and Sumithrin (302.9 to >365.5 times) in all adults of the strains tested, whereas low to high levels of resistance were registered for Tandem (1.4-4.7 times), Temprid (7.3-16.7 times), and Sumithion (1.2-14.6 times) for adults of all bed bug strains. For first instars, resistance to the former two formulations were high to very high (31.4-118.1 times). In contrast, they showed lower resistance to Tandem, Temprid, and Sumithion (1.0-10.2 times). An immersion method used to test on bed bug eggs found high to very high resistance toward all tested formulations. Results demonstrate that the resistance level varies between bed bug developmental stages.
  6. Dang K, Toi CS, Lilly DG, Lee CY, Naylor R, Tawatsin A, et al.
    Pest Manag Sci, 2015 Jul;71(7):1015-20.
    PMID: 25132449 DOI: 10.1002/ps.3880
    Bed bugs [both Cimex hemipterus (F.) and Cimex lectularius L.] are highly resistant to pyrethroids worldwide. An important resistance mechanism known as 'knockdown resistance' (kdr) is caused by genetic point mutations on the voltage-gated sodium channel (VGSC) gene. Previous studies have identified two point mutations (V419L and L925I) on the VGSC gene in C. lectularius that are responsible for kdr-type resistance. However, the kdr mutations in C. hemipterus have not been investigated.
  7. Wu W, Ding D, Zhao Q, Xiao Z, Luo J, Ganguli M, et al.
    Alzheimers Dement, 2023 Jan;19(1):107-122.
    PMID: 35290713 DOI: 10.1002/alz.12628
    INTRODUCTION: Though consistent evidence suggests that physical activity may delay dementia onset, the duration and amount of activity required remains unclear.

    METHODS: We harmonized longitudinal data of 11,988 participants from 10 cohorts in eight countries to examine the dose-response relationship between late-life physical activity and incident dementia among older adults.

    RESULTS: Using no physical activity as a reference, dementia risk decreased with duration of physical activity up to 3.1 to 6.0 hours/week (hazard ratio [HR] 0.88, 95% confidence interval [CI] 0.67 to 1.15 for 0.1 to 3.0 hours/week; HR 0.68, 95% CI 0.52 to 0.89 for 3.1 to 6.0 hours/week), but plateaued with higher duration. For the amount of physical activity, a similar pattern of dose-response curve was observed, with an inflection point of 9.1 to 18.0 metabolic equivalent value (MET)-hours/week (HR 0.92, 95% CI 0.70 to 1.22 for 0.1 to 9.0 MET-hours/week; HR 0.70, 95% CI 0.53 to 0.93 for 9.1 to 18.0 MET-hours/week).

    DISCUSSION: This cross-national analysis suggests that performing 3.1 to 6.0 hours of physical activity and expending 9.1 to 18.0/MET-hours of energy per week may reduce dementia risk.

  8. Makkar SR, Lipnicki DM, Crawford JD, Kochan NA, Castro-Costa E, Lima-Costa MF, et al.
    J Gerontol A Biol Sci Med Sci, 2020 09 25;75(10):1863-1873.
    PMID: 32396611 DOI: 10.1093/gerona/glaa116
    We aimed to examine the relationship between Apolipoprotein E ε4 (APOE*4) carriage on cognitive decline, and whether these associations were moderated by sex, baseline age, ethnicity, and vascular risk factors. Participants were 19,225 individuals aged 54-103 years from 15 longitudinal cohort studies with a mean follow-up duration ranging between 1.2 and 10.7 years. Two-step individual participant data meta-analysis was used to pool results of study-wise analyses predicting memory and general cognitive decline from carriage of one or two APOE*4 alleles, and moderation of these associations by age, sex, vascular risk factors, and ethnicity. Separate pooled estimates were calculated in both men and women who were younger (ie, 62 years) and older (ie, 80 years) at baseline. Results showed that APOE*4 carriage was related to faster general cognitive decline in women, and faster memory decline in men. A stronger dose-dependent effect was observed in older men, with faster general cognitive and memory decline in those carrying two versus one APOE*4 allele. Vascular risk factors were related to an increased effect of APOE*4 on memory decline in younger women, but a weaker effect of APOE*4 on general cognitive decline in older men. The relationship between APOE*4 carriage and memory decline was larger in older-aged Asians than Whites. In sum, APOE*4 is related to cognitive decline in men and women, although these effects are enhanced by age and carriage of two APOE*4 alleles in men, a higher numbers of vascular risk factors during the early stages of late adulthood in women, and Asian ethnicity.
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