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1 ne) is a formerly used and highly neurotoxic rodenticide.
2 reas but was supressed in areas treated with rodenticides.
3 for the Federal Insecticide, Fungicide, and Rodenticide Act, and recommended for the Toxic Substance
4 y, effects of low-level exposure to multiple rodenticides, and quantitative data on the magnitude of
7 e, routine application of some anticoagulant rodenticides (ARs) may be at a crossroad due to new regu
9 e, mosquito repellents and the superwarfarin rodenticides can help protect children from significant
10 fect that local selection with anticoagulant rodenticides has had on microsatellite marker variation
11 Cys, that confer resistance to anticoagulant rodenticides in house mice and a new missense mutation A
12 ntrogressed allele after the introduction of rodenticides in the 1950s, we found signatures of select
13 ing of genotypes expressing an anticoagulant-rodenticide-insensitive vitamin K 2,3-epoxide reductase
15 ew) activity increased in areas treated with rodenticides (likely in response to lower levels of rat
16 ding the Vkorc1 gene, which is implicated in rodenticide resistance, and olfactory receptor genes.
17 wide IPM program consisted of application of rodenticide, sealing entry points, trap placement, targe
18 pest management consisted of application of rodenticide, sealing of holes that could serve as entry
19 219 and the genomic background revealed that rodenticide selection has overwhelmed drift-mediated pop
23 rin, warfarin-like anticoagulants, or potent rodenticides ("superwarfarins"), such as brodifacoum.
24 Use of the highly toxic and easily prepared rodenticide tetramethylenedisulfotetramine (TETS) was ba
25 Rum, Scotland, and tested whether localised rodenticide treatments (to control introduced Norway rat
26 nformation on common mosquito repellents and rodenticides used in households and discusses their toxi
28 Ingestion of yellow phosphorus-containing rodenticides (YPR) or firecrackers is an important cause