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1 ighted exposure-days (p for trend = 0.03) to alachlor.
4 uate the exposure-response relations between alachlor and cancer incidence controlled for the effects
6 to identify the degradation intermediates of alachlor and then proposed a possible alachlor degradati
7 ordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes
8 ee chloroacetanilide herbicides (acetochlor, alachlor, and metolachlor) and one chloroacetamide herbi
10 dings suggest a possible association between alachlor application and incidence of lymphohematopoieti
11 emoglobin (Hb)- and serum-protein adducts of alachlor as potential biomarkers of alachlor exposure, a
13 acid, 3-phenoxybenozic acid, 4-nitrophenol, alachlor, atrazine, azoxystrobin, chlorpyrifos, diazinon
14 sis of a herbicide test mixture (composed of alachlor, atrazine, butachlor, hexachlorocyclopentadiene
17 uic acid (PCA) can significantly promote the alachlor degradation in the Fe(III)/H2O2 Fenton oxidatio
18 tes of alachlor and then proposed a possible alachlor degradation mechanism in this novel Fenton oxid
19 on of protocatechuic acid could increase the alachlor degradation rate by 10000 times in this Fenton
23 ducts of alachlor as potential biomarkers of alachlor exposure, a genotoxic and carcinogenic herbicid
27 among pesticide applicators with exposure to alachlor in the Agricultural Health Study, a prospective
28 blood from female CD rats was incubated with alachlor in vitro at concentrations up to 300 microM.
29 ay provides a new approach for biomonitoring alachlor levels in experimental animals and has the pote
32 increased lifetime days of pesticide use for alachlor (p = 0.002), 2,4-dichlorophenoxyacetic acid (2,
33 the observation that cleavage of S-cysteinyl alachlor-protein adducts by methanesulfonic acid gave th
34 lide herbicides metolachlor, acetochlor, and alachlor, the chloroacetamide herbicide dimethenamid, an
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