ライフサイエンスコーパス: aldicarb

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1 nimals to the acetylcholinesterase inhibitor aldicarb.

2 ere is an accelerated rate of contraction on aldicarb.

3 ffects of an acetylcholinesterase inhibitor, aldicarb.

4 bition of egg laying and fails to respond to aldicarb.

5 gus using the acetylcholinesterase inhibitor aldicarb.

6 nimals to the acetylcholinesterase inhibitor aldicarb.

7 stance to the acetylcholinesterase inhibitor aldicarb.

8 ytic response to a cholinesterase inhibitor, aldicarb.

9 Carbamate insecticide screens often include aldicarb and its oxidative metabolites, aldicarb sulfoxi

10 adult worms are incubated in the presence of aldicarb and scored for the time-course of aldicarb-indu

11 istant to the acetylcholinesterase inhibitor aldicarb, and they exhibit reduced swimming rates in liq

12 Recoveries of aldicarb, ASX and ASN from excreta were of 79% +/- 5.4,

13 Since aldicarb, ASX, and ASN are normally detectable in organ

14 HPLC postcolumn derivitization to determine aldicarb, ASX, and ASN from avian excreta and from gastr

15 or no embryo toxicity (cyanazine, picloram, aldicarb, azinphos-methyl, dieldrin, diquat dibromide, e

16 sol, ethylacrylate, malathion, chlorpyrifos, aldicarb, carbofuran, carbaryl, 2,4-dichlorophenol, 2,4,

17 vity, with either mutations or the inhibitor aldicarb, decreased egg laying.

18 lly exhibit a change in their sensitivity to aldicarb (either increased sensitivity for enhancements

19 es an important forensic tool for evaluating aldicarb exposures.

20 se reducing their function results in strong aldicarb hypersensitivity and hyperactive locomotion.

21 istant to the acetylcholinesterase inhibitor aldicarb, indicating that cholinergic transmission is im

22 ghtened drug responsiveness was caused by an aldicarb-induced increase in muscle ACR-16 acetylcholine

23 ng the DVA mechanoreceptor (TRP-4) decreased aldicarb-induced NLP-12 secretion and blocked aldicarb-i

24 f aldicarb and scored for the time-course of aldicarb-induced paralysis.

25 with increased PKC-1 activity had more rapid aldicarb-induced paralysis.

26 ailure) and also with altered sensitivity to aldicarb-induced paralysis.

27 Aldicarb-induced potentiation was eliminated by mutation

28 ldicarb-induced NLP-12 secretion and blocked aldicarb-induced synaptic potentiation.

29 treatment with the cholinesterase inhibitor aldicarb induces a form of presynaptic potentiation wher

30 e rate of animal contraction when exposed to aldicarb is controlled by the balance between excitatory

31 les are primary transformation products from aldicarb, its sulfoxide, or its sulfone.

32 Aldicarb nitrile, ASX nitrile, and ASN nitrile recoverie

33 se reducing their function results in strong aldicarb resistance and slow locomotion rates.

34 G(q)alpha signaling network by screening for aldicarb-resistant mutants with phenotypes similar to eg

35 By contrast, genetic analysis of aldicarb responses and imaging of fluorescently tagged n

36 nalysis of a YFP-tagged NLP-12 suggests that aldicarb stimulates DVA secretion of NLP-12.

37 al assays using the cholinesterase inhibitor aldicarb suggest that VAs and GOA-1 similarly downregula

38 istant to the acetylcholinesterase inhibitor aldicarb, suggesting that cholinergic transmission was g

39 e metabolites, aldicarb sulfoxide (ASX), and aldicarb sulfone (ASN).

40 lude aldicarb and its oxidative metabolites, aldicarb sulfoxide (ASX), and aldicarb sulfone (ASN).

41 stance to the acetylcholinesterase inhibitor aldicarb, they are significantly hypersensitive to the a

42 tivity to an acetylcholinesterase inhibitor, aldicarb, uncovering deficiencies in inhibitory neurotra

43 nduced by the acetylcholinesterase inhibitor aldicarb, whereas mutants with increased PKC-1 activity

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