ライフサイエンスコーパス: hot plate

1 r using a commercially available printer and hot plate.

2 when a liquid droplet is self-vaporized on a hot plate.

3 eption were determined with the 52 degrees C hot plate, 52 degrees C warm-water tail-flick and the Ha

4 Surprisingly, on the hot plate (55 degrees C), the COX-1-deficient heterozygo

5 showed reduced pain sensitivity in both the hot plate and formalin tests.

6 and morphine dependent flush as well as the hot plate and spinal nerve ligation (SNL) models of acut

7 ion, compound 20 was also studied in the rat hot plate and spinal nerve ligation (SNL) models of acut

8 rozygous mice with wild-type controls in the hot plate and stretching tests for analgesia.

9 eption were presently studied in rats on the hot plate and tail flick tests.

10 aged rats displayed longer latencies in the hot plate and the high-intensity tail flick assays (hypo

11 rats partially restored the responses in the hot plate and von Frey hair assays.

12 Using the hot-plate and conditioned place preference test, we inve

13 exhibited normal thermal nociception in the hot-plate and tail-flick tests, and had similar olfactor

14 enhancement of baseline latency in both the hot-plate and warm-water tail-withdrawal tests.

15 inistered to mice, SR-17018 does not lead to hot plate antinociceptive tolerance, receptor desensitiz

16 , potently increased withdrawal latency in a hot plate assay (a test of analgesia) at intrathecal dos

17 show potent analgesic activity in the mouse hot-plate assay following either intraperitoneal (i.p.)

18 nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 mi

19 suppression of acute nociception (i.e., the hot-plate assay) when morphine pre-exposed rats were com

20 0% inhibition at 20 and 10 microg/kg in the hot-plate assay, respectively.

21 ivity was evaluated using the tail flick and hot plate assays for thermal pain and the Von Frey assay

22 e activity (acetic acid-induced writhing and hot plate assays), leading to the identification of a se

23 , acoustic startle, prepulse inhibition, and hot plate assays.

24 in increased efficacy in the tail-flick and hot-plate assays of antinociception.

25 logical activity in the mouse tail-flick and hot-plate assays, and for hypothermia and locomotor acti

26 antinociception in the mouse tail-flick and hot-plate assays, engender nicotine-like responding in r

27 iminished in the radiant heat tail-flick and hot-plate assays.

28 The heating mechanisms of hot plate evaporation and microwave-assisted evaporation

29 classically volatile analytes occurred using hot plate evaporation.

30 y sensitive nanostructured metal oxide micro hot plate gas sensors by utilizing an innovative multifr

31 O3 and H2O2 mixture by microwave-assisted or hot-plate heating, a partial decomposition by means of s

32 male Sprague-Dawley rats were tested in the hot plate, high- and low-intensity radiant heat tail fli

33 ced near-maximal antinociception on both the hot plate (HP) and tail flick (TF) nociceptive tests.

34 treatment alone also significantly increased hot-plate latencies and reduced gait support and stride

35 prevented the change in nerve conduction and hot-plate latencies.

36 njection of morphine produced an increase in hot plate latency in all groups except rats pretreated w

37 Results indicated that hot-plate latency increased during the first 2 days of n

38 8 antagonized the increase in tail-flick and hot-plate latency produced by either dose of baclofen.

39 -pretreated rats did not alter tail-flick or hot-plate latency.

40 roscale encapsulation technique consisted of hot plate magnetic stirrer.

41 lid wax on the surface of the paper, and the hot plate melts the wax so that it penetrates the full t

42 nd tissue digestates were evaporated using a hot plate method and a newly developed reduced-pressure

43 e selectively deposited on elements of micro hot plate (microHP) arrays.

44 tinociception activity in the tail-flick and hot-plate models of acute pain and for their ability to

45 The longer reaction times on the hot plate of COX-1-deficient heterozygotes are difficult

46 e also sensitive to NMDA antagonism, but not hot plate or tail flick latencies, which were insensitiv

47 ignificantly reduce nociceptive responses in hot plate or tail flick tests of homozygous mu receptor

48 enotype, and appear to be hypoalgesic in the hot plate paradigm.

49 ntagonists in the tail-flick test versus the hot-plate procedure.

50 injection of mice with CCL3 decreased their hot-plate response latency.

51 ia using tail-flick (spinal involvement) and hot-plate (supraspinal effect) tests, respectively; the

52 ty (von Frey hair), and thermal sensitivity (hot plate/tail flick).

53 elevated plus-maze, defensive freezing, and hot-plate task performance were observed.

54 0.05) thermal hypoalgesia measured using the hot plate test (52 degrees C): the mean (+/-S.D.) hind p

55 e effect of nitrous oxide (N(2)O) in the rat hot plate test is sensitive to antagonism by antisera ag

56 In the hot plate test only E139 had antinociceptive activity.

57 ) and morphine was studied in rats using the hot plate test to determine if there is synergism betwee

58 complete elimination of the antinociceptive (hot plate test) effects of ethanol, oxotremorine, nicoti

59 k test, acetic acid-induced writhing models, hot plate test, and formalin-induced analgesia, along wi

60 With the exception of DPDPE in the hot plate test, isobolographic analysis revealed that th

61 geenan-induced paw oedema model), analgesic (hot plate test, tail-flick test, acetic acid-induced wri

62 aminone, has antinociceptive activity in the hot plate test.

63 of NT69L and morphine was synergistic in the hot plate test.

64 combined effect of NT69L and morphine in the hot plate test.

65 in the formalin paw test or responses in the hot plate test.

66 e responsiveness to nociceptive stimulus, in hot plate test.

67 as tested in animal models for pain (thermal-hot plate test; visceral-acetic acid-induced writhing te

68 ced writhing test (0.6 vs. 0.1-0.5%), in the hot-plate test (52.5 and 55 vs. 50 degrees C), and in te

69 increased the pain threshold in mice in the hot-plate test at 2 and 50 mg/kg.

70 increased the latency to paw licking in the hot-plate test but only at doses that impaired motor fun

71 animal, Go-deficient mice are hyperalgesic (hot-plate test) and display a severe motor control impai

72 In the hot-plate test, a measure of supraspinal nociception, mo

73 me tolerant to morphine as determined in the hot-plate test, a paradigm that primarily assesses supra

74 op morphine antinociceptive tolerance in the hot-plate test, further indicating that the betaarr2 pro

75 In the hot-plate test, intrathecal administration of N-acetyl-p

76 Similar to the hot-plate test, mice showed licking or jumping responses

77 more potent in the tail-flick assay than the hot-plate test.

78 ection, reduces nociceptive threshold in the hot-plate test.

79 this model, as assessed by the 58 degrees C hot-plate test.

80 ly (Experiment 2) followed 20 min later with hot-plate testing.

81 isplayed shorter latencies on tail flick and hot plate tests for spinal and supraspinal nociceptive r

82 antinociceptive activity in the formalin and hot plate tests that are dependent on GABA receptors.

83 -3-en-1-oate (BRG 19) using the formalin and hot plate tests.

84 erception were observed using the rotarod or hot-plate tests, and there was no change in GABA(A)-rece

85 cotine antagonist in both the tail-flick and hot-plate tests, whereas 8a was an antagonist only in th

86 t, but not that using the foot-withdrawal or hot-plate tests.

87 and increasing-temperature (3 degrees C/min) hot-plate tests.

88 ymer has been integrated into a microfluidic hot plate that can be programmed to adsorb and desorb pr

89 T-jump is introduced through a substrate (a "hot plate" type arrangement) because only the substrate

90 more time-consuming conventional oven ashing/hot plate wet digestion method.