ライフサイエンスコーパス: toxic dose

1 at concentrations of 5mug/mL, well below the toxic dose.

2 n human overdose patients and rats receiving toxic doses.

3 oncentrations orders of magnitude lower than toxic doses.

4 at concentration regimes far lower than the toxic doses.

5 n to cause centrilobular hepatic necrosis at toxic doses.

6 ts from pathogenic fungi or attack them with toxic doses.

7 s for hematological neoplasms at lower, less toxic, doses.

8 endent response from mouse Y1 adrenal cells (toxic dose 10 vs. 300 pg/well).

9 In separate groups of rats, non-toxic doses (50 and 250 microg/kg) of the acetylcholines

10 ign has higher risks of exposing patients to toxic doses above the MTD than the modified toxicity pro

11 evidence for treatments with lower and less toxic doses and broadening the application of PI to othe

12 The oral toxic dose causing illness in 50% of those exposed to me

13 potential efficacy of a few compounds at non-toxic doses could not be excluded.

14 Chlorthiazide's toxic dose for 50% of animals tested (TD50) could not be

15 in human tissues; to identify effective non-toxic doses for more extensive clinical testing; and to

16 DM) chemotherapy, which utilizes lower, less toxic, doses given on a close regular basis over prolong

17 showed an improved therapeutic range (active/toxic dose in mg/kg body weight) of 1/5 mg/kg for tTF-NG

18 wing administration of either therapeutic or toxic doses, in particular within a patient context.

19 letely inactive at both tolerable and highly toxic dose levels.

20 only marginally active when given at highly toxic dose levels.

21 However, in cortical cultures exposed to a toxic dose of Abeta (50 microM), Zn at concentrations of

22 iver failure was induced in BALB/c mice by a toxic dose of acetaminophen (APAP).

23 Urine samples from rats treated with a toxic dose of acetyl fentanyl contained high concentrati

24 c RXRalpha knockout mice were treated with a toxic dose of APAP (500 mg/kg i.p.).

25 C57BL/6 mice were given an intraperitoneal toxic dose of APAP (500 mg/kg), which caused severe acut

26 T knockout (MET KO) mice were administered a toxic dose of APAP and assessed for liver injury/regener

27 C57BL/6 mice were administered a toxic dose of APAP intraperitoneally to cause liver inju

28 tocytes and C57BL/6 mice were administered a toxic dose of APAP with or without SP600125, a chemical

29 ndrial pathway of apoptosis using a slightly toxic dose of DAC may therefore be a strategy for treati

30 The median estimated toxic dose of DEG was 1.34 mL/kg (range, 0.22-4.42 mL/kg

31 tion decline and injury induced in mice by a toxic dose of endotoxin.

32 ring HBO2 exposure indicates a threshold for toxic dose of HBO2 and how it may be related to toleranc

33 We injected rats with a moderate non-toxic dose of MDMA (9 mg/kg) during social interaction,

34 ts strongly suggest that a pharmacologically toxic dose of MKT-077 minimally affects the overall func

35 e exposure of LRRK2 transgenic mice to a sub-toxic dose of MPTP resulted in severe motor impairment,

36 n vivo administration of a pharmacologically toxic dose of the lipophilic cationic compound, MKT-077,

37 Treatment of HK with a non-toxic dose of UVA rapidly increased NADPH oxidase activi

38 In murine xenograft models, non-toxic doses of 17-AAG markedly reduced the expression of

39 ine (DFO) to mice prior to administration of toxic doses of 6-OHDA resulted in a decrease in activity

40 /kg, i.p.) 10 min prior to administration of toxic doses of 6OHDA (350 or 400 mg/kg, i.p.) resulted i

41 ture (XANES) studies have now shown that non-toxic doses of [Cr3 O(OCOEt)6 (OH2 )3 ](+) (A), a prospe

42 g cells (CFCs) in methylcellulose containing toxic doses of aerolysin (1 x 10(-9) M).

43 d effects on target molecules in response to toxic doses of APAP; however, the primary Ca2+ target re

44 eporter gene expression, but required mildly toxic doses of cationic lipid, and resulted in some loss

45 me c release when exposed either to OE or to toxic doses of ceramide.

46 dministration of otherwise myeloablative and toxic doses of chemotherapy and for reconstitution of an

47 s stimulated new uptake route, following non-toxic doses of dielectric barrier discharge CAP.

48 ced by up to 50 x in the presence of low non-toxic doses of formate.

49 on by HbLDL increased resistance of cells to toxic doses of hemin or t-BuOOH.

50 was much greater than that produced by more toxic doses of ionizing radiation.

51 red when endothelial cells were treated with toxic doses of LPC-C18:0 or minimally modified low densi

52 ex vivo TNF-alpha response to large, highly toxic doses of LPS (p < .05).

53 es are capable of adapting to and tolerating toxic doses of LT.

54 increased the viability of the cells against toxic doses of menadione or H2O2.

55 These results suggest that toxic doses of METH that cause loss of presynaptic DA ma

56 D1 receptors labeled with [3H]SCH23390 after toxic doses of METH that were shown to cause marked depl

57 s thus support the notion that injections of toxic doses of METH trigger the activation of the progra

58 suggest that c-fos induction in response to toxic doses of methamphetamine might be involved in prot

59 table event when an individual is exposed to toxic doses of some compounds or as an unpredictable eve

60 DNA cross-links, are induced in response to toxic doses of the agents that produce these lesions.

61 oduction in identified dopaminergic neurons, toxic doses of the Complex I inhibitor rotenone did not.

62 The low sub-toxic doses of the studied compounds greatly affected th

63 udy, for the first time, we assessed the non-toxic doses of the triterpene saponins (ginsenoside-Rb3

64 with oAbeta to produce these effects, as sub-toxic doses of the two peptides combined lead to LTP and

65 fects of NSAIDs or/and may allow lower, less toxic doses of these drugs to be used.

66 Toxic doses of TNF-alpha failed to alter EPCR mRNA level

67 Treatment for 96 hours with toxic doses of vitamin D caused widespread calcification

68 Both sediments elicited a toxic dose-response by H. azteca early in the aging proc

69 h IL-1 alpha followed by CPT-11 at minimally toxic doses significantly (5-6-fold) enhanced antitumor

70 We conclude that at the toxic doses studied, NMDA receptor activation results pr

71 Instead of applying a toxic dose, we attempted to monitor the effects of AgNPs