ライフサイエンスコーパス: cardiotoxic

1 produce high response rates but may also be cardiotoxic.

2 k or whether certain manifestations are more cardiotoxic.

3 and during normal (1 microM, n = 6) and high cardiotoxic (50 microM, n = 11) dose infusions of the di

4 ot be 1 facet of depression that is the most cardiotoxic across all contexts.

5 ype TRalpha(wt), that is associated with the cardiotoxic actions of T3.

6 erns similar to that seen with several known cardiotoxic agents such as doxorubicin.

7 BRs) catalyze reduction of anthracyclines to cardiotoxic alcohol metabolites.

8 The use of less cardiotoxic alternatives, such as liposomal doxorubicin,

9 ared with doxorubicin, daunorubicin was less cardiotoxic among survivors of childhood cancer than mos

10 cumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and d

11 mor growth and demonstrated markedly reduced cardiotoxic and nephrotoxic effects, as well as better t

12 ture, particularly ways that could avoid the cardiotoxic and neurotoxic effects of current agents suc

13 e dissolved phase of runoff (e.g., PAHs) are cardiotoxic and that soil bioretention protects against

14 Here we demonstrate that the cardiotoxic anticancer agent doxorubicin (adriamycin) in

15 Doxorubicin (Dox), a cardiotoxic antineoplastic drug, disrupts the cardiac-sp

16 Doxorubicin, a cardiotoxic antineoplastic, disrupts the cardiac-specifi

17 se results indicate that previously regarded cardiotoxic cancer therapy adversely increases thoracic

18 ostication of patients receiving potentially cardiotoxic cancer therapy has involved relatively small

19 re related to prior receipt of a potentially cardiotoxic cancer treatment regimen.

20 ticularly in patients with prior exposure to cardiotoxic chemotherapies e.g., anthracyclines.

21 may lead to changes in the administration of cardiotoxic chemotherapies.

22 related to the administration of potentially cardiotoxic chemotherapy in human subjects.

23 re and 3 months after initiating potentially cardiotoxic chemotherapy using blinded, unpaired analysi

24 es 3 months after the receipt of potentially cardiotoxic chemotherapy.

25 tion in human subjects receiving potentially cardiotoxic chemotherapy.

26 Epirubicin (EPI) is less cardiotoxic compared with other canonical anthracyclines

27 tress and thereby cardiac injury, as a model cardiotoxic compound and observed changes in the Mrp1 ex

28 increase in carbonylation under Dox-induced cardiotoxic conditions in a spontaneously hypertensive r

29 ified specific serum proteins oxidized under cardiotoxic conditions.

30 ellular calcium overload, and the release of cardiotoxic cytokines.

31 t was less efficacious with the higher, more cardiotoxic dose of DOX.

32 ancer efficacy and cardiotoxicity, we tested cardiotoxic doxorubicin alone and in combination with an

33 that reproduces susceptibility to develop a cardiotoxic drug response.

34 afish model of cardiomyopathy induced with a cardiotoxic drug.

35 iduals exhibit different susceptibilities to cardiotoxic drugs and that use of disease-specific hiPSC

36 monstrated increased susceptibility to known cardiotoxic drugs as measured by action potential durati

37 ve courses of chemotherapy agents with known cardiotoxic effects (including anthracyclines, taxanes,

38 for the first time, that 3NPA has important cardiotoxic effects as well as neurotoxic effects, and t

39 These cardiotoxic effects can be acute, such as changes in ele

40 Cardiotoxic effects can occur immediately during adminis

41 ervations: The old paradigm of anthracycline cardiotoxic effects is replaced by new insights that ant

42 at Edg-mediated Sph1P negative inotropic and cardiotoxic effects may play important roles in acute my

43 lated cardiomyopathy in mice, resembling the cardiotoxic effects observed in a subset of breast cance

44 n appearing more susceptible than men to the cardiotoxic effects of alcohol.

45 that oxidized myocardial CaMKII mediates the cardiotoxic effects of aldosterone on the cardiac matrix

46 a new therapeutic target in ameliorating the cardiotoxic effects of DOX treatment in cancer patients.

47 supporting the idea that Bnip3 underlies the cardiotoxic effects of DOX.

48 Despite the known cardiotoxic effects of doxorubicin and other anthracycli

49 The cardiotoxic effects of doxorubicin are cumulative, which

50 These results suggest that the cardiotoxic effects of doxorubicin develop from mitochon

51 may be further explored in view of potential cardiotoxic effects of FLT3-targeting anticancer therapy

52 ikely to be the primary target for the known cardiotoxic effects of other, related antihistamines.

53 ing that oxidative stress may exacerbate the cardiotoxic effects of the PLN(R9C) mutant.

54 The on-target cardiotoxic effects of trastuzumab were owing to a prosu

55 logical mechanisms underlying such potential cardiotoxic effects remain unclear.

56 Prevention of anthracycline cardiotoxic effects should be based on inhibiting or deg

57 However, imatinib also has cardiotoxic effects traceable to its impact on the C-Abl

58 No acute cardiotoxic effects were observed with either treatment,

59 Cardiotoxic effects were reported in 15 (5%) of 291 chil

60 icity of anthracyclines while reducing their cardiotoxic effects, we have developed a novel class of

61 ak may contribute to AMT's proarrhythmic and cardiotoxic effects, which may be counteracted by interv

62 are at increased risk of trastuzumab-related cardiotoxic effects.

63 ores, myofibrillar degeneration, and related cardiotoxic effects.

64 omarkers have allowed for early detection of cardiotoxic effects.

65 on for the prevention of trastuzumab-related cardiotoxic effects.

66 drawn even later from the marketplace due to cardiotoxic effects.

67 oprotective agents may prevent some of these cardiotoxic effects.

68 ficial in preventing the development of late cardiotoxic effects.

69 ER2/neu) correlates with trastuzumab-related cardiotoxic effects.

70 al sites, or for i.v. therapeutics or during cardiotoxic episodes.

71 uary, 2004, following clinically significant cardiotoxic events (nine events in eight of 77 patients)

72 breast cancer, and proved to be excessively cardiotoxic for use in the adjuvant setting.

73 Cardiotoxic free radicals are generated by ischemia-repe

74 peptide angiotensin II (Ang II) is a potent cardiotoxic hormone whose actions have been well studied

75 ibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose effects can be prevented by l-

76 Anthracyclines are cardiotoxic; however, there are limited data characteriz

77 iac inflammatory reactions, showing that the cardiotoxic IFN-gamma effect operative in SAP-IFN-gamma

78 They also were less cardiotoxic in cell culture.

79 dy, we tested the hypothesis that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotec

80 linical study suggested that imatinib may be cardiotoxic in some patients.

81 and utilization leads to the accumulation of cardiotoxic lipid species, and to establish a mouse mode

82 cardiotoxicity, we compared potentially less cardiotoxic liposomal daunorubicin (L-DNR) to idarubicin

83 Our findings demonstrate a cardiotoxic mechanism by which crude oil affects the reg

84 e showed decreased circulating levels of the cardiotoxic metabolite, doxorubicinol, after administrat

85 sequent decrease in the concentration of its cardiotoxic metabolite.

86 d did not (no risk [NR]) receive potentially cardiotoxic modalities, and with values expected for com

87 in association with other drugs that may be cardiotoxic or for patients with conduction disorders.

88 However, the precise identity of cardiotoxic PAHs, and the mechanisms underlying contract

89 Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubi

90 Its antitumor and cardiotoxic properties have been ascribed to anthracycli

91 rexpressing Beclin 1 manifested an amplified cardiotoxic response.

92 ence for the role of catalase in doxorubicin cardiotoxic responses.

93 hat particular levels of hyperkalemia confer cardiotoxic risk have been challenged by several reports

94 otheraputic use of antineoplastic drugs with cardiotoxic side effects (i.e., doxorubicin).

95 However, due to its extensive cardiotoxic side effects a lifetime cumulative dose limi

96 For example, cardiotoxic side effects of the cancer drug imatinib mig

97 ugs is restricted owing to potentially fatal cardiotoxic side effects.

98 n is an effective anticancer drug with known cardiotoxic side effects.

99 ts clinical use is limited because of severe cardiotoxic side effects.

100 ut its application is limited because of its cardiotoxic side effects.

101 bb, Princeton, NJ) and r-verapamil, the less cardiotoxic stereoisomer, in heavily pretreated patients

102 Ropivacaine is less cardiotoxic than bupivacaine and, at low concentrations,

103 Lidocaine is generally considered much less cardiotoxic than other local anesthetics and is used com

104 as the advantage of being significantly less cardiotoxic than racemic bupivacaine, which suggests tha

105 Childhood cancer survivors treated with cardiotoxic therapies are recommended to have routine ca

106 Childhood Cancer Survivor Study who received cardiotoxic therapy and reported no history of cardiomyo

107 ociated with cardiovascular risk factors and cardiotoxic therapy were assessed in multivariable Poiss

108 in any survivor who has received potentially cardiotoxic therapy.

109 rove the care of oncology patients receiving cardiotoxic therapy.

110 act ERK axis, which blunted the induction of cardiotoxic transcripts, in part by enhanced serine 273

111 hildhood cancer with and without exposure to cardiotoxic treatments at a median of 11 years after dia

112 increased in other cancer populations where cardiotoxic treatments have been used.

113 Childhood cancer survivors not receiving cardiotoxic treatments nevertheless have cardiovascular

114 The use of potentially cardiotoxic treatments should be reconsidered for high-r

115 gavon, United Kingdom) is effective and less cardiotoxic, which is important in this setting.