ライフサイエンスコーパス: drug toxicity

1 factors able to protect sensitive cells from drug toxicity.

2 a questionnaire to assess their awareness of drug toxicity.

3 activation but did not protect cells against drug toxicity.

4 ocellular-cholestatic injury compatible with drug toxicity.

5 assisted reproduction or potential sites of drug toxicity.

6 hemagglutinin (HA)-specific T cells, and the drug toxicity.

7 le neutropenia was 1.4%; no patients died of drug toxicity.

8 eeded to be euthanized early due to signs of drug toxicity.

9 nd to prevent graft loss due to rejection or drug toxicity.

10 to an understanding of the cellular basis of drug toxicity.

11 econdary antibody responses, and (3) minimal drug toxicity.

12 hly intervals to evaluate weight changes and drug toxicity.

13 failure is a rare but devastating result of drug toxicity.

14 the development of diabetes with no apparent drug toxicity.

15 improvement for 6 months with no significant drug toxicity.

16 ng a structural basis for Pol gamma-mediated drug toxicity.

17 nge, and none had other clinical evidence of drug toxicity.

18 tion, opportunistic infections, and possible drug toxicity.

19 two groups discontinued treatment because of drug toxicity.

20 ment for two years without evidence of major drug toxicity.

21 ite symptoms of arthritis and no evidence of drug toxicity.

22 etformin, potentially increasing the risk of drug toxicity.

23 bulky peritoneal tumors and reduced systemic drug toxicity.

24 trolyte disorders, uremic complications, and drug toxicity.

25 a basis for understanding Pol gamma-mediated drug toxicity.

26 causes, preventions, and treatments for this drug toxicity.

27 treatment, poor management of treatment, and drug toxicity.

28 bitor to be used for the purpose of reducing drug toxicity.

29 pment of models of disease, drug action, and drug toxicity.

30 us terminating both psychoactive effects and drug toxicity.

31 -gp inhibitors, thus increasing the risk for drug toxicity.

32 y localised in the context of organ-specific drug toxicity.

33 ld be considered a potential risk factor for drug toxicity.

34 .9% (5 of 567), and 2 deaths were related to drug toxicity.

35 ted drugs in the intestine, thereby reducing drug toxicity.

36 n1 expression blocked autophagy and enhanced drug toxicity.

37 of hiCE that may have utility in modulating drug toxicity.

38 f islets infused into the portal veins or to drug toxicity.

39 reproducible, early and sensitive measure of drug toxicity.

40 PERK) allowing dormant tumor cells to resist drug toxicity.

41 There was no graft loss from rejection or drug toxicity.

42 of food restrictions, virologic failure, or drug toxicities.

43 ry effects of CMV as well as consequences of drug toxicities.

44 t monthly intervals to evaluate appetite and drug toxicities.

45 large suppressed individual and combination drug toxicities.

46 1) compared with controls without noticeable drug toxicities.

47 day episodes of calcineurin inhibitor (CNI) drug toxicity (9.2% vs. 35.3%, P=0.003).

48 Most importantly, to avoid drug toxicities, a larger formulary is needed in resourc

49 ossible etiologies include immunosuppressive drug toxicity, acute cellular rejection, viral hepatitis

50 ulation, these etiologies often coexist with drug toxicities and metabolic abnormalities that complic

51 erm graft survival owing to a combination of drug toxicities and the emergence of chronic alloimmune

52 ver injury represents the combined result of drug toxicity and a potent innate immune response that f

53 tumor imaging to long-term cell tracking, to drug toxicity and bacterial infection imaging for fluore

54 -human immunodeficiency virus (HIV) therapy, drug toxicity and emergence of drug-resistant isolates d

55 anner will determine their susceptibility to drug toxicity and harm.

56 he concept that central venulitis represents drug toxicity and indicate instead that it is a form of

57 medicinal chemistry and can be confounded by drug toxicity and off-target activities of the test mole

58 NA resulting from chemotherapy may influence drug toxicity and survival in response to treatment.

59 se in patients, the problems associated with drug toxicity and the development of resistance means th

60 hreatening complications from antiretroviral drug toxicity and the immune reconstitution inflammatory

61 se to chemotherapy has been hampered by free drug toxicity and the low bioavailability of nano-formul

62 espite recent advances in antiviral therapy, drug toxicity and unwanted side effects render effective

63 resulting in interindividual variability of drug toxicity and/or efficacy.

64 reduced pain, significantly relieved common drug toxicities, and improved survival in patients with

65 ts due to interactions among drugs, additive drug toxicities, and the continued need for combination

66 accessibility to viral reservoirs, long-term drug toxicities, and treatment failures are limitations

67 ts emerging treatment options, side effects, drug toxicities, and treatment-induced depression.

68 lude chronic immune rejection, inflammation, drug toxicity, and chronic kidney injury from secondary

69 erosis, Crohn's disease, ulcerative colitis, drug toxicity, and even autism.

70 n metabolism, liver injury, gene regulation, drug toxicity, and hepatotropic infections.

71 or 6 months for primary outcomes: mortality, drug toxicity, and immune reconstitution inflammatory sy

72 he degree of drug retention, their intrinsic drug toxicity, and individual susceptibility, PPH could

73 l (HgbA1C, hypertension, serum cholesterol), drug toxicity, and infection also were measured.

74 ood tests for causes of hepatitis other than drug toxicity, and liver biopsy in two patients.

75 causes of hepatitis and cirrhosis other than drug toxicity, and liver biopsy.

76 with disease due to endocrine, immunologic, drug toxicity, and other causes were excluded.

77 disease, injury from prolonged preservation, drug toxicity, and underlying recipient disease.

78 could reduce nonsteroidal anti-inflammatory drug toxicity, and, most recently, development of classe

79 y be due to hypoxemia, emboli, inflammation, drug toxicity, and/or other etiologies.

80 This drug toxicity appears to occur by 2 different mechanisti

81 se results suggest a method to predict which drug toxicities are most amenable to treatment and infor

82 Drug toxicities are the main causes of posttransplant ne

83 hoice of an optimal PEP drug regimen, record drug toxicities arising from specific PEP regimens, and

84 Drug toxicities associated with HAART lend urgency to th

85 of Beclin1 or autophagy-related 5 suppressed drug toxicity by approximately 40%.

86 gene or microinjected Ras protein increased drug toxicity by approximately threefold in actively cyc

87 There was no evidence of drug toxicity by clinical examination, electroretinograp

88 It has been documented that drug toxicities can be mitigated through nanoparticle fo

89 Our model also incorporates drug toxicity constraints by tracking the dynamics of pa

90 Idiosyncratic drug toxicity, defined as toxicity that is dose independ

91 t with HAART is challenging given cumulative drug toxicities, difficulties with adherence to complica

92 ntracellular pathogens can be complicated by drug toxicity, drug resistance, and the need for prolong

93 mulations showed that the increased risk for drug toxicity extends many days beyond the end of the co

94 V related or tuberculosis related, including drug toxicity; factors associated with mortality were la

95 increased IOP, or evidence of procedural or drug toxicity following injection of TA into the SCS in

96 Sound exposures, infections, drug toxicity, genetic disorders, and aging all can caus

97 mmunity, alloimmunity, and immunosuppressive drug toxicity, highlighting the potential for better out

98 risky behavior; and monitoring for potential drug toxicities, HIV acquisition, and antiretroviral dru

99 ration of larger doses of MTX by alleviating drug toxicity in normal cells and tissues that are drug

100 native compensatory mechanisms to counteract drug toxicity in some of the mutants.

101 er-related conditions, viral infections, and drug toxicity in South and Central America.

102 The drug toxicity in the ocular tissues was assessed by hist

103 s-6+hamKu86 cells, albeit exhibiting similar drug toxicity in these two cell lines.

104 may partially account for the high rates of drug toxicity in this population.

105 pplications to model liver diseases and test drug toxicity in vitro.

106 s), disease progression (in 4 patients), and drug toxicity (in 2 patients).

107 ith or without azathioprine or patients with drug toxicity include the use of cyclosporine, tacrolimu

108 ycle phase and oncogenic signaling influence drug toxicity independently of alterations in topo IIalp

109 s of acquired neutropenia including systemic drug toxicity, infection, and autoimmune disease were ex

110 Drug toxicity is a long-standing concern of modern medic

111 Drug toxicity is an important factor that contributes si

112 The observed drug toxicity is believed to involve the formation of an

113 contributes to tumorigenesis or antimitotic drug toxicity is not well defined.

114 ase), osteoporosis prevention and treatment, drug toxicity monitoring, renal disease, and reproductiv

115 (ATN) (n = 8), chronic rejection (n = 6), or drug toxicity (n = 3).

116 ncidental diagnosis at nephrectomy (n=2), or drug toxicity (n=1).

117 osis: AR, n=15; chronic rejection (CR), n=8; drug toxicity, n=4; urinary leak, n=2; recurrence of pri

118 of treatment, unless transplantation ensued, drug toxicity necessitated withdrawal, or the patient de

119 ng-term graft dysfunction, immunosuppressive drug toxicity, need for multiple donors, and increased r

120 onsequences in pharmacogenomics and variable drug toxicity observed in human populations.

121 ft dysfunction from other causes (infection, drug toxicity, obstruction) were associated with values

122 ort such use and even less information about drug toxicity or interactions.

123 ologic, immunologic, or clinical failure and drug toxicity or intolerance.

124 lated to recurrent disease, viral hepatitis, drug toxicity, or graft ischemia.

125 iver (frequency and severity of seizures and drug toxicity) (P<0.001).

126 have been abandoned owing to concerns about drug toxicity, particularly in stroke.

127 Viral drug toxicity, resistance, and an increasing immunosuppr

128 sed combination therapy in order to minimize drug toxicity, resistance, and costs in the face of ulti

129 ATP1B3 null mutations may confer substantial drug toxicity risks.

130 describe future applications for preclinical drug toxicity screening, drug design, and development.

131 e and development and provide a platform for drug toxicity screens and identification of novel pharma

132 ac disorders to model differences in cardiac drug toxicity susceptibility for patients of different g

133 these cells would accelerate haematopoietic drug toxicity testing and treatment of patients with blo

134 for a wide range of applications, including drug toxicity testing, cell transplantation, and patient

135 pplications, including cell transplantation, drug toxicity testing, patient-specific disease modeling

136 t, tissue engineering, disease modeling, and drug toxicity testing.

137 tabolizer is often more likely to experience drug toxicity than a rapid metabolizer.

138 ommon site for nonsteroidal antiinflammatory drug toxicity than the gastroduodenal mucosa.

139 n of tuberculosis drugs and a higher risk of drug toxicity than tuberculosis patients without diabete

140 ancer treatments are impacted by concomitant drug toxicities that could potentially limit therapeutic

141 creasing neurologic injury, may also lead to drug toxicity that may limit its benefit.

142 es have consistently shown value in reducing drug toxicity, their use has not always translated into

143 r microenvironment will significantly reduce drug toxicity to normal tissues.

144 y a reduction in angiogenesis areas, without drug toxicity to the normal CAM vasculature.

145 Nonsteroidal antiinflammatory drug toxicity to the small intestine is common.

146 Drug toxicity toward Muller cells, retinal pigment epith

147 otection, and rescue experiments in rats, of drug toxicity treatment with clinically relevant timing

148 The samples associated with drug toxicity, urological problems, or recurrence of pri

149 herapy (ART) include poor patient adherence, drug toxicities, viral resistance, and failure to penetr

150 Drug toxicity was assessed over this same time period by

151 h related to graft loss or immunosuppressive drug toxicity was attributed a maximum weight of 100.

152 nducing signal complex (DISC) formation, and drug toxicity was blocked by knockdown of CD95 or overex

153 The incidence of IRIS, and drug toxicity was not significantly different between tr

154 No evidence of drug toxicity was observed during the 4-week period of t

155 Systemic drug toxicity was short-lived, easily managed, and relat

156 g, iron/vitamin deficiencies, hemolysis, and drug toxicities, were ruled out.

157 ome of these effects are related directly to drug toxicity, whereas others are related to secondary e

158 completion of 6 months of treatment with no drug toxicity while maintaining 50% improvement in compo

159 pressing Delta105-125 PrP are susceptible to drug toxicity within minutes, suggesting that the mutant

160 sion dosing modification to further minimize drug toxicity without sacrificing regimen efficacy.