ライフサイエンスコーパス: drug toxicity

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

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

3 c mechanism of action of the drug as well as drug toxicity.

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

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

6 factors able to protect sensitive cells from drug toxicity.

7 a questionnaire to assess their awareness of drug toxicity.

8 activation but did not protect cells against drug toxicity.

9 ocellular-cholestatic injury compatible with drug toxicity.

10 assisted reproduction or potential sites of drug toxicity.

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

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

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

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

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

16 hly intervals to evaluate weight changes and drug toxicity.

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

18 argets, and to explain poly-pharmacology and drug toxicity.

19 the development of diabetes with no apparent drug toxicity.

20 improvement for 6 months with no significant drug toxicity.

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

22 tion, opportunistic infections, and possible drug toxicity.

23 two groups discontinued treatment because of drug toxicity.

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

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

26 murine studies for anti-cancer efficacy and drug toxicity.

27 proved transplantation outcomes with reduced drug toxicity.

28 f tumor response and progression, as well as drug toxicity.

29 both the treatment of cancer and controlling drug toxicity.

30 sential for understanding renal diseases and drug toxicity.

31 xic amounts of nanoparticles, which restored drug toxicity.

32 ischemia/reperfusion, oxidative stress, and drug toxicity.

33 ly and that OPA1 LKO protects the liver from drug toxicity.

34 ytostatic and tissue specific, which reduces drug toxicity.

35 ite significant infectious complications and drug toxicity.

36 trolyte disorders, uremic complications, and drug toxicity.

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

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

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

40 reproducible, early and sensitive measure of drug toxicity.

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

42 ome to improve response to therapy or reduce drug toxicity.

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

44 etformin, potentially increasing the risk of drug toxicity.

45 bulky peritoneal tumors and reduced systemic drug toxicity.

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

47 or enhanced tumor targeting and reduction of drug toxicity.

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

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

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

51 us terminating both psychoactive effects and drug toxicity.

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

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

54 .9% (5 of 567), and 2 deaths were related to drug toxicity.

55 n1 expression blocked autophagy and enhanced drug toxicity.

56 1) compared with controls without noticeable drug toxicities.

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

58 t monthly intervals to evaluate appetite and drug toxicities.

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

60 large suppressed individual and combination drug toxicities.

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

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

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

64 , autoimmune skin conditions, wound healing, drug toxicity, aging, and antiaging, SoC aims to circumv

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

66 bility, assess response to treatment, detect drug toxicities and recurrences.

67 to use PROTAC technology to reduce on-target drug toxicities and rescue the therapeutic potential of

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

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

70 However, long-term drug toxicity and associated complications necessitate i

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

72 The most efficient way of studying drug toxicity and efficacy requires high-resolution imag

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

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

75 term outcomes remain suboptimal, hampered by drug toxicity and immune-mediated injury, the leading ca

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

77 erogeneity in drug response that can lead to drug toxicity and ineffective treatment, making CYP2D6 o

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

79 caveats associated with their use, including drug toxicity and resistance.

80 Improving treatment outcomes while reducing drug toxicity and shortening the treatment duration to ~

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

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

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

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

85 changes therapeutically have been stymied by drug toxicity and tumour cell plasticity.

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

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

88 ng drugs and metabolites sharing reactivity, drug toxicities, and drug targets.

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

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

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

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

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

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

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

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

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

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

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

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

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

102 monitoring response to therapy, detection of drug toxicity, and patient selection for clinical trials

103 ologic features of cardiomyopathy, potential drug toxicity, and survival.

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

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

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

107 This drug toxicity appears to occur by 2 different mechanisti

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

109 Drug toxicities are the main causes of posttransplant ne

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

111 Drug toxicities associated with HAART lend urgency to th

112 ling more robust and reliable predictions of drug toxicity, bioactivity, and physicochemical properti

113 and serve as a reliable means for assessing drug toxicity, but the implementation is limited by the

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

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

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

117 erial beta-glucuronidase (GUS) enzymes cause drug toxicity by reversing Phase II glucuronidation in t

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

119 igns of LSCD, particularly in patients where drug toxicity can be aggravated due to impaired hepatic

120 per screening to evaluate drug efficacy and drug toxicity caused by a therapeutic.

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

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

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

124 ll as difficulties posed by drug resistance, drug toxicity, disease monitoring, and metastatic evolut

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

126 D) has limited efficacy towards treatment of drug toxicity due to strong drug-protein binding.

127 NAFLD having utility for compound screening, drug toxicity evaluation, and assessment of gene regulat

128 With regards to drug toxicity, everolimus alone led to a modest degree o

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

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

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

132 ition during HD is a potential treatment for drug toxicities for which current recommendations exclud

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

134 Common causes of ALF in adults include drug toxicity, hepatotropic and non-hepatotropic viruses

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

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

137 may result in immune-mediated idiosyncratic drug toxicity (IDT).

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

139 ism with NUDT15 polymorphism associated with drug toxicity in patients.

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

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

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

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

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

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

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

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

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

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

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

151 Drug toxicity is an important factor that contributes si

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

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

154 ce on therapeutic drug monitoring to predict drug toxicity is scarce.

155 g globally, with limited antifungal classes, drug toxicity issues, and the rapid emergence of multidr

156 an autologous source for cardiac repair and drug toxicity, it is vital to understand the functionali

157 he ipilimumab group were attributed to study drug toxicity (marrow aplasia in one patient and colitis

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

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

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

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

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

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

164 the nivolumab arm, two were related to study drug toxicity; no deaths occurred in the placebo arm.

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

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

167 However, drug toxicity occurred frequently in both arms.

168 No new deaths due to study drug toxicity occurred since the 32.9-month median follo

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

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

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

172 such as serious and rarely fatal infections, drug toxicities overlapping with irAEs and the risk of c

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

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

175 d that these vascular cells exhibit distinct drug toxicity patterns, which are linked to divergent th

176 e in many tasks, including drug repurposing, drug toxicity prediction and target gene-disease priorit

177 s been widely used to aid in drug screening, drug toxicity prediction, quantitative structure-activit

178 elial injury, including allograft rejection, drug toxicity, recurrent infections and postrenal obstru

179 Patients with sarcoidosis and drug toxicity-related ILD were excluded.

180 Viral drug toxicity, resistance, and an increasing immunosuppr

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

182 ATP1B3 null mutations may confer substantial drug toxicity risks.

183 IHP-1), have been used for decades to permit drug toxicity screening and studies into potential AKI m

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

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

186 r tissue engineering, cell preservation, and drug toxicity study.

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

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

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

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

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

192 rdless of biofabrication method), performing drug toxicity-testing, and testing pharmaceutical effica

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

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

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

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

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

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

199 of a more comprehensive approach to studying drug toxicity through longitudinal profiling of the huma

200 o alternative to animal models for assessing drug toxicity, thus reducing expensive and invasive anim

201 utic agents to cancer cells while minimizing drug toxicity to normal cells and off-targeting effects,

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

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

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

205 Drug toxicity toward Muller cells, retinal pigment epith

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

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

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

209 Drug toxicity was assessed over this same time period by

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

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

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

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

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

215 Acute drug toxicity was the most common cause of death in each

216 Study drug toxicity was the reported cause of death in five (1

217 Deaths due to study drug toxicity were reported in two (1%) patients in the

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

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

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

221 nation of immunosuppressive therapy to avoid drug toxicity, with concurrent acceptance of the allogra

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

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