ライフサイエンスコーパス: multiple drug

1 to substantial changes in susceptibility to multiple drugs.

2 al target for increasing chemosensitivity to multiple drugs.

3 ence to a minimum of 6 months treatment with multiple drugs.

4 the pervasiveness of cross-resistance across multiple drugs.

5 d the first view of any MDR protein bound to multiple drugs.

6 toms was strongly associated with the use of multiple drugs.

7 selected the largest studies that evaluated multiple drugs.

8 ffects than coadministration of a mixture of multiple drugs.

9 origin or the cancer subtypes for single or multiple drugs.

10 NTCP is also a target of multiple drugs.

11 of a single-target drug or a combination of multiple drugs.

12 x system like DrrAB contains specificity for multiple drugs.

13 Ferumoxytol) can be utilized to carry one or multiple drugs.

14 preferentially associated with resistance to multiple drugs.

15 hs, especially when the child was exposed to multiple drugs.

16 urs within a year and exhibits resistance to multiple drugs.

17 complications arising from administration of multiple drugs.

18 particular drug and shared in resistance to multiple drugs.

19 election of pathogenic bacteria resistant to multiple drugs.

20 eported to be associated with alcoholism and multiple drug abuse and dependence.

21 siological response, and reduced reliance on multiple drug administration regimens.

22 ants lacking Pmr1 show growth sensitivity to multiple drugs (amiodarone, wortmannin, sulfometuron met

23 eed for lifelong coagulation monitoring, and multiple drug and diet interactions.

24 The ability to evaluate and cross-compare multiple drugs and drug combinations simultaneously in l

25 tability and allowed data to be obtained for multiple drugs and experimental conditions over hundreds

26 Multiple drugs and infectious agents can trigger the dis

27 ecent identification of strains resistant to multiple drugs and the potential use of Y. pestis as an

28 Multiple drugs are available for this purpose.

29 phenotypes, named accelerated resistance to multiple drugs (ARMD), raise important questions about t

30 tly inferring unknown DDIs from a network of multiple drug-based similarities and known interactions.

31 e labeling data also suggest the presence of multiple drug binding sites in ABCG2.

32 essful drugs target large gene families with multiple drug binding sites.

33 was a prospective trial of 41 patients with multiple drug class-resistant HIV who were randomized to

34 sms promoting the emergence of resistance to multiple drug classes have not been described in this or

35 As multiple drug classes progress in development, combinati

36 Despite the availability of multiple drug classes that modulate glycemia effectively

37 reat since it readily acquires resistance to multiple drug classes, including triazoles and/or echino

38 he Enterobacteriaceae are often resistant to multiple drug classes, making therapy of urinary infecti

39 ctive single agents, doublets, triplets, and multiple drug combination chemotherapy.

40 out, we analyzed hundreds of mutations under multiple drug conditions and found that the effects of m

41 ociated with major diseases and resistant to multiple drugs could be routinely delivered to individua

42 responsiveness to simultaneous microdoses of multiple drugs directly in a patient's tumor.

43 other classes of cytotoxic drugs, we applied multiple drug effect/combination index (CI) isobologram

44 idrug resistance (MDR), which is mediated by multiple drug efflux ATP-binding cassette (ABC) transpor

45 ubation in an asthmatic adolescent receiving multiple drugs for anesthesia, in whom no sensitization

46 ases like HIV, pediatric patients are taking multiple drugs for effective treatments.

47 indamycin, penicillin plus erythromycin, and multiple drugs (>/=3 antibiotics) was significantly lowe

48 methods, the ability of Sav1866 to transport multiple drugs has not been described.

49 between genetic mutations and resistance to multiple drugs have not been systematically evaluated.

50 itivity reactions have tendencies to develop multiple drug hypersensitivities (MDH).

51 f the Theme II transplant models depended on multiple drug immunosuppression (Theme III, Immunology),

52 Current therapy rests on multiple-drug immunosuppression but its prognostic influ

53 on was added to the tacrolimus-steroid-based multiple drug immunosuppressions.

54 he speed for screening and identification of multiple drugs in equine plasma for doping control analy

55 course (6 to 9 mo) intermittent therapy with multiple drugs including isoniazid, ethambutol, pyrazina

56 Increasing resistance to multiple drugs, including quinolones, is associated with

57 taphylococcus aureus, protects the cell from multiple drugs, including quinolones.

58 K intake, common genetic polymorphisms, and multiple drug interactions that affect its pharmacodynam

59 ngular vaccine with the potential to display multiple drug-like antigens; thus two haptens were synth

60 IM-MS evidenced ADC multiple drug loading, collisional cross sections measur

61 sporter is the efflux of spermidine, whereas multiple drugs may be recognized by Blt merely opportuni

62 tor (CAR; NR1I3) regulates the expression of multiple drug-metabolizing enzymes and transporters in l

63 By use of data-dependent product ion scans, multiple drugs of abuse could be detected in a single dr

64 cocaine exposure, yet locomotor responses to multiple drugs of abuse were unaltered in the KO mice.

65 echanisms underlying behavioral responses to multiple drugs of abuse.

66 ore intensive continuation chemotherapy with multiple drug pairs administered in weekly rotation.

67 Multiple drug pairs identified in this study, including

68 Shorter multiple-drug preventive regimens have been proposed.

69 of an efflux pump that reduces the effect of multiple drugs provides an alternative pathway to sequen

70 y analyses examined the risk associated with multiple-drug regimens, including stimulants and antidep

71 tor and anti-interleukin-1], anti-CD-18, and multiple-drug regimes [combination of anti-tumor necrosi

72 h unexpected thrombocytopenia who are taking multiple drugs remains a difficult clinical problem.

73 The increase in bacterial resistance to multiple drugs represents a serious and growing health r

74 centration was reversed by agents that block multiple drug resistance (MDR) and by the UIC2 anti-Pgp

75 Multiple drug resistance (MDR) as a result of overexpres

76 The murine multiple drug resistance (mdr) gene, mdr1a, encodes a 17

77 to enhance therapeutic efficacy by silencing multiple drug resistance (MDR) genes and resensitizing r

78 In a search for improved multiple drug resistance (MDR) modulators, we identified

79 sterone's ability to inhibit the activity of multiple drug resistance (MDR) P-glycoproteins.

80 pression of P-glycoprotein (P-gp) can confer multiple drug resistance (MDR) phenotype on cancer cells

81 therapeutic small interfering RNA (siRNA) to multiple drug resistance (MDR) tumors.

82 transplantation were related to CYP3AP1 and multiple drug resistance (MDR)-1 genotypes determined by

83 safety and efficacy of transfer of the human multiple drug resistance (MDR1, MDR) gene into hematopoi

84 idermal growth factor receptor (EGFR), human multiple drug resistance 1 (MDR-1) and human proliferati

85 ase chain reaction (RT-PCR) amplification of multiple drug resistance 1 (MDR1) mRNA from high prolife

86 M1 is a substrate for P-glycoprotein and the multiple drug resistance 2 transporter.

87 Rapid development of multiple drug resistance against current therapies is a

88 ew antimicrotubule compound that circumvents multiple drug resistance and so may be useful in the tre

89 mosomal genes implicated in cell physiology, multiple drug resistance and virulence.

90 Multiple drug resistance due to P-glycoprotein (P-gp) ex

91 omology with components of fimbrial operons, multiple drug resistance efflux pumps and a haemolysin.

92 r drug accumulation, or amplification of the multiple drug resistance gene (MDR).

93 rmal growth factor receptor (EGFR) and human multiple drug resistance gene (MDR-1).

94 drugs used for selection in combination with multiple drug resistance gene 1 (MDR1) could have an enh

95 ith an amphotropic retrovirus containing the multiple drug resistance gene leads to gene transfer not

96 wo plasmids, R1 and RP4, both of which carry multiple drug resistance genes and were shown to impose

97 n region V of CMV pol can, therefore, confer multiple drug resistance in a clinical isolate.

98 B operon is a regulatory locus that controls multiple drug resistance in Escherichia coli.

99 Prospective analysis of the role of multiple drug resistance in localized osteosarcoma did n

100 lle called vault, and has been implicated in multiple drug resistance in many cancer cell lines and p

101 nal infections may play an important role in multiple drug resistance in Mycobacterium avium infectio

102 lyzed prospectively to determine the role of multiple drug resistance in osteosarcoma.

103 many standard cytotoxic agents by means of a multiple drug resistance mechanism, remained quite susce

104 However, multiple drug resistance mechanisms can still emerge.

105 explore the hypothesis that the existence of multiple drug resistance mechanisms in different patient

106 r the taxanes in their ability to circumvent multiple drug resistance mechanisms.

107 All patients failing therapy showed multiple drug resistance mutations in different compartm

108 d reverse transcriptase sequences containing multiple drug resistance mutations, amplified from patie

109 nd that activates the ATPase activity of the multiple drug resistance P-glycoprotein, activated the m

110 of the MDR1 gene has been implicated in the multiple drug resistance phenotype expressed by many can

111 extrusion mechanisms including expression of multiple drug resistance proteins.

112 any neurological diseases, and the resulting multiple drug resistance represents a major clinical cha

113 her, our results support the hypothesis that multiple drug resistance to AEDs involves cerebrovascula

114 PB) cells, genetically marked with the human multiple drug resistance transgene (MDR1) were used for

115 The ATPase activity of the multiple drug resistance transporter Mdr1 (P-glycoprotei

116 n of the gene ABCB1 (also known as MDR1, for multiple drug resistance) in HeLa cells.

117 le CT18 carries two plasmids, one conferring multiple drug resistance, Ty2 has no plasmids and is sen

118 nt transformation and conferring tumors with multiple drug resistance.

119 is, angiogenesis, response to infection, and multiple drug resistance.

120 and paclitaxel in the context of tumors with multiple drug resistance.

121 in the PDR1-101 transcription factor confers multiple drug resistance.

122 of cancer stem-like cells (CSC) that exhibit multiple drug resistance.

123 quisition of mutations in the development of multiple drug resistance.

124 sing candidate for treatment of cancers with multiple drug resistance.

125 n, which codes for the Vibrio cholerae VceAB multiple-drug resistance (MDR) efflux pump, and vceR, wh

126 MATE transporters also mediate multiple-drug resistance (MDR) in bacteria and mammals,

127 Although poorly understood, in common with multiple-drug resistance (MDR) in tumors, MHR is associa

128 The multiple-drug resistance (MDR) transporter P-glycoprotei

129 recombination could contribute to high-level multiple-drug resistance and that this process must be c

130 ments often involve sequential selection for multiple-drug resistance in single ES cell lines, we hav

131 nt viruses and performed linkage analysis of multiple-drug resistance mutations.

132 in the proportion of T cells expressing the multiple-drug resistance pump P-glycoprotein.

133 Multiple drug-resistance bacteria (MDRB) infection is on

134 It harbors multiple drug-resistance elements including a truncated

135 Multiple drug-resistance interpretation algorithms have

136 lop resistance through stepwise selection of multiple drug-resistance mechanisms.

137 CT18 harbours a 218,150-bp multiple-drug-resistance incH1 plasmid (pHCM1), and a 10

138 Whole-genome sequencing of a multiple drug resistant (MDR) ST313 NTS isolate, D23580,

139 l resistance to antibiotics, particularly to multiple drug resistant antibiotics, is becoming cause f

140 170-glycoprotein efflux pump associated with multiple drug resistant cancer cells.

141 has inhibitory activity against P-gp 170, a multiple drug resistant gene product.

142 Since the 1990s the rising incidence of multiple drug resistant TB, particularly in the context

143 ts an economical donor for the production of multiple-drug resistant MEFs.

144 oduct sansalvamide A that are potent against multiple drug-resistant colon cancer cell lines.

145 ide A as a privileged structure for treating multiple drug-resistant colon cancers.

146 alvamide A as an excellent lead for treating multiple drug-resistant colon cancers.

147 amine the efficacy of protegrin-1 in killing multiple drug-resistant microbes isolated from human bur

148 significantly associated with development of multiple drug-resistant organisms in IAI (P=0.032).

149 otics within 2 weeks before transplantation, multiple drug-resistant organisms often caused IAI.

150 such as increased levels of glutathione and multiple drug-resistant protein 4, these effects are unl

151 Against KB/7d cells (a pleiotrophic multiple drug-resistant subclone selected with etoposide

152 esent day thrust for new drugs to counteract multiple drug-resistant tuberculosis.

153 cent detection and recognition of widespread multiple-drug-resistant (MDR) and extensively drug-resis

154 ent of the major facilitator (MF) VceAB-VceC multiple-drug-resistant (MDR) efflux pump of Vibrio chol

155 se, viruses carrying various combinations of multiple-drug-resistant (MDR) mutations predominated wit

156 When concentrations of CBZ found in multiple-drug-resistant brain were directly applied to h

157 Of note is the response of slices from human multiple-drug-resistant brain, which was greater than in

158 f HIV infection, particularly infection with multiple-drug-resistant isolates.

159 ing standard antibiotics with protegrin-1 on multiple-drug-resistant microbial organisms isolated fro

160 ce of anaerobic bacteremia and prevalence of multiple-drug-resistant microorganisms.

161 In this paper, we have characterized a multiple-drug-resistant mutant of the HIV-1 protease tha

162 osocomial pathogen with a high prevalence of multiple-drug-resistant strains, causing pneumonia and s

163 me of a S. typhi (CT18) that is resistant to multiple drugs, revealing the presence of hundreds of in

164 Furthermore, there are multiple drug reviews and prevalence studies.

165 Multiple drug scaffolds were simultaneously docked into

166 howed significant negative correlations with multiple drugs, suggesting a mechanism of drug resistanc

167 Multiple drug target analysis (MDTA) used in doping cont

168 Based on the prediction of multiple drug target pathway activation, we derive a com

169 he BET inhibitor JQ1 combined favorably with multiple drugs targeting B-cell receptor signaling, one

170 Single agents against multiple drug targets are of increasing interest.

171 At cytotoxic concentrations, amiloride has multiple drug targets including inhibition of NHE1 and s

172 The efficacy of engaging multiple drug targets using bispecific antibodies (BsAbs

173 omated design of ligands against profiles of multiple drug targets.

174 anocarriers which simultaneously incorporate multiple drugs that affect different pathways and act th

175 compliance with life-style modifications and multiple drug therapies should be explored.

176 EM is a complication of multiple drug therapy in patients awaiting heart transpl

177 obilized, tethered to devices, and receiving multiple drugs to facilitate the entire process.

178 Since use of multiple drugs to treat psychiatric patients is increasi

179 codes the primary transcription activator of multiple drug transporter genes in S. cerevisiae, includ

180 ngle cell phosphoquantitation in response to multiple drug treatment conditions and using limited pri

181 However, for long-term multiple-drug treatments, complications can arise from s

182 ected locally, through subsequent failure of multiple drugs until introduction of artemisinin combina

183 sed in cell lines selected for resistance to multiple drugs used to treat acute leukemia.

184 naptic 5-HT inactivation and the targets for multiple drugs used to treat psychiatric disorders.

185 ons (mostly malaria and typhoid), and giving multiple drugs was common.

186 on to the development of HIV-1 resistance to multiple drugs was investigated.

187 ts are often given continuous treatment with multiple drugs well into old age.

188 rror (chloramphenicol), and 15 minor errors (multiple drugs) were observed.

189 red, conversion to another active form; (ii) multiple drugs within a treatment combination; (iii) dif

190 ns also facilitates opportunities to combine multiple drugs within one delivery platform, as well as