ライフサイエンスコーパス: rifampicin

1 of Mycobacterium smegmatis to challenge with rifampicin.

2 tude as spontaneous resistance to drugs like rifampicin.

3 plets containing TAG and in its tolerance of rifampicin.

4 tant to host RNA polymerase (RNAP) inhibitor rifampicin.

5 10-fold induction in response to PXR agonist rifampicin.

6 the current frontline anti-tuberculosis drug rifampicin.

7 growth advantage in the presence of the drug rifampicin.

8 ance frequencies compared to clinically used rifampicin.

9 increase in concentration of the antibiotic rifampicin.

10 eudomonas aeruginosa adapt to the antibiotic rifampicin.

11 strated increased binding in the presence of rifampicin.

12 f histone H4, in response to the PXR agonist rifampicin.

13 but that many of these are not inducible by rifampicin.

14 monotherapy and in combination therapy with rifampicin.

15 se with resistance to at least isoniazid and rifampicin.

16 one that is resistant to both isoniazid and rifampicin.

17 herapies with 3 to 4 months of isoniazid and rifampicin.

18 the former necessitating discontinuation of rifampicin.

19 n ~0.0067 mg/ml, clarithromycin ~0.05 mg/ml, rifampicin ~0.002 mg/ml) could be defined for healthy vo

20 g, isoniazid, pyrazinamide, and SQ109; 63 to rifampicin 10 mg/kg, isoniazid, pyrazinamide, and moxifl

21 oniazid, pyrazinamide, and ethambutol; 59 to rifampicin 10 mg/kg, isoniazid, pyrazinamide, SQ109; 57

22 9-month antituberculosis regimen (containing rifampicin 10 mg/kg/day) with an intensified regimen wit

23 with an intensified regimen with higher-dose rifampicin (15 mg/kg/day) and levofloxacin (20 mg/kg/day

24 mg/kg, isoniazid, pyrazinamide, SQ109; 57 to rifampicin 20 mg/kg, isoniazid, pyrazinamide, and SQ109;

25 er-generated permuted block randomisation to rifampicin 300 mg twice daily or matching placebo (50 mg

26 patients to different treatment arms (63 to rifampicin 35 mg/kg, isoniazid, pyrazinamide, and ethamb

27 e hypothesis that the use of higher doses of rifampicin (35 mg/kg) will significantly reduce treatmen

28 r a daily standard control regimen (10 mg/kg rifampicin, 5 mg/kg isoniazid, 25 mg/kg pyrazinamide, an

29 intravenously, or colistin (as above), plus rifampicin 600 mg every 12 hours intravenously.

30 sation list to receive 2 weeks of adjunctive rifampicin (600 mg or 900 mg per day according to weight

31 iotic rifampicin (RIF) to 2'-N-hydroxy-4-oxo-rifampicin, a metabolite with much lower antimicrobial a

32 Among these compounds, rifampicin, a well-known antibiotic, showed the stronges

33 followed by 4 months of daily isoniazid and rifampicin; a 4-month regimen in which the isoniazid in

34 Dose escalation of rifampicin achieves >90% Wolbachia depletion in time per

35 The inhibitory effects of rifampicin against amyloid-beta and tau oligomers were e

36 es also showed potency comparable to that of rifampicin against the nonreplicating streptomycin-starv

37 Rifampicin also inhibited cytochrome c release from the

38 ere found to bind to PXREs in the absence of rifampicin, although binding was stronger after rifampic

39 In addition, rifampicin, an inhibitor of host RNA polymerase, restore

40 observed when spa19 cells were treated with rifampicin, an inhibitor of the chloroplast RNA polymera

41 dpoint was 0.5 points (SD 0.7) per month for rifampicin and 0.5 points (0.5) per month for placebo (d

42 participants were randomly assigned: 370 to rifampicin and 388 to placebo.

43 we randomly assigned 100 participants (50 to rifampicin and 50 to placebo).

44 Previously observed effects of rifampicin and chloramphenicol indicate that transcripti

45 ue 9 and 16 at 4 mug/mL decreased the MIC of rifampicin and clarithromycin against the same pathogens

46 ck lamA are more uniform and more rapid with rifampicin and drugs that target the cell wall.

47 Large doses of rifampicin and fluoroquinolones might improve outcome, a

48 e to penicillin G, amoxicillin, doxycycline, rifampicin and gentamicin.

49 as mediating macrophage-induced tolerance to rifampicin and intracellular growth.

50 icin susceptible (INH-R), and susceptible to rifampicin and isoniazid (INH-S + RIF-S).

51 The predicted resistance to rifampicin and isoniazid exceeded 90% sensitivity and sp

52 All patients received rifampicin and isoniazid for 6 months reinforced with py

53 acterium tuberculosis isolate susceptible to rifampicin and isoniazid recovered <3 months after MDR t

54 , treatment of the mice with the antibiotics rifampicin and isoniazid, as expected, resulted in effec

55 andard antituberculosis treatment, including rifampicin and isoniazid.

56 due to M. tuberculosis resistant to at least rifampicin and isoniazid.

57 n with existing first-line chemotherapeutics rifampicin and isoniazid.

58 s with the human OATP1B1 and -1B3 substrates rifampicin and pravastatin and demonstrated a reduced li

59 lity, we show that the key sterilizing drugs rifampicin and pyrazinamide efficiently penetrate the si

60 ications reversed tolerance to isoniazid and rifampicin and slowed intracellular growth.

61 inically used tuberculosis drugs, isoniazid, rifampicin and streptomycin.

62 or clarithromycin, 19% for amikacin, 18% for rifampicin, and 11% for moxifloxacin.

63 The patient was treated with doxycycline, rifampicin, and gentamicin, and underwent surgical repai

64 nteract with OATPs, including cyclosporin A, rifampicin, and glibenclamide, each demonstrated concent

65 evolution of resistance to fluoroquinolones, rifampicin, and macrolides was observed to occur on mult

66 Together, phenytoin, rifampicin, and monocrotaline caused further endothelial

67 Phenytoin, rifampicin, and monocrotaline produced injury in hepatoc

68 included 2 months of ethambutol, isoniazid, rifampicin, and pyrazinamide administered daily followed

69 id this for isoniazid, kanamycin, ofloxacin, rifampicin, and streptomycin resistance in Mycobacterium

70 d livers, differentiated hepatocytes, and in rifampicin- and phenobarbital-induced hepatocytes.

71 l)oxime (CITCO)], pregnane X receptor (PXR) [rifampicin], and peroxisome proliferator-activated recep

72 However, the effects of oxidized and reduced rifampicin are similar, in that neither prevents amyloid

73 ation rate was observed in the colistin plus rifampicin arm (P = .034).

74 ost-treatment follow-up: one in the 35 mg/kg rifampicin arm and none in the moxifloxacin arm.

75 tudies have highlighted the potential use of rifampicin as an inhibitor of amyloid formation by a var

76 th the first-line anti-tubercular antibiotic rifampicin, as well as with the antibiotic metronidazole

77 In 13-month-old Tg2576 mice, oral rifampicin at 0.5 mg/day for 1 month decreased amyloid-b

78 In the Morris water maze, rifampicin at 1 mg/day improved memory of the mice to a

79 ng Xpert MTB/RIF (Mycobacterium tuberculosis/rifampicin) automated testing on induced sputum (IS) is

80 g factors, is affected by amino acids of the Rifampicin-binding pocket, suggesting altered RNA cappin

81 n-allopathic practitioners do not treat with rifampicin, but because of the high rates of inappropria

82 rvival on media containing nalidixic acid or rifampicin, but did not have an increased mutation rate

83 ed resistance to isoniazid, streptomycin and rifampicin by around 1973, indicating continuous circula

84 Functional analysis further revealed that rifampicin can enhance lipid accumulation in human prima

85 at elevated exposures of orally-administered rifampicin can lead to Wolbachia depletions from filaria

86 The data indicate that rifampicin cannot be used to test the relative toxicity

87 Pharmacodynamic indices for rifampicin, clarithromycin, amikacin, and moxifloxacin a

88 combination therapy with three antibiotics: rifampicin, clofazimine, and dapsone.

89 If isoniazid Cmax was <4.6 mg/L and rifampicin Cmax/MIC <28, the isoniazid concentration had

90 tive interactions between isoniazid Cmax and rifampicin Cmax/MIC ratio on 2-month culture conversion.

91 ses using MARS identified isoniazid Cmax and rifampicin Cmax/MIC thresholds below which there is conc

92 were done before the introduction of modern rifampicin-containing antituberculosis chemotherapy.

93 analysis that only included trials that used rifampicin-containing regimens, the results were similar

94 afety in humans, these results indicate that rifampicin could be a promising, ready-to-use medicine f

95 e initially tested five candidate compounds: rifampicin, curcumin, epigallocatechin-3-gallate, myrice

96 In addition, rifampicin decreased the level of p62/sequestosome-1 in

97 Doxycycline and rifampicin deplete essential Wolbachia from filarial nem

98 We show that rifampicin does not prevent amyloid formation by IAPP an

99 novel p-cyanoPhe analogue of IAPP shows that rifampicin does not significantly affect the kinetics of

100 Our results show that rifampicin does not slow or halt progression of multiple

101 onsible for resistance of M. tuberculosis to rifampicin drug, and discriminating them from wild-type

102 Rifampicin even accumulates in necrotic caseum, a critic

103 As these regimens omit isoniazid, rifampicin, fluoroquinolones and injectable aminoglycosi

104 These mice were given phenytoin and rifampicin for 3 days, after which monocrotaline was giv

105 hs or longer (OR, 0.52 [CrI, 0.41 to 0.66]), rifampicin for 3 to 4 months (OR, 0.41 [CrI, 0.18 to 0.8

106 The PXR ligand rifampicin further increased the expression of CYP3A4, a

107 triguing new data to suggest higher doses of rifampicin given intravenously may improve the survival.

108 Three (6%) of 50 participants in the rifampicin group and 12 (24%) of 50 in the placebo group

109 of study termination, 49 participants in the rifampicin group and 50 in the placebo group had follow-

110 Four participants in the rifampicin group and five in the placebo group withdrew

111 n in liquid media was faster in the 35 mg/kg rifampicin group than in the control group (median 48 da

112 erved; however, 63 (17%) participants in the rifampicin group versus 39 (10%) in the placebo group ha

113 e was 0.62 points [SD 0.85] per month in the rifampicin group vs 0.47 points [0.48] per month in the

114 rrent evidence suggests that the minocycline-rifampicin-impregnated CVC appears to be the most effect

115 conducted in human hepatocytes treated with rifampicin in order to identify new pregnane-X receptor

116 e aimed to assess the safety and efficacy of rifampicin in patients with multiple system atrophy.

117 tibiotics ciprofloxacin, clarithromycin, and rifampicin in the case of suspected allergies to antibio

118 y used to detect resistance to isoniazid and rifampicin in the diagnosis of MDR-TB, has good diagnost

119 dren and pregnant/breastfeeding women, as is rifampicin in the latter group with the additional spect

120 dditional putative compensatory mutations to rifampicin in this dataset.

121 ning TAG and develop phenotypic tolerance to rifampicin in two in vitro models of dormancy including

122 with high levels of resistance to rifampin (rifampicin) in Mycobacterium tuberculosis isolates that

123 y of antibiotics (doxycycline, oxacillin and rifampicin) in preventing Staphylococcus aureus biofilms

124 In LS180 human intestinal cells, rifampicin increased UGT2A3 mRNA by more than 4.5-fold c

125 Rifampicin inhibited CXL more significantly than aminogu

126 In a mouse model of multiple system atrophy, rifampicin inhibited formation of alpha-synuclein fibril

127 Under cell-free conditions, rifampicin inhibited oligomer formation of amyloid-beta,

128 ese data suggest that the inducing effect of rifampicin is counterbalanced by a concentration-dependa

129 Rifampicin is unstable in aqueous solution and is readil

130 ected) were intensively sampled to determine rifampicin, isoniazid, and pyrazinamide plasma concentra

131 Antituberculosis therapy (rifampicin, isoniazid, ethambutol and pyrazinamide) was

132 ingredients (APIs) ampicillin, amoxicillin, rifampicin, isoniazid, ethambutol, and pyrazinamide and

133 4 months (OR, 0.41 [CrI, 0.18 to 0.86]), and rifampicin-isoniazid regimens for 3 to 4 months (OR, 0.5

134 nly regimens (OR, 0.41 [CrI, 0.19 to 0.85]), rifampicin-isoniazid regimens of 3 to 4 months (OR, 0.53

135 to 4 months (OR, 0.53 [CrI, 0.36 to 0.78]), rifampicin-isoniazid-pyrazinamide regimens (OR, 0.35 [Cr

136 loration of body fluids with higher doses of rifampicin it was not possible to mask patients and clin

137 n plates containing lethal concentrations of rifampicin, kanamycin, and nalidixic acid.

138 The bactericidal drugs isoniazid and rifampicin kill greater than 99% of exponentially growin

139 Concurrent administration of rifampicin led to 68%, 23%, and 10% decreases in C(max)

140 Twenty-six percent of patients had Cmax of rifampicin <8 mg/L, pyrazinamide <35 mg/L, and isoniazid

141 The prototypical PXR activator rifampicin markedly induced the mRNA and protein express

142 Rifampicin monooxygenase (RIFMO) catalyzes the N-hydroxy

143 (26.7%) patients, MDR in 15 (4.7%) patients, rifampicin monoresistance in 1 patient (0.3%), and INH-S

144 Acquired isoniazid and rifampicin monoresistance occurred in 1 in 1018 and 1 in

145 country level with isoniazid monoresistance, rifampicin monoresistance, multidrug resistance (MDR), f

146 and safety of 6-month isoniazid monotherapy, rifampicin monotherapy, and combination therapies with 3

147 mpicin, or ertapenem followed by combination rifampicin, moxifloxacin, and metronidazole for 6 months

148 f doxorubicin transport by Hoechst 33342 and rifampicin occurs by a competitive mechanism, whereas ve

149 rates (including verapamil, vinblastine, and rifampicin) of the well studied multidrug transporters i

150 tations that confer resistance to isoniazid, rifampicin, ofloxacin and streptomycin.

151 to 72 months (OR, 0.50 [CrI, 0.41 to 0.62]), rifampicin-only regimens (OR, 0.41 [CrI, 0.19 to 0.85]),

152 , paenipeptins, alone or in combination with rifampicin or clarithromycin, are promising candidates f

153 b) and sterilizes Mtb in vitro combined with rifampicin or isoniazid.

154 on mouse models both alone and combined with rifampicin or isoniazid.

155 roportion cured for 3-mo regimens containing rifampicin or rifapentine was 19-100%.

156 terial is observed by LDPI-MS in response to rifampicin or trimethoprim antibiotic treatment.

157 eatment with combinations of clindamycin and rifampicin, or ertapenem followed by combination rifampi

158 atio to receive (all orally) either 35 mg/kg rifampicin per day with 15-20 mg/kg ethambutol, 20 mg/kg

159 n per day with 400 mg moxifloxacin, 20 mg/kg rifampicin per day with 300 mg SQ109, 10 mg/kg rifampici

160 fampicin per day with 300 mg SQ109, 10 mg/kg rifampicin per day with 300 mg SQ109, or a daily standar

161 er day with 15-20 mg/kg ethambutol, 20 mg/kg rifampicin per day with 400 mg moxifloxacin, 20 mg/kg ri

162 y 14 weeks of 5 mg/kg isoniazid and 10 mg/kg rifampicin per day.

163 Mice were treated with rifampicin, phenytoin, and monocrotaline.

164 e of MDR and XDR occurring 20 y (rpoB L452P [rifampicin]; pncA 1 bp insertion [pyrazinamide]; 1984 [9

165 nd intestine (CXD2), as well as induction by rifampicin (pregnane X receptor).

166 other small thiols with either isoniazid or rifampicin prevents the formation of drug-tolerant and d

167 h high probability, but combining ADEP4 with rifampicin produced complete eradication of Staphylococc

168 INTERPRETATION: Adjunctive rifampicin provided no overall benefit over standard ant

169 ed use of first line antibiotics (isoniazid, rifampicin, pyrazinamide, and ethambutol) is efficient t

170 regimens (OR, 0.35 [CrI, 0.19 to 0.61]), and rifampicin-pyrazinamide regimens (OR, 0.53 [CrI, 0.33 to

171 sceptible pulmonary tuberculosis, isoniazid, rifampicin, PZA, and ethambutol (HRZE regimen).

172 he two most potent agents, isoniazid (H) and rifampicin (R), would usually prompt therapeutic modific

173 in regimen (moxifloxacin [M], isoniazid [H], rifampicin [R], pyrazinamide [Z], ethambutol [E]) or the

174 APPOSK mice at 0.5 and 1 mg/day for 1 month, rifampicin reduced the accumulation of amyloid-beta olig

175 ssed whether the combination of colistin and rifampicin reduced the mortality of XDR A. baumannii inf

176 Risk factors for acquired rifampicin resistance (ARR) in human immunodeficiency vi

177 interval [CI], 8.25-44.7; P < .001), initial rifampicin resistance (OR, 35.9; 95% CI, 8.61-150; P < .

178 Isoniazid resistance evolved before rifampicin resistance 46 times, whereas rifampicin resis

179 mingly arose before mutations that conferred rifampicin resistance across all of the lineages, geogra

180 The simple genetics of rifampicin resistance allowed us to determine the geneti

181 lecular diagnostics that include markers for rifampicin resistance alone will be insufficient to iden

182 detection of smear-negative tuberculosis and rifampicin resistance and to estimate and compare Xpert

183 The rifampicin resistance determinant region (RRDR) of rpoB

184 fore rifampicin resistance 46 times, whereas rifampicin resistance evolved prior to isoniazid only tw

185 s targets to detect the mycobacteria and the rifampicin resistance from gDNA directly extracted from

186 for detection of pulmonary tuberculosis and rifampicin resistance in children younger than 16 years

187 ated the incidence of acquired isoniazid and rifampicin resistance in rifampicin-susceptible tubercul

188 is article, we show that the average cost of rifampicin resistance in the pathogenic bacterium Pseudo

189 The Xpert MTB/RIF assay detected rifampicin resistance in three GLA samples: two confirme

190 Rifampicin resistance in Xpert-positive patients was inf

191 i (K-12 and B strains), the mutation rate to rifampicin resistance is plastic and inversely related t

192 (78%) in the katG codon and the most common rifampicin resistance mutation was S531L (68%) in the rp

193 tivities and specificities for isoniazid and rifampicin resistance of the tools were high, whereas th

194 Patients without evidence of rifampicin resistance on phenotypic test who took at lea

195 he sensitivity of Xpert MTB/RIF in detecting rifampicin resistance to 93.8%.

196 These results show that the cost of rifampicin resistance varies with demand for the mutated

197 pooled sensitivity and specificity to detect rifampicin resistance was 86% (95% credible interval 53-

198 Rifampicin resistance was detected for the first time in

199 Rifampicin resistance was detected in 3 eyes by rpoB gen

200 ection: RpoB H(4)(8)(1)Y, which is linked to rifampicin resistance, and RelA F(1)(2)(8)Y, which is as

201 s improved the detection of tuberculosis and rifampicin resistance, but its sensitivity is inadequate

202 resistance was significantly associated with rifampicin resistance, this drug may still be effective

203 resistance was significantly associated with rifampicin resistance.

204 carried a rare rpoB mutation associated with rifampicin resistance.

205 detection of Mycobacterium tuberculosis and rifampicin resistance.

206 cs employed in South Africa that assess only rifampicin resistance.

207 ected to rpoB gene sequencing to demonstrate rifampicin resistance.

208 t of Xpert for detection of tuberculosis and rifampicin resistance.

209 les rapid detection of tuberculosis (TB) and rifampicin resistance.

210 ite increased rates of inducible mutation to rifampicin resistance.

211 a and Xpert performed similarly in detecting rifampicin resistance.

212 tra and Xpert specificities for detection of rifampicin resistance.

213 ed MDR strains had compensatory mutations of rifampicin resistance.

214 antiretroviral therapy was 10%, with limited rifampicin resistance.

215 ents and in settings with high prevalence of rifampicin resistance.

216 alent, but it allowed for rapid detection of rifampicin resistance.

217 In a rifampicin-sensitive to rifampicin-resistance assay that detects base substituti

218 risk group were only included in analyses of rifampicin-resistance detection.

219 ound only in isolates carrying a common rpoB rifampicin-resistance mutation, may play a role in fitne

220 soniazid resistant, and 1 in 23 if initially rifampicin resistant.

221 Losses were substantially higher among rifampicin- resistant cases, with only 22% successfully

222 Rifampicin-resistant (Rif(r)) isolates were stable, sugg

223 ermutation by sequencing rpoB in spontaneous rifampicin-resistant (Rif(R)) mutants.

224 various novel rifampicin-susceptible (RS) or rifampicin-resistant (RR) TB regimens that differed on s

225 llent antibacterial activity against several rifampicin-resistant M. tuberculosis strains.

226 ory mutations in the RNA polymerase genes of rifampicin-resistant M. tuberculosis, the etiologic agen

227 s transcription from late phiKZ promoters in rifampicin-resistant manner.

228 features from a cohort of streptomycin- and rifampicin-resistant mutants grown in the absence of ant

229 We hypothesize that ORF64 encodes rifampicin-resistant phage RNAP that recognizes early ph

230 In vivo experiments revealed the presence of rifampicin-resistant RNA polymerizing activity in infect

231 -resistant Mycobacterium leprae, including a rifampicin-resistant strain, is reported.

232 ng pocket, suggesting altered RNA capping in Rifampicin-resistant strains.

233 However, GeneXpert identified rifampicin-resistant TB in one patient, who was initiall

234 South Africa has a large burden of rifampicin-resistant tuberculosis (RR-TB), with 18,734 p

235 Xpert MTB/RIF (Xpert) detects rifampicin-resistant tuberculosis (RR-tuberculosis), ena

236 B/RIF assay for detecting culture-confirmed, rifampicin-resistant tuberculosis was 81.3% (95% CI, 53.

237 till be effective in 19-63% of patients with rifampicin-resistant tuberculosis.

238 deficiency virus (HIV)-coinfected cases) and rifampicin-resistant tuberculosis.

239 Thus, rifampicin response is complex and due to a combination

240 st optimized the size, surface modification [rifampicin (RF) conjugation], and concentration (2.5 nM)

241 Rifampicin (RF) is known for its ability to enhance the

242 Co-therapy with rifampicin (RIF) and isoniazid (INH) used to treat tuber

243 ection and highly sensitive determination of rifampicin (RIF) by square wave adsorptive stripping vol

244 Rifampicin (RIF) induces UGT1A1, an enzyme involved in r

245 primary hepatocytes to the human PXR agonist rifampicin (RIF) on expression of target genes involved

246 Given our finding that PXR activation by rifampicin (RIF) represses the estrogen sulfotransferase

247 tion of Mycobacterium tuberculosis (MTB) and rifampicin (RIF) resistance, was endorsed by WHO in Dece

248 roxylation of the natural product antibiotic rifampicin (RIF) to 2'-N-hydroxy-4-oxo-rifampicin, a met

249 Wolbachia but synergized with minocycline or rifampicin (RIF) to deplete symbionts, block embryogenes

250 latent animals with a combination of INH and rifampicin (RIF) was highly effective at preventing reac

251 We have developed a tissue model for rifampicin (RIF), an antibiotic used to treat tuberculos

252 osis (TB) chemotherapeutics isoniazid (INH), rifampicin (RIF), and pyrazinamide (PZA) have been label

253 with the pregnane X receptor (PXR) activator rifampicin (RIF), human hepatocellular carcinoma HepG2-d

254 n the presence of both -82T-->C mutation and rifampicin (RIF)-activated PXR.

255 Rifampicin (RMP) significantly reduced itch intensity an

256 gnificant decreases were shown by miconazole-rifampicin (RR, 0.14 [95% CI, .05-.36]), 5-fluorouracil

257 SI reduction was associated with minocycline-rifampicin (RR, 0.29 [95% CI, .16-.52]) and silver (RR,

258 [95% HPD: 1974-1992]) and 10 y (rpoB D435G [rifampicin]; rrs 1400 [kanamycin]; gyrA A90V [ofloxacin]

259 In a rifampicin-sensitive to rifampicin-resistance assay that

260 Patients with newly diagnosed, rifampicin-sensitive, previously untreated pulmonary tub

261 These results indicate that, at present, rifampicin should not be routinely combined with colisti

262 Treatment with rifampicin shows that active transcription is necessary

263 prototypical pregnane X receptor activator, rifampicin, significantly reversed decitabine-induced AB

264 n of vitamin D(3) to the human PXR activator rifampicin; SMRT increased its dissociation as this rati

265 n of urinary catheters with a combination of rifampicin, sparfloxacin and triclosan.

266 are essential antituberculosis drugs in new rifampicin-sparing regimens.

267 stranslation rates, which result in enhanced rifampicin-specific phenotypic resistance.

268 Discordant rifampicin susceptibility results of Xpert MTB/RIF and m

269 ctively identify subpopulations with altered rifampicin susceptibility.

270 tidrug resistant (MDR), isoniazid resistant, rifampicin susceptible (INH-R), and susceptible to rifam

271 We modeled the introduction of various novel rifampicin-susceptible (RS) or rifampicin-resistant (RR)

272 ysis included patients with newly diagnosed, rifampicin-susceptible pulmonary tuberculosis, with and

273 uired isoniazid and rifampicin resistance in rifampicin-susceptible tuberculosis in a setting of high

274 GeneXpert MTB/RIF-confirmed patients with rifampicin-susceptible tuberculosis were recruited at an

275 ophene and the antibiotics, tetracycline and rifampicin, that target the apicoplast inhibited LS deve

276 After isoniazid and rifampin (rifampicin), the next pivotal drug class in Mycobacteriu

277 ng trials more often evaluated regimens with rifampicin throughout and intermittent regimens, and pat

278 Addition of rifampicin to colistin may be synergistic in vitro.

279 -day mortality is not reduced by addition of rifampicin to colistin.

280 ges and subsequent bacterial release enabled rifampicin to effectively kill Mtb at concentrations tha

281 also modified when the cells are exposed to rifampicin (transcription inhibitor), nalidixic acid (gy

282 enome between vegetative cells, gametes, and rifampicin-treated cells by quantitative PCR, we found t

283 in BBD-treated mice were lower than those in rifampicin-treated mice.

284 e (untreated, bile duct-ligated, vehicle- or rifampicin-treated) and strain-matched knockout mice una

285 tween tether-induced initiation blocking and rifampicin treatment and the role of programmed changes

286 Rifampicin treatment to 14-15-month-old tau609 mice at 0

287 sites in gametes that were also sensitive to rifampicin treatment.

288 ampicin, although binding was stronger after rifampicin treatment.

289 )Tc-mebrofenin disposition was altered after rifampicin treatments.

290 nking unacylated tridecaptin A1 (H-TriA1) to rifampicin, vancomycin, and erythromycin enhanced their

291 ek 12, 62 (17%) of participants who received rifampicin versus 71 (18%) who received placebo experien

292 A dose of 35 mg/kg rifampicin was safe, reduced the time to culture convers

293 INTERPRETATION: A dose of 35 mg/kg rifampicin was safe, reduced the time to culture convers

294 y considerably in fitness in the presence of rifampicin were challenged with adapting to a high dose

295 ibitors of AGE formation, aminoguanidine and rifampicin, were applied during CXL in the treatment sol

296 that clinically relevant dose elevations of rifampicin, which have recently been determined as safe

297 Rifampicin, which inhibits bacterial RNA polymerase, pro

298 mycin) or can not be widely recommended (eg, rifampicin, which is the key drug to treat tuberculosis)

299 cated for ultra-trace level determination of rifampicin with very low detection limit (4.55x10(-17)M)

300 We tested the hypothesis that adjunctive rifampicin would reduce bacteriologically confirmed trea