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1 s of S. aureus in infected mice treated with rifampin.
2 sistance of a poxvirus to the antiviral drug rifampin.
3 sis resistant to at least both isoniazid and rifampin.
4 nt in the presence of the assembly inhibitor rifampin.
5 e negative pharmacokinetic interactions with rifampin.
6 tween PDE-Is (cilostazol and sildenafil) and rifampin.
7 Nine patients were treated with TMP-SMX and rifampin.
8 esistant mutants were not cross-resistant to rifampin.
9 and absence of the RNA polymerase inhibitor rifampin.
10 d maybe also a potential benefit from adding rifampin.
11 One patient was taking only rifampin.
12 trifugation, was hindered in the presence of rifampin.
13 as 95.1% concordance with INH and 96.1% with rifampin.
14 e CarD protein did not affect sensitivity to rifampin.
15 m, gentamicin, tigecycline, doxycycline, and rifampin.
16 os instead of azithromycin, doxycycline, and rifampin.
17 und 26 is also shown to work in synergy with rifampin.
18 g beta-lactams, and 37% of patients received rifampin.
19 ine than in subjects receiving standard-dose rifampin.
20 gher rates of hepatotoxicity than placebo or rifampin.
21 starved cells but killed those generated by rifampin.
22 r 11 drugs: isoniazid (0.03 to 0.12 mug/ml), rifampin (0.03 to 0.25 mug/ml), ethambutol (0.25 to 2 mu
24 of removable components (0.60), early use of rifampin (0.98 per day of treatment within the first 30
26 09 if initially susceptible to isoniazid and rifampin, 1 in 113 if initially isoniazid resistant, and
27 assigned rifapentine 10, 15, or 20 mg/kg or rifampin 10 mg/kg daily for 8 weeks (intensive phase), w
28 e randomized to rifapentine 10 mg/kg/dose or rifampin 10 mg/kg/dose, administered 5 days per week for
29 ing the MDR-TB assay were 100% and 92.3% for rifampin, 100% and 93.8% for isoniazid, 91.6% and 94.4%
31 ntensified regimen that included higher-dose rifampin (15 mg per kilogram per day) and levofloxacin (
32 ental groups with 15 patients each receiving rifampin 20, 25, 30, and 35 mg/kg, respectively, for 14
33 oniazid (6H), three months of isoniazid plus rifampin (3RH) and three months of isoniazid plus rifape
34 plus isoniazid (900 mg) weekly for 12 weeks, rifampin (600 mg) plus isoniazid (900 mg) twice weekly f
36 ic ineligibility were similar across groups (rifampin, 8.2%; rifapentine 10, 15, or 20 mg/kg, 3.4, 2.
37 results were 94.3% for isoniazid, 98.7% for rifampin, 97.6% for quinolones (ofloxacin, levofloxacin,
38 0)Z and HR(160)Z therapy regimens showed for rifampin a C(max) of 16.2 and 157.3 mg/L, an AUC(0-24h)
45 y contributed to the detection of phenotypic rifampin and fluoroquinolone resistance with negligible
46 Using catheters coated with minocycline and rifampin and implementing infection control precautions.
47 in primary human hepatocytes was induced by rifampin and inhibited by CYP3A4-specific inhibitors.
49 y for Mycobacterium tuberculosis complex and rifampin and isoniazid resistance detection on clinical
50 ve genotypic susceptibility results for both rifampin and isoniazid were seen in 26% of MTBDRplus tes
51 ntensive phase and was continued, along with rifampin and isoniazid, during the continuation phase.
52 zinamide, and ethambutol followed by 4 mo of rifampin and isoniazid, with a 4-mo clofazimine-containi
55 or uvrD increased spontaneous resistance to rifampin and nalidixic acid, and MMC/uvrD double mutants
56 ly bactericidal (isoniazid) and sterilizing (rifampin and pyrazinamide), and ethambutol to help preve
57 had concentration-dependent antagonism with rifampin and pyrazinamide, with an adjusted odds ratio f
58 tor of hPXR expression and the hPXR agonists rifampin and rilpivirine are chemical suppressors of miR
62 acts had isolates resistant to isoniazid and rifampin, and 41 (36.6%) contacts had isolates with resu
63 three-times-weekly therapy with a macrolide, rifampin, and ethambutol is a reasonable initial treatme
66 folP1, rpoB, and gyrA, targets for dapsone, rifampin, and fluoroquinolones, real-time PCR-HRM assays
68 cin, trimethoprim, gentamicin, fusidic acid, rifampin, and mupirocin) performed by the routine clinic
69 , concurrent use of amiodarone, fluconazole, rifampin, and phenytoin compared with the use of NOACs a
70 Concurrent use of amiodarone, fluconazole, rifampin, and phenytoin with NOACs had a significant inc
71 high between-child variability of isoniazid, rifampin, and pyrazinamide concentrations: 110 (77%) com
72 tal pharmacokinetic parameters of isoniazid, rifampin, and pyrazinamide were identified for each pati
73 gimens to the standard regimen of isoniazid, rifampin, and pyrazinamide, based on exponential decline
76 izing effect, with inoculum spiked with 0.5% rifampin- and isoniazid-resistant isogenic strains in so
77 erestingly, the antibiotics thiostrepton and rifampin are fast acting and might target additional pro
79 rved with the combination of polymyxin B and rifampin as well as with polymyxin B and doxycycline, re
82 ncentration-time curve (AUC) </= 363 mg.h/L, rifampin AUC </= 13 mg.h/L, and isoniazid AUC </= 52 mg.
86 quinolones and in those receiving a standard rifampin-based regimen in an interleukin-2 (IL-2) trial.
87 region, an 81-base pair region encoding the rifampin binding site on the beta subunit of RNA polymer
90 en the virus was passaged in the presence of rifampin but was lost in the absence of the drug, sugges
91 sceptible to chloramphenicol, penicillin and rifampin, but almost 60% of isolates characterized in So
92 levofloxacin, ethambutol, azithromycin, and rifampin (CLEAR) regimen or a comparative placebo regime
94 SA and MRSA prognoses, although the specific rifampin combinations may have had different efficacies.
96 ange in antigen production when treated with rifampin, demonstrating drug susceptibility and resistan
98 97]); 65.66 for NOAC use alone vs 103.14 for rifampin (difference, 36.90 [99% CI, 1.59-72.22); and 56
105 robial activity and safety of rifapentine vs rifampin during the first 8 weeks of pulmonary tuberculo
106 ortion susceptibility results for isoniazid, rifampin, ethambutol, streptomycin, amikacin, kanamycin,
107 rs should ideally evaluate for resistance to rifampin, fluoroquinolones, isoniazid, and pyrazinamide
108 ultured isolates phenotypically resistant to rifampin, fluoroquinolones, or aminoglycosides, but for
109 ents receiving the standard dose of 10 mg/kg rifampin, followed by consecutive experimental groups wi
111 erythromycin, clarithromycin, azithromycin, rifampin, gentamicin, and doxycycline against 101 isolat
112 media occurred in 110 of 169 (65.1%) in the rifampin group and 133 of 196 (67.9%) in the rifapentine
113 ed in 145 of 174 participants (83.3%) in the rifampin group and 171 of 198 participants (86.4%) in th
114 erapy, 40 of 254 participants (15.7%) in the rifampin group and 40 of 275 participants (14.5%) in the
115 ere negative in 81.3% of participants in the rifampin group versus 92.5% (P = 0.097), 89.4% (P = 0.29
116 Liquid cultures were negative in 56.3% (rifampin group) versus 74.6% (P = 0.042), 69.7% (P = 0.1
120 Change in resistance to tetracycline and rifampin in clinically relevant staphylococcal isolates
122 indicate that MD-2 is a important target of rifampin in its inhibition of innate immune function and
124 lococci clinical isolates to tetracycline or rifampin in the intensive care unit and on a hospitalwid
125 staphylococcal isolates to tetracycline and rifampin in the intensive care unit or throughout the ho
127 bacterial survival rates in the presence of rifampin in vitro, while deletion significantly decrease
128 te mechanism for resistance of poxviruses to rifampin, indicates a direct relationship between A17 le
131 ciated with species typing and resistance to rifampin, isoniazid and fluoroquinolone antibiotics.
133 among M. tuberculosis isolates resistant to rifampin, isoniazid, and fluoroquinolones, respectively.
135 s from the Philippines for susceptibility to rifampin, isoniazid, and ofloxacin by using the conventi
137 own to retain their anti-TB activity against rifampin, isoniazid, and streptomycin resistant Mtb stra
138 ith resistance to four types of antibiotics (rifampin, isoniazid, fluoroquinolones, and aminoglycosid
139 lofazimine-containing regimen: 2 mo of daily rifampin, isoniazid, pyrazinamide, and clofazimine follo
140 egimen for TB treatment, i.e., 2 mo of daily rifampin, isoniazid, pyrazinamide, and ethambutol follow
141 iazid group, 2.9 per 100 person-years in the rifampin-isoniazid group, and 2.7 per 100 person-years i
146 , rpoB mutant progeny strains with confirmed rifampin monoresistance following antitubercular therapy
147 ese isolates, with their known resistance to rifampin, NGS of pncA improved PZA resistance detection
148 (SNPs) that confer resistance to isoniazid, rifampin, ofloxacin, and moxifloxacin occur the most fre
149 r-positive specimens resistant to isoniazid, rifampin, or both according to the GenoType MTBDRplus as
151 tration-time curve <11.95 mg/L x hour and/or rifampin peak <3.10 mg/L were the best predictors of the
153 uberculosis regimen (which included 10 mg of rifampin per kilogram of body weight per day) with an in
154 imulations have suggested that isoniazid and rifampin pharmacokinetic variability best explained poor
156 instead of azithromycin; 2) azithromycin and rifampin plus placebo instead of doxycycline; or 3) plac
158 ulosis were treated with regimens containing rifampin, pyrazinamide, and ethambutol +/- a FQ for a me
159 One group of patients received isoniazid, rifampin, pyrazinamide, and ethambutol for 8 weeks, foll
160 and bactericidal effect rates for isoniazid, rifampin, pyrazinamide, and ethambutol were the same in
162 for MAC identification; 97.4% and 98.7% for rifampin(r) TB identification; 60.6% and 100% for isonia
164 ce for hepatoxicity comparing isoniazid with rifampin ranged from 3% to 7%, with a pooled RR of 3.29
165 ot significantly more active than a standard rifampin regimen, by the surrogate endpoint of culture s
168 CI], 82.4% to 97.9%) sensitive for detecting rifampin resistance and 99.7% (95% CI, 98.3% to 99.9%) s
170 ts suggested that Rv2629 could be a cause of rifampin resistance and a valuable target for rifampin r
171 f M. tuberculosis The specific links between rifampin resistance and named lipid factors provide diag
172 pxB grown as a biofilm showed no increase in rifampin resistance compared to the same cells grown pla
173 ted for samples referred for confirmation of rifampin resistance detected by the Cepheid Xpert MTB/RI
176 largely determined by mutations in an 80-bp rifampin resistance determining region (RRDR) of the rpo
177 berculosis DNA and mutations associated with rifampin resistance in 5 of 7 participants with rifampin
178 iation was found between the 191C allele and rifampin resistance in an analysis that included the SCG
182 Tests of 23 different commonly occurring rifampin resistance mutations demonstrated that all 23 (
183 d in both genetic backgrounds, we found that rifampin resistance mutations lead to altered concentrat
186 lecular beacon assay should greatly simplify rifampin resistance testing in clinical laboratories.
187 performance of the Xpert assay for detecting rifampin resistance using phenotypic drug sensitivity te
189 sensitivity of the Xpert assay for detecting rifampin resistance was assessed in vitro by testing cul
193 this assay's sensitivity and specificity for rifampin resistance were 85.7% (95% CI, 57.2, 98.2) and
194 DR-Plus, the sensitivity and specificity for rifampin resistance were 91.7% and 96.6%, respectively,
196 fers ofloxacin resistance) and rpoB (confers rifampin resistance) had significantly more breakpoints
197 the acquisition of missense mutations in the rifampin resistance-determining region, an 81-base pair
204 ified 222/225 rifampin-resistant isolates as rifampin resistant (sensitivity, 98.7%; 95% CI, 95.8 to
207 Consequently, we found that the frequency of rifampin-resistant (Rif(r)) mutants is dramatically incr
208 tiate between DNA sequences of wild-type and rifampin-resistant (Rif(r)) Mycobacterium tuberculosis (
209 equencing-based drug resistance screening of rifampin-resistant (rifampin(r)), isoniazid(r), and pyra
211 629 A191C mutations were present in 99.1% of rifampin-resistant and 0% of rifampin-susceptible clinic
212 The 191C allele was present in 30/98 (30.6%) rifampin-resistant isolates and 25/148 (16.9%) rifampin-
216 vitro-derived recombinants of ofloxacin- and rifampin-resistant L(1) and D strains, respectively, gro
218 unctive transferrin reduced the emergence of rifampin-resistant mutants of S. aureus in infected mice
219 posure yielded considerably lower numbers of rifampin-resistant mutants than cultures of the wild typ
220 mately 10,000 cell wall lipids in a panel of rifampin-resistant mutants within two genetically distin
221 ng a principal screening tool for diagnosing rifampin-resistant Mycobacterium tuberculosis complex (M
222 to their superior affinity for wild-type and rifampin-resistant Mycobacterium tuberculosis RNA polyme
224 to DD Mtb generation, an effect lacking in a rifampin-resistant strain with a mutation in rpoB, which
225 acteristic remodeling of cell wall lipids in rifampin-resistant strains of M. tuberculosis The specif
230 sis (wild type) to those of their respective rifampin-resistant, rpoB mutant progeny strains with con
231 iepileptic drugs and the antimicrobial agent rifampin, resulting in drug-induced osteomalacia, which
232 henotypic DST (true resistance) was 100% for rifampin (RIF) (14/14), 90.0% for isoniazid (INH) (36/40
233 of a highly conserved regulatory motif, the rifampin (RIF) -associated element (RAE), which is found
234 promoter were targeted for the detection of rifampin (RIF) and isoniazid (INH) resistance, respectiv
242 ires daily administration of combinations of rifampin (RIF), isoniazid [isonicotinylhydrazine (INH)],
243 eptibility testing (DST) to isoniazid (INH), rifampin (RIF), moxifloxacin (MOX), ofloxacin (OFX), ami
244 merase (rpoB) gene that confer resistance to rifampin (RIF), the treatment of choice for tuberculosis
245 ere offered 9-month isoniazid (INH), 4-month rifampin (RIF), weekly rifapentine/isoniazid (RPT/INH) f
251 Nigerian HIV-infected individuals (7.0% for rifampin [RIF] and 9.3% for RIF or isoniazid [INH]).
252 ex (MTBC)-negative, MTBC-positive (including rifampin [RIF] susceptible and RIF resistant), and nontu
253 orrelation with high levels of resistance to rifampin (rifampicin) in Mycobacterium tuberculosis isol
256 mance of GeneChip in detecting resistance to rifampin (RMP) and isoniazid (INH) and in detecting mult
258 ined their activity against isoniazid (INH), rifampin (RMP), and streptomycin (SM) resistant Mtb stra
259 s used in the United States-isoniazid (INH), rifampin (RMP), ethambutol (EMB), and pyrazinamide (PZA)
263 treatment of healthy volunteers (n = 6) with rifampin selectively induced CYP3A4-dependent 4beta,25(O
265 s 18 to 65 years of age with smear-positive, rifampin-sensitive, newly diagnosed pulmonary tuberculos
266 tion curves and peak serum concentrations of rifampin showed a more than proportional increase with d
268 22/429 (98%) accurate results for isoniazid, rifampin, streptomycin, ethambutol, amikacin, kanamycin,
269 and 335/336 rifampin-susceptible isolates as rifampin susceptible (specificity, 99.7%; 95% CI, 95.8 t
270 ent in 99.1% of rifampin-resistant and 0% of rifampin-susceptible clinical Mycobacterium tuberculosis
271 fampin-resistant isolates and 25/148 (16.9%) rifampin-susceptible isolates and was more common in iso
272 y, 98.7%; 95% CI, 95.8 to 99.6%) and 335/336 rifampin-susceptible isolates as rifampin susceptible (s
274 utation in rpoB, which encodes the canonical rifampin target, the beta subunit of RNA polymerase.
275 transcriptional and translational inhibitors rifampin, tetracycline, and erythromycin were found to b
276 xycycline, linezolid, meropenem, penicillin, rifampin, tetracycline, trimethoprim-sulfamethoxazole, a
278 nfer a survival advantage in the presence of rifampin, they may alter the normal process of transcrip
280 trimethoprim-sulfamethoxazole (TMP-SMX) and rifampin, TMP-SMX alone, rifampin alone, or tetracycline
281 mice exhibit tolerance to both isoniazid and rifampin to a degree proportional to the activation stat
283 inhibitor of NQO1 dicoumarol synergized with rifampin to promote intracellular killing of mycobacteri
287 r step by repression of A14 expression or by rifampin treatment, A11 colocalized with virion membrane
289 (adjusted OR, 5.65; 95% CI, 0.93-34.47), and rifampin use (adjusted OR, 4.56; 95% CI, 0.74-27) were a
290 etween catheters coated with minocycline and rifampin use and a decrease in central line-associated b
291 nsplantation, cytomegalovirus infection, and rifampin use) when compared with none of these factors c
292 seven different antibiotics (ciprofloxacin, rifampin, vancomycin, ampicillin, sulfamethoxazole, gent
293 vity during the first 28 days of therapy and rifampin was active against dormant bacilli after the es
295 a substrate for CYP3A4, which is induced by rifampin, we evaluated the pharmacokinetic/pharmacodynam
296 ns of amikacin, doripenem, levofloxacin, and rifampin were quantitatively assessed using a validated
297 , 9200 catheters coated with minocycline and rifampin were used hospitalwide over a total of 511,520
298 ect of catheters coated with minocycline and rifampin with and without other infection control precau
299 -month course of intermittent rifapentine or rifampin with isoniazid nor continuous isoniazid was sup
300 here was a nonlinear increase in exposure to rifampin without an apparent ceiling effect and a greate
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