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1 MDR and XDR tuberculosis are associated with high morbid
2 MDR and XDR-TB isolates were significantly more likely t
3 MDR is typically associated with transmembrane proteins
4 MDR(+) cells were frequently observed in leukemic blast
5 MDR-TB was defined as culture-confirmed TB disease with
10 into leukemic blast cells with MDR activity (MDR(+)) and leukemic blast cells without MDR activity (M
13 Furthermore, the strategy that co-administer MDR-ABCB1 inhibitor to overcome the resistance of one FD
14 tics with improved in vitro activity against MDR pathogens using recently updated guidelines for acti
15 the hybrid possesses potent activity against MDR, P. aeruginosa isolates the activity that can be syn
16 bacterial activity, in vivo efficacy against MDR A. baumannii infections and promising preclinical sa
20 oquinolones have high resistance rates among MDR uropathogens and are being strongly discouraged as f
22 d evidence of the phenotypes predicted by an MDR result (fundus albipunctatus due to RDH5 and variega
23 for the incidence density of candidemia and MDR BSI (+0.018 cases per 1000 OBDs per quarter; 95% con
24 ity rate of hospital-acquired candidemia and MDR BSI through sustained reduction in antibiotic use.
27 tal infection control practices for MRSA and MDR-AB (ie, contact precautions, private room/cohorting,
32 b IC50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb patient isolates IC50 = 140 nM) and favorable ph
35 ual per-capita incidence of tuberculosis and MDR-tuberculosis by HC, with a rate of MDR-tuberculosis
36 improve patients' health, protect background MDR TB drugs, and decrease transmission, but would likel
39 that capsular switching has occurred between MDR vaccine serotypes belonging to ST156 (e.g., 9V, 14,
41 approaches in treating infections caused by MDR bacteria will be heavily influenced by a precision m
45 ple therapeutic agents, but also help bypass MDR pathways, which are conducive for the efficient deli
46 31 (TCG/TTG) and katG 315 (AGC/ACC)] causing MDR-TB and verification of loss of the respective wild t
47 of common carbapenemase genes using a Check-MDR CT101 microarray (Check-Points, Wageningen, the Neth
51 ) and repurposed (linezolid and clofazimine) MDR-TB drugs and the new shorter MDR-TB regimen in child
54 wever, we found that pyrazinamide-containing MDR-LTBI regimens often resulted in treatment discontinu
55 ood circulation and effectively downregulate MDR gene expression in vivo to enhance chemotherapeutic
56 tallopeptidases, multidrug-resistant efflux (MDR) pumps, TonB-dependent receptors and many proteins o
58 a serotype Reading isolates were extensively MDR, suggesting a strong association between serotype an
62 sus the least-affected HC; (2) high risk for MDR-tuberculosis in a region spanning several HCs (odds
63 apy where bacteriophages exert selection for MDR bacteria to become increasingly sensitive to traditi
64 obial drugs are in advanced trial stages for MDR tuberculosis, and two new antimicrobial drug candida
67 treated compared with those not treated for MDR-LTBI; 10 presented outcomes only for treated contact
70 uced risk of TB incidence with treatment for MDR-LTBI, suggesting effectiveness in prevention of prog
71 ted great promise as potential treatment for MDR-related tumors based on the synergistic effects of P
73 owever, pronounced variability in functional MDR activity between leukemic blasts was observed, with
77 20 adults with AML whose leukemic blasts had MDR activity against the anthracyline daunorubicin (DNR)
78 (5%) of 7982 patients with tuberculosis had MDR tuberculosis and 324 (88%) of these had isolates ava
80 t multiple-case and 88 single-case household MDR strains were analyzed for 10 specific drug resistanc
81 characteristics associated with decreases in MDR-AB rates, greater compliance with the MDR-AB prevent
88 reventive strategies (such as prophylaxis in MDR and XDR contacts), palliative and patient-orientated
90 says that can distinguish the variability in MDR activity between individual leukemic blasts are lack
91 ercentage of XDR tuberculosis among incident MDR tuberculosis to increase, reaching 8.9% (95% predict
92 is reports to forecast estimates of incident MDR and XDR tuberculosis and the percentage of incident
93 tuberculosis and the percentage of incident MDR and XDR tuberculosis caused by acquired drug resista
97 ohort study of adult patients that initiated MDR-TB treatment with individualized regimens between Se
99 ugs, these are DS (drug sensitive isolates), MDR (multi-drug resistant isolates) and XDR (extremely d
100 Among all invasive serotype 35B isolates, MDR isolates increased significantly, from 2.9% (1/35) t
107 bafetinib reversed ABCB1- and ABCG2-mediated MDR by blocking the drug efflux function of these transp
115 significant reduction in the acquisition of MDR A. baumannii (RR, 0.28 [95% CI, .18-.43] and 0.48 [9
116 2.33, 4.36); and (3) spatial aggregation of MDR-tuberculosis genotypes, suggesting localized transmi
119 ends in four countries with a high burden of MDR tuberculosis: India, the Philippines, Russia, and So
121 (95% SI: 246, 558), with 46% being cases of MDR-TB, while incorporating programmatic management of M
128 composition, transmission, and evolution of MDR- and XDR-TB in Belarus and will enable improved diag
129 and the genetic composition and evolution of MDR- and XDR-TB in the region, we sequenced and analyzed
130 ng pathway, leading to reduced expression of MDR transporters and thereby an increased accumulation o
131 approach, we estimated that the majority of MDR-TB was due to the recent transmission of already-res
132 ile incorporating programmatic management of MDR-TB into these programs reduced incidence to 233 case
139 The comparative gene expression profile of MDR E. coli 381 and the reference human strain E. coli A
141 s and MDR-tuberculosis by HC, with a rate of MDR-tuberculosis 89 times greater (95% confidence interv
142 tance rates are needed to stop the spread of MDR and XDR tuberculosis in countries with a high burden
150 onses and resistance during various types of MDR-P. aeruginosa infections is needed to define ceftolo
151 robial resistance and the emergence of other MDR pathogens, such as malaria, HIV, and Gram-negative b
154 etics, the use of Pgp inhibitors to overcome MDR in the clinical setting remains elusive despite prom
157 ll discuss the mechanism of NO in overcoming MDR and recent progress of combined NO and drug delivery
158 ly sensitized ABCB1 and ABCG2 overexpressing MDR cells to their anticancer substrates and increased t
162 ere was 42%-55% underestimation of pediatric MDR-TB cases when using only culture-confirmed case defi
163 rtain potential underestimation of pediatric MDR-TB, we surveyed high-burden states for clinically di
164 This review fills a gap in the pediatric MDR-TB literature by providing practice-based recommenda
165 sulting in underestimation of true pediatric MDR-TB burden in the United States using strictly bacter
168 ving Effective TB Treatment Study to predict MDR and XDR tuberculosis trends in four countries with a
171 rated that the various mechanisms regulating MDR in HCC cells are calcium dependent through the TRPC6
173 les that confer multiple disease resistance (MDR) are valuable in crop improvement, although the mole
175 s tendency to develop multi-drug resistance (MDR), whose various underlying mechanisms make it diffic
177 ncer cells can develop multidrug resistance (MDR) after prolonged exposure to chemotherapeutic drugs,
178 n hospitals, including multidrug resistance (MDR) and its association with serious infectious disease
180 e of DOX and overcomes multidrug resistance (MDR) in cancer cells, producing a remarkably improved th
182 rotein (Pgp) increases multidrug resistance (MDR) in cancer, which greatly impedes satisfactory clini
185 gies to overcome tumor multidrug resistance (MDR) is to deliver anticancer drug along with P-glycopro
188 f treatment failure is multidrug resistance (MDR) mediated by the ABCB1, ABCC1, and ABCG2 drug-efflux
190 tumors show intrinsic multidrug resistance (MDR) or inevitably acquire such when treated with antica
191 er, the development of multidrug resistance (MDR) restricts the efficacy of current chemotherapeutic
193 in the development of multidrug resistance (MDR), a major obstacle for successful chemotherapy in ca
194 of the main causes of multidrug resistance (MDR), being capable of effluxing many chemotherapeutics.
195 mpicin monoresistance, multidrug resistance (MDR), fluoroquinolone-resistant multidrug resistance, se
197 s is a major factor in multidrug resistance (MDR), which makes these pumps important antibacterial dr
198 the expression of 377 multidrug resistance (MDR)-associated genes in two independent cohorts of pati
201 ncreased prevalence of multidrug resistance (MDR; 94% compared to 60% in layers), including prevalenc
202 ents to infection with multi-drug resistant (MDR) bacteria are determined by many complex factors.
205 ased the proportion of multi-drug resistant (MDR) Salmonella from day 4 through day 26, which was the
207 nd the epidemiology of multi-drug-resistant (MDR) Escherichia coli (using blaNDM and mcr-1 as marker
208 ded for the analysis of multidrug resistant (MDR) and extensively drug resistant (XDR) Mtb strains th
212 ries were predefined as multidrug resistant (MDR), isoniazid resistant, rifampicin susceptible (INH-R
213 actam resistance during multidrug resistant (MDR)-Pseudomonas aeruginosa infections are limited.
219 he increasing burden of multidrug-resistant (MDR) and extensively drug-resistant (XDR) tuberculosis.
220 density of Candida and multidrug-resistant (MDR) bacteria bloodstream infections (BSIs) and their cr
224 systems are absent from multidrug-resistant (MDR) Enterococcus faecalis, which only possess an orphan
225 se antibiotics includes multidrug-resistant (MDR) gram-negative bacteria (GNB), including Pseudomonas
229 interventions to treat multidrug-resistant (MDR) Pseudomonas aeruginosa infections are severely limi
231 inadequate treatment of multidrug-resistant (MDR) tuberculosis (i.e., acquired resistance) versus tho
232 r contact to infectious multidrug-resistant (MDR) tuberculosis (TB) are lacking because published dat
234 recent transmission of multidrug-resistant (MDR) tuberculosis and identify potential risk factors fo
236 se regimen for treating multidrug-resistant (MDR) tuberculosis was recently recommended by the World
238 s treatment options for multidrug-resistant (MDR) uropathogens are limited, clinicians need to be awa
239 012 muM; SI >/= 16000), multidrug-resistant (MDR), and extensively drug-resistant (XDR) Mycobacterium
240 oprim-sulfamethoxazole (multidrug resistant [MDR]) was limited to Typhi isolates, primarily acquired
241 y toxic chemosensitizing agents that reverse MDR effects, which has raised expectations in the develo
243 the cytotoxicity and the ability to reverse MDR was tested with the chemotherapeutic agents SN-38 an
245 oup), which included monogenic disease risk (MDR) results (associated with Mendelian disorders), carr
250 uberculosis (TB) and multidrug-resistant TB (MDR-TB) are major health problems in Western Province, P
251 berculosis (TB) and multi-drug resistant TB (MDR-TB), repurposing FDA (U.S. Food and Drug Administrat
253 results show that SIPI has higher power than MDR (Multifactor Dimensionality Reduction), AA_Full, Gen
256 ound 13 showed moderate activity against the MDR Gram-negative strains, with MICs in the range of 16-
264 in MDR-AB rates, greater compliance with the MDR-AB prevention bundle did not lead to reductions in M
266 with the synergistic sensitization of those MDR tumor cells to conventional chemotherapeutic agents,
268 ents with hospital-acquired infection due to MDR bacteria in Thailand in 2010 represented excess mort
270 To address the need for new agents to treat MDR P. aeruginosa, we focused on inhibiting the first co
271 spread of multidrug-resistant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR
276 han 30% of multidrug-resistant tuberculosis (MDR-TB) patients are currently diagnosed, due to laborat
279 better antimicrobial performance against two MDR isolates of Pseudomonas aeruginosa and Acinetobacter
281 n the few MDR loci that are well-understood, MDR is conditioned by diverse mechanisms at the locus an
282 itical information about the highly virulent MDR E. coli strain of poultry origin and warrant further
288 tion, fold-increase of DNR accumulation with MDR inhibition, ease of cell trapping, and ease of maint
290 ategorization into leukemic blast cells with MDR activity (MDR(+)) and leukemic blast cells without M
292 y between leukemic blasts was observed, with MDR(+) cells not infrequently seen in some patients that
294 stricting bedaquiline usage to patients with MDR plus additional resistance and withholding bedaquili
295 g bedaquiline available to all patients with MDR TB, restricting bedaquiline usage to patients with M
298 successful in treating 71% of patients with MDR-P. aeruginosa infections, most of whom had pneumonia
299 rospective cohort study of 172 subjects with MDR/extensively drug-resistant TB subjects and sequenced
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