ライフサイエンスコーパス: CRE

1 CRE analysis in urine samples displayed excellent result

2 CRE incidence was determined based on detection of CRE,

3 CRE infections originate from almost all ACHs and half o

4 CRE prevalence was higher in facilities that manage vent

5 CRE was attributed to a facility based on timing of cult

6 CRE were clustered into isolated bradycardia (IB), isola

7 CRE-positive adult inpatients were prospectively recruit

8 CREs show tissue- and cell-type specificity and disease-

9 ctSCAN-SMS identified 10 CREs and 12 TREs as novel candidate REs of the Oct4 gene

10 Delaying the intervention until the 20th CRE detection resulted in substantial delays in achievin

11 further developed a cell-based assay (the 3'CRE-REP assay) to yield recombinants throughout the non-

12 Among 430 CRE isolates from the 249 subjects, 307(71.3%) were CPE,

13 Prospectively, 45 CRE isolates were encountered over a 3-month period, inc

14 cilities and nursing homes experiencing >= 5 CRE acquisitions annually decreased from 35 to 11 during

15 ere highly similar, averting 2,976 and 2,789 CRE transmission events, respectively (72.2% and 77.0% o

16 A transgenic mouse containing a CRE-recombinase inducible CAG promoter driven CD9 protei

17 we examined the gene expression profile of a CRE Escherichia coli clinical isolate that is sensitive

18 KO) mice) and the traced lineages by using a CRE-dependent TdTomato reporter.

19 mapped a subnetwork of TFs associated with a CRE that may contribute to UPR management.

20 -specific viral injections of AAV-GFP or AAV-CRE in CREB(loxP/loxP) animals, behavioral testing measu

21 more post-LT dialysis sessions and acquired CRE before LT evolved with post-LT CRE infection.

22 ction, whereas 119 (30.8%) patients acquired CRE after LT.

23 hrough December 2015, 5265 patients acquired CRE in LTCFs.

24 Patients who acquired CRE before LT had a high risk of developing CRE infectio

25 ngle experiment, enabling comparisons across CREs within and between gene clusters.

26 tilizing different sets of co-factors across CREs, we hypothesize that global p53 activity is guarded

27 ely integrates information from co-activated CREs, similar cells, and publicly available regulome dat

28 Active CREs are imbedded in open chromatin that are accessible

29 A subset of active CREs and TREs physically interact with the Oct4 promoter

30 ysis reveals that a greater number of active CREs than active TREs are evolutionarily conserved betwe

31 es; specifically, a greater number of active CREs, compared with active TREs, physically interact wit

32 filing, based on the observation that active CREs produce ncRNAs.

33 Among all CRE-CRAB-CRPsA EPOC studies, the most frequent intervent

34 IC established a real-time repository of all CRE carriers and events of acquisition, supervised infor

35 PlantDHS provides a platform to predict all CREs associated with individual genes from three model p

36 operation under stop-flow mode, which allows CRE to passively diffuse across the AEM.

37 uced the number of new carriers by 11.7% and CRE prevalence by 7.6% over a 3-year period.

38 mase (ESBL)-producing Enterobacteriaceae and CRE carriage among solid organ transplant recipients to

39 brated to achieve realistic patient flow and CRE transmission and detection rates.

40 nd between FC levels (a fecal indictor), and CRE (r = 0.924; p = 0.005), blaNDM-1 (r = 0.934, p = 0.0

41 infection, targeted patient notification and CRE screening cultures were performed.

42 rity of the REs are functionally active, and CREs are more active than TREs in controlling Oct4 gene

43 The PDIs, TF networks, and CREs identified in our work are foundational resources f

44 ten implemented using a multimodal approach (CRE: 10/11; CRAB: 4/5; CRPsA: 3/3).

45 interrupted time series analyses, assessing CRE (n = 11; 65%), CRAB (n = 5; 29%) and CRPsA (n = 3; 1

46 Thus, multiple, causal, mutually associated CRE variants can underlie GWAS signals.

47 nd carbapenem-resistant Entero-bacteriaceae (CRE) bloodstream infections.

48 Through population-based CRE surveillance in the 8-county Atlanta (GA) metropolit

49 tifs and local sequence context on p53-bound CRE activity.

50 Our data indicate that p53-bound CREs are both positively and negatively affected by alte

51 tors and local sequences acting at p53-bound CREs are comparatively understudied.

52 Briefly, CRE diffuses through an anion-exchange membrane (AEM) fr

53 mids or crossed with tamoxifen inducible CAG-CRE-ER(T2) or nestin-CRE-ER(T2) mice.

54 er (TIGER) mouse was electroporated with CAG-CRE plasmids or crossed with tamoxifen inducible CAG-CRE

55 of a registry that tracked patients carrying CRE to help guide infection prevention and control.

56 ity against OXA-CRAB as well as SBL-carrying CRE pathogens.

57 We identified 13 causal CRE variants using allelic reporter activity, cardiomyoc

58 entified at least one high-confidence causal CRE variant for each of the five sentinel hits that coul

59 cting AAV8-DIO-hM(4)Di into the LHb and CAV2-CRE (a retrograde viral vector) into one of the three ta

60 Clinical CRE trend among adult inpatients showed stabilization fo

61 ating the intervention at the first clinical CRE detection in the LTACH, cumulative CRE transmissions

62 inery from a representative Escherichia coli CRE isolate as well as a fluorescent reporter gene to ea

63 quantify regulatory divergence, we compared CRE activity across species by testing differential ChIP

64 Conserved CRE function is associated with sequence conservation, p

65 Conversely, only 16% of conserved CREs overlap TEs.

66 We further demonstrate that conserved CREs bind master regulators, suggesting that while CREs

67 endent program of gene expression containing CRE binding sites, which includes activity-regulated gen

68 n patients with carbapenemase-producing (CP)-CRE compared with non-CP-CRE bacteremia.

69 CP-CRE isolates were more likely to have meropenem minimum

70 including 191 retrospective isolates (122 CP-CRE and 69 non-CP isolates) as well as 45 prospective cl

71 l as 45 prospective clinical isolates (15 CP-CRE and 30 non-CP-CRE) obtained over a 3-month period.

72 teremia during the study period: 37 (45%) CP-CRE and 46 (55%) non-CP-CRE.

73 ze cutoff that best discriminated between CP-CRE and members of the family Enterobacteriaceae that do

74 carbapenem-resistant Enterobacteriaceae (CP-CRE) is an important element of the effort to prevent an

75 4 days were more than 4 times greater for CP-CRE compared with non-CP-CRE bacteremic patients (adjust

76 typic and molecular methods available for CP-CRE detection.

77 period, including 15 CPE (33%) and 30 non-CP-CRE (67%).

78 that CP-CRE may be more virulent than non-CP-CRE and are associated with poorer outcomes.

79 mase-producing (CP)-CRE compared with non-CP-CRE bacteremia.

80 imes greater for CP-CRE compared with non-CP-CRE bacteremic patients (adjusted odds ratio, 4.92; 95%

81 n the CP-CRE group and 6 (13%) in the non-CP-CRE group.

82 rations (MICs) >/=16 microg/mL, while non-CP-CRE isolates were more likely to have meropenem MICs </=

83 ler class A, B, and D carbapenemases, non-CP-CRE isolates, and carbapenem-susceptible isolates were i

84 likely due to restricted inclusion of non-CP-CRE to assess the specificity of the assays.

85 e clinical isolates (15 CP-CRE and 30 non-CP-CRE) obtained over a 3-month period.

86 period: 37 (45%) CP-CRE and 46 (55%) non-CP-CRE.

87 Reliable detection of CP-CRE is the first step in combating this problem.

88 The majority of CP-CRE isolates were bla KPC (92%), followed by bla NDM (5%

89 Our findings suggest that CP-CRE may be more virulent than non-CP-CRE and are associa

90 within 14 days, including 12 (32%) in the CP-CRE group and 6 (13%) in the non-CP-CRE group.

91 for the analytical detection of creatinine (CRE) in undiluted human urine.

92 nical CRE detection in the LTACH, cumulative CRE transmissions over 5 years across all 10 facilities

93 ctivity of novel Nrl-dependent ncRNA-defined CREs in developing cones.

94 molecular mechanisms underlying TF-dependent CRE activity.

95 elationships among human- and animal-derived CRE were assessed using whole-genome sequencing-based mo

96 The point prevalence of newly detected CRE carriage in post-acute care hospitals decreased from

97 CRE before LT had a high risk of developing CRE infection (P < 0.001).

98 The impact of different CRE types and clinical variables on %Delta was evaluated

99 REs), yet functional analysis of gene-distal CREs such as enhancers remains challenging.

100 rther contributes to cerebral hypoxia during CRE.

101 g a critical cis-acting replication element (CRE) from the polyprotein coding region to the 3' non-co

102 protein (p-CREB), and cAMP response element (CRE)-Luc, or PDGF-induced cyclin D1 expression.

103 utilizing different cis-regulatory elements (CRE) within the TAD.

104 nteractions between cis-regulatory elements (CREs) and regulatory proteins.

105 code, that is, the cis-regulatory elements (CREs) and their combinations that regulate plant -Fe-res

106 H3K4me1) to profile cis-regulatory elements (CREs) and using RNA-seq to characterize gene expression

107 Cis-regulatory elements (CREs) are commonly recognized by correlative chromatin f

108 ndreds of synthetic cis-regulatory elements (CREs) comprised of combinations of binding sites for plu

109 ies of a variety of cis-regulatory elements (CREs) in ER stress-responsive gene promoters.

110 ities of individual cis-regulatory elements (CREs) in individual cells or rare cell subpopulations.

111 ify the location of cis regulatory elements (CREs) including promoters and enhancers.

112 cell type-specific cis-regulatory elements (CREs) is crucial for understanding development and disea

113 ighly enriched with cis-regulatory elements (CREs) linked to developmental processes, whereas BiP3 pr

114 quence variation in cis-regulatory elements (CREs) modulating a target gene's expression as the major

115 ription factors and cis-regulatory elements (CREs) orchestrates the dynamic and diverse genetic progr

116 gh rearrangement of cis-regulatory elements (CREs) remains unclear.

117 yet the presumptive cis-regulatory elements (CREs) that control color patterning remain unknown.

118 ed maps of putative cis-regulatory elements (CREs) using publicly available open chromatin data for t

119 e binding of p53 to cis-regulatory elements (CREs), which are non-coding segments of DNA that spatial

120 and the gene's own cis-regulatory elements (CREs), which remain unknown for most of the genes.

121 roximal and -distal cis-regulatory elements (CREs), yet functional analysis of gene-distal CREs such

122 omatin structure at cis-regulatory elements (CREs).

123 Cis-regulatory elements (CREs, e.g., promoters and enhancers) regulate gene expre

124 , which acts through cAMP response elements (CREs), suggesting that SM may also act to counteract DHX

125 waters, respectively, implying that elevated CRE and blaNDM-1 are of patient origin.

126 mpartment termed common recycling endosomes (CRE).

127 scuss carbapenem-resistant Enterobacterales (CRE) and carbapenem-resistant organisms (CROs).

128 ainst carbapenem-resistant Enterobacterales (CRE) carrying class A, C, and D SBLs; however, none of t

129 utive carbapenem-resistant Enterobacterales (CRE; 58 isolates) and non-glucose-fermenting GNB (50 iso

130 Carbapenem-resistant Enterobacteriaceae (CRE) are a serious public health threat.

131 Carbapenem-resistant Enterobacteriaceae (CRE) are among the most severe threats to the antibiotic

132 Carbapenem-resistant Enterobacteriaceae (CRE) are an urgent threat with potential for rapid sprea

133 Carbapenem-resistant Enterobacteriaceae (CRE) are associated with considerable mortality.

134 Carbapenem-resistant Enterobacteriaceae (CRE) are high-priority bacterial pathogens targeted for

135 Carbapenem-resistant Enterobacteriaceae (CRE) are multidrug-resistant pathogens for which new tre

136 of carbapenem-resistant Enterobacteriaceae (CRE) carriers.

137 ing carbapenem-resistant Enterobacteriaceae (CRE) clinical isolates, we reveal the underlying basis f

138 of carbapenem-resistant Enterobacteriaceae (CRE) has been increasing in Singapore.

139 of carbapenem-resistant Enterobacteriaceae (CRE) has risen substantially, and the study of CRE resis

140 of carbapenem-resistant Enterobacteriaceae (CRE) in both humans and animals poses a global threat to

141 of carbapenem-resistant Enterobacteriaceae (CRE) in healthcare facilities, contributing to rapid reg

142 of carbapenem-resistant Enterobacteriaceae (CRE) in sentinel US hospitals.

143 in carbapenem-resistant Enterobacteriaceae (CRE) infections has created a global health emergency, u

144 ith carbapenem-resistant Enterobacteriaceae (CRE) infections were treated with meropenem-vaborbactam.

145 mia carbapenem-resistant Enterobacteriaceae (CRE) infections.

146 Carbapenem-resistant Enterobacteriaceae (CRE) is an emergent microorganism of infections after li

147 by carbapenem-resistant Enterobacteriaceae (CRE) is crucial for proper treatment and infection contr

148 of carbapenem-resistant Enterobacteriaceae (CRE) isolates were evaluated, including 191 retrospectiv

149 Carbapenem-resistant Enterobacteriaceae (CRE) spread regionally throughout healthcare facilities

150 and carbapenem-resistant Enterobacteriaceae (CRE) using nares, skin (axilla/groin), and peri-rectal s

151 Carbapenem-resistant Enterobacteriaceae (CRE), Acinetobacter baumannii (CRAB), and Pseudomonas ae

152 C), carbapenem-resistant Enterobacteriaceae (CRE), blaNDM-1, and selected extended-spectrum beta-lact

153 to carbapenem-resistant Enterobacteriaceae (CRE), leading to higher rates of clinical cure, decrease

154 ven carbapenem-resistant Enterobacteriaceae (CRE)-infected patients were treated with ceftazidime-avi

155 ing carbapenem-resistant Enterobacteriaceae (CRE).

156 and carbapenem-resistant Enterobacteriaceae (CRE).

157 rly carbapenem-resistant Enterobacteriaceae (CREs), present a major and growing threat to human healt

158 Carbapenem-resistant Enterobacteriacieae (CRE) isolates were evaluated with polymerase chain react

159 to a second reservoir, containing the enzyme CRE deiminase.

160 id not detect a change in the rates of ESBL, CRE and MDR Pseudomonas aeruginosa following ASP.

161 ifferent types of cardio-respiratory events (CRE) in preterm infants during postnatal transition, as

162 , also defined as cardio-respiratory events (CRE), in preterm neonates during postnatal transition.

163 Newly evolved CREs are enriched in immune response and neurodevelopmen

164 Newly evolved CREs are enriched in young transposable elements (TEs),

165 actors, relatively few studies have examined CRE pathogens through changes in gene expression.

166 Amelx-iCre mice displayed exclusive CRE-mediated recombination in incisor and molar amelobla

167 Some regions have experienced CRE outbreaks that were likely amplified by frequent tra

168 transfer network; other factors may explain CRE patient movement in these facilities.

169 Here, we determine how two extragenic CREs that are prominent in epithelial cells in the lung,

170 Surveillance cultures for CRE were collected immediately before LT and weekly ther

171 itive clinical and surveillance cultures for CRE were estimated based on mandatory data submitted to

172 is study was to analyze the risk factors for CRE acquisition and infection after LT.

173 Other risk factors for CRE infection were acquisition of CRE post-LT, Model for

174 acetate, ethyl isovalerate and guaiacol for CRE.

175 me, the presented analytical methodology for CRE detection is translated into an all-solid-state plat

176 LT, 68 (17.6%) patients tested positive for CRE, 11 (16.2%) of those patients having CRE infection,

177 , the CRE sensor appears to be promising for CRE analysis in both urine and blood.

178 ee region, including active surveillance for CRE carriers and enhanced isolation of identified carrie

179 t Carba-R assay make it a potential tool for CRE detection and identification directly in sputum spec

180 ive approaches for rapid phenotypic ASTs for CREs are urgently needed.

181 e-associated variants are often enriched for CREs in the tissues and cells that pertain to a given di

182 rter screens in cardiomyocyte cell lines for CREs overlapping nearly all common variants associated w

183 r-related gene overexpression resulting from CRE reorganization (e.g., enhancer hijacking) by integra

184 for CRE, 11 (16.2%) of those patients having CRE infection, whereas 119 (30.8%) patients acquired CRE

185 We noted 6 SNFs with high CRE-derived betweenness but low Medicare-derived between

186 Higher CRE rates were observed among facilities with greater pa

187 pted a chemogenetic approach using a 5-HT2CR(CRE) line to clarify the function of subset of 5-HT2C re

188 g of CRTC1 to the transcriptional complex in CRE/TATA-containing promoters to engage activity-depende

189 rvention resulted in a sustained decrease in CRE incidence and prevalence in LTCFs.

190 and bolA potentiated carbapenem efficacy in CRE E. coli, whereas inhibition of the genes flhC and yg

191 own to be affected by pathogenic variants in CREs, to establish a roadmap for characterizing regulato

192 During 2016, 283 incident CRE cases with concurrent or prior year facility stays w

193 nd other Gram-negative infections, including CREs, in the presence of numerous common resistance dete

194 racy for estimating activities of individual CREs.

195 ing transcription factor-1, and CREB-induced CRE modulator proteins in kidney nuclear preparations.

196 achieved by delivery of ligand cross-linked CRE protein to the skin of transgenic reporter mice, but

197 lineage, with 63% of the tested human liver CREs showing similar activity across species.

198 ialysis was the only risk factor for post-LT CRE acquisition.

199 Post-LT CRE infection was identified in 59 (15.7%) Klebsiella pn

200 acquired CRE before LT evolved with post-LT CRE infection.

201 deletion of hepcidin in myeloid cells (LysM(CRE/+)/ Hamp(f/f)) improved cardiac function.

202 n a linear range of response from 1 to 50 mM CRE concentration.

203 ere were 83 unique episodes of monomicrobial CRE bacteremia during the study period: 37 (45%) CP-CRE

204 tamoxifen inducible CAG-CRE-ER(T2) or nestin-CRE-ER(T2) mice.

205 rnered large reductions in the number of new CRE carriers.

206 rovided the most benefits for preventing new CRE carriers, if this is not feasible, it may be worthwh

207 The new CRE biosensor exhibits a Nernstian slope, within a linea

208 ble predictors of mortality in nonbacteremia CRE infections.

209 enerating Slc26a9(P2ACre) mice, and observed CRE activity throughout the otic epithelium and neurons,

210 n urgent need of new antibiotics, and 55% of CRE isolates from larger hospitals carried at least one

211 t antibiotics were distinct, and over 88% of CRE isolates exhibited heteroresistance to multiple anti

212 actors for CRE infection were acquisition of CRE post-LT, Model for End-Stage Liver Disease score gre

213 fers strongly correlated with betweenness of CRE case-transfer data in ACHs (r = 0.75; P < .01) and L

214 rea hospitals, together with a collection of CRE from a single California hospital, to define the fre

215 rders of magnitude greater concentrations of CRE bacteria and blaNDM-1 than local sewers (depending o

216 cidence was determined based on detection of CRE, either during LTFC stay or on admission to another

217 tributing to rapid regional dissemination of CRE.

218 the prevalence, risk factors, and drivers of CRE transmission between humans and their backyard anima

219 d the clinical and molecular epidemiology of CRE among adult inpatients in Singapore.

220 In this article, we discuss the evolution of CRE, with a focus on the epidemiology of the CPE pandemi

221 enomatous polyposis coli) upon expression of CRE recombinase in the liver and monitored their effects

222 uring transition, the haemodynamic impact of CRE is influenced not only by the event type, but also b

223 Incidence of CRE clinical cultures among adult inpatients plateaued f

224 ur framework enables systematic inference of CRE rearrangements mediating dysregulation in cancer.

225 interchangeable with regard to management of CRE infections, and clinicians need to be aware of their

226 ineating underlying resistance mechanisms of CRE to direct antibiotic treatment decisions.

227 est isolates of the 3 causative pathogens of CRE infections using ceftriaxone (CRO), ertapenem (ETP),

228 eillance unit, we assessed the prevalence of CRE at the household level and examined the factors asso

229 tact precautions increased the prevalence of CRE from 0% to 8.0% countywide over 10 years.

230 mpact of detecting increasing proportions of CRE carriers.

231 nt between facilities to model the spread of CRE within a region.

232 proportions of carriers has on the spread of CRE.

233 E) has risen substantially, and the study of CRE resistance mechanisms has become increasingly import

234 However, the transmission of CRE between humans and animals has not yet been well stu

235 ng asymptomatic carriage and transmission of CRE.

236 olecular composition of the vast majority of CREs in chromatin remains unknown.

237 To better understand the role of CREs in neuropsychiatric disorders we applied the Assay

238 revention and control (IPC) interventions on CRE-CRAB-CRPsA in inpatient healthcare facilities to inf

239 Pan-otic CRE drivers enable gene regulation throughout the otic p

240 des a useful complement to existing pan-otic CRE drivers, particularly for postnatal analyses.

241 Furthermore, extant pan-otic CREs recombine in auditory and vestibular brain nuclei,

242 analogous mice generated with other pan-otic CREs, these were viable.

243 iling to identify rod and cone photoreceptor CREs from wild-type and mutant mouse retinas, defined by

244 y LTACH-focused intervention in a previously CRE-free region, including active surveillance for CRE c

245 associated with non-carbapenemase-producing CRE (NCPE) (n = 88) compared with CPE (n = 161) subjects

246 ty, whereas recruitment of CRTC1 to proximal CRE/TATA promoters depends on neuronal activity.

247 ent genes containing promoters with proximal CRE/TATA sequences, such as c-fos, Dusp1, Nr4a1, Nr4a2 a

248 Nr4a2 and Ptgs2, but not genes with proximal CRE/TATA-less promoters (e.g. Nr4a3, Presenilin-1 and Pr

249 clustering, we identified over 100 putative CREs (pCREs) that predicted -Fe-induced gene expression

250 We aggregate variants within these putative CREs within 50 Kb of the start or end of 'expressed' gen

251 ely drug-resistant organism registry reduced CRE spread, even when only 25% of the largest Illinois f

252 lly a highly efficient strategy for reducing CRE transmissions across an entire region, particularly

253 an essential public health tool in reducing CRE in healthcare facilities.

254 f transcription factors in order to regulate CRE activity.

255 LKB1 from ISCs in mice using Lgr5-regulated CRE-ERT2 (Lkb1(Lgr5-KO) mice) and the traced lineages by

256 promoters were enriched with stress related CREs.

257 ajor role of the carbon catabolite repressor CRE-1 in regulating the expression of major facilitator

258 ments within the ~12-kb cis-region (cis-REs; CREs) of the Oct4 gene locus, as well as genome-wide 2,6

259 Vinagre de Condado de Huelva Reserva (CRE) showed a stronger percentage of 'chemical' impact o

260 nsive element 1), a known grass -Fe response CRE.

261 rivative defective in sequence-specific RNAP-CRE interactions.

262 We prospectively sampled CRE from hospitalized patients from three Boston-area ho

263 tosis, which can be rescued by cell-specific CRE-mediated expression of wild-type FUS within motor ne

264 interactions distinguish cell type-specific CRE activity.

265 housands of candidate rod- and cone-specific CREs, and identified motifs for rod- and cone-specific T

266 We hypothesized that context-specific CREs could be identified by context-specific non-coding

267 for the identification of cell type-specific CREs and the discovery of molecular mechanisms underlyin

268 Targeted CRE-mediated recombination was achieved by delivery of l

269 ore work is necessary in this direction, the CRE sensor appears to be promising for CRE analysis in b

270 with marginal overlap between strains in the CRE and CSE clades.

271 se time (15-60 min) primarily depends on the CRE diffusion across the AEM.

272 These data reveal that the CRE architecture of BiP promoters potentially define the

273 e identified a subset of SNFs central to the CRE transfer network but not the Medicare transfer netwo

274 ra-otic gene-of-interest expression with the CRE lineage can compromise viability and impede auditory

275 There, CRE reacts with the enzyme, and the formation of ammoniu

276 unique contributions to regulation by these CREs.

277 e frequency and linear distribution of these CREs produced two phylogenetic branches that further res

278 (72%) of the variance in expression of these CREs.

279 e use CRISPR/Cas9 technology to remove these CREs from the endogenous locus in human bronchial epithe

280 We showed earlier that these CREs, located at -44 and -35 kb upstream of the promoter

281 on of CFTR, likely through occupancy at this CRE and the gene promoter.

282 ated from 2016 Medicare data and compared to CRE-transfer derived centrality metrics by Spearman corr

283 mechanism that involves CRTC1 recruitment to CRE promoters.

284 ent of cerebral oxygen status in response to CRE, whereas the brain-sparing remodelling of the fetal

285 tional period, the haemodynamic responses to CRE are influenced by the event type and by specific neo

286 r strategies to prevent, diagnose, and treat CRE infections in LMICs.

287 bial culturing found 18 to 41% of wastewater CRE isolates (n = 1447) were on the WHO "critical pathog

288 For example, it is unknown what CREs underlie the zebrafish mpp5b(ponli) (ponli) and cru

289 Trends held when CRE was already present in the region.

290 We sought to determine whether CRE resistance mechanism determination is prognostically

291 ying a conditional Braf(CAT) allele in which CRE-mediated recombination leads to co-expression of BRA

292 ind master regulators, suggesting that while CREs contribute to species adaptation to the environment

293 with CSE bloodstream infection and 123 with CRE bloodstream infection.

294 vel and examined the factors associated with CRE carriage through a detailed questionnaire.

295 d 35% (43 of 123 patients) for patients with CRE bloodstream infection.

296 In a cohort of 475 patients with CRE infections, a PBS >=4 was associated with mortality

297 egulate gene expression, and variants within CREs can modulate disease risk.

298 Genetic variation within CREs plays a central role in phenotypic variation in com

299 Wnt4-CRE-driven megalin/LRP2 ablation in cystinotic mice effi

300 s achieved by a Cre-LoxP strategy using Wnt4-CRE.