ライフサイエンスコーパス: CRE

1 CRE exposure during viral infection in early life induce

2 CRE for this study were identified by evaluating the ant

3 CRE identification results were available in 18 h compar

4 CRE-positive adult inpatients were prospectively recruit

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

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

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

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

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

10 Among 599 CRE cases in 481 individuals, 520 (86.8%; 95% CI, 84.1%-

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

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

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

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

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

16 molecular assays to more rapidly administer CRE-active therapy and the development of new antimicrob

17 ed empirical regimens are not active against CRE.

18 w antimicrobial agents with activity against CRE.

19 f databases that allow investigation for all CREs.

20 DHSs are indicative of all CREs, including promoters, enhancers, silencers, insulat

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

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

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

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

25 Mutagenesis of the NFAT and CRE binding sites, respectively, inhibited the effects o

26 ly source, targeted patient notification and CRE screening cultures were performed.

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

28 The overall annual CRE incidence rate per 100<000 population was 2.93 (95%

29 hout increased infection control approaches, CRE would become endemic in nearly all Orange County hea

30 seasonal and regional variability in Arctic CRE of order 10 W m(-2).

31 le-stranded sequences when proteins, such as CRE-binding protein, are bound to an adjacent cis-regula

32 onse element (CRE) site and a novel -248 ATF/CRE modifier (ACM) element.

33 e also examined the ability of the CHAC1 ATF/CRE and ACM sequences to bind ATF4 and ATF3 using immuno

34 lation through its binding to a putative ATF/CRE composite site within the PCK2 promoter functioning

35 n CHAC1 promoter in the proximity of the ATF/CRE and ACM using ChIP.

36 Population-based CRE incidence, site-specific standardized incidence rati

37 ely terminate in the canonical UU donated by CRE(2C)-mediated uridylylation of VPg, we hypothesized t

38 urther investigated the expression driven by CREs comprised of homotypic chains of KLF4 binding sites

39 n setting the levels of expression driven by CREs in ES cells.

40 ture technology to instead capture candidate CREs, thereby tiling across the targeted regions and mar

41 In response to immunization, Emu(CycD1)CD19(CRE)Bim(fl/fl) mice manifested selective expansion of th

42 Clinical CRE trend among adult inpatients showed stabilization fo

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

44 urrent antimicrobial armamentarium to combat CRE is extremely limited, a multifaceted approach that i

45 We combined CRE case information from the Illinois extensively drug-

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

47 at correlated with the presence of consensus CRE sequences in the TSS region.

48 Conserved CRE function is associated with sequence conservation, p

49 CREBH binds to the evolutionally conserved CRE-BP binding elements located in the enhancer region o

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

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

52 jection with unmodified or lesion-containing CRE, but not scrambled CRE or scrambled CRE with a G/U m

53 ompletely prevented access to G/U-containing CRE by UNG2 and, therefore, to base excision repair, whe

54 we show how temperature and humidity control CRE through competing influences between the mid- and fa

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

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

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

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

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

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

61 carbapenem-resistant Enterobacteriaceae (CP-CRE) are a significant clinical and public health concer

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

63 4 days were more than 4 times greater for CP-CRE compared with non-CP-CRE bacteremic patients (adjust

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Using the same 16 mutations in the CVB3 CRE(2C) structure that were considered lethal for this v

81 EB1 and DNA glycosylases compete for damaged CRE in vitro and in vivo, thus blocking DNA repair and r

82 poration and AAV viral vectors, we delivered CRE-DOG to multiple GFP mouse lines, which led to effect

83 ients (97.2%), while the CDC method detected CRE in 56 of 72 (77.8%).

84 SOT) recipients in CRE-endemic areas develop CRE infection, and the infection site correlates with th

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

86 ecially valuable in the detection of distant CREs that are located away from promoters.

87 The infrared cloud radiative effect (CRE) at the surface is modulated by cloud properties; ho

88 The net cloud radiative effects (CREs) over Antarctica are increased by +7.4 Wm(-2), and

89 e pairs (bp) of a RHOcis-regulatory element (CRE) and demonstrate Rho specific transcriptional silenc

90 irus functions as a cis-replicating element (CRE).

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

92 A cis-acting replication element (CRE) in the 2C protein-coding region [CRE(2C)] templates

93 (CREB) to a conserved cAMP response element (CRE) contiguous with the NFAT binding site in the FGF-23

94 ation mediated by the cAMP response element (CRE) in reporter gene studies (10-fold vs. control; n =

95 ression: the -267 ATF/cAMP response element (CRE) site and a novel -248 ATF/CRE modifier (ACM) elemen

96 ein 1 (PCBP1) recognized the C-rich element (CRE) in the 3' UTR of sortilin mRNA, and depletion of PC

97 cription bubble ("core recognition element," CRE).

98 oters and other cis-regulatory DNA elements (CREs).

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

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

101 equence variants in cis-regulatory elements (CREs) are suspected etiological causes of complex disord

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

103 ors (TFs) to cis-acting regulatory elements (CREs) in DNA play crucial roles in directing gene expres

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

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

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

107 nctionally distinct cis-regulatory elements (CREs).

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

109 ion is regulated by cis-regulatory elements (CREs, i.e., enhancers, promoters, and silencers) and the

110 [RARE], cyclic AMP [cAMP] response elements [CRE], NF-kappaB binding sites [kB], serum response eleme

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

112 mpartment termed common recycling endosomes (CRE).

113 differentiation operate through the enhancer CRE-kB-RARE core in strengthening induction of HCMV MIE

114 Carbapenem-resistant Enterobacteriaceae (CRE) are a concern for health care in the United States

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

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

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

118 Carbapenem-resistant Enterobacteriaceae (CRE) are emerging global pathogens.

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

120 Carbapenem-resistant Enterobacteriaceae (CRE) are increasingly reported worldwide as a cause of i

121 ing carbapenem-resistant Enterobacteriaceae (CRE) breakpoints might have resulted in 1,821 additional

122 ing carbapenem-resistant Enterobacteriaceae (CRE) can be difficult.

123 of carbapenem-resistant Enterobacteriaceae (CRE) from 300 rectal swab specimens obtained from patien

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

125 ong carbapenem-resistant Enterobacteriaceae (CRE) has infrequently been reported in the United States

126 Carbapenem-resistant Enterobacteriaceae (CRE) have spread globally and represent a serious and gr

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

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

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

130 Carbapenem-resistant Enterobacteriaceae (CRE) producing the New Delhi metallo-beta-lactamase (NDM

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

132 Carbapenem-resistant Enterobacteriaceae (CRE), a group of pathogens resistant to most antibiotics

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

134 ii, carbapenem-resistant Enterobacteriaceae (CRE), extended-spectrum beta-lactamase (ESBL)-producing

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

136 ing carbapenem-resistant Enterobacteriaceae (CRE).

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

138 Newly evolved CREs are enriched in immune response and neurodevelopmen

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

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

141 ) and exposed to low-dose cockroach extract (CRE) in early and later life, and airway inflammation, r

142 hospitals (LTACHs) predicted higher facility CRE rates.

143 d from bone marrow of Nes-GFP mice following CRE challenge.

144 OGG1 and CREB1 reversibly competed for CRE containing an degrees G/C pair.

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

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

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

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

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

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

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

152 migration induced by conditioned medium from CRE-challenged human epithelium in air/liquid interface

153 fR recycles to the basolateral membrane from CRE, Megalin, like pIgR, traffics to subapical Rab11-pos

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

155 Furthermore, CRE-DOG enabled optogenetic control of these neurons.

156 ipulation, Cre recombinase dependent on GFP (CRE-DOG), a split component system that uses GFP and its

157 Of the 300 patients, 72 (24%) harbored CRE and were PCR positive for KPC enzymes.

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

159 Higher CRE rates were observed among facilities with greater pa

160 statewide patient-sharing network had higher CRE burden.

161 ients with LTACHs was associated with higher CRE rates, but this association may have been due to cha

162 e is modulated by cloud properties; however, CRE also depends on humidity because clouds emit at wave

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

164 At constant relative humidity, CRE does not decrease with increasing temperature/absolu

165 that could have been avoided by identifying CRE and initiating contact precautions.

166 ories delineating procedures for identifying CRE and carbapenemase production.

167 tedly high rates of resistance to CAZ-AVI in CRE bloodstream isolates at our institution associated w

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

169 (unit of degree) conferred a 6% increase in CRE rate in rural facilities (relative risk [RR] = 1.056

170 d constant, we calculate recent increases in CRE of 1-5 W m(-2) in autumn and winter, which are proje

171 y purification (TRAP) of mRNA populations in CRE-expressing cells.

172 and carbapenemase-encoding genes present in CRE isolated from patients at a Californian tertiary hea

173 f solid organ transplant (SOT) recipients in CRE-endemic areas develop CRE infection, and the infecti

174 ntrations similar to those found to increase CRE-mediated gene expression in hippocampal neurons.

175 have the potential to add to the increasing CRE burden.

176 show that two other functionally independent CRE variants, one binding Gata2 and the other binding Ra

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

178 and found that MSCs significantly inhibited CRE-induced inflammatory cytokine secretion (IL-4, IL-13

179 discharge dataset to predict facility-level CRE rates, adjusting for hospital size and geographic ch

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

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

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

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

184 Many CREs contained functional (i.e., activating or silencing

185 We incubated 39-mer CRE-containing double-stranded oligonucleotides with rec

186 investigated the role of MSCs in modulating CRE-induced T cell response and found that MSCs signific

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

188 Most CRE cases were isolated from a urine source, and were as

189 While the wt genome with the mutated CRE(2C) displays suppressed replication levels similar t

190 parental CVB3 strain containing the mutated CRE(2C) drives the de novo generation of genomic deletio

191 However, only the G/U mispair in native CRE resulted in substantial developmental abnormalities,

192 ying these mutations with a nonuridylylating CRE(2C) are viable.

193 During the intervention, nosocomial CRE acquisition in acute care declined from a monthly hi

194 ensitivity tests confirm that Southern Ocean CREs are strongly sensitive to mixed-phase clouds colder

195 encoding gene was found in 81.7% (94/115) of CRE and included bla(KPC) (78.3%), bla(NDM-1) (0.9%), an

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

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

198 Cases of CRE were defined as carbapenem-nonsusceptible (excluding

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

200 idence that the presence of a combination of CRE variants synergistically reduces RET expression and

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

202 a research-use-only PCR for the detection of CRE in rectal surveillance specimens.

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

204 Assessment of the US epidemiology of CRE is needed to inform national prevention efforts.

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

206 Incidence of CRE clinical cultures among adult inpatients plateaued f

207 illance system in 7 states, the incidence of CRE was 2.93 per 100<000 population.

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

209 n serum and p-Smad2/3 expression in lungs of CRE-treated mice.

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

211 ikely identifies hospitals at higher risk of CRE exposure, enabling focused clinical and public healt

212 ) was identified in more than one species of CRE cultured from the same patient in four cases.

213 ions (2011-2012), we simulated the spread of CRE throughout Orange County health-care facilities unde

214 The spread of CRE to transplant recipients and patients with hematolog

215 lkit would not completely stop the spread of CRE, it would cut its spread substantially, by half.

216 cked or neutralized, whereas substitution of CRE with exogenous IL-33 recapitulated the phenotype obs

217 and laboratory-based active surveillance of CRE conducted among individuals living in 1 of 7 US metr

218 ng asymptomatic carriage and transmission of CRE.

219 ification and functional characterization of CREs and associated epigenetic modulation.

220 egions and markedly increasing the length of CREs that can be readily assayed.

221 f genomic data that predict the locations of CREs, but a bottleneck lies in functionally interpreting

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

223 n mutation analysis for multiplex parsing of CREs.

224 allel functional analysis of a wide range of CREs in any organ or species that can be infected by AAV

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

226 Centrality had a greater effect on CRE rates in rural counties, which do not have LTACHs.

227 This strategy relies on CRE recombinase-dependent activation of an EGFP-tagged L

228 PVM infection or CRE exposure alone did not induce disease, whereas PVM/C

229 By comparing our CRE-seq results to a comprehensive set of genome annotat

230 and active surveillance is needed to prevent CRE infections in immunocompromised hosts.

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

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

233 Previous NDM-producing CRE clusters have been attributed to person-to-person tr

234 en exposure and acquisition of NDM-producing CRE; results of environmental cultures and organism typi

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

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

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

238 e created PV-M1 knockout mice by crossing PV-CRE and floxed M1 mice.

239 HC PV cells, visualized by crossing PV-CRE mice with Rosa26YFP mice, were anatomically identifi

240 recapitulated the phenotype observed in PVM/CRE-coexposed mice.

241 re alone did not induce disease, whereas PVM/CRE coexposure acted synergistically to induce the hallm

242 oved and mHtt expression was terminated (Q97(CRE)).

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

244 ement (CRE) in the 2C protein-coding region [CRE(2C)] templates the addition of two uridine residues

245 Our findings establish RNAP-CRE interactions are a functional determinant of TSS sel

246 ile of the RNAP derivative defective in RNAP-CRE interactions differed from that of WT RNAP, in a man

247 ng, 5' mNET-seq, we assessed effects of RNAP-CRE interactions at natural promoters in Escherichia col

248 readout, MASTER, we assessed effects of RNAP-CRE interactions on TSS selection in vitro and in vivo f

249 investigated whether sequence-specific RNAP-CRE interactions affect TSS selection.

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

251 nscriptional pausing and establish that RNAP-CRE interactions modulate pausing.

252 We propose that RNAP-CRE interactions modulate the position of the downstream

253 and we identified 39 promoters at which RNAP-CRE interactions determine TSS selection.

254 Centers for Disease Control and Prevention's CRE toolkit would not completely stop the spread of CRE,

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

256 or lesion-containing CRE, but not scrambled CRE or scrambled CRE with a G/U mispair, resulted in inc

257 ning CRE, but not scrambled CRE or scrambled CRE with a G/U mispair, resulted in increased embryo dea

258 g the CREB1 binding site consensus sequence (CRE) sequence (TGACGTCA).

259 performed cis-regulatory element sequencing (CRE-seq).

260 ve been largely restricted to assaying short CREs in a limited repertoire of cultured cell types.

261 VSCMs before (Apoe(-/-)Akt1(fl/fl)Sm22alpha(CRE)) and after (Apoe(-/-)Akt1(fl/fl)SM-MHC-CreER(T2E))

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

263 ning this mouse line with cell type-specific CRE-driver lines, we identified distinct cellular respon

264 We compared the Remel Spectra CRE agar plate to CDC standard methodology for the isola

265 Remel Spectra CRE agar plates can provide useful means for a fast and

266 The Remel Spectra CRE plates detected KPC-type CRE in isolates from 70 of

267 In 23% (5/22) of clinical successes, CRE infections recurred within 90 days.

268 P promoter deletion constructs revealed that CRE-like and G-box sequences in the region between -170

269 The CRE standardized incidence ratio was significantly highe

270 tertypic and intratypic recombination in the CRE-REP assay and using a range of polymerase variants i

271 in (CREB) and was eliminated by mutating the CRE-binding site on the COX-2 promoter.

272 bserved in a CVB3-TD strain, mutation of the CRE(2C) function in a CVB3-TD strain does not further de

273 duced the FSK-induced phosphorylation of the CRE-binding protein (CREB) measured on Western blots (co

274 We found that the CRE and kB combination sets the preinduction enhancer to

275 ifferentiated NTera2, we also found that the CRE-kB combination functions as initiator and amplifier

276 transactivates Etv2 gene expression via the CRE motif.

277 system due to the poor replication of these CRE-deficient viruses.

278 unique contributions to regulation by these CREs.

279 (72%) of the variance in expression of these CREs.

280 Integrity of this CRE, designated SL9266 (alternatively 5BSL3.2), is criti

281 n was unaffected by UNG2 when CREB1 bound to CRE, but was greatly reduced by prior UNG2 exposure.

282 mechanism that involves CRTC1 recruitment to CRE promoters.

283 t and reliable method for detecting KPC-type CRE and for accelerated institution of appropriate infec

284 e Remel Spectra CRE plates detected KPC-type CRE in isolates from 70 of 72 patients (97.2%), while th

285 le CVB can replicate without a uridylylating CRE(2C), the replication rate suffers significantly.

286 pothesized that a functional (uridylylating) CRE(2C) would be unnecessary for CVB-TD replication.

287 f canonical NF-kappaB in the epidermis using CRE-mediated deletion of p65 and c-Rel in keratinocytes.

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

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

290 These features were ameliorated when CRE-induced IL-33 release was blocked or neutralized, wh

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

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

293 f 91 cases (27.5%; 95% CI, 18.1%-36.8%) with CRE isolated from normally sterile sites.

294 apical recycling pathway of epithelia, with CRE as its apical sorting station.

295 A separate cohort was injected with CRE-dependent AAV vectors expressing diphtheria toxin (D

296 injected in FC (prelimbic/precingulate) with CRE-dependent adeno-associated viral (AAV) vector encodi

297 factor I (NFI), SOX, and FOX families, with CREs often densely bound by several of these different T

298 The CpG islet within CRE was modified to contain a G/U or 8-oxoG ( degrees G)

299 DNA lesions within CRE modulate CREB1 binding negatively and positively.

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