ライフサイエンスコーパス: beta-lactam

1 antibiotics that inhibit PG synthases (e.g., beta-lactams).

2 actamases, thereby restoring activity of the beta-lactam.

3 h are able to hydrolyze nearly all available beta-lactams.

4 s with delayed hypersensitivity reactions to beta-lactams.

5 adjuvants that preserve the efficacy of the beta-lactams.

6 quickly quantify the pathogen's response to beta-lactams.

7 ly treated with ertapenem or antipseudomonal beta-lactams.

8 er implicated in the Staudinger synthesis of beta-lactams.

9 t can be targeted by antibiotics such as the beta-lactams.

10 one of the highly effective antibacterials, beta-lactams.

11 rturbed evolved prior to the clinical use of beta-lactams.

12 BPs as enzymes and not merely the targets of beta-lactam acylation.

13 ctane (DBO) scaffold restore the activity of beta-lactams against pathogenic bacteria, including thos

14 Initial beta-lactam agent administered as either IV push or IV p

15 US population has reported allergies to the beta-lactam agent penicillin, with higher rates reported

16 Like other beta-lactam agents, the principal bactericidal activity

17 ce are widespread, and algorithms to clarify beta-lactam allergy and optimize antibiotic use were des

18 ic assessment tool in patients with reported beta-lactam allergy resulted in a pronounced and sustain

19 beta-lactam allergy skin testing (BLAST) is recommended

20 A beta-lactam allergy was the second most common reason.

21 valuation of patients reporting a penicillin/beta-lactam allergy.

22 resistant to multiple antibiotics, including beta-lactams, aminoglycosides, fluoroquinolones, and pol

23 t the generality of our approach, we use the beta-lactam ampicillin to predict target molecule occupa

24 gradation of three representative classes of beta-lactams (ampicillin, cefotaxime, and meropenem) and

25 The effect of the N-ligand as well as beta-lactam and aldehyde structures on the yield and ste

26 th amoxicillin or amoxicillin/clavulanate, a beta-lactam and beta-lactamase inhibitor, respectively.

27 mecA provides a widespread advantage across beta-lactam and non beta-lactam antibiotics, non-antibio

28 de beta-lactamase allows for reassessment of beta-lactams and beta-lactamases role in humans.

29 rompting us to investigate synergism between beta-lactams and DCS.

30 nB substrates will suffer from the fact that beta-lactams and fluoroquinolones coselect resistance to

31 d inhibition of MBLs by beta-lactams and non-beta-lactams and illustrate the utility of PrOF NMR for

32 for the mechanisms and inhibition of MBLs by beta-lactams and non-beta-lactams and illustrate the uti

33 has increased accessibility upon exposure to beta-lactams and that a judiciously chosen surfactant pe

34 The role of other broad-spectrum beta-lactams and the likelihood of ampC induction by oth

35 fied beta-lactamases and the potentiation of beta-lactam antibacterial activity, indicating that DBO

36 Patients with reported beta lactam antibiotic allergies (BLA) are more likely t

37 orted BLA was associated with greater use of beta lactam antibiotic alternatives.

38 ity can be co-regulated with production of a beta-lactam antibiotic (carbapenem carboxylate) and a li

39 Bacteria are known to evade beta-lactam antibiotic action by producing beta-lactamas

40 Patients with reported beta-lactam antibiotic allergies (BLAs) are more likely

41 orted BLA was associated with greater use of beta-lactam antibiotic alternatives.

42 ions reveals weak binding events between the beta-lactam antibiotic ampicillin and the porin PorB fro

43 itional antienterococcal antibiotic and/or a beta-lactam antibiotic at any time during treatment were

44 The beta-lactam antibiotic ceftazidime is one of the handful

45 We hypothesized that subtherapeutic beta-lactam antibiotic exposure, determined by the pharm

46 determine therapeutic versus subtherapeutic beta-lactam antibiotic exposure.

47 These inhibitors compete with the beta-lactam antibiotic for the same binding site on the

48 romising agent for use in combination with a beta-lactam antibiotic for the treatment of a wide range

49 Combining standard therapy with a beta-lactam antibiotic has been associated with reduced

50 g in opening of the active site, whereby the beta-lactam antibiotic now is enabled to bind to the act

51 a membrane-bound protein marker that confers beta-lactam antibiotic resistance.

52 Metampicillin is a beta-lactam antibiotic that is prepared by the reaction

53 l resistance (AMR) facilitated by widespread beta-lactam antibiotic use.

54 l disturbance, severe neutropenia, and prior beta-lactam antibiotic use.

55 from sepsis diagnosis to administration of a beta-lactam antibiotic was 48 minutes (19-96 min) versus

56 two antibacterials, namely, cefadroxil (CFD, beta-lactam antibiotic) and doxycycline (DXC, tetracycli

57 P. carotovorum ATCC39048 produces the beta-lactam antibiotic, 1-carbapen-2-em-3-carboxylic aci

58 ity in the nanomolar range for ampicillin, a beta-lactam antibiotic, used as biorecognition elements

59 imitation, a high-quality genome sequence of beta-lactam antibiotic-producing Streptomyces clavuliger

60 m September to November 2017 and 2) received beta-lactam antibiotic.

61 ing antibiotic resistance upon exposure to a beta-lactam antibiotic.

62 (AKI) compared with vancomycin plus 1 other beta-lactam antibiotic.

63 beta-lactam antibiotics act on bacterial cell walls and

64 e penicillin-based sulfones 1-7 to repurpose beta-lactam antibiotics activity with bacterial species

65 of these are able to rescue the activity of beta-lactam antibiotics against carbapenem-resistant Aci

66 emonstrated that 20 restored the activity of beta-lactam antibiotics against carbapenem-resistant Pse

67 of several important drug classes, including beta-lactam antibiotics and antiviral and antineoplastic

68 heriae resistant to penicillin and all other beta-lactam antibiotics and describe a novel mechanism o

69 fely facilitate more rapid administration of beta-lactam antibiotics and may allow for better complia

70 We found that critical frontline beta-lactam antibiotics antagonize fluconazole activity.

71 beta-Lactam antibiotics are among the safest and most ef

72 beta-lactam antibiotics are associated with a variety of

73 Intravenous beta-lactam antibiotics are considered to confer a high

74 PBP2a effectively discriminates against the beta-lactam antibiotics as potential inhibitors, and in

75 sepsis diagnosis to first-dose completion of beta-lactam antibiotics between IV push and IV piggyback

76 d that these 2-AI molecules also potentiated beta-lactam antibiotics by affecting mycobacterial prote

77 ed to play a key role in the biosynthesis of beta-lactam antibiotics by isopenicillin N-synthase (IPN

78 P. aeruginosa developed resistance to beta-lactam antibiotics during evolution, when grown wit

79 enes has remained universally susceptible to beta-lactam antibiotics for 70 years.

80 with significantly reduced susceptibility to beta-lactam antibiotics have been recently described.

81 the promise of such a biosensor to determine beta-lactam antibiotics in aqueous solutions by using am

82 Resistance to beta-lactam antibiotics in Gram-negative bacteria is com

83 inding protein 2X (PBP2X), a major target of beta-lactam antibiotics in pathogenic bacteria.

84 fore deciding not to use penicillin or other beta-lactam antibiotics is an important tool for antimic

85 MRSA resistance to beta-lactam antibiotics is mediated by two divergons tha

86 An important mechanism of resistance to beta-lactam antibiotics is via their beta-lactamase-cata

87 Resistance to beta-lactam antibiotics mediated by metallo-beta-lactama

88 Combinations of beta-lactam antibiotics show promise in overcoming MDR P

89 of its infection has been accomplished using beta-lactam antibiotics such as the penicillins and the

90 Penicillin refers to a group of beta-lactam antibiotics that are the first-line treatmen

91 the phenotypic resistance profile, including beta-lactam antibiotics that were used to treat ESBL-pos

92 ogical efforts to preserve the future of the beta-lactam antibiotics through a better understanding o

93 Serine active-site beta-lactamases hydrolyze beta-lactam antibiotics through the formation of a coval

94 at was designed to be given with intravenous beta-lactam antibiotics to degrade excess antibiotics in

95 LIs) can be administered in combination with beta-lactam antibiotics to negate the action of the beta

96 exes formed by l,d-transpeptidases with some beta-lactam antibiotics undergo non-hydrolytic fragmenta

97 Proteins related to the degradation of beta-lactam antibiotics were abundant in EVs released fr

98 eported penicillin allergies who receive non-beta-lactam antibiotics when compared to their non-penic

99 sh group was less likely to fail the goal of beta-lactam antibiotics within 1 hour (44.6% vs 57.3%; o

100 acrolide resistance, including resistance to beta-lactam antibiotics, an antibiotic class prescribed

101 acting as the first line of defense against beta-lactam antibiotics, and antibiotic stress leads to

102 actamases (MBLs) degrade a broad spectrum of beta-lactam antibiotics, and are a major disseminating s

103 ceptible bacteria in the presence of several beta-lactam antibiotics, and directly degrade the antibi

104 fection in patients treated with intravenous beta-lactam antibiotics, and our findings support contin

105 ese studies will aid in the synthesis of new beta-lactam antibiotics, beta-lactamase inhibitors, and

106 eus (MRSA), which is resistant to nearly all beta-lactam antibiotics, limiting treatment options.

107 espread advantage across beta-lactam and non beta-lactam antibiotics, non-antibiotic drugs and even d

108 enicillin-binding protein poorly acylated by beta-lactam antibiotics, PBP2a.

109 High-dose drugs, especially beta-lactam antibiotics, RCM and clindamycin, are common

110 a cell wall, or blocking its synthesis with beta-lactam antibiotics, results in an increased flux th

111 ) to combinations of avibactam and different beta-lactam antibiotics, suggest that it may be possible

112 sted the hypothesis that upon treatment with beta-lactam antibiotics, susceptible Enterobacteriaceae

113 actam and zidebactam) potentiate activity of beta-lactam antibiotics, to various extents, against car

114 with increased use of broad-spectrum and non-beta-lactam antibiotics, which results in increased adve

115 in-resistant Staphylococcus aureus (MRSA) to beta-lactam antibiotics.

116 ecreased susceptibility in vitro to multiple beta-lactam antibiotics.

117 get to enhance the susceptibility of MRSA to beta-lactam antibiotics.

118 hreat due to their ability to inactivate all beta-lactam antibiotics.

119 re first described as inactivators of common beta-lactam antibiotics.

120 resistance, rendering bacteria resistant to beta-lactam antibiotics.

121 threaten the clinical utility of almost all beta-lactam antibiotics.

122 reactions, or hypersensitivities to multiple beta-lactam antibiotics.

123 s for L-form growth and non-lytic killing by beta-lactam antibiotics.

124 of these kinases in regulating resistance to beta-lactam antibiotics.

125 reat due to rapidly rising resistance toward beta-lactam antibiotics.

126 k, the mecA gene, confers resistance to many beta-lactam antibiotics.

127 nt in inactivating most of the commonly used beta-lactam antibiotics.

128 disposing factors for immediate reactions to beta-lactam antibiotics.

129 includes vancomycin plus an antipseudomonal beta-lactam (AP-BL).

130 impact of de-escalation from antipseudomonal beta-lactam (APBL) therapy within 48 hours of Enterobact

131 predict drug synergies; for example, certain beta-lactams appear to work cooperatively due to their p

132 h as alpha-quaternary beta-homo prolines and beta-lactams, are also prepared in two- to three-steps f

133 analysis indicated a wide variety of mobile beta-lactam ARGs associated with pathogens downstream of

134 ity of ARGs in general (85.4 versus <2%) and beta-lactam ARGs in particular.

135 needed to explore what effects administering beta-lactam-avibactam combinations have on treating MRSA

136 pression increased susceptibility to several beta-lactam-based antibiotics in strain P. aeruginosa PA

137 By dissecting the structure of beta-lactam-based ligands, a new series of compounds was

138 mycin, ceftaroline, ertapenem, and the novel beta-lactam beta-lactam inhibitor combinations.

139 Avibactam is a non-beta-lactam beta-lactamase inhibitor for treating compli

140 with approximately 32-minute time savings to beta-lactam (beta = -0.60; 95% CI, -0.91 to -0.29) and a

141 Piperacillin-tazobactam (P/T) is a beta-lactam-beta-lactamase inhibitor combination frequen

142 aptomycin, ceftaroline, ertapenem, and novel beta-lactam-beta-lactamase inhibitor combinations from J

143 ltivorans induced by various beta-lactams or beta-lactam-beta-lactamase inhibitor combinations.

144 st) could identify susceptibility to 2 newer beta-lactam/beta-lactamase inhibitor (BL-BLI) combinatio

145 treatment implications, particularly for new beta-lactam/beta-lactamase inhibitor combinations.

146 and imipenem-relebactam (an investigational beta-lactam/beta-lactamase inhibitor).

147 cillin (benzylpenicillin MIC >= 256 mug/ml), beta-lactam/beta-lactamase inhibitors and cephalosporins

148 enicillin-binding protein (PBP) 5 (PBP5) and beta-lactam binding affinity in HOU503 versus R497.

149 cent penicillin derivative, showed increased beta-lactam binding affinity of PBP5 of HOU503 compared

150 and MecR1, which both have an extracellular beta-lactam-binding sensor domain.

151 , the primary transcriptome landscape of the beta-lactam biosynthetic pathway is analyzed, suggesting

152 An accurate diagnosis of beta-lactam (BL) allergy can reduce patient morbidity an

153 n how European allergy specialists deal with beta-lactam (BL) hypersensitivity demonstrated a signifi

154 Mounting evidence suggests the addition of a beta-lactam (BL) to daptomycin (DAP) results in synergis

155 beta-lactams (BLCs) are the most widely used antibiotics

156 ase inhibitor (BLI) drugs, including the non-beta-lactam BLI avibactam (AVI).

157 However, some beta-lactam-BLI combinations have lost their effectivene

158 mproved understanding of the biochemistry of beta-lactam breakdown.

159 reoselective synthesis of highly substituted beta-lactams by intramolecular Tsuji-Trost allylation is

160 selection bias make inferences on effective beta-lactam choices problematic.

161 structures along with new, and improved, PBP-beta-lactam co-structures.

162 Novel beta-lactam combination agents appear to retain active i

163 ICUs and in vitro activities of new beta-lactam combination agents.

164 larvae and the efficacy of twenty-eight dual beta-lactam combination therapies were compared to their

165 d IV vancomycin plus 1 other antipseudomonal beta-lactam combination therapy at 1 of 6 large children

166 study was to determine the efficacy of dual beta-lactam combination treatments derived from eight ap

167 that the enhanced efficacy of these two dual beta-lactam combinations could not be explained by more

168 Five of the dual beta-lactam combinations resulted in greater than 70% su

169 ers of crystal structures, in particular for beta-lactam complexes, and methods such as neutron diffr

170 resistance that emerges in the setting of a beta-lactam compound, (2) stable derepression due to mut

171 we identified mutations that allow growth at beta-lactam concentrations far exceeding those inhibitin

172 Depending on the relative beta-lactam configuration, the reactions occur under kin

173 eta lactamase inhibitors in combination with beta-lactam containing antibiotics is discussed in detai

174 both at the three and seven position of the beta-lactam core structure on the electrochemical finger

175 leading to the efficient formation of chiral beta-lactam derivatives.

176 )/InI-mediated allylations of aldehydes with beta-lactam-derived organoindiums.

177 upplemented with subinhibitory levels of the beta-lactam drug cefoxitin, we find that mecA provides a

178 fic, and some combinations of avibactam with beta-lactam drugs appear to prevent such escape phenotyp

179 actamases can now confer resistance to other beta-lactam drugs, including both cephalosporins and car

180 study, we explored di- and tripeptides with beta-lactam electrophilic warheads as inhibitors of deng

181 This breaks the dogma that beta-lactams enter Gram-negative bacteria only by passiv

182 ted by macrolide but with high prevalence of beta-lactam, fluoroquinolone, and tetracycline resistanc

183 ions.Patients treated with daptomycin plus a beta-lactam for MRSA bloodstream infection had lower odd

184 ng consideration that the adjunctive role of beta-lactams for MRSA in select patients helps elicit fa

185 These data underscore the importance of beta-lactams for SaB, including consideration that the a

186 term (</=60 min) infusion of antipseudomonal beta-lactams for the treatment of patients with sepsis w

187 ATION: Prolonged infusion of antipseudomonal beta-lactams for the treatment of patients with sepsis w

188 the complex was not a competent catalyst for beta-lactam formation.

189 kene-isocyanate cycloaddition method affords beta-lactams from glycals with high regio- and stereosel

190 Patients treated with beta-lactam had higher IL-1beta on day 3 (median +5.6 pg

191 Patients treated with beta-lactam had higher IL-1beta on days 3 (median +5.6 p

192 Data have emerged showing beta-lactams have multidimensional antibacterial effects

193 sistance, penicillin and the wider family of beta-lactams have remained the single most important fam

194 a)) compared with acyl-enzyme complexes with beta-lactams, hindering its function to deprotonate Glu1

195 ting T cells are detectable in patients with beta-lactam hypersensitivity.

196 ssociations between exposure to antibiotics (beta-lactam, imidazole, macrolide, nitrofurantoin, quino

197 We compared the efficacies of a beta-lactam in combination with daptomycin (BL/D-C) and

198 C/EI of beta-lactams in cirrhotic patients with BSI may improve

199 lead to the formation of trans-disubstituted beta-lactams in excellent yields and selectivities.

200 ersus short-term infusion of antipseudomonal beta-lactams in patients with sepsis.

201 DCS resensitized MRSA to beta-lactams in vitro and significantly enhanced MRSA er

202 ary regarding the effectiveness of prolonged beta-lactam infusion.

203 ticularly for MBLs; the likely impact of new beta-lactam:inhibitor combinations and the continuing cl

204 rometry experiments revealed that tripeptide-beta-lactam inhibitors bind to the protease in two disti

205 A key bicyclic beta-lactam intermediate not only serves as the key cont

206 in or daptomycin) plus an antistaphylococcal beta-lactam (intravenous flucloxacillin, cloxacillin, or

207 that hydrolyzes carbapenems, the most potent beta-lactams; known KPC variants differ in turnover of e

208 ine residue for site-specific conjugation to beta-lactam linker-functionalized siRNA.

209 cular interest in whether the superiority of beta-lactams links to key cytokine pathways.

210 ns and the continuing clinical importance of beta-lactams mean that this remains a rewarding research

211 ic site-to-active site communication and for beta-lactam mimicry of the peptidoglycan substrates, as

212 Tripeptides with a (3S)-beta-lactam moiety displayed the highest activity, with

213 tamase inhibitors, and bicyclic carbohydrate-beta-lactam monomers prepared by the alkene-isocyanate m

214 in combination with daptomycin (BL/D-C) and beta-lactam monotherapy (BL-M) in improving clinical out

215 a in the study period; 1019 (71.9%) received beta-lactam monotherapy and 399 (28.1%) received beta-la

216 s with P. aeruginosa bacteremia treated with beta-lactam monotherapy during 2009-2015.

217 Although beta-lactam monotherapy is common, data to guide the cho

218 8 hours, patients were treated with either a beta-lactam (n = 24), including oxacillin, cefazolin, or

219 st 48 h, patients were treated with either a beta-lactam (n=24), including oxacillin, cefazolin, or c

220 omycin with vs without an antistaphylococcal beta-lactam on mortality, bacteremia, relapse, or treatm

221 In all, 70,101 procedures (52,504 beta-lactam only, 5,089 vancomycin only, and 12,508 comb

222 xtracts of B. multivorans induced by various beta-lactams or beta-lactam-beta-lactamase inhibitor com

223 ivation of the most widely used antibiotics, beta-lactams (penicillins, cephalosporines, carbapenems,

224 Use of a beta-lactam plus an oral or parenteral macrolide (azithr

225 Double antibiotic therapy (beta-lactam plus either an aminoglycoside or a fluoroqui

226 -lactam monotherapy and 399 (28.1%) received beta-lactam plus macrolide combination therapy.

227 a infections and confirm that aztreonam-like beta-lactams plus nonclassical beta-lactamase inhibitors

228 mination at 140 degrees C in DMF to afford a beta-lactam product.

229 substitution (S(N)2) reaction to give spiro-beta-lactam-pyrroloquinoline scaffolds 6a-t.

230 ion was developed for the synthesis of spiro-beta-lactam-pyrroloquinolines.

231 minantly belonging to the aminoglycoside and beta-lactam resistance classes.

232 ic distances between isolates with different beta-lactam resistance determinants suggests that the pr

233 worldwide and rapid spread of large spectrum beta-lactam resistance genes such as carbapenemases is d

234 m minimum inhibitory concentration (MIC) and beta-lactam resistance genes with mortality in the MERIN

235 ) methods for the detection of mecA-mediated beta-lactam resistance in 100 human isolates of S. epide

236 xpensive method for detecting PBP2a-mediated beta-lactam resistance in clinically relevant non-SASS f

237 The development of beta-lactam resistance in non-SASS through acquisition a

238 Overcoming beta-lactam resistance in pathogens such as Pseudomonas

239 highly reliable for detecting mecA-mediated beta-lactam resistance in S. epidermidis isolates.

240 reakpoints reliably identified mecA-mediated beta-lactam resistance in S. epidermidis Using mecA PCR

241 f phenotypic methods to detect mecA-mediated beta-lactam resistance in staphylococci is becoming more

242 f laboratory testing to detect mecC-mediated beta-lactam resistance in Staphylococcus aureus Kriegesk

243 istance to erythromycin has been recognised, beta-lactam resistance in toxigenic diphtheria has not b

244 strate viability, the PAD was used to detect beta-lactam resistance in wastewater and sewage and iden

245 genes in the dacB-defective background, the beta-lactam resistance phenotype was abolished, disablin

246 ons in genes that are known to contribute to beta-lactam resistance were identified.

247 es isolates with characterized mechanisms of beta-lactam resistance, 180 clinical isolates from the M

248 , consistent with a first step in developing beta-lactam resistance.

249 , consistent with a first-step in developing beta-lactam resistance.

250 ence of C. diphtheriae BQ11 and mechanism of beta-lactam resistance.

251 Methicillin (beta-lactam) resistance in Staphylococcus epidermidis is

252 ried out in both types of EVs to investigate beta-lactam resistant determinants.

253 The beta-lactams retain a central place in the antibacterial

254 ydrolyze the amide bond of the four-membered beta-lactam ring are the primary resistance mechanism, w

255 The carbapenem bicyclic core consists of a beta-lactam ring fused to a pyrroline ring.

256 The beta-lactam ring represents a valuable moiety that can i

257 covalent, but reversible, interaction of the beta-lactam ring with the catalytic serine, followed by

258 owed by release of the inhibitor with opened beta-lactam ring.

259 to first-generation inhibitors containing a beta-lactam ring.

260 ich are then countered by new generations of beta-lactam structure.

261 ic ring-opening polymerization of a bicyclic beta-lactam sugar monomer.

262 oxamates facilitated syntheses of monocyclic beta-lactams suitable for incorporation of a thiomethyl

263 otypic and phenotypic approaches to identify beta-lactam susceptibility in Escherichia coli, Klebsiel

264 id replacement in PBP2X that confers reduced beta-lactam susceptibility in vitro was more fit, as ass

265 Decreased beta-lactam susceptibility is geographically widespread

266 e nucleic acid quantification to measure the beta-lactam susceptibility phenotype of Ng very rapidly,

267 ains with macrolide resistance and decreased beta-lactam susceptibility was unexpected and is of publ

268 MRSA play a crucial role in the survival of beta-lactam susceptible bacteria by acting as the first

269 ss the impact of peptidoglycan substrates on beta-lactam targeting of transpeptidation, and (d) demon

270 ity to exogenous nucleases after exposure to beta-lactams (termed nuclease-accessibility AST [nuc-aAS

271 Fourteen compounds from 6 classes (beta-lactams, tetracyclines, sulfonamides, fluoroquinolo

272 spectrum, including digesting anticancer and beta-lactams, that can be then used as nutriments.

273 be rapid, but it has not been successful for beta-lactams (the largest antibiotic class used to treat

274 owing beta-lactamase-mediated opening of the beta-lactam, the pyrroline may interconvert between an e

275 ST (pol-aAST), a new phenotypic approach for beta-lactams, the major antibiotic class for gram-negati

276 f the bacterial cell wall are the targets of beta-lactams, the most clinically successful antibiotics

277 nding proteins (PBPs) are the targets of the beta-lactams, the most successful class of antibiotics e

278 S. aureus protects the enzyme targets of the beta-lactams, the penicillin-binding proteins.

279 4.5-fold greater odds of receiving preferred beta-lactam therapy (95% confidence interval, 2.4-8.2; P

280 reviews the tremendous advantages offered by beta-lactam therapy and makes a strong case that the deb

281 Encephalopathy complicates beta-lactam therapy, particularly with impaired renal fu

282 portant contributors to efficacy of DAP plus beta-lactam therapy.

283 acteremia, addition of an antistaphylococcal beta-lactam to standard antibiotic therapy with vancomyc

284 that class D SBL-catalyzed rearrangement of beta-lactams to beta-lactones is important as a resistan

285 beta-lactam treated patients had sharper declines in IL-

286 beta-lactam-treated patients had sharper declines in IL-

287 Therapeutic and subtherapeutic beta-lactam use is associated with different patterns of

288 ed >=24 but <=72 hours of an antipseudomonal beta-lactam/VAN combination: PTZ/VAN, cefepime (CEF)/VAN

289 e risk associated with other antipseudomonal beta-lactam/VAN combinations.

290 SBLs neutralize beta-lactams via a hydrolytically labile covalent acyl-e

291 with cysteine yields enzymes which fragment beta-lactams via a similar mechanism as the l,d-transpep

292 as determined by treating clinicians and the beta-lactam was administered for 7 days.

293 At competing risk analysis, C/EI of beta-lactams was associated with significantly higher ra

294 Resistance to WHO recommended beta-lactams was reported in 614 (68%) of 904 cases and

295 osamides, sulfonamides, aminoglycosides, and beta-lactams were quantified using a Custom qPCR Array o

296 Prolonging the clinical effectiveness of beta-lactams, which remain first-line antibiotics for ma

297 activity of these enzymes, combinations of a beta-lactam with a beta-lactamase inhibitor (BLI) have b

298 bones containing quinoline, pyrrolidone, and beta-lactam with high bond-forming efficiency.

299 ntroduction to the clinic of combinations of beta-lactams with diazabicyclooctanone and cyclic borona

300 s, delivers alpha-alkoxycarbonyl-substituted beta-lactams with outstanding diastereoselectivity.

301 lly with I(2) to form either aryl iodides or beta-lactams within minutes at room temperature.