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1 n the native S. aureus PBPs are inhibited by beta-lactams.
2 one of the highly effective antibacterials, beta-lactams.
3 istance to the carbapenem imipenem and other beta-lactams.
4 anhydride to transform aliphatic amines into beta-lactams.
5 inhibitor could restore the effectiveness of beta-lactams.
6 abolite levels that occur during exposure to beta-lactams.
7 these pathogens test as susceptible to some beta-lactams.
8 L) producing bacteria has limited the use of beta-lactams.
9 allergic reactions to penicillins and other beta-lactams.
10 rturbed evolved prior to the clinical use of beta-lactams.
11 t strains with their inhibition by different beta-lactams.
12 ast bactericidal effect, are not inferior to beta-lactams.
13 olecules that restore sensitivity of MRSA to beta-lactams.
14 he detection ranges were 0.26-3.56 ng/mL for beta-lactams, 0.04-0.98 ng/mL for tetracyclines, 0.08-2.
15 of beta-lactamases, enzymes that inactivate beta-lactams, a class of antibiotics that has been a the
17 gainst Enterobacteriaceae and restoration of beta-lactam activity in a broad range of MDR Gram-negati
18 ying beta-lactam allergies to safely promote beta-lactam administration among these patients is warra
21 adjust both the dose and dosing interval of beta-lactam agents allows the treatment of strains with
23 nam and the tolerability of such alternative beta-lactams, all subjects underwent skin tests with cep
24 ent programs aimed at accurately identifying beta-lactam allergies to safely promote beta-lactam admi
27 e the burden and clinical impact of reported beta-lactam allergy on patients seen by infectious disea
30 sociation study of the genetic predictors of beta-lactam allergy to better understand the underlying
32 us 146/10,215 (1.4%) patients who received a beta-lactam alone (crude RR 0.61, 95% CI 0.45, 0.83).
34 resistant to multiple antibiotics, including beta-lactams, aminoglycosides, fluoroquinolones, and pol
35 s study chooses four classes of antibiotics, beta-lactam (ampicillin and penicillin), quinolone (enox
36 Because combination therapy using both a beta-lactam and a second antibiotic suppressing the smal
37 aceae (3GC-R EB), Dutch guidelines recommend beta-lactam and aminoglycoside combination therapy or ca
38 amide-streptogramin, bacitracin, vancomycin, beta-lactam and aminoglycoside resistance genes were the
39 lin resistance in Staphylococcus aureus, and beta-lactam and co-trimoxazole resistance in Streptococc
41 cation of the two side chains carried by the beta-lactam and the five-membered rings of the carbapene
42 isopenicillin N synthase (IPNS) installs the beta-lactam and thiazolidine rings of the penicillin cor
43 atients with immediate allergic reactions to beta-lactams and 1124 paired control subjects from Spain
44 nditions were lower than those observed with beta-lactams and close to those observed with amikacin.
45 d inhibition of MBLs by beta-lactams and non-beta-lactams and illustrate the utility of PrOF NMR for
46 for the mechanisms and inhibition of MBLs by beta-lactams and non-beta-lactams and illustrate the uti
48 ined and empiric therapy with broad-spectrum beta-lactams and/or aminoglycosides and/or fluoroquinolo
51 b transpeptidase domain is a major target of beta-lactams, and therefore it is important to attain a
56 with vancomycin plus 1 other antipseudomonal beta-lactam antibiotic combination (adjusted odds ratio,
58 athways that have evolved to the three other beta-lactam antibiotic families: penicillin/cephalospori
59 r conditions of induction of resistance to a beta-lactam antibiotic identified two signaling muropept
61 a an active process and was inhibited by the beta-lactam antibiotic oxacillin, which slowed inactivat
62 genum is the main industrial producer of the beta-lactam antibiotic penicillin, the most commonly use
63 erant and hypersensitive patients taking the beta-lactam antibiotic piperacillin and the threshold re
64 every new user of an oral fluoroquinolone or beta-lactam antibiotic prescription with at least 24 mon
65 omal AmpC beta-lactamase is a major cause of beta-lactam antibiotic resistance in the Gram-negative b
66 Here we show that the protein conferring beta-lactam antibiotic resistance, penicillin-binding pr
68 herapy with vancomycin and 1 antipseudomonal beta-lactam antibiotic throughout the first week of hosp
69 demonstrate that bacterial persisters, under beta-lactam antibiotic treatment, show less cytoplasmic
71 d IV vancomycin plus 1 other antipseudomonal beta-lactam antibiotic, 157 patients (8.2%) had antibiot
72 sion of beta-lactamase in the absence of any beta-lactam antibiotic, thus indicating that they serve
75 The paper card can also detect substandard beta lactam antibiotics using an iodometric back-titrati
76 ed in presence of other structurally related beta-lactam antibiotics (amoxicillin, oxacillin, penicil
78 he main bacterial mechanism of resistance to beta-lactam antibiotics and are a significant challenge
79 -beta-lactamases (MBLs) hydrolyze almost all beta-lactam antibiotics and are unaffected by clinically
80 a-lactamases catalyze the hydrolysis of most beta-lactam antibiotics and hence represent a major clin
84 PBP2a effectively discriminates against the beta-lactam antibiotics as potential inhibitors, and in
85 with intermittent dosing, administration of beta-lactam antibiotics by continuous infusion in critic
86 uct complex crystal structures of KPC-2 with beta-lactam antibiotics containing hydrolyzed cefotaxime
87 ant Enterobacteriaceae are resistant to most beta-lactam antibiotics due to the production of the Kle
88 tified that reversed intrinsic resistance to beta-lactam antibiotics in a manner distinct from beta-l
89 amases are enzymes that confer resistance to beta-lactam antibiotics in bacteria, and there is a crit
90 g continuous versus intermittent infusion of beta-lactam antibiotics in critically ill patients with
92 epair and the manifestation of resistance to beta-lactam antibiotics in many Enterobacteriaceae and P
97 Tipper-Strominger hypothesis stipulates that beta-lactam antibiotics mimic the acyl-D-Ala-D-Ala moiet
101 (CLSI) lowered the MIC breakpoints for many beta-lactam antibiotics to enhance detection of known re
102 taphylococcus aureus (MRSA) are resistant to beta-lactam antibiotics, which inhibit bacterial cell wa
112 and 23S rRNA) associated with resistance to beta-lactam antimicrobials, macrolides, or fluoroquinolo
113 val [CI], 1.45-5.42), as was narrow-spectrum beta-lactams (aOR, 3.54; 95% CI, 1.98-6.33), and appropr
114 n Denmark, we quantified four broad-spectrum beta-lactam AR genes (ARG; bla(TEM), bla(SHV), bla(OXA)
117 f exchanging the removable components and of beta-lactams are confirmed and maybe also a potential be
119 ble Staphylococcus aureus (MSSA) infections, beta-lactams are recommended for definitive therapy; how
121 the concern of complex drug responses, many beta-lactams are typically ruled out if ESBL-producing p
122 h as alpha-quaternary beta-homo prolines and beta-lactams, are also prepared in two- to three-steps f
123 ly reduced aminoglycoside, tetracycline, and beta-lactam ARG levels relative to anaerobic units, alth
125 for immediate hypersensitivity reactions to beta-lactams, aspirin, and nonsteroidal anti-inflammator
126 to delineate an advantageous approach toward beta-lactams based on a two-step, one-pot protocol: an i
127 eport the discovery of compound 4a, a potent beta-lactam-based monoacylglycerol lipase (MGL) inhibito
129 hen combined with ceftazidime, the novel non-beta-lactam beta-lactamase inhibitor avibactam provides
131 bactam and ceftazidime/avibactam are 2 novel beta-lactam/beta-lactamase combination antibiotics.
134 tive alternative drugs to carbapenems except beta-lactam/beta-lactamase inhibitors for the treatment
135 sistant to cephalosporins, fluoroquinolones, beta-lactam/beta-lactamase inhibitors, multidrug resista
137 o, 1.65 [95% CI, 1.15-2.37]) and exposure to beta-lactams/beta-lactamase inhibitors (risk ratio, 1.78
139 ections (BSIs) in patients presenting with a beta-lactam (BL) allergy is often a difficult decision g
140 ests (DPT) are commonly performed as part of beta-lactam (BL) allergy workup, in case of negative ski
144 y trapping experiments, thus confirming that beta-lactams can be designed that are capable of releasi
147 serovar Typhi strain with resistance against beta-lactams, cephalosporins (extended-spectrum beta-lac
148 robial resistance determinants for different beta-lactams, ciprofloxacin, and tetracyclines on multip
150 d IV vancomycin plus 1 other antipseudomonal beta-lactam combination therapy at 1 of 6 large children
151 genes, were used to predict resistance to 4 beta-lactams commonly used in the empiric treatment of n
154 s vancomycin, bacitracin, daptomycin and the beta-lactam-containing penicillins, cephalosporins and n
155 ours; P = .01) and increased narrow-spectrum beta-lactam (control 42 hours, rmPCR 71 hours, rmPCR/AS
156 Using quantitative modeling, we show that beta-lactams could still effectively treat pathogens pro
158 , particularly plasmid-encoded resistance to beta lactam drugs, poses an increasing threat to human h
159 ubgraphs were noted, one containing the five beta-lactam drugs and the other containing both sulfonam
161 days), and long treatments (>/=21 days) with beta-lactams, either as monotherapy (0.48) or in combina
162 E), blaNDM-1, and selected extended-spectrum beta-lactam (ESBL) resistant bacteria and genes in 12 ho
163 cephalosporins, which are antibiotics in the beta-lactam family that target cell-wall biosynthesis.
164 ination of vancomycin and antistaphylococcal beta-lactams for methicillin-resistant Staphylococcus au
166 term (</=60 min) infusion of antipseudomonal beta-lactams for the treatment of patients with sepsis w
167 ATION: Prolonged infusion of antipseudomonal beta-lactams for the treatment of patients with sepsis w
168 d multicomponent method for the synthesis of beta-lactams from imines, aryl halides, and CO has been
169 ients who received definitive therapy with a beta-lactam had 35% lower mortality compared with patien
170 Patients who received empiric therapy with a beta-lactam had similar mortality compared with those wh
171 's repertoire that can be activated with the beta-lactam hapten and/or an imbalance in immune regulat
174 e groups of enzymes, their substrates and of beta-lactams have led to the conclusion that beta-lactam
175 ose who especially require these alternative beta-lactams, however, we recommend pretreatment skin te
179 study was to use piperacillin as a model of beta-lactam hypersensitivity to study the nature of the
182 tazidime) complexes with PBP2a-each with the beta-lactam in the allosteric site-defined (with precedi
183 D platforms for detecting resistance against beta-lactams in 72 highly resistant isolates of Escheric
184 lead to the formation of trans-disubstituted beta-lactams in excellent yields and selectivities.
185 ing corresponding alpha-alkylidene-beta-aryl-beta-lactams in good isolated yields (41-83%) with exclu
189 of cardiac procedures showed superiority of beta-lactams in preventing superficial and deep chest SS
190 of E. coli PBP1b bound to multiple different beta-lactams in the transpeptidase active site and compl
192 trate the direct incorporation of monocyclic beta-lactams into a variety of molecular architectures.
195 lar to mecA, mecC confers resistance against beta-lactams, leading to the phenotype of methicillin-re
196 dical reasons) with beta-lactam monotherapy, beta-lactam-macrolide combination therapy, or fluoroquin
199 ic site-to-active site communication and for beta-lactam mimicry of the peptidoglycan substrates, as
200 ne are epidemiology of allergic reactions to beta-lactams, molecular structure, formulations availabl
203 al (n = 1737) demonstrated noninferiority of beta-lactam monotherapy (n = 506) vs beta-lactam plus ma
204 a in the study period; 1019 (71.9%) received beta-lactam monotherapy and 399 (28.1%) received beta-la
206 of hospital stay between children receiving beta-lactam monotherapy and combination therapy (median,
207 ombination therapy conferred no benefit over beta-lactam monotherapy for children hospitalized with c
208 hically confirmed pneumonia and who received beta-lactam monotherapy or beta-lactam plus macrolide co
209 580) failed to demonstrate noninferiority of beta-lactam monotherapy vs beta-lactam plus macrolide co
211 llowing deviations for medical reasons) with beta-lactam monotherapy, beta-lactam-macrolide combinati
217 determinants of immediate reactions (IR) to beta-lactams (n = 19), NAR against aspirin (n = 12) and
219 troduction of the compactin pathway into the beta-lactam-negative P. chrysogenum DS50662, a new cytoc
221 uce and secrete the antibiotic penicillin, a beta-lactam nonribosomal peptide, by taking genes from a
222 133 putative instances of resistance to the beta-lactams of interest identified by WGS, only 87 (65%
225 ose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide alters both host and microbiota
227 s failed to demonstrate clinical benefits of beta lactam plus aminoglycoside combination therapy comp
229 rity of beta-lactam monotherapy (n = 506) vs beta-lactam plus macrolide combination therapy (n = 566)
230 effectiveness of beta-lactam monotherapy vs beta-lactam plus macrolide combination therapy among a c
232 pneumonia, antibiotic therapy consisting of beta-lactam plus macrolide combination therapy or fluoro
233 dy populations of 1188 to 24,780) found that beta-lactam plus macrolide combination therapy was assoc
234 noninferiority of beta-lactam monotherapy vs beta-lactam plus macrolide combination therapy, with an
239 a infections and confirm that aztreonam-like beta-lactams plus nonclassical beta-lactamase inhibitors
240 fluoroquinolone prescription compared with a beta-lactam prescription using multivariate regression w
244 nal linkage between specific determinants of beta-lactam resistance (e.g. beta-lactamase) and redox p
245 lead to antibiotic resistance; for example, beta-lactam resistance by L,D-transpeptidase activities.
247 aluated for identification of PBP2a-mediated beta-lactam resistance in human and animal clinical isol
249 f laboratory testing to detect mecC-mediated beta-lactam resistance in Staphylococcus aureus Kriegesk
250 strate viability, the PAD was used to detect beta-lactam resistance in wastewater and sewage and iden
257 ence of two oxidative cyclizations, with the beta-lactam ring being installed first and the thiazolid
258 is fully compatible with the highly unstable beta-lactam ring of carbapenems and that the triazole ri
260 he pro-S-CCys,beta-H bond for closure of the beta-lactam ring, and the CVal,beta-H bond for installat
262 etween these enzymes' active site structure, beta-lactam specificity and metal content.Carbapenem-res
263 ted under the reaction conditions, including beta-lactam-, steroid-, and sugar-derived ones, leading
265 attractive entry to a variety of monocyclic beta-lactam structures related to monobactams and nocard
267 e mechanistic aspects of how Mtb responds to beta-lactams such as Amoxicillin in combination with Cla
268 t was the widespread use of first generation beta-lactams such as penicillin in the years prior to th
269 mation and increases antibiotic tolerance to beta-lactams, suggesting that HQNO-dependent cell autoly
270 oxamates facilitated syntheses of monocyclic beta-lactams suitable for incorporation of a thiomethyl
271 ell-based time-kill assays show BTZs restore beta-lactam susceptibility of Escherichia coli-producing
272 en optimized for inactivation of the unusual beta-lactam targets of Mycobacterium tuberculosis or for
274 Gold-catalyzed hydroarylation reaction of beta-lactam-tethered allenyl indoles gives azeto-oxepino
275 s detection of four families of antibiotics (beta-lactams, tetracyclines, quinolones and sulfonamides
276 qualitative analysis, the cut-off values of beta-lactams, tetracyclines, quinolones and sulfonamides
277 4.5-fold greater odds of receiving preferred beta-lactam therapy (95% confidence interval, 2.4-8.2; P
278 ne periods, 50% (124/246) received preferred beta-lactam therapy based on history, compared with 60%
279 In contrast, patients who received preferred beta-lactam therapy had a similar risk of adverse events
284 ders, patients who did not receive preferred beta-lactam therapy were at greater risk of adverse even
285 al ASPs resulted in greater use of preferred beta-lactam therapy without increasing the risk of adver
290 allows cell-wall biosynthesis, the target of beta-lactams, to continue even in the presence of typica
292 he majority of cases were treated with other beta-lactams, trimethoprim-sulfamethoxazole, or vancomyc
293 ceipt of 2 antimicrobials (vancomycin plus a beta-lactam) versus either single agent alone (vancomyci
300 d annulations allowed the formation of fused beta-lactams without harming the sensitive four-membered
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