The beta-lactamase stability and interactions of imipenem were analysed in comparison with those of cefazolin, cefuroxime, cefoxitin, cefotaxime, ceftazidime, mezlocillin, piperacillin and penicillin G for a set of representative beta-lactamases. These enzymes included penicillinases such as those obtained from Staphylococcus aureus, Escherichia coli and other Enterobacteriaceae (TEM-1 and similar enzymes) (group A); cephalosporinases produced by Esch. coli (Amp C type), Serratia liquefaciens, Enterobacter cloacae, Pseudomonas aeruginosa (group B); and beta-lactamases produced by Klebsiella spp., Proteus vulgaris and Bacteroides fragilis and with a high hydrolytic activity for the newer cephalosporins (group C). Enzymes of group A were demonstrated to be highly active against penicillins and also against the early cephalosporins; enzymes of group B showed hydrolytic activity for all other tested compounds, including the newer cephalosporins and cephamycins, but not imipenem, whereas enzymes of group C were highly active against the new cephalosporins but not against cephamycins and imipenem. In conclusion, imipenem shows a moderate affinity for all these enzymes but no detectable hydrolysis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1093/jac/18.supplement_e.1 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Contribution of Blood Biomarkers to Multiple Sclerosis Diagnosis.
Neurol Neuroimmunol Neuroinflamm
March 2025
Servei de Neurologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Background And Objectives: Invasive procedures may delay the diagnostic process in multiple sclerosis (MS). We investigated the added value of serum neurofilament light chain (sNfL), glial fibrillary acidic protein (sGFAP), chitinase-3-like 1 (sCHI3L1), and the immune responses to the Epstein-Barr virus-encoded nuclear antigen 1 to current MS diagnostic criteria.
Methods: In this multicentric study, we selected patients from 2 prospective cohorts presenting a clinically isolated syndrome (CIS).
Specific immunohistochemical expression of Mmp-26 in prostatic adenocarcinoma.
An Acad Bras Cienc
January 2025
Universidade Federal de Pernambuco, Departamento de Histologia e Embriologia, Av. Prof. Moraes Rego, 1235, Cidade Universitária, 50760-420 Recife, PE, Brazil.
Matrix metalloproteinases (MMP) have been identified as biomarkers for several diseases, including cancer. The increase in the expression of these enzymes has been related to greater tumor aggressiveness. MMP-26 is expressed constitutively in the endometrium and some cancer cells of epithelial origin.
View Article and Find Full Text PDFThe relationship between insulin resistance and fibroblast growth factor 23 in patients with non-diabetic pre-dialysis chronic kidney disease: a cross-sectional study.
Sao Paulo Med J
January 2025
Associate Professor, Department of Nephrology, Ankara Bilkent City Hospital, Ankara, Turkey.
Background: Insulin resistance often occurs in patients with chronic kidney disease (CKD) owing to mineral and bone metabolism disorders. Fibroblast growth factor (FGF)-23 and soluble klotho (s-KL) play crucial roles in linking CKD with mineral and bone metabolism.
Objective: This study aimed to examine the relationship between insulin resistance and FGF-23 and s-KL in patients with non-diabetic pre-dialysis patients with CKD.
AGER-dependent macropinocytosis drives resistance to KRAS-G12D-targeted therapy in advanced pancreatic cancer.
Sci Transl Med
January 2025
Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Pancreatic ductal adenocarcinoma (PDAC) driven by the mutation presents a formidable health challenge because of limited treatment options. MRTX1133 is a highly selective and first-in-class KRAS-G12D inhibitor under clinical development. Here, we report that the advanced glycosylation end product-specific receptor (AGER) plays a key role in mediating MRTX1133 resistance in PDAC cells.
View Article and Find Full Text PDFNitroxyl protects H9C2 cells from H/R-induced damage and inhibits autophagy via PI3K/Akt/mTOR pathway.
PLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!