Related Experiment Video

Updated: Aug 18, 2026

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method
12:03

Antimicrobial Synergy Testing by the Inkjet Printer-assisted Automated Checkerboard Array and the Manual Time-kill Method

Published on: April 18, 2019

Adverse reactions and interactions with newer cephalosporin and cephamycin antibiotics

S R Norrby

    Medical Toxicology
    |January 1, 1986
    PubMed

    More Related Videos

    Quadruple-Checkerboard: A Modification of the Three-Dimensional Checkerboard for Studying Drug Combinations11:15

    Quadruple-Checkerboard: A Modification of the Three-Dimensional Checkerboard for Studying Drug Combinations

    Published on: July 24, 2021

    Assay Development for High-Throughput Drug Screening Against Mycobacteria07:50

    Assay Development for High-Throughput Drug Screening Against Mycobacteria

    Published on: October 25, 2024

    Related Concept Videos

    Combined Effects of Drugs: Synergism01:27

    Combined Effects of Drugs: Synergism

    Synergism is a useful mechanism where combining two or more drugs is more effective than each constituent used alone. Such combinations are also called supra-additive interactions. The drugs collectively enhance the final therapeutic effect by acting on different targets. Another advantage is that the low dose of each constituent drug is sufficient to achieve the desired effect. This helps reduce the duration of therapy and lower the adverse effects of these drugs.
    Such synergistic combinations...
    Pharmacokinetics: Drug–Drug Interactions01:25

    Pharmacokinetics: Drug–Drug Interactions

    Drug interactions occur when the pharmacological effect of one drug is altered by another substance, either enhancing or diminishing its activity. The drug whose activity is altered is known as the object drug, and the substance causing the alteration is called the agent drug or the precipitant. The net effects of these interactions are mostly undesirable, leading to decreased effectiveness or increased adverse effects. In rare cases, interactions can be beneficial, such as the enhanced...
    Drug toxicity: Drug–Drug Interaction01:30

    Drug toxicity: Drug–Drug Interaction

    Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
    Mechanism of Antibiotic Resistance in MRSA01:25

    Mechanism of Antibiotic Resistance in MRSA

    Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
    Inhibitors of Bacterial Protein Synthesis01:25

    Inhibitors of Bacterial Protein Synthesis

    Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
    Inhibitors of Bacterial DNA Synthesis01:28

    Inhibitors of Bacterial DNA Synthesis

    Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...