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A permanent electric dipole orients itself along an external electric field. This rotation can be quantified by defining the potential energy because the external torque does work in rotating it. Then, the potential energy is minimum at the parallel configuration and maximum at the antiparallel configuration. While the former is a stable equilibrium, the latter is an unstable equilibrium.
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The fact that emfs are induced in circuits implies that work is being done on the conduction electrons in the wires. What can possibly be the source of this work? We know that it’s neither a battery nor a magnetic field, as a battery does not have to be present in a circuit where current is induced, and magnetic fields never do any work on moving charges. The source of the work is in fact an electric field that is induced in the wires. For example, if a stationary conductor is placed in a...
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Updated: Feb 13, 2026

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Fluoropyrimidine-induced cardiotoxicity.

Ilaria Depetris1, Donatella Marino1, Alessandro Bonzano2

  • 1Medical Oncology, Candiolo Cancer Institute, FPO, IRCCS, Candiolo, Italy; Department of Oncology, University of Turin, Italy.

Critical Reviews in Oncology/Hematology
|March 18, 2018
PubMed
Summary
This summary is machine-generated.

Fluoropyrimidine drugs, like 5-fluorouracil, can cause heart toxicity (FIC), a rare but serious side effect. This review details FIC

Keywords:
5-FluorouracilCapecitabineCardiac toxicityCardiotoxicityFICFluoropyrimidinesUridine triacetateVistogard(®)

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Area of Science:

  • Oncology
  • Cardiology
  • Pharmacology

Background:

  • Fluoropyrimidines (5-fluorouracil, capecitabine) are essential antimetabolites for cancer treatment.
  • While common toxicities are known, fluoropyrimidine-induced cardiotoxicity (FIC) lacks comprehensive characterization.
  • FIC is an infrequent yet potentially life-threatening adverse effect.

Purpose of the Study:

  • To review the current knowledge on fluoropyrimidine-induced cardiotoxicity (FIC).
  • To explore pathogenetic models, risk factors, and diagnostic approaches for FIC.
  • To discuss current and future treatment strategies for FIC.

Main Methods:

  • Literature review of studies on fluoropyrimidine-induced cardiotoxicity.
  • Analysis of proposed pathogenetic mechanisms, including vasospasm, cellular damage, and metabolic factors.
  • Evaluation of diagnostic markers (laboratory, ECG, imaging) and therapeutic interventions.

Main Results:

  • Several pathogenetic models for FIC are proposed, involving coronary vasospasm, endothelial/cardiomyocyte damage, toxic metabolites, and DPD deficiency.
  • Risk and predictive factors for FIC are identified.
  • Diagnostic tools and treatments, including uridine triacetate, are discussed.

Conclusions:

  • FIC is a critical toxicity requiring further research and improved diagnostic/therapeutic strategies.
  • Understanding FIC mechanisms and risk factors is crucial for patient management.
  • Future research directions include microRNA technology for FIC detection.